objections to march 29, 2017 order denying pan/nrdc ...jun 05, 2017 · tolerances and cancel all...

June 5, 2017 Docket No. EPA-HQ-OPP-2007-1005

Submitted by:

Earthjustice

Objectors:

Pesticide Action Network

Natural Resources Defense Council

United Farm Workers

California Rural Legal Assistance Foundation

Farmworker Association of Florida

Farmworker Justice

GreenLatinos

Labor Council for Latin American Advancement

League of United Latin American Citizens

Learning Disabilities Association of America

National Hispanic Medical Association

Pineros y Campesinos Unidos del Noroeste

Objections to March 29, 2017 Order Denying PAN/NRDC

Petition to Revoke All Tolerances and Cancel All Registrations for

the Pesticide Chlorpyrifos

i

TABLE OF CONTENTS

INTRODUCTION AND SUMMARY ........................................................................................... 1

PRELIMINARY MATTERS.......................................................................................................... 3

I. NO FEE REQUIRED ..........................................................................................................3

II. THE ADMINISTRATIVE RECORD .................................................................................3

III. NO EVIDENTIARY HEARING IS NEEDED IN LIGHT OF THE PURELY SCIENTIFIC ISSUES RAISED IN THESE OBJECTIONS...............................................4

BACKGROUND ............................................................................................................................ 4

I. THE LEGAL FRAMEWORK REQUIRES PROTECTION, PARTICULARLY OF CHILDREN, FROM HARMFUL PESTICIDES ................................................................4

A. The FFDCA Mandates Elimination of Harmful Pesticides From Our Food Supply ......................................................................................................................4

B. Pesticide Use on Food Crops Is Regulated Under Overlapping Provisions of the Federal Insecticide, Rodenticide and Fungicide Act .........................................6

II. EPA’S RE-REGISTRATION OF CHLORPYRIFOS .........................................................7

A. Chlorpyrifos .............................................................................................................7

B. EPA’s Re-registration Determinations for Chlorpyrifos .........................................8

III. ADVOCACY TO CONVINCE EPA TO PROTECT CHILDREN FROM DRIFT AND NEURODEVELOPMENTAL HARM FROM CHLORPYRIFOS EXPOSURES .......................................................................................................................9

IV. EPA’S ACTIONS IN RESPONSE TO THE 2007 PETITION .........................................11

A. Inhalation Exposures through Pesticide Drift and Volatilization ..........................12

1. EPA Has Appropriately Taken Steps to Reduce Exposures From Spray Drift, But These Steps Fail to Protect Children From Unsafe Exposures to Chlorpyrifos Through Drift....................................................................... 12

2. EPA Initially Found Harmful Exposures From Volatilization, But Reversed Course Based on Dow Studies That Have Been Heavily Criticized ................................................................................................... 13

B. EPA Found that Chlorpyrifos Exposures are Correlated with Harm to the Developing Brain at Exposures Far Below EPA’s Regulatory Endpoint ..............14

ii

V. THE UNREASONABLE DELAY LITIGATION ............................................................17

VI. EPA PROPOSED TO REVOKE ALL TOLERANCES BECAUSE IT FOUND CHLORPYRIFOS UNSAFE .............................................................................................20

VII. EPA FOUND SERIOUS HARM, PARTICULARLY TO CHILDREN, AT LOWER EXPOSURES IN ITS MOST RECENT ASSESSMENTS ...............................................21

VIII. THE ORDER DENYING THE 2007 PETITION .............................................................23

OBJECTIONS............................................................................................................................... 25

I. EPA’S DENIAL OF THE 2007 PETITION IS ILLEGAL BECAUSE EPA CANNOT MAINTAIN TOLERANCES IN THE FACE OF ITS FINDINGS THAT CHLORPYRIFOS IS UNSAFE ........................................................................................25

A. EPA Found Unsafe Drinking Water Contamination from Chlorpyrifos Using Poisoning Risks as the Regulatory Endpoint .........................................................26

B. EPA Found All Exposures to Chlorpyrifos to be Unsafe When it Sought to Protect Against Damage to Children’s Developing Brains ...................................27

C. EPA’s Findings that Chlorpyrifos is Unsafe Compel the Administrator to Revoke All Chlorpyrifos Food Tolerances ............................................................28

II. EPA’S RATIONALE FOR LEAVING CHLORPYRIFOS TOLERANCES IN PLACE IS LEGALLY AND SCIENTIFICALLY INDEFENSIBLE ...............................29

A. EPA Cannot Rely on Its 2006 Safety Finding When It Has Since Determined Based on Mounting Scientific Evidence that Chlorpyrifos Damages Children’s Brains and is Unsafe ............................................................................29

B. Scientific Uncertainty is Not a Legally Permissible Reason to Leave Chlorpyrifos Tolerances in Place ...........................................................................30

1. The Science Underlying EPA’s Findings that Chlorpyrifos is Unsafe is Well-Settled .............................................................................................. 30

2. Congress Directed EPA to Revoke Tolerances if Scientific Uncertainty Precludes Finding the Pesticide Safe. ....................................................... 31

3. The Pruitt Order Fails to Address Significant Concerns Raised in Comments that EPA’s 2014 Risk Assessment and Proposed Revocation Fail to Protect Children. ............................................................................ 33

C. Widespread Use of Chlorpyrifos in Agriculture is Legally Irrelevant Because Congress Made Protecting Food Safety and Preventing Neurodevelopmental Harm to Children Paramount. ................................................................................36

iii

D. The Deadline for Completing Registration Review for All Older Pesticides is Not A License to Maintain Tolerances for Pesticides That are Unsafe .................37

CONCLUSION ............................................................................................................................. 39

1

OBJECTIONS TO MARCH 29, 2017 ORDER DENYING PAN/NRDC PETITION TO REVOKE ALL TOLERANCES AND CANCEL ALL REGISTRATIONS FOR THE

PESTICIDE CHLORPYRIFOS

INTRODUCTION AND SUMMARY

These objections seek: (1) reversal of the Environmental Protection Agency’s (“EPA’s”) March 29, 2017 Order denying a 2007 petition to revoke all food tolerances for chlorpyrifos, a neurotoxic pesticide; and (2) an immediate final order revoking all chlorpyrifos tolerances. These objections are filed on behalf of Pesticide Action Network (“PAN”), Natural Resources Defense Council (“NRDC”), United Farm Workers, California Rural Legal Assistance Foundation, Farmworker Association of Florida, Farmworker Justice, GreenLatinos, Labor Council for Latin American Advancement, League of United Latin American Citizens, Learning Disabilities Association of America, National Hispanic Medical Association, and Pineros y Campesinos Unidos del Noroeste, by Earthjustice (collectively “Objectors”).

PAN and NRDC filed the petition in 2007 asking EPA to revoke chlorpyrifos food tolerances and cancel all food uses of the pesticide. Petition to Revoke All Tolerances and Cancel All Registrations for the Pesticide Chlorpyrifos (Sept. 12, 2017) (“2007 Petition”) (EPA-HQ-OPP-2007-1005-0005). The 2007 Petition sought action by EPA on two critical issues left unaddressed when EPA re-registered chlorpyrifos in 2001 and 2006: (1) the growing scientific evidence that chlorpyrifos causes damage to children’s brains from prenatal and early childhood exposures and that it does so at lower exposure levels than what EPA used in re-registering chlorpyrifos; and (2) harmful exposures to chlorpyrifos from pesticide drift and volatilization, which EPA never addressed in re-registering chlorpyrifos, despite numerous reported pesticide poisonings from chlorpyrifos every year and air monitoring detecting chlorpyrifos in school yards and residential neighborhoods in harmful amounts.

PAN and NRDC filed the 2007 Petition under the Federal Food, Drug and Cosmetic Act (“FFDCA”), which prescribes the required procedural and substantive outcomes. Procedurally, EPA may issue a proposed or final rule revoking the tolerances or an order denying the petition. 21 U.S.C. § 346a(d)(4)(A). Substantively, the FFDCA makes food safety the highest priority and constrains EPA’s discretion accordingly. EPA may leave a tolerance in effect for a pesticide “only if the Administrator determines the tolerance is safe.” Id. § 346a(b)(2)(A)(i). Conversely, the Administrator “shall modify or revoke a tolerance if the Administrator determines it is not safe.” Id. The Act further constrains EPA by defining “safe” to mean that “the Administrator has determined that there is a reasonable certainty that no harm will result from aggregate exposure” to the pesticide. Id. § 346a(b)(2)(A)(ii).

As early as 2000, EPA noted that laboratory studies consistently showed that the developing brain can be harmed by low-level exposures to chlorpyrifos.1 When EPA began to review the studies correlating chlorpyrifos exposures with damage to children’s brains in response to the 2007 Petition, it found such a correlation. It submitted its analysis to EPA’s

1 EPA, Human Health Risk Assessment: Chlorpyrifos (June 8, 2000) at 131 (“Results of multiple studies have consistently shown that the developing brain is susceptible to chlorpyrifos treatment.”).

2

Scientific Advisory Panel (“SAP”) on multiple occasions beginning in 2008, and each time, the SAP confirmed EPA’s conclusion that early life exposures to chlorpyrifos pose a risk of long-lasting, adverse cognitive, behavioral, and motor impairments. And both EPA and the SAP found that the exposures associated with serious damage to children’s brains were far below the regulatory endpoint used by EPA in its 2001 and 2006 re-registration determinations and in establishing the chlorpyrifos tolerances currently in effect. See infra at 14-16.

These reviews culminated in EPA’s official finding in its revised human health risk assessment, released in 2014, that chlorpyrifos causes long-lasting damage to children’s brains at exposures lower than EPA’s regulatory endpoint. See infra at 16-17. The 2014 risk assessment also documented unsafe chlorpyrifos exposures from drinking water contamination. In 2015, EPA proposed to revoke all chlorpyrifos tolerances based on these findings. 80 Fed. Reg. 69,080 (Nov. 6, 2015). In the proposed revocation rule, EPA explicitly and repeatedly found chlorpyrifos unsafe. Id. at 69,081-083, 69,097, 69,103, 69,105-106.

At the same time, the proposed revocation rule noted that EPA’s 2014 risk assessment was under-protective in a fundamental way. EPA had not changed its regulatory endpoint, which continued to be based on poisoning risks, even though lower chlorpyrifos exposures caused brain impairments. EPA recognized that its 2014 risk assessment and 2015 proposed tolerance revocation did not address the greatest risks and most sensitive endpoint, as EPA policy requires.

EPA, therefore, continued to explore ways to establish an exposure limit that would protect children from neurodevelopmental harm. Each method it explored revealed more serious risks from chlorpyrifos than the 2014 risk assessment. In November 2016, EPA released its second revised human health risk assessment using a regulatory endpoint designed to guard against damage to children’s brains. That risk assessment found unsafe exposures from every way that people come into contact with chlorpyrifos —on food, in drinking water, through pesticide drift, and from applying the pesticide or working in fields that had recently been sprayed.2 EPA indicated it had found no chlorpyrifos uses that meet the FFDCA safety standard and all chlorpyrifos tolerances would need to be revoked. 81 Fed. Reg. 81,049, 81,050 (Nov. 17, 2016).

While the FFDCA does not establish a timeline for resolving petitions to revoke tolerances, EPA, like all federal agencies, must respond to administrative petitions “within a reasonable time.” 5 U.S.C. § 555(b). EPA fell far short of this obligation with respect to the 2007 Petition to ban all food uses of chlorpyrifos. In 2015, the Ninth Circuit Court of Appeals found EPA guilty of “egregious” unreasonable delay and issued a writ of mandamus setting deadlines for EPA to take action. In re PANNA v. EPA, 798 F.3d 809, 811 (9th Cir. 2015). When EPA found that chlorpyrifos poses such serious risks that a nationwide ban was warranted, the court became persuaded that the time for study had passed and the time for action had arrived. Id. at 814. The court gave EPA a March 31, 2017 deadline to take final action on the 2007 Petition.

Something changed as that deadline approached, but it was neither the science, nor the legal mandates. A newly inaugurated President appointed a new EPA Administrator, Mr. Scott 2 Chlorpyrifos: Revised Human Health Risk Assessment for Registration Review (Nov. 3, 2016) (EPA-HQ-OPP-2015-0653-0454).

3

Pruitt, and it fell to him to meet the court-ordered March 31, 2017 deadline. Administrator Pruitt chose not to finalize the revocation order, even though he could not make the safety findings required to keep chlorpyrifos in place. He decided to put off regulatory action. He issued an order on March 29, 2017, denominated “Chlorpyrifos: Order denying PANNA and NRDC’s petition to revoke tolerances.” 82 Fed. Reg. 16,581 (Apr. 5, 2017) (“Pruitt Order”). That Order, however, did not determine that the 2007 Petition should or could be denied on its merits. Nor did it make the safety findings required by law to take that course of action. Instead, the Pruitt Order postpones taking final action on the proposed tolerance revocation rule until some unspecified future time that could be five or more years off.

Such a postponement violates the FFDCA’s substantive mandates. It leaves chlorpyrifos tolerances in place, but EPA has the authority to do so only if it finds chlorpyrifos safe. EPA has, however, repeatedly found chlorpyrifos to be unsafe. Under the FFDCA, EPA must revoke tolerances if it determines the tolerances unsafe. Revoking all chlorpyrifos tolerances is the only legally and scientifically defensible course of action. These objections ask EPA to rule on these objections within 60 days and revoke all chlorpyrifos on an expeditious basis.

PRELIMINARY MATTERS

I. NO FEE REQUIRED

Counsel for Objectors spoke with EPA’s Office of General Counsel on June 1, 2017, and was informed that the fee described in 40 CFR 178.25(a)(5) is not required because EPA is prohibited from collecting such fees at this time. See 21 U.S.C. § 346a(m)(3) (“PROHIBITION. During the period beginning on October 1, 2007, and ending on September 30, 2017, the Administrator shall not collect any tolerance fees under paragraph (1).”). Therefore, no fee accompanies these objections.

II. THE ADMINISTRATIVE RECORD

Since completing re-registration of chlorpyrifos in 2006, EPA has engaged in extensive reviews and a rulemaking process regarding chlorpyrifos registrations and tolerances and has established three related dockets. The first docket, EPA-HQ-OPP-2007-1005, was opened in response to the 2007 Petition. The second docket, EPA-HQ-OPP-2008-0850, was opened when EPA began the registration review process for chlorpyrifos. The third docket, EPA-HQ-OPP-2015-0653, was opened when EPA initiated the tolerance revocation process after determining that chlorpyrifos was unsafe. EPA cites all three dockets as being relevant to its denial decision. 82 Fed. Reg. 16,581, 16,582 (Mar. 29, 2017). As such, all three dockets must be considered part of the administrative record for reviewing these objections to EPA’s denial of the 2007 Petition.

In September 2016, many of the Objectors filed a Petition for Emergency and Ordinary Suspension of Chlorpyrifos Uses that Pose Unacceptable Risks to Workers and Petition to Cancel All Uses of Chlorpyrifos. After EPA released a revised human health risk assessment in November 2016 finding all food uses of chlorpyrifos unsafe, these groups withdrew the portion of the petition seeking an immediate suspension of chlorpyrifos uses that pose unacceptable risks to workers because revocation of chlorpyrifos food tolerances seemed inevitable and would end the uses and the associated harm to workers. The portion of the petition seeking cancellation of chlorpyrifos uses remains before EPA. EPA never opened a docket for the suspension and

4

cancellation petition, but the petition and supporting declaration and exhibits were submitted through comments to docket EPA-HQ-OPP-2015-0653 and are part of the record.3

Additionally, the administrative record must include all communications regarding chlorpyrifos between EPA (including the post-2016 election transition and beachhead teams) and Dow Agrosciences, CropLife America, the U.S. Department of Agriculture, and any other entity or agency that communicated with EPA outside of the public comment process. 4 See, e.g., Bar MK Ranches v. Yuetter, 994 F.2d 735, 739 (10th Cir. 1993) (“The complete administrative record consists of all documents and materials directly or indirectly considered by the agency”).

III. NO EVIDENTIARY HEARING IS NEEDED IN LIGHT OF THE PURLEY SCIENTIFIC ISSUES RAISED IN THESE OBJECTIONS

The Objectors do not seek an evidentiary hearing because these objections present purely legal issues, namely whether EPA can leave chlorpyrifos tolerances in place when it has found chlorpyrifos unsafe. The FFDCA requires EPA to revoke chlorpyrifos tolerances in these circumstances and no evidentiary hearing is needed to do so.

BACKGROUND

I. THE LEGAL FRAMEWORK REQUIRES PROTECTION, PARTICULARLY OF CHILDREN, FROM HARMFUL PESTICIDES

A. The FFDCA Mandates Elimination of Harmful Pesticides From Our Food Supply

EPA regulates allowable contaminants, including pesticides, in our food supply under the FFDCA. For a pesticide to be permitted on food and imported or sold in interstate commerce, EPA must issue a tolerance that establishes the maximum residue of a pesticide allowed on food. 21 U.S.C. § 346a(b) & (c). EPA may “establish or leave in effect a tolerance for a pesticide chemical residue in or on a food only if the Administrator determines that the tolerance is safe.” Id. § 346a(b)(2)(A)(i).

The Food Quality Protection Act (“FQPA”), passed unanimously in 1996, amended the FFDCA to require that EPA “ensure that there is a reasonable certainty that no harm will result to infants and children from aggregate exposure” to pesticides. 21 U.S.C. § 346a(b)(2)(C)(ii)(I), (II).

3 Earthjustice, et al., Comments on EPA Proposal to Revoke Chlorpyrifos Tolerances (Jan. 17, 2017) (EPA-HQ-OPP-2015-0653-0661). The Petition for Emergency and Ordinary Suspension of Chlorpyrifos Uses that Pose Unacceptable Risks to Workers and Petition to Cancel All Uses of Chlorpyrifos and the Declaration of Philip J. Landrigan, M.D., M.Sc. in Support of Petition to Suspend and Cancel Chlorpyrifos Uses were submitted as attachments to these comments. 4 Earthjustice, on behalf of PAN, submitted a Freedom of Information Act (“FOIA”) request to EPA for these documents on March 15, 2017. EPA failed to substantively respond to that request within the statutory timeline, and to date has not released any documents related to PAN’s FOIA request. On May 10, 2017, PAN filed a FOIA lawsuit against EPA seeking production of the requested records. Pesticide Action Network of North America v. U.S. Environmental Protection Agency, 3:17-cv-02706-SK (N.D. Cal. filed May 10, 2017).

5

The 1996 passage of the FQPA responded to a seminal 1993 National Academy of Sciences (“NAS”) report criticizing EPA for regulating pesticides based on the effects on a 150-pound adult male.5 It documented the ways that children are not “little adults” but have unique exposures from the foods they eat, their play, and their metabolism. For example, a 6-month old child drinks seven times more per body weight than an adult, inhales twice as much air, and puts its hands in its mouth more than is common later in life. The report also highlighted the windows of vulnerability — in utero, infancy, and adolescence — where children are particularly susceptible to the impacts of chemicals on their development. Chemical exposures can damage the developing brain at exposures less than those that affect adults.

The NAS recommended that EPA revamp and strengthen its regulation of pesticides to account for children’s vulnerabilities, consumption patterns, and exposures. Because it would take time to fill gaps in knowledge, safeguards and methodologies, the NAS recommended that additional protection be afforded in the form of “uncertainty” or “safety factors.” The NAS first described how EPA has regularly used uncertainty factors and then proposed an additional uncertainty factor for toxicity to infants and children and where data are incomplete on such toxicity or on children’s exposures:

In the absence of data to the contrary, there should be a presumption of greater toxicity to infants and children. To validate this presumption, the sensitivity of mature and immature individuals should be studied systematically to expand the current limited data base on relative sensitivity.

NAS Report at 9-10.

Heeding the NAS recommendations, the FQPA directs EPA to afford added protection to children based on their exposure patterns, their special sensitivities, such as during early or adolescent development, and gaps in available data to assess such risks. 21 U.S.C. § 346a(b)(2)(C)-(D). The statute explicitly requires EPA to assess the risk that a pesticide poses particularly to infants and children. 21 U.S.C. § 346a(b)(2)(C). Before EPA can establish a tolerance, the agency shall “ensure that there is a reasonable certainty that no harm will result to infants and children from aggregate exposure” to the pesticide, and shall “publish a specific determination regarding the safety of the pesticide chemical residue for infants and children.” Id. §§ 346a(b)(2)(C)(ii)(I) & (II). In ensuring that the statutory safety standard is met, EPA must consider available information concerning “the special susceptibility of infants and children,” including “neurological differences between infants and children and adults, and effects of in utero exposure to pesticide chemicals.” Id. § 346a(b)(2)(C)(i)(II). EPA must also base its tolerance decision on available information about “food consumption patterns unique to infants and children.” Id. §§ 346a(b)(2)(C)(i)(I) & (III).

One of the FQPA’s key provisions is the requirement that EPA use an additional margin of safety to protect infants and children when establishing tolerances. The statute requires that: “an additional tenfold margin of safety for the pesticide chemical residue and other sources of exposure shall be applied for infants and children to take into account potential pre -and post-

5 National Research Council, Pesticides: Diets of Infants and Children (1993) (“NAS Report”), https://www.nap.edu/catalog/2126/pesticides-in-the-diets-of-infants-and-children.

6

natal toxicity and completeness of the data with respect to exposure and toxicity to infants and children.” 21 U.S.C. § 346a(b)(2)(C). EPA can depart from this requirement and use a different margin of safety “only if, on the basis of reliable data, such margin will be safe for infants and children.” Id.

In addition, because “[e]xposure to pesticide residues from ambient air sources is generally higher in areas close to agricultural lands,” and “[b]ecause infants and children are subject to nondietary sources of exposure to pesticides,” the NAS found that “it is important to consider total exposures to pesticides from all sources combined.” NAS Report at 307, 309, 319. The FQPA requires EPA to “ensure that there is a reasonable certainty that no harm will result to infants and children from aggregate exposure” to a pesticide from all sources. 21 U.S.C. § 346a(b)(2)(C)(ii)(I), (II) (emphasis added). “Aggregate exposure” includes “all anticipated dietary exposures and all other exposures for which there is reliable information,” including pesticide drift exposures. 21 U.S.C. § 346a(b)(2)(A)(ii); see also id. § 346a(b)(2)(D)(vi). The FQPA, therefore, requires an assessment based on aggregation of all exposures to a pesticide whether from eating foods, drinking water with residues of the pesticide, or contacting pesticide residues in and around the home or other places where people can be exposed. Id. § 346a(b)(2)(A)(ii), (C)(i)(I), (D)(vi). The FQPA also requires EPA to assess and protect against unsafe risks posed by cumulative exposures to all pesticides that share a “common mechanism of toxicity,” as is the case with pesticides in the organophosphate family. See id. § 346a(b)(2)(C)(i)(III)-(D)(v).

B. Pesticide Use on Food Crops Is Regulated Under Overlapping Provisions of the Federal Insecticide, Rodenticide and Fungicide Act

EPA regulates use of pesticides in the United States under the Federal Insecticide, Rodenticide and Fungicide Act (“FIFRA”). Under FIFRA, EPA must establish a registration before a pesticide may generally be sold or used in the United States. 7 U.S.C. § 136a(a). To register or re-register a pesticide, EPA must determine that its use “will not generally cause unreasonable adverse effects on the environment,” which includes risks to human health. Id. § 136a(c)(5)(D); see id. § 136(bb) (definition of “unreasonable adverse effects”). EPA has the authority to cancel a pesticide registration if the pesticide use “causes unreasonable adverse effects on the environment.” Id. § 136d(b).

The two statutes’ safety standards are intertwined through FIFRA’s definition of “unreasonable adverse effects,” which includes “a human dietary risk from residues that result from a use of a pesticide in or on any food inconsistent with the [FQPA] standard.” 7 U.S.C. § 136(bb)(2). In other words, a pesticide may not be registered for a food use unless a food tolerance is in place, and whenever a food tolerance is revoked, the registration for use of the pesticide on that food crop must be cancelled. Because of this interdependence, the FQPA directs EPA to coordinate FQPA actions to revoke tolerances with any related, necessary FIFRA action. 21 U.S.C. § 346a(l).

Congress gave EPA a ten-year deadline, which ended in August 2006, to bring all food-use pesticides into compliance with these protective mandates. 21 U.S.C. § 346a(q)(1). The August 2006 deadline applied to both tolerances established under the FFDCA, as amended by the FQPA, and re-registration decisions under FIFRA.

7

To ensure that pesticides in use in the United States continue to meet the FQPA and FIFRA standards in light of the development of scientific methodologies and available scientific information on health effects and exposures, Congress required periodic review of pesticides every 15 years, but provided: “Nothing in this subsection shall prohibit the Administrator from undertaking any other review of a pesticide ….” 7 U.S.C. § 136a(g) and § 136a(g)(1)(C). The first round of registration reviews of older pesticides, which includes chlorpyrifos, must be completed by October 1, 2022. Id. § 136a(g)(1)(A)(iii)(I).

II. EPA’S RE-REGISTRATION OF CHLORPYRIFOS

A. Chlorpyrifos

Chlorpyrifos is a widely used organophosphate pesticide first registered by EPA in 1965. It is used on an extensive variety of crops, including fruit and nut trees, vegetables, wheat, alfalfa, and corn. In 2006-2012, chlorpyrifos was applied to more than half of the country’s apple and broccoli crops, 45% of onion, 46% of walnut, and 41% of cauliflower crops.6 Five to eight million pounds are used annually in agriculture, including one million pounds on both corn and soybeans.7

Organophosphate chemicals were developed as nerve agents in World War II and adapted for use as insecticides after the war. They have deleterious effects on people who come into contact with them when they are used as insecticides.

Chlorpyrifos is acutely toxic and causes a significant number of acute pesticide poisoning incidents every year. Chlorpyrifos and other organophosphate pesticides do this by suppressing the activity of an enzyme called acetylcholinesterase, which regulates nerve impulses throughout the body. When cholinesterase activity is inhibited, nerves are over-stimulated, causing people to experience symptoms such as headaches, nausea, abdominal cramps, dizziness, difficulty breathing, vomiting, diarrhea, tremors, muscle spasms, seizures, skin rashes, and sometimes convulsions, respiratory paralysis, comas, and even death in extreme cases.

Widespread use of chlorpyrifos has exposed people through the air, in drinking water, and through the foods they eat. Monitoring by the California Department of Pesticide Regulation showed chlorpyrifos as having one of the highest number of detections in its 2011-2015 air monitoring, and water monitoring detected chlorpyrifos in 17.7% of samples, with 9.9%

6 EPA, Chlorpyrifos Evaluation of the Potential Risks from Spray Drift and the Impact of Potential Risk Reduction Measures at 7 & Appendix C (July 13, 2012) (EPA-HQ-OPP-2008-0850-0105). 7 Id.

8

exceeding the state’s concentration limit.8 In 2015, 61% of the air samples taken at a high school detected chlorpyrifos.9

In addition to poisonings, a growing body of published scientific research from both animal and epidemiology studies links exposure to chlorpyrifos with causing neurodevelopmental harm to children’s brains. Children’s brains are particularly vulnerable to damage from low-dose exposures because the placenta is not a barrier to passage of many toxic chemicals, including chlorpyrifos, from the mother to the fetus. An extensive body of published animal studies reveals cognitive, motor control, and social behavior impacts from chlorpyrifos exposures.

Additional evidence of neurodevelopmental harm from chlorpyrifos has come from three population cohorts that were studied by university research teams as part of the NIH-funded network of Centers for Children’s Environmental Health. A research team at University of California-Berkeley followed a cohort of children born to farmworkers in Salinas Valley in California. A Mount Sinai School of Medicine study observed a New York City Hispanic population. A research team at Columbia University followed African American and Dominican children in New York City. The three studies each enrolled pregnant women and conducted long-term birth-cohort studies. Even though the studies were conducted in different parts of the country on different populations with different types of exposures, they produced strongly convergent results. All found that prenatal exposures to pesticides were statistically significantly correlated with cognitive impairments that persist into the school years, and the Columbia study was specific to chlorpyrifos. Prenatal exposures correlate with lasting functional harm to children’s brains in the form of reduced IQ, loss of working memory, attention deficit disorders, and delayed motor development. Chlorpyrifos also has been found to cause physical changes in brain structure that may have long-lasting effects. Children living near agricultural fields suffer disproportionately from these effects. The Declaration of Philip J. Landrigan, M.D., M.Sc., who led the 1993 study that produced the NAS Report, describes the lines of evidence documenting damage to children’s developing brains from chlorpyrifos and the other organophosphates (attached as Exhibit 1).

B. EPA’s Re-registration Determinations for Chlorpyrifos

EPA used a two-part process for re-registering chlorpyrifos and the other organophosphate pesticides. First, it conducted risk assessments and made interim re-registration determinations for the individual organophosphates, which it did in 2001 for chlorpyrifos. Second, it conducted a cumulative risk assessment of all the organophosphates,

8 Vidrio, E., Wofford, P., Segawa, R., Schreider, J. March 2013. Air Monitoring Network Results for 2011. Vol. 1. California Environmental Protection Agency, Department of Pesticide Regulation, http://www.cdpr.ca.gov/docs/emon/airinit/amn_vol1_final.pdf; and Zhang X., Starner K., Spurlock F. 2012. Analysis of Chlorpyrifos Agricultural Use in Regions of Frequent Surface Water Detections in California, USA . California Department of Pesticide Regulation, Environmental Monitoring Branch, Surface Water Protection Program. http://www.cdpr.ca.gov/docs/emon/pubs/ehapreps/analysis_memos/zhang_chlorpyrifos_report.pdf. 9 http://www.cdpr.ca.gov/docs/emon/airinit/amn_2015_report_final.pdf (Shafter High School).

9

which it completed in 2006. The cumulative risk assessment did not result in changes in the interim re-registration and tolerance determinations for chlorpyrifos.

In its risk assessment for chlorpyrifos (as with the other organophosphates), EPA identified a level of 10% cholinesterase inhibition in red blood cells as the endpoint it would use in determining whether chlorpyrifos exposures violate the regulatory standards. In assessing risks from aggregate exposures to chlorpyrifos, EPA determined that home uses had to be cancelled. Children crawling on treated carpets and hugging pets after flea treatments faced unsafe exposures. Seeing the writing on the wall, the chemical makers agreed to cancel homeowner uses of chlorpyrifos in 2000.

EPA, however, never assessed the extent to which children in agricultural communities are exposed to chlorpyrifos through drift from agricultural sites to schools, day cares, playfields, and homes, or through residues their parents take home on their clothes. The failure to assess risks to and protect children in farmworker communities, who are primarily Latino and low-income, evinced a double standard that raises serious environmental justice concerns.

Nor did EPA protect the fetus and young children from neurodevelopmental harm, despite acknowledging in its 2000 human health risk assessment for chlorpyrifos that the fetus and young children are more sensitive to chlorpyrifos and that multiple studies consistently showed that the developing brain can be harmed by chlorpyrifos exposures.10

PAN, NRDC, and others commented on EPA’s 2001 interim re-registration determination for chlorpyrifos, urging EPA to address pesticide drift and the mounting evidence of neuro-developmental impacts to children at low doses. The New York Attorney General also submitted comments emphasizing that the interim re-registration determination underestimated the risks of chlorpyrifos, particularly to children, and failed to make a finding that the pesticide is “safe” and complied with the FQPA.11 The comments cited studies that suggested “that there is no level of exposure to chlorpyrifos that is without adverse effects on developmental neurotoxicity in the young….”12 In 2006, after releasing its cumulative organophosphate risk assessment, EPA finalized its re-registration of chlorpyrifos without protecting children from drift or neurodevelopmental harm from chlorpyrifos and without addressing the public comments.

III. ADVOCACY TO CONVINCE EPA TO PROTECT CHILDREN FROM DRIFT AND NEURODEVELOPMENTAL HARM FROM CHLORPYRIFOS EXPOSURES

Farmworker and health advocates pursued three legal avenues to rectify EPA’s failure to

10 See NRDC Comments on Chlorpyrifos Interim Reregistration Decision (Jan. 14, 2002) (Docket ID No. OPP-34203G), attached Exhibit 2, (citing Human Health Risk Assessment - Chlorpyrifos (June 8, 2000), available at https://archive.epa.gov/scipoly/sap/meetings/web/pdf/hed_ra.pdf). 11 Attorney General of the State of New York, comments on Chlorpyrifos Interim Reregistration Eligibility Decision and Interim Risk Management Decision pursuant to 66 Fed. Reg. 57,073-074 (Nov. 14, 2001) at 2, attached Exhibit 3. 12 Id. at 19.

10

protect children from the hazards posed by chlorpyrifos. First, UFW, PAN, PCUN, and others, represented by Earthjustice and Farmworker Justice filed a federal district court challenge to the 2001 chlorpyrifos interim re-registration decision, in part, for failing to protect children and other bystanders from pesticide drift and failing to cancel uses that expose workers to admittedly excessive poisoning risks.13 The parties negotiated principles on which the case could be settled with an EPA commitment to make a new regulatory decision for chlorpyrifos by 2010 that would address drift exposures to children and other bystanders. However, after the Ninth Circuit ruled in a case of first impression that challenges to FIFRA registration determinations must be brought in the courts of appeals within 60 days of the decision, the settlement fell apart.14

Second, PAN, UFW, PCUN, California Rural Legal Assistance Foundation, and others, represented by Earthjustice, and Farmworker Justice, petitioned EPA to address pesticide drift as mandated by the FQPA.15 The Kids’ Petition highlighted EPA’s violation of its legal duty to protect children from all aggregate exposures to each pesticide in tolerance and re-registration determinations and asked EPA to expedite adoption of mitigation for airborne routes of exposure to organophosphates and n-methyl carbamates, another pesticide that suppresses cholinesterase, because of the heightened poisoning risks posed by these classes of pesticides. In March 2014, EPA responded to the petition, acknowledging its legal obligation to address pesticide drift under the FQPA and FIFRA. However, EPA indicated it would not protect children from drift until it reviewed pesticide registrations and tolerance decisions individually in registration review, and it refused to impose interim protections.16 The petitioners filed administrative objections, which have not been resolved.17

Third, on September 12, 2007, PAN and NRDC submitted a petition asking EPA to ban chlorpyrifos based on the mounting evidence of risks from chlorpyrifos that were left unaddressed in EPA’s 2001 and 2006 regulatory decisions. At its heart, the 2007 Petition raised two issues:

1. The 2007 Petition (at 17-21) challenged EPA’s failure to account for risks to children and bystanders from chlorpyrifos drift and volatilization, as required by the FQPA. In support of this obligation, the petition presented the California Air Resources Board’s air monitoring reports and data, which documented concentrations above EPA’s levels of

13 UFW v. Administrator, EPA, No. 07-3950-JF (N.D. Cal. filed Aug. 1, 2007). 14 UFW v. Administrator, Stipulation of Voluntary Dismissal, Dkt. 98, No. 07-3950-JF (N.D. Cal. filed April 27, 2010); see UFW v. Administrator, EPA, 592 F.3d 1080 (9th Cir. 2010) (challenges to registration decisions must be brought in courts of appeals within 60 days, rather than in district court under a six-year statute of limitations as had previously been the case). 15 See Pesticides In The Air – Kids At Risk: Petition to EPA to Protect Children From Pesticide Drift (October 13, 2009) (the “Kids’ Petition”) (EPA-HQ-OPP-2009-0825-0002). 16 Agency Response to Pesticides In The Air – Kids At Risk: Petition to EPA to Protect Children From Pesticide Drift (March 31, 2014) at 2, 32-33 (“Agency Response to Kids’ Petition”) (EPA-HQ-OPP-2009-0825-0084). 17 UFW, et al., Written Objections to EPA’s Response to Pesticides in the Air – Kids at Risk: Petition to EPA to Protect Children From Pesticide Drift (May 28, 2014). A court challenge to the decision not to impose interim protection was rejected. PAN v. U.S.E.P.A., No. 14-71514 (9th Cir.).

11

concern near fields and in schoolyards, and community air monitoring, which showed widespread contamination in multiple locations and over a period of years, including in schoolyards.18

2. The 2007 Petition (at 6-9, 11-16) compiled the mounting evidence documenting serious cognitive and behavioral effects from low-dose chlorpyrifos exposures, including peer-reviewed scientific studies showing that children and infants exposed to chlorpyrifos exhibit long-lasting, and possibly permanent, impaired cognitive and behavioral development from early life exposure. The Petition cited concerns raised by members of EPA’s Scientific Advisory Panel that EPA had failed to account for scientific evidence showing brain impacts from early life exposures to chlorpyrifos at lower doses than those used by EPA in its regulatory decisions. Id. at 13, 22-23.

IV. EPA’S ACTIONS IN RESPONSE TO THE 2007 PETITION

EPA has long recognized that organophosphates generally, and chlorpyrifos in particular, raise significant health issues. For this reason and because it would be reviewing the novel, complex scientific issues raised in the 2007 Petition and developing new scientific methodologies to do so, EPA decided to move up the registration review of chlorpyrifos in order to complete it several years in advance of the 2022 deadline.19 EPA initiated the chlorpyrifos registration review and projected it would result in proposed regulatory decisions in 2014 and final ones in 2015. Chlorpyrifos Final Work Plan: Registration Review (Sept. 2009). PAN objected to the lengthy timetable, stating that uncertainties with respect to aspects of chlorpyrifos toxicity do not justify delaying action to protect children.20

As described above, the 2007 Petition sought a ban on use of chlorpyrifos on food based primarily on the need to protect children: (1) from exposure to chlorpyrifos from drift and volatilization; and (2) from exposures that could harm the developing brain. The petition raised other issues as well, which EPA separated from the two core issues. When faced with unreasonable delay litigation (see infra), EPA issued partial denials on various secondary issues, such as delays in completing endocrine disruption studies, cancer risks, that over-reliance on industry studies, and exporting chlorpyrifos to other countries.21

18 Petition to Revoke All Tolerances and Cancel All Registrations for the Pesticide Chlorpyrifos at 17-21 (September 12, 2007), EPA-HQ-OPP-2007-1005. 19 Declaration of Jack Housenger, Director of Health Effects Division of EPA’s Office of Pesticide Programs ¶ 13, in In re PANNA, No. 12-71125 (9th Cir. July 23, 2012). 20 Pesticide Action Network Comments (May 18, 2009) (EPA-HQ-OPP-2008-0850-0010). 21 EPA’s Partial Response to Chlorpyrifos Petition by NRDC & PANNA, letter from Dr. Steven Bradbury, Director, EPA Office of Pesticide Programs, to Aaron Colangelo and Margaret Reeves, Ph.D (July 16, 2012) (EPA-HQ-OPP-2007-1005-0095); Chlorpyrifos July 2014 Partial Petition Response, letter from Jack E. Housenger, Director, EPA Office of Pesticide Programs, to Aaron Colangelo and Margaret Reeves, Ph.D (July 15, 2014) (EPA-HQ-OPP-2007-1005-0098).

12

As to the heart of the petition, EPA engaged in several rounds of scientific review, solicited input from its Scientific Advisory Panel on numerous occasions, and developed methodologies to analyze, quantify, and for drift, to mitigate the risks.

A. Inhalation Exposures through Pesticide Drift and Volatilization

EPA’s 2001 re-registration determination for chlorpyrifos ignored exposures through pesticide drift and volatilization on the theory that such exposures were exempted from the FQPA as occupational exposures. In responding to the Kids’ Petition and in its preliminary human health risk assessment released in 2011, EPA acknowledged its legal obligation to assess and protect against drift and volatilization as aggregate exposures. Agency Response to Kids’ Petition at 2, 32-34; 2011 PHHRA at 71-75. EPA committed to address such exposures in responding to the 2007 Petition and its registration review of chlorpyrifos and other pesticides.

1. EPA Has Appropriately Taken Steps to Reduce Exposures From Spray Drift, But These Steps Fail to Protect Children From Unsafe Exposures to Chlorpyrifos Through Drift

EPA has developed a standard methodology for assessing a pesticide’s propensity to drift from the point of application offsite to schools, homes, day cares, playfields, and other places people gather and will be exposed. EPA models inhalation exposures from aerial applications, but for groundboom and airblast applications, it focuses only on dermal exposures when people come into contact with residues deposited on the ground. EPA justifies this omission because current pesticide labels prohibit applying pesticides in a manner that will allow drift to contact people. Public comments objected to this approach because of the extensive evidence that drift is reaching people and causing poisonings, thereby demonstrating that the label prohibition is not preventing harmful spray drift.22

EPA applied its standard methodology in assessing chlorpyrifos and found that chlorpyrifos can drift in harmful amounts. To protect children and other bystanders, EPA convinced the registrants to change chlorpyrifos labels by December 2012 to reduce application rates for aerial spraying, change nozzle types and droplet sizes, and impose no-spray buffers around sensitive sites frequented by non-occupational bystanders, especially children. Such sites include “residential lawns, pedestrian sidewalks, outdoor recreational areas such as school grounds, athletic fields, parks and all property associated with buildings occupied by humans for residential or commercial purposes. Sensitive sites include homes, farmworker housing, or other residential buildings, schools, day care centers, nursing homes, and hospitals.”23 The buffers are 10 feet for groundboom spraying, 10 feet for airblast applications, enlarged to 25-50 feet for large volume, medium or coarse droplet applications, and 10-100 feet for aerial spraying.

22 Farmworker and Conservation Comments on Chlorpyrifos Revised Human Health Risk Assessment (Apr. 30, 2015) at 47 (“2015 Farmworker Comments”) (EPA-HQ-OPP-2008-0850-0848) (citing Centers for Disease Control and Prevention investigation of pesticide drift causing poisonings of 20 workers between 30-350 feet from the application site). 23 EPA, Chlorpyrifos – Evaluation of the Potential Risks from Spray Drift and the Impact of Potential Risk Reduction Measures (July 13, 2012) at 3.

13

In an interim response to the 2007 Petition, EPA stated that it was partially granting the Petition with respect to inhalation exposure risks and was reducing risks from primary spray drift by limiting application rates and imposing buffer zones around sensitive sites adjacent to agricultural applications.24

2. EPA Initially Found Harmful Exposures From Volatilization, But Reversed Course Based on Dow Studies That Have Been Heavily Criticized

EPA assessed risks from volatilization in its 2011 Preliminary Human Health Risk Assessment (“2011 PHHRA”) based on ambient and application site monitoring. EPA’s assessment showed that one-quarter of the acute ambient air concentrations resulted in risks of concern to residential bystanders, as did over half of the acute application site concentrations and most of the short- and intermediate-term application site concentrations.25

In 2013, drawing on methods used to assess bystander inhalation risks from fumigant pesticides and recommendations from a December 2009 Scientific Advisory Panel meeting, EPA conducted an assessment of volatilization risks from chlorpyrifos. EPA found that chlorpyrifos applied to fields can volatilize and harm people nearly a mile away (and likely farther): “Given the current available information and the state of the science concerning the volatilization of pesticides, this preliminary risk assessment indicates risks of concern are exceeded for bystanders.”26 EPA identified buffer zones that would be required to reduce off-site concentrations to safe levels. For example, for oranges, the average application rate is so high (greater than 2 pounds of active ingredient/acre) that the maximum buffers would need to be between 1,476 and 4,724 feet and whole field buffers would need to range from 623-2,838 feet, so large that continued use of chlorpyrifos would be infeasible.27

EPA subsequently reversed course based on two studies conducted by Dow AgroSciences, which purport to show that people will not experience adverse effects from volatilization exposures. Without submitting the studies to its Scientific Advisory Panel or obtaining other peer review, EPA accepted the studies and found that chlorpyrifos poses no risk of cholinesterase inhibition from volatilization. On July 15, 2014, EPA provided a partial response indicating that EPA will deny the volatilization component of the petition based on the

24 Chlorpyrifos Petition – December 2012 Response, letter from Dr. Steven Bradbury, Director, EPA Office of Pesticide Programs, to Aaron Colangelo and Margaret Reeves, Ph.D (Dec. 18, 2012) (EPA-HQ-OPP-2007-1005-0096). 25 Chlorpyrifos Preliminary Human Health Assessment for Registration Review (June 30, 2011) at 55 (EPA-HQ-OPP-2008-0850-0025). 26 Chlorpyrifos: Preliminary Evaluation of the Potential Risks from Volatilization (Jan. 31, 2013) at 55 (assessment based on a study that measured the effects of aerosolized chlorpyrifos – the form chlorpyrifos takes when applied as a spray – and not the vapor form it takes after volatilization) (EPA-HQ-OPP-2008-0850-0114). 27 Id. at 32-46.

14

Dow studies on chlorpyrifos vapors, as opposed to aerosols, which could have produced the monitoring concerns noted in 2011 and the risks of concern in the 2013 assessment.28

Public comments objected to EPA’s use of the Dow studies without subjecting them to peer review. 2015 Farmworker Comments at 32-33. Comments explained that the Dow studies ignored the effects of temperature, soil moisture, and individual variation and submitted biomonitoring and incident reports showing poisoning incidents at distances as far away as one-half mile from the application site. Id. at 50-58. Comments also pointed out the lack of controls in the Dow study that demonstrated that the experiment was capable of successfully producing or detecting cholinesterase inhibition. Without such controls, the study results cannot be interpreted or used to claim that chlorpyrifos volatilization does not produce cholinesterase inhibition.29

B. EPA Found that Chlorpyrifos Exposures are Correlated with Harm to the Developing Brain at Exposures Far Below EPA’s Regulatory Endpoint

As long ago as 2000, EPA noted that animal studies reveal that the developing fetus and young animals are more susceptible to chlorpyrifos than adults. Since that time, the scientific evidence of harm to children’s brains from chlorpyrifos exposures has grown, with dozens of peer-reviewed scientific articles documenting statistically significant correlations between early life exposures and neurodevelopmental harm.

To respond to the 2007 Petition, EPA conducted a series of transparent and iterative reviews of the extensive scientific literature, including both animal and epidemiology studies, regarding neurodevelopmental harm from chlorpyrifos. It convened its Scientific Advisory Panel (“SAP”) several times to review its assessments.

In 2008, EPA convened its SAP to review the significant new data since EPA’s 2000 risk assessment. The SAP found that laboratory studies show that “gestational or early postnatal exposures can lead to neurochemical and behavioral alterations that persist into adulthood,” including long-term neurobehavioral changes in motor and cognitive behaviors. 2008 SAP Report at 11-12. 30 The Panel found that “chlorpyrifos likely played a role in the birth and neurodevelopmental outcomes noted in the three cohort studies,” and found the Columbia study the most sound and appropriate for use in assessing developmental toxicity of chlorpyrifos. Id. at 12, 37; see also id. at 43 (“chlorpyrifos is likely associated with adverse neurodevelopmental outcomes.”). Finally, Panel members noted that the exposures in the Columbia study were below EPA’s regulatory endpoint and of concern in light of evidence demonstrating that low levels of exposure to toxicants like lead, mercury, and PCBs are now known to produce significant adverse effects when they were previously thought to be harmful only at high levels. 28 Chlorpyrifos July 2014 Partial Petition Response, letter from Jack E. Housenger, Director, EPA Office of Pesticide Programs, to Aaron Colangelo and Margaret Reeves, Ph.D (July 15, 2014). 29 2015 Farmworker Comments at 51; Earthjustice, et al., Comments on EPA Proposal to Revoke Chlorpyrifos Tolerances (Jan. 17, 2017) at 21-22. 30 FIFRA SAP Meeting Minutes No. 2008-04, A Set of Scientific Issues Being Considered by the EPA Regarding: The Agency’s Evaluation of the Toxicity Profile of Chlorpyrifos (Sept. 2008), available at https://www.regulations.gov/document?D=EPA-HQ-OPP-2008-0274-0064.

15

Id. at 43.

In 2010, EPA convened its SAP to address how to incorporate epidemiology and incident data into risk assessments. EPA had developed a draft framework for incorporating epidemiology and human incident data into human health risk assessment. The Panel reviewed the draft and provided factors to be used to evaluate the quality of epidemiology studies, and identified ways such studies could be used in risk assessment.31

In July 2011, EPA released its Preliminary Human Health Risk Assessment, which confirmed, as the 2007 Petition claimed was legally required, the need to address drift, volatilization, and health impacts to children at low doses.32 The assessment expressed concern that current tolerances may not afford sufficient protection to children from drinking water and drift exposures, particularly infants. Reader’s Guide at 2-3; 2011 PHHRA at 17. As to the mounting evidence of neurodevelopmental impacts, EPA concluded that “chlorpyrifos likely played a role in long term neurological effects from early exposures that were evaluated in the epidemiology studies.” Reader’s Guide at 2-3. Despite these statements, EPA proposed to reduce the FQPA 10X safety factor to 1X, i.e., to eliminate it. Numerous comments opposed eliminating the FQPA 10X safety factor, including comments submitted by the California Department of Pesticide Regulation observing that developmental neurotoxicity may be a more sensitive endpoint than cholinesterase inhibition and “[p]rotection against brain cholinesterase inhibition alone may be insufficient to protect against such effects.”33

In 2012, EPA convened its SAP to review EPA’s more comprehensive analysis of the neurotoxicity of chlorpyrifos. In its report, the SAP noted significant, long-term adverse effects on neurobehavioral development from chlorpyrifos in laboratory animal studies. It found that the epidemiology “studies show some consistent associations relating exposure measures to abnormal reflexes in the newborn, pervasive development disorder at 24 or 36 months, mental development at 7-9 years, and attention and behavior problems at 3 and 5 years of age.” 2012 SAP at 17.34 The Panel concurred with EPA and the 2008 SAP that “chlorpyrifos likely plays a role in impacting the neurodevelopmental outcomes examined in the three cohort studies,” id. at 18, and it noted that “multiple lines of evidence suggest chlorpyrifos can affect neurodevelopment at levels lower than those associated with AChE inhibition.” Id. at 19. Because the mode of action has not been identified, the SAP believed the cohort studies do not readily lend themselves as the basis for establishing the point of departure. However, the Panel expressed concern over EPA’s focus on 10% cholinesterase inhibition because there is no 31 FIFRA SAP Meeting Minutes No. 2010-03, A Set of Scientific Issues Being Considered by the EPA Regarding: Draft Framework and Case Studies on Atrazine, Human Incidents, and the Agricultural Health Study: Incorporation of Epidemiology and Human Incident Data into Human Health Risk Assessment (Feb. 2010), available at https://www.regulations.gov/document?D=EPA-HQ-OPP-2009-0851-0059. 32 EPA, Reader’s Guide to the Preliminary Human Health Risk Assessment for Chlorpyrifos at 1-3 (July 1, 2011) (“Reader’s Guide”) (EPA-HQ-OPP-2008-0850-0027). 33 Comment submitted by California Department of Pesticide Regulation to EPA (Sept. 30, 2011) at 3 (EPA-HQ-OPP-2008-0850-0099). 34 FIFRA SAP Meeting Minutes No. 2012-04, A Set of Scientific Issues Being Considered by the EPA Regarding: Chlorpyrifos Health Effects (Apr. 2012), available at https://www.regulations.gov/document?D=EPA-HQ-OPP-2012-0040-0029.

16

mechanism whereby a 10% AChE activity reduction in pregnant women would be responsible for a cognitive defect or developmental delay in their offspring.” Id. at 25. The Panel advised EPA to explore ways to use the Columbia study to inform dose-response relationships. Id. at 19.

In December 2014, EPA released its Revised Human Health Risk Assessment for Chlorpyrifos (“2014 RHHRA”) 35 and acknowledged the strong convergence in the findings from the animal studies and the three mother-child cohort studies. It found that the laboratory animal studies indicated “that gestational and/or postnatal exposure may cause persistent behavioral effects into adulthood.” 2014 RHHRA at 25; see id. at 26 (“upon review of the published literature a pattern of neurodevelopmental adverse outcomes emerges.”). It called the cohort studies “strong studies which support a conclusion that chlorpyrifos likely played a role in these outcomes.” Id. at 33. More specifically, the studies:

consistently identified associations with neurodevelopmental outcomes in relation to chlorpyrifos exposure. There is evidence of delays in mental development in infants (24-36 months), attention problems and pervasive developmental disorder in early childhood, and intelligence decrements in school age children who were exposed to chlorpyrifos or OP during gestation. Investigators reported strong measures of statistical association across several of these evaluations (odds ratios 2-4 fold increased in some instances) and observed evidence of exposure-response trends in some instances, e.g., intelligence measures.

Id at 42. EPA concluded “that these lines of evidence together support a conclusion that exposure to chlorpyrifos results in adverse neurodevelopmental outcomes in humans, at least under some conditions.” Id. at 49. EPA also concluded that the range of exposures in the epidemiology studies were too low to result in cholinesterase inhibition. Id.; see id. at 47 (“it is unlikely that [cholinesterase] would have been inhibited by any meaningful or measureable amount, if at all” in the studies). EPA noted that the mode of action by which chlorpyrifos causes long-lasting damage to children’s brains is uncertain, as is the particular exposure level at which such effects occur (apart from knowing it is lower than EPA’s regulatory endpoint based on cholinesterase inhibition). Based on these uncertainties, EPA retained the FQPA 10X safety factor for infants, children, youth, and women of child-bearing years. Id. at 49.

EPA continued to use cholinesterase inhibition as its regulatory endpoint in its 2014 risk assessment, despite acknowledging that the harm to children’s brains occurred at lower exposures and is therefore the most sensitive endpoint. EPA then used a model developed by Dow Agrosciences (called a physiologically based pharmacokinetic or PBPK model) to estimate doses in people associated with cholinesterase inhibition. Because the model uses human data, at least in part, EPA decided it could eliminate the traditional 10X safety factor that accounts for uncertainty in extrapolating from animal tests to human impacts (inter-species safety factor). It also reduced by half or more the other traditional 10X safety factor designed to account for variability and sensitivity within human populations (intra-species factor), believing that the human data and the model incorporate such human variability.

35 Chlorpyrifos: Revised Human Health Risk Assessment for Registration Review (Dec. 29, 2014) (EPA-HQ-OPP-2008-0850-0195).

17

Public comments objected to the reduction of these traditional safety factors because the Dow model estimates exposures associated with the cholinesterase inhibition endpoint, and neurodevelopmental harm occurred from prenatal exposures far below those that would result in 10% cholinesterase inhibition.36 In addition, EPA’s Scientific Advisory Panel had found serious problems with the Dow model in 2011, yet EPA never submitted the model, as subsequently modified, for further review by the Panel, nor did EPA explain how the modifications corrected the problems identified by the 2011 SAP. 2011 SAP at 11, 13-17.37 The model uses data from two studies that deliberately dosed people, and EPA cannot rely on such deliberate human testing without ensuring the tests meet rigorous ethical and scientific standards. 40 C.F.R. §§ 26.1701-.1706. Comments objected to EPA’s use of the Dow model because EPA did not obtain review of the studies under current legal standards by its Human Studies Review Board and because of ethical flaws in using Dow employees in one study and in its misleading informed consent, as well as scientific deficiencies. 2015 Farmworker Comments at 36-42.

Even though the 2014 RHHRA used an endpoint that fails to protect children from neurodevelopmental harm and shrunk the traditional safety factors, it found that a substantial number of chlorpyrifos uses will result in exposures that exceed EPA’s drinking water levels of concern. 80 Fed. Reg. at 69,083. EPA determined that the drinking water exceedances were likely to be conservative because its modeling is validated by empirical water monitoring data and its modeling is based on a single application.38

V. THE UNREASONABLE DELAY LITIGATION

It took a series of unreasonable delay lawsuits to obtain EPA action on the 2007 Petition. Shortly after PAN filed the 2007 Petition, EPA found that the petition met the legal requirements for FFDCA petitions and published a notice in the Federal Register requesting public comments. 72 Fed. Reg. 58,845 (Oct. 17, 2007). After three years passed without a response to the 2007 Petition, PAN and NRDC filed an unreasonable delay lawsuit, which they settled based on EPA’s commitment to respond to the Petition by the end of November 2011. NRDC v. EPA, No. 10-05590-CM, Dkt. No. 17, at 2-3 (S.D.N.Y. Dec. 21, 2010) (Stipulation).

After EPA missed the 2011 deadline, PAN and NRDC brought a second delay lawsuit. EPA issued a partial response to the 2007 Petition, promising a complete final response in

36 2015 Farmworker Comments at 28-32. See also, Comment submitted by Elaine M. Faustman, Ph.D. DABT, on behalf of the Institute of Risk Analysis and Risk Communication and the Center for Child Environmental Health Risks Resarch at the University of Washington (EPA-HQ-OPP-2008-0850-0829); Comment submitted by Robin M. Whyatt, Professor, Columbia University, Dale Hattis, Research Professor, Clark University and Theodore Slotkin, Duke University School of Medicine (EPA-HQ-OPP-2008-0850-0510). 37 FIFRA SAP Meeting Minutes No. 2011-03, A Set of Scientific Issues Being Considered by the EPA Regarding Chlorpyrifos Physiologically Based Pharmacokinetic and Pharmacodynamis (PBPK/PD) Modeling Linked to Cumulative and Aggregate Rise Evaluation System (CARES) (Feb. 2011), available at https://www.regulations.gov/document?D=EPA-HQ-OPP-2010-0588-0038. 38 Chlorpyrifos: Updated Drinking Water Assessment for Registration Review (Dec. 23, 2014) (EPA-HQ-OPP-2008-0850-0198).

18

December 2012.39 While EPA’s first interim response addressed six points made in the 2007 Petition, it did not determine whether EPA would ban chlorpyrifos. See id. The only practical effect of EPA’s July 2012 partial decision consisted of EPA’s announcement that the chlorpyrifos registrants had agreed to a spray drift mitigation package that calls for small no-spray buffers (most were only ten feet) around school grounds, homes, residential lawns, athletic fields, nursing homes, hospitals, sidewalks, and other places frequented by bystanders.40 EPA then missed the December 2012 deadline for issuing a response to the 2007 Petition, but it promised a final response by February 2014.41

In 2013, the Ninth Circuit Court of Appeals decided not to order EPA to respond to the 2007 Petition because the agency had “set forth a concrete timeline for final agency action that would resolve the 2007 Petition by February 2014.” In re PANNA, 532 F. App’x 649, 651 (9th Cir. 2013).

EPA missed its February 2014 deadline. In July 2014, EPA issued another partial response and reversed its earlier preliminary determination that chlorpyrifos volatilization presents risks that warrant large, no-spray buffers (in some instances many thousands of feet) around schools, homes, and other places frequented by people. EPA based this reversal on two new studies conducted by Dow AgroSciences LLC, the primary chlorpyrifos registrant.42 In that partial response, EPA indicated that it planned to release a revised human health risk assessment for public comment in December 2014, along with either a proposed rule revoking tolerances for chlorpyrifos or a proposed order denying the 2007 Petition, and that it would issue any final denial of the 2007 Petition by the summer of 2015.

After EPA missed its February 2014 deadline, PAN and NRDC filed a third unreasonable delay case seeking a writ of mandamus from the Ninth Circuit directing EPA to act. When the case was argued on June 4, 2015, EPA told the court that it would complete its preliminary review of the public comments on the 2014 risk assessment by June 30, 2015 and determine whether it would deny or grant the 2007 Petition, in whole or in part. On June 10, 2015, the court ordered EPA to file a status report by June 30, 2015 informing the court which path it would take and proposing a timeline for final resolution of the 2007 Petition. In re PANNA, 790 F.3d 875 (9th Cir. 2015). EPA’s June 30, 2015 status report revealed that EPA had become convinced that revocation of all chlorpyrifos food tolerances was warranted because of drinking 39 EPA’s Partial Response to Chlorpyrifos Petition by NRDC & PANNA, letter from Dr. Steven Bradbury, Director, EPA Office of Pesticide Programs, to Aaron Colangelo and Margaret Reeves, Ph.D (July 16, 2012). 40 Id. (citing Chlorpyrifos – Evaluation of the Potential Risks from Spray Drift and the Impact of Potential Risk Reduction Measures (July 13, 2012) at 3). 41 See Chlorpyrifos Petition – December 2012 Response, letter from Dr. Steven Bradbury, Director, EPA Office of Pesticide Programs, to Aaron Colangelo and Margaret Reeves, Ph.D (Dec. 18, 2012) (EPA-HQ-OPP-2007-1005-0096); Chlorpyrifos Petition – January 2013 Response, letter from Dr. Steven Bradbury, Director, EPA Office of Pesticide Programs, to Aaron Colangelo and Margaret Reeves, Ph.D (Jan. 25, 2013) (EPA-HQ-OPP-2007-1005-0097); EPA Response to Petition for Writ of Mandamus, in In re PANNA, No. 12-71125 (9th Cir. July 24, 2012). 42 Chlorpyrifos July 2014 Partial Petition Response, letter from Jack E. Housenger, Director, EPA Office of Pesticide Programs, to Aaron Colangelo and Margaret Reeves, Ph.D (July 15, 2014) at 2-5.

19

water contamination. Because it offered no definitive timetable for initiating and completing such a revocation rule, PAN and NRDC asked the Court to do so.

In August 2015, the Ninth Circuit issued a writ of mandamus setting deadlines for EPA action. The decision began as follows:

Although filibustering may be a venerable tradition in the United States Senate, it is frowned upon in administrative agencies tasked with protecting human health. Pesticide Action Network North America and the Natural Resources Defense Council have been waiting for years for the United States Environmental Protection Agency to respond to their administrative petition requesting a ban on the pesticide chlorpyrifos. Instead, they've received a litany of partial status reports, missed deadlines, and vague promises of future action. We recognize the scientific complexity inherent in evaluating the safety of pesticides and the competing interests that the agency must juggle. However, EPA's ambiguous plan to possibly issue a proposed rule nearly nine years after receiving the administrative petition is too little, too late. This delay is egregious and warrants mandamus relief. We order EPA to issue a full and final response to the petition no later than October 31, 2015.

In re PANNA, 798 F.3d 809, 811 (9th Cir. 2015); see id. at 813 (“Issuing a writ of mandamus is necessary to end this cycle of incomplete responses, missed deadlines, and unreasonable delay.”).

The court explained that the circumstances had changed in two significant respects since the court rejected the earlier request in 2013. First, in 2006, after residential uses had ended, EPA had found the remaining chlorpyrifos uses to be safe and it had not overturned those findings in its 2011 preliminary human health risk assessment. That changed in 2014 when EPA found agricultural uses of chlorpyrifos unsafe due to drinking water contamination and also noted serious risks to farmworkers who apply chlorpyrifos or who enter fields after chlorpyrifos has been sprayed. The court found that “EPA offers no acceptable justification for the considerable human health interests prejudiced by the delay. In view of EPA’s own assessment of the dangers to human health posed by this pesticide, we have little difficulty concluding it should be compelled to act quickly to resolve the administrative petition.” Id. at 814.

Second, EPA told the court that complex regulatory proceedings may be needed to effectuate a chlorpyrifos ban. While it indicated it would try to negotiate a settlement with the registrants, if voluntary action did not eliminate unsafe exposures, EPA would need to take regulatory action to revoke chlorpyrifos food tolerances. Yet EPA offered the court no concrete timeline for proposing, let alone finalizing, a tolerance revocation rule. Calling this approach “a roadmap for further delay,” the court concluded that EPA had “stretched the ‘rule of reason’ beyond its limits.” Id.

The court ordered EPA either to initiate a tolerance revocation rulemaking or deny the 2007 Petition by October 31, 2015, and if it proposed to revoke tolerances, to provide a timeline for finalizing that proposed rule. Id. at 815. After EPA proposed to revoke all chlorpyrifos tolerances, the court directed EPA to take final action on that proposal by December 30, 2016. In re PANNA, No. 14-72794, Order (9th Cir. Dec. 10, 2015). The court also directed EPA to file

20

a status report on June 30, 2016, detailing the steps taken to meet the final deadline and indicating that the court would extend the deadline only if EPA showed that extraordinary circumstances made compliance impracticable. Id.

EPA sought an additional six months to conduct further scientific review, referring to its efforts to quantify the exposures associated with damage to children’s brains for use in a quantitative risk assessment and to continue its assessment of drinking water risks. The court denied the request, calling it “another variation on a theme ‘of partial reports, missed deadlines, and vague promises of future action’ that has been repeated for the past nine years.” In re PANNA, No. 14-72794, Order (9th Cir. Aug. 12, 2016). The court found no justification for further delay in responding “to the pressing health concerns presented by chlorpyrifos.” Id.; see id. (“a claim of premature rulemaking has come and gone.”). The court nonetheless gave EPA until March 31, 2017 to take final action and stated: “This is the final extension, and the court will not grant any further extensions.” Id.

VI. EPA PROPOSED TO REVOKE ALL TOLERANCES BECAUSE IT FOUND CHLORPYRIFOS UNSAFE

In October 2015, EPA proposed to revoke all chlorpyrifos tolerances because of drinking water contamination. 80 Fed. Reg. 69,080 (Nov. 6, 2015). EPA concluded that it “is unable to conclude that the risk from aggregate exposure from the use of chlorpyrifos meets the safety standard of the Federal Food, Drug, and Cosmetic Act (FFDCA).” Id.; see also id. at 69,081 (“EPA cannot, at this time, determine that aggregate exposure to residues of chlorpyrifos, including all anticipated dietary exposures and all non-occupational exposures for which there is reliable information, are safe.”). “Because EPA is unable to determine at this time that aggregate exposures to chlorpyrifos are safe, EPA is proposing to revoke these tolerances in response to a Petition from PANNA and the Natural Resources Defense Council (NRDC) to revoke all chlorpyrifos tolerances….” Id. at 69,081. Drinking water contamination proved to be the impetus for the proposed revocation. EPA relied on its 2014 risk assessment, which it called “a highly sophisticated assessment of hazard and exposure to chlorpyrifos and its oxon.” Id. at 69,082. Based on that assessment, EPA determined that multiple chlorpyrifos uses exceed EPA’s drinking water level of concern with considerable frequency and present a risk of concern with infants most at risk. Id. at 69,082-83. EPA found all chlorpyrifos uses under current labels to be unsafe. Id. at 69,083. The proposed rule held open the possibility that registrants and growers might be able to submit additional information and propose label modifications to prevent some watersheds from being at risk from certain chlorpyrifos uses. Id. at 69,080. The proposed rule also acknowledged that the 2014 risk assessment was under-protective of children because it was based on cholinesterase inhibition and the harm to children’s brains is associated with lower exposures. EPA indicated that it would continue to review the evidence of long-lasting neurodevelopmental harm to children from low-level exposures and to try to incorporate that evidence into its risk assessment and regulatory determination. In public comments to EPA, farmworker and health advocates submitted recently published scientific articles that continued to strengthen the correlation between low-level

21

chlorpyrifos exposures and damage to children’s brains, and also found lung damage in 11-year olds and tremors that could impair their ability to draw and write.43 The comments continued to urge EPA to develop an endpoint or restore the traditional safety factors to protect children from this harm, and conducted calculations based on the 2014 risk assessment to add such protection, which showed that exposures are unsafe from food alone, all drinking water, and from drift at distances greater than those covered by the spray drift buffers put in place in 2012. The comments cited evidence that chlorpyrifos travels further, including a Washington incident when workers were sickened by chlorpyrifos being applied about a mile from their worksite.44 VII. EPA FOUND SERIOUS HARM, PARTICULARLY TO CHILDREN, AT LOWER

EXPOSURES IN ITS MOST RECENT ASSESSMENTS

To protect against damage to children’s brains from low-level exposures and to ensure that its regulatory actions are based on the most sensitive endpoint, consistent with longstanding EPA policy, EPA sought to identify a regulatory endpoint from the Columbia study that correlated chlorpyrifos exposures with serious harm to children’s brains. 45 In 2016, EPA used measurements of chlorpyrifos in cord blood from the Columbia study to derive a more protective endpoint that would protect against adverse brain impacts, heeding a recommendation of the 2012 SAP. EPA submitted its analysis to the SAP for review. Even though the SAP did not support EPA’s particular methodology for deriving such an endpoint, the SAP concurred with EPA’s conclusion in the 2014 risk assessment that the 10% cholinesterase inhibition endpoint is not protective because damage to children’s brains occurred at lower doses and EPA should take steps to protect against this harm. 2016 SAP at 18, 52-53.46

In November 2016, EPA released its 2016 Chlorpyrifos Revised Human Health Risk Assessment (“2016 RHHRA”).47 EPA derived a regulatory endpoint based on neurodevelopmental effects because the Agency had determined that neurodevelopmental harm to fetuses occurred when pregnant mothers were exposed to far lower doses of chlorpyrifos than what produces 10% cholinesterase inhibition. 2016 RHHRA at 13. EPA considered all lines of

43 Earthjustice, et al Comments on EPA Proposal to Revoke Chlorpyrifos Tolerances (Jan. 5, 2016) at 7 (EPA-HQ-OPP-2015-0653-0390). 44 Id. at 21 (citing Washington State Department of Health Comments (May 8, 2015) (EPA-HQ-OPP-2008-0850-0842)). 45 Also, as EPA continued to review the scientific evidence correlating low-level exposures to chlorpyrifos and other organophosphates with damage to children’s brains, it reiterated and expanded its findings substantiating this harm to all organophosphates, given that they share a common mechanism of toxicity, and extensive scientific evidence correlates organophosphates with adverse neurodevelopmental effects. See Literature Review on Neurodevelopment Effects and FQPA Safety Factor Determination for the Organophosphate Pesticides (Sept. 2015), available at https://www.regulations.gov/%23!documentDetail;D=EPA-HQ-OPP-2008-0440-0039. 46 FIFRA Scientific Advisory Panel Minutes No. 2016-01, A Set of Scientific Issues Being Considered by the EPA Regarding Chlorpyrifos:Analysis of Biomonitoring Data) (Apr. 2016), available at https://www.regulations.gov/document?D=EPA-HQ-OPP-2016-0062-0140. 47 Chlorpyrifos Revised Human Health Risk Assessment (Nov. 3, 2016) (EPA-HQ-OPP-2015-0653-0454).

22

evidence, including human epidemiological and animal toxicological studies in making its determination to change its endpoint. 81 Fed. Reg. 81,049, 81,050 (Nov. 17, 2016) (agreeing with Scientific Advisory Panel that existing point of departure based on 10% cholinesterase inhibition is “not sufficiently health protective”). EPA also retained the FQPA 10X safety factor to account for uncertainty in using a lowest-observable adverse effect level in the absence of a no-observable adverse effect level. 2016 RHHRA at 22.48

In establishing an updated regulatory endpoint, EPA used the physiologically based pharmacokinetic (“PBPK”) model developed by Dow AgroSciences as a tool to analyze exposure estimates. EPA followed the recommendation of the 2016 Scientific Advisory Panel and used the PBPK model to predict a time-weighted average blood concentration for women in the Columbia cohort. 2016 RHHRA at 16-17. EPA applied the average blood concentration to females, infants, and young children, which was supported by data from animal studies showing that both the pre- and post-natal periods are windows of susceptibility.49

Using this more appropriate endpoint, EPA found that chlorpyrifos presents unacceptable safety risks through exposures from food, drinking water, spray drift, and occupational activities. Food-only exposures for chlorpyrifos were found to be unsafe for all population subgroups analyzed, with young children having the highest risks of concern. 2016 RHHRA at 23. While the adult subgroup had an alarming risk estimate at 62 times the safe level of exposure, the risk estimate for children ages 1-2 was more than double that of adults at 140 times safe levels. Id. Additionally, EPA’s revised assessment did not result in any changes to its finding that “the majority of estimated drinking water exposures from currently registered uses, including water exposures from non-food uses, continue to exceed safe levels even taking into account more refined drinking water exposures.” 81 Fed. Reg. at 81,050. Regarding spray drift, EPA found unsafe levels of chlorpyrifos from the field’s edge to distances of more than 300 feet from where the pesticide is sprayed and unsafe levels in the ambient air recorded in air monitoring performed in agricultural communities in California and Washington. 2016 RHHRA at 31. EPA also found unacceptable risks to all farmworkers who mix and apply chlorpyrifos, even with maximum levels of personal protective equipment or engineering controls. 2016 RHHRA at 36-37. Moreover, even though current labels allow workers to re-enter the fields within 1-5 days after pesticide spraying to weed, irrigate, and pick crops, EPA found that, on average, re-entry intervals of at least 18 days were needed to protect workers from risks of concern. Id. at 38. After releasing the 2016 RHHRA, EPA reopened the comment period for its proposal to revoke chlorpyrifos food tolerances, noting that:

48 EPA’s longstanding risk assessment methods apply an additional uncertainty or safety factor when the scientific studies do not identify a no-observable adverse effect level. EPA then uses and extrapolates from the lowest-observable adverse effects level, and adds a safety factor to guard against exposing people to the observed adverse effects. EPA Office of Pesticide Programs, Determination of the Appropriate FQPA Safety Factor(s) in Tolerance Assessment at 9 (Feb. 28, 2002) (https://www.epa.gov/sites/production/files/2015-07/documents/determ.pdf). 49 EPA reviewed animal studies and found at in its 2014 Revised Human Health Risk Assessment for Chlorpyrifos that, “There is a considerable and growing body of literature on the effects of chlorpyrifos on the developing brain of laboratory animals (rats and mice) indicating that gestational and/or postnatal exposure may cause persistent behavioral effects into adulthood. These data provide support for the susceptibility of the developing mammalian brain to chlorpyrifos exposure.” 2014 RHHRA at 25-26.

23

EPA’s revised analyses do not result in a change to the EPA’s proposal to revoke all tolerances but it does modify the methods and risk assessment used to support that finding in accordance with the advice of the SAP. The revised analysis indicates that expected residues of chlorpyrifos on most individual food crops exceed the ‘‘reasonable certainty of no harm’’ safety standard under the Federal Food, Drug, and Cosmetic Act (FFDCA). In addition, the majority of estimated drinking water exposures from currently registered uses, including water exposures from non-food uses, continue to exceed safe levels even taking into account more refined drinking water exposures. Accordingly, based on current labeled uses, the agency’s analysis provided in this notice continues to indicate that the risk from the potential aggregate exposure does not meet the FFDCA safety standard. EPA can only retain chlorpyrifos tolerances if it is able to conclude that such tolerances are safe. EPA has not identified a set of currently registered uses that meets the FFDCA safety standard because it is likely only a limited number of food uses alone, and in combination with predicted drinking water exposures, would meet the standard. Further, EPA has not received any proposals for mitigation that registrants may be willing to undertake that would allow the EPA to retain any of the tolerances subject to this rulemaking.

81 Fed. Reg. at 81,050.

This was the state of the record as the March 31, 2017 court-ordered deadline approached. EPA had found chlorpyrifos unsafe due to drinking water contamination in 2014, leading to the 2015 proposal to revoke all tolerances. No mitigation or further analysis lessened the risks. To the contrary, as EPA conducted further assessment to determine what action is necessary to guard against damage to children’s developing brains, it found unsafe exposures every way people come into contact with chlorpyrifos whether in food, in drinking water, or in the air. And young children are most at risk. The fate of chlorpyrifos had been all but sealed. VIII. THE ORDER DENYING THE 2007 PETITION

Instead of finalizing the proposed revocation order based on its findings that chlorpyrifos is unsafe, on March 29, 2017, the new EPA Administrator, Scott Pruitt, issued an order on March 29, 2017, entitled “Chlorpyrifos: Order Denying PANNA and NRDC Petition to Revoke Tolerances” (“Pruitt Order”), 82 Fed. Reg. 16,581, 16,583 (Apr. 5, 2017). The Pruitt Order finalized the interim responses EPA had previously provided addressing spray drift, volatilization, endocrine disruption screening, cancer risks, export hazards, and other issues. The Pruitt Order reiterated the interim responses, even where subsequent EPA action had reversed or severely undermined the rationale for the earlier partial response based on further analysis or new scientific evidence. For example, EPA defended dispensing with the FQPA 10X safety factor for chlorpyrifos, even though it decided in 2014 that the FQPA safety factor had to be retained in full. Id. at 16,588-89. EPA also repeated its earlier justification for not considering genetic vulnerability to chlorpyrifos, even though the Dow model used in EPA’s 2014 and 2016 risk assessments incorporated such genetic variability into its metrics. Id. at 16,585-86. And EPA adhered to its incomplete assessment and mitigation for spray drift and volatilization,

24

without ever acknowledging, let alone addressing, the public comments criticizing EPA’s approach as legally and scientifically flawed.

With the exception of the FIFRA export claim not at issue here, EPA had indicated that it would not make its interim, partial responses final, unless PAN and NRDC requested that it do so. See id. at 16,583, 16,585. PAN and NRDC did not ask EPA to make the partial responses final because the heart of the 2007 Petition — neurodevelopmental harm to children from chlorpyrifos at low doses — remains unresolved. Resolution of that issue in a manner that protects children would lead to revocation of chlorpyrifos tolerances and eliminate the need for objections and further proceedings. Moreover, EPA had not addressed the comments submitted by PAN, NRDC, and others, criticizing the spray drift mitigation and interim volatilization determination because they were based on poisoning risks and not damage to children’s brains at lower doses. Nor had EPA yet addressed comments making the case that EPA: (1) had illegally ignored direct drift and inhalation exposures in its spray drift assessment and mitigation; and (2) had backtracked from its volatilization assessment documenting unsafe exposures far from the application site based on two scientifically flawed Dow studies.

PAN and NRDC believed that EPA would follow the law and science, and revoke all chlorpyrifos tolerances once it developed a regulatory endpoint and risk assessments that would protect children from neurodevelopmental harm, and once it addressed the public comments revealing serious flaws in its approach to spray drift and volatilization. While EPA did revise its human health risk assessment in 2016 based on a regulatory endpoint designed to prevent low-level exposures associated with brain damage to children, the Pruitt Order made no final decisions and took no final action based on that assessment or any other approach that would protect children’s brains. Nor did the Pruitt Order address the public comments revealing flaws that made its treatment of spray drift and volatilization to date under-protective, particularly of children.

As to the one issue EPA had not previously resolved — neurodevelopmental harm from chlorpyrifos — the Pruitt Order made no substantive determination. Despite EPA’s repeated findings that chlorpyrifos is unsafe, the Pruitt Order did not finalize the tolerance revocation rule. Instead, the Pruitt Order postponed such action based on the Administrator’s preference to engage in further study of the harm to children’s brains from chlorpyrifos before finalizing the October 2015 proposed revocation rule or taking an alternative regulatory path. Id. at 16,590. Without any elaboration, the Pruitt Order asserted vaguely that comments received in response to the October 2015 proposed rule and its November 2016 risk assessment suggest some stakeholders believe uncertainty persists about the use of epidemiological data in risk assessments. Id.

EPA framed its delay in deciding whether to revoke chlorpyrifos food tolerances as a reprioritization of the chlorpyrifos registration review schedule developed by earlier administrations. Id. EPA asserts that, while the Ninth Circuit’s order compelled a response to the 2007 Petition, the court “cannot compel EPA to complete the registration review of chlorpyrifos in advance of the October 1, 2022 deadline” for registration review of all older pesticides. Id.

Acknowledging that it is not legally a relevant factor, the Pruitt Order nonetheless stated: “it is important to note that for many decades chlorpyrifos has been and remains one of the most

25

widely used pesticides in the United States” and that a decision to remove the pesticide from the market would be a “significant policy choice.” Id. Citing the significance of the decision and uncertainty regarding the correlation between chlorpyrifos and adverse neurodevelopmental effects, the Pruitt Order expressed the Administrator’s preference to engage in further study before finalizing any regulatory action. Id.

Within a week of EPA’s Pruitt Order, PAN and NRDC filed a motion with the Ninth Circuit seeking further mandamus relief because EPA had essentially given itself an open-ended extension of time to make chlorpyrifos tolerance decisions, rather than take action on the 2007 Petition and EPA’s findings that chlorpyrifos is unsafe. Specifically, PAN and NRDC asked the Ninth Circuit to give EPA a 30-day deadline to take final regulatory action by either: (1) revoking chlorpyrifos tolerances based on its findings that chlorpyrifos is unsafe; or (2) denying the 2007 Petition if EPA could find chlorpyrifos safe. The motion also asked the court to establish a deadline for EPA to resolve any objections filed contesting its final tolerance action. The motion was fully briefed on May 5, 2017. If the Ninth Circuit fully grants the motion, it will moot these objections.

OBJECTIONS

The EPA Administrator’s decision to leave chlorpyrifos tolerances in place cannot stand for two reasons. First, the decision violates the law, which allows the Administrator to leave tolerances in place only if he finds the pesticide safe. EPA has repeatedly found chlorpyrifos unsafe. The Administrator therefore lacks the legal authority to retain tolerances for this harmful pesticide. Second, the Administrator’s rationale for putting off regulatory action on chlorpyrifos is indefensible under both the law, given EPA’s findings chlorpyrifos is unsafe, which flow from the solid and extensive scientific evidence before the agency. The Pruitt Order should be reversed, and EPA should issue a final revocation rule on an expeditious basis. It should take EPA no longer than 60 days to rule on these objections because they present purely legal issues, and EPA has an obligation to resolve objections “as soon as practicable”. See 21 U.S.C. § 346a(g)(2)(c) (EPA Administrator must issue an order on objections “as soon as practicable”).

I. EPA’S DENIAL OF THE 2007 PETITION IS ILLEGAL BECAUSE EPA CANNOT MAINTAIN TOLERANCES IN THE FACE OF ITS FINDINGS THAT CHLORPYRIFOS IS UNSAFE

EPA’s decision to leave chlorpyrifos tolerances in place violates the law and exceeds the Administrator’s legal authority. Under the FFDCA, the EPA Administrator “may establish or leave in effect a tolerance for a pesticide chemical residue in or on food only if the Administrator determines that the tolerance is safe.” 21 U.S.C. § 346a(b)(2)(A)(i) (emphasis added). “Safe” means the Administrator has determined that there is a reasonable certainty of no harm from aggregate exposures to the pesticide chemical residue. Id. § 346a(b)(2)(A)(ii). The law spells out the consequences of an inability to make the required safety finding in a way that leaves no discretion: “The Administrator shall modify or revoke a tolerance if the Administrator determines it is not safe.” Id. § 346a(b)(2)(A)(i) (emphasis added). Because EPA has repeatedly found chlorpyrifos to be unsafe, the Administrator must revoke all food tolerances for chlorpyrifos.

26

EPA first found unsafe drinking water exposures and proposed to revoke all chlorpyrifos tolerances on this basis, which is addressed in A below. When EPA took steps to protect children from neurodevelopmental harm, it found chlorpyrifos unsafe every way people are exposed to it, which is addressed in B below.

A. EPA Found Unsafe Drinking Water Contamination from Chlorpyrifos Using Poisoning Risks as the Regulatory Endpoint

After years of study and several rounds of review by its Scientific Advisory Panel, EPA has made an unbroken series of findings that chlorpyrifos harms children’s brains at lower exposures than those used by EPA in its previous risk assessments and regulatory decision. EPA’s analysis of the scientific evidence and several SAP reviews culminated in the 2014 risk assessment, which found that chlorpyrifos causes harm to children’s brains from prenatal exposures and that this harm occurs at exposures far lower than EPA’s regulatory endpoint, 10% red-blood cell cholinesterase inhibition. This finding, coupled with uncertainties about the precise low-level exposures that damage children’s developing brains, led EPA to retain the FQPA tenfold margin of safety to protect children from neurodevelopmental harm. The 2014 risk assessment documented drinking water contamination from chlorpyrifos that exposed children to unsafe levels of the pesticide. 2014 RHHRA at 48-49, 95-96. In October 2015, EPA proposed to revoke all tolerances because it could not “determine that aggregate exposure to residues of chlorpyrifos, including all anticipated dietary exposures and all other non-occupational exposures for which there is reliable information, are safe.” 80 Fed. Reg. 69,080, 69,081 (Nov. 6, 2015). EPA explained:

Section 408(d) of the FFDCA, 21 U.S.C. 346a(d), authorizes EPA to revoke tolerances in response to administrative petitions submitted by any person. Because EPA is unable to determine at this time that aggregate exposures to chlorpyrifos are safe, EPA is proposing to revoke these tolerances in response to a Petition from PANNA and the Natural Resources Defense Council (NRDC) to revoke all chlorpyrifos tolerances . . ..This proposal also implements the agency findings made during the registration review process required by section 3(g) of FIFRA (7 U.S.C. 136(a)(g)) which EPA is conducting in parallel with its petition response.

Id. EPA’s proposal to revoke chlorpyrifos tolerances is replete with findings that chlorpyrifos is unsafe:

EPA cannot determine that current dietary exposures to chlorpyrifos are safe within the meaning of FFDCA section 408(b)(2)(A). [Id. at 69,106.]

EPA cannot find that any current tolerances are safe and is therefore proposing to revoke all chlorpyrifos tolerances. [Id.]

[F]ood exposures, when aggregated with residential exposures and potentially more significant drinking water exposures do present a significant risk concern and support revocation of all chlorpyrifos tolerances. [Id. at 69,097.]

27

[W]e cannot make a safety finding based on drinking water exposure. [Id. at 69,106.]

See also Declaration of Richard P. Keigwin, Jr., EPA Office of Pesticide Programs, ¶ 5, in In re PANNA, No. 14-72794, Dkt. No. 25-2 (9th Cir. Oct. 29, 2015) (proposed rule is “based on EPA’s conclusion that it could not make the ‘reasonable certainty of harm’ finding”).

B. EPA Found All Exposures to Chlorpyrifos to be Unsafe When it Sought to Protect Against Damage to Children’s Developing Brains

EPA’s findings that chlorpyrifos is unsafe flow from the 2014 risk assessment, which uses 10% red blood cell cholinesterase inhibition as the regulatory endpoint. That risk assessment, however, contained a pivotal, and troubling, finding: the damage to children’s brains in the mother-child cohort studies occurred from exposures that were too low to produce cholinesterase inhibition. 2014 RHHRA at 47, 49. In its proposal to revoke chlorpyrifos tolerances, EPA indicated it would heed the SAP’s advice and try to reconstruct the exposures correlated with adverse brain impacts in the Columbia study or find some other method to protect against this type of harm. This attempt to identify exposures linked to damage to the developing brain is consistent with EPA’s policy to ensure that its risk assessments are designed to identify and protect the most sensitive endpoint. While the 2016 SAP did not agree with EPA’s first effort to reconstruct the exposure levels based on cord blood samples from the Columbia study, it agreed with EPA that the harmful brain impacts occurred at exposures far below EPA’s regulatory endpoint based on cholinesterase inhibition and that EPA should be more protective to guard against such impacts. 2016 SAP at 18, 52-53.

EPA’s second effort, released in November 2016, was based in large part on Dow’s PBPK model and showed that people will be at risk of harm from virtually every use and every way that people are exposed to chlorpyrifos, with children, and particularly 1 to 2- year olds, most at risk. 2016 RHHRA at 23. With the lower endpoint, the 2016 risk assessment revealed even higher and more pervasive risks from chlorpyrifos:

All food exposures exceed safe levels, with the most exposed population - children 1-2 years of age - exposed to 140 times what EPA deems to be safe.

Use of chlorpyrifos contaminates drinking water.

Drift of pesticides from the fields expose children to unsafe levels of chlorpyrifos within 300 or more feet of the fields where the pesticide is sprayed. Children could be exposed to harmful drift at schools, day cares, in their homes, and at playgrounds.

For children between 1 to 2- years old, all 11 acute ambient air concentrations assessed resulted in risks of concern. For adults, all but one of the 11 steady state ambient air concentrations assessed resulted in risks of concern.

All workers who mix and apply chlorpyrifos pesticides are exposed to levels greater than what EPA deems to be safe.

28

Field workers are currently allowed to re-enter fields within 1-5 days after pesticide spraying, but unsafe exposures continue on average for 18 days after applications.

Id. at 23-24, 30-33.

Not surprisingly, EPA found based on the 2016 risk assessment:

The revised analysis indicates that expected residues of chlorpyrifos on most individual food crops exceed the ‘reasonable certainty of no harm’ safety standard under the Federal Food, Drug, and Cosmetic Act (FFDCA). In addition, the majority of estimated drinking water exposures from currently registered uses, including water exposures from non-food uses, continue to exceed safe levels even taking into account more refined drinking water exposures. Accordingly, based on current labeled uses, the agency’s analysis provided in this notice continues to indicate that the risk from the potential aggregate exposure does not meet the FFDCA safety standard. EPA can only retain chlorpyrifos tolerances if it is able to conclude that such tolerances are safe. EPA has not identified a set of currently registered uses that meets the FFDCA safety standard . . . .Further, EPA has not received any proposals for mitigation that registrants may be willing to undertake that would allow the EPA to retain any of the tolerances subject to this rulemaking.

81 Fed. Reg. 81,049, 81,050 (Nov. 17, 2016) (citing 2016 RHHRA).

C. EPA’s Findings that Chlorpyrifos is Unsafe Compel the Administrator to Revoke All Chlorpyrifos Food Tolerances

In the face of these findings, which build upon the 2014 risk assessment and 2015 tolerance revocation proposal, the EPA Administrator has a legal obligation to revoke all chlorpyrifos tolerances. This is the only legally defensible course of action under the law, which allows the Administrator to leave a tolerance in place “only if the Administrator determines that the tolerance is safe.” 21 U.S.C. § 346a(b)(2)(A)(i). Beginning in 2014, EPA has repeatedly stated that it cannot find chlorpyrifos safe and it has since found chlorpyrifos unsafe every way that people are exposed to it. In the face of these findings, the law is clear: “the Administrator shall modify or revoke a tolerance if the Administrator determines it is not safe.” Id.

This mandatory obligation is reinforced by the FFDCA’s provisions laying out the “actions” the Administrator is authorized and directed to take on a petition to revoke tolerances. The FFDCA provides that the Administrator “shall” take one of three permissible actions:

(i) issue a final regulation (which may vary from that sought by the petition) establishing, modifying, or revoking a tolerance for the pesticide chemical residue …(which final regulation shall be issued without further notice and without further period for public comment);

29

(ii) issue a proposed regulation under subsection (e) of this section and thereafter issue a final regulation under such subsection; or

(iii) issue an order denying the petition.

Id. § 346a(d)(4)(A).

These actions are stated in the alternative, meaning they are mutually exclusive paths the Administrator may take on a petition or specific part of a petition. The second option starts with a proposed regulation and proceeds to a final regulation after notice and public comment. Here, in contrast, EPA proposed to revoke chlorpyrifos tolerances, but did not finalize that regulation. He left the proposed revocation rule intact, awaiting further final action. Administrator Pruitt then issued an order purporting to deny the 2007 Petition, but without withdrawing the proposed regulation because he did not resolve the merits of the 2007 Petition. The FFDCA does not allow the Administrator to take these two mutually exclusive actions on the same issue concurrently. For this reason as well, the Administrator acted in blatant violation of the law by denying the 2007 Petition and leaving chlorpyrifos tolerances in place.

II. EPA’S RATIONALE FOR LEAVING CHLORPYRIFOS TOLERANCES IN PLACE IS LEGALLY AND SCIENTIFICALLY INDEFENSIBLE

The Pruitt Order offers several reasons for delaying action on chlorpyrifos tolerances for many years, possibly until October 1, 2022. None can legally justify defying the clear legal mandate to revoke tolerances because EPA cannot find chlorpyrifos safe.

A. EPA Cannot Rely on Its 2006 Safety Finding When It Has Since Determined Based on Mounting Scientific Evidence that Chlorpyrifos Damages Children’s Brains and is Unsafe

The 2007 Petition sought to compel EPA to address and act on scientific evidence and routes of exposure disregarded in its old risk assessments used in re-registering chlorpyrifos in 2001 and 2006. Oddly, the Pruitt Order defends the 2006 cumulative risk assessment based on the science then available as if time stood still. See, e.g.,82 Fed. Reg. at 16,589 (“the Agency is confident that its assessment for chlorpyrifos in 2006 was reasonably based on the best available science at the time of the assessment”) (emphasis added). To state the obvious, it is no longer 2006. EPA must address the extensive and ever-growing evidence of serious brain damage to children from chlorpyrifos, developed over the past 11 years. See 21 U.S.C. § 346a(d)(4) (EPA must assess available information); id. § 346a(b)(2)(C)-(D) (EPA must consider available information concerning such factors as toxicity, population sensitivities, and children’s exposures).

The Pruitt Order also depicts much of the 2007 Petition as a challenge to the 2006 re-registration determination when the heart of the Petition sought action on issues EPA had sidestepped in 2006, namely drift, volatilization, and damage to the developing brain. See 82 Fed. Reg. at 16,590. At one point, the Pruitt Order defends eliminating the FQPA 10X safety factor, even though EPA decided in 2014 that it must retain that safety factor due to gaps in information needed to protect infants and children. Id. at 16,588. The Pruitt Order asserts that PAN and NRDC failed to show that using a FQPA 10X safety factor would show chlorpyrifos is unsafe. Id. That statement is mind-boggling in light of EPA’s findings in its 2014 and 2016 risk

30

assessments (that retain a FQPA 10X safety factor) that chlorpyrifos is unsafe, which compels revocation of all chlorpyrifos tolerances.

EPA cannot continue to rely on its 2006 safety finding in light of the Agency’s and multiple SAP’s subsequent findings that chlorpyrifos fails to meet the FQPA safety standard based on an extensive body of peer-reviewed toxicological and epidemiological studies correlating neurodevelopmental harm to fetuses and children with chlorpyrifos exposure. As the Ninth Circuit Court of Appeals noted, EPA “has backtracked significantly from” its 2006 pronouncement of safety when it found chlorpyrifos unsafe in its 2014 risk assessment and determined its tolerances needed to be revoked. In re PANNA v. EPA, 798 F.3d at 814. The FQPA gives EPA only two options: the Agency must find that chlorpyrifos is safe based on the evidence currently before it in order to retain chlorpyrifos tolerances, which it cannot do, or it must revoke tolerances based on its findings that chlorpyrifos is unsafe. Hiding behind stale 2006 findings that have since been reversed based on numerous, definitive studies and EPA and SAP findings is not an option.

B. Scientific Uncertainty is Not a Legally Permissible Reason to Leave Chlorpyrifos Tolerances in Place

The primary justification offered in the Pruitt Order for failing to revoke chlorpyrifos tolerances in the face of its prior findings that chlorpyrifos exposures are unsafe is that the Administrator prefers to engage in further study. 82 Fed. Reg. at 16,590 (“EPA’s preference is to fully explore approaches raised by the SAP and commenters on the proposed rule, and possibly seek additional peer review of EPA’s risk assessment prior to finalizing any regulatory action in the course of registration review.”). The Pruitt Order states that:

EPA has concluded that, despite several years of study, the science addressing neurodevelopmental effects remains unresolved and that further evaluation of the science during the remaining time for completion of registration review is warranted to achieve greater certainty as to whether the potential exists for adverse neurodevelopmental effects to occur from current human exposures to chlorpyrifos. EPA has therefore concluded that it will not complete the human health portion of the registration review or any associated tolerance revocation of chlorpyrifos without first attempting to come to a clearer scientific resolution of those issues.

82 Fed. Reg. at 16,583; see also id. at 16,590 (“the science on this question is not resolved and would likely benefit from further inquiry.”).

1. The Science Underlying EPA’s Findings that Chlorpyrifos is Unsafe is Well-Settled

In putting off action on the 2007 Petition and its proposal to revoke chlorpyrifos tolerances, the Pruitt Order alludes generally to scientific uncertainties, ignoring how much progress has been made in assessing the mounting scientific evidence of neurodevelopmental harm from chlorpyrifos exposures and the weight of the scientific evidence. EPA and the SAP have consistently found that chlorpyrifos causes damage to children’s developing brains and that this damage has resulted from exposures that are far lower than EPA’s regulatory endpoint. The

31

chlorpyrifos tolerances currently in place do not protect against these adverse brain impacts. On this point, assertions of scientific uncertainty ring hollow given the overwhelming scientific evidence and the unbroken EPA and SAP findings.

When EPA convened its SAP in 2008 to review post-re-registration science, the SAP found that prenatal and early postnatal chlorpyrifos exposures can produce long-lasting cognitive and motor impairments. 2008 SAP Report at 11-12. The SAP also found that the exposures associated with this serious harm were below EPA’s regulatory endpoint. Id. at 43-44. In 2012, the SAP again found, based on more extensive scientific review, that chlorpyrifos is associated with abnormal reflexes, mental deficiencies, and attention and behavioral problems from exposures lower than those associated with cholinesterase inhibition, EPA’s regulatory endpoint. 2012 SAP at 17, 19. Even the 2016 SAP, which disagreed with EPA’s first attempt to quantify exposures correlated with such brain damage, agreed that chlorpyrifos harms children’s brains at exposures far below EPA’s regulatory endpoint and that EPA needs to be more protective than its 2014 risk assessment. 2016 SAP 18, 52-53.

EPA’s risk assessments have, since 2011, similarly found correlations between low-level chlorpyrifos exposures and long-lasting harm to children’s brains. The 2011 PHHRA found that chlorpyrifos played a role in causing such neurodevelopmental harm. 2011 PHHRA at 8. The 2014 RHHRA made even stronger findings from multiple lines of evidence that chlorpyrifos results in neurodevelopmental harms to children, such as reduced IQ, delays in mental development, and attention disorders, and that the exposures associated with these brain impairments were too low to produce cholinesterase inhibition. 2014 RHHRA at 41-43, 46.

There may be scientific uncertainty on other issues, but not as to these uncontestable findings. And these findings alone revealed in the 2014 RHHRA that chlorpyrifos is unsafe due to drinking water contamination. Id. at 48-49, 95-96.

Scientific uncertainty remains as to the mode of action by which chlorpyrifos damages children’s brains and the exact dose at which such effects occur. EPA does not need to know the precise mode of action to know that harm is occurring and that the statutory safety standard is being violated. See id. at 48. Nor does EPA need to know the precise dose at which neurodevelopmental harm occurs, given that such harm is occurring at exposures so far below the regulatory endpoint supporting the current chlorpyrifos tolerances that EPA cannot identify a safe exposure level. As explained below, Congress has prescribed how EPA must deal with such uncertainties in protecting the safety of our food supply and preventing harm to children.

2. Congress Directed EPA to Revoke Tolerances if Scientific Uncertainty Precludes Finding the Pesticide Safe.

Congress has established a statutory standard that precludes delaying protection, particularly to children, due to scientific uncertainty when there is evidence of harm. This direction manifests itself in three ways.

First, EPA can “leave in effect a tolerance for a pesticide chemical residue in or on a food only if the Administrator determines that the tolerance is safe.” 21 U.S.C. § 346a(b)(2)(A)(i). An affirmative finding of safety is a prerequisite to establishing or retaining a tolerance. And if EPA determines a pesticide is not safe, “[t]he Administrator shall modify or revoke a tolerance.”

32

Id. (emphasis added). EPA acknowledged the statutory mandates in its proposed revocation rule, stating: “It is important to stress, however, that because the FFDCA is a safety standard, EPA can only retain chlorpyrifos tolerances if it is able to conclude that such tolerances are safe.” 80 Fed Reg. 69,080 (Nov. 6, 2015). Explicitly requiring a safety finding to retain a tolerance reinforces longstanding precedent that places the burden of proof on EPA and industry registrants seeking to retain food tolerances to prove safety. See Envtl. Def. Fund, Inc. v. U.S. Dep’t of Health, Ed. & Welfare, 428 F.2d 1083, 1092 n.27 (D.C. Cir. 1970) (following petition for revocation, burden of establishing the safety of any tolerance is on those seeking to permit a residue).50 EPA is mistaken in asserting in the Pruitt Order that petitioners bear the burden of proving that chlorpyrifos is unsafe. 82 Fed. Reg. at 16,587-88.51 When EPA adhered to the regulatory safety standard and burdens, it proposed to revoke all chlorpyrifos tolerances.

Second, “safe” means that EPA “has determined that there is a reasonable certainty that no harm will result from aggregate exposure to the pesticide chemical residue….” 21 U.S.C. § 346a(b)(2)(A)(ii). Not only must EPA make a safety finding to retain a tolerance, it must find a reasonable certainty of no harm. The fact that chlorpyrifos is associated with serious brain damage at low doses makes it impossible for EPA to find a reasonable certainty of no harm from exposures allowed under the current tolerances.

Third, other FQPA provisions further specify how EPA must deal with scientific uncertainty. The FQPA directs EPA to act on the basis of available information on the special susceptibility of infants and children, including neurological differences between adults and infants and children, and EPA must apply an additional tenfold margin of safety to account for gaps in data or evidence of pre- or post-natal toxicity to children. 21 U.S.C. § 346a(b)(2)(C).

50 The court’s reasoning (id.) applies with even greater force to the FFDCA standard, as amended by the FQPA.

Section 408 of the FDCA authorizes the Secretary of HEW to establish tolerances for pesticide residues on or in raw agricultural commodities ‘to the extent necessary to protect the public health.’ The section also authorizes the setting of a zero tolerance (no residue) level ‘if the scientific data before the Secretary does not justify the establishment of a greater tolerance.’ We need not pause to plumb the obvious ambiguities in this language since both Senate and House Committee Reports make the intended meaning of this section indisputably clear:

‘Before any pesticide-chemical residue may remain in or on a raw agricultural commodity, scientific data must be presented to show that the pesticide-chemical residue is safe from the standpoint of the food consumer. The burden is on the person proposing the tolerance or exemption to establish the safety of such pesticide-chemical residue.’

51 The Pruitt Order states that EPA proposed to revoke all chlorpyrifos tolerances based in part on uncertainty surrounding the correlation between chlorpyrifos exposures and longlasting neurodevelopmental harm. 82 Fed. Reg. at 16,583, 16,590. However, EPA proposed to revoke chlorpyrifos tolerances because it could not find chlorpyrifos safe. To the extent the Pruitt Order is referring to the requirement that EPA be able to find safety in order to retain tolerances, that is what Congress has mandated.

33

Congress specifically directed EPA to act to protect children where scientific evidence shows they are at risk of harm and it will take time to fill in gaps in the data. In 2014, EPA retained the FQPA tenfold safety factor because of gaps in scientific information on the mode of action and exposure levels by which chlorpyrifos causes damage to children’s brains. It recognized, however, that the 2014 risk assessment was under-protective because it continued to use cholinesterase inhibition as the regulatory endpoint, and that brain damage to children has resulted from lower exposure levels. In the face of this evidence, EPA also recognized that it needed to lower its regulatory endpoint or have additional safety factors to protect children’s brains, and the 2016 SAP concurred. 2016 RHHRA at 13-14; 2016 SAP at 18-19. The uncertainties go to the precise exposure level to use or additional safety factors to include in establishing a brain-protective regulatory endpoint. That uncertainty offers no reason to retain tolerances, however. In 2014, even using a poisoning regulatory endpoint that is not protective of children’s brains, EPA found chlorpyrifos unsafe due to drinking water contamination. When it developed a regulatory endpoint that would protect children’s brains, it found chlorpyrifos unsafe every way people are exposed to it with young children exposed to 140 times safe levels in food.52 More study will simply confirm how hazardous and devastating this pesticide can be. Congress decided not to expose children to such risks by precluding EPA from maintaining tolerances when it cannot find a reasonable certainty of no harm from the pesticide.

3. The Pruitt Order Fails to Address Significant Concerns Raised in Comments that EPA’s 2014 Risk Assessment and Proposed Revocation Fail to Protect Children.

The Pruitt Order indicates that EPA decided that the science regarding neurodevelopmental harm from chlorpyrifos remains unresolved and warrants further study before final regulatory action “[f]ollowing a review of comments” on the proposed revocation and 2016 risk assessment. 82 Fed. Reg. at 16,583. While it is typical for EPA to prepare a response to comments as part of a rulemaking, no response to comments document is in the administrative records for the chlorpyrifos registration review or the proposed revocation. Agencies need to “consider and respond to significant comments received during the period for public comment” on proposed rules. Perez v. Mortgage Bankers Ass’n, 135 S. Ct. 1199, 1203 (2015); see also 5 U.S.C. § 553(c) (agency must give consideration to relevant matter, including data and arguments submitted during the comment period on proposed rules). Of particular relevance to this proceeding, when resolving a petition to revoke tolerances and deciding to leave a tolerance in effect, EPA must consider “information available to the Administrator” and specifically information relevant to such statutorily mandated considerations as pre- and post-natal neurotoxicity, children’s exposures, population sensitivities, and gaps in

52 If scientific uncertainties prevent EPA from identifying an acceptable exposure level that will prevent damage to children’s brains, EPA must use additional safety factors due to pre-natal and post-natal neurotoxicity from chlorpyrifos. See Earthjustice, et al., Comments on EPA Proposal to Revoke Chlorpyrifos Tolerances (Jan. 17, 2017) at 2-11; 2016 SAP 18-19.

34

information. 21 U.S.C. § 346a(b)(2)(C)-(D) and § 346a(d)(4)(A); see also Dichlorvos (DDVP); Order Denying NRDC's Objections and Requests for Hearing, 73 Fed. Reg. 42683, 42696 (July 23, 2008) (EPA recognizes its obligation to provide a reasoned explanation for its treatment of significant comments when acting on petitions to revoke tolerances). While EPA has apparently heeded some unspecified and vaguely referenced comments from Dow Agrosciences and others who want to retain chlorpyrifos tolerances, it is silent as to the multiple and extensive comments offering scientific reasons why the 2014 risk assessment and proposed revocation do not protect children and violate governing legal standards. Particularly formidable are the numerous, well-supported comments from scientists, health professionals, and farmworker and health advocates making the case that EPA is failing to protect against the most sensitive health effect — harm to children’s developing brains – because the 2014 risk assessment and proposed revocation use 10% cholinesterase inhibition as the regulatory endpoint.53 If EPA had either lowered its regulatory endpoint or used the traditional and FQPA safety factors to guard against such brain impairments, it would have, as it did in 2016, found unsafe exposures in food, from drift 300 feet or more from the application site, and in drinking water nationwide. 2016 RHHRA at 23-24, 30-33.54 In denying the 2007 Petition, EPA did not disavow its prior findings that chlorpyrifos is unsafe. Nor could it credibly do so in light of the overwhelming scientific evidence correlating low-level chlorpyrifos exposures with damage to children’s developing brains. If EPA were to modify the particular brain-protective endpoint used in the 2016 risk assessment, it would need to ensure that the endpoint selected, possibly coupled with additional safety factors, would produce a risk assessment that protects children from permanent brain damage from chlorpyrifos exposures. The only way EPA can ensure there is reasonable certainty of no harm from chlorpyrifos exposures is to account for the evidence of such harm from exposures far below the regulatory endpoint underpinning the current tolerances.

53 See, e.g., 2015 Farmworker Comments; Comments to EPA from Environmental Health Scientists and Healthcare Professionals in support of EPA’s 2016 Revised Human Health Risk Assessment and the 2015 proposed tolerance revocation for chlorpyrifos (Jan. 17, 2017) (EPA-HQ-OPP-2015-0653-0587); Comments to EPA submitted on behalf of University of California, Davis scientists with the UC Davis Environmental Health Sciences Center and the UC Davis Center for Children’s Environmental Health in support of EPA’s 2016 Revised Human Health Risk Assessment in conjunction with the 2015 proposed rulemaking to revoke tolerances for chlorpyrifos (Jan. 17, 2017) (EPA-HQ-OPP-2015-0653-0640); Comments to EPA from Environmental Health Scientists and Healthcare Professionals in support of EPA’s Proposal to Revoke Chlorpyrifos Food Residue Tolerances (Jan. 5, 2016) (EPA-HQ-OPP-2015-0653-0374); Comment submitted by Harry Wang, Vice-President, Physicians for Social Responsibility/Sacramento (Apr. 30, 2015) (EPA-HQ-OPP-2008-0850-0834). 54 See also Earthjustice, et al., Comments on EPA Proposal to Revoke Chlorpyrifos Tolerances (Jan. 5, 2016) at 8-10 (If EPA had used a 1000X safety factor, it would have found risks of concern to all children from food, even without using an endpoint that reflects the harm to the developing brain, with children 1-2 years old facing the highest risks, more than 2 times EPA’s level of concern.).

35

Public comments raised several other significant issues that EPA would need to address if it persists in leaving chlorpyrifos tolerances in place in response to the 2007 Petition.55 First, the farmworker and health advocate comments disputed EPA’s legal authority to ignore inhalation exposures from chlorpyrifos spraying, which EPA tried to justify because the labels prohibit allowing a pesticide to drift onto people. Chlorpyrifos drift poisons people every year, documenting that the label prohibition is ineffective and greater safeguards are needed to provide reasonable certainty of no harm. 2015 Farmworker Comments at 43-49. Second, while EPA recognized in its 2011 preliminary risk assessment that chlorpyrifos has a propensity to volatilize after application and move large distances as vapor, and that buffers as large as 4000 feet may be necessary to prevent harm from exposures to chlorpyrifos vapors, it ultimately disregarded volatilization exposures based on two rat studies submitted by Dow Agrosciences that purport to show that it is impossible to inhale enough chlorpyrifos to produce an adverse effect. Public comments pointed out that the Dow studies suffer from significant flaws because they fail to address temperature and soil moisture impacts on volatilization, individual variation, a lack of controls to ensure the experiment could detect cholinesterase inhibition, and biomonitoring and incident data showing harmful exposures at distances as large as one-half mile from application sites. 2015 Farmworker Comments at 50-58. Third, the comments submitted California incident data documenting poisonings from chlorpyrifos at far greater distances than the spray drift buffers put in place by the registrants in 2012. These real-life impacts show that reasonable certainty of harm persists. This year on Cinco de Mayo, roughly one dozen farmworkers in Kern County, California, were poisoned and a total of 50 put at risk from spray drift of what has been reported to be chlorpyrifos.56 Local news described how "twelve people reported symptoms of vomiting [and] nausea and one person fainted.” Id. The farmworkers were harvesting cabbage at a farm that does not use chlorpyrifos when drift from a nearby field led workers to complain of “a bad odor, nausea and vomiting.”57 Following the incident, the Kern County Department of Agriculture and Measurement Standards stated that testing was still underway, but confirmed that they are investigating a ground application of chlorpyrifos that took place one-half mile from where the poisoning occurred. Fourth, not only did EPA continue to use poisoning as its regulatory endpoint, it used a model developed by Dow AgroSciences to try to pinpoint the exposures that will produce 10% cholinesterase inhibition in people. Public comments objected to use of the model because, in February 2011, EPA’s Scientific Advisory Panel found numerous flaws in the model, using terms like “very problematic,” “cursory,” “overstated,” “inadequate,” ”inaccurate,” “imprecise,”

55 Objectors incorporate by reference all comments submitted by Objectors under docket numbers EPA-HQ-OPP-2007-1005, EPA-HQ-OPP-2008-0850, and EPA-HQ-OPP-2015-0653. 56 Tom Philpott, Trump's EPA Greenlights a Nasty Chemical. A Month Later, It Poisons a Bunch of Farmworkers., Mother Jones (May 15, 2017, 6:00 AM) http://www.motherjones.com/environment/2017/05/california-farm-workers-just-got-poisoned-nasty-pesticide-greenlghted-trump. 57 Oliver Milman, Pesticide that Trump’s EPA refused to ban blamed for sickening farm workers, The Guardian (May 17, 2017, 7:00 AM), https://www.theguardian.com/environment/2017/may/17/pesticide-trump-ban-california-farm-workers-sick.

36

and “incomplete.” 58 Dow made some changes in the model, but EPA did not obtain another review by its Scientific Advisory Panel. In addition, the model is based on ethically and scientifically deficient studies. Congress has required that human testing must meet minimal ethical and scientific standards before EPA can rely on such tests. An EPA ethics advisor found that the key Dow human study fell short of meeting informed consent requirements, and EPA’s Human Studies Review Board found the study scientifically deficient in two respects that have not been corrected. EPA has since strengthened its regulatory standards governing use of intentional human dosing studies, yet EPA failed to resubmit the study to the Human Studies Review Board. EPA has provided no credible basis for relying on human testing without subjecting it to such scrutiny and without confronting the earlier findings of ethical and scientific shortcomings. 2015 Farmworker Comments at 36-42.

Based on the Dow model, EPA eliminated the inter-species safety factor altogether, and it shrank the intra-species safety factor from 10X to 4X-5X for children, although it retained a 10X for women of childbearing age since the Dow model lacks data reflecting how a pregnant woman’s body processes chlorpyrifos. The result — under the 2014 risk assessment —EPA will allow chlorpyrifos exposures to be an order of magnitude higher for pregnant women and even higher still for children than would be allowed if traditional safety factors had been retained. Comments argued that EPA cannot use Dow’s model to eliminate or reduce the safety factors in light of the neurodevelopmental effects that occur at lower doses than those used in the model. 2015 Farmworker Comments at 28-32. If EPA had heeded these comments and had retained the traditional safety factors, it would have found in 2014 that chlorpyrifos is unsafe on food as well as in drinking water, and that children are at even greater risk from chlorpyrifos drift and workers from handling the pesticide or re-entering fields shortly after chlorpyrifos spraying.

C. Widespread Use of Chlorpyrifos in Agriculture is Legally Irrelevant Because Congress Made Protecting Food Safety and Preventing Neurodevelopmental Harm to Children Paramount.

The Pruitt Order states:

Although not a legal consideration, it is important to recognize that for many decades chlorpyrifos has been and remains one of the most widely used pesticides in the United States, making any decision to retain or remove this pesticide from the market an extremely significant policy choice.

82 Fed. Reg. at 16,590; see also id. at 16,584 (“chlorpyrifos is currently the only cost-effective choice for control of certain insect pests.”). The Pruitt Order then cites the significance of the decision as a reason for further study of the risks before taking final regulatory action. Id. EPA issued a press release on the Pruitt Order noting that chlorpyrifos is “one of the most widely used pesticides in the world” and quoting EPA Administrator Scott Pruitt as saying, “We need to provide regulatory certainty to the thousands of American farms that rely on

58 Meeting minutes, report, and background material is available in Docket EPA-HQ-OPP-2010-0588 and on the SAP meetings website at: http://www.epa.gov/scipoly/sap/meetings/2011/021511meeting.html.

37

chlorpyrifos.” The EPA press release included a statement from Sheryl Kunickis, director of the Office of Pest Management Policy at the U.S. Department of Agriculture (“USDA”), endorsing the Pruitt Order because it “frees American farmers from significant trade disruptions that could have been caused by an unnecessary, unilateral revocation of chlorpyrifos tolerances in the United States.”59 EPA released another press statement on April 5, 2017, compiling statements from USDA and various agricultural associations praising EPA’s decision not to ban chlorpyrifos.60 As the Pruitt Order acknowledges, however, EPA must make food tolerance decisions based on safety and in particular whether EPA can find that there is a reasonable certainty of no harm from the pesticide. Congress decided long ago that the safety of our food cannot be sacrificed, and in 1996, it expanded that mandate to aggregate exposures to a pesticide in food, drinking water, and pesticide drift. EPA cannot leave tolerances in place in the absence of a finding of safety, no matter how widely used the pesticide is.61 Indeed, widespread use of chlorpyrifos cuts the other way because its use exposes children and communities throughout the country to poisoning and brain damage risks, making the Administrator’s decision to delay protections even more egregious.

D. The Deadline for Completing Registration Review for All Older Pesticides is Not A License to Maintain Tolerances for Pesticides That are Unsafe

As a final reason for denying the 2007 Petition and leaving chlorpyrifos tolerances in place, EPA claims the right to re-order the priorities that had been set by previous administrations. It asserts that it can put off deciding whether to revoke chlorpyrifos tolerances for years as long as it does so before October 1, 2022, the deadline for completing registration review of all older pesticides. 82 Fed. Reg. 16,581, 16,590 (April 5, 2017); see 7 U.S.C. § 136a (g)(1)(A)(iii)(I) (registration review deadline). This position is indefensible because it ignores other legal mandates and the scientific evidence that precludes the safety finding that is necessary to leave chlorpyrifos tolerances in place.

59 Press Release, U.S. EPA, EPA Administrator Pruitt Denies Petition to Ban Widely Used Pesticide (Mar. 29, 2017), https://www.epa.gov/newsreleases/epa-administrator-pruitt-denies-petition-ban-widely-used-pesticide-0. 60 Press Release, U.S. EPA, Agriculture Community Reacts to Recent EPA Action (Apr. 5, 2017), https://www.epa.gov/newsreleases/agriculture-community-reacts-recent-epa-action. 61 Chlorpyrifos usage has declined over time, as many farmers have shifted to less toxic alternatives, even before EPA’s proposal to revoke chlorpyrifos tolerances. Annual agricultural pesticide use data compiled by the U.S. Geological Survey’s Pesticide National Synthesis Project show that, since the mid-1990s, chlorpyrifos use has declined. https://water.usgs.gov/nawqa/pnsp/usage/maps/show_map.php year=2014&map=CHLORPYRIFOS&hilo=L&disp=Chlorpyrifos. Additionally, in California, the combined use of chlorpyrifos in alfalfa, almonds, citrus, and cotton decreased from 2006 -2012. While overall use increased in 2013 and 2014, it remained below the amount used in 2006. “Identifying and Managing Critical Uses of Chlorpyrifos Against Key Pests of Alfalfa, Almonds, Citrus and Cotton” (UC IPM report for CA DPR), August 31, 2016 at 3.

38

Under the FFDCA, any person may file a petition to revoke tolerances. 21 U.S.C. § 346a(d)(1). The Administrator must give the petition due consideration and issue either a proposed or final regulation to revoke the tolerances or an order denying the petition. Id. § 346a(d)(4)(A). While the FFDCA does not establish a specific deadline for acting on petitions to revoke tolerances, the Administrative Procedure Act requires that federal agencies respond to petitions “within a reasonable time.” 5 U.S.C. § 555(b). In 2015, the Ninth Circuit held that EPA’s delay in responding to the 2007 Petition was unreasonable and “egregious” and set a timeline for EPA to respond. In re Pesticide Action Network North America v. EPA, 798 F.3d 809, 811 (9th Cir. 2015). In 2016, the court reiterated its concerns over any further delay, stating that any “claim of premature rulemaking has come and gone.” In re PANNA, No. 14-72794, Order (9th Cir. Aug. 12, 2016). The fact that Congress established an October 1, 2022, deadline for EPA to complete registration review of all older pesticides is no license for EPA to continue to exacerbate its unreasonable delay in acting on the 2007 Petition seeking revocation of chlorpyrifos tolerances. First, the registration review provision states that: “Nothing in this subsection shall prohibit the Administrator from undertaking any other review of a pesticide . . .” 7 U.S.C. § 136a(g)(1)(C). This clause prohibits EPA from relying on the registration review deadline to forestall other legally required or scientifically compelled regulatory action. Second, it is FIFRA, not the FFDCA, that establishes the registration review process. While registration review will include an assessment of food and drinking water risks and determine whether food tolerances may be retained or must be revoked, registration review is far broader in scope than the issues arising under the FFDCA. It will examine all uses of a pesticide, not only food uses, and risks to wildlife, waterbodies, and workers in addition to food and drinking water. In addition, FFDCA tolerance determinations must be made solely on the basis of safety, while nonfood use decisions under FIFRA are based on a balancing of risks and benefits. Compare 21 U.S.C. § 346a(b)(2)(A)(i) & (ii) (FFDCA standard and determination of safety), with 7 U.S.C. § 136(bb) (FIFRA definition of “unreasonable adverse effects on the environment”). Even where EPA accelerates food safety determinations, as it had done for chlorpyrifos, other FIFRA assessments and decisions lie ahead and remain subject to the 2022 registration review deadline. EPA’s review of chlorpyrifos has proceeded to a point of no return. The agency developed methods for addressing spray drift, volatilization, and epidemiology studies, and released human health risk assessments that document unsafe exposures from chlorpyrifos. EPA made findings that chlorpyrifos is unsafe in 2014 directed at drinking water contamination, see, e.g., 80 Fed. Reg. 69,080, and expanded those findings in November 2016 to every way people are exposed to chlorpyrifos. 81 Fed. Reg. at 81,050. The law is clear. EPA can leave food tolerances in place only if it can find the pesticide safe. Because EPA has found chlorpyrifos to be unsafe, it lacks the authority to retain the food tolerances. It cannot lawfully issue an order denying the 2007 Petition, but instead must comply with the FFDCA mandate to revoke tolerances for this unsafe pesticide. In claiming the authority to postpone revoking chlorpyrifos tolerances despite its own scientific findings, EPA cites the prerogative of a new presidential administration to make policy choices that differ from its predecessor, citing Fed. Commc’n Comm’n v. Fox Television

39

Stations, 556 U.S. 502 (2009). 82 Fed. Reg. at 16,589. Fox Television, however, requires agencies to provide a reasoned explanation that comports with Motor Vehicles Mfrs. Ass’n v. State Farm Mut. Automobile Ins. Co., 463 U.S. 43 (1983), and to address prior factual findings and circumstances that underlay the earlier agency decision. 556 U.S. at 515-16. EPA provided no such explanation, and it has not disavowed its previous findings that chlorpyrifos is unsafe. Nor could it given the extensive scientific record documenting the damage chlorpyrifos causes to children’s brains at low-level exposures. Whatever leeway a new administration has to make its own policy choices does not extend to factual determinations, like EPA’s findings that chlorpyrifos is unsafe. Nor does that latitude allow the new administration to break the law by leaving tolerances in place in the face of findings of such serious harm to children.

CONCLUSION

For these reasons, EPA must reverse the Pruitt Order and revoke all chlorpyrifos tolerances. This misguided Order and the delay it has spurred threaten to expose countless children and communities to chlorpyrifos well into the future. People will needlessly suffer from poisonings from chlorpyrifos drift. Parents will watch their children struggle with attention disorders and impaired brain functioning that hinders their ability to learn and play, and the children will experience lifelong deficits that make it harder for them to achieve their full potential and dreams. Prolonging revocation of chlorpyrifos tolerances, as required by the law and science, is not only unlawful, but also callous and heartless. EPA should rule on these objections within 60 days and expedite revocation of all chlorpyrifos tolerance.

Submitted by:

Patti A. Goldman Marisa C. Ordonia Kristen L. Boyles Earthjustice 705 Second Avenue, Suite 203 Seattle, Washington 98104 (206) 343-7340 [email protected] [email protected] [email protected]

On behalf of: Kristin Schafer Executive Director Pesticide Action Network 1611 Telegraph Ave, Suite 1200 Oakland, CA 94612

Erik D. Olson Director, Health & Environment Program Natural Resources Defense Council 111 Sutter Street, 21st floor San Francisco, CA 94104

mailto:[email protected]

40

Anne Katten Pesticide and Work Safety Project Director California Rural Legal Assistance Foundation 2210 K Street, Suite 201 Sacramento, CA 95816

Hector E. Sanchez Executive Director Labor Council for Latin American Advancement 815 16th Street, NW, 3rd Floor Washington, DC 20006

Patricia M. Lillie President Learning Disabilities Association of America 4156 Library Road Pittsburgh, PA 15234

/s/ Erik Nicholson Erik Nicholson, National Vice President United Farm Workers 29700 Woodford-Tehachapi Road P.O. Box 62 Keene, CA 93531

/s/ Ramon Ramirez Ramon Ramirez, President Pineros y Campesinos Unidos del Noroeste 300 Young St. Woodburn, OR 97071

/s/ Virginia Ruiz Virginia Ruiz Director of Occp’l & Environmental Health Farmworker Justice 1126 16th St NW # 270 Washington, DC 20036

/s/ Brent Wilkes Brent Wilkes, Executive Director League of United Latin American Citizens 1133 19th Street, NW, Suite 1000 Washington, DC 20036

/s/ Jeannie Economos Jeannie Economos Pesticide Safety and Environmental Health Project Coordinator Farmworker Association of Florida 1264 Apopka Boulevard Apopka, FL 32703

/s/ Elena Rios Elena Rios, MD, MSPH, President National Hispanic Medical Association 1920 L St NW #725 Washington, DC 20036

/s/ Mark Magana Mark Magana, President and CEO GreenLatinos 801 Pennsylvania Avenue NW, Suite 1010 Washington, DC 20036

Exhibit 1

1

DECLARATION OF PHILIP J. LANDRIGAN, M.D., M.SC. IN SUPPORT OF

PETITION TO SUSPEND AND CANCEL CHLORPYRIFOS USES

I, Philip J. Landrigan, M.D., M.Sc., hereby declare and state as follows:

1. I submit this declaration in support of the petition to cancel and suspend

chlorpyrifos uses that is being submitted by Earthjustice on behalf of United Farm Workers and

other farmworker advocates.

PROFESSIONAL BACKGROUND AND EXPERTISE

2. I am a pediatrician and epidemiologist, and I am board certified in occupational

medicine, general preventive medicine and pediatrics. I have been a member of the faculty of

the Icahn School of Medicine at Mount Sinai since 1985 and am currently a professor of

preventive medicine and a professor of pediatrics. I am also the Dean for Global Health, a

position I have held since 2010.

3. I obtained my medical degree from Harvard Medical School in 1967. I completed

an internship at Cleveland Metropolitan General Hospital and a residency in pediatrics at Boston

Children's Hospital. In 1977, I received a Diploma of Industrial Health from the University of

London and a Master of Science degree in Occupational Medicine from the London School of

Hygiene and Tropical Medicine. My CV is attached as Exhibit 1.

4. I served for 15 years as an Epidemic Intelligence Service Officer and medical

epidemiologist at the Centers for Disease Control and Prevention (CDC) and the National

Institute for Occupational Safety and Health (NIOSH). I directed the national program in

occupational epidemiology for NIOSH from 1979-1985. I have been awarded numerous honors

throughout my career, including the Meritorious Service Medal of the U.S. Public Health Service

in 1985.

2

5. From 2000 to 2002, I served on the Armed Forces Epidemiological Board, and

from 1996 to 2005, in the Medical Corps of the U.S. Naval Reserve. I retired from the United

States Navy in 2005 at the rank of Captain (O-6) and continue to serve as Surgeon General of the

New York Naval Militia, the naval component of the New York National Guard.

6. I was elected a member of the Institute of Medicine of the National Academy of

Sciences in 1987. I have chaired committees at the National Academy of Sciences (NAS) on

Environmental Neurotoxicology and on Pesticides in the Diets of Infants and Children. From

1997 to 1998, I served as Senior Advisor on Children's Health to the Administrator of the U.S.

Environmental Protection Agency (EPA) and was instrumental in helping to establish a new

Office of Children's Health Protection at EPA.

7. I am editor in chief of the Annals of Global Health, deputy editor of the American

Journal of Industrial Medicine, and an associate editor of Environmental Health Perspectives.

8. I have studied the impacts of toxic chemicals, including pesticides, on children’s

health for over thirty years. I have published more than 500 scientific papers and five books, on

subjects including epidemiology, occupational health, environmental neurotoxicity, and

children’s health. I have extensive knowledge and expertise in environmental and occupational

medicine, epidemiology, environmental neurotoxicity, and the effects of pesticides and other

chemicals on children through my education, training, professional experience, involvement in

applicable peer-reviewed research, and my ongoing review of the pertinent medical and

scientific literature.

CHILDREN’S VULNERABILITY TO PESTICIDES

9. A key policy breakthrough occurred over the past three decades with the

discovery that children are far more sensitive than adults to toxic chemicals in the environment.

3

This finding led to the recognition that chemical exposures early in life are significant yet

preventable causes of disease in children and adults.

10. In the 1970s, my research showed that 60% of children living within one mile of

ASARCO's El Paso smelting plant had elevated blood lead levels and that even small amounts of

lead exposure lowered a child's IQ. My research showed that lead can cause brain damage to

children at levels too low to clinically detect signs and symptoms. This phenomenon is now

called “subclinical toxicity.” These studies contributed importantly to the U.S. federal

government’s decision to phase out lead components from gasoline and regulate the lead content

of paint in the 1970s.

11. I led a five-year study as chair of the NAS Committee that published Pesticides in

the Diets of Infants and Children in 1993.1 This pivotal study showed that infants and children,

including infants in the womb, are much more sensitive to pesticides and other toxic chemicals

than adults and documented four differences between children and adults that contribute to

children’s heightened susceptibility to chemicals in the environment. The following description

of this work is taken from an article that I co-authored with Dr. Lynn R. Goldman, “Children’s

Vulnerability to Toxic Chemicals: A Challenge and Opportunity to Strengthen Health and

Environmental Policy,” Health Affairs 30, no.5 (2011): 842-850 (Exhibit 2):

First, children have greater exposures to toxic chemicals for their body weight than

adults. A six-month-old infant drinks seven times more water per pound than an adult,

and children take in three to four times more calories per pound than adults. The air

intake per pound of an infant is twice that of an adult. These differences result in

children being disproportionately exposed to toxic chemicals in air, food, and water.

Children’s hand-to-mouth behavior and play on the ground further magnify their

exposures.

1 National Research Council. Pesticides in the Diets of Infants and Children. Washington, DC:

National Academy Press, 1993.

4

Second, children’s metabolic pathways are immature, and a child’s ability to metabolize

toxic chemicals is different from an adult’s. In some instances, infants are at lower risk

than adults because they cannot convert chemicals to their toxic forms. More commonly,

however, children are more vulnerable because they lack the enzymes needed to break

down and remove toxic chemicals from the body.

Third, children’s early developmental processes are easily disrupted. Rapid, complex,

and highly choreographed development takes place in prenatal life and in the first years

after birth, continuing more slowly throughout childhood into puberty. In the brain, for

example, billions of cells must form, move to their assigned positions, and establish

trillions of precise interconnections. Likewise, development of the reproductive organs is

guided by a complex and precisely timed sequence of chemical messages and is shaped

by maternal and fetal hormones.

Recent research in pediatrics and developmental toxicology has elaborated the concept of

“windows of vulnerability.” These are critical periods in early development when

exposures to even minute doses of toxic chemicals—levels that would have no adverse

effect on an adult—can disrupt organ formation and cause lifelong functional

impairments. . . .These windows of vulnerability have no equivalent in adult life.

Fourth, children have more time than adults to develop chronic diseases. Many diseases

triggered by toxic chemicals, such as cancer and neurodegenerative diseases, are now

understood to evolve through multistage, multiyear processes that may be initiated by

exposures in infancy.

12. Since the 1993 publication of the NAS report, peer-reviewed research continues

to document the developing human brain’s unique vulnerability to toxic chemical exposures, and

to confirm that major windows of developmental vulnerability occur in utero, during infancy,

and in early childhood. During these sensitive life stages, exposure to pesticides and other

chemicals can cause permanent brain injury at levels of exposure far below those which would

have an effect in adults.

13. A fetus in the womb is at risk of exposure to pesticides and other toxic chemicals

because of both exposure and vulnerabilities. In terms of exposure, the placenta does not block

the passage of many toxic chemicals from the maternal to the fetal circulation. In fact, more than

200 chemicals have been detected in infants’ umbilical cord blood, meaning they have passed

from the mother’s circulation to the baby’s circulation prior to birth. In terms of susceptibility,

5

several prenatal developmental processes have been shown to enhance the vulnerability of the

fetus in the womb to toxic chemicals.

14. Prior to the publication of the NAS report, virtually all environmental policy in

the United States had focused on assessment of risk to the average adult man weighing 150

pounds. Little attention was paid to the unique risks faced by infants, children, or other

vulnerable groups within the population.

15. The core findings and recommendations of the NAS report were incorporated into

the 1996 Food Quality Protection Act (FQPA), which revamped federal pesticide laws. The

FQPA changed risk assessment by requiring the use of child-protective safety factors to account

for children’s exposures and unique susceptibilities and to account also for gaps in data, and by

requiring consideration of aggregate exposures to a pesticide via multiple routes, including diet,

drinking water, and interaction with pesticide residues through play and other activities. It also

required evaluation of cumulative effects of multiple pesticides that have the same mechanism of

toxicity.

16. Implementation of the new standards led to bans on residential applications of two

very widely used organophosphate insecticides: chlorpyrifos and diazinon. These bans were

triggered by recognition of these compounds’ neurodevelopmental toxicity to children and

documentation of their long residence time in indoor environments. FQPA implementation also

led to a cumulative risk assessment for all organophosphates because they have a common

mechanism of toxicity, as discussed below.

NEURODEVELOPMENTAL HARM TO CHILDREN’S BRAINS FROM CHLORPYRIFOS

AND OTHER ORGANOPHOSPHATES

17. Chlorpyrifos, like other organophosphate pesticides (OPs), causes acute

poisonings by inhibiting the enzyme acetylcholinesterase (AChE), which regulates nerve

6

impulses. When cholinesterase is inhibited, it leads rapidly to overt symptoms of cholinergic

hyperstimulation. The symptoms include nausea, headaches, skin rashes, eye irritation,

vomiting, dizziness, seizures, coma, and death, depending on the dose and the toxicity of the

product. When EPA conducted risk assessments on the organophosphates in the 1990s through

2006, it set human exposure limits based on detection of AChE inhibition. Specifically, it uses

10% red-blood cell AChE inhibition as its regulatory endpoint, called its point of departure.

18. A growing body of scientific evidence has documented neurodevelopmental harm

to the developing brain from organophosphates, including chlorpyrifos. This evidence comes

both from animal and epidemiology studies. EPA has compiled and reviewed the published

studies in its Revised Human Health Risk Assessment for Chlorpyrifos Registration Review

(Dec. 29, 2014) (RHHRA), and in its Literature Review on Neurodevelopmental Effects &

FQPA Safety Factor Determination for the Organophosphate Pesticides (Sept. 15, 2015).

19. Numerous scientific studies have documented neurodevelopmental harm from

prenatal and early postnatal exposures to chlorpyrifos. Animal studies have found disruption in

neuronal development, neurotransmitter systems and synaptic function, as well as behavioral and

cognitive impairments following low-dose perinatal chlorpyrifos exposure. Neurobehavioral

effects include impairment on maze performance, locomotion, and balance in neonates exposed

in utero or during postnatal life.

20. Direct evidence that chlorpyrifos can cause neurodevelopmental harm to

children’s brains comes from three epidemiology studies conducted respectively at Columbia

University, University of California-Berkeley, and Mount Sinai School of Medicine. These

universities conducted this research through their Centers for Children’s Environmental Health

and Disease Prevention Research.

7

21. These Centers are part of an NIH-funded, competitively awarded national

network of such Centers established to increase scientific understanding of the impacts of toxic

exposures on children. The Berkeley study studied children of farmworkers in the Salinas

Valley of California, the Mount Sinai study observed a New York City Hispanic population

whose exposures were primarily residential, and the Columbia study examined African-

American and Dominican children in New York City, whose exposures were similarly

residential.

22. These three Centers have been conducting long-term birth-cohort studies in which

pregnant women are enrolled during their pregnancies. Their environmental exposures during

pregnancy are recorded through objective measures like blood and urine samples, dust and air

samples, and cord blood. Chlorpyrifos exposure during pregnancy was measured through

analysis of chlorpyrifos’ metabolic breakdown products in maternal urine samples. Even though

these three studies were conducted in distinct geographic regions of the country, on different

populations, with different routes of exposure, and using different biomarkers, they produced

strongly convergent results. All studies found cognitive impairments that persist into school

years from OP exposures. The Columbia study was specific to chlorpyrifos. It found that

prenatal exposure to chlorpyrifos resulted in the birth of babies with reduced head circumference.

Reduction in head circumference at birth is a measure of delayed or reduced brain growth during

pregnancy and is an effect seen also in infants exposed in the womb to Zika virus. In the

Columbia study, the degree of reduction in head circumference was proportional to the degree of

maternal exposure to chlorpyrifos during pregnancy. The impact of chlorpyrifos on head

circumference was no longer observed after the ban on residential application of chlorpyrifos

was imposed.

8

23. Follow-up studies of the babies in these three studies have found that prenatal

exposures have persistent deleterious effects on cognitive function through 7 years of age. The

brain impairments observed in these infants and children include reduction in motor function,

decreases in working and visual memory, processing speed, verbal comprehension, perceptual

reasoning, and diminished IQ. The studies also documented neurobehavioral problems,

including increased risk of attention deficit hyperactivity disorder, pervasive developmental

disorder, and behaviors typical of the autism spectrum. Certain subpopulations demonstrate

greater susceptibility, including children of farmworkers and those who have reduced capacity to

detoxify OPs. Some studies found elevated risks of respiratory symptoms consistent with

asthma. And recently, a study using magnetic resonance imaging found that even low to

moderate levels of prenatal exposure to chlorpyrifos may lead to long-term, potentially

irreversible changes in the structure of the developing brain, causing thinning of the cerebral

cortex.

24. These studies found damage to children’s brains from exposures to chlorpyrifos

that produced no or less than 1% red-blood cell cholinesterase inhibition. In other words, the

harm to the developing brain and nervous systems occurred at exposures substantially below

EPA’s regulatory limit, which is based on exposures that are high enough to inhibit

cholinesterase in adults. EPA acknowledged in its 2014 revised human health risk assessment on

chlorpyrifos that the neurodevelopmental harm to children’s brains occurred at lower doses than

its regulatory endpoint.

EPA’S RISK ASSESSMENTS DO NOT PROTECT AGAINST BRAIN DAMAGE TO

CHILDREN

25. Even though EPA has acknowledged that neurodevelopmental harm to children

occurs at exposures that produce no or only minimal cholinesterase inhibition, EPA has

9

continued to set its exposure limits based on cholinesterase inhibition. It continues to use 10%

red-blood cell cholinesterase inhibition as the endpoint in its risk assessments, even though the

mothers in the Columbia study who gave birth to infants with brain injury exhibited less than 1%

cholinesterase inhibition or no inhibition at all.

26. Safety factors are used in risk assessment and standard-setting to account for

uncertainties. In setting a standard or tolerance for a pesticide, EPA will begin the risk

assessment by identifying an exposure level that produces no adverse effect as its endpoint. This

is called the no observable adverse effect level. If some adverse effects are observed at that

exposure level, EPA will add a three-fold safety factor. EPA then typically uses a tenfold safety

factor to account for uncertainties in extrapolating from animal studies to people, and a second

tenfold safety factor to account for differences among human populations due to such factors as

genetic predisposition and other stressors. Finally, the FQPA requires EPA to use a third tenfold

“child-protective” safety factor when there is either evidence that children are especially

vulnerable to a chemical or when there are gaps in data concerning children’s exposures or

vulnerabilities. For OPs, EPA has retained a 10X child-protective FQPA safety factor because of

the published evidence that these chemicals cause neurodevelopmental harm to infants and

children.

27. For chlorpyrifos, however, EPA departed from this usual practice and instead

relied on the Dow Agrosciences Company’s pharmacokinetic-pharmacodynamic (PBPK) model

of OP toxicity, which tries to pinpoint the exposures that will produce 10% cholinesterase

inhibition. The Dow model is drawn largely from human studies that included deliberate dosing

of people. Many of these studies were conducted in countries outside of the United States. Use

of human studies in risk assessment poses significant ethical and scientific issues, and the Dow

10

human studies have been criticized for not meeting the informed consent standards that would be

required in the US and also for scientific deficiencies. Because the Dow model uses human data,

it obviates the need to extrapolate data from animals to humans. In relying on the Dow data, EPA

therefore dispensed with the 10X inter-species safety factor for all populations except for women

of child-bearing years. For women of child-bearing years, EPA retained the 10X intra-species

safety factor because Dow did not have human data for this population.

EPA’S RISK ASSESSMENTS DO NOT PROTECT WORKERS OCUPATIONALLY

EXPOSED TO CHLORPYRIFOS AND DO NOT PROTECT THE CHILDREN IN THE

WOMB OF PREGNANT WOMEN WORKERS

28. In their assessments of risk from occupational exposures to chlorpyrifos, EPA

identified risks of concern for over half of the handler exposure scenarios. EPA states that

additional engineering controls or protective gear could eliminate the risks of concern for 27 of

these activities, but notes that 126 would remain of concern regardless of the level of personal

protective equipment or environmental controls. EPA also found that protection of agricultural

field workers against chlorpyrifos toxicity would need longer re-entry intervals to reduce risks.

29. For many of the handler exposure scenarios, EPA found Margins of Exposure

(MOEs) of less than 10 and for some scenarios the MOEs were close to or even less than 1. In

other words, EPA estimates that worker exposures from these activities likely would result in

10% cholinesterase inhibition. In these scenarios, the current EPA standard manifestly fails to

protect worker health or to comply with the fundamental intent of the Occupational Safety &

Health Act of 1970 (OSHA) which states that every worker has the “right to a safe and healthful

workplace.”

30. EPA has acknowledged that its regulatory end point is underprotective. It has

proposed using umbilical cord blood chlorpyrifos levels from the Columbia study to develop a

more protective end point based on loss of working memory. It convened a Scientific Advisory

11

Panel (SAP) to review this proposal. The SAP did not support developing a point of departure

based on a single study, but it did agree that EPA’s approach of using 10% cholinesterase

inhibition as the regulatory endpoint was underprotective.

31. The California Department of Pesticide Regulation (DPR) prepared its own risk

assessment of chlorpyrifos which was modeled on EPA’s approach and like EPA incorporated

10% cholinesterase inhibition, Dow’s PBPK model, and the reduced safety factors. California’s

Office of Environmental Health Hazard Assessment (OEHHA), which routinely reviews

pesticide standards proposed by DPR to ensure that they protect worker health, conducted a

scientific peer review of DPR’s human health risk assessments on chlorpyrifos and released its

review in June 2016. OEHHA found that the 10% cholinesterase inhibition end point and the

reduced safety factors proposed by the DPR failed to adequately protect human health and

therefore failed to comply with occupational safety and health legislation. OEHHA

recommended using a total uncertainty factor of 1000X or 3000X to protect the health of

workers occupationally exposed to chlorpyrifos.

32. Any occupational exposure standard for chlorpyrifos needs to take cognizance of

the fact that the workforce may include pregnant women workers (who may not yet realize that

they are pregnant) and that pregnant women workers who are occupationally exposed to

chlorpyrifos will unwittingly pass any chlorpyrifos that they absorb into the bodies of their

unborn children where the chlorpyrifos will cause irreversible brain damage. To prevent this

sequence of events, EPA should at a minimum use safety factors that total 1000X. Moreover, an

additional 3X uncertainty factor is warranted over and above the 1000X safety factor because

10% cholinesterase inhibition cannot be considered a “no observable adverse effect level” in

12

light of the finding that neurodevelopmental harm to the fetus can result at exposure levels below

this outdated limit value.

PREVENTING BRAIN DAMAGE TO CHILDREN FROM TOXIC CHEMICAL

EXPOSURES YIELDS SIGNIFICANT COST SAVINGS

33. Neurobehavioral development disorders affect 10-15% of births in the United

States, and the prevalence of attention deficit hyperactivity disorder, autism and other

neurodevelopmental disorders is increasing in the US and worldwide. Subclinical decrements in

brain function are even more common. All of these disabilities can have serious consequences

for individuals, such as diminished quality of life, reduced academic achievement, behavioral

disruptions, and they also have consequences for society in the form of the diminished economic

productivity of affected children and the increased risk that these children will grow up to

become unemployed, underemployed and institutionalized or incarcerated adults. Environmental

exposures play a role in many, if not most, of these developmental disorders as genetic factors

account for only approximately 30-40% of them.

34. Preventing exposures to chemicals can yield great economic savings. While it is

difficult to precisely quantify the harm from neurodevelopmental disorders and the cost savings

that result from their prevention, several studies suggest that both are quite large. To estimate

the contribution of environmental pollutants to the prevalence and costs of disease in American

children, investigators at Mount Sinai School of Medicine examined four categories of illness:

lead poisoning, asthma, cancer, and neurobehavioral disorders. Based on prevalence, the

environmentally attributable fraction of each disease, and national economic data, they

calculated that the total annual costs of these diseases attributable to environmental exposures is

$54.9 billion (range $48.8 billion to $64.8 billion): $43.4 billion for lead poisoning, $2.0 billion

for asthma, $0.3 billion for childhood cancer, and $9.2 billion for neurobehavioral disorders.

13

Because of the difficulties inherent in assessing the full economic consequences of

neurobehavioral impairments, it is likely that these estimates are low.

35. After the phase-out of lead in gasoline from 1976 and 1990, the mean blood lead

level of American children decreased by more than 90% (to below 2 micrograms per deciliter

today), and the incidence of childhood lead poisoning also fell by more than 90%. A further

consequence of the reduction in exposure to lead was that the mean IQ of American children has

increased. Children born in the United States today are estimated to have IQ scores that, on

average, are 2.2–4.7 points higher than those of children born in the early 1970s. And because

each 1-point gain in population mean IQ is associated with an estimated 2% increase in

productivity over a lifetime, the gain in population IQ is estimated to have produced a national

economic benefit of $110–$319 billion in each annual cohort of babies born in the United States

since the 1980s.

36. Dr. David Bellinger, a professor of neurology at Harvard Medical School,

published a paper in 2012, which estimated that Americans have collectively forfeited 41 million

IQ points as a result of exposure to lead, mercury, and OPs. He calculated a total loss of 16.9

million IQ points due to exposure to OPs.2

EPA’S APPROACH TO WORKER RISK MITIGATION IS UNDERPROTECTIVE AND AT

ODDS WITH STANDARD OCCUPATIONAL HEALTH PRACTICE

37. When EPA identifies a risk of concern, it explores as a first priority whether use

of personal protective equipment will eliminate the risk. If personal protective equipment is

found not to be protective, EPA then asks whether engineering controls or administrative

controls such as restricted re-entry intervals will eliminate the risk. Only if the risk of concern

2 D.C. Bellinger, “A Strategy for Comparing Contributions of Environmental Chemicals and

Other Risk Factors to Neurodevelopment of Children,” Environmental Health Perspectives, Vol.

120, No. 4, pp.501-507 (April 2012).

14

remains after implementation of all such mitigation does EPA explore eliminating the exposure

or shifting to less harmful alternative chemicals or application methods.

38. EPA’s approach is backwards and wrong. It violates standard, long-established

occupational health practice. It fails to protect worker health.

39. In the field of occupational safety and health, regulators adhere to a hierarchy of

controls that prioritizes prevention of exposure – not use of personal protection. Regulators start

by asking whether the exposure can be eliminated altogether or whether other less toxic

chemicals can be substituted. If those approaches are found not to be feasible, the regulator will

look to engineering controls such as machine-guarding or administrative controls such as longer

re-entry times to sprayed fields. The regulator will turn to personal protective equipment only as

a last resort, because personal protective equipment has been shown repeatedly over the decades

to be far less effective at worker protection than product substitution, engineering controls and

administrative controls. A final reason for not relying on personal protective equipment is that

such equipment degrades workers’ ability to function and increases risk of heat stress and heat

stroke. Thus double-layers of clothing, gloves, and respirators likely impede mobility and

contribute to heat and respiratory stress of pesticide handlers working in hot temperatures during

summer growing seasons.

40. OSHA has adhered to this prioritization for decades. The lead standard is

illustrative. EPA refused to rely on personal protective equipment, and on respirators in

particular, because they fail to eliminate exposure, provides inadequate protection, and creates

additional hazards by interfering with vision and mobility. The 1978 lead standard is replete

with findings that respirators afford inadequate protection. OSHA required respirators in

15

addition to engineering controls to afford workers additional protection during the time it would

take to fully implement the controls. 43 Fed. Reg. 52,952 (Nov. 14, 1978).

41. For decades, EPA has adopted a wrong-headed strategy for mitigating worker

exposures to chlorpyrifos and other toxic pesticides that relies first and foremost on personal

protective equipment. By relying on this inadequate strategy and by relying on personal

protective equipment that has been shown to confer highly inadequate protection, EPA has

allowed workers to be exposed to harmful levels of chlorpyrifos. By relying on this ineffective

strategy, EPA has allowed pregnant women workers to be occupationally exposed to levels of

chlorpyrifos that can result in fetal brain damage to infants in the womb. Sound occupational

health principles require engineering or administrative controls, where effective, or elimination

of the exposure, where engineering or administrative controls are not effective.

I declare under penalty of perjury that the foregoing is true and correct.

Executed on this 7th day of September 2016, in New York, New York.

________________________________________

Philip J. Landrigan, M.D., M.Sc.

1

August 2016

CURRICULUM VITAE Philip J. Landrigan, M.D., M.Sc., D.I.H., F.A.A.P., F.A.C.P.M.

ACADEMIC APPOINTMENTS Current: Icahn School of Medicine at Mount Sinai, Dean for Global Health, 2010-Present Icahn School of Medicine at Mount Sinai, Professor, Department of Preventive Medicine, 1990-Present Icahn School of Medicine at Mount Sinai, Professor of Pediatrics, 1985-Present Previous: Icahn School of Medicine at Mount Sinai, Ethel H. Wise Professor and Chairman,

Department of Preventive Medicine, 1990-2015. Icahn School of Medicine at Mount Sinai, Director, Division of Environmental and Occupational Medicine, Department of Community and Preventive Medicine, 1985-1990. U.S. Environmental Protection Agency, Senior Advisor to the Administrator on Children's Health and the Environment, 1997-1998. (Sabbatical position) National Institute for Occupational Safety and Health, Director, Division of Surveillance, Hazard Evaluations and Field Studies, 1979-1985. Centers for Disease Control and Prevention

Chief, Environmental Hazards Activity, Bureau of Epidemiology, 1974-1979. Director, Research and Development, Bureau of Smallpox Eradication, 1973-1974. Epidemic Intelligence Service (EIS) Officer, 1970-1973.

Adjunct Positions:

Harvard School of Public Health, Adjunct Professor of Environmental Health, 2010-present; Visiting Lecturer on Occupational Health, 1981-2010

Harvard Medical School, Clinical Instructor in Pediatrics, 1969-1970; Visiting Lecturer on Preventive Medicine and Clinical Epidemiology, 1982-Present

University of Washington School of Public Health and Community Medicine, Auxilary Clinical Professor of Environmental Health, 1983-2013

University of Cincinnati, Department of Environmental Health, College of Medicine, Assistant Clinical Professor of Environmental Health, 1981-1986

London School of Hygiene and Tropical Medicine, Visiting Fellow, TUC Institute of Occupational Health, 1976-1977

EDUCATION High School: Boston Latin School, 1959 College: Boston College, A.B. (magna cum laude), 1963 Medical School: Harvard Medical School, M.D., 1967 POSTDOCTORAL TRAINING Internship: Cleveland Metropolitan General Hospital, 1967-1968 Residency: Children's Hospital Medical Center, Boston, (Pediatrics), 1968-1970 Post Graduate: London School of Hygiene & Tropical Medicine, 1976-77 Diploma of Industrial Health (England), 1977 Master of Science in Occupational Medicine, University of London (with distinction), 1977

2

CERTIFICATION American Board of Pediatrics - 1973 American Board of Preventive Medicine: General Preventive Medicine - l979 Occupational Medicine - 1983 MEDICAL LICENSURE Massachusetts #31277, 1967 - present New York #162034, 1985 - present INSTITUTE OF MEDICINE Institute of Medicine, National Academy of Sciences, Elected to membership, 1987 HONORS/AWARDS

Asbestos Disease Awareness Association – Dr. Irving Selikoff Lifetime Achievement Award, 2016 Grassroots Environmental Education, Award for Outstanding Leadership in Children’s Environmental

Health, 2015 Boston College – Distinguished Alumni Research Award, 2014 Boston Latin School - Distinguished Graduate Award, 2014 University of Medicine & Dentistry of New Jersey - Senator Frank R. Lautenberg Annual Award in

Public Health, 2011 Hearst Foundation, The Daily Green – The Heart of Green Award, 2010 The New York Academy of Medicine – The Stephen Smith Medal for Lifetime Achievement in Public

Health, 2009 U.S. Environmental Protection Agency, Region II – Environmental Quality Award on behalf of Mount

Sinai Medical Center, 2009 Westchester County (NY). Sustainability Award for Service on Westchester County Global Warming

Task Force, 2009 Student Physicians for Social Responsibility. Lifetime Achievement Award, 2009 Women’s City Club of New York. Civic Spirit Award, 2009 Boston College. Alumni Award for Professional Excellence, 2008 Collegium Ramazzini. Irving J. Selikoff Award, 2008

Healthy Schools Network, Inc. Healthy Schools Hero Award, 2008 Westchester Children’s Association. Edith Macy Award for Distinguished Service, 2008

Children’s Health Environmental Coalition. Lifetime Achievement Award, 2006 U.S. Environmental Protection Agency. Child Health Champion Award, 2006

Huntington Breast Cancer Action Coalition. Humanities Award for Children’s Health Protection, 2005 Icahn School of Medicine at Mount Sinai. J. Lester Gabrilove Award, 2005 American College of Occupational and Environmental Medicine. Health Achievement in Occupational Medicine Award, 2005

National Nutritional Foods Association. Rachel Carson Environmental Award, 2005 Federated Conservationists of Westchester County. Super Hero Award for Children’s Health, 2005 Physicians for Social Responsibility, Los Angeles Chapter. Socially Responsible Medicine Award,

2004 Organic Style Magazine. Environmental Power List, 2004 Finnish Institute for Occupational Health. Jorma Rantanen Award, 2003

American Public Health Association, David P. Rall Award for Advocacy in Public Health, 2003 Castle Connolly Ltd.-America’s Top Doctor. Preventive Medicine. New York Metropolitan Area

and United States 2001, 2002, 2003, 2004, 2005, 2006, 2007, 2008, 2009, 2010, 2011, 2012, 2013, 2014 and 2015

3

HONORS/AWARDS (cont)

Public Health Association of New York City, Haven Emerson Award, 2002 National Institute for Occupational Safety & Health, James Keogh Award, 2002 Icahn School of Medicine at Mount Sinai, Jacobi Medallion, 2002 Environmental Advocates (New York), Award for Environmental Advocacy on Behalf of Children, 2000

American Conference of Governmental Industrial Hygienists, William Steiger Memorial Award, 2000 Russian Academy of Medical Science, Elected as Foreign Member, 2000 Earth Day New York, Award for Excellence in Environmental Medicine, 1999

Mothers & Others for a Livable Planet, Award for Advocacy on Behalf of the Health of Children, 1999 American College of Preventive Medicine, Katherine Boucot Sturgis Award, 1999 International Society for Occupational and Environmental Health, Vernon Houk Award, 1998 New Jersey Environmental Federation Certificate of Recognition. Environmental Achievement Award, 1998 Physicians for Social Responsibility, Broad Street Pump Award in Environmental Health, 1996 International Association of Fire Fighters, Occupational Health and Safety Award, 1995 American Public Health Association, Herbert L. Needleman Medal and Award for Scientific Contributions and Advocacy on Behalf of Children, 1995 United Brotherhood of Carpenters, William Sidell Presidential Award, 1995 New England College of Occupational and Environmental Medicine, Harriet Hardy Award,

1993 New York Committee for Occupational Safety and Health, Annual Honoree, 1985

United States Navy Navy & Marine Corps Commendation Medal (3 awards), 2002, 2003 and 2005 National Defense Service Medal, 2003 Secretary of Defense Medal for Outstanding Public Service, 2002

U.S. Public Health Service Meritorious Service Medal, 1985 Group Citation as Member of Beryllium Review Panel, 1978 Career Development Award, 1976

U.S. Department of Health, Education and Welfare, Volunteer Award, 1973 HONORARY DEGREES: Mount Sinai School of Medicine, Doctor of Science (honoris causa), 2007 OTHER PROFESSIONAL APPOINTMENTS:

American College of Preventive Medicine Fellow, 2003-present Physicians for Social Responsibility, Board of Directors 1996-1999; Board of Sponsors, 1994-95 New York Academy of Medicine, Elected Fellow, 1991 American College of Occupational and Environmental Medicine, Fellow, 1986 Herman Biggs Society, Member, 1986-1992 International Commission on Occupational Health, Member, 1985-present Collegium Ramazzini, Fellow, 1983-present President, 1997-present American College of Epidemiology, Fellow, 1983-present Board of Directors, 1990 - 1993 American Epidemiological Society, Elected Member, 1982-present American Public Health Association, Member, 1982-present Occupational Health Section, Chair, 1989-90

4

OTHER PROFESSIONAL APPOINTMENTS: (cont)

Society for Epidemiologic Research, Member, 1978-present Royal Society of Medicine, Elected Fellow, 1977 American Academy of Pediatrics, Fellow, 1975-present New York Occupational Medicine Association, Member 1985-present Board of Directors, 1988-1990 New York Academy of Sciences, Fellow 2002-present

COMMITTEES: The White House Presidential Advisory Committee on Gulf War Veterans' Illnesses, 1995-1996 American Academy of Pediatrics Committee on Environmental Hazards, 1976-1987. Chairman, 1983-1987 National Research Council Institute of Medicine, Chairman, Interest Group (14) Environmental and Occupational Health and

Toxicology, 2009-2011 National Academy of Sciences, Board on Sustainable Development, 1995-1998 National Academy of Sciences, Committee on the Scientific Issues Surrounding the Regulation of Pesticides in the Diets of Infants and Children, Chairman, 1988-1992 National Academy of Sciences, Committee on Neurotoxicology in Risk Assessment, 1987-1989 National Academy of Sciences, Committee on the Epidemiology of Air Pollutants, Vice-Chairman, 1984-1985 National Academy of Sciences, Assembly of Life Sciences, 1981-1982; Commission on Life Sciences, 1982-1984 National Academy of Sciences, Panel on the Proposed Air Force Study of Herbicide Agent Orange, 1979-1980 Institute of Medicine, Committee for a Planning Study for an Ongoing Study of Costs of Environment-Related Health Effects, 1979-1980 National Academy of Sciences, Assembly of Life Sciences. Board on Toxicology and Environmental Health Hazards, 1978-1987; Vice-Chairman, 1981-1984 National Institutes of Health/U.S. Public Health Service National Institutes of Health, National Institute of Environmental Health Sciences, External Clinical Advisory Council, 2009-present

National Institute of Child Health and Human Development, Federal Advisory Committee to the National Children’s Study, 2003-2005

National Institute of Child Health and Human Development, National Children’s Study, Executive Steering Committee, 2007-2009

Food and Drug Administration, Ranch Hand Advisory Committee, 2000-2001 National Institute for Occupational Safety and Health, Board of Scientific Counselors, 1995-1997 National Institutes of Health, Study Section on Epidemiology and Disease Control, 1986-1990 National Institute of Environmental Health Sciences, Third Task Force for Research Planning in the Environmental Health Sciences; Chairman, Subtask Force on Research Strategies for Prevention of and Intervention in Environmentally Produced Disease, 1983-1984

Department of Defense Armed Forces Epidemiological Board, 2000-2002

5

COMMITTEES: (cont) State and Local Government New York State, Governor’s Advisory Committee on Safety and Healthy New York Foods, 2015-2016 State of New York, Advisory Council on Children’s Environmental Health, Co-Chair 2009-present State of New York, Advisory Council on Lead Poisoning Prevention, 2009-present Westchester County, New York, Westchester County Global Warming Task Force, 2006-2008 City of New York, Weapons of Mass Destruction (WMD) Advisory Group, 2002-2008

State of New York, Health Research Science Board, 1997-present State of New York, Public Health Priorities Committee, 1996 State of New York, New York State Advisory Council on Lead Poisoning Prevention, Chairman, 1993-2004 City of New York, Mayor's Lead Paint Poisoning Advisory Committee, 1991-1993 State of New York, Asbestos Advisory Board, Chair, 1987-present State of New Jersey, Meadowlands Cancer Advisory Board, Chair, 1987-1989 State of New York, Governor's Blue Ribbon Committee on the Love Canal, 1978-1979

Academic Cornell University, Dean's Advisory Council in Veterinary Medicine, 1996-1997 Mickey Leland National Urban Air Toxics Research Center, National Advisory Committee, 1994-1995 New York Academy of Medicine, Working Group on Housing and Health, 1987-1989; Chairman, 1989 New York Lung Association, Research and Scientific Advisory Committee, 1986-1989. Board of Directors, 1987-1990 Association of University Programs in Occupational Health and Safety, 1985-Present; President, 1986-1988 Milbank Memorial Foundation, Technical Board, 1986-1988 Harvard School of Public Health, Occupational Health Program, Residency Review Committee, 1981-1983; Chairman, 1981 International Organizations World Health Organization. Contributor to the WHO Publication: “Guidelines on Studies in Environmental Epidemiology” (Environmental Health Criteria, No. 27), 1984. International Agency for Research on Cancer, service as member of Working Groups on Cancer Assessment, volume 29 (benezene), 1981; volume 42 (silica), 1986; voume 87 (lead), 2005; volume 98, (firefighting) 2007; volume 100 (asbestos). 2011. Environmental Organizations Healthy Child, Healthy World, Board of Directors, 1996-present Children's Environmental Health Network, Board of Directors, 1995-present Environmental Health Foundation, Board of Directors, 1993-1996 INFORM, Board of Directors, 1991-2003 Labor Unions International Brotherhood of Teamsters, National Health and Safety Advisory Committee, 1994-2002 George Meany Center for Labor Studies, Board of Trustees, 1994-1997 United Brotherhood of Carpenters, National Health and Safety Fund, Medical Advisory Committee, 1990 -2000; Chairman, 1994-2000

6

COMMITTEES: (cont) Labor Unions United Automobile Workers (UAW) - Chrysler Corporation, Joint Scientific Advisory Committee, Member, 1990-2006 International Association of Fire Fighters, John Redmond Foundation, Medical Advisory Committee, 1989-present Other Organizations Health Insurance Plan (HIP) of Greater New York, Board of Directors, 1992-1994 American Legion, Science Panel, Chairman, 1988-2000 Editorial Boards Editor-in-Chief: Annals of Global Health, 2013-present Deputy Editor: American Journal of Industrial Medicine, 2007-present Associate Editor: Environmental Health Perspectives, 2002-present Editorial Board: Journal of Public Health Management and Practice, 1995-1996 Editor-in-Chief: American Journal of Industrial Medicine, 1992-2006; Consulting Editor, 1979-1992 Editorial Board: New Solutions: A Journal of Environmental and Occupational Health Policy, 1990-present Editorial Board: The PSR Quarterly, 1990-1994 Editorial Board: American Journal of Public Health, 1987-1993 Editor-in-Chief: Environmental Research, 1987-1994 Senior Editor: Environmental Research, 1985-1987 Editorial Board: Annual Review of Public Health, 1984-1990 Consulting Editor: Archives of Environmental Health, 1982-present National Service United States Naval Reserve, Medical Corps, 1996-2005 LCDR (0-4) 1996-98; CDR (0-5) 1998 – 2004; CAPT (0-6) 2004-2005. Retired January 1, 2005. United States Public Health Service, Commissioned Corps, 1970-1995. LCDR (0-4) to CAPT (0-6). New York Naval Militia 2000-present; CAPT (0-6); Surgeon General. GRANT SUPPORT ACTIVE: Blacksmith Institute (Landrigan, PI) 01/01/12 – 12/23/17 $45,000 Assessing the Disease Burden of Hazardous Waste Sites The purpose of this contract is to support the development of a series of scientific papers that will assess the health burden associated with human exposure to hazardous waste sites in the developing world. 2011-N-13318 (Lucchini, PI) 07/01/11 – 12/31/16 CDC $28,422,550 World Trade Center Data and Coordination Center This project is the coordinating center for a multicenter program providing monitoring and treatment to volunteers who assisted in the recovery and cleanup after the 9/11 attack. Role: Co-Investigator

7

Completed Research Support: 1T32HD049311 (Landrigan, PI) 05/01/07 - 07/01/13 NICHD $323,002 Research Training Program in Environmental Pediatrics The goal of this interdisciplinary research training program is to train the next generation of physician-researchers and academic leaders in environmental pediatrics. C-010124 NYS DoH Landrigan (PI) 4/1/09 – 3/31/12; Lucchini (PI) 4/1/12 – present World Trade Center Responders Data and Coordinating Center. This program has collected, analyzed and published medical monitoring and treatment data collected clinically on 30,000 9/11 responders evaluated at five Clinical Centers in the New York metropolitan area. NIH-HHSN27520080031C (Landrigan, PI) 09/28/08 - 09/27/13 (Monroe) NIH National Children’s Study Vanguard Centers This project will recruit 1250 live births into a NICHD study of social, behavioral and environmental factors and their impact on childhood health, growth and development. The Queens Vanguard Center is one of the first six sites selected to pilot the NCS, which will follow more than 100,000 children across the United States from birth until age 21. U10-OH08232 CDC Landrigan (PI) 6/1/04 – 3/31/12; Lucchini (PI) 4/1/12 - present New York/New Jersey Education Research Center in Occupational Safety & Health. The goal of this multi-institutional program is to train professionals from multiple disciplines - medicine, nursing, industrial hygiene and industrial safety - to be future leaders in occupational health and safety. Children’s Environmental Health Center - Inner City Toxicants, Child Growth and Development Co-Principal Investigator EPA RD831711-01 11/1/03 – 10/31/10 NIEHS P01 ES009584 11/1/98 – 10/31/10

8

ORIGINAL, PEER-REVIEWED PUBLICATIONS

1. Lovejoy FH Jr, Marcuse EK, Landrigan PJ: Two examples of purpura factitia. Clinica Pediatr 10:183-184, 1971.

2. Landrigan PJ, Conrad JL: Current status of measles in the United States. J Infect Dis 124:620-622, 1971.

3. Landrigan PJ: Epidemic measles in a divided city. JAMA 221:567-570, 1972.

4. Hattwick MA, Hochberg FH, Landrigan PJ, Gregg MG: Skunk-associated human rabies. JAMA 222:44-50, 1972.

5. Grand MG, Wyll SA, Gehlbach SH, Landrigan PJ, Judelsohn RG, Zendel SA, Witte JJ: Clinical reactions following rubella vaccination: A prospective analysis of joint, muscular, and neuritic symptoms. JAMA 220:1569-1572, 1972.

6. Landrigan PJ, Griesbach PH: Measles - In previously vaccinated children in Illinois. Illinois Med J 141:367-372, 1972.

7. Tarlin L, Landrigan PJ, Babineau R, Alpert JJ: A comparison of the antipyretic effect of acetaminophen and aspirin: Another approach to poison prevention. Am J Dis Child 124:880-882, 1972.

8. Landrigan PJ, Witte JJ: Neurologic disorders following live measles-virus vaccination. JAMA 223:1459-1462, 1973.

9. Landrigan PJ, Murphy KB, Meyer HM, Parkman PD, Eddins DL, Witte JJ: Combined measles-rubella vaccines: virus dose and serologic response. Am J Dis Child 125:65-67, 1973.

10. Landrigan PJ, Huber DH, Murphy GC, Creech WB, Bryan JA: The protective efficacy of immune serum globulin in hepatitis A: A statistical approach. JAMA 223:74-75, 1973.

11. Landrigan PJ, Bresnan M, Berenberg W: Behr's syndrome: Familial optic atrophy, spastic diplegia, and ataxia. Develop Med Child Neurol 15:41-47, 1973.

12. Brandling-Bennett AD, Landrigan PJ, Baker EL: Failure of vaccinated school children to transmit measles. JAMA 224:616-618, 1973.

13. Barthel WF, Smrek AL, Angel GP, Liddle JA, Landrigan PJ, Gehlbach SH, Chisholm JJ: Modified Delves' cup atomic absorption determination of lead in blood. J Official Analyst Chemists 56:1252-1256, 1973.

14. Schluederberg A, Lamm SH, Landrigan PJ, Black FL: Measles immunity in children vaccinated before one year of age. Am J Epidemiol 97:402-409, 1973.

15. Landrigan PJ, Stoffels MA, Anderson E, Witte JJ: Epidemic rubella in adolescent boys - clinical features and results of vaccination. JAMA 227:1283-1287, 1974.

16. Marshall R, Habicht JP, Landrigan PJ, Foege WH, Delgado H: Effectiveness of measles vaccine given simultaneously with DTP. J Trop Pediatr 20:126-129, 1974.

17. Landrigan PJ, Navarro E, Eddins D: Epidemiologic assessment of a nationwide multiple antigen vaccine campaign. J Trop Pediatr 20:135-140, 1974.

18. Landrigan PJ, Gehlbach SH, Rosenblum BF, Shoults JM, Candelaria RM, Barthel WF, Liddle JA, Smrek AL, Staehling NW, Sanders JF: Epidemic lead absorption near an ore smelter: the role of particulate lead. New Engl J Med 292:123-129, 1975.

19. Landrigan PJ, Whitworth RH, Baloh RW, Barthel WF, Staehling NW, Rosenblum BF: Neuropsychological dysfunction in children with chronic low-level lead absorption. Lancet 1:708-712, 1975.

9

ORIGINAL, PEER-REVIEWED PUBLICATIONS (cont)

20. Landrigan PJ, McKinney AS, Hopkins LC, Rhodes WW Jr, Price WA, Cox DH: Chronic lead absorption - result of poor ventilation in an outdoor pistol range. JAMA 234:394-397, 1975.

21. Wallace RB, Landrigan PJ, Smith EA, Pifer J, Teller B, Foster SO: Trial of a reduced dose of measles vaccine in Nigerian children. Bull WHO 53:361-364, 1976.

22. Landrigan PJ, Baker EL, Feldman RH, Cox DH, Eden KV, Orenstein WA, Mather JA, Yankel AJ, VonLindern IH: Increased lead absorption with anemia and slowed nerve conduction in children near a lead smelter. J Pediatr 85:904-910, 1976.

23. Levine RJ, Moore RM, McLaren CD, Barthel WF, Landrigan PJ: Occupational lead poisoning, animal deaths, and environmental contamination at a scrap smelter. Am J Public Health 66:548-552, 1976.

24. Baker EL, Folland DS, Taylor TA, Frank M, Peterson W, Lovejoy G, Cox D, Housworth J, Landrigan PJ: Lead poisoning in children of lead workers: Home contamination with industrial dust. New Engl J Med 296:260-261, 1977.

25. Diggory HJP, Landrigan PJ, Latimer KP, Ellington AC, Kimbrough RD, Liddle JA, Cline AE, Smrek AL: Fatal parathion poisoning caused by contamination of flour in international commerce. Am J Epidemiol 106:145-153, 1977.

26. Winegar DA, Levy BS, Andrews JS Jr, Landrigan PJ, Scruton WH, Krause MJ: Chronic occupational exposure to lead: an evaluation of the health of smelter workers. J Occup Med 19:603-606, 1977.

27. Baker EL, Smrek A, Kimbrough RD, Hudgins M, Landrigan PJ, Liddle JA: Hereditary cholinesterase deficiency: A report of a family with two rare genotypes. Clinical Genetics 12:134-138, 1977.

28. Baker EL Jr, Hayes CG, Landrigan PJ, Handke JL, Leger RT, Housworth WJ, Harrington JM: A nationwide survey of heavy metal absorption in children living near primary copper, lead and zinc smelters. Am J Epidemiol 106:261-273, 1977.

29. Baker EL, Field PH, Basteyns BJ, Skinner GH, Bertozzi PE, Landrigan PJ: Phenol poisoning due to contaminated drinking water. Arch Environ Health 33:89-94, 1978.

30. Wysowski DK, Landrigan PJ, Ferguson SW, Fontaine RE, Liddle JA: Cadmium exposure in a community near a smelter. Am J Epidemiol 107:27-35, 1978.

31. Cannon SB, Veazey JM, Jackson RS, Burse VW, Hayes C, Straub WE, Landrigan PJ: Epidemic kepone poisoning in chemical workers. Am J Epidemiol 107:529-537, 1978.

32. Harrington JM, Craun GF, Meigs JW, Landrigan PJ, Flannery JT, Woodhull RS: An investigation of the use of asbestos cement pipe for public water supply and the incidence of gastrointestinal cancer in Connecticut 1935-1973. Am J Epidemiol 107:96-103, 1978.

33. Baker EL, Peterson WA, Holtz J, Mann JM, Coleman C, Landrigan PJ: Subacute cadmium intoxication in jewelry workers: An evaluation of diagnostic procedures. Arch Environ Health 34:173-177, 1979.

34. Morse DL, Baker EL, Landrigan PJ: Cut flowers: A potential pesticide hazard. Am J Public Health 69:53-56, 1979.

35. Morse DL, Watson WN, Housworth J, Witherell LE, Landrigan, PJ: Exposure of children to lead in drinking water. Am J Public Health 69:711-712, 1979.

36. Morse DL, Kominsky JR, Wisseman CL III, Landrigan PJ: Occupational exposure to hexachlorocyclopentadiene: How safe is sewage? JAMA 241:2177-2179, 1979.

10


37. Morse DL, Landrigan PJ, Rosenblum BF, Housworth J: El Paso revisited: epidemiologic follow-up of an

environmental lead problem. JAMA 242:739-741, 1979.

38. Morse DL, Harrington JM, Kelter A, Housworth J, Landrigan PJ: Arsenic exposure in multiple environmental media in children near a smelter. Clin Toxicol 14:389-399, 1979.

39. Landrigan PJ, Wilcox KR Jr, Silva J Jr, Humphrey HEB, Kauffman C, Heath CW Jr: Cohort study of Michigan residents exposed to polybrominated biphenyls: epidemiologic and immunologic findings. Ann NY Acad Sci 320:284-294, 1979.

40. Baker EL, Landrigan PJ, Barbour AG, Cox DH, Folland DS, Ligo RN, Throckmorton J: Occupational lead poisoning in the United States: Clinical and biochemical findings related to blood lead levels. Br J Ind Med 36:314-322, 1979.

41. Silva J, Kauffman CA, Simon DG, Landrigan PJ, Humphrey HEB, Heath CW, Wilcox ER, VanAmburg G, Kaslow RA, Hoff K: Lymphocyte function in humans exposed to polybrominated biphenyls. J Recituloendothelial Soc 26:341-347, 1979.

42. Englender SJ, Landrigan PJ, Atwood RB, Clarkson TW: Organic mercury exposure from fungicide-contaminated eggs. Arch Environ Health 35:224-228, 1980.

43. Baker EL, Landrigan PJ, Glueck CJ, Zack MM, Liddle JA, Burse VW, Housworth WF, Bayse DD, Needham LL: Metabolic consequences of exposure to polychlorinated biphenyls (PCBs) in sewage sludge. Am J Epidemiol 112:553-563, 1980.

44. Landrigan PJ, Tamblyn PB, Nelson M, Kerndt P, Kronoveter KJ, Zack MM: Lead exposure in stained glass workers. Am J Ind Med 11:177-180, 1980.

45. Wilson R, Lovejoy FH, Jaeger RJ, Landrigan PJ: Acute phosphine poisoning aboard a grain freighter: epidemiologic, clinical, and pathological findings. JAMA 244:148-150, 1980.

46. Rosenberg MJ, Landrigan PJ, Hahn JL, Crowley S: Low-level arsenic exposure in wood processing plants. Am J Ind Med 1:99-108, 1980.

47. Nelson DB, Kimbrough ED, Landrigan PJ, Hayes AW, Yang GC, Benanides J: Aflatoxin and Reye's Syndrome: A case-control study. Pediatrics 66:865-869, 1980.

48. Hassan A, Velasques E, Belmar R, Coye M, Drucker E, Landrigan PJ, Michaels D, Sidel KB: Mercury poisoning in Nicaragua: A case study of the export of environmental and occupational health hazards by a multinational corporation. Int J Health Serv 11:221-226, 1981.

49. Halperin W, Landrigan PJ, Altman R, Iaci AW, Morse DL, Needham LL: Chemical fire at toxic waste disposal plant: Epidemiologic study of exposure to smoke and fumes. J New Jersey Med Soc 78:592-594, 1981.

50. Rinsky RA, Zumwalde RD, Waxweiler RJ, Murray WE, Bierbaum PJ: Landrigan PJ, Terpilak M, Cox C: Cancer mortality at a naval nuclear shipyard. Lancet 1:231-235, 1981.

51. Froneberg B, Johnson PL, Landrigan PJ: Respiratory illness caused by overheating of polyvinyl chloride. Br J Ind Med 39:239-243, 1982.

52. Landrigan PJ, Baker EL, Himmelstein JS, Stein GF, Weddig JP, Straub WE: Exposure to lead from the Mystic River Bridge - The dilemma of deleading. New Engl J Med 306:673-676, 1982.

53. Schulte PA, Singal M, Stringer WT, Kominsky JR, Landrigan PJ: The efficacy of a population-based comparison group in cross-sectional occupational health studies. Am J Epidemiol 116:981-989, 1982.

11


54. Landrigan PJ, Costello RJ, Stringer WT: Occupational exposure to arsine: An epidemiologic reappraisal of current standards. Scand J Work Environ Health 8:169-177, 1982.

55. Halperin WE, Goodman M, Stayner L, Elliott LJ, Keenyside RA, Landrigan PJ: Nasal cancer in a worker exposed to formaldehyde. JAMA 249:510-512, 1983.

56. Landrigan PJ, Powell KE, James LM, Taylor PR: Paraquat and marijuana: epidemiologic risk assessment. Am J Public Health 73:784-788, 1983.

57. Kreiss K, Zack MM, Landrigan PJ, Feldman RG, Niles CA, Chirico-Post J, Sax DS, Boyd MH, Cox DH: Neurologic evaluation of a population exposed to arsenic in Alaskan well water. Arch Environ Health 38:116-121, 1983.

58. Landrigan PJ, Miller BP: The Arjenyattah Epidemic: Home interview data and toxicological aspects. Lancet 2:1474-1475, 1983.

59. Horan JM, Kurt T, Landrigan PJ, Melius JM, Singal M: Neurologic dysfunction from exposure to 2-t-butylazo-2-hydroxy-5-methylhexane (BHMH): A new occupational neuropathy. Am J Public Health 75:513-517, 1985.

60. Selevan SG, Landrigan PJ, Stern FB, Jones JH: Mortality of lead smelter workers. Am J Epidemiol 122:673-683, 1985.

61. Robins JM, Landrigan PJ, Robis TG, Fine LJ: Decision-making under uncertainty in the setting of environmental health regulations. J Public Health Policy 3:322-328, 1985.

62. Landrigan PJ, Straub WE: Occupational lead exposure aboard a tall ship. Am J Ind Med 8:233-239, 1985.

63. Landrigan PJ, Cherniack MG, Lewis FA, Catlett LR: Silicosis in a grey iron foundry: The persistence of an ancient disease. Scand J Work Environ Health 12:32-39, 1986.

64. Liss GM, Halperin WE, Landrigan PJ: Occupational asthma in a home pieceworker. Arch Environ Health 41:359-326, 1986.

65. Stern FB, Waxweiler RA, Beaumont JJ, Lee ST, Halperin WE, Zumwalde RD, Bierbaum PJ, Rinsky RA, Landrigan PJ, Murray WE: A case-control study of leukemia at a naval nuclear shipyard. Am J Epidemiol 123: 980-992, 1986.

66. Wielopolski K, Ellis KJ, Vaswani AN, Cohn SH, Greenberg A, Puschett JB, Parkinson DK, Fetterolf DE, Landrigan PJ: In vivo bone lead measurements: A rapid monitoring method for cumulative lead exposure. Am J Ind Med 9:221-226, 1986.

67. Greenberg A, Parkinson DK, Fetterolf DE, Ellis KJ, Wielopolski L, Vaswani AN, Cohn SH, Landrigan PJ, Puschett JB: Effects of elevated lead and cadmium burdens on renal function and calcium metabolism. Arch Environ Health 4:69-76, 1986.

68. Landrigan PJ, Stein GF, Kominsky JR, Ruhe RL, Watanabe AS: Common source community and industrial exposure to trichloroethylene. Arch Environ Health 42:327-332, 1987.

69. Rinsky RA, Smith AB, Hornung R, Filloon TG, Young RJ, Okun AH, Landrigan PJ: Benzene and Leukemia: An epidemiologic risk assessment. New Engl J Med 316:1044-1050, 1987.

12


70. Schwartz E, Landrigan PJ: Use of court records for supplementing occupational disease surveillance. Am J Public Health 77:1457-1458, 1987.

71. Rinsky RA, Melius JM, Hornung RW, Zumwalde RD, Waxweiler RJ, Landrigan PJ, Bierbaum PJ, Murray WE Jr: Case-control study of lung cancer in civilian employees at the Portsmouth Naval Shipyard, Kittery, Maine. Am J Epidemiol 127:55-64, 1988.

72. Schwartz J, Landrigan PJ, Feldman RG, Silbergeld EK, Baker EL Jr, VonLindern IH: Threshold effect in lead-induced peripheral neuropathy. Pediatrics 112:12-17, 1988.

73. Kraut A, Lilis R, Marcus M, Valciukas JA, Wolff MS, Landrigan PJ: Neurotoxic effects of solvent exposure on sewage treatment workers. Arch Environ Health 43:263-268, 1988.

74. Nicholson WJ, Landrigan PJ: Quantitative assessment of lives lost due to delay in regulation of occupational exposure to benzene. Environ Health Perspect 82:185-188, 1989.

75. Landrigan PJ, Halper LA, Silbergeld EK: Toxic air pollution across a state line: Implications for the siting of resource recovery facilities. J Public Health Policy 10:309-323, 1989.

76. Marino PE, Franzblau A, Lilis R, Landrigan PJ: Acute lead poisoning in construction workers - The failure of current protective standards. Arch Environ Health 44:140-145. 1989.

77. Fahs MC, Markowitz SB, Fischer E, Shapiro J, Landrigan PJ: The health costs of occupational disease in New York State. Am J Ind Med 16:437-449, 1989.

78. Landrigan PJ, Markowitz SB: Current magnitude of occupational disease in the United States: Estimates from New York State. Ann NY Acad Sci 572:27-45, 1989.

79. Wolff MS, Herbert R, Marcus M, Rivera M, Landrigan PJ, Andrews LR: PAH residues on skin in relation to air levels among roofers. Arch Environ Health 44:157-163, 1989.

80. Markowitz S, Landrigan P: The magnitude of the occupational disease problem: An investigation in New York State. Toxicol Ind Health 5:9-30, 1989.

81. Lilienfeld DE, Chan E, Ehland J, Godbold J, Landrigan PJ, Marsh G, Perl DP: Rising mortality from motoneuron disease in the U.S.A., 1962-1984. Lancet 1:710-713, 1989.

82. Elliott LJ, Halperin WE, Landrigan PJ: Perspectives on opportunities toward a hazard-free bioprocessing environment. In: Bioprocessing Safety: Worker and Community Safety and Health Considerations, ASTM STP 1051, WC Hyer Jr (ed). Philadelphia: American Society for Testing and Materials, pp 20-26, 1990.

83. Schwartz J, Landrigan PJ, Baker EL Jr, Orenstein WA, VonLindern IH: Lead-induced anemia: Dose-response relationships and evidence for a threshold. Am J Public Health 80:165-168, 1990.

84. Marino PE, Landrigan PJ, Graef J, Nussbaum A, Bayan G, Boch K, Boch S: A case report of lead paint poisoning during renovation of a Victorian farm house. Am J Public Health 80:1183-1185, 1990.

85. Herbert R, Marcus M, Wolff MS, Perera FP, Andrews L, Godbold JH, Rivera M, Stefanidis M, Quing Lu X, Landrigan PJ, Santella RM: Detection of DNA adducts in white blood cells of roofers by 32P Postlabeling. In: Complex Mixtures and Cancer Risk. Lyon: International Agency for Research on Cancer. (Eds) H Vainio, M. Sorsa & AJ McMichael, pp 205-214, 1990.

86. Lilienfeld DE, Chan E, Ehland J, Godbold J, Landrigan PJ, Marsh G, Perl DP: Two decades of increasing mortality from Parkinson's disease among the nation's elderly. Arch Neurol 47:731-734, 1990.

87. Herbert R, Marcus M, Wolff MS, Perera FP, Andrews L, Godbold JH, Rivera M, Stefanidis M, Lu Q-X, Landrigan PJ, Santella RM: Detection of adducts of deoxyribonucleic acid in white blood cells of roofers by 32P-postlabeling: Relationship of adduct levels to measures of polycyclic aromatic hydrocarbon exposure. Scand J Work Environ Health 16:135-143, 1990.

13


88. Lilienfeld DE, Chan E, Ehland J, Godbold J, Landrigan PJ, Marsh G: Mortality from pulmonary embolism in the United States: 1962-1984. Chest 98:1067-1072, 1990.

89. Kraut A, Chan E, Lioy PJ, Cohen FB, Goldstein BD, Landrigan PJ: Epidemiologic investigation of a cancer cluster in professional football players. Environ Res 56:131-143, 1991.

90. Rosenstock L, Rest KM, Benson JA Jr, Cannella JM, Cohen J, Cullen MR, Davidoff F, Landrigan PJ, Reynolds RC, Clever LH, Goldstein BD: Occupational and Environmental Medicine -- Meeting the Growing Need for Clinical Services (Special Article). New Engl J Med 325:924-927, 1991.

91. Johanning E, Wilder DG, Landrigan PJ, Pope MH: Whole-Body vibration exposure in subway cars and review of adverse health effects. J Occup Med 33:605-612, 1991.

92. Ehrlich R, Kattan M, Godbold J, Saltzberg DS, Grimm KT, Landrigan PJ, Lilienfeld DE: Childhood asthma and passive smoking: urinary cotinine as a biomarker of exposure. Am Rev Respir Dis 145:594-599, 1992.

93. Murata K, Landrigan PJ, Araki S: Effects of age, heart rate, gender, tobacco and alcohol ingestion on RR interval variability in human ECG. J Autonomic Nervous System 37:199-206, 1992.

94. Steenland K, Selevan S, Landrigan P: The mortality of lead smelter workers: an update. Am J Public Health 82:164l-1644, 1992.

95. McConnell R, Anderson K, Russell W, Anderson KE, Clapp R, Silbergeld EK, Landrigan PJ: Angiosarcoma, porphyria cutanea tarda and probable chloracne in a worker exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin-contaminated waste oil. Br J Ind Med 50:699-703, 1993.

96. Belville R, Pollack SH, Godbold JH, Landrigan PJ: Occupational injuries among working adolescents in New York State. JAMA 269:2754-2759 1993.

97. Markowitz SB, Nunez CM, Klitzman S, Munshi AA, Kim WS, Eisinger J, Landrigan PJ: Lead Poisoning Due to Hai Ge Fen. The porphyrin content of individual erythrocytes. JAMA 271:932-934, 1994.

98. Herbert R, Gerr F, Luo J, Harris-Abbott D, Landrigan PJ: Peripheral neurologic abnormalities among roofing workers: sentinel case and clinical screening. Arch Environ Health 50:349-354, 1995.

99. Lightdale JR, Oken E, Klein WM, Landrigan PJ, Welty TK: Psychosocial barriers to health promotion in a American Indian population. American Indian and Alaska Native Mental Health Research 7:34-49, 1997.

100. Herbert R, Plattus B, Kellogg L, Luo J, Marcus M, Mascolo A, Landrigan PJ: The union health center: A working model of clinical care linked to preventive occupational health services. Am J Ind Med 31:263-273, 1997.

101. Smith D, Herbert R, Schechter C, Phillips R, Diamond J, Carroll S, Weiner J, Dahms TE, Landrigan P: Occupational Coronary Heart Disease Among Bridge and Tunnel Officers. Canadian J Cardiol 13(Supp B):76B, 1997.

102. Leigh JP, Markowitz SB, Fahs M, Shin C, Landrigan PJ: Occupational injury and illness in the United States. Estimates of costs, morbidity, and mortality. Arch Intern Med 157:1557-1568, 1997.

103. Claudio L, Torres T, Sanjurjo E, Sherman LR, Landrigan PJ: Environmental Health Sciences Education - A Tool For Achieving Environmental Equity and Protecting Children. Environ Health Perspect 106:849-855, 1998.

104. Joellenbeck LM, Landrigan PJ, Larson EL: Gulf War Veterans' Illnesses: A Case Study in Causal Inference. Environ Res 79:71-81, 1998.

14


105. Ehrlich R, Robins T, Jordaan E, Miller S, Mbuli S, Selby P, Wynchank S, Cantrell A, De Broe M, D'Haese P, Todd AC, Landrigan PJ: Lead absorption and renal dysfunction in a South African battery factory. Occup Environ Med 55:453-460, 1998.

106. Claudio L, Tulton L, Doucette J, Landrigan PJ: Socioeconomic factors and asthma hospitalization rates in New York City. J Asthma 36:343-350, 1999.

107. Landrigan PJ, Claudio L, Markowitz SB, Berkowitz GS, Brenner BL, Romero H, Wetmur JG, Matte TD, Gore AC, Godbold JH, Wolff MS: Pesticides and inner-city children: Exposures, risks, and prevention. Environ Health Perspect 107 (Suppl 3):431-437, 1999.

108. Landrigan PJ, Suk WA, Amler RW: Chemical wastes, children's health, and the Superfund Basic Research Program. (Commentary). Environ Health Perspect 107:423-427, 1999.

109. Landrigan PJ: Risk assessment for children and other sensitive populations. In: Uncertainty in the Risk Assessment of Environmental and Occupational Hazards. Annals of the New York Academy of Sciences 895:1-9, 1999.

110. Marcus M, McChesney R, Golden A, Landrigan PJ: Video Display Terminals and Miscarriages. J Am Wom Med Assoc 55:84-88, 2000.

111. Forman J, Moline J, Cernichiari E, Sayegh S, Torres JC, Landrigan MM, Hudson J, Adel HN, Landrigan PJ: A cluster of pediatric metallic mercury cases treated with meso-2,3-Dimercaptosuccinic acid (DMSA). Environ Health Perspect 108: 575-577, 2000.

112. Herbert R, Schechter C, Smith DA, Phillips R, Diamond J, Carroll S, Weiner J, Dahms TE, Landrigan PJ: Occupational Coronary Heart Disease among Bridge and Tunnel Officers. Arch Environ Health 55:152-163, 2000.

113. Berkowitz GS, Wolff MS, Matte T, Susser E, Landrigan PJ: The Rationale for a National Prospective Cohort Study of Environmental Exposure and Childhood Development. Environ Res 85:59-68, 2001.

114. Landrigan PJ, Schechter CB, Lipton JM, Fahs MC, Schwartz J. Environmental pollutants and disease in American children: Estimates of morbidity, mortality and costs for lead poisoning, asthma, cancer and developmental disabilities. Environ Health Perspect 110:721-728, 2002.

115. Etzel RA, Crain EF, Gitterman BA, Oberg C, Scheidt P, Landrigan PJ: Pediatric Environmental Health Competencies for Specialists. Ambulatory Pediatrics 3:60-63, 2003.

116. Berkowitz GS, Obel J, Deych E, Lapinski R, Godbold J, Liu Z, Landrigan PJ, Wolff MS. Exposure to indoor pesticides during pregnancy in a multiethnic urban cohort. Environ Health Perspect 111:79-84, 2003.

117. Berkowitz GS, Wolff MS, Janevic TM, Holzman IR, Yehuda R, Landrigan PJ. The World Trade Center Disaster and Intrauterine Growth Restriction. (Research Letter) JAMA 290:595-596, 2003.

118. Brenner BL, Markowitz S, Rivera M, Romero H, Weeks M, Sanchez E, Deych E, Garg A, Godbold J, Wolff MS, Landrigan PJ, Berkowitz G. Integrated Pest Management in an Urban Community – A Successful Partnership for Prevention. Environ Health Perspect 111:1649-1653, 2003.

119. Landrigan PJ, Kimmel CA, Correa A, Eskenazi B. Children’s Health and the Environment: Public Health Issues and Challenges for Risk Assessment. Environ Health Perspect 112:257-265, 2003.

120. Landrigan P, Garg A, Droller DBJ. Assessing the Effects of Endocrine Disruptors in the National Children’s Study. Environ Health Perspect 111:1678-1682, 2003.

121. Fewtrell LJ, Prüss A, Landrigan P, Ayuso-Mateos JL. Estimating the global burden of disease from environmental lead exposure. Environ Res 94:120-133, 2004.

15


122. Landrigan PJ, Lioy PJ, Berkowitz G, Chen LC, Chillrud SN, Georgopoulos PG, Geyh AS, Levin S, Perera F, Rappaport SM, Small C, Thurston G. Health and Environmental Consequences of the World Trade Center Disaster. The NIEHS World Trade Center Working Group. Environ Health Perspect 112:731-739, 2004.

123. Trasande L, Schechter C, Landrigan PJ: Public Health and Economic Consequences of Methyl Mercury Toxicity to the Developing Brain. Environ Health Perspect 113:590-596, 2005.

124. Landrigan PJ, Sonawane B, Butler RN, Trasande L, Callan R, Droller D. Early Environmental Origins of Neurodegenerative Disease in Later Life. Environ Health Perspect 113:1230-1233, 2005.

125. Smith DA, Ness EM, Herbert R, Schechter CB, Phillips RA, Diamond JA, Landrigan PJ. Abdominal diameter index: a more powerful anthropometric measure for prevalent coronary heart disease risk in adult males. Diabetes, Obesity & Metabolism (in press), 2005.

126. Gobeille A, Morland K, Bopp R, Godbold J, Landrigan PJ: Body Burdens of Mercury in Lower Hudson River Area Anglers. Env Res 101:205-212, 2006.

127. Morland KB, Landrigan PJ, Sjödin A, Gobeille AK, Jones RS, McGahee EE, Needham LL, Patterson DG, Jr. Body Burdens of Polybrominated Diphenyl Ethers among Urban Anglers. Environ Health Perspect 113:1689-1692, 2005.

128. Boscarino JA, Adams RE, Foa EB, Landrigan PJ: A Propensity Score Analysis of Brief Worksite Crisis Interventions after the World Trade Center Disaster: Implications for Intervention and Research. Med Care 44:454-462, 2006.

129. Trasande L, Schechter C, Haynes KA, Landrigan PJ: Applying cost analyses to inform environmental health policy: mercury as a case study. Annals of the New York Academy of Sciences 1076: 911-923, 2006.

130. Golden AL, Berkowitz GS, Wolff MS, Godbold JH, Afilaka A, Chillrud SN, Bopp RF, Simpson HJ, Landrigan PJ. Body Burdens of Persistent Pollutants in Hudson River Anglers. Environ Res (submitted), 2005.

131. Trasande L, Schechter C, Haynes KA, Landrigan PJ. Mental Retardation and Prenatal Methylmercury Toxicity. Am J Ind Med 153-158, 2006.

132. Trasande L, Cronk CE, Leuthner SR, Hewitt JB, Durkin M, McElroy J, Anderson HA, Landrigan PJ. The NationaChildren’s Study and the Children of Wisconsin. Wisconsin Medical Journal 105(2):45-49, 2006.

133. Trasande L, Schapiro ML, Falk R, Haynes KA, Behrmann A, Vohmann M, Stremski ES, Eisenberg C, Evenstad C, Anderson HA, Landrigan PJ. Pediatrician Attitudes and Knowledge of Environmental Health in Wisconsin. Wisconsin Medical Journal 105(2):50-54, 2006.

134. Trasande L, Boscarino J, Graber N, Falk R, Schechter C, Galvez, M, Dunkel G, Geslani J, Moline J, Kaplan-Liss E, Miller RK, Korfmacher K, Carpenter D, Forman J, Balk SJ, Laraque D, Frumkin H, Landrigan PJ. The Environment in Pediatric Practice: A Study of New York Pediatricians’ Attitudes, Beliefs, and Practices towards Children’s Environmental Health. J Urban Health 83(4):760-772, 2006.

135. Grandjean P, Landrigan PJ. Developmental neurotoxicity of industrial chemicals: A silent pandemic. Lancet 368(9553):2167-2178, 2006.

136. Landrigan PJ, Trasande L, Thorpe LE, Gwynn C, Lioy PJ, D’Alton ME, Lipkind HS, Swanson J, Wadhwa PD, Clark EB, Rauh VA, Perera FP, Susser E. The National Children’s Study: A 21-year prospective study of 100,000 American children. Pediatrics 118(5):2173-2186, 2006.

137. Herbert R, Moline J, Skloot G, Metzger K, Baron S, Luft B, Markowitz S, Udasin I, Harrison D, Stein D, Todd A, Enright P, Stellman JM, Landrigan PJ, Levin S. The World Trade Center Disaster and the Health of Workers: Five-Year Assessment of a Unique Medical Screening Program. Environ Health Perspect 114:1853-1858, 2006.

138. Landrigan PJ, Woolf AD, Gitterman B, Lanphear B, Forman J, Karr C, Moshier EL, Steiner JF, Godbold J, Crain E. The Ambulatory Pediatric Association Fellowship in Pediatric Environmental Health: A Five-Year Assessment. Environ Health Perspect 115:1383-1387, 2007.

16


139. Chemtob CM, Conroy DL, Hochauser CJ, Laraque D, Banks J, Schmeidler J, Cruz MD, Nelson WC, Landrigan PJ. Children who lost a parent as a result of the terrorist attacks of September 11, 2001: Registry construction and population description. Death Studies 31:87-100, 2007.

140. Magdo HS, Forman J, Graber N, Newman B, Satlin L, Amler R, Winston JA, Landrigan PJ. Grand Rounds: Nephrotoxicity in a Young Child Exposed to Uranium from Contaminated Well Water. Environ Health Perspect 115(8):1237-1241, 2007.

141. Moline JM, Herbert R, Levin S, Stein D, Luft BJ, Udasin IG, Landrigan PJ. WTC Medical Monitoring and Treatment Program: Comprehensive Health Care Response in Aftermath of Disaster. Mount Sinai J Med 75:67-75, 2008.

142. Stellman JM, Smith RP, Katz CL, Sharma V, Charney DS, Herbert R, Moline J, Luft BJ, Markowitz S, Udasin I, Harrison D, Baron S, Landrigan PJ, Levin SM, Southwick S. Enduring Mental Health Morbidity and Social Function Impairment in World Trade Center Rescue, Recovery and Cleanup Workers: The Psychological Dimension of an Environmental Health Disaster. Environ Health Perspect, 116(9):1248-1253, 2008.

143. Rauh VA, Landrigan PJ, Claudio L. Housing and Health: Intersection of Poverty and Environmental Exposure. Ann N Y Acad Sci 1136:276-288, 2008.

144. Trasande L, Cronk C, Durkin M, Weiss M, Schoeller DA, Gall EA, Hewitt JB, Carrel AL, Landrigan PJ, Gillman MW. Environment and Obesity in the National Children’s Study. Environ Health Perspect 117:159-166, 2009. PMID: 19270782

145. Moline JM, Herbert R, Crowley L, Troy K, Hodgman E, Ghukla G, Udasin I, Luft B, Wallenstein S, Landrigan P, Savitz DA. Multiple Myeloma in World Trade Center Responders: A Case Series. J Occup Environ Med 2009 Aug;51(8):896-902. PMID: 19620891

146. Zajac L, Sprecher E, Landrigan PJ, Trasande L. A systematic review of U.S. state environmental legislation and regulation with regards to the prevention of neurodevelopmental disabilities and asthma. Environmental Health 2:9, 2009. doi: 10.1186/1476-069X-8-9.PMID: 19323818

147. Tornheim JA, Morland KB, Landrigan PJ, Enrique Cifuentes. Water Privatization, Water Source, and Pediatric Diarrhea in Bolivia. Int J Occup Environ Health 15:241-248, 2009. PMID: 19323818

148. Lioy PJ, Isukapalli SS, Trasande L, Thorpe L, Dellarco M, Weisel C, Georgopoulos PG, Yung C, Brown M, Landrigan P. Using National and Local Extant Data to Characterize Environmental Exposures in the National Children’s Study (NCS): Queens County, New York. Environ Health Perspect 117:1494-1504, 2009. PMID: 20019897

149. Miodovnik A, Landrigan PJ. The U.S. Food and Drug Administration Risk Assessment on Lead in Women’s and Children’s Vitamins is Based on Outdated Assumptions. (Commentary) Environ Health Perspect 17:1021-1022, 2009.

150. Landrigan PJ. What causes autism? Exploring the environmental contribution. Curr Opin Pediatr 2010, 22(2):219-25. Review. DOI: 10.1097/MOP.0b013e328336eb9a PMID: 20087185

151. Trasande L, Cortes JE, Landrigan PJ, Abercrombie MI, Bopp RF, Cifuentes E. Methylmercury exposure in a subsistence fishing community in Lake Chapala, Mexico: an ecological approach. Environ Health 9:1-10, 2010. doi: 10.1186/1476-069X-9-1. PMID 20064246

152. Cifuentes E, Trasande L, Ramirez M, Landrigan PJ. A qualitative analysis of environmental policy and children’s health in Mexico. Environ Health 9:14, 2010. PMID: 20331868

153. Fleisch A, Sheffield P, Chinn C, Edelstein B, Landrigan P. Bisphenol A and Related Compounds in Dental Materials. Pediatrics 126:760–768, 2010. PMID: 20819896

17


154. Landrigan PJ, Rauh VA, Galvez MP. Environmental Justice and the Health of Children. Mount Sinai J Med 77:178-187, 2010.

155. Sheffield PE, Landrigan PJ. Global climate Change and Children’s Helath: Threats and Strategies for Prevention. Environ Health Perspect 113(3):291-298, 2011. PMID 20947468

156. Crowley LE, Herbert R, Moline JM, Wallenstein S, Shukla G, Schechter C, Skloot GS, Udasin I, Luft BJ, Harrison D, Shapiro M, Wong K, Sacks HS, Landrigan PJ, Teirstein AS. “Sarcoid Like” Granulomatous Pulmonary Disease in World Trade Center Disaster Responders. Am J Ind Med 54:175-184, 2011.

157. Landrigan PJ, Goldman LR. Children’s Vulnerability to Toxic Chemicals: A Challenge and Opportunity to Strengthen Health and Environmental Policy. Health Affairs 30(5):842-850, 2011.

158. Landrigan PJ, Ripp J, Murphy RJC, Claudio L, Jao J, Hexom B, Bloom HG, Shirazian T, Elahi E, Koplan JP. New Academic Partnerships in Global Health: Innovations at Mount Sinai School of Medicine. Mount Sinai J Med. 78:470-482, 2011.

159. Camargo MC, Stayner LT, Straif K, Reina M, Al-Alem U, Demers PA, Landrigan PJ. Occupational Exposure to Asbestos and Risk of Ovarian Cancer: A Meta-Analysis. Environ Health Perspect 119(9):1211-7, 2011.

160. Wisnivesky JP, Teitelbaum S, Todd A, Boffetta P, Crane M, Crowley L, Dellenbaugh C, Harrison D, Herbert R, Hyun K, Jeon Y, Kaplan J, Katz C, Levin S, Luft B, Markowitz S, Moline J, Osbay F, Pietrzak R, Shapiro M, Sharma V, Skloot G, Southwick S, Stevenson L, Udasin I, Wallenstein S, Landrigan PJ. Persistence of multiple illnesses in World Trade Center rescue and recovery workers: a cohort study. Lancet 378: 888–897, 2011.

161. Woskie S, Hyyun K, Freund A, Stevenson L, Park BY, Baron S, Herbert R, de Hernandez MS, Teitelbaum S, de la Hoz, RE, Wisnivesky JP, Landrigan PJ. World Trade Center Disaster: Assessment of Responder Occupations, Work Locations and Job Tasks. Am J Ind Med 54:681-695, 2011.

162. Kim H, Herbert R, Landrigan P, Markowitz SB, Moline JM, Savitz DA, Todd AC, Udasin IG, Wisnivesky JP. Increased Rates of Asthma Among World Trade Center Disaster Responders. Am J Ind Med 55:44-53, 2012.

163. Caravanos J, Chatham-Stephens K, Ericson BC, Landrigan PJ, Fuller R. The Burden of Disease from Pediatric Lead Exposure at Hazardous Waste Sites in 7 Asian Countries. Environ Res 120:119-125, 2012. http://dx.doi.org/10.1016/j.envres.2012.06.006.

164. Isukapalli S, Brinkerhoff CJ, Xu S, Dellarco M, Landrigan PJ, Lioy PJ, Georgopoulos PG. Exposure Indices for the National Children’s Study: Application to inhalation exposures in Queens County, NY. J Expo Sci Environ Epidemiol, 2012. doi:10.1038/jes.2012.99 PMID: 23072768.

165. Pietrzak RH, Schechter CB, Bromet EJ, Katz CL, Reissman DB, Ozbay F, Sharma V, Crane M, Harrison D, Herbert R, Levin SM, Luft BJ, Moline JM, Stellman JM, Udasin IG, Landrigan PJ, Southwick SM. The burden of full and subsyndromal posttraumatic stress disorder among police involved in the World Trade Center rescue and recovery effort. J Psych Research 46:835-842, 2012.

166. Lucchini RG, Crane MA, Crowley L, Globina Y, Milek DJ, Boffetta P, Landrigan PJ. The World Trade Center health surveillance program: results of the first 10 years and implications for prevention. G Ital Med Lav Erg, 34:3, Suppl 539-533, 2012.

167. Pietrzak RH, Feder A, Singh R, Schechter CB, Bromet EJ, Katz CL, Reissman DB, Ozbay F, Sharma V, Crane M, Harrison D, Herbert R, Levin SM, Luft BJ, Moline JM, Stellman JM, Udasin IG, Landrigan, PJ, Southwick S M. Trajectories of PTSD risk and resilience in World Trade Center responders: An 8-year prospective cohort study. Psychological Medicine, pp 1-15, April 2013. DOI: http://dx.doi.org/10.1017/S0033291713000597

18


168. Schwartz AW, Clarfield AM, Doucette JT, Valinsky L, Karpati T, Landrigan PJ, Sternberg SA. Dispartities in pneumococcal and influenza immunization among older adults in Israel: A cross-sectional analysis of socio-demographic barriers to vaccination. Preventive Medicine 56:337-340, 2013.

http://dx.doi.org/10.1016/j.ypmed.2013.01.019 169. Pietrzak RH, Feder A, Schechter CB, Singh R, Cancelmo L, Bromet EJ, Katz CL, Reissman DB, Ozbay

F, Sharma V, Crane M, Harrison D, Herbert R, Levin SM, Luft BJ, Moline JM, Stellman JM, Udasin IG, El-Gabalawy R, Landrigan PJ, Southwick SM. Dimensional structure and course of post-traumatic stress symptomatology in World Trade Center responders. (Original Article) Psychological Medicine, pp 1-14. Cambrindge University Press, 2013.

170. Ericson B, Caravanos J, Chatham-Stephens, Landrigan P, Fuller R. Approaches to systematic assessment of environmental exposures posed at hazardous waste sites in the developing world: the Toxic Sites Identification Program. Environ Monit Assess 185:1755-1766, 2013. PMID: 22592783.

171. Chatham-Stephens K, Caravanos J, Ericson B, Sunga-Amparo J, Susilorini B, Sharma P, Landrigan PJ, Fuller R. Burden of Disease from Toxic Waste Sites in India, Indonesia, and the Philippines in 2010. Environ Health Perspect 121:791-796, 2013.

172. Solan S, Wallenstein S, Shapiro M, Teitelbaum SL, Stevenson L, Kochman A, Kaplan J, Dellenbaugh C, Kahn A, Biro FN, Crane M, Crowley L, Gabrilove J, Gonsalves L, Harrison D, Herbert R, Luft B, Markowitz SB, Moline J, Niu X, Sacks H, Shukla G, Udasin I, Lucchini RG, Boffetta P, Landrigan PJ. Cancer Incidence in World Trade Center Rescue and Recovery Workers; 2001-2008. Environ Health Perspect 121:699-704, 2013.

173. Espina C, Porta M, Schüz, Aguado IH, Percival RB, Dora C, Slevin T, Guzman JR, Meredith T, Landrigan PJ, Neira M. Environmental and Occupational Interventions for Primary Prevention of Cancer: A Cross-Sectorial Policy Framework. Environ Health Perspect 121:420-426, 2013.

174. Individual Scientists. Statement in Response to Asbestos Industry Efforts to Prevent a Ban on Asbestos in Pakistan: Chrysotile Asbestos Use is Not Safe and Must Be Banned. (Letter to Editor). Arch Environ Occup Health 68:243-249, 2013.

175. Grandjean P, Landrigan PJ. Neurobehavioural effects of developmental toxicity. Lancet Neurol 13:330-338, 2014.

176. Tolins M, Ruchirawat M, Landrigan P. The Developmental Neurotoxicity of Arsenic: Cognitive and Behavioral Consequences of Early Life Exposure. Annals of Global Health 80:303-314, 2014.

177. Landrigan PJ, Fuller R. Environmental pollution: An enormous and invisible burden on health systems in low- and middle-income countries. World Hospitals and Health Services 4:35-40, 2014.

178. Chatham-Stephens K, Caravanos J, Ericson B, Landrigan P, Fuller R. The pediatric burden of disease form lead exposure at toxic waste sites in low and middle income countries. Environ Research 132:379-383, 2014.

179. Georgopoulos PG, Brinkerhoff CJ, Isukapalli S, Dellarco M, Landrigan PJ, Lioy PJ. A tiered framework for risk-relevant chacterization and ranking of chemical exposures: applications to the National Children’s Study (NCS). Risk Analysis 34:1299-1316, 2014.

180. Laborde A, Tomasina F, Bianchi F, Bruné M-N, Buka I, Comba P, Corra L, Cori L, Dufffert CM, Harari R, Iavarone I, McDiarmid MA, Gray KA, Sly PD, Soares A, Suk WA, Landrigan PJ. Children’s Health in Latin America: The Influence of Environmental Exposures. Environ Health Perspect 123:201-209, 2015. In print: http://dx.doi.org/10.1289/ehp.1408292

181. Sly P, Carpenter D, Van den Berg M, Stein R, Landrigan P, Brune-Drisse MN, Suk W. Health consequences of environmental exposures: What is an environmental disease? Lancet 2015, in press.

19


182. Landrigan P, Ruchirawat M, Silva E, Huo X, Diaz-Barriga F, Zar H, King M, Ha EH, Asante KA, Ahanchian H. Health consequences of environmental exposures in early life: Changing global patterns of exposure and disease with data from the CEH WHO collaborating centers’ network. Lancet 2015, in press.

183. E-Waste and Harm to Vulnerable Populations: A Growing Global Problem. Heacock M, Kelly CB, Asante KA, Birnbaum LS, Bergman AL, Bruné M-N, Buka I, Carpenter DO, Chen A, Huo X, Kamel M, Landrigan PJ, Magalini F, Diaz-Barriga F, Neira M, Omar M, Pascale A, Ruchirawat M, Sly L, Sly PD, van den Berg M, Suk W. (Commentary). Environ Health Perspect 124:550-555, 2016. DOI:10.1289/ehp.1509699.

184. Li Q, Kappil MA, Li A, Dassanyake PS, Darrah TH, Friedman AE, Friedman M, Lambertini L, Landrigan P, Stodgell CJ, Xia Y, Nanes JA, Aagaard KM, Schadt EE, Murray JC, Clark EB, Dole N, Culhane J, Swanson J, Varner M, Moye J, Kasten C, Miller RK, Chen J. Exploring the associations between microRNA expression profiles and environmental pollutants in human placenta from the National Children’s Study (NCS). Epigenetics 10:793-802, 2015.

185. Heindel JJ, Balbus J, Birnbaum L, Brune-Drisse MN, Grandjean P, Gray K, Landrigan PJ, Sly PD, Suk W, Cory Slechta D, Thompson C, Hanson M. Developmental Origins of Health and Disease: Integrating Environmental Influences. Endocrinology, Mini Review 1-5, 2015. PMID: 26241070.

186. Landrigan PJ, Wright RO, Cordero JF, Eaton DL, Goldstein BD, Hennig B, Maier RM, Ozonoff DM, Smith MT, Tukey RH. The NIEHS Superfund Research Program: 25 Years of Translational Research for Public Health. (Commentary). Environ Health Perspect 123:909-918, 2015.

187. Feder A, Mota N, Salim R, Rodriguez J, Singh R, Schaffer J, Schechter C, Cancelmo L, Bromet EJ, Katz CL, Reissman DB, Ozbay F, Kotov R, Crane M, Harrison DJ, Herbert R, Levin SM, Luft BJ, Moline JM, Stellman JM, Udasin IG, Landrigan PJ, Zvolensky MJ, Yehuda R, Southwick SM, Pietrzak RH. Risk, Coping and PTSD Symptom Trajectories in World Trade Center Responders. Journal of Psychiatric Research 2016, in press.

BOOKS

1. Landrigan PJ, Selikoff IJ (editors). Occupational Health in the 1990's: Developing a Platform for Disease Prevention. Annals NY Academy of Sciences: 572 1-296, 1989.

2. Landrigan PJ. (Chair): Environmental Neurotoxicology. Commission on Life Sciences, National Research Council. Washington: National Academy Press, 1992.

3. Landrigan PJ (Chair): Pesticides in the Diets of Infants and Children. Committee on Pesticides in the Diets of Infants and Children. Board on Agriculture, and Commission on Life Sciences. National Research Council. Washington: National Academy Press, 1993.

4. Landrigan PJ, Needleman HL: Raising Children Toxic Free. How to Keep Your Child Safe From Lead, Asbestos, Pesticides and Other Environmental Hazards. New York: Farrar, Straus and Giroux, 1994.

5. Araki S: Neurobehavioral Methods and Effects in Occupational and Environmental Health. Ed. Araki S, Associate Eds. Gilioli R, Landrigan PJ, Yokoyama K. Academic Press, New York, 1994.

6. Leigh JP, Markowitz S, Fahs M, Landrigan P: Costs of Occupational Injuries and Illnesses. Ann Arbor: The University of Michigan Press, 2000.

7. Landrigan PJ, Needleman HL, Landrigan M. Raising Healthy Children in a Toxic World: 101 Smart Solutions for Every Family. Emmaus PA: Rodale Press, 2002.

8. Mehlman MA, Bingham E, Landrigan PJ, Soffritti M, Belpoggi F, Melnick RL. Carcinogenesis Bioassays and Protecting Public Health. Commemorating the lifework of Cesare Maltoni and colleagues. Annals of the New York Academy of Sciences (Vol. 982), New York, NY. GYAT/B-M Press, 2002.

9. Landrigan PJ, Etzel RA (Editors). Textbook of Children's Environmental Health. London: Oxford University Press, November 2013.

20

OTHER PUBLICATIONS: REVIEW ARTICLES, CONFERENCE PROCEEDINGS, BOOK CHAPTERS,

COMMENTARIES, EDITORIALS, LETTERS TO EDITOR, ABSTRACTS & POSTERS

1. Landrigan PJ: Measles (Rubella). In: Immunization Against Disease – 1972. Center for Disease Control, 1972.

2. Landrigan PJ: Can measles vaccine cause hearing loss? JAMA 219:92, 1973.

3. McLaren GC, Barthel WF, Landrigan PJ: Screening for lead poisoning: Measurements and methodology. (Letter) Pediatrics 52:303, 1973.

4. Landrigan PJ: The exposure of children to lead from industry: Epidemiology and health consequences. In: Proceedings of National Conference on Health Effects of Occupational Lead and Arsenic Exposure, Chicago, February 24-25, 1975. HEW Pub. No. (NIOSH) 76-134, pp 147-156.

5. Landrigan PJ, Earl JL, Chow TJ: Biogeochemical studies of lead isotopes near a smelter. In: Proceedings of the Second International Conference on Stable Isotopes, Oak Brook, Illinois, October 20-23, 1975.

6. Bridbord K, Wagoner J, Blejer H, Landrigan PJ, Lemen R: The role of epidemiology in assessing the health effects of metals. In: Proceedings of the International Conference on Environmental Sensing and Assessment, Las Vegas, Nevada, September 14, 1975.

7. Landrigan PJ, Baker EL: Increased lead absorption with anemia and subclinical neuropsychologic dysfunction in children near two lead smelters. In: Proceedings of the International Conference on Heavy Metals in the Environment, Toronto, Ontario, Canada, October 27-31, 1975.

8. Landrigan PJ, Carter CD, Modlin FJ, Henderson RH, Edwards PQ: Infectious disease in adolescence. In: Adolescent Medicine Topics, Vol. I, (Ed) Ralph I. Lopez. New York: Spectrum Publications, 1976.

9. Landrigan PJ, Feldman RG, Baker EL, Coski CL, Hayes MK, Bernstein R, Cohen S: Lead absorption and slowed nerve conduction in children near a leadsmelter. (Abstract) Neurology 26:391-392, 1976.

10. Baker EL, Landrigan PJ, Harrington JM: Perspectives on environmental health: Vignettes from recent epidemiologic investigations. In: Toxic Torts: Tort Actions for Cancer and Lung Disease Due to Environmental Pollution. (Eds) Rheingold PD, Landau NJ, Canavan MM. Washington: The Association for Trial Lawyers of America, 1977.

11. Landrigan PJ, Baker EL: Child health and environmental lead. Letter to the Editor. Brit Med J 1:836, 1977.

12. Landrigan PJ, Baker EL: Reply to a note concerning the papers of Landrigan and associates. Letter to the Editor. Peds 91:515, 1977.

13. Baker EL, Landrigan PJ, Glueck CJ, Zack MM, Liddle JA, Burse VW: Metabolic consequences on population exposure to polychlorinated biphenyls. (Abstract) Clin Res 26:657A, 1978.

13.1 Miller RW, Brent RL, Brown AK, Finberg L, Frantz C, Goldbloom VC, Heavenrich RM, Peebles TC, Stevenson JL, Jr., Falk H, Knelson JH, Landrigan PJ, Rogan, WJ. National Standad for Airborne Lead: Committee on Environmental Hazards. Peds 62:1070-1071, 1978.

14. Landrigan PJ: Neurologic effects of exposure to lead. Letter to the Editor. Peds 94:504-505, 1979.

15. Landrigan PJ, Whitworth RH, Feldman RG: Neurotoxicologic evaluations of children with chronic increased lead absorption. (Abstract) In: Proceedings of the International Conference on Critical Current Issues in Environmental Health Hazard. Tel Aviv, Israel; 4-7, p 112, March 1979.

16. Landrigan PJ, Baker EL: Occupational lead poisoning: Clinical and biochemical findings related to blood lead levels. (Abstract) Am J Epidemiol 110:357, 1979.

21


COMMENTARIES, EDITORIALS, LETTERS TO EDITOR, ABSTRACTS & POSTERS (cont)

17. Landrigan PJ, Baker EL, Whitworth RH, Feldman RG: Neuroepidemiologic evaluations of children with chronic increased lead absorption. In: Low Level Lead Exposure: The Clinical Implications of Current Research. (Ed) Needleman HL. New York: Raven Press, 1980, pp 17-33.

18. Landrigan PJ, Kreiss K, Xintaras C, Feldman RG, Heath CW: Clinical epidemiology of occupational neurotoxic disease. Neurobehav Toxicology 2:43-48, 1980.

19. Landrigan PJ: General population exposure to environmental concentrations of halogenated biphenyls. Chapter 9A. Halogenated Biphenyls, Terphenyls, Napthalenes, Dibenzodioxins, and Related Products. (Ed) Kimbrough RD. Amsterdam: Elsevier, 1980, pp 267-286.

20. Halperin WE, Landrigan PJ: No time for vertigo. (Letter) New Engl J Med 303:467, 1980.

21. Landrigan PJ, Baker EL: Exposure of children to heavy metals from smelters: Epidemiology and toxic consequences. Environ Res 25:204-244, 1981.

22. Landrigan PJ: Arsenic: State of the Art. Am J Ind Med 2:5-14, 1981.

23. Needleman HL, Landrigan PJ: The health effects of low level exposure to lead. Annual Rev Publ Health 2:277-298, 1981.

24. Landrigan PJ, Harrington JM: Gynecomastia. (Letter) New Engl J Med 304:234-235, 1981.

25. Landrigan PJ, Hayes CG, Graham MG: Sources of lead for lead workers' children - A directory of scrap smelters. Appendix. Pediatrics 68:228-230, 1981.

26. Landrigan PJ, Gross RL: Chemical wastes - Illegal hazards and legal remedies. (Editorial) Am J Public Health 71:985-987, 1981.

27. Landrigan PJ: Toxic exposures and psychiatric diseases: An epidemiologic approach. In: Proceedings of the Third World Congress of Biological Psychiatry, Stockholm, 1981. Amsterdam: Elsevier North Holland Biomedical Press, 1981, pp 108-113.

28. Waxweiler RJ, Landrigan PJ, Infante P, Shapiro R: Introduction to Conference to Re-Evaluate the Toxicity of Vinyl Chloride Monomer, Poly (Vinyl Chloride) and Structural Analogs. Environ Health Perspect 41:1, 1981.

29. Landrigan PJ: Recent advances in the assessment of workplace exposure - Epidemiologic linkage of medical and environmental data. J Environ Sci Health A17:499-513, 1982.

30. Landrigan PJ: Increased lead absorption with anemia and slowed nerve conduction in children near a lead smelter. In: Proceedings of an International Workshop on Plans for Clinical and Epidemiologic Follow-up after Area-Wide Chemical Contamination. Washington, DC: National Academy of Sciences, 1982, pp 74-84.

31. Landrigan PJ: Cohort study of Michigan residents exposed to polybrominated biphenyls: Epidemiologic and immunologic findings. In: Proceedings of an International Workshop on Plans for Clinical and Epidemiologic Follow-up after Area-Wide Chemical Contamination. Washington, DC: National Academy of Sciences, 1982, pp 99-112.

32. Landrigan PJ: Epidemiology of lead and other metal poisonings in children. In: Chemical and Radiation Hazards to Children. Report of the 84th Ross Conference on Pediatric Research. Columbus, Ohio: Ross Laboratories, 1982, pp 40-49.

33. Landrigan PJ: Lead study results questioned. (Letter) Pediatrics 69:248, 1982.

22



34. Landrigan PJ: Cancer: The Right to Know. (Guest Editorial) The Cincinnati Enquirer, April 2, 1982.

35. Landrigan PJ: Occupational and community exposures to toxic metals - lead, cadmium, mercury and arsenic. Western J Med 137:532-539, 1982.

36. Landrigan PJ, Rinsky RA, Waxweiler RJ: Epidemiologic assessment of occupational illness caused by exposures to petrochemicals. Proceedings of the Seventh Alaska Health Congress, 1982, pp 84-96.

37. Landrigan PJ, Cohen ML, Dowdle W, Elliott LJ, Halperin WE: Medical surveillance of biotechnology workers: Report of the CDC/NIOSH Ad Hoc Working Group on Medical Surveillance for Industrial Applications of Biotechnology. NIH Recombinant DNA Technical Bulletin 5:133-138, 1982.

38. Landrigan PJ: Epidemiologic approaches to persons with exposure to waste chemicals. Environ Health Perspect 48:93-97, 1983.

39. Landrigan PJ, Melius JM, Rosenberg MJ, Coye MJ, Binkin NJ: Reproductive hazards in the workplace: Development of epidemiologic research. Scand J Work Environ Health 9:83-88, 1983.

40. Landrigan PJ: Toxic exposures and psychiatric disease – Lessons from the epidemiology of cancer. Acta Psychiatrica Scandinavica 67 Suppl 303:6-15, 1983.

41. Landrigan PJ, Baker EL: Epidemiological aspects of occupational lead poisoning. J Univ Occup Environ Health (Japan) 5 Suppl:145-155, 1983.

42. Rinsky RA, Landrigan PJ: Data on lung cancer in radiation workers. (Letter) Proc Royal Soc Med 76:324-325, 1983.

43. Landrigan PJ: Occupational and pediatric aspects of lead toxicity. Veterinary and Human Toxicology 25(Suppl):1-6, 1983.

44. Landrigan PJ: Lead Exposure, Lead Absorption and Lead Toxicity in the Children of Port Pirie: A Second Opinion. Report to the Minister of Health of South Australia. Adelaide, 1983.

45. Landrigan PJ, Rinsky RA: The contribution of epidemiology to the development of disease prevention policy. In: Proceedings of a Conference on Health-Related Claims: Can the Tort and Compensation Systems Cope? Arlington, VA: National Legal Center for the Public Interest, 1983, pp 56-75.

46. Landrigan PJ: Arsenic. Chapter 41. In: Environmental and Occupational Medicine. (Ed) Rom WN. Boston: Little, Brown and Co., 1983.

47. Landrigan PJ, Bridbord K: Additional exposure routes. In: Changing Metal Cycles and Health. Dahlem Konferenzen. (Ed) Nriagu JO. Berlin:Springer-Verlag, 1984.

48. Landrigan PJ, Harrington JM, Elliott LK: The Biotechnology Industry. In: Recent Advances in Occupational Health. Vol. 2. (Ed) Harrington JM. London: Churchill, Livingstone, 1984, pp 3-13.

49. Landrigan PJ, Meinhardt TJ, Gordon J, Lipscomb JA, Berg JR, Mazzuckelli LR, Lewis TR, Lemen RA: Ethylene oxide: An overview of toxicologic and epidemiologic research. Am J Ind Med 6:103-116, 1984.

50. Landrigan PJ, Bainbridge JK, Melius JM: Multidisciplinary approach to prevention and health monitoring: Role of individual disciplines. Medical Inspectors/Medical Officers. In: Assessment of Toxic Agents at the Workplace - Roles of Ambient and Biological Monitoring. (Eds) Berlin A, Yodaiken RE, Henman BA. Boston: Kluwer Academic Publishers (for the Commission of the European Communities), 1984.

51. Landrigan PJ, Houk VN: EPA Review of Lead Study. Letter to the Editor. Science 223:118, 1984.

23



52. Moody L, Halperin WE, Fingerhut MA, Landrigan PJ: The chronic health effects of occupational exposure to dioxins: Unanswered questions. (Editorial) Am J Ind Med 5:157-160, 1984.

53. Landrigan PJ, Goyer RA, Clarkson TW, Sandler DP, Smith JH, Thun MJ, Weeden RP: The work-relatedness of renal disease and summary of the work group on renal disease. Arch Environ Health 39:225-230, 250, 1984.

54. Landrigan PJ, Rinsky RA: The application of epidemiology to the prevention of occupational cancer. J Toxicol 22:209-238, 1984.

55. Reeve GR, Halperin WE, Landrigan PJ: Brain tumor investigations in Texas. In: Proceedings of a Conference on Cancer in Texas. San Antonio: January 1984.

56. Landrigan PJ, Rinsky RA, Melius JM, Thun MJ: Approaches to the estimation of exposure in occupational and environmental epidemiology. Proceedings of the Banbury Center Conference on Risk Quantitation and Regulatory Policy, 1984.

57. Landrigan PJ, Froines JR, Mahaffey KR: Body lead burden: A summary of epidemiological data on its relation to environmental sources and toxic effects. Chapter 14. In: Dietary and Environmental Lead: Human Health Effects. (Ed) Mahaffey KR. Amsterdam: Elsevier Scientific Publishers, 1985.

58. Landrigan PJ: The importance of occupational cohorts in chronic disease epidemiology. Chairman's Remarks. NCI Monograph 67; 83, 1985.

59. Melius JM, Landrigan PJ: Occupational Health. In: Introduction to Environmental Health. (Ed) Blumenthal DS. New York: Springer Publishing Company, 1985.

60. Landrigan PJ: The uses of epidemiology in the study of neurotoxic pollutants - Lessons from the workplace. Int J Mental Health 14:44-63, 1985.

61. Brigham CR, Landrigan PJ: Safety and health in boat building and repair. Am J Ind Med 8:169-182, 1985.

62. Baker EL Jr, Smith TJ, Landrigan PJ: The neurotoxicity of industrial solvents: A review of the literature. Am J Ind Med 8:207-217, 1985.

63. Landrigan PJ: Academic occupational health and environmental medicine: Current directions. Bull NY Acad Med 61:901-916, 1985.

64. Landrigan PJ, Gehlbach SH, Graef JW, Hanson JW, Nathenson G: Smokeless Tobacco - A carcinogenic hazard to children. Committee on Environmental Hazards, American Academy of Pediatrics. Pediatrics 76:1009-1011, 1985.

65. Rosenstock L, Landrigan PJ: Occupational Health: The intersection between clinical medicine and public health. Ann Rev Pub Health 7:337-356, 1986.

66. Landrigan PJ, Robbins A: Foreword to The Hawk's Nest Incident: America's Worst Industrial Disaster. Cherniack MG. New Haven: Yale University Press, 1986.

67. Boardman B, Greaves I, Levenstein C, Landrigan PJ: The Pattern of White House Budget Office Decisions in Environmental Health Research: A Statistical Analysis. Report to Subcommittee on Oversight and Investigations, Committee on Energy and Commerce, U.S. House of Representatives and to the American Public Health Association. September 29, 1986.

68. Wilkinson CW, Landrigan PJ, Eck J: Violent deaths: The mortality experience of police officers. (Abstract) Presented at the Annual Meeting of the Epidemiology Section of the International Commission on Occupational Health, Los Angeles, CA, September 1986.

24

OTHER PUBLICATIONS: REVIEW ARTICLES, CONFERENCE PROCEEDINGS, BOOK CHAPTERS, COMMENTARIES,

EDITORIALS, LETTERS TO EDITOR, ABSTRACTS & POSTERS (cont)

69. Landrigan PJ: Epidemiologic and toxicologic analyses of the neurotoxicity of new materials. (Abstract) Presented at a Symposium on Health and Safety of New Technologies, "Workplace 2000." Boston, November 13-14, 1986.

70. Landrigan PJ, DiLiberti JH, Graef JW, Hanson JW, Nathenson G: Involuntary Smoking - A Hazard to Children. Committee on Environmental Hazards, American Academy of Pediatrics. Pediatrics 77:755-757, 1986.

71. Nelson N, Levine RJ, Albert RE, Blair AE, Griesemer RA, Landrigan PJ, Stayner LT, Swenberg JA: Contribution of Formaldehyde to Respiratory Cancer. Environ Health Perspect 70:23-35, 1986.

72. Cone JE, Reeve GR, Landrigan PJ: Clinical and epidemiologic studies. In: Toxic Substances and Human Risk - Principles of data interpretation. (Eds) Tardiff RB, Rodricks JV. New York: Plenum Press 1987, pp 95-120.

73. Hoel DG, Landrigan PJ: Comprehensive evaluation of human data. Chapter 7. In: Toxic Substances and Human Risk - Principles of data interpretation. Principles for the Evaluation of Toxic Hazards to Human Health. (Eds) Tardiff RB, Rodricks JV. New York: Plenum Press 1987, pp 121-130.

74. Landrigan PJ, Graef JW: Pediatric lead poisoning in 1987 - The silent epidemic continues. (Editorial) Pediatrics 719:582-583, 1987.

75. Landrigan PJ, Selikoff IJ: Primary prevention against occupational carcinogens. In: Cancer Risks: Strategies for Elimination. (Ed) P Bannasch. Springer-Verlag: Berlin, Heidelberg, New York, London, Paris, Tokyo, 1987.

76. Landrigan PJ: Silicosis. Occupational Medicine. State of the Art Reviews 2:319-326, 1987.

77. Landrigan PJ: Occupational leukemia. State of the Art Reviews 2:179-188, 1987.

78. Landrigan PJ: Principles for application of porphyrin markers in epidemiological studies. Ann NY Acad Sci 514:323-326, 1987.

79. Needleman HL, Rosen J, Piomelli S, Landrigan PJ, Graef J: The hazards of benign(?) neglect of elevated blood lead levels. Letter to the Editor. Am J Dis Child 141:941-942, 1987.

80. Landrigan PJ: Benzene and Leukemia. (Editorial) Am J Ind Med 11:605-606, 1987.

81. Wilkinson CW, Landrigan PJ, Eck JE: The contribution of bullet-proof vests and worker training to reduction of line-of-duty deaths in police officers. (Abstract) Presented at the Annual Meeting of the Society of Occupational and Environmental Health, 1987.

82. Landrigan PJ, DiLiberti JH, Graef JW, Jackson RJ, Nathenson G: Statement on Asbestos Exposure in Schools. Committee on Environmental Hazards, American Academy of Pediatrics. Pediatrics 79:301-305, 1987.

83. Landrigan PJ, DiLiberti JH, Gehlbach SH, Graef JW, Hanson JW, Jackson RJ, Nathenson G: Statement on Childhood Lead Poisoning. American Academy of Pediatrics, Committee on Environmental Hazards, Committee on Accident and Poison Prevention. Pediatrics 79:457-465, 1987.

84. Rinsky RA, Smith AB, Hornung R, Okun AH, Landrigan PJ: Benzene and Leukemia. (Letter) New Engl J Med 317:1027-1029, 1987.

85. Levin SM, Baker DB, Landrigan PJ, Monaghan SV, Frumin E, Brathwaite M, Towne M: Testicular cancer in leather tanners exposed to dimethyl formamide. (Letter) Lancet 2:1154, 1987.

25



86. Goldstein B, Gibson J, Henderson R, Hobbie J, Landrigan PJ, Mattison D, Perera F, Pfitzer E, Silbergeld E, Wogan G: Biological markers in environmental health research. Environ Health Perspect 74:3-9, 1987.

87. Landrigan PJ: Relation of body burden measures to ambient measures. In: Epidemiology and Health Risk Assessment. (Eds) L Gordis and CH Libauer. Oxford University Press, New York, 1988 pp 139-147.

88. Christiani DC, Melius JM, Landrigan PJ, Coye MJ, Wegman DH: Control of Occupational Disease in the U.S.A. (in Chinese). Chinese J Occup Health 4:314-320, 1988.

89. Landrigan PJ, Baker D, Needleman HL: Lead poisoning in automobile radiator mechanics. (Letter) New Engl J Med 318:320-321, 1988.

90. Selevan SG, Landrigan PJ, Stern FB, Jones JH: Brief Report: Lead and hypertension in a mortality study of lead smelter workers. Environ Health Perspect 78:65-66, 1988.

91. Landrigan PJ, Goldstein EA: Smoke gets in our eyes. New York Newsday, p 62, March 1, 1988.

92. Epstein SS, Swartz JB, Bailar J, Bingham E, Dahlsten DL, Infante PR, Landrigan PJ, Nicholson WJ, Lappé M, Moreno M, Legator M, Mirer F, Moure R, Silverstein M, Ozonoff D, Paigen B, Warren J: April 17, 1987 Ames Article. (Letter) Science 240:1043-1045, 1988.

93. Landrigan PJ, Perera FP: Controversy in the regulation of formaldehyde. (Editorial) Am J Ind Med 14:375-377, 1988.

94. Baker D, Levin SM, Landrigan PJ, Frumin E, Brathwaite M, Towne W: Testicular cancer, industrial bronchitis, and dermatitis among leather tanning workers. (Abstract) Proceedings of Annual Meeting, American Public Health Association, Boston, Nov. 13-17, 1988.

95. Lilis R, Landrigan PJ: Renal and Urinary Tract Disorders. (Chapter) In: Occupational Health-Recognizing and Preventing Work-Related Disease. Levy BS, Wegman DH (eds). Boston: Little, Brown and Co., 2nd edition, 1988, pp. 465-476.

96. Landrigan PJ: Epidemiologic assessment of lead absorption associated with incineration of municipal waste. (Abstract) Proceedings of Annual Meeting of American Public Health Association, Nov. 13-17, 1988.

97. Landrigan PJ: Assessment of the health hazards of lead. In: Proceedings of a One Earth Forum on Managing Hazardous Materials, René Dubos Center for Human Environments. New York City, May 25-26, 1988.

98. Landrigan PJ: Critical review of epidemiology studies on the human carcinogenicity of formaldehyde. Proceedings of the Annual Meeting of the Collegium Ramazzini, Carpi, Italy, December 1, 1988.

99. Landrigan PJ: Lead: Assessing its health hazards. Health and Environ Digest 2:1-3, July 1988.

100. Frumin E, Brathwaite M, Towne W, Levin SM, Baker DB, Monaghan SV, Landrigan PJ, Marshall EG, Melius JM: Testicular cancer in leather workers - Fulton County, New York. MMWR 38:105-114, 1988.

101. Rinsky RA, Hornung R, Landrigan PJ: Benzene and leukemia: A review of the literature and a risk assessment. (Letter) Am J Epidemiol 129:1084-1086, 1989.

102. Morawetz JS, Landrigan PJ: A cluster of traumatic occupational deaths at a foundry, 1974-1986. MMWR 38:293-297, 1989.

26



103. Landrigan PJ: The incompletely studied hazards of waste incineration. (Editorial) Am J Ind Med 15:243-244, 1989.

104. Landrigan PJ: The toxicity of lead at low dose. (Editorial) Br J Ind Med 46:593-596, 1989.

105. Jackson RJ, DiLiberti JH, Landrigan PJ, Nathenson G, Needleman HL, Brown AK, Etzel RA, Falk H, Miller RW, Rogan W: American Academy of Pediatrics, Committee on Environmental Hazards: Radon exposure: A hazard to children. Pediatrics 83:799-802, 1989.

106. Herbert RH, Luo J, Marcus M, Landrigan PJ: The failure of workers compensation statistics to monitor work-related illness in garment workers. (Abstract) Proceedings of Annual Meeting of the American Public Health Association, Chicago, Illinois, October 1989.

107. Landrigan PJ: Improving the surveillance of occupational disease. (Editorial) Am J Public Health 79:1601-1602, 1989.

108. Landrigan PJ: Does formaldehyde cause cancer? A review of the evidence. Health & Environ Digest 3:1-3, 1989.

109. Landrigan PJ: Occupational Health in New York State. Proceedings of the Julia M. Jones Preventive Medicine Day. New York: New York Lung Association, October 18, 1989, pp 10-12.

110. Landrigan PJ: Critical assessment of epidemiologic studies on the human carcinogenicity of 1,3-butadiene. Environ Health Perspect 86:143-147, 1990.

111. Landrigan PJ: Prevention of toxic environmental illness in the twenty-first century. Environ Health Perspect 86:197-199, 1990.

112. Baker DB, Landrigan PJ: Occupationally related disorders. Med Clin North Am 74:441-460, 1990.

113. Landrigan PJ: Current issues in the epidemiology and toxicology of occupational exposure to lead. Environ Health Perspect 89:61-66, 1990.

114. Pollack SH, Landrigan PJ, Mallino DL: Child Labor in the 1990: Prevalence and Health Hazards. Ann Rev Public Health 11:359-375, 1990.

115. Landrigan PJ: Health effects of environmental toxins in deficient housing. Bull New York Academy of Medicine 66:491-499, 1990.

116. Landrigan PJ: Housing and Health: Conclusions and challenges for the future. Bull New York Academy of Medicine 66:587-591, 1990.

117. Ehrlich RI, Kattan M, Saltzberg DS, Grimm KT, Landrigan PJ, Lilienfeld DE: Passive smoking and urinary cotinine levels in acute and non-acute asthmatics. (Abstract) Proceedings of the American Pediatric Society/Society for Pediatric Research, 1990.

118. Kraut A, Chan E, Landrigan PJ: Comparison of cost of searching for data on deaths: National Death Index vs. Social Security Administration. (Abstract) Proceedings of the 118th Annual Meeting of American Public Health Association, New York, 1990.

119. Pollack S, Belville R, McConnell R, Landrigan PJ: Rates of work-related injury requiring hospitalization among teenagers in New York City. (Abstract) Proceedings of the 118th Annual Meeting of American Public Health Association, New York, 1990.

120. Pollack S, McConnell R, Gallelli M, Schmidt J, Obregon R, Landrigan PJ: Pesticide exposure and working conditions among migrant farmworker children in Western New York State. (Abstract) Proceedings of the 118th Annual Meeting of American Public Health Association, New York, 1990.

27



121. Landrigan PJ: Proposal for reduction of the case definition for childhood lead poisoning. (Abstract) Proceedings of the 118th Annual Meeting of American Public Health Association, New York, 1990.

122. Nicholson WJ, Johnson EM, Harington JS, Melius JM, Landrigan PJ: Mesothelioma in the Quebec chrysotile mining and milling area. (Letter) Science 248:796-799, 1990.

123. Levin SM, Landrigan PJ: Tollbooth Syndrome. (Letter) The New York Times, Tuesday, April 1, 1990.

124. Landrigan PJ, Silbergeld E, Froines JR, Pfeffer RM: Lead in the Modern Workplace. (Editorial) Am J Public Health 80:907-908, 1990.

125. Pollack S, Landrigan P, McConnell R, Belleville R: Epidemiologic studies on the health hazards of child labor. (Abstract) Proceedings of the 23rd International Congress on Occupational Health, Montreal, 1990.

126. Tamblyn PB, Landrigan PJ, Nelson M, Kerndt P, Kronoveter K, Zack MM: Lead exposure in stained glass workers. J Environ Pathology, Toxicology and Oncology, 10:63-66, 1990.

127. Markowitz SB, Landrigan PJ: Occupational Lung Disease: Diagnosis, Surveillance, and Prevention. Current Issues in Respiratory Public Health: II. 3:219-232, 1990.

128. Landrigan PJ: Out Sick, Toxins at Work. Harvard Medical Alumni Bulletin. Summer: 42-47, 1990.

129. Landrigan P, Kazemi H: Asbestos and cancer. (Letter) The Economist 316:7670, September 1, 1990.

130. Lilienfeld DE, Perl DP, Landrigan PJ, Chan E, Godbold JH, Marsh G, Ehland J: Increasing mortality from motor neuron disease in the United States during the past two decades. New Advances in Toxicology and Epidemiology. F. Clifford Rose & Forbes H. Norris (Eds). Smith-Gordon, 1990.

131. Lilienfeld DE, Sekkor D, Simpson S, Perl DP, Ehland J, Marsh G, Chan E, Godbold J, Landrigan PJ: Parkinsonism death rates by race, sex and geography: A 1980s update. Neuroepidemiology 9:243-247, 1990.

132. Landrigan PJ: Child labor law violations. California Pediatrician, Fall 1990, pp. 35-36.

133. Landrigan PJ: Recent developments in the toxicology and epidemiology of lead. Tokyo J Med Sc 97:170-172, 1990.

134. Landrigan PJ, Baker DB: Workers. In: Occupational Health. Vol. 3, 2nd Ed., Chapter 27, Oxford Textbook of Public Health. Holland WW, Detels R, Knox G (Eds) Oxford University Press: Oxford, New York, Toronto, pp 449-465, 1991.

135. Landrigan PJ: Strategies for epidemiologic studies of lead in bone in occupationally exposed populations. Environ Health Perspect 91:81-86, 1991.

136. Landrigan PJ, Campbell CC: Chemical and Physical Agents. Chapter 17. In Fetal and Neonatal Effects of Maternal Disease. (Editors) Avron Y. Sweet and Edwin G. Brown. St. Louis: 1991, Mosby Year Book, pp 414-447.

137. Landrigan PJ: Current issues in the epidemiology and toxicology of occupational exposure to lead (in Russian). Gigiena Truda 6:25-29, 1991.

138. Pollack SH, Landrigan P, Mallino DL: Child Labor in the 1990’s: Prevalence and Health Hazards. Ann Rev Public Health 11:359-375, 1990.

139. Silbergeld EK, Landrigan PJ, Froines JR, Pfeffer RM: The occupational lead standard: A goal unachieved, a process in need of repair. New Solutions 1:20-30, 1991.

28



140. Gerr F, Letz R, Landrigan PJ: Upper-extremity musculoskeletal disorders of occupational origin. Annu Rev Public Health 12:543-566, 1991.

141. Pollack SH, Landrigan PJ, Rubinstein H: Child Labor. Chapter in III. Environmental Health, Maxcy-Rosenau-Last Textbook of Public Health, 13th edition, 1991, pp. 576-583.

142. Landrigan PJ, Baker DB: Using Occupational History to Pinpoint the Diagnosis. Geriatrics 46:61-67, 1991.

143. Landrigan PJ, Baker DB: The recognition and control of occupational disease. JAMA 266:676-680, 1991.

144. Belville R, Pollack SH, Landrigan PJ: Adolescent work-related injury award rates in New York State. (Abstract). Proceedings of Annual Meeting of the American Public Health Association, 1991.

145. Pollack SH, Belville R, Landrigan PJ: Work-related head injuries in children. (Abstract). Proceedings of Annual Meeting of the American Public Health Association Meeting, 1991.

146. Landrigan PJ: Preface. In: The Third Wave of Asbestos Disease: Exposure to Asbestos in Place. PJ Landrigan, H Kazemi, IJ Selikoff IJ (Eds). Ann NY Acad Sci 643:xv-xvi, 1991.

147. Landrigan PJ: A Population of Children at Risk of Exposure to Asbestos in Place. In: The Third Wave of Asbestos Disease: Exposure to Asbestos in Place. PJ Landrigan, H Kazemi, IJ Selikoff IJ (Eds). Ann NY Acad Sci 643:283-286, 1991.

148. Markowitz S, Garibaldi K, Lilis R, Landrigan PJ: Asbestos Exposure and Fire Fighting. In: The Third Wave of Asbestos Disease: Exposure to Asbestos in Place. PJ Landrigan, H Kazemi, IJ Selikoff (Eds). Ann NY Acad Sci 643:573-577, 1991.

149. Landrigan PJ: Occupational Surveillance -- Needs and Priorities. Presented at Occupational Surveillance Conference, University of Massachusetts, Amherst, MA, April 29, 1991.

150. Landrigan PJ: Current Issues in the Epidemiology and Toxicology of Occupational Exposure to Lead. Toxicol Ind Health 7:9-14, 1991.

151. Mendelson MH, Short L, Schechter C, Meyers BR, Rodriguez M, Cohen S, Lozada J, Button G, Sacks H, Decambre M, Landrigan P, Hirschman SZ: Comparative cross-over study of a needleless heparin lock system vs. a conventional heparin lock: impact on complications, sharps injuries and cost (Abstract). Accepted for presentation at 32nd lnterscience Conference on Antimicrobial Agents and Chemotherapy. American Society of Microbiology. Anaheim, CA, October, 1992.

152. Landrigan PJ: Arsenic. Chapter 59. In: Environmental and Occupational Medicine, 2nd Edition. Rom WN (Editor). Boston: Little, Brown & Company, 1992, pp. 773-779.

153. Landrigan PJ: Benzene. Chapter 67. In: Environmental and Occupational Medicine, 2nd Edition. Rom WN (Editor). Boston: Little, Brown & Company, 1992, pp. 861-871.

154. Landrigan PJ: Formaldehyde. Chapter 68. In: Environmental and Occupational Medicine, 2nd Edition. Rom WN (Editor) Boston: Little, Brown & Company, 1992, pp. 867-871.

155. Landrigan PJ: Ethylene Oxide. Chapter 87. In: Environmental and Occupational Medicine, 2nd Edition. Rom WN (Editor) Boston: Little, Brown & Company, 1992, pp. 1033-1039.

156. Landrigan PJ, Pollack SH, Belville R: Child Labor. Chapter 118. In: Environmental and Occupational Medicine (Second edition): A Guide to their Recognition. Rom WN (Ed). Boston: Little, Brown & Co., 1992, pp.1365-1370.

29



157. Selikoff IJ, Landrigan PJ: The third epidemiological revolution. (Editorial) J Occup Med and Toxicol 1:vii-viii, 1992.

158. Bertin JE, Ashford NA, Bellinger D, Landrigan PJ, Legator MS, Mattison DR, McBeath WH, Rosen JF, Stellman JM: The Goal: Safety and Equality. (Editorial) Am J Ind Med 21:463-465, 1992.

159. Landrigan PJ: Environmental disease - a preventable epidemic (Commentary). Am J Public Health 82:941-943, 1992.

160. Landrigan PJ: Current status of occupational disease in the United States (Editorial). J Occup Med Toxicol 1:97-100, 1992.

161. Kraut A, Chan E, Landrigan PJ: The costs of searching for deaths: National Death Index vs Social Security Administration. (Letter) Am J Public Health 82:760, 1992.

162. Landrigan PJ: Risk assessment for 1,3-butadiene. (Letter) Science 257:1330-1331, 1992.

163. Landrigan PJ, Markowitz SB: The case for OSHA reform (Guest Editorial). New Solutions 3:3-7, 1992.

164. Bates DV, Gotsch AR, Pharm D, Brooks S, Landrigan PJ, Hankinson JL, Merchant JA: Prevention of occupational lung diseases. Chest (Supplement) 102:257S-276S, 1992.

165. Selikoff IJ, Landrigan PJ: The third epidemiological revolution. (Letter), Eur J Epidemiol 8:625-626, 1992.

166. Landrigan PJ: Assessment of the Health Hazards of Lead. In: Management of Hazardous Agents. Eds. LeVine DG and Upton AC. Industrial and Regulatory Approaches, Vol. 1, pp1992.

167. Kraut A, Chan E, Abe T, Hall NEL, Landrigan PJ: Completeness of Case Ascertainment of the State Cancer Registry. J Med Soc NJ 89:772-773, 1992.

168. Landrigan PJ: Environmental pollution and health. (Letter), Lancet 340:1220, 1992.

169. Landrigan PJ, Pollack SH, Belville R, Godbold JG: Child labor in the United States: Historical Background and Current Crisis. Mount Sinai J Med 59:498-503, 1992.

170. Landrigan PJ, Curran A: Lead - A Ubiquitous Hazard. Environ Res 59:279-280, 1992.

171. Landrigan PJ: Summary of Workshop: Prevention Strategies for Neurotoxicology. Environ Res 60:63-64, 1993.

172. Baker DB, Landrigan PJ: Occupational Exposures and Human Health. In: Critical Condition: Human Health and the Environment. Chivian E., McCally M, Hu H, Haines A., Editors. Cambridge: MIT Press, 1993.

173. Landrigan PJ: Protecting children from pesticides. (Letter) Washington Post, April 9, 1993.

174. Landrigan PJ, Pollack SH, Belville R, Godbold JH: Health Hazards of Child Labor. Wallace Public Health and Preventive Medicine, 14th edition. Public Health and Preventive Medicine pp. 697-698.

175. Landrigan PJ: Protecting our nervous system from toxic chemicals. Headline News, Science Views II, Ed. Jarmul D., Washington, D.C. National Academy Press, pp. 56-58, 1993.

30



176. Todd AC, Landrigan PJ, Bloch P: Workshop on the X-ray fluorescence of lead in bone: Conclusions, recommendations and summary. Neurotoxicology 14:145-154, 1993.

177. Landrigan PJ, Belville R: The dangers of illegal child labor. (Editorial). Am J Dis Child 147:1029-1030, 1993.

178. Landrigan PJ: Child Labor: A re-emergent threat. (Editorial). Am J Ind Med 24:267-268, 1993.

179. Landrigan PJ: Asbestos anxiety. Op-Ed Page, The New York Times, September 7, 1993.

179.1 Landrigan PJ: Health Risks of Creosotes. Questions & Answers. JAMA 269:1309, 1993.

180. Todd AC, Landrigan PJ: X-ray fluorescence analysis of lead in bone. Environ Health Perspect 101:494-495, 1993.

181. Landrigan PJ: Critical assessment of epidemiological studies on the carcinogenicity of 1,3-butadiene and styrene. In: Butadine and Styrene: Assessment of Health Hazards, IARC Scientific Publication No. 127, Sorsa M, Peltonen K, Vainio H and Hemminki K (eds.). Lyon, International Agency for Research on Cancer, pp. 375-388, 1993.

182. Committee on Environmental Health, American Academy of Pediatrics: Ambient Air Pollution: Respiratory hazards to children. Needleman HL, Jackson RJ, Landrigan PJ, Lipsett M. Pediatrics, 91:1210-1213, 1993.

183. Landrigan PJ, Graham DG, Thomas RD: Strategies for the prevention of environmental neurotoxic illness. Environ Res 61:157-163, 1993.

184. Landrigan PJ: Overview of Industrial Chemical Exposures. Environ Res 63:1-15, 1993.

185. Landrigan PJ, Pollack SH, Belville R, Godbold JH: Child Labor: Epidemiology and Health Risks. Maternal and Child Health. Wallace H (Editor). Third Party Publishing Co., pp. 73-81, 1994.

186. Landrigan PJ: Lead poisoning. Chapter in Current Diagnosis in Neurology. (Ed. Feldmann E). Mosby-Year Book, Inc., St. Louis, pp. 206-209, 1994.

187. Landrigan PJ, Baker DB, Markowitz SB, Nicholson WJ: Cancer Prevention in the Workplace. (Chapter 22) In: The Science and Practice of Cancer Prevention and Control. Greenwald P, Kramer BS, Weed DL, Editors. New York: Marcel-Dekker, 1994, pp. 393-410.

188. Lilis R, Landrigan PJ: Renal and Urinary Tract Disorders. Chapter for Occupational Health (3rd ed). Wegman DH and Levy B, Editors. Boston: Little, Brown & Co., 1994, Chapter 31, pp. 599-616.

189. Landrigan PJ, Graham DG, Thomas RD: Environmental neurotoxic illness: Research for Prevention. Environ Health Perspect 102(suppl 2):117-121, 1994.

190. Landrigan PJ, Todd AC: Lead poisoning. Conferences and Reviews. West J Med 161:153-159, 1994.

191. Landrigan PJ, Pollack SH, Godbold JG, Belville R: Child Labor: Risks and Prospects for Prevention. In: The Identification and Control of Environmental and Occupational Diseases. Mehlman MA and Upton A (eds), A Tribute to Professor Irving J. Selikoff (1915-1992), pp. 559-569.

31



192. Landrigan PJ, Pollack SH, Godbold JG, Belville R: The health and safety hazards of child labor. In Child Labor in the United States, ed. Newman J. New York: National Child Labor Committee, pp. 13-15, 1994.

193. Landrigan PJ: Principles of Occupational and Environmental Medicine. In Cecil Textbook of Medicine, 20th ed., Bennet JC, Plum F, eds. Philadelphia: WB Saunders Co., 1994, pp. 56-59.

194. Landrigan PJ, Todd AC: Direct measurement of lead in bone: A promising biomarker. (Editorial). JAMA 271:239-240, 1994.

195. Landrigan PJ: Perspective on Pesticides. Encyclopaedia Britannica, Medical and Health Annual, pp. 250-254, 1994.

196. McCally M, Chivian E, Landrigan PJ: More on critical condition: Human health and the environment. (Letter) New Engl J Med 330:1161-1162, 1994.

197. Nicholson WJ, Landrigan PJ: The carcinogenicity of chrysotile asbestos. Advances in Modern Environmental Toxicology, Mehlman M and Upton A (eds.). Princeton Scientific Publishing Co., Princeton, NJ, pp. 407-423, 1994.

198. Nicholson WJ, Landrigan PJ: Human health effects of polychlorinated biphenyls. In: Dioxins and Health. Schecter A., Editor. Plenum Publishing Corp., New York, NY, pp. 487-524, 1994.

199. Landrigan PJ: Disclosure of interest: A time for clarity. (Editorial) Am J Ind Med 26:281-282, 1994.

200. McDiarmid MA, Collins MD, Landrigan PJ: G. II. "Environmental Toxins in Child Health." In Proceedings of "Child Health in the Inner-City IV:" Issues and Answers for the `90s. Washington, D.C.: Department of Pediatrics and Child Health, Howard University College of Medicine, 1994, pp. 283-288

201. Chisholm J, Goldstein G, Cory-Slechta D, Weiss B, Landrigan P, Mushak P, Needleman HL, Rice D, Rosen J, Silbergeld E: Lead Debate Goes On. (Letter) Pediatrics 84:408-410, 1994.

202. Wolff MS, Landrigan PJ: Environmental Estrogens. (Letter) Science 266:525-528, 28 Oct., 1994.

203. Landrigan PJ, Golden AL, Markowitz SB: Occupational Cancer in New York City Firefighters. New York: United Firefighters Association and United Fire Officers Association, 1994.

204. Landrigan PJ, Rowe JW, Fahs MC, Silver A, Cornbill R: The Mount Sinai Health of the Public Program. Abstract. Proceedings of the Annual Meeting of the American Public Health Association, 1994.

204.1 Landrigan PJ: Lead. Chapter 30.9 Textbook of Clinical Occupational and Environmental Medicine, 2nd edition. (Eds) Cullen M, Rosenstock L, 1994, pp. 745-754.

205. Markowitz SB, Li AK, Landrigan PJ: In: Reply: Lead poisoning due to Hai Ge Fen. (Letter). JAMA 273:24-25, 1995.

206. Landrigan PJ, Pollack SH, Belville R, Godbold J: Child labor. Pediatric Annals 24:657-662, 1995.

207. Landrigan PJ, Pollack SH, Godbold JH, Belville R: Occupational injuries--epidemiology, prevention, treatment. In: Adolescent Medicine. State-of-the-Art Reviews 6:207-214, 1995.

208. Landrigan PJ, Pollack SH: Committee on Environmental Health. American Academy of Pediatrics. Statement on the Hazards of Child Labor. Pediatrics 95:311-313, 1995.

209. Landrigan PJ, Baker D: The clinical recognition of occupational and environmental disease. The Mount Sinai J Med 62:406-411, 1995.

32



210. Landrigan PJ, Todd AC: Lead poisoning alert--False alarm? (Letter). West J Med 162:474-475, 1995.

211. Herbert R, Landrigan P: When Work is a Health Hazard. New York Newsday, Op-Ed, Thursday, April 27, 1995.

212. Landrigan PJ: Disclosure of interest: responses from our readers. (Editorial). Am J Ind Med 28:581-582, 1995.

213. Landrigan PJ: Risk assessment and cost/benefit analysis for new regulations. New Solutions 5:85-91, 1995.

214. Landrigan PJ: Book Review: Environmental Medicine, Integrating a Missing Element into Medical Education, by Rall DP and Pope AM. Nature Medicine 1:709, 1995.

215. Landrigan PJ: Pesticides in the Diets of Infants and Children: The Report from the National Academy of Sciences Two Years Later. EPA Journal, fall 1995.

216. Landrigan PJ: Comments on a “Survey of Lead Exposure Around a Closed Lead Smelter.” (Letter) Pediatrics 95:550-554, 1995.

217. Landrigan PJ, Carlson JE: Environmental Policy and Children's Health. The Future of Children 5:34-52, 1995.

218. Brandt-Rauf PW, Landrigan PJ: Budget cuts are grave to NIOSH. (Editorial). Am J Ind Med 28:457-458, 1995.

219. Landrigan PJ, Todd AC, Wedeen RP: Lead poisoning. Mount Sinai J Med 62:360-364, 1995.

220. Landrigan PJ: Childhood leukemias. (Letter) New Engl J Med 333:1286, 1995.

221. Golden AL, Markowitz SB, Landrigan PJ: The risk of cancer in firefighters. Occupational Medicine: State of the Art Reviews 10:803-820, 1995.

222. Todd AC, Wetmur JG, Moline JM, Godbold JH, Levin SM, Landrigan PJ: Unraveling the chronic toxicity of lead: an essential priority for environmental health. Environ Health Perspect 104 (Supplement I):141-146, 1996.

223. Landrigan PJ: Public health. The Amicus Journal. Washington, D.C.: Natural Resources Defense Council, Winter 1996, pp. 37-40.

224. Landrigan PJ: Risk. (Letter) Smithsonian, p. 18, January 1996.

225. Landrigan PJ: Benzene and blood: one hundred years of evidence. (Editorial) Am J Ind Med 29:225-226, 1996.

226. Needleman HL, Landrigan PJ: Toxins at the pump. New York Times, Op-Ed, March 13, 1996.

227. Nicholson WJ, Landrigan PJ: Asbestos: a status report. Current Issues in Public Health 2:118-123, 1996.

228. Landrigan PJ: Asbestos-related cancer. (Letter) CA 46:254-255, 1996.

229. Landrigan PJ: Occupational Illness (Commentary). Abstracts of Clinical Care Guidelines, 8:15-18, 1996.

230. Claudio L, Wetmur, JG, Landrigan PJ: Genetic susceptibility to lead neurotoxicity. (Abstract). Presented at the 124th Annual Meeting of the American Public Health Association, New York, November, 1996, Session 2019, p. 155.

231. Landrigan PJ: Risk assessment, risk management, and right to know - the three R's of child-centered environmental health policy. (Abstract). Presented at the 124th Annual Meeting of the American Public Health Association, New York, November, 1996, Session 3084, p. 426.

232. Landrigan PJ: Lead levels, home dust, and proximity to lead smelters (Letter). Pediatrics 97:603-604, 1996.

33



233. Landrigan PJ: The prevention of occupational cancer (Editorial). CA 46:67-69, 1996.

234. Baker D, Landrigan PJ: Workers. In: The Practice of Public Health. Vol. 3, Chapter 20. Detels R, Holland WW, McEwen J, Omenn GS (Eds) Oxford University Press: Oxford, New York, Toronto, pp 1413-1430, 1997.

235. Landrigan PJ: Angiosarcoma of the liver among polyvinyl chloride workers - Kentucky. (Editorial). MMWR 46:99-101, 1997.

236. Smith DA, Ness K, Herbert R, Schechter C, Phillips R, Diamond J, Landrigan P: Saggital abdominal diameter/thigh circumference and waist hip ratio highly correlated. Mount Sinai J Med 64:32, 1997.

237. Smith D, Herbert R, Schechter C, Phillips R, Diamond J, Dahms TE, Landrigan P: Occupational coronary heart disease among Bridge and Tunnel Officers. (Abstract) Can J Cardiology Vol. 13, Supplement B, p. 76B, June 1997.

238. Smith D, Herbert R, Schechter C, Phillips R, Diamond J, Dahms TE, Landrigan P: Occupational coronary heart disease among Bridge and Tunnel Officers. (Poster) Fourth International Conference on Preventive Cardiology, Montreal, Canada, June 1997.

239. Landrigan PJ, Needleman HL: Environmental neurotoxins and children's development. NCJW Journal 20:22-27, 1997.

240. Landrigan PJ: Identification of Gulf War Syndrome: Methodological Issues and Medical Illnesses. (Letters in reply). JAMA 278:383-387, 1997.

241. Landrigan PJ, Clark NL: Unions help reduce lead risk among workers. Forum for Applied Research and Public Policy, p 151, summer 1997.

242. Landrigan PJ, McCammon JB: Child labor still with us after all these years. Public Health Rep 112:466-473, 1997.

243. Landrigan PJ: Children’s Health and the Environment – The First Herbert L. Needleman Award Lecture. Maternal and Child Health Journal 1:61-64, 1997.

244. Landrigan PJ: Recent Developments in the Toxicology and Epidemiology of Lead. (eds.) Araki S, Yokoyama K, Journal Public Hygiene 50 years in Tokyo University, pp. 45-47, 1997.

245. Landrigan PJ, McCally M: Public health education at universities in the United States. Ibid, pp. 206-207, 1997

246. Landrigan PJ: Illness in Gulf War veterans: causes and consequences. (Editorial). JAMA 277:259-261, 1997.

247. Landrigan PJ, Claudio L: Heart rate variability: a new physiologic marker of autonomic neurotoxicity. (Editorial). J Pediatrics 130:725-729, 1997.

248. Landrigan PJ: Illness in Gulf War Veterans: Causes and Consequences. The Journal of the American International Health Council 1:49-51, 1998.

249. Landrigan PJ: Environmental hazards for children. Report of the Twenty-Seventh Ross Roundtable on Critical Approaches to Common Pediatric Problems in Collaboration with the Ambulatory Pediatric Association. Environmental Health, November 19, 1996, Int J Occup Med and Environ Health 11:189-194, 1998.

34



250. Rall D, Landrigan PJ: Of Apples and Alar. Letter to the Editor, Washington Post, January 13, 1998.

251. Osinubi OYO, Landrigan PJ: Book Review: Occupational, Industrial and Environmental Toxicology. Eds. Greenberg MI, Hamilton RJ and Philips SD. Am J Ind Med 33:99, 1998.

252. Landrigan PJ, Claudio L, McConnell R: Pesticides. Chapter. In: Environmental Toxicants-Human Exposures and Their Health Effects, Lippmann M (ed). New York: Van Nostrand Reinhold, 1998.

253. Landrigan PJ: Asbestos--still a carcinogen. (Editorial) New Engl J Med 338:1618-1619, 1998.

254. Landrigan PJ, Etzel R: Chemical Pollutants. Chapter 719 In: Nelson Textbook of Pediatrics, 16th edition, Behrman R et al., Editors. Philadelphia: WB Saunders Co., 1998, pp. 2152-2154.

255. Landrigan PJ, Carlson JE, Bearer CF, Cranmer JS, Bullard RD, Etzel RA, Groopman J, McLachlan JA, Perera FP, Reigart JR, Robison L, Schell L, Suk, WA: Children's Health and the Environment: A New Agenda for Prevention Research. Environ Health Perspect 106:787-793, 1998.

256. Landrigan PJ, Goldman LR: Response to the Report of the Canadian Ad Hoc Panel on Pesticides and Cancer Risk. (Letter to the Editor). Cancer 83:1057-1058, 1998.

257. Landrigan PJ, Lashof JC, Hamburg DA: Gulf War Syndrome Illness in veterans. (Letter). Am J Epidemiol 148:404-407, 1998.

258. Landrigan PJ, Costa Dias E, Sokas RK: Health hazards of child labor demographics. Chapter 32 - Vulnerable Populations. In: International Occupational and Environmental Medicine. Eds. Herzstein JA, Bunn WB, Fleming LE, Harrington JM, Jeyaratnam J, Gardner IR. pp. 531-542.

259. Landrigan PJ: Is Gulf War Syndrome due to stress? The evidence reexamined" (letter to editor). Am J Epidemiol 148:404-405, 1998.

260. Landrigan PJ: Pesticides Harm Kids (letter to editor), New York Times, July 7, 1998.

261. Galson SK, Carroquino MJ, Landrigan PJ: Introduction to Conference on Preventable Causes of Cancer in Children. Environ Health Perspect 106:865, 1998.

262. Carroquino MJ, Galson SK, Licht J, Amler RW, Perera FP, Claxton LD, Landrigan PJ: The U.S. EPA Conference on Preventable Causes of Cancer in Children: A Research Agenda. Environ Health Perspect 106:867-873, 1998.

263. Landrigan PJ, Etzel RA: Children. Chapter 35. In: Primary Care Guide to Occupational and Environmental Medicine. Eds: Hashimoto D, Atkins S, Christiani D, Davis A, Leiken J, St. Louis: Mosby, 1998.

264. Landrigan PJ: Risk Assessment for Children and other Sensitive Populations. (Abstract) Presented at Collegium Ramazzini Conference on Risk Assessment, Bologna, Italy, Sept. 25-26, 1998.

265. Landrigan PJ: Nonoccupational exposure to chrysotile asbestos and the risk of lung cancer (letter to the editor). New Engl J Medicine 339:999-1002, 1998.

266. Landrigan PJ: Foreword: Occupational and Environmental Medicine. In Occupational and Environmental Neurotoxicology (Ed. Feldman, RG), Lippincott-Raven, Philadelphia-New York, p. ix, 1998.

267. Landrigan PJ: Exposure to dimethylmercury (letter to the editor). New Engl J Med 339:1243-1244, 1998.

268. Landrigan, PJ: Illness in Gulf War Veterans: Causes and Consequences. The Journal of the American International Health Council 1:49-51, 1998.

269. Landrigan PJ, Nicholson WJ, Suzuki Y, LaDou J: The hazards of chrysotile asbestos: A critical review. Ind Health 37:271-280, 1999.

35



270. Landrigan PJ: The impact of environmental toxins on children's learning and behavior. The Aspen Institute Congressional Program, May 6, 1999.

271. Landrigan PJ: ACPM, Mount Sinai to Tackle Children's Environmental Health Issues. ACPM Newsletter, Spring 1999.

272. Landrigan PJ: Child Labor. Chpater 10. In: Ambulatory Pediatrics 5th Edition. M Green, RJ Haggerty, M Weitzman (eds). W.B. Saunders Company, 1999 pp. 28-31.

273. Landrigan PJ: Asthma in American children. Congressional staff briefing: Asthma and the Environment: Protecting Our Children, Washington, D.C., May 27, 1999.

274. Landrigan PJ: Why Not Use It All? (Letter to the editor). Environ Health Perspect 107:A546, 1999.

275. Landrigan PJ: Malathion may be a necessary evil. (Op-Ed) Newsday, Sept. 14, 1999.

276. Moline J, Landrigan PJ: Insights on asthma at work. (Book Review) The Lancet 354:1217, 1999.

277. Landrigan, PJ: Pesticides. Chapter 20. In: Handbook of Pediatric Environmental Health. R Etzel, S Balk, (eds). Elk Grove, Illinois: American Academy of Pediatrics, 1999. pp. 193-214.

278. Landrigan, PJ: Doctor’s orders: healthy kids need a healthy planet. Creation Care. Spring, 1999, pp.6-7, 17-18.

279. Landrigan, PJ: Children’s health and the environment. Eur J Oncol 4:661-664, 1999.

280. Landrigan PJ, Claudio L, McConnell R: Pesticides. Chapter 21. In: Environmental Toxicants: Human Exposures and Their Health Effects, Lippmann M (ed). New York: John Wiley & Sons, Inc., 2000 pp. 725-739.

281. Herbert R, Landrigan PJ: Work-related death: a continuing epidemic. (Editorial) Am J Public Health 90:541-545, 2000.

282. McChesney R, Marcus M, O’Connor JF, Golden A, Landrigan P: The determination of early pregnancy loss using measurement of human chorionic gonadotropin (hCG) – related forms with a modified urine specimen collection protocol. (Abstract) Am J Epidemiol 151:S49, 2000.

283. Weiss B, Landrigan P: The developing brain and the environment: an introduction. Environ Health Perspect 108 (Supplement):373-374, June 2000.

284. Landrigan PJ, Boffetta P, Apostoli P: The reproductive toxicity and carcinogenicity of lead: a critical review. Am J Ind Med 38: 231-243, 2000.

285. Landrigan PJ: Principles of Occupational and Environmental Medicine. In: Cecil Textbook of Medicine, 21st edition. Goldman L, editor. Philadelphia: W.B. Saunders Co, 2000.

286. Moline JM, Golden AL, Bar-Chama N, Smith E, Rauch ME, Chapin RE, Perreault SD, Schrader SM, Suk WA, Landrigan PJ: Exposure to hazardous substances and male reproductive health: A research framework. Environ Health Perspect 108:803-813, 2000.

287. Landrigan PJ, Martiney JA: Fleet Hospital Fort Dix Battles West Nile Virus. Naval Reserve Association News 47:28, 2000.

288. Carpenter DO, Chew FT, Damstra T, Lam LH, Landrigan PJ, Makalinao I, Peralta GL, Suk WA: Environmental Threats to the Health of Children: The Asian Perspective. Environ Health Perspect 108:989-992, 2000.

289. Landrigan PJ, Wolfe S, Oakley GP Jr: Bad Policy, Worse Medicine. (Commentary) Pediatrics 106(6):1482-1483, 2000.

290. Landrigan, PJ, et al: Gesundheit von Kindern und Umwelt: Eine neue Agenda für präventive Forschung. Kinder-Gesundheit-Umwelt-Krankheit 47-73, 2000.

290.1 Landrigan PJ: A year of passage. Am J Ind Med 38:483-484, 2000.

36



291. Landrigan PJ: Pediatric Lead Poisoning: Is There a Threshold? (Commentary). Public Health Reports 115:530-531, 2000.

292. Landrigan PJ: Pesticides, PCBs, and the Risk to Children. Contemporary Pediatrics 18(2):110-126, 2001.

293. Landrigan PJ: Pesticides and polychlorinated biphenyls (PCBs): An analysis of the evidence that they impair children’s neurobehavioral development. Molecular Genetics and Metabolism 73:11-17, 2001.

294. Landrigan PJ: Bernardino Ramazzini: perpetuating the lesson of the Master. The diagnosis and prevention of occupational and environmental illness. (Editorial). Eur J Oncol 6:235-237, 2001.

295. Landrigan PJ: Pesticides and polychlorinated biphenyls (PCBs): An analysis of the evidence that they impair children’s neurobehavioral development. Jap Journal of Occup Med and Traumatology 49:89-97, 2001.

296. Landrigan PJ, Markowitz S, Baker DB: Cancer Prevention in the Workplace. In: Cancer Prevention and Control, eds, Greenwald P, Kramer BS, Weed DL. 2nd Edition. New York: Marcel Dekker, 2001.

297. Landrigan PJ, Golden AL: Hudson River bass pose danger to fetuses (Letter to the editor). The Journal News (Westchester County, NY) 2001.

298. Landrigan PJ, Crain E, Etzel R, Gitterman B, Oberg C, Scheidt P: The need for a new subspecialty in environmental pediatrics. (Abstract) Presented at Global Forum for Children’s Environmental Health, Washington DC, 7-11 September 2001.

299. Landrigan PJ, Golden A, Berkowitz G, Wolff M, Godbold J: Body Burdens of Persistent Pollutants in Hudson River Anglers. (Abstract) Presented at Global Forum for Children’s Environmental Health, Washington DC, 7-11 September 2001.

300. Forman J, Satlin L, Amler RW, Winston JA, Fleissner ML, Toal B, Landrigan PJ: Environmental Uranium Contamination of Well Water Associated with Beta-2-Microblobulinuria. (Abstract) Presented at Global Forum for Children’s Environmental Health, Washington DC, 7-11 September 2001.

301. LaDou J, Landrigan P, Bailar JC III, Foa V, Frank A: A call for an international ban on asbestos. (Commentary). Can Med Assoc J 164:489-490, 2001.

302. Landrigan PJ: Children’s Environmental Health: An Overview. Washington DC: Population Reference Bureau, 2001.

303. Todd AC, Carroll S, Landrigan PJ: Key issues in childhood lead exposure in the USA. Urban Health and Development Bulletin of the South African Medical Research Council, 2001.

304. Mehlman MA, Soffritti M, Landrigan PJ: In: Memoriam: Professor Cesare Maltoni (1930-2001). Am J Ind Med 40:1-2, 2001.

305. Landrigan PJ: MMT, déjà vu and national security. Am J Ind Med 39:434-435, 2001.

306. Landrigan PJ: PCB cleanup must begin now (Letter). The Journal News, (Westchester County, NY) August 2, 2001.

307. Landrigan PJ, Mattison DR, Boardman B, Bruckner JV, Jackson RJ, Karol MH, Krewski D, Weil WB: Children’s Health, Susceptibility and Regulatory Approaches to Reducing Risk from Chemical Carcinogens. (Letter to the Editor). Environ Health Perspect 109:A412-A413, 2001.

308. Mehlman MA, Landrigan PJ, Soffritti M: In Memoriam Professor Cesare Maltoni (1930-2001) Int J Occup Environ Health 7:254, 2001.

309. Landrigan PJ: Health Consequences of the September 11 Attacks. (Editorial) Environ Health Perspect 109:A514-A515, 2001.

37



310. Sonawane B, Landrigan P, Olin S: Children’s Environmental Health Risk Assessment: Issues and Challenges. (Abstract) Presented at Society for Risk Assessment, 2001.

311. Landrigan PJ: Children’s Environmental Health: Lessons from the Past and Prospects for the Future. Pediatr Clin North Am 48:1319-1330, 2001.

312. Wolff MS, Landrigan PJ: Organochlorine Chemicals and Children’s Health. (Editorial). J Pediatr 140:10-13, 2002.

313. LaDou J, Landrigan P, Bailar III, JC, Foa V, Frank A: A call for an international ban on asbestos. Public Health Rev 29:241-246, 2001.

314. Landrigan PJ, Sonawane B, Mattison D, McCally M, Garg A: Chemical Contaminants in Breast Milk and their Impacts on Children’s Health: An Overview. Environ Health Perspect 110:A313-A315, 2002.

315. Landrigan PJ, Garg A: Chronic Effects of Toxic Environmental Exposures on Children’s Health. Presented at the WHO/AAPCC Symposium on Children’s Health and Environmental Toxicology: New Challenges for Toxicologists and Poison Centers. Montreal, Canada. Clin Toxicol 40:449-456, 2002.

316. Claudio L, Garg A, Landrigan PJ: Addressing Environmental Health Issues. In: Terrorism and Public Health. Levy B, Sidel V, eds., Oxford University Press, New York, pp. 69-79, 2002.

317. Landrigan PJ: Confronting the health consequences of the World Trade Center attacks (Abstract). Presenting at the Environment of the 130th Annual Meeting, Philadelphia PA, 9-13 November 2002.

318. Garg A, Landrigan PJ: Children’s Environmental Health: New Gains in Science and Policy. Annals of the American Academy of Political and Social Science 584:135-144, 2002.

319. Landrigan PJ, Garg A: Public Health: What’s Next? The Green Guide 90:4, 2002.

320. Landrigan PJ, Garg A: Climate Change and Infectious Diseases. The Green Guide 91:4, 2002.

321. Landrigan PJ: New Year, New Faces. Am J Ind Med 42:164-166, 2002.

322. Landrigan PJ: Foreword: Pest Control in Public Housing, Schools and Parks: Urban Children at Risk. In: State of New York, Attorney General Eliot Spitzer. Environmental Protection Bureau, 2002.

323. Landrigan PJ: Strong Chemicals, Strong Action, Strong Control. The CHEC Report, issue #8, 2002.

324. Landrigan PJ: The Worldwide Problem of Lead in Petrol. (Editorial). Bull World Health Organ 80(10):768, 2002.

325. Landrigan PJ, Garg A: Vulnerable Populations. In: . McCally M., ed., The MIT Press, Cambridge, Massachusetts, pp. 257-271, 2002.

326. Eskenazi B, Landrigan PJ: Environmental Health Perspects and children’s environmental health. (Editorial) Environ Health Perspect 110:A559-A560, 2002.

327. Landrigan PJ: Lessons Learned: Worker Health and Safety Since September 11, 2001. Am J Ind Med 42:530-531, 2002.

328. Etzel RA, Landrigan PJ: Letter from the Guest Editors. Ambulatory Pediatrics 3:16-17, 2003.

329. Adamu M, Morland K, Golden A, Godbold J, Moshier E, Wolff M, Landrigan P: Body Burden of Pollutants from Fish Consumption (Abstract). In: Proceedings of the 2003 Annual Meeting of the Society of Epidemiologic Research; Am J Epidemiol 157:S085, 2003.

38



330. Landrigan PJ: Indoor Air Quality: A Doctor’s Viewpoint. The CHEC Report, issue #9, 2003.

331. Galvez M, Brenner B, Rivera M, Teitelbaum S, Moskowitz H, Claudio L, Berkowitz T, Wolff M, Forman J, Landrigan PJ: Exposure Assessment of Environmental Risk Factors for Overweight/Obesity in Urban Children. (Abstract) Presented the annual meeting of Pediatric Academy Societies, Seattle, WA, 2003.

332. Landrigan PJ, McCally M, Oleskey C: Ethics of Pesticide Testing in Humans. Environ Health Perspectives 111:A750, 2003.

333. Landrigan P, Garg A, Droller DBJ: Assessing the Effects of Endocrine Disruptors in the National Children’s Study. Environ Health Perspect 111:1678-1682, 2003.

334. Landrigan PJ, Schechter CB, Lipton JM, Fahs, Schwartz J: Estimated Costs of Environmental Disease: Response to Rigas (Correspondence). Environ Health Perspect 111:A145, 2003.

335. Landrigan PJ, Goldman L: Another View of Children’s Health. (Editorial). Chemical & Engineering News 81:3, 2003.

336. Landrigan PJ, Goldman L: Prenatal methylmercury exposure in the Seychelles – 3rd reply. (Letter) Lancet 362:666, 2003.

337. Suk WA, Ruchirawat KM, Balakrishnan K, Berger M, Carpenter D, Damstra T, deGarbino Pronczuk J, Koh D, Landrigan PJ, Makalinao I, Sly PD, Xu Y, Zheng BS: Environmental Threats to Children’s Health in southeast Asia and the Western Pacific. Environ Health Perspect 111:1340-1347, 2003.

338. Landrigan PJ: A Doctor’s Viewpoint: Why Air Pollutants Harm Kids. The CHEC Report, issue 12, Fall 2003.

339. Galvez MP, Frieden TR, Landrigan PJ: Obesity in the 21st Century. (Editorial) Environ Health Perspect 111:A684-A685, 2003.

340. Edwards ES, Green N, Henry CJ, Landrigan PJ, Swartz D: Tracking Children’s Health to Age 21. (Letter) Science 302:781, 2003.

341. Landrigan PJ, Droller DBJ: The Burden of Obesity Among Young Urban People. The Green Guide 98, 2003.

342. Etzel RA, Balk SJ, Reigart JR, Landrigan PJ: Environmental Health for Practicing Pediatricians. Indian Pediatrics 853-860, 2003.

343. The Council of Science Editors and the International Committee of Medical Journal Editors. Correspondence about Publication Ethics and Regulatory Toxicology and Pharmacology. Special Contributions. Int J Occup Environ Health 9:386-389, 2003.

344. Landrigan PJ: Principles of Occupational and Environmental Medicine. Chapter 18. In: Cecil Textbook of Medicine, 22nd edition. Eds, Goldman L, Ausiello D. Philadelphia: W.B. Saunders Co, pp 81-85, 2003.

345. Galvez MP, Vanable L, Forman JA, Landrigan PJ, Akeredolu E, Leighton J, Nagin D, Yip W, Simmonds K: A case of childhood lead poisoning from commercially manufactured European ceramic dinnerware, New York City, 2003 (Abstract). Presented at the Annual Meeting of Pediatric Academic Societies, San Francisco, CA, May 2004.

346. Needleman HL, Landrigan P: What level of lead in blood is toxic for a child. (Letter) Am J Public Health 94:8, 2004.

347. Landrigan PJ, Slutsky J: Are Learning Disabilities Linked to Environmental Toxins? Learning Disabilities Journal 15:7-12, 2004.

39



348. Landrigan P: Dr. T.K. Joshi and Asbestos in India: A Message from the Collegium Ramazzini. Am J Ind Med 45:125-128, 2004.

349. Landrigan PJ: Environmental Factors and Pediatric Disease: New Developments in Research and Education. J San Francisco Medical Society 77:18-19 & 26, 2004.

350. Goldman L, Falk H, Landrigan PJ, Balk SJ, Reigart JR, Etzel RA: Environmental Pediatrics and its Impact on Government Health Policy. Pediatrics 113:1146-1157, 2004.

351. Landrigan PJ: Children As A Vulnerable Population. Int J Occup Med Environ Health 17:175-177, 2004.

352. Landrigan PJ, Steenland K, Richter E: Olav Axelson, MD. Am J Ind Med 45:582-583, 2004.

353. Landrigan PJ: New faces. Am J Ind Med 45:584-585, 2004.

354. Landrigan PJ, Trasande L: Applying the precautionary principle in environmental risk assessment to children. In: The Precautionary Principle: protecting public health, the environment and the future of our children. Martuzzi M, Tickner JA, eds, 2004. pp. 121-143.

355. Galvez M, Vanable L, Forman JA, Landrigan PJ, Akeredolu E, Leighton J, Nagin D: Childhood Lead Poisoning from Commercially Manufactured European Ceramic Dinnerware – New York City, 2003. MMWR 53:585-586, 2004.

356. Landrigan PJ: The WTC Disaster: Landrigan’s Response. (Correspondence). Environ Health Perspect 112:A607, 2004.

357. Trasande L, Landrigan PJ: The National Children’s Study: A Critical National Investment. (Editorial). Environ Health Perspect 112:A789-A790, 2004.

358. Landrigan PJ, Garg A: Children are not little adults. Chapter 1. In: WHO Handbook on Children’s Health and the Environment. A global perspective. Geneva. Pronczuk-Garbino J, ed, pp. 3-16: WHO, 2005.

359. Landrigan PJ: A public health project in Ghana. African Newsletter on Occupational Health and Safety 14:47, 2004.

360. Moline J, Landrigan P: Lead. Chapter 39.8. In: Textbook of Occupational and Environmental Medicine, 2nd edition. Rosenstock L, Cullen M, Brodkin D, Redlich C, eds, pp. 967-978, 2005.

361. Landrigan PJ, Trasande L: More kids chronically ill. Poughkeepsie Journal, January 2, 2005.

362. Landrigan PJ, Soffritti M: Collegium Ramazzini Statement on Darfur. Am J Ind Med 47:193-194, 2005.

363. Landrigan PJ: Environmental Threats to Children’s Health – The Promise of the National Children’s Study. New England College of Occupational and Environmental Medicine (NECOEM Reporter) 2:1-2, 2005.

364. Galvez M, Forman J, Landrigan PJ: Children. Chapter 28. In: Environmental Health: From Global to Local. Frumkin H, ed, pp. 805-845, 2005.

365. Landrigan PJ, Soffritti M: Collegium Ramazzini Call for an International Ban on Asbestos. Am J Ind Med 47:471-474, 2005.

366. Landrigan PJ, Soffritti M: Collegium Ramazzini Statement on the Tokyo Declaration Banning Asbestos. Am J Ind Med 48:89-90, 2005.

367. Landrigan PJ, Tamburlini G. Children’s Health and the Environment: A Transatlantic Dialogue. (Editorial) Environ Health Perspect 113:A646-A647, 2005.

40



368. Landrigan PJ, Newman B. Children and other high-risk workers as a special challenge to occupational health services. SJWEH Suppl 1:43-45, 2005.

369. Landrigan PJ. Environmental Exposures and Children’s Health Challenges. Zero to Three 26:8-10, 2005.

370. Pirisi A. Profile: Philip Landrigan: children’s health crusader. Lancet 365:1301, 2005.

371. Landrigan PJ, Claudio L. Pesticides. Chapter 21. In: Environmental Toxicants: Human Exposures and Their Health Effects. Lippman M (ed.). 2nd Edition. New York: John Wiley, 2005.

372. Landrigan PJ, Golden AL, Simpson HJ. Toxic substances and their impacts on human health in the Hudson River Watershed. Chaper 28. In: The Hudson River Estuary. Levinton J, Waldman J (eds). Cambridge University Press, 2006.

373. Landrigan PJ, Kotelchuck D, Grandjean P. Principles for Prevention of the Toxicity of Metals. Chapter 16. For inclusion in: Handbook of Toxicity of Metals. Nordberg GF, Fowler BA, Nordberg M, Friberg LT (eds). Academic Press, Inc. 2007.

374. Landrigan PJ, Benbrook CM. Impacts of the Food Quality Protection Act on Children’s Exposures to Pesticides. Presented at the AAAS Symposium on Opportunities and Initiatives to Minimize Children’s Exposures to Pesticides. St. Louis, Missouri, February 19, 2006.

375. Landrigan PJ. Essays in Public Health and Preventive Medicine. Mount Sinai J Med 73:564, 2006.

376. Landrigan PJ. Environmental Pediatrics and the Ecological Imperative. (Editorial) EcoHealth 3:75-76, 2006.

377. Landrigan PJ, Trasande L. Economic Implications of Metal Neurotoxicity. Presented at an International Workshop on Neurotoxic Metals: Lead, Mercury and Manganese from Research to Prevention. Brescia, Italy, June 17-18, 2006.

378. Landrigan PJ. Our Most Vulnerable. Chapter 12. In: Child Honouring. How to Turn this World Around. Cavoukian R, Olfman S (eds). Praeger Publishers, 2006.

379. Landrigan PJ, Pronczuk DeGarbino J, Newman B. Introduction. In: Living in a Chemical World. Ann NY Acad Sci xvii-xviii, 2006. Framing the Future in Light of the Past. In: Living in a Chemical World. Ann NY Acad Sci 1-3, 2006.

380. Landrigan PJ. Ruth Lilis (1926-2006). Am J Ind Med 49:607-608, 2006.

381. Landrigan PJ, Forman JA. Chemical Pollutants. Chapter 707. In: Nelson Textbook of Pediatrics. Kliegman, Behrman, Jenson, Stanton (eds.). 18th Edition. Philadelphia, PA: Saunders Elsevier, Inc., pp. 2906-2909, 2007.

382. Landrigan PJ, Nordberg M, Lucchini R, Nordberg G, Grandjean P, Iregren A, Alessio L. The Declaration of Brescia on Prevention of the Neurotoxicity of Metals. Am J Ind Med 50:709-711, 2007.

383. Tornheim JA, Morland KB, Landrigan PJ Cifuentes E. Diarrheal Disease Burden Attributable to Water Privatization in Bolivia. (Poster). Presented at CMCA Conference, December 7, 2006.

384. Landrigan PJ. Doctor David V. Bates (1922-2006). Eur J Oncol 11:265, 2006.

385. Robbins A, Landrigan PJ. Safer, Healthier Workers: Advances in Occupational Disease and Injury Prevention. Chapter 10. In: Silent Victories. Ward JW, Warren C (eds). Oxford University Press, pp 209-229, 2007.

41



386. Landrigan PJ. The 2nd ADAO Asbestos Conference Proceedings. Preface. Am J Ind Med 50:51, 2007.

387. Landrigan PJ. Valediction. (Editorial) Am J Ind Med 50:243-244, 2007.

388. Landrigan PJ. Benzene. Chapter 71. In: Environmental and Occupational Medicine, Fourth Edition, edited by William N. Rom, Lippincott-Raven Publishers, Philadelphia, 2007.

389. Landrigan PJ, Claudio L. Pesticides. Chapter 24. In: Environmental Toxicants. Lippman M (ed.). Third Edition. John Wiley & Sons Inc., 2009.

390. Trasande L, Landrigan PJ, Schechter CB, Bopp RF. Methylmercury and the Developing Brain. (Letter to the editor) Environ Health Perspect 115:A396-A397, 2007. PMID: 17687420

391. Grandjean P, Bellinger D, Bergman A, Cordier S, Davey-Smith G, Eskenazi B, Gee D, Gray K, Hanson M, van den Hazel P, Heindel JJ, Heinzow B, Hertz-Picciotto I, Hu H, Huang T T-K, Jensen TK, Landrigan PJ, McMillen IC, Murata K, Ritz B, Schoeters G, Skakkebaek NE, Skerfving S, Weihe P. The Faroes Statement: Human Health Effects of Developmental Exposure to Chemicals in Our Environment. Basic & Clinical Pharmacology & Toxicology 102: 73-75, 2008. PMID: 18226057

392. Landrigan PJ, Trasande L, Swanson JM. Genetics, Altruism and the National Children’s Study. Am J of Med Genetics Part A 146A:294-296, 2008. PMID: 18203190

393. Pollack SH, Landrigan PJ. Health Hazards of Child Labor. Chapter 45. In: Public Health & Preventive Medicine. Wallace RB (ed). 15th Edition. McGraw Hill, 2007.

394. Landrigan PJ. The Unique Vulnerability of the Developing Human Brain to Early Neurotoxic Exposures. Volume 1. In: The Sixth Princess Chulabhorn International Science Congress: The Interface of Chemistry and Biology in the “Omics” Era: Environment & Health and Drug Discovery. Amarin Printing and Publishing Public Company Limited. Plenary Lecture, Bangkok, Thailand, November 2007.

395. Landrigan PJ. Developmental Neurotoxicity of Industrial Chemicals and Pediatric Bipolar Disorder: A Call to Research. Chapter 9. In: Bipolar Children. Olfman, S (ed). Praeger Publishers, 2007.

396. Landrigan PJ, Trasande L. Mercury in sushi. New York Times. (Letter to the Editor). January 28, 2008.

397. Brown RC, Bullock MB, Landrigan PJ, Sonawane B. Children’s Environmental Health: Issues and Challenges. In: Encyclopedia of Environmental Health. Sonawane B, Brown R (eds). Elsevier Ltd, submitted 2008.

398. Patton RM, Arthur T, Bain EI, Balbus J, Landrigan PJ, et al. Open Letter to Stephen Johnson, Administrator, U.S. Environmental Protection Agency: Ban Endosulfan. Int J Occup and Environ Health 14:236-239, 2008.

399. Landrigan PJ. Foreword. Environmental Threats to Healthy Aging With a Closer Look at Alzheimer’s & Parkinson’s Diseases. Boston: Greater Boston Physician for Social Responsibility pp 6-7, 2008.

400. Landrigan PJ. Emerging Technologies. Chapter. In: American Academy of Pediatrics, Pediatric Environmental Health, Third Edition. Etzel, Ruth (ed). Submitted 2008.

401. Landrigan PJ. Artificial Turf Fields Pose Safety Issues. The Journal News. (Letter to the Editor). December 11, 2008.

402. Landrigan PJ, Forman J, Galvez M, Newman B, Engel SM, Chemtob C. Impact of September 11 World Trade Center Disaster on Children and Pregnant Women. Mount Sinai J Med 75:129-134, 2008.

403. Galvez MP, Forman J, Landrigan PJ. Children. Chapter 25. In: Environmental Health: From Global to Local. Frumkin H (ed). Second Edition, 2009.

42



404. Landrigan PJ, Bullock M. Integrated Pest Management (IPM) Can Cost-Effectively Reduce Pesticide Exposures in the Urban Environment. (Abstract). Presented at Translating Science to Policy Protecting Children’s Environmental Health at The Columbia Center for Children’s Environmental Health In collaboration with WE ACT for Environmental Justice, New York, NY, March 30, 2009.

405. Sheffield PE, Knowlton K, Kinney PL, Landrigan PJ. The Effect of Climate Change on Pediatric Respiratory Hospitalizations: a Glimpse into the Future. (Abstract). Presented at the Pediatric Academic Societies meeting, Baltimore, MD, May 3, 2009.

406. Schwartz AW. Socio-demographic Predictors of Influenza and Pneumonia Non-Vaccination among Elderly Israelis. INSPIRE final presentations. Mentor: Landrigan PJ: Mount Sinai School of Medicine, November 18, 2009.

407. Stayner LT, Camargo MC, Reina M, Al-Alem U, Straif K, Landrigan PJ. A meta-analysis of the association between asbestos exposure and the risk of ovarian cancer. (Abstract). Presented at the EPICOH meeting, Taiwan, Republic of China, 2009.

408. Landrigan PJ. Foreword: Leadership. In: Leadership Essentials for Emergency Medical Services. American Academy of Orthopaedic Surgeons. Jones and Bartlett Publishers, LLC. Brophy, John R., 2010.

409. Landrigan P. Counting Roaches. Reducing Pesticide Exposures via Integrated Pest Management. San Francisco Medical Society. Medicine and the Environment, p 32, April 2010.

410. Landrigan PJ. The Making of a Medical Epidemiologist. In: Medicine Science and Dreams. The Making of Physician-Scientists. Chapter 16. Springer. Schwartz, David A. (ed). 2010.

411. Landrigan PJ, Satlin LM, Boffetta P. Why Are We Subsidizing Childhood Obesity? New York Times, Op-Ed, October 2010.

412. Landrigan PJ, Trasande L. The U.S. National Children’s Study: A 21-Year Prospective Study of 100,000 American Children. (Abstract). Presented at the Excellence in Paediatrics conference, London, UK, December 2-4, 2010.

413. LaDou J, Castleman B, Frank A, Gochfeld M, Greenberg M, Huff J, Joshi TK, Landrigan PJ, Lemen R, Myers J, Soffritti M, Soskolne CL, Takahashi K, Teitelbaum D, Terracini B, Watterson A. The case for global ban on asbestos. Environ Health perspect 118:897-901, 2010. PMID: 20601329

414. Takaro TK, Davis D, Van Rensburg SJ, Arroyo Aguiliar RS, Algranti E, Bailar JC 3rd, Belpoggi F, Berlin M, Bhattacharya S, Bonnier Viger YV, Brophy J, Bustinza R, Cameron RB, Dement JM, Egilman D, Castleman B, Chaturvedi S, Cherniack M, Choudhury H, Demers PA, Digangi J, Digon A, Edwards JG, Englund A, Erikson B, Corréa Filho HR, Franco G, Frank AL, Freund A, Gee D, Giordano A, Gochfeld M, Kern DG, Keifer M, Khatter K, Kjuus H, Keith M, Koo LC, Kumar A, LaDou J, Landrigan PJ, Lemen RA, Last JM, Lee CW, Leigh J, Levin SM, Lippman A, Madrid GA, McCulloch J, McDiarmid MA, Merchant JA, Monforton C, Morse T, Muir DC, Mukerjee D, Mulloy KB, Myers J, Nuwayhid I, Orris P, Ozonoff D, Paek D, Patra M, Pelclová D, Pepper L, Poje GV, Rahman Q, Reyes B, Robinson BW, Rodriguez E, Rose C, Rosenman KD, Rosenstock L, Ruchirawat M, Rydzyński K, Schneider J, Silverstein B, Siqueira CE, Slatin C, Soffritti M, Soskoline C, Sparer J, Stayner LT, Takaro TK, Tarkowski S, Teitelbaum DT, Tompa A, Trosic I, Turcotte F, Vilela RA, Waterman YR, Watterson A, Wegman DH, Welch LS, Woitowitz HJ, Yanri Z, Zavariz C. Scientists Appeal Tighter to Quebec Premier Charest to stop exporting asbestos to the developing world. Int J Occup Environ Health 16:239-246, 2010. PMID 20465068

43



415. Lee HH, Milam EC, Claudio L, Landrigan PJ, Crane M. Addressing Environmental Health Issues. In: Terrorism and Public Health. 2nd Edition. Levy and Sidel (eds). 2011.

416. Landrigan PJ, Morland K, La Merrill MA. Environment and Heart Disease. In: Hurst’s The Heart. 13th Edition. The McGraw-Hill Companies, Inc. Fuster, Walsh & Harrington (eds). 2011.

417. Landrigan PJ, Miodovnik A. Children’s Health and the Environment: An Overview. Mount Sinai J Med 78:1-10, 2011.

418. Galvez M, Landrigan PJ. Q. and A.: PCBs in School Classrooms. The New York Times, Friday, February 18, 2011.

419. Carroquino MJ, Posada M, Landrigan PJ. Environmental Toxicology: Children at Risk. Encyclopedia of Sustainability Science and Technology, DOI 10.1007/978-1-4419-0851-3. 2011

420. Morland KB, Evenson KR, Bordowitz R, Godbold JH, Granieri EC, Spark A, Landrigan PJ. Methods for the Assessment of Food and Physical Activity Environments: Brooklyn Seniors and the Built Environment (BSBE) Study. (Abstract). Presented at the International Society of Environmental Epidemiology (ISEE), Barcelona, Spain 2011.

421. Landrigan PJ, Goldman LR. Protecting Children from Pesticides and Other Toxic Chemicals. J Expo Sci Environ Epidemiol 21:119-120, 2011.

422. Landrigan PJ. Tighter Regulations to Protect the Nation’s Children. People & Places. Health Affairs 30(5):851, 2011.

423. Landrigan PJ, Garcia CE, Neira M. Global Prevention of Environmental and Occupational Cancer. Editorial. Environ Health Perspect 119(7):A280-A281, 2011.

424. Landrigan PJ, Forman JA. Chemical Pollutants. Chapter 700. In: Nelson Textbook of Pediatrics. Kliegman, Stanton, Behrman, St. Geme, Schor (eds.). 19th Edition. Philadelphia, PA: Saunders Elsevier, Inc., pp. 2448-, 2011.

425. Landrigan PJ, Espina C, Neira M. In Favor of Controlling Proven, but Not Probable, Causes of Cancer : Landrigan et al. Respond. Environ Health Perspect 119(11) :A469-A470, 2011.

426. Crane MA, Milek DJ, Ripp J, Globina Y, Seifu L, Landrigan PJ. The Lessons of September 11. Ind Health 49 :673-676, 2011.

427. Chatham-Stephen KM, Mann M, Schwartz AW, Landrigan PJ. First, Do No Harm. Children’s Environmental Health in Schools. American Educator, pp 22-31, Winter 2011-2012.

428. Lee HH, Milam E, Claudio L, Landrigan PJ, Crane MA. Investigating the Health Consequences of the World Trade Center Attack. Chapter 4. In: Terrorism and Public Health. Levy BS, Sidel VW (eds). 2nd Edition. Oxford University Press, pp. 67-79, 2011.

429. Schwartz AW, Landrigan PJ. Bisphenol A in Thermal Paper Receipts: An Opportunity for Evidence-Based Prevention. Environ Health Perspect 120:A14-A15, 2012.

430. Landrigan PJ. Mommy Dearest – Salute, Maloney! New York Post (Letter to the Editor). May 13, 2012.

431. LandriganPJ. Emerging Technologies and Materials. In: Pediatric Environmental Health. Chapter 50. Etzel RA (ed). 3rd Edition. American Academy of Pediatrics, pp. 749-755, 2012.

432. Landrigan PJ, Lambertini L, Birnbaum LS. A Research Strategy to Discover the Environmental Causes of Autism and Neurodevelopmental Disabilities. Environ Health Perspect 120:A258-A259, 2012.

44



433. Landrigan PJ, Kellner CH. Lead-Based Paint (image). Environ Health Perspect 120; A268, 2012.

434. Landrigan PJ. Chemicals and Bladder Cancer. (Editorial Commentary) The Journal of Urology 189: 52, 2013.

435. Straif K, Stayner L, Demers PA, Landrigan PJ. Use of Meta-analyses by IARC Working Groups. (Correspondence). Environ Health Perspectives 120:A342-A343, 2012.

436. Landrigan PJ. The hidden costs of environmental contamination. (Editorial). Eur Respir J 40:286-288, 2012.

437. Huey RB, Landrigan P. Recommendation of Crews D and Gore AC: Epigenetic synthesis: a need for a new paradigm for evolution in a contaminated world. (Commentary) F1000 Biol Rep 2012, 4(18). Faculty of 1000, 02 Oct 2012; DOI: 10.3410/f.717957733.793462153. f1000.com/prime/717957733#eval793462153 Epigenet

438. Chatham-Stephens K, Caravanos J, Ericson B, Landrigan P, Fuller R. Burden of Disease from Toxic Waste Sites in India, Indonesia, and the Philippines in 2010. (Poster). 2013 Annual Meeting of the Pediatric Academic Socieities, Washington, DC, May 2013.

439. Solan S, Wallenstein S, Shapiro M, Teitelbaum SL, Stevenson L, Kochman A, Kaplan J, Dellenbaugh C, Kahn A, Biro FN, Crane M, Crowley L, Gabrilove J, Gonsalves L, Harrison D, Herbert R, Luft B, Markowitz SB, Moline J, Niu X, Sacks H, Shukla G, Udasin I, Lucchini RG, Boffetta P, Landrigan PJ. Cancer Incidence in World Trade Center Rescue and Recovery Workers; 2001-2008. (Poster). 2013 Annual Meeting of the council of State and Territorial Eidemiologists, Pasadena, CA, June 2013.

440. Bellinger DC, Burger J, Cade TJ, Cory-Slechta DA, Finkelstein M, Hu H, Kosnett M, Landrigan PJ, Lanphear B, Pokras MA, Redig PT, Rideout BA, Silbergeld E, Wright R, Smith DR. Health Risks from Lead-Based Ammunition in the Environment. (Editorial) Environ Health Perspect 121:A178-A179, 2013.

441. Darrah TH, Whiate AM, Campbell ME, Miller RK, CJ, Katzman PJ, Ruffolo L, Weidenborner P, Culhane J, Wadlinger S, Landrigan P, Littman L, Thiex N, Specker B, Swanson J, Dole N, Eucker B, Clark EB, Varner M, Taggart E, Moye J. Understanding the Trace Metal Composition of Human Placenta from the National Children’s Study (NCS). (Abstract). Presented at the Teratology Society Meeting, Tucson, Arizona, June 2013.

442. Salafia CM, Dalton JL, Misra D, Stodgell CJ, Katzman PJ, Ruffolo L, Culhane J, Wadlinger S, Torres C, Landrigan P, Littman L, Sheffield P, Leuthner S, Szabo S, Thiex N, Specker B, Swanson J, Dole N, Thorp J, Eucker B, Clark EB, Varner MW, Taggart E, Durkin MS, Sandoval M-N, Moye J, Miller RK. The Chronic Surface Vascular Network in Human Placenta: Quantifying Structure to Estimate Gestational Stressors and Life Course Risks, Autism Spectrum Disorder (ASD) As a Model for Future Analyses: National Children’s Study and EARLI. (Abstract). Presented at the Teratology Society Meeting, Tucson, Arizona, June 2013.

443. Alberti A. Taking a History: A profile of Philip Landrigan. Harvard Medicine Magazine, May 2013. 444. Landrigan PJ, Goldman LR. Chemical Safety, Health Care Costs and the Affordable Care Act. Am J Ind

Med (Comment). Published online (wileyonlinelibrary.com) DOI10.1002/ajim.22268;1-3, 2013. 445. Landrigan PJ. State’s children deserve health excellence centers. Network would diagnose diseases of

environmental orgin, provide outreach. (Op-ed). Albany Times Union December 13, 2013. 446. Landrigan PJ, Wright RO, Birnbaum LS. Mercury Toxicity in Children. (Letter to Editor). Science

342:1447, 2013.

45



447. Hao K, Narzo AD, Chen J, Schadt EE, Littman L, Landrigan P, Aagaard Kjersti, Hobbs C, Clark EB, Varner M, Dole N, Culhane J, Swanson J, Thiex N, Murry J, Moye J, Kasten C, Stodgell CH, Miller RK, National Children’s Study Placenta Consortium. Expression Quantitative Trait Loci in Placenta Tissues from the National Children’s Study Reveal Developmental Origins of Human Complex Diseases. (Abstract). Presented at the IFPA meeting, Paris, France, 2014.

448. Dassanayake PS, Xia Y, Nanes J, Ranasinghe P, Li A, Stodgell CJ, Clark EB, Varner M, Landrigan P, Dole N, Culhane J, Thiex N, Swanson J, Moye J, Miller RK on behalf of the National Children’s Study Placenta Consortium. Emerging and Legacy environmental Organic Pollutants in Placenta Specimens collected in the National Children’s Study-Human Placenta Project. (Abstract). Presented at the14th Annual Workshop on Brominated and other Flame Retardants, 2014.

449. Boffetta P, Georgopoulos PG, Giacalone J, Wallenstein S, Lucchini R, Lioy PJ, Landrigan P. Cancer Risk in World Trade Center Rescue and Recovery Workers. (Poster). Presented at the 105th Annual Meeting of the American Association for Cancer Research, San Diego, CA, April 5-9, 2014.

450. Stodgell C, Salamone L, Murry J, Chen J, Lambertini L, Schadt E, Littman L, Landrigan P, Aagaard KM, Hobbs C, Clark E, Varner M, Dole N, Culhane J, Swanson J, Thiex N, Busch T, Kasten C, Moye J. Lack of Correlation between Placenta Gene Expression and RNA Integrity Number (RIN) or Time to Collection. (Poster). Presented at International Federation of Placenta Associations, Paris, France, September 9-12, 2014.

451. Friedman A, Friedman M, Miller RK, Stodgell C, Littman L, Landrigan P, Clark EB, Varner M, Dole N, Culhane J, Swanson J, Thiex N, Moye J, National Children’s Study Placenta Consortium. Quantitative Analysis of Bisphenol A in Human Placental Tissue from Nine Counties Across the U.S.: National Children’s Study (NCS). (Abstract). Presented at International Federation of Placenta Associations, Paris, France, September 9-12, 2014.

452. Miller RK, Darrah TH, Landrigan P, Walker C, Szabo S, Moye J. Environmental Exposures During Pregnancy: A National Children’s Study Formative Research Experience. (Abstract). To be Presented at The Teratology Society, Bellevue, Washington, June 28-July 2, 2014.

453. Anandaraja NA, Roth R, Landrigan PJ. Chapter 25: Building a Global Health Education Program in an Urban School of Medicine. In: The Role of Anesthesiology in Global Health: A Comprehensive Guide, eds. Roth R, Frost EAM, Gevirtz C, Atcheson CLH; pp. 331-344, Springer, New York, NY, 2014.

454. Friedman A, Friedman M, Miller RK, Stodgell C, Littman L, Landrigan P, Clark EB, Varner M, Dole N, Culhane J, Swanson J, Thiex N, Moye J, National Children’s Study Placenta Consortium. Quantitative Analysis of Bisphenol A in Human Placental Tissue from Nine Counties Across the U.S.: National Children’s Study (NCS). (Poster). Presented at International Federation of Placenta Associations, Paris, France, September 9-12, 2014.

455. Nordberg GF, Fowler BA, Nordberg M, Landrigan PJ. Prevention of the Toxic Effects of Metals Contained in Batteries and E-Waste/Waste Electric and Electronic Equipment (WEEE). (Poster). Presented at Annual Meeting of the Collegium Ramazzini, Carpi, Italy, October 24-26, 2014.

456. Landrigan PJ, Fuller R. Environmental Pollution and Occupational Health in a Changing World. (Commentary) Ann Glob Health 80:245-246, 2014.

457. Crane MA, Cho HG, Landrigan PJ. Implications of the World Trade Center Health Program (WTCHP) for the Public Health Response to the Great East Japan Earthquake. Industrial Health 52:5-12, 2014.

46

OTHER PUBLICATIONS:

REVIEW ARTICLES, CONFERENCE PROCEEDINGS, BOOK CHAPTERS, COMMENTARIES, EDITORIALS, LETTERS TO EDITOR, ABSTRACTS & POSTERS (cont)

458. Sly PD, Neira M, Collman G, Carpenter DO, Landrigan PJ, Van Den Berg M, Barriga FD, Ruchirawat M, Laborde A, Pascale A, Heacock M, Dalmau MT, Suk WA. Networking to advance progress in children’s environmental health. (Commentary) Lancet Glob Health 2:e129-e130, 2014.

458a.Landrigan PJ. The Role of Environmental Exposures in the Aetiology of Autism. A Retrospective View of the Last Decade: New Results and New Frontiers for the Future. Proceedings of the XXIX International Conference, The Person with Autism spectrum Disorders: Animinating Hope-Second Session. New Synod Hall, Vatican City, November 20-22, 2014. Dolentium Hominum N. Journal of the Pontifical Council for Health Care Workers 86:35-41, 2014.

459. Landrigan PJ, Narula J. Introducing the Annals of Global Health. Ann Glob Health 80:1-2, 2014. 460. Landrigan PJ, Lucchini RG, Kotelchuck D, Grandjean P. Principles for Prevention of the Toxic Effects of

Metals. In: Handbook on the Toxicology of Metals. Chapter 24. Nordberg GF, Fowler BA, Nordberg M (Eds). Volume I: General Considerations, 4th Edition. Academic Press, pp. 507-528, 2015.

461. A Report by Greater Boston Physicians for Social Responsibility. In Harm’s Way: Toxic Threats to Child Development (Foreword) May, 2000.

462. Nordberg GF, Fowler BA, Nordberg M, Landrigan PJ. Prevention of the Toxic Effects of Metals Contained in Batteries and E-Waste Electric and Electronic Equipment (WEEE). (Abstract). Presented at ICOH Congress in Korea in 2015.

463. Li Q, Kappil M, Li A, Dassanayke DMA, Darrah T, Friedman AE, Friedman M, Lambertini L, Landrigan P, Stodgell CJ, Aagaard K, Schadt E, Murry J, Clark EB, Done N, Culhane J, Swanson J, Varner M, Moye J, Kasten C, Miller RK, Chen J, National Children’s Study Consortium. Exploring the associations between microRNA expression profiles and environmental pollutants in human placenta from the National Children’s Study (NCS). (Abstract). Presented at the 55th Annual Teratology Society meeting in Montreal, QC, Canada, June 27-July 1, 2015.

464. Landrigan PJ, Suk WA. Jenny Pronczuk de Garbino: AGlobal Champion for Children’s Health. (Editorial). Environ Health Perspect 123:A52-A53, 2015.

465. Landrigan PJ, Baker DB. The National Children's Study: End or New Beginning? New Engl J Med, 372:1486-1487, 2015.

466. Ringen K, Landrigan PJ, Stull O, Duffy R, Melius J, McDiarmid MA. Occupational safety and health protections agains Ebola virus disease. Am J Ind Med, 2015. DOI: 10.1002/AJIM.22467. PubMed PMID: 25950864.

467. Landrigan PJ, Forman JA. Chemical Pollutants. Chapter 719. In: Nelson Textbook of Pediatrics. Kliegman, Stanton, St Geme III, Schor (eds). 20th Edition, Volume 2. Philadelphia, PA: Elsevier, pp. 3427-3431, 2015.

468. Landrigan PJ, Fuller R. Global health and environmental pollution. (Editorial). Int J Public Health 60:761-762, 2015. DOI: 10.1007/s00038-015-0706-7.

469. Landrigan PJ. Irving J. Selikoff, MD January 15, 1915-May 20, 1992. Am J IndMed 58:1015-1016, 2015. doi: 10.1002/ajim.22488. [Epub ahead of print] PubMed PMID: 26333886.

470. Landrigan PJ, Fuller R, Horton R. Environmental pollution, health, and development: A Lancet-Global Alliance on Health and Pollution-Icahn School of Medicine at Mount Sinai Commission. (Comment) Lancet 386:1429-1431, 2015.

471. Landrigan PJ, Benbrook C. GMOs, Herbicides, and Public Health. NEJM 373:693-694, 2015. 472. Landrigan PJ. Children’s Environmental Health: A Brief History. Acad Pediatr 16:1-9, 2016; doi:

10.1016/j.acap.2015.10.002.

47



473. Lucchini RG, Landrigan PJ. Occupational Health and Safety in the Expanding Economies: Severe

Challenges and the Need for Action Through Education and Training. (Editorial) Annals of Global Health 81:463-464, 2015.

474. Landrigan PJ. Emerging Technologies and Materials. Chapter 52. For inclusion in: American Academy of Pediatrics. Handbook of Pediatric Environmental Health, 4th edition, 2016.

475. Landrigan PJ. Environment and Heart Disease. Chapter 105. For inclusion in: Fuster V. (editor). Hurst’s, The Heart, 14th edition, 2016.

476. Miller MD, Marty MA, Landrigan PJ. Children’s Environmental Health – Beyond National Boundaries. In: Our Shrinking Globe: Implications for Child Safety. Sheety AK (ed). Pediatr Clin N Am 63:149-165, 2016. http://dx.doi.org/10.1016/j.pcl.2015.08.008

477. Landrigan PJ. Eula Bingham, PhD: Former Assistant Secretary for Occupational Safety and Health, US Department of Labor. Am J Ind Med 59:81-83, 2016. Doi:10.1002/ajim.22515. PubMed PMID: 26768757.

478. Landrigan PJ. The Effects of Nox On Our Health. Features & Investigations-Car Emissions, It’s not just diesel. Expert Review. Which? 20-23, February 2016.

479. Portier CJ, Armstrong BK, Baguley BC, Baur X, Belyaev I, Bellé R, Belpoggi F, Biggeri A, Bosland MC, Bruzzi P, Budnik LT, Bugge MD, Burns K, Calaf GM, Carpenter DO, Carpenter HM, López-

Carrillo L, Clapp R, Cocco P, Consonni D, Comba P, Craft E, Dalvie MA, Davis D, Demers PA, De Roos AJ, DeWitt J, Forastiere F, Freedman JH, Fritschi L, Gaus C, Gohlke JM, Goldberg M, Greiser E, Hansen J, Hardell L, Hauptmann M, Huang W, Huff J, James MO, Jameson CW, Kortenkamp A,Kopp-Schneider A, Kromhout H, Larramendy ML, Landrigan PJ, Lash LH, Leszczynski D, Lynch CF, Magnani C, Mandrioli D, Martin FL, Merler E, Michelozzi P, Miligi L, Miller AB, Mirabelli D, Mirer FE, Naidoo S, Perry MJ, Petronio MG, Pirastu R, Portier RJ, Ramos KS, Robertson LW, Rodriguez T, Röösli M, Ross MK, Roy D, Rusyn I, Saldiva P, Sass J, Savolainen K, Scheepers PT, Sergi C, Silbergeld EK, Smith MT, Stewart BW, Sutton P, Tateo F, Terracini B, Thielmann HW, Thomas DB, Vainio H, Vena JE, Vineis P, Weiderpass E, Weisenburger DD, Woodruff TJ, Yorifuji T, Yu IJ, Zambon P, Zeeb H, Zhou SF. Differences in the carcinogenic evaluation of glyphosate between the International Agency for Research on Cancer (IARC) and the European Food Safety Authority (EFSA). J Epidemiol Community Health, 2016. pii: jech-2015-207005. doi: 10.1136/jech-2015-207005. [Epub ahead of print]PubMed PMID: 26941213.

480. Myers JP, Antoniou MN, Blumberg B, Carroll L, Colborn T, Everett LG, Hansen M, Landrigan PJ, Lanphear BP, Mesnage R, Vanderberg LN, vom Saal FS, Welshons WV, Benbrook CM. Concerns over use of glyphosate-based herbicides and risks associated with exposures: a consensus statement. (Review). Environmental Health 15:19, 2016. DOI 10.1186/s12940-016-01177-0.

481. Suk WA, Ahanchian H, Asante KA, Carpenter DO, Diaz-Barriga F, Ha E-H, Huo X, King M, Ruchirawat M, da Silva ER, Sly L, Sly PD, Stein RT, van de Berg M, Zar H, Landrigan PJ. Environmental Pollution: An Under-recognized Threat to Children’s Health, Especially in Low- and Middle-Income Countries. (Brief Communication) Environ Health Perspect 124:A41-A45, 2016.

482. Landrigan PJ, Fuller R. Pollution, Health and Development: The Need for a New Paradigm. Rev Environ Health 31:121-124, 2016. pii:/j/reveh.ahead-of-print/reveh-2015-0070/reveh-2015-0070.xml. doi:10.1515/reveh-2015-0070. [Epub ahead of print] PubMed PMID: 26943599. 483. Landrigan PJ, Bellinger D. How to Finally End Lead Poisoning in America. Time Magazine, 2016.

http://time.com/4286726/lead-poisoning-in-america/ 484. TENDR Statement Authors. Project TENDR: Targeting environmental Neuro-Developmental Risks.

The TENDR Consensus Statement. (Brief Communication) Environ Health Perspect 124:A118-A122, 2016.

48

INVITED LECTURES/PRESENTATIONS Visiting Professorships and Lectureships: University of Utah, Wallace Stegner Lecturer, 2012 Harvard School of Public Health, The James L. Whittenberger Lecturer, 2009 University of Kentucky, Inaugural John P. Wyatt Lecturer in Environmental Health and Disease, 2008 University of Minnesota, School of Public Health, Richard G. Bond Memorial Lecture, 2007 James P. Keogh, MD Memorial, Lecturer in Occupational Medicine, University of Maryland School of Medicine, 2006 Royal College of Physicians (London), Faculty of Occupational Medicine, Richard Schilling Memorial Lecturer, 2000 University of Rochester, 44th Annual Paul W. Beaven Lecturer, 2000 Centers for Disease Control and Prevention, Langmuir Memorial Lecturer, 1999 Mayo Clinic, Department of Pediatrics, Amberg-Helmholtz Lecturer in Pediatrics, 1998 Duke University Medical School, Visiting Professor, NIEHS Clinical Training Program in Environmental Medicine, 1995 National University of Singapore, Visiting External Examiner in Occupational Medicine, 1994 Medical College of Pennsylvania, Catherine Boucot Sturgis Visiting Professor in Community and Preventive Medicine, March 1992 University of Cape Town Medical School, Visiting Professor, Department of Community Health, March 1992 University of Tokyo, Visiting Professor of the University, July 1990 University of Tokyo, Visiting Professor of the Faculty of Medicine, September 1989

Exhibit 2

1

January 14, 2002

Public Information and Records Integrity Branch

Information Resources and Services Division (7502C)

Office of Pesticide Programs

Environmental Protection Agency

1200 Pennsylvania Ave., N.W.

Washington, DC 20460

Docket Number: OPP-34203G

Submitted by Email: [email protected]

RE: Comments on the Chlorpyrifos Interim Reregistration Eligibility Decision Document

(IRED)

Federal Register: November 14, 2001; Volume 66, Number 220, Pages 57073-57074

Dear Sir or Madam:

We submit the following comments on behalf of the Natural Resources Defense Council

(NRDC), the World Wildlife Fund (WWF), and the Farmworker Justice Fund, Inc. NRDC uses

law, science, and the support of more than 500,000 members nationwide to protect the planet's

wildlife and wild places and to ensure a safe and healthy environment for all living things.

NRDC has no direct or indirect financial or fiduciary interest in the manufacture or sale of

chlorpyrifos. WWF is a non-profit organization with over 1.2 million members in the United

States. WWF is dedicated to using the best available scientific knowledge to preserve the

diversity and abundance of life on Earth by conserving endangered spaces, safeguarding

endangered species, and addressing global threats to the planet's web of life. The Farmworker

Justice Fund, Inc. is a national, nonprofit advocacy center that seeks to improve living and

working conditions for migrant and seasonal farmworkers and their families. For the past two

decades, it has urged the EPA to reduce or eliminate the use of hazardous pesticides.

mailto:[email protected]

2

Unless otherwise noted or referenced, all page number references in the text of these comments

refer to the Interim Reregistration Eligibility Decision (IRED) for Chlorpyrifos, Case No. 0100.

SUMMARY OF COMMENTS:

ALL CHLORPYRIFOS TOLERANCES MUST BE REVOKED & CHLORPYRIFOS

MUST BE CANCELLED

EPA has found that there is not a “no observable effect level” (NOEL), or even a “no observable

adverse effect level” (NOAEL), for the developmental effects of chlorpyrifos on young animals,

and therefore on human infants and children. In other words, EPA has no scientific basis upon

which to conclude that there is a fully safe level at which infants and children will not suffer

developmental harm due to chlorpyrifos exposure. Moreover, EPA has no basis to derive a Q* or

to use any other quantitative risk assessment methodology that will derive a negligible risk level

(i.e. 1 in 1 million lifetime risk) for chlorpyrifos’ developmental effects. Therefore, EPA simply

cannot make a legal finding that any specific chlorpyrifos level on food is “safe” for infants and

children, or that there is a “reasonable certainty of no harm” to infants and children, at any

specific level. Thus, as a legal matter, under FFDCA §408(b)(2), EPA must revoke all tolerances

and cancel all food uses, for chlorpyrifos.

Moreover, even assuming for the sake of argument that EPA may set tolerances for chlorpyrifos,

notwithstanding the legal prohibition on EPA’s setting a tolerance for a substance that has no

NOEL or NOAEL (and for which a Q* cannot be derived and therefore a cancer-like risk

assessment is impossible), EPA has failed to adequately apply safety factors and to consider

many routes of exposure in the IRED. EPA must apply not only the traditional two 10-fold safety

factors for interspecies variability and for intra-species variability, but also must apply an

additional safety factor of at least 10 for gaps in exposure data, assumptions, and underestimates

of risk, as detailed in these comments, and an FQPA safety factor of at least 30 to account for

potential pre-and post-natal toxicity to infants and children (10X) and to account for significant

gaps in exposure data for infants and children and the lack of a NOEL (3X). EPA has failed to

adequately consider important exposure routes for millions of infants and children, including

children living on farms and who accompany their parents into farm fields (see discussion of farm

children below), exposure from mosquito spraying, drift, and drinking water. Moreover, EPA has

failed to consider cumulative exposure to organophosphates and carbamates that have a common

mechanism of toxicity.

3

Finally, EPA must cancel all uses of chlorpyrifos under FIFRA. All food uses must be cancelled

due to excessive risk and the cancellation of all tolerances under the FFDCA. Even if

theoretically an extremely low tolerance could be set for chlorpyrifos after application of all

appropriate safety factors, the chemical would have to be applied at such low rates and in such a

manner that it would not be efficacious. Moreover, the food and non-food uses of chlorpyrifos

result in worker exposure; non-occupational drift, air, and water exposure; other non-food human

exposure; and ecological risks that pose “unreasonable adverse effects on the environment” and

thus must result in cancellation of all uses of chlorpyrifos.

INTRODUCTION

Uses and Risks of Chlorpyrifos

Chlorpyrifos is an organophosphate pesticide used at approximately 21-24 million pounds active

ingredient (a.i.) annually in the United States. In addition to food crops, chlorpyrifos is used as a

cattle eartag, as a treatment for lawns, turf, and ornamentals, and for pasture, woodland, and

lots/farmsteads. Turf use accounts for 2.5 million pounds annually. By agreement with the

registrants (June, 2000)i, almost all the residential uses (including household, schools, parks) of

chlorpyrifos are being cancelled; public health uses such as mosquito and “childproof” ant-and-

roach bait are residential uses that remain eligible for reregistration (IRED p.8). Termite control

accounted for 5 million pounds annually, and is slated to be withdrawn or phased-out (prohibited

Dec. 31, 2005; IRED p.7). These voluntary phase-outs are predicted to eliminate almost half the

annual chlorpyrifos use in the United States (IRED p.12). Prior to these phase-outs, chlorpyrifos

was the fourth most commonly used pesticide in US households, and comprised a full 25% of

pesticide pounds in residential settings. However, these voluntary phase-outs and withdrawals in

the US will not reduce the amount of chlorpyrifos exported annually, which has remained steady

at approximately 8-9 million pounds annually since 1997.ii

Non-agricultural outdoor uses remaining include golf courses (rate of application reduction), road

medians, food processing plants, manufacturing plants, ship holds, railbox cars, and non-

structural wood treatments such as fenceposts, utility poles, landscape timber, poles, posts, and

processed wood products (IRED p.10). NRDC believes that many of these remaining uses,

especially wood treatments, pose significant exposure risks to children.

4

Chlorpyrifos is used in highest amounts on corn (5.53 million lbs a.i.), cotton (670 thousand),

apples (550 thousand), alfalfa (480 thousand), oranges (460 thousand), and peanuts (316

thousand). Crops with the highest percentage of crop treated are Brussels sprouts (73%),

cranberries (46%), apples (44%), broccoli (41%), and cauliflower (31%). This list includes some

of the foods most consumed by children, making children’s exposure risk particularly high.iii

Chlorpyrifos is applied aerially, by chemigation, groundboom, hand wand, airblast sprayer, and

other methods.

The EPA risk summary speculates that dietary risk, acute and chronic, would now be below the

Agency’s level of concern, presuming full compliance with risk mitigation recommendations.

Prior to mitigation, EPA admits that acute exposures exceed the level of concern for infants,

toddlers, children, and females. After mitigation, EPA believes that these risk groups no longer

exceed the level of concern (IRED p.19).

However, there are considerable risks remaining for workers, even presuming full compliance

with so-called “mitigation measures.” For mixers, loaders, and applicators some risks remain

elevated, even assuming that maximum personal protection equipment (PPE) and engineering

controls are used. In real life, however, maximum recommended PPE is often not used. Under

many scenarios current restricted entry intervals (REIs) also are insufficient.iv The IRED notes

that risks may be mitigated by a combination of additional PPE and engineering controls, and by

reductions in application rates (IRED p.3). Again, past experience shows that recommended

application rates, along with recommended PPE controls, are often disregarded. Post application

risks, also exceeding the level of concern, may be mitigated by reducing application rates and by

lengthening REIs. Again, this is unlikely to be sufficient to protect worker risk.

Furthermore, in measuring the extent of exposure and in determining aggregate exposure, EPA

should acknowledge farmworker children to be a major, identifiable subgroup of consumers

whose unique, increased level of exposures must be taken into account. These nearly 1,000,000

children are deserving of protection under the “reasonable certainty of no harm” health standard

under the law.

Although EPA says the drinking water risk is below the level of concern, the Agency notes that

there have been cases of high levels of drinking water well contamination associated with

localized applications of chlorpyrifos as a subterranean termiticide. This is being addressed, EPA

5

says, by eliminating all termiticidal uses. However, despite EPA’s assertions that only

termiticidal use leads to water contamination problems, USGS and others have found

contamination of ground and surface water with chlorpyrifos and its metabolites, and EPA’s own

modeling shows that it is likely that in certain areas of heavy use, chlorpyrifos (and its

metabolites) present significant water risks. There is no evidence that the water risks of

chlorpyrifos and its metabolites are limited to termiticidal use. This evidence of surface and

groundwater contamination with chlorpyrifos is discussed below.

Drift/Air Exposure

In certain "sentinel" populations, such as farmworker children who live in a pesticide-rich

environment, registered, non-residential, non-dietary sources may account for most of a child’s

exposure to pesticides, regardless of whether there is registered indoor use. Pesticides applied

aerially must be assessed for its effects on people affected by pesticide drift or sloppy application.

Reports in the medical literature describe numerous preventable illnesses and deaths among

children with such “take-home” exposures. NRDC’s report, Trouble on the Farm, documents the

scientific evidence supporting the potential for take-home exposures from pesticides, even when

not registered for residential use (this report is hereby incorporated by reference). These

exposures are particularly important for children given their greater potential susceptibility, hand-

to-mouth behavior and other behaviors in the home.

Significant concentrations of organophosphate pesticides (of at least 1.0 ng/m3, and at least 2.4

ng/m3 in one site in California) have been detected in winter fog, outside of the growing season

(Glotfelty and others, 1987;v Seiber and others, 1993

vi). This phenomenon may be due to

volatilization or wind erosion, as is the case for other pesticides (Glotfelty and others, 1990c; Wu,

1981).vii

Evidence suggests that photochemical reactions lead to the production of oxygen

analogs (oxons) of chlorpyrifos in air during daylight, which are incorporated into the nighttime

fog (Glotfelty and others, 1990aviii

). Chlorpyrifos has been detected in rain at concentrations up

to 180 ng/L, in air up to 199/ng/m3, and in fog up to 14,200 ng/L.

ix The maximum concentration

found in rain frequently exceeded EPA's water quality criteria for freshwater aquatic organisms

(83 ng/L – acute; 41 ng/L - chronic).x In addition, several studies have shown that drift is a

significant concern. Thus, EPA must consider airborne exposure as a source in conducting its

assessment of risk.

Ecological Risks

6

Ecological risks from chlorpyrifos use remain extremely worrisome; the Agency notes high risks,

acute and reproductive toxicity, to birds, fish, mammals, and aquatic invertebrates. Some risk

quotients exceed 1000 times the acceptable limit (IRED pp. 52-58). It is highly toxic to honey

bees, which are killed if present even within 24 hours after application (IRED p. 54). Given that

animals and insects, and especially honeybees, pollinate over ¾ of the staple crop plants

worldwide, and have an estimated economic value to world agriculture of $200 billion annually,

it is no surprise that any decline in honeybee populations is considered a serious threat to world

food supplies.xi The IRED states that mitigation will require reduced application rates, increased

retreatment intervals, reduced seasonal maximum allowable rates, and no-spray setback zones

(IRED, p. 4). NRDC believes that these recommendations are unlikely to be adhered to, as

discussed further in these comments. EPA estimates that risks to invertebrates will remain of

concern, despite these mitigation efforts. Further, bioconcentration of chlorpyrifos will likely

pose an acute and reproductive risk to aquatic birds and mammals, in spite of mitigation efforts.

EPA’s Decision

The Agency’s IRED concludes that chlorpyrifos may be reregistered under the Federal

Insecticide, Fungicide, and Rodenticide Act (FIFRA) for agricultural uses because the registrants

agreed to cancel most residential uses, and because EPA intends to require some mitigation

measures for the remaining agricultural uses. Under the Federal Food, Drug and Cosmetic Act

(FFDCA), EPA relies on the same rationale to keep in effect those tolerances that the registrant

continues to support.

The IRED states that with the addition of label restrictions and amendments detailed in the IRED,

all currently registered uses of chlorpyrifos except open-pour dust formulations may continue. In

the current IRED, EPA says the tolerance for tomatoes will be revoked, and tolerances for apples

and grapes will be lowered to 0.01 ppm each (IRED p.18). In an effort to further mitigate

elevated ecological risk, the IRED recommends some crop-specific measures, including reducing

the maximal number of liquid applications per season as follows: alfalfa, from eight to four;

citrus, to two; corn, to three, with a reduced application rate from 7.5 to 3 lbs a.i./A; cotton, from

six to three, with a reduced application rate from 6 to 3 lbs a.i./A. Further, spray drift warnings

and no-spray zones will be included on labels.

The Agency has determined that, with presumed full compliance with mitigation

recommendations, a 10X FQPA factor for infants, children, and females aged 13-50 (IRED p.16),

7

and a 100X uncertainty factor for acute and chronic reference doses (IRED p.15) will provide a

sufficient margin of safety.

EPA CANNOT LAWFULLY ESTABLISH OR LEAVE IN EFFECT TOLERANCES FOR

CHLORPYRIFOS

EPA has found that there is no NOEL or NOAEL for the developmental effects of chlorpyrifos

on human infants and children. EPA therefore has no scientific basis upon which to conclude that

there is a fully safe level at which infants and children will not suffer developmental harm

because of chlorpyrifos exposure. Moreover, EPA has no basis to derive a Q* or to use any other

quantitative risk assessment methodology that will derive a negligible risk level (i.e. 1 in 1

million lifetime risk) for chlorpyrifos’ developmental effects. Therefore, EPA simply cannot

make a legal finding that any specific chlorpyrifos level on food is “safe” for infants and children,

or that there is a “reasonable certainty of no harm” to infants and children, at any specific level.

Thus, as a matter of law, under FFDCA §408(b)(2), EPA must revoke all tolerances, and cancel

all food uses, for chlorpyrifos.

Even assuming for the sake of argument that EPA can set tolerances for chlorpyrifos,

notwithstanding the legal prohibition on EPA’s setting a tolerance for a substance that has no

NOEL or NOAEL (and for which a Q* cannot be derived and therefore a cancer-like risk

assessment is impossible), EPA has failed adequately to apply safety factors and to consider

many routes of exposure in the IRED. EPA must apply not only the traditional two 10-fold safety

factors for interspecies variability and for intra-species variability, but also must apply an

additional safety factor of at least 10 for the data gaps and buried assumptions that underestimate

risk, as detailed further below, and an FQPA safety factor of at least 30 to account for potential

pre-and post-natal toxicity to infants and children (10X) and to account for significant gaps in

exposure data for infants and children and the lack of a NOEL (3X). EPA has failed adequately

to consider important exposure routes for millions of infants and children, including children

living on farms and who accompany their parents into farm fields (see farm children section

below), exposure from mosquito spraying, drift, and drinking water exposure. Moreover, EPA

has failed to consider cumulative exposure to organophosphates and carbamates that have a

common mechanism of toxicity; under FFDCA §408(b)(2), no tolerance may be established or

left in place without considering such cumulative risks.

8

EPA must cancel all uses of chlorpyrifos under FIFRA. All food uses must be cancelled due to

excessive risk and the cancellation of all tolerances under the FFDCA. Even if theoretically an

extremely low tolerance could be set for chlorpyrifos after application of all appropriate safety

factors, the chemical would have to be applied at such low rates an in such a manner that it would

not be efficacious. Moreover, the food and non-food uses of chlorpyrifos result in worker

exposure; non-occupational drift, air, and water exposure; other non-food human exposure; and

ecological risks that pose “unreasonable adverse effects on the environment” and thus must result

in cancellation of all uses of chlorpyrifos.

CHLORPYRIFOS TOXICITY CONSIDERATIONS

The Agency has seriously underestimated the risks posed by chlorpyrifos use, thereby

undermining its conclusion that chlorpyrifos can continue to be used in a way that prevents

“unreasonable adverse effects on the environment,” FIFRA § 3(c)(5), and provides “a reasonable

certainty that no harm will result from aggregate exposure to the pesticide chemical residue,”

FFDCA § 408(b)(2)(A). EPA rationalized the continued use of chlorpyrifos for agriculture

applications, because EPA considers that dietary risks are not of concern, residential risks are no

longer of concern due to voluntary withdrawals of household uses, and EPA considers that risks

posed to workers and the environment are acceptable, although they exceed the level of concern

in a number of scenarios.

While supporting the voluntary withdrawals of residential uses, schools, and parks, which is

predicted to reduce by half the total pounds of chlorpyrifos used annually, NRDC takes issue with

the above assumptions. Our concern about exposure to chlorpyrifos remains high,

notwithstanding EPA’s intended cancellation and mitigation actions. Unfortunately, the Agency

has understated the adverse health effects caused by chlorpyrifos, the amount of exposure that

people endure without effect, and the amount of chlorpyrifos to which people are exposed. With

chlorpyrifos and other developmental neurotoxic chemicals, risk to the fetus, infant, and child

comes primarily from the timing of exposure. Even a very small dose, for even a short duration,

during a developmental period of vulnerability will result in permanent neural dysfunction. There

is no demonstrated reliable threshold of safety for this highly toxic chemical, as indicated in the

IRED, where a no-effect level could not be determined for developmental neurotoxicityxii

(IRED

p. 15-16). In addition, the Agency has overestimated the effectiveness of some mitigation

recommendations. First, EPA assumes that pesticide applicators will reliably use personal

protective equipment (PPE) and will always abide by specified re-entry intervals (REIs) – a

9

waiting time between applying the product and returning to the field – even though these

mitigation measures are not enforced and are commonly ignored. Second, the Agency does not

adequately account for “take-home” exposures from agriculture uses (domestic contact with

pesticides tracked home on the clothes, shoes, and skin of workers) or exposures from spray drift

(wind-blown pesticides from field or aerial applications that subsequently impact people). These

points are described in greater detail in NRDC’s comments submitted to the Agency October 16,

2000.xiii

There is demonstrated evidence of neuropathology and increased vulnerability of fetuses when

exposed to chlorpyrifos (IRED p. 16; Makris et al.xiv

). However, given that in these experiments

neuropathology was seen in the neonates at the lowest dose tested, these studies were unable to

identify an offspring NOAEL in the DNT (IRED p. 16). In that study, structural alterations in

brain development, which would result in permanent brain dysfunction, were seen at the lowest

doses tested (IRED p. 17), strongly indicating that a 10X FQPA margin of safety is insufficient to

protect fetuses, neonates, and children from irreversible chlorpyrifos-induced brain damage.

Furthermore, Congress was clear in stating that under the FQPA, EPA must establish tolerances

based on a No Effect Level (NOEL); not the NOAEL. If there is no NOEL, EPA cannot simply

assume that there is a safe level based upon no evidence, and then apply safety factors. Whereas

Congress did allow EPA to consider setting tolerances for non-threshold carcinogens at a level

that poses no greater than a 1 in 1 million lifetime cancer risk, EPA has no scientific basis upon

which to set a tolerance for chlorpyrifos that would pose a 1 in 1 million risk of suffering

developmental problems, cannot establish a NOEL, and thus cannot set or leave in place a

tolerance for chlorpyrifos.

Of additional concern, the chlorpyrifos metabolite, TCP, is more persistent than the parent

compound (IRED p.20), is of greater toxic potency to fetuses than adults (IRED p.16), and

exceeds chronic DWLOCs for children (IRED p.16). The toxicity of the chlorpyrifos metabolite

was not considered in the chlorpyrifos dietary assessment (IRED p.17). This omission represents

a very serious risk to tens of thousands of exposed vulnerable fetuses, neonates, and children.

Given these very serious concerns, NRDC believes that EPA simply cannot establish or leave in

effect any tolerance for chlorpyrifos. Assuming arguendo that EPA can do so, at a minimum EPA

must use an additional 30X FQPA margin of safety – in addition to the other uncertainty factors –

to protect children and to account for demonstrated fetotoxicity, uncertainty in extrapolating from

10

effect-levels to NOAELs, and very substantial gaps in exposure and toxicity data (detailed in

these comments). The current IRED recommends an uncertainty factor of 100X for the acute and

chronic reference dose (IRED p. 15). NRDC believes that if the agency decides to establish

tolerances notwithstanding the lack of NOELs (a decision that we believe would not be lawful),

the Agency is clearly obligated to apply a 1000X UF, in addition to a 30X FQPA margin of

safety, comprised of: 10X for interspecies extrapolation, 10X for intraspecies variability, and 10X

to adjust for the lack of consideration of metabolite-induced toxicity, uncertainty in extrapolating

from subchronic to lifetime effects, and uncertainty associated with other non-conservative

assumptions detailed in these comments.xv

NRDC believes that there are no “safe” levels of

chlorpyrifos for fetuses, infants, and children, as demonstrated by the Agency’s own DNT

studies. Exposure to the developing nervous system to neurotoxic chemicals during periods of

heightened vulnerability, even at low levels or short durations, will disrupt normal structure and

function and will cause permanent disruption of neural function (see numerous papers by Abou-

Donia et al, and Slotkin et al xvi).

DEVELOPMENTAL TOXICITY OF CHLORPYRIFOS IS UNDERESTIMATED

The action of chlorpyrifos as a developmental neurotoxic chemical is undisputed. The EPA

human health risk assessment of chlorpyrifos states:

In conclusion, the weight of the evidence raises concern for an increase in both the

sensitivity and susceptibility of the fetus or young animal to adverse biochemical,

morphological, or behavioral alterations from chlorpyrifos treatment during brain

development. With respect to cholinesterase inhibition, an increase in sensitivity of the

young compared to adults was seen all along the dose response curve, even at relatively

low doses. There is a clear differential response (2- to ~5-fold ) in the young compared to

the adult animal after an acute treatment to a relatively low dose of chlorpyrifos. There is

also increased sensitivity found after repeated dosing (up to 9-fold), but at the LD10 and

MTD. It is important to point out that an uncertainty remains concerning the magnitude

of the differential response, given that newborn animals (less than PND 7) have not been

characterized for sensitivity. Results of multiple studies have consistently shown that the

developing brain is susceptible to chlorpyrifos treatment. Effects on the developing CNS

that are indicative of the unique susceptibility to the young animal include changes in

macromolecular synthesis, altered cell signaling and muscarinic receptor down

regulation, as well as morphological alterations in brain development. An uncertainty

remains regarding the NOAELs for the susceptibility effects. The effects observed raise a

11

high degree of concern that the fetus or young animal is particularly susceptible to

adverse outcome if exposed to chlorpyrifos.xvii

A substantial body of scientific evidence exists demonstrating the fetotoxic, neurotoxic, and

immunotoxic properties of chlorpyrifos and its oxon metabolite, with treatment in utero or

perinatal resulting in permanent damage to the nervous system (see numerous papers by Abou-

Donia et al, and Slotkin et al xviii). NRDC is extremely concerned, in light of the experimentally

demonstrated, permanent, effects of chlorpyrifos in the developing nervous system, that the

chlorpyrifos IRED has underestimated risk, used central tendency estimates, used non-

conservative assumptions, and ignored data gaps in estimating exposure risk. These concerns are

detailed further below.

The IRED Does Not Account for the Toxicity of Metabolites and Stereoisomers

Though EPA has abundant data for dietary exposure to chlorpyrifos, its PDP and FDA databases

only include monitoring data for residues of the chlorpyrifos parent compound. As stated in the

IRED, the Agency has concluded that the primary metabolite of chlorpyrifos, 3,5,6-trichloro-2-

pyridinol (TCP), does not induce cholinesterase inhibition, and exhibits effects only at doses

higher than those producing ChEI with chlorpyrifos, and therefore, is less toxic than chlorpyrifos

(58 Fed. Reg. 19,354(April 14, 1993)) (IRED p. 16). However, compared with chlorpyrifos, TCP

is stated to be “more mobile and significantly more persistent in many soils, especially under

anaerobic conditions” (IRED p.20). Further, the Agency states in the IRED that, “upper-bound

estimated environmental concentrations of TCP exceeded chronic DWLOCs for children” (IRED

p. 16). This is especially disconcerting, given the “evidence of increased susceptibility of rabbit

fetuses relative to dams” (IRED p.16). Recently published experimental evidence of the toxicity

of chlorpyrifos oxon and TCP in animalsxix, and in a human cell linexx emphasize the need for

inclusion of metabolites in the risk assessment. The impact of these metabolites on developing

animals – where even short-lived compounds could conceivably have irreversible effects on the

nervous system – heightens the need for prudence in carrying out cumulative assessments. EPA

appears to have no requirement for chemical-specific pharmacokinetic studies in fetal animals

that would aid in discerning the contribution of toxic metabolites, such as the chlorpyrifos oxon

and TCP, to children’s risk. Until data are available that are specific to parent

compound/metabolite mixtures for chlorpyrifos, from all exposure sources, any risk assessment

involving this chemical would be incomplete, and likely less protective of public health than is

required by law. Under FQPA, EPA is to set tolerances so as to "ensure that there is a reasonable

12

certainty that no harm will result to infants and children from aggregate exposure to the pesticide

chemical residue.”xxi

NRDC therefore asserts that the Agency is unjustified in its determination

that “residues of TCP are not of concern for the chlorpyrifos dietary assessment,” and “can

therefore be excluded from the tolerance expression.” (IRED p. 17).

Buried Assumptions Underestimate Risk

Many OP assessments contain buried or outdated assumptions that receive little or no recognition

in the risk characterization, despite their less-than-health-protective impact on final risk estimates.

These assumptions tend towards a lesser, rather than a greater, certainty of no harm to infants and

children. EPA should acknowledge as much. Outside scientists have criticized many of these

assumptions as not being sufficiently protective.xxii

Some specific examples from the chlorpyrifos and other OP assessments, drawn from the draft

SOPs, illustrate the problem better:

EPA assumes all “toddlers,” aged 1 to 6 years, weigh 33 pounds (15 kg). EPA bases its

assumption on the mean or average weight for three year-olds. Because home pesticide

exposures and risks are calculated on a per pound basis, EPA’s baseline assumption about

a toddler’s weight will tend toward risk estimates that understate true risks for smaller

toddlers and younger infants whose brains and nervous systems are developing more

rapidly and are therefore more vulnerable than those of older children.

EPA bases its estimate of a toddler’s exposure to a chlorpyrifos-contaminated surface

due to hand-to-mouth activity on the ludicrous assumption that this activity occurs just

1.56 times per hour. Then-Assistant Administrator L. Goldman, a pediatrician, as well as

EPA’s latest scientific advisory panel all singled out this assumption as being particularly

inadequate. The latter panel also indicated that assessment of a child’s mouthing behavior

would be incomplete if it focused only on hand-to-mouth exposures. Children put objects

other than fingers in their mouth, and these objects may carry pesticide residues and be

ingested. Children also eat “feral” food — food that’s dropped on the floor and which

picks up residues from contaminated linoleum, carpet or other household surfaces. In

any case, the hand-to-mouth value EPA currently uses as its “conservative” assumption is

roughly 16 times lower than the value obtained from a recent study of 30 children. Those

children put fingers in their mouths 26 times per hour on average, with some children

showing the behavior up to 70 times per hourxxiii

. While EPA has proposed to change its

guidelines to a value of 20 times per hour, this is still an average value. Moreover, until

13

the change is final, the agency continues to use the dramatically low value of 1.56 times

per hour — a value which any parent will recognize as ridiculously low.

Since FQPA’s mandate for a reasonable certainty of no harm means that EPA must set tolerances

so as to fully protect even exceptionally exposed children (i.e. EPA must set tolerances to protect

all children, including all “major identifiable subgroups” of children at greater risk), and not

merely the average child, use of these central tendency estimates are inappropriate. These

concerns apply equally to the characterization of risk from residential exposure of agriculture

uses such as spray drift, residential residue track-in, exposures to farm worker children, and

exposures to children in and around schools.

It is clear the above central tendency assumptions are not health-protective of more highly-

exposed and susceptible populations; EPA must stop making any claims of conservatism, and

should instead acknowledge that current assessments using the draft standard operating

procedures may be likely to understate true exposure for many children.

Reliance on Unenforced and Unreliable Mitigation Downplays Exposure

It is disturbing that the risks to workers for mixing, loading and applying chlorpyrifos to

agriculture crops exceed safe levels, even when presuming full compliance with mitigation

recommendations. Furthermore, it is widely recognized that training and monitoring workers for

use of PPE is inadequate, and moreover, workers in hot fields often cannot tolerate PPE. EPA

therefore should not assume that PPE will mitigate the risk from certain scenarios when real life

experience suggests PPE cannot be relied upon. These particular chemical uses may not be

found "safe", and by definition cause "unreasonable adverse effects on the environment" under

FIFRA. Therefore EPA should issue a Notice of Intent to Cancel (NOIC) and proposal to revoke

their tolerances.

The Agency has proposed to mitigate occupational risks partially through lengthening the re-entry

interval (REI) for most crops. Although this seems at face value to be a health-protective step, in

practice it has no mitigation value whatsoever. There is no enforcement for REIs, and therefore,

lengthening such REIs, like requirements for increased PPE, are routinely ignoredxxiv

. Poor

compliance with a mitigation effort that may sound reasonable on paper will not protect exposed

individuals. It is clearly stated under FIFRA §3(C)(5) that “The Administrator shall register a

pesticide if the Administrator determines that…..when used in accordance with widespread and

14

commonly recognized practice it will not generally cause unreasonable adverse effects on the

environment”. This passage illustrates that EPA cannot rely on mitigation methods, such as PPE

and REIs, which are unenforced and poorly followed.

Exporting Hazards

Although chlorpyrifos is listed as a “restricted use” pesticide in the US, it is exported in high

volume: 7 to 9 million pounds annually since 1997 (8,570,694 in 2000).xxv

In fact, a recent article

by C. Smith states that, according to customs records, between the years 1997 through –2000,

nearly 65 million pounds of severely restricted or forbidden pesticides in the United States were

exported; more than 22 tons per day. More than 55% of these products were exported to

developing countries for agriculture use. The International Labor Organization estimates that 60

to 90% of children estimated to be working in Africa (80 million), Asia (152 million), and Latin

America (17 million) are working in agriculture. These children are exposed to toxic pesticides

in the fields, from drinking and washing water, through contaminated clothing, and in their

homes.xxvi

The U.N. Commission on Human Rights stated that “[a]llowing the export of products

recognized to be harmful is immoral.”xxvii

The mitigation requirements in this IRED include

respirators with an organic-vapor removing cartridge and a pesticide-approved prefilter,

chemical-resistant outerclothes, enclosed-cab machinery, emergency equipment readily available,

and storage containments for discarding single-use chemically-resistant overclothes. It is

inconceivable that these are “readily available” to mixers, loaders, applicators, and fieldworkers

in developing countries. Clearly, new labeling requirements will have no mitigation effects for

these men, women, and children workers.

No Estimate of Risk Associated with Greenhouse and Nursery Uses

Of further concern, the IRED states that post application risks to nursery and greenhouse workers

were unassessed, due to lack of data (IRED pp. 40, 89). This lack of data is insufficient

justification to ignore the obvious risk of such registered uses. NRDC maintains that this must be

considered an important gap in data required to conduct a complete risk assessment, and

contributes to the underestimation (in this case, complete ignorance) of risk in this IRED.

RISK TO FARMWORKER CHILDREN

Farmworker Children Are an Identifiable High-Risk Group

In measuring the extent of exposure and in determining aggregate exposure, EPA should

acknowledge farmworker children to be a major, identifiable subgroup of consumers whose

15

unique, increased level of exposures must be taken into account.xxviii

NRDC’s report, Trouble on

the Farm, documents the scientific evidence supporting the potential for take-home exposures

from pesticides, even when not registered for residential use (this report is hereby incorporated by

reference). These exposures are particularly important for children given their greater potential

susceptibility, hand-to-mouth behavior and other behaviors in the home. These nearly 1,000,000

children are deserving of protection under the “reasonable certainty of no harm” health standard

under the law.

EPA’s refusal to apply a sufficient margin of safety for children (at least 30X) in its chlorpyrifos

assessment is inconsistent with the need for additional protections for the fetuses of pregnant

farmworker women who may be exposed while their mothers are at work, and the risks facing

neonates who are brought to the fields to accompany their parents due to lack of day care. These

babies, who face exposure to an extremely potent neurotoxin at vulnerable stages of development

are not employees and may not be disregarded on the grounds they face an occupational risk

(Farmworker Justice Fund, Comments to the EPA’s Pesticide Docket on the Preliminary Risk

Assessment for Chlorpyrifos, December 23, 1999).

The legal analysis submitted by Farmworker Justice Fund to the Pesticides Docket for the

chlorpyrifos risk assessment remains relevant:

“In setting, modifying or revoking tolerances, the FQPA directs the EPA to consider,

inter alia, ‘available information concerning the … effects of in utero exposure to

pesticide chemicals.’ § 408 (b)(2)(C)(I)(II). In the case of threshold effects, FQPA also

directs the EPA to add an additional 10-fold (or other) margin of safety for infants and

children ‘to take into account potential pre- and post-natal toxicity and completeness of

the data with respect to exposure and toxicity to infants and children.’ Id. at

408(b)(2)(C)(ii). In explaining its method of implementing the 10-fold safety factor to

the SAP, the EPA expressly stated that it would not consider prenatal exposures to the

unborn children of pregnant farmworker women because such exposures are

‘occupational’ and hence, not within the contemplation of the FQPA. See Presentation

for the FIFRA Scientific Advisory Panel by Office of Pesticide Programs, Health Effects

Division on FQPA Safety Factor for Infants and Children (March 1998). The statutory

language which directs the EPA to consider the effects of ‘in utero’ or ‘pre-natal’

exposures to pesticides makes no exception for occupational exposures. Nor could such

an exception make sense since it is patent that a fetus or unborn child cannot work. In an

16

analogous context, the California Supreme Court has held that a child, who was injured in

utero when his pregnant mother was exposed to carbon monoxide at work, could not be

prevented from filing suit in tort by the workers compensation bar, which prohibits an

employee from suing his or her employer. Snyder v. Michael’s Stores Inc, 16 Cal.4th

991, 945 P.2d 781, 68 Cal.Rptr.2d 476 (1997). The Court dismissed the notion that the

unborn child could be deemed an ‘employee’ as ‘wholly without merit.’ The Court also

noted that every other court to consider this question - except one - had reached the same

conclusion (and the only exception was a lower California court whose decision was

effectively overruled by the Snyder case). Since an unborn child cannot be an

‘employee,’ its pesticide exposure cannot be ‘occupational.’”

Thus, any prenatal exposure to the fetuses of farmworkers must be considered in the

determination to set the FQPA margin of safety for infants and children. Although the Agency

applied a 10X FQPA factor, given the extremely neurotoxic action of chlorpyrifos, the

demonstrated increased vulnerability of fetuses and neonates, and the lack of a NOEL,xxix

NRDC

maintains that this is woefully insufficient to provide a margin of safety for these vulnerable sub-

groups.

Drift and Take-Home Exposures to Chlorpyrifos

Even setting aside the issue of whether an unborn child in a farmworker mother’s womb is

exposed as a result of “occupational” activity when the mother is in the fields, it is clear beyond

peradventure that EPA must consider fetal and childhood exposure of farm children and fetuses

as a result of drift, take-home exposure, drinking water exposure in farm areas, in-field “day

care,” and other farm child exposure resulting from proximity to the fields. These comments are

discussed in detail in the NRDC Report Trouble on the Farm.xxx

The scientific literature and common sense demonstrate that children and others experience

substantial potential exposures through drift from crop spraying, and through take-home

exposures when, for example, pesticides are exhaled from parents' lungs or brought home on

boots, work clothes, etc. xxxi

xxxii

Pesticides used on lawns, gardens and nearby farms end up in

soil and are tracked into the home on shoes and pets. One common lawn herbicide, 2,4-D, has

been found to persist in carpet dust up to a year after lawn application.xxxiii

For methyl-parathion,

for example, 34% of original residues remained in clothes even after 10 launderings—a level high

17

enough to kill insects and present a health risk to humans.xxxiv

Chlorpyrifos is expected to cause

long-lasting take-home exposure problems (IRED p. 41).

EPA’s current policy, as stated in the spray and dust drift label policy, is clear. The Agency is

obligated to protect public health from all pesticide exposures, including those resulting from

spray and dust drift:

“EPA's position on pesticide drift is that applicators must not allow pesticide spray or

dust to drift from the application site and contact people, animals, and certain sensitive

sites, including structures people occupy at any time and the associated property, parks

and recreation areas, nontarget crops, aquatic and wetland areas, woodlands, pastures, or

rangelands. The Agency believes this is prudent public policy. It sets high but appropriate

standards for applicators to protect people and the environment.”xxxv

In certain "sentinel" populations, such as farmworker children who live in a pesticide-rich

environment, these non-dietary sources may account for most of a child’s exposure regardless of

whether there is registered indoor use. Reports in the medical literature describe numerous

preventable illnesses and deaths among children with such “take-home” exposures. NRDC’s

report, Trouble on the Farm, documents the scientific evidence supporting the potential for take-

home exposures from pesticides, even when not registered for residential use (this report is

hereby incorporated by reference). These exposures are particularly important for children given

their greater potential susceptibility, hand-to-mouth behavior and other behaviors in the home.

EPA is now considering building into its pesticide risk assessments the fact that worker risks may

"spill over" to the families of workers and to fetuses that workers may carry on and off the job.

For example, pregnant women working or living on or near farms may very well have pesticide

exposures that clearly fall within the purview of the FFDCA section 408 aggregate safe exposure

requirement—particularly (but not exclusively) when the exposures occur off the work site due to

take–home/drift exposures. Current EPA practice, including the current chlorpyrifos risk

assessment, is to consider an additional FQPA 10X margin of safety, when applicable, only to

consumers of food crops and not to exposed workers and their families. Given the certainty of

drift and take–home exposures with many pesticides, including chlorpyrifos, the Agency is

obligated to expand its exposure assessment to include these risks from agriculture use. EPA’s

failure to incorporate these real-life exposures into its risk assessments will result in final risk

estimates that are not adequately protective of human health. If data are lacking to quantify such

18

exposures, it is essential to incorporate an additional margin of safety to assure that use of the

chemical is consistent with a reasonable certainty of no harm to children until more precise data

can be generated, as required by the FQPA.

As detailed in the above discussion, it is invalid to presume, as the IRED does, that by canceling

residential uses of chlorpyrifos, there will no longer be a risk of exposure to fetuses and children.

NRDC asserts that so long as agriculture uses remain, the risk of exposure to fetuses and children

is certain.

DIETARY EXPOSURE IS UNDERESTIMATED

EPA’s Acute Dietary Exposure Estimate Is Flawed and Unlawful

For chlorpyrifos, as with other OPs, the Agency used estimates of the percentage of crops treated

(%CT) from BEAD (Biological Economic Analysis Division) to derive the acute dietary risk

estimate, rather than assuming the more conservative approach of 100% crop treated (IRED p. 18;

Acute dietary risk assessmentxxxvi

). Using %CT in estimating acute risk violates governing law.

The FQPA specifically authorized EPA to consider the percent of crop treated (%CT) “when

assessing chronic dietary risk . . . only if the Administrator” makes four specific findings about

data reliability. FFDCA § 408 (b)(2)(F) (emphasis added). By contrast, the law nowhere allows

EPA to use %CT in assessing acute dietary risk. Of course, the law’s distinction between chronic

and acute risks makes perfect sense. Congress understood that the likelihood that a person will

experience harm from chronic exposures over time could be affected by the overall percentage of

that crop treated with that chemical. On the other hand, in examining the acute harm resulting

from a single exposure, it is irrelevant whether a large or small percentage of that crop was

treated with that pesticide. Any amount of a crop treated at a level causing acute harm could not

be characterized as assuring a “reasonable certainty of no harm,” making it completely

inappropriate and unlawful to use %CT in assessing acute dietary risks. Using %CT to assess

acute risk is in direct violation of the FQPA.

In the case of chlorpyrifos, BEAD estimated a maximum of 53% crop treated for apples, and only

1% CT for grapes.xxxvii

By using %CT, rather than assuming 100% CT, the Agency has

underestimated risk for affected individuals by as much as 100X for grapes (used 1%CT), and

1.8X for apples (used 53% CT). This is especially important given that the mitigation measures

proposed in this IRED include reducing tolerances for both apples (currently 1.5 ppm) and grapes

(currently 0.5 ppm) to 0.01 ppm. Simple math reveals that the Agency has underestimated the

19

risk estimate for grapes by 100X, and then reduced the tolerance by 50X, resulting in an overall

increase by 50X in allowable risk. For apples, the Agency has underestimated risk by 50X, and

then reduced the tolerance by 150X, resulting in a real-reduction of only 100X. Since apples and

grapes are acknowledged to be the largest contributors to dietary exposure (especially for

children), this is extremely worrisomexxxviii

(IRED p. 18). Further, the acute dietary risk

assessment for chlorpyrifos indicates that without mitigation, exposure from residues on fresh

apples exceeds the allowable risk for children 1-6 yrs by over 300X (aPAD=364%)xxxix

(IRED p.

19), rendering the above 50X increase completely inappropriate and the above 100X reduction

wholly inadequate.

The mitigation proposed, which is limited to the above described insufficient tolerance changes

and new labeling requirements, which are unenforced and poorly adhered to, is unlikely to result

in any substantial reductions in exposure.

Drinking Water Exposures Do Not Account for Toxic Metabolites

For drinking water, the chlorpyrifos metabolite TCP is not included in the tolerance expression,

despite being identified in a number of environmental fate studies. Compared with chlorpyrifos,

TCP is stated to be “more mobile and significantly more persistent in many soils, especially under

anaerobic conditions” (IRED p.20). Further, the Agency states in the IRED that, “upper-bound

estimated environmental concentrations of TCP exceeded chronic DWLOCs for children” (IRED

p. 16). This is especially disconcerting, given the “evidence of increased susceptibility of rabbit

fetuses relative to dams” (IRED p.16). Given the demonstrated evidence of exposure to TCP in

food and drinking water, and the increased vulnerability of children and pregnant women, NRDC

believes the Agency is unjustified in not including TCP exposure in its tolerance assessment.

Under FQPA, drinking water exposures (through ingestion, inhalation, and dermal absorption

from hand-washing and showers) at least must be estimated. "Refinement" of drinking water data

in a risk assessment may be an appropriate long-term goal, but it is scientifically unjustified for

EPA to intentionally circumscribe the scope of the risk assessment by ignoring these exposures in

the interim. Where EPA lacks drinking water monitoring data for specific chemicals or toxic

metabolites, it should make quantitative or qualitative estimates and be frank in its description of

both the assumptions, the uncertainties, and the limitations of the data.

20

Inclusion of complete, real-world drinking water exposures to chlorpyrifos and its metabolites

such as TCP at sites of maximum likely exposure in an aggregate exposure assessment is critical

for two additional reasons. First, EPA decision-makers should be presented with a risk

assessment that reflects the entire range of real-life exposures to the chemical in question.

Second, because exposure to OP-contaminated drinking water will tend to add to the estimated

risk, its inclusion in the preliminary risk assessment is necessary to demonstrate, in the most

transparent way, the urgency of taking immediate steps to reduce that risk. When EPA fails to

incorporate real-life drinking water OP exposures into its risk assessments, it will tend toward

risk estimates that are less than health-protective. If data are lacking to quantify drinking water

exposure to individual OPs, the use of an additional 10X margin of safety is essential to assure

that use of the chemical is consistent with a reasonable certainty of no harm to children until more

precise data can be generated.

Water Monitoring Data Is Not Designed to Detect Peak Levels

The IRED states that surface water estimates were based on the USGS NAWQA monitoring data,

which reported the maximum dissolved chlorpyrifos concentration was 0.4 ppb (IRED p.21).

Surface Water

Combined USGS data for state, local, national, and multi-state studies that measured chlorpyrifos

concentrations in surface water detected the pesticide at 7 of 108 (6%) sites sampled.xl Most of

these data do not include TCP or other chlorpyrifos metabolites. Chlorpyrifos has medium

runoff potential due to its relatively low water solubility, 2 mg/L, (Becker and others, 1989xli

;

Goss, 1992xlii

), though some of its metabolites are more soluble and persistent A chlorpyrifos

flux as a percentage of use of 0.15 has been measured in the Minnesota River.xliii

Chlorpyrifos is

also, of course, used in non-agricultural settings, and can thus drift or runoff directly into surface

water bodies in areas of high population density. In two out of nine studies that measured

chlorpyrifos concentrations in surface waters, its concentration exceeded EPA's water quality

criteria for aquatic organisms in some samples (0.083 μg/L [83 ng/L] – acute; 0.041 μg/L [41

ng/L] – chronic).xliv,xlv,xlvi,xlvii

Ground Water

Data from the Mid-Continent Pesticide Studyxlviii

shows that chlorpyrifos was present in the

ground water in 4.2% of the wells sampled.xlix

Cohen and others (1990) found the chlorpyrifos

transformation product 3,5,6-Thrichloro-2-pyridinol in ground water in Cape Cod, Mass.l

21

Chlorpyrifos has been detected in 0.6% of wells sampled, according to the U.S. EPA's Pesticides

in Ground Water Database.li Long (1989) detected chlorpyrifos in the ground water of 30% of 56

sites examined beneath pesticide mixing and loading facilities in Illinois.lii The maximum

concentration detected was 0.5 μg/L. Habecker (1989)liii

detected a maximum surface soil

concentration of chlorpyrifos of 41,000 μg/kg at pesticide mixing and loading sites in Wisconsin.

Krapac and othersliv

detected a maximum surface soil concentration of 26,000 μg/kg at

agrichemical facilities in Illinois.

EPA Must Consider Exposures at Areas of High Water Contamination.

With the exception of the extraordinarily high exposures that would be suggested by the data for

mixing and loading areas, these monitoring data generally are not targeted to areas of anticipated

maximum exposure, which are the areas that FQPA requires that EPA consider in setting “safe”

tolerances considering aggregate exposure. EPA, therefore, must at least estimate such maximum

exposure levels using modeling.

Using the PRZM/EXAMS screening model, estimated 90-day average and peak chlorpyrifos

concentrations were 6.7 and 40 ppb respectively. However, EPA did not rely upon these model

estimates. Rather, the IRED estimated acute exposures at 0.026 to 0.4 ppb, based on the 95th

percentile of the monitoring data. This is a full 100X lower than the 40 ppb estimate derived from

the PRZM/EXAMS model.

NRDC contends that, contrary to the assertions of conservatism in the IRED (IRED pp. 21-22),

these estimates likely underestimate actual levels substantially. Water monitoring sample sites

are not necessarily correlated with chlorpyrifos use sites, and in particular, may miss sites where

multiple fields are treated with chlorpyrifos resulting in pooled runoff into a common water

source. In fact, the IRED states, “it is not clear that they [monitoring data] represent the most

vulnerable groundwater where chlorpyrifos is used most intensively” (IRED p.22). Monitoring of

surface water is likely to be subject to the same problem. Levels of chlorpyrifos in pooled runoff

sites are likely to be many times higher than single field sites. Similarly, data collection is not

timed to correspond with worst-case scenarios, such as closely following chlorpyrifos

applications, or following large storm runoff events, and thus most often misses these highly toxic

environmental exposures.

AGGREGATE RISK ESTIMATE IS INADEQUATE

22

Under the FFDCA, a pesticide tolerance can only be established if “there is a reasonable certainty

that no harm will result from aggregate exposure to the pesticide chemical residue, including all

anticipated dietary exposures and other exposures for which there are reliable information.”

FFDCA § 408(b)(2)(A)(ii). Aggregate exposure is the total exposure to a single chemical or its

residues that may occur from dietary (i.e., food and drinking water), residential and other non-

occupational sources, and from all known or plausible exposure routes (oral, dermal and

inhalation).

The FQPA requires assessment of both dietary and non-dietary, non-occupational pesticide

exposures in the aggregate, and FIFRA demands that EPA protect against pesticides’

unreasonable health and environmental effects. Both good science and public health protection

demand routine assessment of aggregate exposure because real-world exposures aggregate – that

is, pesticides are used in a wide variety of settings and formulations likely to result in multiple

exposure sources. Yet EPA has failed to do an adequate aggregate assessment in its chlorpyrifos

assessment.

In addition to food and water exposures, the aggregate assessment must take into account

exposures due to air drift and migration of contaminated soil, especially in agricultural areas,

residential exposures from registered uses (including golf courses, greenhouses, and nurseries),

residential “take-home” exposures to families of those directly exposed to the OP through its

agricultural uses, as well as exposures from uses that do not conform with the label, where there

is an indication that these uses occur.

When lacking actual data on any these various sources of non-dietary exposure, EPA should not

simply assume that the particular route of exposure is unimportant or nonexistent, as it has chosen

to do with respect to chlorpyrifos. For example, in the chlorpyrifos IRED, the Agency has ignored

the contribution to risk from chlorpyrifos metabolites, which are highly toxic and persistent

(IRED p.17), from spray drift and take-home exposures associated with agriculture uses (IRED p.

41), and from greenhouse and nursery uses (IRED p. 40). The risk characterization should clearly

note that failure to include all possible routes of exposure will tend to bias final estimates of

aggregate risk so that they will understate rather than overstate true risks. In other words, EPA’s

risk estimates are less rather than more protective of public health. Moreover, when there are not

actual data to confirm the absence of exposure to a pesticide across any particular route, EPA

must incorporate an additional safety factor to account for this lack of complete exposure data.

23

LEVEL OF REGULATION MUST ENSURE A REASONABLE CERTAINTY OF NO

HARM FOR ALL FETUSES, INFANTS, AND CHILDREN

EPA may not sacrifice the hundreds or thousands of children who may exceed the reference dose

for a particular OP. Under FQPA, the burden is upon the advocate of a tolerance to prove (and

upon EPA to find) that there is a reasonable certainty that no children will be harmed in EPA ’s

pesticide decisions. Thus, if the best evidence suggests that hundreds or even thousands of

children will exceed the reference dose for an OP, EPA is forbidden by statute to find a

reasonable certainty of no harm to these particular infants and children, and the Agency should

not issue a tolerance at that level.

Instead, in EPA’s proposed approach – which is styled as a “highly refined” Monte Carlo risk

analysis – the agency regulates dietary residues of individual OPs at the 99.9th percentile. EPA

seeks to mask in this approach the fact that even regulation at the 99.9th percentile, for a pesticide

commonly used on a ubiquitous children’s food, means that 0.1% of all American children under

age six (around 24,000 children in all) could exceed the chronic RfD every day, based on the best

information available to the agency. Further, a child exposed to multiple organophosphate

pesticides may fall within the 99.9th percentile for one, but lie above the safety threshold when

cumulative OP risks are calculated. No reading of the statute will support any approach that

allows hundreds or thousands of children to exceed the reference dose. Regulating dietary

residues of chlorpyrifos at the 99.9th percentile directly violates the plain statutory language of the

FQPA.

HUMAN TESTING

In 1999, chlorpyrifos registrants submitted to EPA a never-published, non peer-reviewed study in

which volunteers had been intentionally dosed with chlorpyrifos for the purpose of discovering a

no-effect level, and therefore influencing regulatory levels for this nerve system poison.lv In

previous years, human tests of chlorpyrifos have been performed on small groups of prison

“volunteers” as well, and the results submitted for consideration by EPA. The human tests

submitted by chlorpyrifos registrants should be rejected by EPA. The purpose of using results

from human testing is to justify the establishment of less stringent safety standards. Intentionally

dosing human subjects with known poisons – with no medical benefit to the subjects –is illegal,

unethical, and unscientific.

24

Human testing of pesticides violates the Nuremberg Code, adopted by American judges in the

wake of the Nuremberg “Doctors Trials” of Nazis following World War II. The Nuremberg Code

has been relied on by state and federal courts as establishing rock bottom minimum legal

standards for human testing. Furthermore, EPA’s consideration of the chlorpyrifos human tests

would clearly be unethical and in contravention of the Helsinki Declaration, the Common Rule,

FIFRA, and the EPA Scientific Advisory Panel/Science Advisory Board report on human testing.

Finally, the scientific value of the results of the chlorpyrifos human tests is negligible at best.

The tests involved so few subjects that the risks to the broader population –especially the most

vulnerable subgroups – cannot be meaningfully assessed. The IRB process used to justify the

tests, the “voluntary” consent process used, and many other aspects of the chlorpyrifos human

tests were in clear violation of ethical and legal requirements of the Nuremberg Code, Helsinki

Declaration, the Common Rule, FIFRA, and the EPA Scientific Advisory Panel/Science Advisory

Board report on human testing.

We note that, in December 2001, the Agency requested that the National Academy of Sciences

conduct a review of the scientific and ethical issues posed by use of these studies.lvi

The Agency

has stated that during the Academy’s deliberations, and until a policy is in place, the Agency will

not consider or rely on any such studies, whether previously or newly submitted.lvii

NRDC urges

the Agency to adhere to this position, and to refrain from any consideration of these studies. EPA

must reject the use of human tests, consistent with sound scientific practice and pursuant to

EPA’s ethical and legal obligations.

Thank you for the opportunity to provide these comments.

Respectfully submitted,

Jennifer Sass, Ph.D.

Senior Scientist


1200 New York Avenue, NW, Suite 400


202-289-6868

Erik Olson

Senior Attorney


1200 New York Avenue, NW, Suite 400


25

202-289-6868

Shelley Davis, Attorney

Co-Executive Director

Farmworker Justice Fund, Inc.

Washington, DC

202-783-2628

Kristina Thayer, PhD

Program Scientist

Wildlife and Contaminants Program

World Wildlife Fund

Washington, D.C.

202-822-3473

Sarah Lynch, Ph.D.

Senior Program Officer

Center for Conservation Innovation

World Wildlife Fund

Washington, D.C.

202-778-9781

i USEPA. Chlorpyrifos revised risk assessment and agreement with registrants. June 2000.

Available electronically at http://www.epa.gov/pesticides/op/chlorpyrifos/agreement.pdf ii Smith, C. 2001. Pesticide exports from U.S. ports, 1997-2000. Int J Occ Environ Health, 7(4):

266-274. Table 6, data from California EPA. iii Consumers Union of US, Inc. Washington, DC. 1998. Worst First; High-risk insecticides,

children’s foods and safer alternatives. p. 13 iv Kate Hallward, Anne Katten, Margaret Reeves and Kristin Schafer, Facing Poison in the

Fields: California Farmworkers and Pesticides (1999); Shelley Davis and Rebecca Schleifer,

Indifference to Safety (1999)

Columbia Legal Services, Enforcement of Farm Worker Pesticide Protection in Washington State

(November 1998) vv Glotfelty, J.E., Seiber, J.N., and Liljedahl, L.A., 1987, Pesticides in fog: Nature, v. 325, pp.

602-605. vi Seiber, J.N., Wilson, B.W., and McChesney, M.M., 1993, Air and fog deposition residues of

four organophosphorus insecticides used on dormant orchards in the San Joaquin valley,

California: Envrion, Sci. Technol., v. 27, no. 10, pp. 2236-2243. vii Majewski et al, 1995, supra, at 135; Wu, T.L., 1981, Atrazine residues in estuarine water and

the aerial deposition of atrazine into Rhode River, Maryland: J. Water, Air, Soil Poll., v. 15, pp.

173-184. viii Majewski et al, supra, at 144; Glotfelty, D.E., Majewski, M.S., and Seiber, J.N., 1990,

Distribution of several organophosphorus insecticides and their oxygen analogs in a foggy

atmosphere: Environ. Sci. Technol., v. 24, no. 3, pp. 353-357. ix Majewski et al, 1995, supra, at 159t. x Ibid at 159t, 161. xi Smith, op cit.

xii Makris S, Raffaele K, Sette W, Seed J. A retrospective analysis of twelve developmental

26

neurotoxicity studies submitted to the USEPA Office of Prevention, Pesticides, and Toxic

Substances (OPPTS). Draft 11/12/98. xiii

NRDC comments submitted by A. Quintero to the Chlorpyrifos Docket: OPP-34203C,

October 16, 2000. xiv

Makris S, Raffaele K, Sette W, Seed J. A retrospective analysis of twelve developmental

neurotoxicity studies submitted to the USEPA Office of Prevention, Pesticides, and Toxic

Substances (OPPTS). Draft 11/12/98. xv

this list of buried assumptions and underestimates of risk is similar to that cited in the EPA

Trichloroethylene Health Risk Assessment, Review Draft, August, 2001, section 1.4 xvi

Huff RA, Abu-Qare AW, Abou-Donia MB. Effects of sub-chronic in vivo chlorpyrifos

exposure on muscarinic receptors and adenylate cyclase of rat striatum. Arch Toxicol. 2001

Oct;75(8):480-6

Navarro HA, Basta PV, Seidler FJ, Slotkin TA. Neonatal chlorpyrifos administration elicits

deficits in immune function in adulthood: a neural effect? Brain Res Dev Brain Res. 2001 Oct

24;130(2):249-52.

Levin ED, Addy N, Nakajima A, Christopher NC, Seidler FJ, Slotkin TA. Persistent behavioral

consequences of neonatal chlorpyrifos exposure in rats. Brain Res Dev Brain Res. 2001 Sep

23;130(1):83-9.

Slotkin TA, Cousins MM, Tate CA, Seidler FJ. Persistent cholinergic presynaptic deficits after

neonatal chlorpyrifos exposure. Brain Res. 2001 Jun 1;902(2):229-43. xvii

EPA. Human health risk assessment: Chlorpyrifos. June 8, 2000. p 131 xviii

Huff RA, Abu-Qare AW, Abou-Donia MB. Effects of sub-chronic in vivo chlorpyrifos

exposure on muscarinic receptors and adenylate cyclase of rat striatum. Arch Toxicol. 2001

Oct;75(8):480-6

Navarro HA, Basta PV, Seidler FJ, Slotkin TA. Neonatal chlorpyrifos administration elicits

deficits in immune function in adulthood: a neural effect? Brain Res Dev Brain Res. 2001 Oct

24;130(2):249-52.

Levin ED, Addy N, Nakajima A, Christopher NC, Seidler FJ, Slotkin TA. Persistent behavioral

consequences of neonatal chlorpyrifos exposure in rats. Brain Res Dev Brain Res. 2001 Sep

23;130(1):83-9.

Slotkin TA, Cousins MM, Tate CA, Seidler FJ. Persistent cholinergic presynaptic deficits after

neonatal chlorpyrifos exposure. Brain Res. 2001 Jun 1;902(2):229-43. xix

Huff RA, Abou-Donia MB. In vitro effect of chlorpyrifos oxon on muscarinic receptors and

adenylate cyclase. Neurotoxicology. 1995 Summer;16(2):281-90.

Huff RA, Corcoran JJ, Anderson JK, Abou-Donia MB. Chlorpyrifos oxon binds directly to

muscarinic receptors and inhibits cAMP accumulation in rat striatum. J Pharmacol Exp Ther.

1994 Apr;269(1):329-35. xx

Qiao D, Seidler FJ, Slotkin TA. Developmental neurotoxicity of chlorpyrifos modeled in vitro:

comparative effects of metabolites and other cholinesterase inhibitors on DNA synthesis in PC12

and C6 cells.

Environ Health Perspect. 2001 Sep;109(9):909-13. xxi

FFDCA Sec. 408 (a)(2)(C )(ii)(I)

xxii USEPA, Report of The Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA)

Scientific Advisory Panel (SAP), meeting on September 9, 1997, A Set of Scientific Issues Being

Considered by the Agency in Connection with the Exposure Assessment Methodologies for

Residential Scenarios, Office of Science Policy Coordination

xxiii USEPA, Overview of Issues Related to the Standard Operating Procedures for Residential

Exposure Assessment, Presented to the FIFRA Scientific Advisory Panel on September 21, 1999,

Office of Pesticide Programs, August 5, 1999, p. 66 xxiv

Kate Hallward, Anne Katten, Margaret Reeves and Kristin Schafer, Facing Poison in the

27

Fields: California Farmworkers and Pesticides (1999); Shelley Davis and Rebecca Schleifer,

Indifference to Safety (1999)

Columbia Legal Services, Enforcement of Farm Worker Pesticide Protection in Washington State

(November 1998) xxv

Smith, C. 2001. Pesticide exports from U.S. ports, 1997-2000. Int J Occ Environ Health, 7(4):

266-274. Table 6, data from California EPA. xxvi

US Newswire. 2001. U.N. human rights investigator deems U.S. export of banned pesticides

‘immoral’. December 17, 16 :09. http://www.usnewswire.com xxvii

U.N. Special Rapporteur Fatma Zora Ouhachi-Vesely. In : US newswire, December 17,

2001. op cit. xxviii

Lu C, Fenske RA, Simcox NJ, Kalman D. Pesticide exposure of children in an agricultural

community: evidence of household proximity to farmland and take home exposure pathways.

Environ Res. 2000 Nov;84(3):290-302. xxix

Makris et al. op cit. xxx Solomon GM, Mott L. 1998. Trouble on the farm: Growing up with pesticides in agricultural

communities. Report by the Natural Resources Defense Council.

xxxi Mott, L, Our Children at Risk: The 5 Worst Environmental Threats to Their Health, Natural

Resources Defense Council, San Francisco, CA, 1997

xxxii Fenske RA, Lu C, Simcox NJ, Loewenherz C, Touchstone J, Moate TF, Allen EH, Kissel

JC. 2000. Strategies for assessing children’s organophosphorus pesticide exposures in

agricultural communities. J Expo Anal Environ Epidemiol, 10 (6 Pt 2): 662-671

xxxiii Nishioka, M. et al., "Measuring Transport of Lawn Applied Herbicide Acids from Turf to

Home: Correlation of Dislodgeable 2,4-D Turf Residues with Carpet Dust and Carpet Surface

Residues," Env. Sci. and Tech. 30(11), pp. 3313-3320, 1996

xxxiv Solomon, G, Trouble on the Farm: Growing Up with Pesticides in Agricultural

Communities, 1998, citing Laughlin, J, Gold R, Laundering Pesticide Contaminated Clothing,

University of Nebraska, Lincoln xxxv

EPA. Draft pesticide registration notice spray and dust drift label statements for pesticide

products. Draft PR notice 2001-X (8/9/01). 66 Fed. Reg. 57098-57099. xxxvi

EPA. Chlorpyrifos. Acute dietary risk assessment for chlorpyrifos, revised after public

comments; Chemical No. 59101; DP Barcode D263890. June 22, 2000. xxxvii

EPA. Chlorpyrifos. Acute dietary risk assessment for chlorpyrifos, revised after public

comments; Chemical No. 59101; DP Barcode D263890. June 22, 2000. see p.10 for apples, and

p. 12 for grapes. xxxviii

ibid, p. 2-3, in bold. xxxix

ibid, p. 3, Table 1. xl Larson, Steven J., Capel, Paul D., and Majewski, M.S., 1997, Pesticides in Surface Waters:

Distribution, Trends, and Governing Factors. Chelsea, MI: Ann Arbor Press, 373 p. 19. xli Becker, R.L., Herzfeld, D., Ostlie, K.R., and Stamm-Katovich, E.J., 1989, Pesticides: Surface

runoff. leaching, and exposure concerns: University of Minnesota, Minnesota Extension Service

Publication AG-BU-3911, 32 p. xlii Goss, D.W., 1992, Screening procedure for soil and pesticides relative to potential water

quality impacts: Weed Technol., v. 6, pp. 701-708. xliii Larson et al, 1997, supra, at p. 192-93 xliv Ibid at p. 264-65 xlv Radtke, D.B., Kepner, W.G., and Effertz, R.J., 1988, Reconnaissance investigation of water

quality, bottom sediment, and biota associated with irrigation drainage in the Lower Colorado

River valley, Arizona, California, and Nevada, 1986-87: U.S. Geological Survey Water-

Resources Investigation Report 88-4002, 77 p. xlvi Richards, R.P., and Baker, D.B., 1993, Pesticide concentration patterns in agricultural drainage

28

networks in the Lake Erie Basin: Environ. Toxicol. Chem., v. 12, no. 1, pp. 13-26 xlvii Baker, D.B., 1988, Sediment, nutrient and pesticide transport in selected Lower Great Lakes

tributaries: U.S. Environmental Protection Agency, Great Lakes National Program Office Report

1, EPA-905/4-88-001, 225 p. xlviii Burkart, M.R., and Kolpin, D.W., 1993, Hydrologic and land-use factors associated with

herbicides and nitrate in near-surface aquifers: J. Environ. Qual., v. 22, no. 4, pp. 646-656. xlix

Barbas, J.E., and Resek, E.A., 1996, Pesticides in Ground Water: Distribution, Trends, and

Governing Factors. Chelsea, MI: Ann Arbor Press, 588 p., at p. 98-9 l Ibid at 101; Cohen, S.Z., Nickerson, S., Maxey, R., Dupuy, A., Jr., and Senita, J.A., 1990, A

ground water monitoring study for pesticides and nitrates associated with golf courses on Cape

Cod: Ground Water Monitor. Rev., v. 10, no. 1, pp. 160-173. li Barbas & Resek, supra, at p. 167 lii Long, T., 1989, Groundwater contamination in the vicinity of agrichemical mixing and loading

facilities, in Illinois Agricultural Pesticides Conference: Proceedings: University of Illinois,

College of Agricultural Consumer and Environmental Services, Urbana-Champaign, Ill., pp. 139-

149; Barbas & Resek at 327. liii Habecker, M.A., 1989, Environmental contamination at Wisconsin pesticide mixing/loading

facilities: Case study, investigation and remedial action evaluation: Wisconsin Department of

Agriculture, Trade and Consumer Protection, Agricultural Resource Management Division,

Madison, Wis., 80 p. liv Krapac, I.G., Roy, W.R., Smyth, C.A., and Barnhardt, M.L., 1993, Occurrence and distribution

of pesticides in soil at agrichemical facilities in Illinois, in Agrichemical facility site

contamination study: Illinois Department of Agriculture, Springfield, Ill., variously paged.

lv Kisicki JC. 1999. A rising dose toxicology study to determine the No-Observable-Effect-

Levels (NOEL) for erythrocyte acetylcholinesterase (AChE) inhibition and chloinergic signs and

symptoms of chlorpyrifos at three dose levels. Dow AgroSciences LLC, study ID: DR# K-

044793-284. FOIA RIN-0938-00 to NRDC. lvi

Letter from S. Johnson, Assistant Administrator, EPA to National Academy of Sciences.

December 14, 2001. Available electronically at www.epa.gov/epahome/headline3_121401.htm lvii EPA newsroom. December 14, 2001.

Exhibit 3

© 0

STATE of NEW YORK

OFFICE OF THE ATTORNEY GENERAL

ELIOT SPITZERDIVISION OF PUBLIC ADVOCACY

Attorney GeneralENVIRONMENTAL PROTECTION BUREAU

. January 30, 2002

Public Information and Records Integrity BranchInformation Resources and Services Division (7502C)Office ofPesticide ProgramsEnvironmental Protection Agency1200 Pennsylvania Ave., N.W.Washington, D.C. 20460

Re: Chiorpyrifos Interim Reregistration Eligibility Decision and

Interim Risk Management Decision;Docket Control Number OPP-34203G

Dear Sir or Madam:

The Attorney General of the State of New York submits these comments onthe Environmental Protection Agency’ s chiorpyrifos Interim ReregistrationEligibility Decision and Interim Risk Management Decision (hereinaftercollectively “IRED”) pursuant to the November 1 4, 200 1 federal Register notice(66 fed. Reg. 57,073-57,074). These comments supplement the AttorneyGeneral’s December 27, 1999 comments (amended January 3, 2000) (OPP-34203),and October 20, 2000 comments (OPP-34203C) on the preliminary and revisedhealth and ecological risk assessments for chlorpyrifos. These comments aresubmitted pursuant to an extension granted by the project manager, Tom Myers.

The Capitol, Albany, NY 12224 • (518) 474-8096 • Fax (518) 473-2534

2

I. Introduction

The IRED proposes to establish and/or leave in effect chlorpyrifostolerances, or allowable residues, from 0.0 1 to 1 5 milligrams per kilogram (mg/kg)or parts per million (ppm) on a variety of foods. Many of these foods are widelyconsumed by children. for the reasons set forth below, the tolerances proposed inthe IRED are not safe and will result in unreasonable adverse impacts on humanhealth and the environment. The IRED therefore fails to fulfill the requirements ofthe federal Insecticide, Fungicide and Rodenticide Act (“FIFRA”) and the FederalFood Drug and Cosmetic Act, as amended by the Food Quality Protection Act(“FQPA”). Both FIFRA and the FQPA require that EPA ensure that humanexposures to chlorpyrifos residues in food are safe and are protective of bothhuman health and the environment. Continued agricultural use of chiorpyrifos onfood crops presents unacceptable risks to human health and the environment evenif the mitigation measures proposed in the IRED are fully implemented. Moreover,the WED fails to address the ecological threats posed by continued use ofchlorpyrifos. Chlorpyrifos products therefore should not be deemed eligible forreregistration for use on food and the IRED does not support such a determination.

II. Summary of the Attorney General’s Comments on the IRED

A. The FQPA requires that EPA find chlorpyrifos “safe” for useon food before determining eligibility.

The IRED does not set forth a finding that chlorpyrifos is “safe.” Such afinding of safety is a necessary, legal prerequisite under the FQPA for EPA toallow chlorpyrifos to remain in widespread use on food in the United States. As setforth in recent scientific studies, chlorpyrifos residues on foods, even at the lowestlevels, may cause adverse health effects and therefore are not safe, particularly forchildren. The IRED does not set forth a finding of safety and, indeed, does notsupport such a finding.

B. The FQPA requires that EPA consider cumulative risksand endocrine disruption effects before determining eligibility.

EPA’s failure to complete either a cumulative risk assessment for allorganophosphates or an endocrine disruption screening program results in an

3

understatement of the risks posed by chlorpyrifos. In the absence of thisinformation, EPA cannot find that tolerances are safe or determine that chiorpyrifosproducts are eligible for reregistration.

C. FIFRA requires that EPA find no unreasonable adverse effectson human health and the environment from chiorpyrifos.

The IRED fails to set forth a level of exposure that will have no effect onhuman health and ignores documented ecological impacts from single exposures.There is strong evidence of adverse effects on the young at the lowest doses tested.Establishing a level at which no effects on the young are seen is critical todetermining whether adverse effects are unreasonable under FIFRA’s standard forreregistration. The IRED also ignores documented ecological impacts fromwildlife exposures to chlorpyrifos. The IRED does not support a finding ofeligibility under FIFRA.

D. The IRED fails to protect against the ecological risks posed bychlorpvrifos and violates the Endangered Species Act.

The Endangered Species Act (“ESA”) mandates that EPA consider whetheragricultural and other uses of chlorpyrifos jeopardizes endangered and threatenedspecies. EPA apparently has not consulted with the U.S. Fish and Wildlife Service(“fWS”) and has disregarded the biological opinions issued by FWS finding thatendangered and threatened species are seriously jeopardized by the continued useof chiorpyrifos. The IRED does not propose actions specifically designed toprotect endangered and threatened species and therefore is in violation of therequirements of the E$A.

E. The IRED’s inadequate analysis ofhuman health risks does not justifyEPA’s finding that chlorpvrifos is eligible for reregistration.

The IRED and the underlying health and environmental risk assessments onwhich it is based are inadequate to support a finding ofreregistration eligibilitybecause EPA has not accurately evaluated dietary exposure and consequently hasfailed to adequately assess human health risks.

4

F. The IRED does not establish a level at which no adverse effects are

observed and fails to apply an additional “safety” or uncertainty factor

to account for this deficiency.

The data suggest that there is no level of exposure to chlorpyrifos that is

without adverse effects on developmental neurotoxicity in the young, and it is

impossible to establish a true “No Observed Adverse Effect Level” (“NOAEL”) for

chiorpyrifos. The IRED instead utilizes a “Lowest Observed Adverse Effect

Level” (“LOAEL”) in analyzing developmental neurotoxicity adverse effects of

chlorpyrifos exposure (IRED, p. 1 6). The use of a LOAEL is inadequate to

accurately assess risk, and, at the very least, requires application of an additional

tenfold “safety” or uncertainty factor.

G. The IRED underestimates human exposure.

The IRED fails to assess the widespread presence of chlorpyrifos residue in

more than one third of the foods, tested by the United States Food and Drug

Administration (“FDA”) as a part ofits annual “Total Diet Study.” Many of the

foods with chlorpyrifos residues are baby foods. The IRED also significantly

undervalues human exposure by failing to consider residue data showing repeated

exceedances of statutory tolerance levels and the presence of chlorpyrifos on foods

widely consumed by children for which no tolerance has been set (e.g., carrots,

celery, potatoes and other foods).

H. The IRED fails to address the persistent illegal presence of

chlorpyrifos on foods for which no tolerances are established.

The IRED does not address the persistent and illegal use of chlorpyrifos on

foods for which no tolerance is set and erroneously fails to include residues on

these foods in calculating dietary exposure. The presence of chlorpyrifos residue

on these foods is a “presumptive tolerance violation” and, as a matter of law, are

considered “unsafe.”

5

I. The IRED’s reregistration eligibility finding was predetermined by the

June 2000 Memorandum ofAgreement between EPA and Registrants.

The June 2000 MOA between EPA and the registrants predetermined the

outcome of the entire chiorpyrifos reregistration process, but specifically the results

reached in the IRED and the previously-issued risk assessment. This

predetermined result was reached without the benefit ofpublic review and

comment and is not in conformance with the procedural requirements of FIFRA.

J. The IRED contains inadequate risk mitigation measures with respect

to dietary exposure. occupational and ecological exposure and risks.

The IRED does not address the continued unacceptable dietary, occupational

and ecological exposures even assuming there will be strict compliance with all

proposed, albeit unenforceable, mitigation measures. More importantly, the IRED

incorrectly assumes that the mitigation measures will be adequate not only to

protect workers but to protect the general population (including women, children

and infants) and ecological receptors as well. There simply is no evidence in the

record that the mitigation measures will significantly reduce the unacceptable risks

to human health and the environment required by the FQPA and FIFRA.

K. The IRED’s attempt at Codex harmonization is flawed.

The IRED’s attempt to harmonize the EPA-set U.S. tolerances for

chiorpyrifos with the often vastly different international standards will increase

exposure and risk to human health in the United States from both domestic and

imported foods. The IRED does not consider adopting the Codex international

standards that are more stringent than the U.S. tolerances. The IRED also fails to

propose measures to assure that chlorpyrifos residues on imported food do not

exceed the U.S. tolerances.

III. Background

Chlorpyrifos is the most widely used organophosphate insecticide in the

United States. It is used to control insects on an extensive variety of food crops for

human consumption and on feed crops for animal consumption. The annual total

domestic usage of chiorpyrifos in the United States for the years 1 987 through

.6

1 998 was approximately 2 1 to 24 million pounds of the active ingredient (ai)

tIRED, p. 1 ). The largest agricultural applications of chiorpyrifos are on corn

(about 5.5 million pounds ai).

Chiorpyrifos is a developmental neurotoxin. That is, it impairs brain and

central nervous system development. Chiorpyrifos shares with other

organophosphates a common mechanism of toxicity that adversely impacts human

health.

Chiorpyrifos was first registered in 1 965 . Registered uses since then have

included its use on food and feed crops, golf courses and green houses, and its use

for structural termite control, home and garden pest control, and as a mosquitocide.

Permissible residue levels or numerical “tolerances” for chlorpyrifos are set forth in

EPA’s regulations, 40 C.F.R. § 180.342.

Chlorpyrifos is also used and its residue found on a variety of food crops for

which EPA has not established by regulation a tolerance. These food crops include

cantaloupe, spinach, winter squash, potatoes, celery, carrots, green beans and

lettuce.’ As more fully discussed below, the presence ofchlorpyrifos residues on

these crops is illegal per se and violates the FQPA.2

In 1 999 EPA began the process of assessing the human health and ecological

impacts of chlorpyrifos for the purpose of determining whether chlorpyrifos

products should be reregistered under the FQPA and FIFRA. In October, 1999,

EPA issued a preliminary risk assessment that outlined both the human health and

ecological impacts of chlorpyrifos. On December 29, 1 999, the Attorney General

submitted comments on the preliminary risk assessment and asserted that it was

deficient in several respects.3

1 United States Department ofAgriculture (“USDA”) PDP Residue Data for

Chiorpyrifos, 1993-1999 (Exhibit A).

2 See FQPA Section 408(a)(1), 21 U.S.C. § 346a(a)(1).

3 See Attorney General’s December 29, 1 999 comments and January 3, 2000 amended

comments on EPA Preliminary Risk Assessment.

7

In a June 2000 Memorandum ofAgreement with EPA, the registrants of

chiorpyrifos products agreed to voluntarily cancel registrations for certain uses,

including home and garden uses, termiticide uses, and its use on tomatoes. The

registrants ‘ voluntary cancellation of these uses was contingent upon EPA granting

the pending applications for reregistering chlorpyrifos products that would

continue to be used primarily on food (MOA, ¶J 2-5).

On August 1 6, 2000, EPA issued a final, revised human health and

environmental effects risk assessment for chlorpyrifos as part of FIFRA’s

reregistration process (OPP-34203C). On October 20, 2000, the Attorney General

submitted comments on the revised risk assessment. These comments stated that

continued use of chlorpyrifos on food posed a significant risk to human health and

the environment, that all uses on food should be cancelled, and that reregistrations

should be denied.4 The Attorney General’s comments demonstrated that the risk

assessments were flawed, that chlorpyrifos is not safe for continued agricultural

use, and that it therefore is not eligible for reregistration.

Among the specific points raised in the Attorney General’s comments on the

risk assessments were the following deficiencies:

. Failure to apply appropriate FQPA safety factor.

. Failure to consider the cumulative impacts of chlorpyrifos

exposure when viewed with exposures to otherorganophosphate pesticides.

. failure to consider aggregate exposure pathways from food and

other sources such as air and drinking water.. Data gaps and the absence of sufficient data (e.g. cumulative

risk assessment and endocrine disrupter screening) to support

tolerance decisions and eligibility determination.. Failure to include and consider recent toxicity studies showing

adverse health effects at extremely low levels of exposure and to

apply appropriate uncertainty factors.. Failure to include and consider relevant data showing the

significant adverse ecological impacts on fish and wildlife from

4 See the Attorney General’s October 20, 2000 comments on the final revised risk

assessment. The position in those comments that chiorpyrifos should not be reregistered was set

forth in other public comments, including those of the Natural Resources Defense Council.

0

8

widespread agricultural use.. Underestimation ofpotential human exposures from dietary and

non-dietary sources.. Failure to incorporate environmental justice considerations with

respect to farm worker and minority exposure.. Failure to assess the, chiorpyrifos metabolite, TCPy.. Failure to assess risks associated with inert ingredients.. Improper methodology in assessing risk.. Failure to demonstrate the effectiveness ofproposed mitigation

measures to reduce exposure and risk.

On September 28, 2001, EPA issued the IRED finding chiorpyrifos eligible

for reregistration and continued use on food. The IRED does not address or correct

the deficiencies set forth in the Attorney General’s previous comments on the risk

assessments and does not respond to those and other comments submitted by

interested parties. Despite the opportunity in the IRED to correct deficiencies in

the human health and ecological risk assessments, EPA is continuing an apparently

undeterred course to reregister chiorpyrifos products for use on food in violation of

both FIFRA and the FQPA.

Iv. Summary of the IRED’s Findings

The IRED proposes to establish and/or leave in effect chlorpyrifos residue

levels or tolerances on food ofbetween 0.01 and 15 ppm (IRED, Table 29, pp. 67-

7 1). Thus, the IRED determined that agricultural use of chlorpyrifos on food and

feed crops will continue. In addition to registered uses for food and feed crops, the

IRED determined that chlorpyrifos will continue to be used on golf courses, in

greenhouses, for non-structural wood treatments such as utility poles and fence

posts, and as a mosquitocide (IRED Executive Summary p. 1). Use ofproducts for

pre-construction structural termite control also will be allowed to continue (IRED

p. 1). The IRED recites that, pursuant to the June 2000 MOA with the registrants,

the use of chlorpyrifos as a post-construction termiticide is being phased out

(IRED,pp. 12-13).

9

The IRED proposes to leave in effect chlorpyrifos tolerances currently

allowed by regulation for the following foods:

almonds peppers

asparagus pumpkins

bananas radishes

beets rutabagas

broccoli soybeans

Brussels sprouts strawberries

cabbage sweet potatoes

cattle meat turnips

cauliflower turnip greens

Chinese cabbage walnuts

citrus fruits wheat

corn peppermint and spearmint oil

cucumbers goats meat (including

dried beans byproducts e.g., cheese)

eggs pork meat (including

figs byproducts, e.g. bacon

kiwi fruit and sausage)

milk all poultry products (including

onions chicken and turkey)

peaches sheep meat (including

peanuts byproducts e.g., cheese)

pearsplums

(IRED, Table 29, pp. 67-71).

The IRED proposes to establish by regulation new chiorpyrifos tolerances

for the following foods:apple pomace lettuce

clover macadamia nuts

cotton, gin byproducts pecans

dried grapes raspberries

filberts wheat, hay

grass, hay, forage and seed aspirated grain fractions

.10

(IRED, Table 29, pp. 67-73)

The IRED proposes to lower tolerances for the following foods:

apples sunflower seeds

citrus oil sorghum (fodder, grain and

corn oil forage)

sweet corn vegetables, leafy, Brassica

grapes

(IRED, Table 29, pp. 67-7 1).

Finally, the IRED proposes to revoke tolerances for the following foods:

blueberries peas, forage

caneberries sapote

cherimoya seed and pod vegetables (okra

dates and dill)

feijoa (pineapple guava) snap beans, forage

leeks sorghum milling fractions

lima beans, forage soybean, forage

mushrooms sugarcane

nectarines tomatoes

(IRED, Table 29, pp. 67-7 1)

The IRED proposes mitigation measures to reduce the unacceptable risk

posed by chiorpyrifos including elimination of termiticide uses and use on certain

foods, label changes providing for reduced application rates and buffer zones, and

worker protection requirements. Relying on the August 2000 revised risk

assessment, the IRED states that implementation of these mitigation measures

should reduce occupational, ecological and dietary risks from food to acceptable

levels (IRED, pp. 75-79; 9 1 -92). The IRED notes that some occupational

exposure to chlorpyrifos from termiticide use continues to pose excessive risks

despite these mitigating measures (IRED, pp. 2; 7). The IRED also notes that, even

from a single application, chiorpyrifos poses a serious ecological threat to many

.11

non-target aquatic and terrestrial animals (IRED, pp. 2; 52-56).

V. The IRED fails to meet the legal requirements of the FQPA,

FIFRA and the E$A

A. The FOPA requires that EPA find chiorpyrifos “safe” for use on food.

As set forth in the IRED (Table 29), most of the existing tolerances for

chiorpyrifos on food set forth in EPA’s current regulations, 40 C.F.R. § 180.342,

will remain in effect. A limited number of tolerances will be lowered or revoked.

The IRED therefore constitutes EPA’s final determination “to establish” and/or “to

leave in effect” tolerances for chlorpyrifos residues on food within the meaning of

FQPA Section 408(B)(2), 21 U.S.C. § 346(a)(B)(2).

The standard governing EPA’s decision to establish or leave in effect a

pesticide tolerance is set forth in FQPA Section 408(b)(2)(A). That section states

that the EPA Administrator “may establish or leave in effect a tolerance for a

pesticide chemical residue in or on food only fthe Administrator determines that

the tolerance is safe. “ 2 1 U.S.C. § 346a(b)(2)(A) (emphasis added).5 Thus, the

FQPA requires EPA to determine the safety of chlorpyrifos tolerances before

establishing or leaving in effect any tolerance, before finding chlorpyrifos eligible

for reregistration under FIFRA, and before allowing it to remain on the market in

widespread use on food. Although the IRED proposes to establish and leave in

effect chlorpyrifos tolerances, it does not find those tolerances “safe.” In fact, the

IRED repeatedly expresses concerns with its safety (IRED, p. 65- 66).

EPA’s attempt to veil the IRED’s final determination to by terming the

reregistration eligibility decision “interim” is belied by the practical effect of the

determination, which is to continue indefinitely the use of chlorpyrifos on food at

essentially the same tolerance levels currently in place. The IRED acknowledges

that the FQPA-required safety determination is not being done at this time (IRED,

p. 66), yet reaches the conclusion that chiorpyrifos is nonetheless eligible for

reregistration. This approach is unacceptable and contrary to the FQPA’s express

5 The term “safe” as used in Section 408(b)(2)(A) means “that the Administrator has

determined that there is a reasonable degree ofcertainty that no harm will resultfrom aggregate

exposure to thepesticide chemical residue. ... “ from a variety of sources. See 21 U.S.C. §346a(b)(2)(A).

.12

mandate to establish or leave in effect a tolerance only after finding, with a

reasonable degree ofcertainty, that it is safe. 21 U.S.C. § 346a(b)(2)(A). The

approach taken in the IRED is clearly not what Congress intended.

In 1 996, the FQPA was passed by Congress with the express intention of

requiring EPA “promptly to commence such [pesticide tolerance re-evaluation]

proceedings as are warranted under FIFRA and the new [FQPA] Section 408 of the

FFDCA, as soon as there is sufficient information with respect to the dietary risk of

a particular active ingredient and no later than when a determination is made as to

whetherpesticides containing a particular active ingredient should or should not

be reregistered.”6 (Emphasis added.) The FQPA’s statutory deadlines are the best

evidence of the urgency with which Congress viewed the much-needed re

evaluation of older pesticides like chlorpyrifos.7 Indeed, the FQPA mandates that

one third of all pesticides be reviewed by August 1 999; the second third by August

2002; and the last third by August 2006. See 21 U.S.C. § 346a(q)(l).8 EPA’s

determination in the IRED to continue the use of chlorpyrifos on food indefinitely,

without a determination as to its safety, is contrary to the letter and the spirit of the

FQPA as set forth in the statute’s legislative history.

The FQPA’s requirement of finding a tolerance “safe” is a threshold

determination without which the process of reregistration eligibility decision-

making under FIFRA should not proceed. Indeed, as detailed below, a similar

standard for reregistering a pesticide is set forth in FIFRA and requires EPA to find

that chlorpyrifos will not cause unreasonable adverse effects on human health and

the environment. 7 U.S.C. § 136a-l(g)(2)(C) [referring to the standard in 7 U.S.C.

§ 1 36a(c)(5)(D)J. The IRED fails to make this finding under FIFRA as well.

6 See H.R. Rep. No. 104-669(I), p. 41 (1996), reprinted in 1996 U.S.C.C.A.N. 1208,

1216.

7 Chiorpyrifos was first registered in 1965 without the benefit ofthe health or ecological

impact data required to register a pesticide today.

8 EPA has not met the first statutory deadline to reassess one third of all pesticides by

August 1999. See FQPA section 408(q)(1)(A), 21 U.S.C. § 346a(q)(1)(A).

13

B. The FQPA requires that EPA consider cumulative risks and endocrine

disruption effects.

The FQPA expressly requires that EPA consider 1) the cumulative risks

posed by chlorpyrifos and other organophosphates with a common mechanism of

toxicity, and 2) the endocrine disrupter effects of chlorpyrifos. 2 1 U.S.C. §346a(b)(2)(D)(v) and (viii). The IRED concedes that neither has been considered

and thereby violates the express requirements of the FQPA.

1 . The IRED fails to consider cumulative risks posed by

chiorpyrifos with other organophosphate pesticides.

The IRED concedes that the chlorpyrifos risk assessment is for only that

individual organophosphate and does not consider the cumulative risks from other

pesticides or substances sharing a common mechanism oftoxicity (IRED, p. 65-

66). This approach is contrary to the FQPA. In establishing or leaving in effect

chlorpyrifos tolerances, FQPA Section 408(b)(2)(D)(v) requires that the EPA

Administrator “shall consider, among other relevant factors . . . available

information concerning the cumulative effects ofsuch residues and other

substances that have a common mechanism oftoxicity.” 21 U.S.C. §346a(b)(2)(D)(v) (emphasis added). In the absence of a cumulative risk assessment

for all organophosphates, the IRED cannot support a finding that chlorpyrifos

tolerances are “safe.”

It is undisputed that chlorpyrifos is one of several organophosphates having

a common mechanism ofneurotoxicity.’° This means that chlorpyrifos and the

other organophosphates adversely affect the brain and central nervous system.

That finding has been made by the Agency for Toxic Substances and Disease

9 Indeed, the IRED itself concedes that, without the cumulative risk assessment, it “does

not fully satisfy the reassessment ofthe existing chlorpyrifos food residue tolerances as called for

by FQPA” (fRED, p. 65).

10 See Handbook ofFediatric Environmental Health, pp. 193-200, R. Etzel, ed. (1991);

see also Agency for Toxic Substances and Disease Registry (ATSDR), Toxicological Profiles of

Chiorpyrifos, p. 10 (CD-ROM) (1997) (Exhibit B, relevant pages only).

14

Registry,” by the National Research Council,’2, and by EPA (IRED, p. 5). The

available scientific literature is replete with studies and data showing the

cumulative toxicity of organophosphates as a chemical group.’3 The IRED

proposes to establish and leave in effect tolerances without considering the

cumulative impact of exposure to all organophosphates. Under the FQPA, this is a

mandatory factor that EPA must consider prior to reaching the tolerance-setting

and eligibility determination set forth in the IRED. The absence of a cumulative

risk assessment makes the IRED’s determination contrary to the express provisions

ofthe FQPA. 21 U.S.C. § 346a(b)(2)(d)(v).

Even in the absence of the required cumulative risk assessment, the

chiorpyrifos data by itself shows that chlorpyrifos exposure, poses excessive

dietary risks, particularly to infants and children. If other organophosphate risks

were also considered (as they would be in a cumulative risk assessment), the

assessment would undoubtedly result in even greater risks. There are clearly

enough scientific data and residue information on chlorpyrifos to conclude that it

poses such a cumulative risk with other organophosphates that it cannot be

considered safe under the FQPA. In fact, the chlorpyrifos data alone are sufficient

to support immediate regulatory action to protect public health by revoking

tolerances on food and denying reregistration.

2. The IRED lacks an evaluation ofpotential endocrinedisruption effects.

Similarly, the IRED fails to consider whether chlorpyrifos may have effects

on the human endocrine system. FQPA Section 408(b)(2)(D)(viii) requires the

EPA Administrator to consider whether chlorpyrifos “may have an effect in

humans that is similar to an effect produced by a naturally occurring estrogen or

other endocrine effects.” 21 U.S.C. 346a(b)(2)(D)(viii). This means that EPA

must consider and determine whether chiorpyrifos has endocrine disruption effects

11 See Agency for Toxic Substances and Disease Registry (ATSDR), “Chlorpyñfos:

Toxicological Profiles (CD-ROM.) (September 1 997) (Exhibit B).

12 See National Research Council, Pesticides in the Diets oflnfants and Children, pp.297-301, (National Academy Press 1993) (Exhibit B, relevant pages only).

131d.

0

15

before establishing or leaving in effect the tolerances and before findingchiorpyrifos eligible for reregistration. 2 1 U. S .C. § 346a(b)(2)(D)(viii). The IREDmerely acknowledges that the endocrine screening program is not complete orfinalized and states that “chiorpyrifos may be subjected to additional screeningand/or testing” in the future to determine its endocrine disruption effects (IRED, p.74). The IRED fails to set forth either a time frame or a process under which this“additional screening andlor testing” will take place.

The IRED does not consider or evaluate whether chlorpyrifos has thepotential to affect and disrupt the endocrine system (IRED, page 74). Recentliterature reports show such adverse impacts.’4 The FQPA requires EPA toconsider this impact in assessing tolerances on food and the IRED’s failure toinclude this factor is contrary to that requirement, 21 U.S.C. § 346a(b)(2)(D)(viii).The evaluation of potential endocrine disrupter risks will necessarily lead to theconclusion that human health risks may be increased.

The IRED notes that chlorpyrifos may be subjected to additional screeningand/or testing to better characterize effects related to endocrine disruption tIRED,

page 74). Chiorpyrifos must be evaluated for potential endocrine disrupter effectsbefore the chiorpyrifos risk assessment can be considered complete and before areregistration eligibility decision is reached.

The IRED fails to meet the mandating requirements ofFQPA. Section408(b)(2)(D)(v) that cumulative and endocrine disruption effects be consideredbefore establishing or leaving in effect a tolerance and before determiningreregistration eligibility. As stated above, these deficiencies are not mitigated byEPA’s denomination ofits determination as “interim,” since the effect ofthe IREDis to leave existing tolerances in place and permit unsafe exposures to continue.

C. FIFRA requires that EPA find no unreasonable adverse effects onhuman health and the environment from continued use of chlorpvrifos.

In addition to not meeting the FQPA standard, the IRED also does not fulfillFIFRA’s legal requirement to find that chiorpyrifos will not cause unreasonable

14 Gore, A., “Environmental toxicant effects on neuroendocñne function,” Endocrine

14(2): 235-246 (2001) (Exhibit B).

16

adverse effects on human health and the environment. FIFRA Sections 3(c) and

4(g) provide that EPA shall reregister a pesticide only after determining that “it will

perform its intended function without unreasonable adverse effects on the

environment.” 7 U.S.C. § 1 36a(c)(5)(C) and § 1 36a- 1 (g)(C). The IRED repeatedly

recognizes strong evidence of adverse impact on both human health and the

environment but, in the face of this evidence, finds chiorpyrifos eligible for

reregistration (IRED, pp. 64-66). The WED’s reregistration eligibility

determination is therefore unsupported by the record and not in conformance with

the legal standard set forth in FIFRA Sections 3(c) and 4(g). 7 U.S.C. § 36(a)(5)(c)

and § 136a-1(g).

D. The IRED fails to protect against the ecological risks posed bychlorpyrifos and violates the Endangered Species Act.

The IRED’s analysis ofthe ecological risks, particularly to endangered

species, is flawed. The IRED states that chiorpyrifos and its degradate, TCP, are

persistent in the environment (IRED, pp. 47-48) and bioaccumulate in tissue

(IRED, p. 52). The WED also states that a single application of chiorpyrifos poses

a “high risk” to numerous species and that multiple applications increase this

already high risk (IRED, p. 52). The IRED notes that the U.S. Fish and Wildlife

Services (“FWS”) has published five opinions in which the agency found that more

than one hundred endangered and threatened species are in jeopardy or are

adversely affected by the use of chiorpyrifos tIRED, p. 53). The WED concludes

that the endangered species levels of concern are significantly exceeded (IRED, p.

53). The IRED recites the significant risks chlorpyrifos poses to numerous other

species (IRED, pp. 53-56) and its “widespread and persistent presence in aquatic

areas throughout the nation.” tIRED, p. 55)

In light ofthe IRED’s recitation ofthe foregoing significant ecological risks,

it is troubling that the IRED then concludes that these risks are outweighed by the

benefits of chiorpyrifos and its continued agricultural use (IRED, p. 65). The IRED

fails to identify the specific benefits of chlorpyrifos, however. The IRED also

attempts to justify its risk/benefit analysis on the basis ofuntried and unproven

“mitigation measures” (IRED, p. 64). These measures will have little impact on

agricultural uses, which represent the most significant routes of ecological

exposure, because the widespread use of chlorpyrifos on food will continue.

17

Because ofthe significant ecological impacts, the IRED’s finding thatchiorpyrifos is eligible for reregistration is contrary to both FIFRA and theEndangered Species Act (“ESA”). FIFRA expressly requires EPA to find thatchiorpyrifos will not cause unreasonable adverse effects on the environment. 7U.S.C. § 1 36a(c)(5). The IRED does not support that finding. Moreover, thesignificant adverse ecological effects of chlorpyrifos, particularly on endangeredspecies, are not outweighed by any benefit by its continued use.

The ESA requires that every federal agency insure that its “action” (such asreregistering a pesticide) is not likely to jeopardize any endangered or threatenedspecies. See 1 6 U.S.C. § 1 536(a)(2). In furtherance of this objective, the ESArequires that EPA confer with the FWS on any action likely to jeopardizeendangered or threatened species. See 1 6 U.S.C. § 1 536(a)(5). After conferring,with EPA, FWS is then required to issue an opinion detailing whether an agency’saction will jeopardize or otherwise affect a species. See 16 U.S.C. § 1536(b)(3)(A).

As the IRED notes (j. 53), the FWS has issued not one butfive biological opinions

finding that chlorpyrifos seriously j eopardizes endangered and threatened species.FWS has not changed those opinions and yet the IRED disregards them entirely inviolation of the ESA. The IRED ‘ s attempt to justify the continued use ofchlorpyrifos by continually pointing to the proposed mitigation measures is without

merit. The IRED simply does not explain how these measures will curtail adverseimpacts on various species.

E. The IRED’s inadequate analysis ofhuman health risks does not justifyEPA’s finding that chlorpyrifos is eligible for reregistration.

The IRED and the underlying health and environmental risk assessments onwhich it is based are inadequate to support a finding ofreregistration eligibilitybecause EPA has not accurately evaluated dietary exposure and consequently hasfailed to adequately assess human health risks. EPA has not evaluated currenttolerances in the context ofrecent scientific studies showing adverse health impactsat the lowest doses evaluated. These adverse impacts such as neurobehavorial anddevelopmental effects are evident at doses lower than those that causecholinesterase inhibition. The IRED therefore utilizes an incorrect endpoint(cholinesterase inhibition) rather than neurobehavorial effects in the youngreflected in recent studies.

18

The dietary risks set forth in the IRED are based on incorrect assumptions

regarding both exposure to chiorpyrifos and the toxic effects of chiorpyrifos on the

young. The dietary risks would be considered unacceptable, and therefore not

“safe” under the FQPA standard, if EPA accurately calculated exposure and

considered newer studies showing toxicity at lower levels of exposure. The IRED

fails to adequately review and assess current tolerances for chlorpyrifos in light of

recent studies and data that show adverse effects particularly on neonatal cognitive

and immune system functions.15 None ofthese studies was able to determine a

dose level at which no adverse effects were seen, indicating that a threshold level

for these effects has not been found. The safety ofthe LOAEL and the current and

proposed tolerances, therefore, cannot be demonstrated.

Under section 408(b)(2)(A)(i) ofthe FQPA, 21 U.S.C. § 346a(b)(2)(A)(i),

EPA may establish or leave in effect a tolerance for pesticide residue on food “only

if the Administrator determines that the tolerance is safe.” To be deemed “safe,”

chlorpyrifos tolerances would have to be eliminated on most foods and/or reduced

so substantially, the formulations and/or application rates changed so drastically,

that it would have questionable efficacy against pests. To be reregistered, a

pesticide must have demonstrated efficacy to control pests at the label application

rate or it cannot be registered. See FIFRA, 7 U.S.C. § 1 36a(c)(5). In short,

chiorpyrifos cannot be found “safe” at the current tolerances that the IRED

proposes to retain but may not be efficacious at reduced application rates. It

therefore is not eligible for reregistration under FIFRA.

F. The IRED does not establish a level at which no adverse effects are

observed and fails to apply an additional safety or uncertainty factor to

account for this deficiency.

Studies cited in the IRED show adverse health effects from chlorpyrifos

exposure at very low levels. The health effect seen in these studies is

cholinesterase inhibition. Cholinesterase inhibition, however, is not the

appropriate “end point.” There are other more subtle neurotoxic adverse effects

beyond cholinesterase inhibition that the IRED does not consider. These adverse

developmental effects on brain function are persistent behavioral consequences and

15 See footnotes 1 6, 1 8-25, infra, and accompanying text.

. 0

19

often are seen over the long term, and are as troubling as cholinesterase

inhibition. 16

The IRED found adequate evidence of susceptibility for infants, children,

and women ofreproductive age to retain the FQPA ten-fold safety factor (IRED,

pp. 1 6- 1 7). In addition to this evidence, however, recently reported studies not

included in the IRED, and apparently not considered by EPA, provide further

compelling evidence of adverse health effects and increased susceptibility of the

young from exposure to chlorpyrifos. These recent studies show neurological and

immune system effects on neonatal animals at the lowest doses tested. Recent data

suggest that there is no level of exposure to chlorpyrifos that is without adverse

effects on developmental neurotoxicity in the young, and it is impossible to

establish a true “No Observed Adverse Effect Level” (“NOAEL”) for chlorpyrifos.

The IRED instead utilizes a “Lowest Observed Adverse Effect Level” (“LOAEL”)

for cholinesterase inhibition only in analyzing developmental neurotoxicity adverse

effects of chlorpyrifos exposure (IRED, p. 1 6). The use of a LOAEL is inadequate

to accurately assess risk and, as detailed below, requires the application of an

additional tenfold “safety” or uncertainty factor because there is no established

level of exposure that is entirely without adverse Moreover, a NOAEL

for cholinesterase inhibition is not the most sensitive end point.

Ofparticular note is a recent research report finding that neonatal exposure

to chlorpyrifos in rats at doses that produce no overt toxicity and no cholinesterase

inhibition, nevertheless elicited both immediate and long-term deficits in

coordination indicative of neurological 18 Indeed, behavioral performance

was affected during the period of exposure to levels as low as 1 mg/kg body weight

16 Levin, E., Addy, N., Nakajima, A., et al., “Persistent behavioral consequences of

neonatal chiorpyrifos exposure in rats,” Developmental Brain Research 130:83-89 (2001).

17 The WED and the FQPA both use the term “safety factor” to refer to a factor meant to

account for the uncertainties in determining risk. That term is interchangeable with the term

“uncertainty factor,” but for purposes ofthese comments the term “safety factor” will be used.

18 Dam, K., $eidler, F., Slotkin, T., “Chlorpyrifos exposure during a critical neonatal

period elicits gender-selective deficits in the development of coordination skills and locomotor

activity.” Developmental Brain Research 121 : 179- 1 87 (2000) (Exhibit B).

..

20

on post-natal days 1 to 4,19 Behavior also was affected in the postweanling period

several weeks after the termination ofexposure.2° The IRED fails to recognize

that, based on the results of this recent study, adverse human health effects caused

by chiorpyrifos exposure may not be immediately detected, may appear well after

exposure, and are observed before cholinesterase inhibition is seen. Accordingly,

cholinesterase inhibition is not the only effect by which to judge the risks ofchlorpyrifos.2’ . .

A second recent report also indicated behavioral alterations in the absence of

classic signs of cholinesterase inhibition or cholinergic toxicity.22 A third study

reports that exposure ofneonatal rats to 1 mg/kg chlorpyrifos produced lasting

changes in neural function and long-term deficits in immune competence.23 Yet

another report shows alterations in behavioral performance at a dose of 1 mg/kg

that persist or emerge long after termination of exposure and well after the

restoration of cholinesterase activity.24 Finally, a recent study found behavioral

effects at a dose of 0.3 mg/kg in weanling rats even though there was no evidence

19

20 jj This study confirms that adverse neonatal effects occur after termination of

exposure and without continued exposure. Further, these behavioral/neurological effects were

evident after dosing the young animals for only 4 days following birth, which indicates that the

time period of exposure may be of critical importance.

21 See Rice, D. and Barone, S., “Critical Periods ofVulnerability For the Developing

Nervous System: Evidence From Human and Animal Models,” Environmental Health

Perspectives 1 08 (Supp. 3), pp. 5 1 1 -533 (2000) (Exhibit B).

22Sanchez-Amate, M., Flores, P., $anchez-Santed, F, “Effects of chiorpyrifos in the plus-

maze model ofanxiety.” Behavioral Pharmacology 12: 285-292 (2001) (Exhibit B).

23Navarro, H., Basta, P., Seidler, F., Slotkin, T., “Neonatal chlorpyrifos administration

elicits deficits in immune function in adulthood: a neural effect?” Developmental Brain

Research 130: 249-252 (2001) (Exhibit B).

24 Slotkin, I., Cousins, M., Tate, C., Seidler, F., “Persistent cholinergic presynaptic

deficits after neonatal chiorpyrifos exposure,” Brain Research 902: 229-243 (2001) (Exhibit B).

.21

of cholinesterase inhibition.25 The IRED fails to recognize that, based on the

findings of these recent studies, exposure to chiorpyrifos causes behavioral impacts

at very low doses and well before cholinesterase inhibition becomes evident.

These studies taken together indicate that a NOAEL has not been

identified, that effects can occur at lower levels than those assumed in the

WED, that adverse effects are seen in the absence of cholinesterase inhibition,

and that chiorpyrifos can cause behavioral, immunological and neurological

effects well after termination of low level exposure. Indeed, this recent

research shows that these potentially serious developmental effects have

demonstrated threshold of exposure.

At a minimum, the studies set forth above demonstrate the need for anadditional safety or uncertainty factor of ten when deriving a reference dose from a

LOAEL instead of a NOAEL. An additional safety factor of ten is a default

assumption that is applied in chemical risk assessments to account for the

uncertainty associated with the use of a LOAEL in place of a NOAEL, and for

other data inadequacies, such as short exposure duration testing for neurological

and developmental effects.26 Using this additional safety factor is consistent with

recent guidelines on the use ofuncertainty factors.27 It is also consistent with

recent developments in the selection of safety or uncertainty factors to account for

interhuman variability in pharmacokinetics and pharmacodynamics.28

25 Jett, Ii, Navoa, R., Beckles, R., et al.,. “Cognitive function and cholinergic

neurochemistry in weanhing rats exposed to chlorpyñfos,” Toxical Applied Pharmacol. 174: 89-

98 (2001) (Exhibit B).

26 See, Casarett & Doull Toxicology: The Basic Science ofPoisons, pp. 80-81,

McGraw-Hill Health Professional Division, Curtis D. Klaassen, ed. (Fifth Edition 1996) (Exhibit

B, relevant pages only).

27 See Dourson, M., Felter, S., Robinson, D., “Evolution ofscience-based uncertainty

factors in noncancer risk assessment.” Regul. Toxicol. Pharmacol. 24: 1 08-120 (1996)

(hereinafter Dourson et al., 1996) (Exhibit B).

28 See Calabrese, E., “Uncertainty factors and inteñndividual variation,” Regul. Toxicol.

Pharmacol. 5: 190-196 (1985); Dourson et al., 1996; Hattis, D., et al. “Human variability in

susceptibility to toxic chemicals - A Preliminary Analysis ofPharmacokinetic Data From Normal

Volunteers,” Risk Anal 7:415-426 (1987); Naumann, B., Weideman, 1995. “Scientific basis for

uncertainty factors used to establish occupational exposure limits for pharmaceutical active

22

This additional safety factor to address the absence of a NOAEL was not

applied in the IRED. The IRED only applies three ten-fold safety factors, or a

safety factor of 1 ,000, when a fourth safety factor is called for. The first ten-fold

safety factor accounts for the variation in sensitivity among the human population

(the intraspecies variation) tIRED, p. 1 5); the second ten-fold safety factor

accounts for the uncertainty involved in extrapolating animal data to humans (the

interspecies variation) (IRED, p. 1 5); and the third ten-fold FQPA safety factor

accounts for the increased sensitivity of infants and children (IRED, p. 1 6). The

addition of fourth ten-fold safety factor is necessary to account for the uncertainties

associated with the failure to establish a NOAEL that derives from the IRED’s use

of cholinesterase inhibition as the sole end point. Indeed, in the context of

pesticide exposure, EPA recognizes the application of this additional ten-fold

safety factor in the absence of a LOAEL but fails to apply it (IRED, p. 6).29 At a

minimum, an additional ten-fold safety factor must be applied, brining the total

safety factor to 1 0,000 ( 1 0 x 1 000), rather than the 1 ,000 safety factor proposed in

the IRED. This is a prudent and rational approach to assessing the risks associated

with chlorpyrifos and is consistent with both the FQPA and well settled approaches

to conducting risk assessments.

If an additional safety factor of ten is applied, many of the assessments

provided in the IRED change, thereby undermining EPA’s conclusion that

chlorpyrifos exposure falls within the “risk cup” and therefore is eligible for

ingredients,” Hun. Ecol. Risk Assess. 1: 590-613 (1995); Renwick, A., “Safety factors and

establishment ofacceptable daily intakes,” Food Add. Contam. 8: 135-150 (1991). Renwick, A.,

“Data-derived safety factors for the evaluation of food additives and environmental

contaminants,” Food Add. Contam. 10: 275-305 (1993). See also recent data on the ratio of

subchronic to chronic NOELs in animal studies: Beck, B., Conolly, R, Dourson, M., et al.,

“Symposium Overview: Improvements in quantitative noncancer risk assessment,” fund. Appi.

Toxicol. 20: 1-14 (1993); United States Environmental Protection Agency, “Methods for

derivation of inhalation reference concentrations and application of inhalation dosimetry,”

Office ofResearch and Development, EPAI600/8-90/066F (1994); and USEPA “Methodology

for Deriving Ambient Water Quality Criteria for the Protection ofHuman Health,” Office of

Water. EPA-822-B-OO-004 (October 2000). Each ofthe foregoing is attached as Exhibit B.

29 The fRED (p. 6), refers to the EPA Notice to Registrants, “Worker Risk Mitigation For

Organophosphate Pesticides,” Pesticide Registration Notice 2000-9, (September 29, 2000). This

EPA Notice recommends the use of an additional safety or uncertainty factor to account for the

use ofa LOAEL rather than a NOAEL (Notice 2000-9, p. 4).

23

reregistration and continued use on food. For example, the acute dietary (foodonly) risk estimates for chiorpyrifos show that for children ages 1 to 6, roughly

estimate post-mitigation exposure to chiorpyrifos will account for 82% of the acute

population adjusted dose (“aPAD”) and 5 1 % of the chronic population adjusted

dose (“cPAD”).3° The IRED concludes that these aPAD and cPAD percentages are

not ofconcem because they are below 100% (see IRED, p. 17-19). With theapplication of the additional safety factor of ten to account for the absence of aNOAEL, the aPAD and cPAD percentages will be significantly increased, resultingin unacceptably high percentages of 820% and 5 1 0%, respectively. These are wellin excess of the percentages of concern identified in the IRED and the “risk cup”

mnneth over.

G. The WED Underestimates Human Exposure.

The IRED fails to assess the presence of chlorpyrifos residue in more than

one third of the foods tested by the United States Food and Drug Administration

(“FDA”) as a part ofits annual “Total Diet Study.”3’ Many ofthe foods containing

chiorpyrifos residues are baby foods.32 The FDA’s data are the best evidence of

direct, repeated and significant childhood dietary exposure. These data are

generally ignored in the IRED, however, which favors analyzing theoretical or

30 The terms aPAD and cPAD are used to characterize the acute, or immediate, and the

chronic, or long term, dietary risk posed by chlorpyñfos.

31 See FDA “Total Diet Study; Summary ofResidues Found, Market Baskets (91-3 -- 99-1 “) (September 2000) (Exhibit C). The FDA tested 3 1 9 foods, including baby foods and other

foods widely consumed by children. Chiorpyrifos residue was found at varying levels in 1 1 0 of

3 19 foods, or in one-third of the foods tested. Examples of the foods tested on which

chiorpyrifos residues were found are: french fries, hamburgers, hot dogs, pizza, potato chips,

carrots, peaches, peanuts, peanut butter, various breads, bagels, doughnuts and Danish pastries,

graham crackers, saltine crackers, egg noodles and macaroni, pancake mix, chocolate chip

cookies, milk chocolate candy bars, fruit flavored cereals, raisin bran cereals, granola, popcorn,

apples, oranges, peaches and pears (Exhibit C). It is reasonable to conclude that most of these

foods may be extensively consumed by children. The RED’s failure to accurately assess this

documented exposure is indicative ofthe WED’s overall inadequacy to support any finding of

“safety” for the proposed tolerances under the FQPA.

32 [j The following baby or “junior” foods were found to have chiorpyrifos residue:

applesauce, strained peaches, pears, rice cereal, teething biscuits, apple cereal, mixed vegetables,

custard pudding and fruit dessert (Exhibit C).

e24

“anticipated” exposures rather than actual exposures.

The IRED also fails to adequately assess occupational exposures. Even

assuming full compliance with mitigation measures for workers (use of maximum

personal protective equipment and engineering controls, lengthening re-entry

intervals, etc.), the IRED states that the exposures and risks to workers are still in

excess oflevels considered acceptable (IRED, pp. 3; 28-40; and 74-75). The IRED

fails to explain why chlorpyrifos is eligible for. reregistration in the face of

continued occupational risks and the recognition that the proposed mitigation

measures will be inadequate to protect workers.

Workers may also inadvertently expose family members by bringing

chlorpyrifos residues home on clothing and personal items. Further, there is no

assessment of exposure to greenhouse and nursery workers due to a lack of data in

this area (IRED, p. 40). These additional exposure scenarios have not been

properly evaluated in the IRED. Indeed, EPA cannot adequately assess

occupational exposure and risk in the absence of additional data.

The IRED also fails to assess exposure to sensitive subpopulations such as

children who work in or live near fields where chlorpyrifos is applied, including

the children of farm workers. Residential areas are very developed near farms at a

rapid pace. These children may be exposed to chlorpyrifos on a body weight basis

at levels substantially in excess of these encountered by adults. Since adult farm

worker populations are already found to be well above acceptable exposure levels

in the IRED (pp. 29 and 40), children living in the same environment can be

presumed to be exposed to even greater unacceptable risks.

As raised in the previous comments of the Attorney General, there is strong

evidence of widespread population exposure to chlorpyrifos as measured by the

presence of the chiorpyrifos metabolite 3 ,5 ,6-trichloro-2-pyridinol (“TCPy”) in

urine. As part ofthe National Human Exposure Assessment Survey TCPy was

detected in urine samples from children age 3 to 1 3 in the general population.33

TCPy was found in 93% ofthe 261 urine samples from children, with a maximum

concentration of 45 micrograms per liter. Notably, TCPy levels were not

33 Adgate, I., Barr, D., Clayton, C., et al., “Measurement ofchildren’s exposure to

pesticides: Analysis ofurinary metabolite levels in a probability-based sample,” Environmental

Health Perspectives, 109(6): 583-590 (2001) (hereinafter Adgate et al., 2001) (Exhibit B).

25

significantly higher for subjects from households reporting greater than average

pesticide use compared with households reporting less frequent pesticide use.

This information strongly suggests that dietary sources are a major exposure

pathway to chiorpyrifos. Elimination ofhome and garden and termiticide uses will

have only marginal benefit to reduce population exposure. Most importantly,

TCPy urinary concentrations were up to two times higher in children than the

levels observed in comparable studies in adults.34 Again, this study reflects the

greater exposures and consequently greater risks to children from chiorpyrifos in

food.

H. The IRED fails to address the persistent illegal presence of

chlorpyrifos on foods for which no tolerances are established.

The IRED does not address the persistent and illegal use of chiorpyrifos on

foods for which no tolerance is set and erroneously fails to include residues on

these foods in calculating dietary exposure. From 1 993 to 1 999, chiorpyrifos

residue repeatedly appeared on foods for which no regulatory tolerance is set.

These foods include apricots, cantaloupe, carrots, celery, olives, olive oil, potatoes,

spinach, and winter squash. The consistent presence of chiorpyrifos in these foods

from 1 993- 1 999 does not represent an aberration or infrequent misuse.

The presence of chlorpyrifos residue on these foods is a “presumptive

tolerance violation” within the meaning of the USDA Pesticide Data Program

Annual Residue Summary, (Exhibit A).36 These foods, as a matter of law, are

considered “unsafe” under FQPA Section 408, 21 U.S.C. § 346a(a)(l). Use on

34 Hill, R., Head, S., Baker, S., et al., “Pesticide residues in urine ofadults living in the

United States: reference range concentrations. Environ. Res. 71 : 99-106 (1995) (hereinafter Hill

et al., 1995) (Exhibit B).

35 See USDA Pesticide Data Program 1993 to 1999 (Exhibit A) and FDA Market Basket

Survey, 1991-1999 (Exhibit C).

36 The USDA refers presumptive tolerance violations in its data to EPA for enforcement.

Despite the presence of chiorpyrifos residues on numerous foods for which no tolerance is set,

neither the registrants nor EPA has taken action to curtail the presence of chlorpyñfos on these

foods for which no tolerance is set or the improper use of chlorpyñfos on these foods by growers.

26

these foods is also illegal under FIFRA. See 7 U.S.C. §136j(a)(l)($) and the

FQPA, 21 U.S.C. § 346a(a)(l).

The IRED fails to assess these additional, non-registered uses nor include

them in estimating dietary exposure. Dietary exposures, therefore, are understated

significantly and the IRED’s “risk cup” calculations are flawed. Most importantly,

the IRED does not propose mitigation measures to curtail future dietary exposures

caused by the illegal presence of chiorpyrifos residues on these foods.

I. EPA’s reregistration eligibility finding was predetermined by the June

2000 Memorandum ofAgreement between EPA and the registrants.

The June 2000 MOA between EPA and the registrants predetermined the

outcome of the entire chiorpyrifos reregistration process, but specifically the results

reached in the IRED and the previously-issued risk assessments. This

predetermined result was reached well before the human health and ecological risk

assessments were completed and the eligibility decision made without the benefit

ofpublic review and comment. This predetermined result is not in conformance

with the procedural and substantive requirements ofthe FQPA and FIFRA.

The public was never notified nor given the opportunity to comment on the

fact that in June 2000 EPA had decided to grant the reregistrations and allow the

continued use of chiorpyrifos products on most foods at the existing tolerances.

The MOA was also not made available electronically from EPA’s website docket.

A party desiring to review the MOA was forced to obtain it directly from EPA.

In the MOA, EPA essentially agreed to approve reregistration applications

for chlorpyrifos products and allow its continued use on food at most of the

existing tolerances in exchange for the registrants’ voluntary cancellation of home

and garden and termiticide uses. (MOA, p. 4, J4 - 5.) The MOA provided that

the registrants’ compliance with the terms of the MOA, including label changes

and other mitigation measures, guaranteed EPA’s approval ofthe reregistration

applications for agricultural products that are used on food. (MOA, 1J4 -5; 12).

In fact, the MOA opens with this commitment by EPA: “EPA has no current

intention to initiate cancellation or suspension proceedings under section 6 of

FIFRA with respect to the issues addressed in this Agreement.” (MOA, p. 1 .) The

term “issues addressed in this Agreement” refers to and includes all products

currently before EPA for reregistration for use on food. These products are listed

. 0

27

in attachments to the MOA (See MOA Appendices B and C).

Thus, well before the full reregistration process was completed, EPA had

reached an agreement with the registrants to continue uses on food without regard

to the well-documented health effects and the pervasive presence of chlorpyrifos on

foods for which it is not approved.37 This predetermined result is contrary to the

mandated public participation provisions ofFIFRA. Moreover, it improperly

impairs EPA’ s statutorily-mandated responsibility to make health-based decisions

related to the safety of chlorpyrifos for use on food. The IRED and the underlying

MOA represent a predetermined result to a supposedly objective and fair process

that appears to place the business interests of the registrants above human health

concerns.

J. The IRED contains inadequate risk mitigation measures. particularly

with respect to dietary. occupational and ecological risks.

The IRED recommends risk mitigation measures (IRED, pp 74-75) but other

than discontinued use on tomatoes and lowering the tolerance on apples, does not

propose mitigation measures that will be effective in actually reducing dietary

exposure. The IRED also recommends mitigation measures to reduce occupational

and ecological risks but lacks any basis for concluding that those measures will be

effective.38 Moreover, the IRED does not propose a regulatory requirement

ensuring that the recommended mitigation measures are implemented and EPA

lacks any enforcement mechanism to assure compliance.

In any event, the recommended mitigation measures are wholly inadequate

to address the risks posed by chlorpyrifos residues on food because the actual

allowable residues will essentially stay the same as current uses. (Compare IRED,

Table 29 with 40 C.F.R. § 180.342.)

37 See (Exhibit ), USDA Pesticide Data Program 1993 to 1999; FDA “Total Diet Study;

Summary ofResidues Found, Market Baskets 91-3 -- 99-1” (September 2000).

3$ These occupational and ecological mitigation measures include reduction in application

rate and number of applications per season, establishing no-spray buffer zones, and increased use

ofpersonal protection equipment for workers.

28

K. The IRED’s Attempt At Codex Harmonization Is flawed

The IRED discusses “harmonizing” the EPA-set, U.S. tolerances with the

Codex Alimentarius Commission’s maximum residue levels (MRLs) (IRED, p. 72).

The Codex MRLs are international food safety standards set under the auspices of

the World Health Organization. These international standards set tolerances for

pesticide residue on food.

The term “harmonization” is undefined and the IRED lacks any discussion of

the standards governing the Codex MRLs. The Codex MRLs are inconsistent with

EPA’s tolerances in for chlorpyrifos (Compare 40 C.F.R. § 1 80.342 with IRED,

Table 30, p. 73). Many of the Codex MRLs for chlorpyrifos are higher (less

stringent) than the current or proposed U.S. tolerances tIRED, p. 73, Table 30).

The IRED’s “harmonization” ofthe Codex MRLs with EPA’s standards may

significantly affect the level of chlorpyrifos residues on foods imported into the

United States and may increase human exposure if tolerances are harmonized

upward. The IRED does not analyze this additional exposure.

In the interest ofharmonization, the IRED proposes raising the tolerance for

dried grapes (or raisins) from the EPA tolerance of 0.5 ppm to the Codex MRL of

1 .0 ppm. (IRED, p. 73, table 30). There is no existing tolerance for dried grapes

in 40 C.F.R. § 1 80.342. The IRED erroneously notes that the U.S. tolerance is 1

ppm, presumably relying on the tolerance for grapes. Raisins are widely

consumed by children. The IRED fails to explain or justify this additional two-fold

increase in exposure to children and does not assess this additional risk in the

context of total dietary exposure. Moreover, there is no requirement that EPA

harmonize U.S. tolerances with the Codex MRLs. Rather, the FQPA requires that

EPA only provide its reasons for departing from the Codex MRLs for imported

foods. See 21 U.S.C. § 346a(b)(4). The departure would be fullyjustified solely

for reasons ofpublic health. Ifharmonization is undertaken, however, EPA must

clearly state its reasons for departing from the U.S. tolerances and provide a

rational basis for doing so. The IRED fails to state any reason whatsoever for

increasing the tolerance for dried grapes.

EPA must require food imports to meet the EPA-set U.S. tolerances. This

must be clarified in the IRED because imported foods reach U.S. markets in

significant amounts tIRED, p. 73). IfEPA intends to “harmonize” U.S. tolerances

with the Codex MRLs, and thereby allow higher chlorpyrifos residues on imported

29

food, the IRED must state that clearly so the public and Congress are aware that the

FQPA and FIFRA will not be complied with and EPA will not enforce its tolerance

regulations.

Notably, although higher for most foods, the Codex MRLs for chlorpyrifos

are lower (and therefore more protective) for some foods, including cabbages,

cauliflower, citrus fruits, cottonseed, lettuce, onions and peppers tIRED, p. 73,

Table 30). Codex MRLs are set based on scientific toxicity data. The IRED fails

to explain why these lower tolerances should not be adopted by EPA or

“harmonized” by changing the U.S. tolerances. The Codex set lower tolerances

clearly would be more protective ofpublic health. This downward

“harmonization” to the lower tolerance also would achieve the objective of

eliminating barriers to trade in U.S. exports that is a cornerstone ofthe General

Agreement on Tariffs and Trade (GATT) and the North America Free Trade

Agreement (NAFTA). The adoption of these lower tolerances is particularly

compelling in light of the deficiencies in the WED noted above.

30

VI. Conclusion

In summary, EPA has not fulfilled the legal mandates in the FQPA, FIFRA

and the ESA to protect public health and the environment. The IRED has

underestimated the risks posed by chiorpyrifos. Accordingly, it cannot be

considered eligible for reregistration.

Should you have any questions about the submitted information, please feel

free to contact us at the numbers listed below.

Very truly yours,

t;ç -ci

Judith S. Schreiber, Ph.DSenior Public Health ScientistEnvironmental Protection Bureau(518) 474-9267

Karen R. KaufmannAssistant Attorney GeneralEnvironmental Protection Bureau(518) 486-4551

F. Leary,Assistant AttorneyEnvironmental Protection Bureau(518) 474-7154

/Yf

31

References

ATSDR 200 1 . Agency for Toxic Substances and Disease Registry. Chiorpyrifos.

Toxicological Profiles for Chiorpyrifos (on CD-ROM). September, 1997.

Adgate, J., Barr, D., Clayton, C., et al., 200 1 . Measurement of children’s exposure

to pesticides: Analysis ofurinary metabolite levels in a probability-based sample.

Environ Health Perspectives 1 09(6) : 583-590.

Beck, B., Conolly, R., Dourson, M. et al., 1993. Symposium Overview.

Improvements in quantitative noncancer risk assessment. Fundamental and

Applied Toxicology 20: 1-14.

Casarett and Doull’s Toxicology the Basic Science ofPoisons 1996. Curtis D.

Klaassen, Editor, Fifth Edition, McGraw-Hill Health Professions Division, New

York.

Calabrese, E. 1985. Uncertainty factors and interindividual variation. Regulatory

Toxicology and Pharmacology 5: 190-196.

Dam, K., Seidler, F., Slotkin, T, 2000. Chiorpyrifos exposure during a critical

neonatal period elicits gender-selective deficits in the development of coordination

skills and locomotor activity. Developmental Brain Research 12 1 : 179-187.

Dourson, M., Felter, S., Robinson, D. 1 996. Evolution of science-based

uncertainty factors in noncancer risk assessment. Regulatory Toxicology and

Pharmacology24: 108-120.

Dourson, M., and Stara, J., 1 983 . Regulatory history and experimental support of

uncertainty (safety) factors, Regulatory Toxicology and Pharmacology 3: 224-238.

Food and Drug Administration, Total Diet Study Summary ofResidues Found,

Market Baskets (9 1 -3 --99- 1), September 2000.

Gore, A., 200 1 . Environmental toxicant effects on neuroendocrine function.

Endocrine 14(2): 235-246.

32

Handbook of Pediatric Environmental Health, 1 999. R. Etzel, Editor. American

Academy of Pediatrics, Elk Grove, IL.

Hattis, D., Erdreich, L., Ballew, M., 1 987. Human variability in susceptibility to

toxic chemicals - A preliminary analysis ofpharmacokinetic data from normal

volunteers. Risk Anal. 7: 4 15-426.

Hill, R., Head, S., Baker, S., et al., 1995. Pesticide residues in urine ofadults living

in the United States: reference range concentrations. Environ. Res. 71 : 99-106.

Jett, D., Navoa, R., Beckles, Ii, et al., 2001. Cognitive function and cholinergic

neurochemistry in weanling rats exposed to chlorpyrifos. Toxical Applied

Pharmacol. 174: 89-98.

Lassiter, EL, Barone, S., Moser, V., et al., 1 999. Gestational exposure to

chlorpyrifos: Dose response profiles for cholinesterase and carboxylesterase

activity. Toxicological Sciences 52: 92-100.

Levin, E., Addy, N., Nakajima, A., et al. 200 1 . Persistent behavioral consequences

ofneonatal chlorpyrifos exposure in rats. Developmental Brain Research 130:83-

89.

National Research Council, Pesticides in the Diets of Infants and Children.

National Academy Press, Washington, D.C. (1993)

Naumann, B., Weideman, 1995. Scientific basis for uncertainty factors used to

establish occupational exposure limits for pharmaceutical active ingredients. Hun.

Ecol. Risk Assess. 1 : 590-6 13.

Navarro, H., Basta, P., Seidler, F., Slotkin, T., 200 1 . Neonatal chlorpyrifos

administration elicits deficits in immune function in adulthood: a neural effect?

Developmental Brain Research 1 30: 249-252.

Renwick, A., 1 99 1 . Safety factors and establishment of acceptable daily intakes.

Food Add. Contam. 8: 135-150.

Renwick, A., 1 993 . Data-derived safety factors for the evaluation of food additives

and environmental contaminants. Food Add. Contam. 10: 275-305.

33

Rice, D., Barone, S. 2000. Critical periods ofvulnerability for the developingnervous system: Evidence from human and animal models. Environmental HealthPerspect. 108($uppl 3): 5 1 1 -533.

Sanchez-Amate, M., Flores, P., Sanchez-$anted, F., 200 1 . Effects of chlorpyrifosin the plus-maze model of anxiety. Behavioral Pharmacology 1 2 : 285-292.

Slotkin, T., Cousins, M., Tate, C., Seidler, F., 2001 . Persistent cholinergicpresynaptic deficits after neonatal chlorpyrifos exposure. Brain Research 902: 229-243.

United States Department of Agriculture. Pesticide Data Program, PesticideResidues on Foods: 1993 to 1999 CD-Rom (January 2000).

USEPA, 1 994. Methods for derivation of inhalation reference concentrations andapplication of inhalation dosimetry. Office of Research and Development.EPA/600/8-90/066F.

USEPA, 2000. United States Environmental Protection Agency. Methodology for

Deriving Ambient Water Quality Criteria for the Protection ofHuman Health.

Office ofWater. EPA-822-B-00-004. October 2000.

objections to march 29, 2017 order denying pan/nrdc ...jun 05, 2017 · tolerances and cancel all...

Documents