heta 98-0347-2758 lockheed martin aeronautical systems ... · heta 98-0347-2758 lockheed martin...

HETA 98-0347-2758Lockheed Martin Aeronautical Systems

Marietta, Georgia

Angela M. Weber, M.S.Helga Daftarian, D.O., M.P.H.

This Health Hazard Evaluation (HHE) report and any recommendations made herein are for the specific facility evaluated and may not be universally applicable. Any recommendations made are not to be considered as final statements of NIOSH policy or of any agency or individual involved. Additional HHE reports are available at http://www.cdc.gov/niosh/hhe/reports



This Health Hazard Evaluation (HHE) report and any recommendations made herein are for the specific facility evaluated and may not be universally applicable. Any recommendations made are not to be considered as final statements of NIOSH policy or of any agency or individual involved.


applicable. Any recommendations made are not to be considered as final statements of NIOSH policy or of any agency or individual involved. Additional HHE reports are available at http://www.cdc.gov/niosh/hhe/reports

http://www.cdc.gov/niosh/hhe/reports



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PREFACEThe Hazard Evaluations and Technical Assistance Branch (HETAB) of the National Institute forOccupational Safety and Health (NIOSH) conducts field investigations of possible health hazards in theworkplace. These investigations are conducted under the authority of Section 20(a)(6) of the OccupationalSafety and Health Act of 1970, 29 U.S.C. 669(a)(6) which authorizes the Secretary of Health and HumanServices, following a written request from any employer or authorized representative of employees, todetermine whether any substance normally found in the place of employment has potentially toxic effectsin such concentrations as used or found.

HETAB also provides, upon request, technical and consultative assistance to Federal, State, and localagencies; labor; industry; and other groups or individuals to control occupational health hazards and toprevent related trauma and disease. Mention of company names or products does not constitute endorsementby NIOSH.

ACKNOWLEDGMENTS AND AVAILABILITY OF REPORTThis report was prepared by Angela Weber and Helga Daftarian of HETAB, Division of Surveillance, HazardEvaluations and Field Studies (DSHEFS). Field assistance was provided by Christopher Reh and MaxKiefer. Desktop publishing was performed by Patricia Lovell. Review and preparation for printing wasperformed by Penny Arthur.

Copies of this report have been sent to employee and management representatives at Lockheed MartinAeronautical Systems and the OSHA Regional Office. This report is not copyrighted and may be freelyreproduced. Single copies of this report will be available for a period of three years from the date of thisreport. To expedite your request, include a self-addressed mailing label along with your written request to:

NIOSH Publications Office4676 Columbia ParkwayCincinnati, Ohio 45226

800-356-4674

After this time, copies may be purchased from the National Technical Information Service (NTIS) at5825 Port Royal Road, Springfield, Virginia 22161. Information regarding the NTIS stock number may beobtained from the NIOSH Publications Office at the Cincinnati address.

For the purpose of informing affected employees, copies of this report shall beposted by the employer in a prominent place accessible to the employees for aperiod of 30 calendar days.

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Health Hazard Evaluation Report 98-0347-2758Lockheed Martin Aeronautical Systems

Marietta, GeorgiaNovember 1999

Angela M. Weber, M.S.Helga Daftarian, D.O., M.P.H.

SUMMARYIn September 1998, the National Institute for Occupational Safety and Health (NIOSH) received a health hazardevaluation (HHE) request from Lockheed Martin Aeronautical Systems (LMAS) in Marietta, Georgia. The jointmanagement and employee request concerned potential office employee exposures to diisocyanate-containingpaints, primers, solvents, and cured and uncured composite materials used during the manufacturing of the F-22fighter jet (office area is located directly above the production area). The request stated that office workers in AreaK of Building 11 had experienced breathing difficulties, asthma, burning eyes, and neurological and memoryimpairment. In response to the request, NIOSH investigators conducted an initial site visit at LMAS on October 30,1998, and returned to conduct medical interviews and a tracer gas ventilation study on February 17-18, 1999.

Employee interviews revealed that approximately 88% of the employees (14 of 16) who had worked in Area Kduring May 1998 reported that they had experienced a variety of symptoms. Symptoms included eye, nose andthroat irritation, cough, wheezing, shortness of breath, chest pain, headache, nausea, dizziness, fatigue,numbness/tingling of the extremities, and skin rashes. All but one of the symptomatic employees reported that theirsymptoms were most pronounced when they were at work and tended to diminish away from work. Medicalrecords were reviewed for 13 of the 14 symptomatic employees. Nine of these employees were eventually referredto a pulmonary specialist and diagnosed with a variety of respiratory conditions attributable to chemical exposurein the workplace (these included seven cases of mild asthma/reactive airway disease, one case of acuteexacerbation of asthma/status asthmaticus, one case of chemical pharyngitis, and two cases of chemicalconjunctivitis).

The tracer gas ventilation study consisted of evaluating the potential for contaminant migration from the first floorproduction area to Area K on the second floor. Specifically, a one-percent concentration of sulfur hexafluoride(SF6) was released in two chemical use areas (paint spray booth and core-clean room), where it was suspected thatcontaminant dissemination to other areas may occur. Additionally, tracer gas was released around one of the airhandling units (AHU), located on the first floor mezzanine level which served Area K to evaluate the potential forcontaminant migration from the autoclave area into the AHU. At the time of the initial site visit, LMAS wasimplementing several engineering controls; therefore, the tracer gas study was used to evaluate these changes.Results indicated that corrective actions to control emissions and migration of chemicals from the paint spray boothand the core-clean room had prevented substances generated in these areas from reaching Area K employees.Tracer gas release around the AHU served two purposes. First, it was determined that Area K is undergoingapproximately four air changes per hour (ACH) which is consistent with a recent test and balancing reportdescribing the ventilation system serving this area. Second, tracer gas entrained into the AHU and supplied to Area

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K indicates that any chemicals, contaminants, or odors generated in this area could potentially expose individualsin Area K.

The results of the medical evaluation appear to indicate that the respiratory symptoms which were beingexperienced by the affected employees who were working in Area K during May 1998 are most consistent withknown exposure to isocyanates at the time the employees’ symptoms became manifest. Possible concomitantexposure to solvents such as MEK or isopropyl alcohol may also explain some of the irritant mucous membraneand respiratory symptoms experienced by Area K employees. However, no specific cause can be identified whichwould explain why some of the employees continued to experience symptoms after being relocated to anotherbuilding. Results from the tracer gas ventilation study indicate that corrective actions to control emissions andmigration of chemicals from the paint spray booth and the core-clean room were successful, while chemicals,contaminants, or odors generated in the near vicinity of the AHU located in the production area could potentiallyexpose individuals in Area K. Recommendations to help prevent and address future indoor environmental qualityconcerns among Area K employees are provided in this report.

Keywords: SIC 381 (Search, Detection, Navigation, Guidance, Aeronautical, and Nautical Systems, Instruments,and Equipment) Indoor Environmental Quality, Indoor Air Quality, IEQ, IAQ, Ventilation, Tracer Gas, SulfurHexafluoride, Composites, Diisocyanate-Containing Paints, Methyl Ethyl Ketone, MEK, Methyl Ethyl IsobutylKetone, MIBK, Isoproponal, Occupational Asthma, Chemical Sensitization, Mucous Membrane Irritation.

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Highlights of the NIOSH Health Hazard Evaluation

Airborne Exposures to Isocyanates and Organic SolventsThe NIOSH Health Hazard Evaluation (HHE) was jointly requested by management and employees from Lockheed MartinAeronautical Systems (LMAS). NIOSH was asked to see if office workers in Area K were becoming ill from isocyanate-basedpaints and organic solvents used in making the F-22 fighter jet. Jets are made in the same building on the first floor directlybelow the offices.

What NIOSH Did

# We talked to employees who were working in Area Kwhen problems started. # We looked at medical records and injury and illnessrecords for Area K employees. # We checked material safety data sheets for chemicalsused on the first floor.# We looked for ways that chemicals on the first floorcould get into Area K through the air. # We reviewed changes LMAS made to the building andthe ventilation to stop air from moving from the first floorinto Area K.# We released tracer gas in selected areas of the firstfloor to see if corrections had stopped air from moving intoArea K.

What NIOSH Found

# Health complaints were most likely caused byexposures to isocyanate paints. # Most of the sick employees in Area K worked near thepaint spray booth exhaust fan room found on the secondfloor. # Further exposure to organic solvents could have causedbreathing problems and eye irritation among Area Kemployees. # Air most likely moved from the paint spray boothexhaust system into Area K before changes were made tothe building and the ventilation system.# After changes were made, tracer gas released in thepaint spray booth did not reach Area K.

# Chemicals and odors found in the air around theventilation unit for Area K could pass through theventilation system to Area K.

What LMAS Managers Can Do

# Don’t use isocyanate paints in the building. # Require the production area to notify LMAS safety andhealth representatives of all activities and changes made tothe process.# Start an indoor air quality management plan to quicklyidentify future problems. # Tell workers about the dangers associated with thechemicals used in the production area. # Encourage Area K employees to quickly report odorsand/or symptoms to LMAS management. # Look into all complaints and explain findings toemployees. # Keep Area K under positive pressure.# Move or enclose the ventilation unit on the first floor tostop chemicals and odors from passing on into Area K.

What LMAS Employees Can Do

# Continue to check with your own doctor if healthproblems continue. # Get permission from your doctor before moving backinto Area K. # Don’t close off supply vents in Area K since thischanges the ventilation system.# Report all odor complaints and/or continuingsymptoms to LMAS management.

CDCCENTERS FOR DISEASE

CONTROLAND PREVENTION

What To Do For More Information:We encourage you to read the full report. If you would like acopy, either ask your health and safety representative to makeyou a copy or call 1-513/841-4252 and ask for HETA Report

# 98-0347-2758

HHE Supplement

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TABLE OF CONTENTSPreface . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ii

Acknowledgments and Availability of Report . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ii

Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . iii

HHE Supplement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . v

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1

Background . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1Indoor Environmental Quality (IEQ) in Area K . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1Building Description . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1Process Description . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2

Methods . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3Medical Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3Environmental Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3

Evaluation Criteria . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4General . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4Agents Used in the Composite Area . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5Isocyanate-Containing Paints . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5Review . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5Health Effects Associated With Isocyanates . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6Methyl Ethyl Ketone (MEK) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7Methyl Isobutyl Ketone (MIBK) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7Isopropanol (Isopropoyl Alcohol) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7

Results . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7Medical Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7Environmental Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9

Discussion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9

Recommendations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11

Health Hazard Evaluation Report No. 98-0037-2758 Page 1

INTRODUCTIONIn September 1998, the National Institute forOccupational Safety and Health (NIOSH) received ahealth hazard evaluation (HHE) request fromLockheed Martin Aeronautical Systems (LMAS) inMarietta, Georgia. The joint management andemployee request concerned potential officeemployee exposures to diisocyanate-containingpaints, primers, solvents, and cured and uncuredcomposite materials used during the manufacturingof the F-22 fighter jet. The request stated that officeworkers in Area K of Building 11 had experiencedbreathing difficulties, asthma, burning eyes, andneurological and memory impairment. In responseto the request, NIOSH investigators conducted aninitial site visit at LMAS on October 30, 1998, andreturned to conduct medical interviews and a tracergas ventilation study on February 17-18, 1999.

BACKGROUNDIndoor Environmental Quality(IEQ) in Area KAn initial IEQ complaint from an employee in AreaK occurred on May 22, 1998. Historicaldocumentation provided by the company physicianindicated that a bottle of cleaning solution(containing limonene) had spilled onto the carpetingin Area K (limonene is a terpene and essential oilthat is a major constituent in oils of orange, lemon,caraway, dill, bergamot, and pine needle. It is usedin flavoring, fragrance and perfume materials, aswell as in solvents and wetting agents). In responseto this complaint, LMAS had the carpeting removeda week later. Shortly after this, in what appeared tobe unrelated to the spill, other Area K workers beganreporting symptoms including respiratory andmucous membrane irritation. Based on the numberof growing odor complaints and symptoms amongArea K workers, LMAS personnel took a number ofactions to better characterize the scope of theproblem, identify possible environmentalexplanations for the intermittent odors, and improvethe workplace environment. In addition, aconsulting firm was hired to evaluate chemicalexposures in Building L-11. Based upon thecompany physician’s recommendation, employees inArea K were relocated to Building L-22 on June 25,1998, due to the continuing presence of unexplained

odors and the persistent symptoms on the part ofseveral employees. Based on the types of symptoms experienced byemployees and the clustering of affected employeesin the vicinity of the mechanical room housing theexhaust fan for the paint spray booth, continuouslow-level exposures to isocyanate-containing paintswas viewed as a potential cause. The mechanicalroom adjacent to Area K was found to be underpositive pressure (air moved from the mechanicalroom into Area K) because the exhaust fans for thepaint spray booth were located within the roominstead of on the roof. Air sampling performed inthe spray paint booth and Area K sections of L-11 bythe consulting firm detected trace amounts ofisocyanates contained in the paints. However,NIOSH investigators reviewed the samplingtechniques and analytical procedures used by theconsulting firm, and concluded that the reportedconcentrations were most likely underestimated.Specifically, the methods employed during theconsultant’s survey (Occupational Safety and HealthAdministration [OSHA] Methods 42 and 47) did nothave the capability to measure the two majorisocyanate compounds (HDI- and MDI-basedpolyisocyanates) present in the 624 and648 polyurethane paints used in Building 11. Inaddition, the OSHA methods are not recommendedwhen sampling for aerosolized isocyanates in spraypainting operations. This review was reported in aletter sent to LMAS by NIOSH on February 10,1999. It should be noted that LMAS haddiscontinued the use of isocyanate-containing paintsbefore the initial NIOSH site visit. In addition to thepaint spray booth exhaust, there was an open catwalkleading from the first floor production area into themechanical room above. Therefore, any chemicalsused in this area, could potentially migrate into AreaK by being drawn into the air handling unit (AHU)serving Area K.

Building DescriptionThe L-11 Building, located on the LMAS campus inMarietta, Georgia, was originally built in the 1970sfor the assembly of jets. In the early 1990s, moreoffice space was added to accommodate theadditional personnel needed for the production of theF-22 fighter jet. Since space on the LMAS campuswas limited based on building security requirements,all personnel (including production, engineering, andadministrative employees) involved with the F-22

Health Hazard Evaluation Report No. 98-0026-2758

composite fabrication process were housed in theL-11 Building.

The 71,000 square feet (ft2) composite area is locatedon the first floor of the L-11 Building. Office spacein L-11 is divided into Areas A through L. All of theoffices (except for Area A) are located on the secondfloor of the building above the manufacturing areas.The 12,000 ft2 office space evaluated by NIOSH(Area K) is located directly above the paint spraybooth. Two separate air handling units (AHU),which share a common outdoor air intake plenum,serve Area K. While one of the AHUs is located onthe roof of the building, the other AHU is located onthe mezzanine level in the manufacturing area.Approximately 70 employees, who were originallyassigned to area K, had been either relocated to otherareas of Building L-11, or to other buildings on theLockheed-Martin campus at the time of the NIOSHsite visit.

Process DescriptionThe composite fabrication in Building L-11 iscomprised of the following steps:

1. Pre-impregnated Composite Material (Prepregs)Preparation. The prepreg composite materialconsists of either unidirectional fibers or wovenfabric that has been impregnated with a resin system.Prepregs used in L-11 contain either 977-3 Epoxynor 5250-4 BMI resins. All prepregs in L-11 arestored below freezing to retard potential chemicalreactions. In preparation to construct a compositepart, the prepreg is cut with a Gerber Cutter to adesired shape.

2. Lay-up. Once the prepreg has been cut to shape,the lay-up process begins. Lay-up is performed in atemperature and humidity controlled clean roomarea. The precut prepreg plies are manually placedon a tool (frame) in layers, and in a specifiedorientation to obtain the desired shape andproperties. Before the prepreg is placed on the tool,the tool is hand-wiped with a solvent soaked rag, anda mold release agent is applied from an aerosol canto the tool to assist in removal of the part followingthe curing cycle.

3. Bagging the Part. After the lay-up is complete, anairtight bagging material is placed over the prepregand sealed to the tool. A vacuum is drawn on thebag to maintain the integrity of the part.

4. Autoclave Cure. The autoclave is used to supportand control the chemical reaction through theapplication of heat and pressure. The part, whileunder vacuum, is placed in the autoclave and heatedto initiate cross-linking (polymerization) and give thecomposite its characteristic properties. The partremains under a vacuum during the curing process.Volatiles generated during the process are drawn off,run through a cold trap, and exhausted to theoutdoors by a vacuum system. The autoclave ispressurized during processing to further consolidatethe laminate and support the chemical reaction. Theautoclave and the vacuum system have independentexhaust systems, and both are exhausted to theoutside. The autoclave is sealed during the curingprocess and is under a nitrogen purge. Once thecuring cycle is complete, the autoclave is exhaustedand the nitrogen is replaced with normal air. Once anormal atmosphere is achieved, the autoclave door isopened and the part is removed.

5. De-bag/Tool Clean-up. Once the initial curingcycle is complete, the part is removed from the bag.The part may undergo further processing in ovens tocomplete the curing cycle. Like the autoclaves, theovens are ventilated directly to the outdoors. Oncethe cure is complete, no further chemical reactionsoccur. After the part is separated from the tool, thetool is cleaned with a solvent-soaked rag to prepareit for its next use.

6. Part Trim/Machining. Composite machiningconsists of mechanical processes (trimming, drilling,sanding, etc.) that may liberate particulate matter.The composite parts are cut into shape with toolsequipped with local exhaust to control the release ofdust. The exhaust system from each machine is tiedinto a central exhaust that is vented to a dustcollector located outside the building.

7. Part Priming/Painting. Once the machining iscomplete, the part is cleaned with a solvent thenprimed and painted. All painting occurs in adedicated paint booth that is directly vented to theoutdoors. The exhaust fan for the paint booth islocated in a mechanical room on the second flooradjacent to Area K.

The employees who worked in the Area K officeswere engaged in strictly administrative duties (whichincluded aerospace procurement contractadministration, cost analysis, logistics analysis,engineering technology management, andsecretarial/clerical duties). The equipment in Area


K was limited to standard office furniture and officesupplies. No smoking was permitted in the Area Koffices.

METHODSOn October 30, 1998, NIOSH held an openingmeeting with management and employeerepresentatives. During this meeting, informationabout NIOSH was provided, and the HHE requestwas discussed. Various operational parametersregarding the use of isocyanate-based paints andorganic solvents, as well as the health problemsbeing reported, were discussed. Following theopening conference, a walk-through evaluation wasconducted in several areas of Building L-11,including three office areas on the second floor andthe composite manufacturing area on the first floor. The follow-up site visit was made on February 17-18, 1999, and consisted of medical interviews andevaluating the potential for contaminant migrationfrom the first floor to Area K on the second floorwith a tracer gas. At the time of the initial site visit,LMAS was in the process of implementing severalengineering controls; therefore, the tracer gas studywas used to evaluate these changes. Because thetracer gas study was conducted after engineeringmodifications were implemented to improve theisolation of Area K, this study only providesinformation on conditions at the time of the site visit.The potential for contaminant migration prior toimplementing the control measures was notdetermined.

Medical EvaluationNIOSH staff conducted individual, confidentialmedical interviews with 28 plant employees duringthe follow-up visit. Employees were selected atrandom from an employee roster provided by thecompany. Employees who were interviewedincluded 15 employees who had worked in Area Kduring May 1998, one L-11 paint spray boothemployee, and 12 additional administrative supportand engineering personnel who worked in otherareas of Building L-11 (including areas A, B, C, D,E, F, and G), as well as Building L-12. The12 additional employees were interviewed in order todetermine whether any similar health effects wereoccurring in any of the other L-11 work areas.Information from the structured interviews addressed

occupational work history, chemical exposures, theuse of personal protective equipment (PPE), historyof health problems/symptoms, medication history,alcohol/tobacco use, and history of chemicalexposures outside of the workplace. Medical recordsfor 15 interviewed employees were obtained fromthe plant medical department and private medicalproviders. Medical records were reviewed for allemployees who reported health problems. EmployeeInjury/Illness Records were also reviewed for anadditional 12 employees who had worked in Area Kduring May 1998, but were unavailable at the time ofthe site visit. A comprehensive list of L-11employee names and each individual’s symptomswas provided by the LMAS occupational medicinephysician, and upon the NIOSH medicalinvestigator’s request, copies of the injury and illnessrecords for these individuals were provided. TheOSHA Log and Summary of Occupational Injuriesand Illnesses (Form 200) for the years 1995-1998were also reviewed.

Environmental EvaluationA one percent (10,000 parts per million [ppm])concentration of sulfur hexafluoride (SF6) innitrogen was released as the source tracer from acompressed gas cylinder equipped with a regulatorand a flow meter. SF6 was released in two chemicaluse areas (paint spray booth and core-clean room)where we suspected that contaminant disseminationto other areas could occur. Additionally, tracer gaswas released around one of the air handling units(AHU), located on the first floor mezzanine level,which served Area K. This test was conducted toevaluate the potential for contaminant migrationfrom the autoclave area into the AHU. Prior to therelease of the gas, a Brüel and Kjaer (B&K) model1302 multi-gas continuous monitor was placedapproximately 20 feet from the door of themechanical room in the southwest corner of Area K.Continuous background sampling prior to the releaseof tracer gas was initiated to establish a baseline.

SF6 is a colorless, odorless, and essentiallychemically inert gas that has ideal properties for useas a tracer. SF6 is not metabolized and is consideredto be toxicologically inert.2 The NIOSHRecommended exposure limit (REL) for SF6 is 1,000ppm as a 10-hour time-weighted average (TWA).1 Inaddition to low toxicity and reactivity, SF6 is easilydetectable at low concentrations. Although SF6 is aheavy gas, at dilute concentrations the overall air


density is not much different from pure air, and thusthe tracer gas will follow room air currents.

The principle of detection by the B & K is infraredabsorption at a specific wavelength with subsequentanalysis via a photoacoustic effect. With thistechnique, sample gas, collected via a teflon samplehose, is pumped into a sample chamber where SF6gas absorbs infrared energy proportional to theconcentration of the gas. The absorbed infraredenergy is released as heat, resulting in a pressureincrease which is measured with a microphone. Themonitor records SF6 concentrations in ppmapproximately every minute. The monitor has adetection limit of approximately 0.05 ppm for SF6.Data collected was logged in the instrument’sinternal memory and subsequently uploaded into apersonal computer. In addition to monitoring in thecontinuous sampling mode, an air sampling bag wasused to collect samples in the core-clean room toverify the calculated concentration. The bag wasfilled using a portable air sampling pump andsubsequently analyzed with the B&K monitor.

The dimensions of the paint booth room and thecore-clean room were determined, and the roomvolume calculated. This information was used todetermine the amount of tracer gas which needed tobe released to generate a concentration of SF6between 10 and 20 ppm. Given a detection limit of0.05 ppm, potential migration to Area K up to amaximum dilution factor of 400 could bedetermined. Prior to each trial, the ventilation ineach area was turned off and the doors closed. Gaswas released at a flow rate of four cubic feet perminute (cfm) until the calculated concentration wasreached. At that time, the gas was shut off and theventilation turned back on. Communication betweenthe point of tracer release and the monitor in Area Kwas established so the specific timing of eachsequence (gas on, gas off, ventilation on) could berecorded. This would allow for the determination ofcontaminant migration, migration time, and thedilution effect.

EVALUATION CRITERIAGeneral As a guide to the evaluation of the hazards posed byworkplace exposures, NIOSH field staff employ

environmental evaluation criteria for the assessmentof a number of chemical and physical agents. Thesecriteria are intended to suggest levels of exposure towhich most workers may be exposed up to 10 hoursper day, 40 hours per week for a working lifetimewithout experiencing adverse health effects. It isimportant, however, to note that not all workers willbe protected from adverse health effects even thoughtheir exposures are maintained below these levels. Asmall percentage may experience adverse healtheffects because of individual susceptibility, a pre-existing medical condition, and/or a hypersensitivity(allergy). In addition, some hazardous substancesmay act in combination with other workplaceexposures, the general environment, or withmedications or personal habits of the worker toproduce health effects even if the occupationalexposures are controlled at the level set by thecriterion. These combined effects are often notconsidered in the evaluation criteria. Also, somesubstances are absorbed by direct contact with theskin and mucous membranes which can potentiallyincrease the overall exposure. Finally, evaluationcriteria may change over the years as newinformation on the toxic effects of an agent becomeavailable.

The primary sources of environmental evaluationcriteria for the workplace are: (1) NIOSH RELs,1(2) the American Conference of GovernmentalIndustrial Hygienists’ (ACGIH®) Threshold LimitValues (TLVs®) and Biological Exposure Indices(BEIs®),2 and (3) the U.S. Department of LaborOSHA Permissible Exposure Limits (PELs).3Employers are encouraged to follow the OSHAlimits, the NIOSH RELs, the ACGIH TLVs, orwhichever are the more protective criterion.

OSHA requires an employer to furnish employees aplace of employment that is free from recognizedhazards that are causing or are likely to cause deathor serious physical harm.4 Thus, employers shouldunderstand that not all hazardous chemicals havespecific OSHA exposure limits such as PELs’s andSTEL’s. An employer is still required by OSHA toprotect their employees from hazards, even in theabsence of a specific OSHA PELs.

TWA exposure refers to the average airborneconcentration of a substance during a normal 8 to10 hour workday. Some substances haverecommended short-term exposure limits (STEL) orceiling values which are intended to supplement the


TWA where there are recognized toxic effects fromhigher exposures over the short-term.

Agents Used in theComposite AreaIsocyanate-Containing PaintsReview

The unique feature common to all diisocyanates isthat they consist of two -N=C=O (isocyanate)functional groups attached to an aromatic oraliphatic parent compound. Because of the highlyunsaturated nature of the isocyanate functionalgroup, the diisocyanates readily react withcompounds containing active hydrogen atoms(nucleophiles). Thus, the diisocyanates readily reactwith water (humidity), alcohols, amines, etc.;diisocyanates also react with themselves to formeither dimers or trimers. When a diisocyanatespecies reacts with a primary, secondary, or tertiaryalcohol, a carbamate (-NHCOO-) group is formedwhich is commonly referred to as a urethane.Reactions involving a diisocyanate species and apolyol result in the formation of cross-linkedpolymers; i.e. polyurethanes. Hence, they are used insurface coatings, polyurethane foams, adhesives,resins, elastomers, binders, and sealants. Manymaterial safety data sheets (MSDS) use isocyanate-related terms interchangeably. For the purpose ofthis report, terms are defined as follows.

Diisocyanates (Monomers): The difunctionalisocyanate species from which polyisocyanates andpolyurethanes are derived. Common examples ofmonomeric isocyanates include 1,6-hexamethylenediisocyanate (HDI), 2,4- and/or 2,6-toluenediisocyanate (TDI), 4,4'-diphenylmethaned i i s o c y a n a t e ( M D I ) , m e t h y l e n ebis(4-yclohexylisocyanate)(HMDI), isophoronediisocyanate (IPDI), and 1,5-naphthalenediisocyanate (NDI). Commercial-grade TDI is an80:20 or 65:35 mixture of the 2,4- and 2,6- isomersof TDI, respectively.

Polyisocyanates: Species possessing free isocyanategroups and derived from monomeric isocyanateseither by directly linking these monomeric units(a homopolymer) or by reacting these monomerswith di- or poly-functional alcohols or amines(a copolymer).

Prepolymers: Species possessing freeisocyanate groups, prepared from the reactionof a polyol with an excess of di- orpolyisocyanate.5 Commercially availableisocyanate products frequently containprepolymers in lieu of more volatileisocyanate monomers.

Oligomeric Isocyanates (Oligomers):Relatively low molecular weightpolyisocyanates.

Intermediates: Species possessing freeisocyanate groups, formed during use of anisocyanate product by partial reaction of theisocyanate species with a polyol.

In general, the types of exposures encounteredduring the use of isocyanates (i.e., monomers,prepolymers, polyisocyanates, and oligomers) in theworkplace are related to the vapor pressures of theindividual compounds. The lower molecular weightisocyanates tend to volatilize at room temperature,creating a vapor inhalation hazard. Conversely, thehigher molecular weight isocyanates do not readilyvolatilize at ambient temperatures, but are still aninhalation hazard if aerosolized or heated in the workenvironment. The latter is important since manyreactions involving isocyanates are exothermic innature, thus providing the heat for volatilization. Toreduce the vapor hazards associated with the lowermolecular weight diisocyanates, prepolymer andpolyisocyanate forms of these diisocyanates weredeveloped and have replaced the monomers in manyproduct formulations.

Isocyanates exist in many different physical forms inthe workplace. Not only are workers potentiallyexposed to the unreacted monomer, prepolymer,polyisocyanate, and/or oligomer species found in agiven product formulation, they can also be exposedto partially reacted isocyanate-containingintermediates formed during polyurethaneproduction. In addition, isocyanate-containingmixtures of vapors and aerosols can be generatedduring the thermal degradation of polyurethanecoatings and plastics. The capability to measure allisocyanate-containing substances in air, whether theyare in monomer, prepolymer, polyisocyanate,oligomer, and/or intermediate forms, is importantwhen assessing a worker's total airborne isocyanateexposure.

Health Effects Associated With Isocyanates


Exposure to isocyanates is irritating to the skin,mucous membranes, eyes, and respiratory tract.6,7

The most common adverse health outcomeassociated with isocyanate exposure is asthma; lessprevalent are contact dermatitis (both irritant andallergic forms) and hypersensitivity pneumonitis(HP).7,8,9 Contact dermatitis can result in symptomssuch as rash, itching, hives, and swelling of theextremities.6,7,9 A worker suspected of havingisocyanate-induced asthma will exhibit thetraditional symptoms of acute airway obstruction(e.g., coughing, wheezing, shortness of breath,tightness in the chest, and nocturnal awakening).6,8,9

An isocyanate-exposed worker may first developasthma-like symptoms or an asthmatic conditionafter a single (acute) exposure, but sensitizationusually takes a few months to several years ofexposure.6,8,10,11,12 The asthmatic reaction may occurminutes after exposure (immediate), several hoursafter exposure (late), or a combination of bothimmediate and late components after exposure(dual).8,11 The late asthmatic reaction is the mostcommon, occurring in approximately 40% ofisocyanate sensitized workers.13 An improvement insymptoms may be observed during periods awayfrom the work environment (weekends,vacations).6,8,11 After sensitization, any exposure,even to levels below an occupational exposure limitor standard, can produce an asthmatic responsewhich may be life threatening. Experience withisocyanates has shown that monomeric,prepolymeric and polyisocyanate species are capableof producing respiratory sensitization in exposedworkers.14,15,16,17,18,19,20,21,22,23,24,25,26,27,28,29,30 Since theintermediates may be chemically similar to thesecompounds, it is reasonable to assume that they mayalso produce this condition. Prevalence estimates forisocyanate-induced asthma in exposed workerpopulations vary considerably: from 5% to 10% indiisocyanate production facilities10,31 to 25% inpolyurethane production plants31,32 and 30% inpolyurethane seat cover operations.33 The scientificliterature contains a limited amount of animal datasuggesting that dermal exposure to diisocyanatesmay produce respiratory sensitization.34,35,36,37 Thisfinding has not been tested in dermally-exposedworkers.

The percentage of sensitized workers with persistentsymptoms of asthma after years of no exposure maybe 50% or higher. Studies have shown that workerswith persistent asthma have a significantly longerduration of symptoms prior to diagnosis, larger

decrements in pulmonary function, and a severedegree of nonspecific bronchial hyperreactivity atdiagnosis.11 These data suggest that prognosis isimproved with early diagnosis of diisocyanate-induced respiratory sensitization and early removalfrom diisocyanate exposure. This emphasizes theneed to minimize workplace exposures, and foractive medical surveillance of all workers potentiallyexposed to diisocyanates.

HP has also been described in workers exposed toisocyanates.38,39,40,41 Currently, the prevalence ofisocyanate-induced HP in the worker population isunknown, and is considered to be rare whencompared to the prevalence rates for isocyanate-induced asthma.9 Whereas asthma is an obstructiverespiratory disease usually affecting the bronchi, HPis a restrictive respiratory disease affecting the lungparenchyma (bronchioles and alveoli). The initialsymptoms associated with isocyanate-induced HPare flu-like, including shortness of breath, non-productive cough, fever, chills, sweats, malaise, andnausea.8,9 After the onset of HP, prolonged and/orrepeated exposures may lead to an irreversibledecline in pulmonary function and lung compliance,and to the development of diffuse interstitialfibrosis.8,9 Early diagnosis is difficult since manyaspects of HP, i.e., the flu-like symptoms and thechanges in pulmonary function are manifestationscommon to many other respiratory diseases andconditions.

A limited number of animal studies havedemonstrated that commercial-grade TDI iscarcinogenic in both rats and mice.42 Statisticallysignificant excesses of liver and pancreatic tumorswere observed in male and female rats and femalemice that received TDI by gavage (route of exposurevia the digestive tract). In addition, a statisticallynon-significant excess in rare brain tumors wereobserved in male rats also treated with TDI bygavage. Also, commercial-grade TDI was found tohave a dose-dependent mutagenic effect on twostrains of Salmonella typhimurium in the presence ofa metabolic activator (S-9 liver fractions from rats orhamsters treated with Aroclor 254).43 Based on theseanimal and in vitro studies, the National Institute forOccupational Safety and Health (NIOSH) concludedthat sufficient evidence exists to classify TDI as apotential occupational carcinogen.44 It is importantto note that no epidemiologic data exists linking TDIexposure to elevated cancer rates in exposedworkers.


In regards to the two types of paints used in Building11, there are currently no recommended exposurelimits for HDI (including HDI-based trimer). TheOSHA and NIOSH ceiling limit for MDI (includingpolymethylenepolyphenyl isocyanate) is set at200 micrograms per cubic meter (µg/m3). TheNIOSH REL and the ACGIH TLV (up to an 8-hourTWA) are set at 50 µg/m3 and 51 µg/m3,respectively.

Methyl Ethyl Ketone (MEK)Methyl ethyl ketone (MEK) is a colorless,flammable organic solvent with a characteristic odorsimilar to acetone and is typically used as a solventin surface coating and synthetic resin industries.2

MEK is absorbed primarily through inhalation andcauses irritation of the eyes, mucous membranes, andskin. At high concentrations, MEK may causecentral nervous system depression. Short-durationinhalation exposure to 100 (ppm) of MEK wasreported to cause slight nose and throat irritation,200 ppm caused mild eye irritation, and 300 ppmwas associated with headaches, and throat irritation,as well as an objectional odor.45 Additional studiesindicate that MEK by itself does not causeneurologic toxicity of the extremities (peripheralneuropathy), but it may potentiate the toxic effects ofsubstances known to cause peripheral neuropathy,such as n-hexane.46,47,48 Continued or prolonged skincontact with MEK liquid can cause dermatitis.45

The National Toxicology Program, an interagencyresearch program, has not found evidence supportingan association between MEK exposure and thedevelopment of cancer in humans or experimentalanimals.49

NIOSH, OSHA, and ACGIH have the sameexposure limit for MEK: a full-shift TWA of200 ppm and a 15-minute STEL of 300 ppm.

Methyl Isobutyl Ketone(MIBK)Used in paints, glues, and as a cleaning agent, MIBKcan irritate the eyes, skin, and mucous membranes.45

Exposures to concentrations between 50 and500 ppm in humans have caused eye irritation,headache, loss of appetite, and weakness.46 Thiscompound has a distinctive camphor-like odor which

is detectable at a level of 100 ppm.45 The NIOSHREL and ACGIH TLV for MIBK are both 50 ppmfor a full-shift TWA and 75 ppm for a 15-minuteSTEL. The OSHA PELS for this chemical is100 ppm for an 8-hour TWA.

Isopropanol (IsopropoylAlcohol)Isopropanol is a colorless, volatile, flammable liquidof low toxicity that is used as a chemicalintermediate, a general purpose solvent, and aningredient in skin lotions, cosmetics, andpharmaceuticals.2,45 The vapor of isopropanol isirritating to the eyes and mucous membranes;inhalation of high concentrations can causedepression of the central nervous system.45,50 Thepotential effects from occupational skin contact withthe liquid are insignificant; cutaneous absorptionshould not contribute to systemic toxicity andgenerally does not produce skin irritation, exceptwith allergic individuals.2,45,50 The inhalationexposure limits established for isopropanol byNIOSH, OSHA, and ACGIH are equivalent. All areset at a full-shift TWA of 400 ppm, and a 15-minuteSTEL of 500 ppm.

RESULTSMedical EvaluationThe average age of the 28 interviewed employeeswas 49 years (range: 26-65 years). Most had workedat LMAS in various administrative positions (such asengineers, engineering technologists, datamanagement, procurement supervisors,secretarial/clerical duties, subcontractors, materieland management specialists, materielrepresentatives, and cost analysts) for three years ormore and were working in their current positions forat least six months. All stated that they worked an8 ½-hour shift. Most stated that their jobs did notrequire the use of PPE. Employees’ use ofworkplace chemicals was confined to standard officesupplies, such as white-out, copier solutions, andgeneral office cleaning supplies.

Of the 28 employees interviewed, 16 stated that theyhad been working in Area K or in the paint bootharea at the time when employee complaints andsymptoms were first reported (May 1998). Three of


the employees who had cubicles closest to themechanical room stated that they were among thefirst to become ill. One of these three employeeswas seen at the LMAS clinic on May 26, 1998, witha chief complaint of acute onset of wheezing while atwork. This individual was diagnosed with an acuteexacerbation of asthma, and was referred to apulmonary specialist three days later. At the time ofthe pulmonary evaluation, a diagnosis of statusasthmaticus was made, and the employee wasadmitted to the hospital the same day. The second ofthe three employees experienced a sore throat andthe acute onset of chest tightness while traveling ona business trip on the afternoon of May 27, 1998.These symptoms began approximately five hoursafter the individual was evaluated in the LMASclinic with a chief complaint of cough and pain uponswallowing which had started the previous day whileat work. The employee presented to the emergencyroom the same evening, and was treated andreleased.

Fourteen of the 16 employees who were working inArea K during May 1998 reported one or more of thefollowing symptoms: eye, nose, and throat irritation,cough, wheezing, shortness of breath, chest pain,headache, nausea, dizziness, fatigue, numbness/andor tingling of the extremities, and skin rash. Of the14 symptomatic employees, 13 stated that thesymptoms they experienced improved with timeaway from work and worsened after returning to theworkplace. Seven of the 14 stated that they hadexperienced acute symptoms (including shortness ofbreath, wheezing, chest tightness, cough, and hoarsevoice) upon briefly reentering their previous workarea in Building L-11. Two of the 14 employees,who have since been relocated to Building L-22,stated that they experienced respiratory symptomsshortly after receiving paperwork which wasoriginally stored in Area K. Six of the 14 employeesstated that they had become “increasingly sensitive”to household chemicals (such as home cleaningsolutions, nail polish remover, indoor-use pesticides,and fertilizers/lawn chemicals); these employeesrelated experiencing an acute onset of mucousmembrane and respiratory irritation symptomsshortly after exposure to these chemicals, withsymptom improvement occurring after cessation ofexposure. None of the symptomatic employeesinterviewed related any participation in hobbies orother non-occupational activities involvingsignificant exposures to chemicals.

Medical records were obtained for 15 of theemployees interviewed. Medical records from theplant medical clinic as well as private medicalprovider records were reviewed. Plant medicalrecords indicated that 12 of the symptomaticemployees had been evaluated for mucousmembrane and upper respiratory irritation secondaryto chemical exposure (characterized as exposure toeither D-limonene, TDI, or MEK between May andJune 1998). Nine of the 12 employees were referredto a pulmonary specialist for further evaluation oftheir respiratory symptoms. Each of the nineemployees underwent a comprehensive pulmonaryevaluation (including history and physicalexamination, pre-and post-bronchodilator pulmonaryfunction testing, diffusion capacity for carbonmonoxide [DLCO] testing, and chest X-ray studies).Of the nine employees evaluated, seven werediagnosed with “reactive airway disease” (plus either“mild obstructive airway disease” or “mild asthma”)secondary to inhalation of chemical sensitizers. Oneemployee with a previous history of asthma wasdiagnosed with an “acute exacerbation ofasthma”/status asthmaticus as a result of presumedworkplace exposure to MEK. Another employeewas d i agn o s e d wi t h a “chemica lpharyngitis/laryngitis” and “vocal cord dysfunction”consistent with exposure to isocyanate-type irritants.According to plant medical records, 8 of the15 symptomatic employees had been placed on classVI permanent work restrictions (i.e., theseemployees were not to reenter Building L-11 withoutprior medical clearance), as a result of exposure tounspecified chemicals in this building. Injury andillness record forms were also reviewed for 12 AreaK employees which NIOSH did not interview.These employees had experienced a variety ofsymptoms suggestive of chemical exposure(including mucous membrane irritation, cough,shortness of breath, headaches, nausea, dizziness,fatigue, skin rash, and numbness of the hands andlegs). All were evaluated in the occupationalmedicine clinic for possible chemical fume exposure.Four individuals underwent chest X-ray andpulmonary function testing as part of their symptomwork-up. The remainder were evaluated by physicalexam, released, and instructed to follow-up asneeded should further symptoms develop.

OSHA 200 log entries for 1995, 1996, 1997, and1998 were reviewed. In 1998, there were 1,519 totalentries noted. Thirty entries (2%) involved fumeexposure (not otherwise specified) involving theeyes, head, chest, lungs, and stomach which were


directly related to exposures in Area K. Themajority of the other injuries and illnesses recordedfor all years involved sprains/strains, lacerations,abrasions, contusions, foreign body injuries, burns,and dermatitis.

Environmental EvaluationTo establish baseline concentrations of SF6 in AreaK, continuous background sampling was conductedover a 25-minute period prior to the release of tracergas in any of the evaluated areas. As seen inFigure 1, background concentrations of SF6 in AreaK ranged from approximately 7.3 x 10-3 ppm to 22.7x 10-3 ppm, with an average concentration of 15.5 x10-3 ppm.

Tracer gas was released in the two chemical useareas of concern: the paint spray booth, and the coreroom where parts are cleaned with MEK. Afterdetermining that the volume of the paint spray boothwas approximately 15,775 cubic feet (ft3), tracer gaswas released for five minutes at four cfm in thebooth, resulting in a calculated concentration ofapproximately 12 ppm prior to turning on theexhaust fan in the booth. Continuous sampling wasconducted over a 22-minute period after turning onthe exhaust fan (see Figure 2). Concentrations of SF6in Area K remained similar to previous baselinemeasurements, ranging from 6.94 x 10-3 ppm to 17.8x 10-3 ppm, with an average concentration of 13.0 x10-3 ppm. These results indicate that tracer gas didnot migrate into the office space of Area K from thepaint spray booth under the environmentalconditions present at the time of the NIOSHevaluation.

SF6 was released for a total of five minutes at 4 cfmin the core room, resulting in a calculatedconcentration of 15.6 ppm (based on an approximateroom volume of 12,840 ft3) prior to activating thelocal exhaust ventilation. As shown in Figure 3,concentrations of SF6 in Area K were alsounchanged during the release of tracer gas in the coreroom. An average concentration of 13.7 x 10-3 ppmwas measured in Area K, with a range from 9.7 x10-3 ppm to 18.1 x 10-3 ppm. To ensure that theappropriate concentration of SF6 was being released,a bag sample was collected in the core room prior toturning on the local exhaust ventilation. The bagsample was found to contain 16 ppm SF6, therebyconfirming the calculated concentrations (seeFigure 4).

In addition to the chemical use areas, tracer gas wasreleased around one of the two AHUs serving AreaK. Since the AHU was situated in an open space onthe mezzanine level of the production area, tracer gaswas released in the proximity of the negativepressure components of the AHU. Unlike theenclosed chemical use areas, for which an initial SF6concentration could be determined, the results fromthis trial only provided information on the potentialfor entrainment and dissemination to Area K. Thedegree of dilution during migration (concentration atsample point versus concentration at the releasepoint) could thus not be determined. Approximatelyone minute after releasing tracer gas around theAHU, concentrations of SF6 in Area K increased to45.7 x 10-3 ppm, in comparison to backgroundconcentrations averaging around 15.0 x 10-3 ppm.After four minutes, the concentration of SF6 in AreaK peaked at 74.7 x 10-3 ppm as shown in Figure 5.Monitoring was continued for approximately onehour after the tracer gas was no longer being releasedto estimate the decay or clearance of SF6 from AreaK. By estimating the curve-fit line of the natural logconcentrations over time, the slope or number ofACH, was calculated to be approximately 4.6 ACH(see Figure 6).

DISCUSSION ANDCONCLUSIONS

Chemicals, including solvents such as MEK, MIBK,isopropyl alcohol, and tolytriazole (a corrosioninhibitor with corrosive and irritant properties) werebeing used on a regular basis in the first floorproduction area located directly below Area Kduring the time period workers first began toexperience symptoms. In addition, paints containingHDI- and MDI-based polyisocyanate compoundswere being used in the paint spray booth. Theconstellation of symptoms (particularly mucousmembrane and respiratory symptoms) reported byArea K employees during interviews, as well as themedical record findings, appear to be consistent withworkplace exposure to either isocyanates or organicsolvents, such as MEK and MIBK.

The predominant symptoms reported by employeeswho were working in Area K during mid-1998 weremucous membrane irritation, respiratory symptoms(including cough, wheezing, shortness of breath,chest discomfort), headache, dizziness, nausea andfatigue. Other symptoms reported included skin


rashes and numbness/tingling of the extremities. Anumber of employees who experienced respiratoryproblems and were referred to a pulmonary specialistfor further evaluation (which included spirometrictesting) were diagnosed with a variety of respiratoryconditions, including reactive airway diseasesecondary to inhalation of respiratory irritants atwork, obstructive airway disease, and presumptiveoccupational asthma. According to the medicalrecords reviewed, one employee was diagnosed withchemical pharyngitis and two employees developedchemical conjunctivitis related to chemical fumeexposure in the workplace.

In summary, the results of the medical evaluationappear to indicate that the respiratory symptomswhich were being experienced by the affectedemployees who were working in Area K during May1998 are most consistent with known exposure toisocyanates at the time the employees’ symptomsbecame manifest. Possible concomitant exposure tosolvents such as MEK and isopropyl alcohol mayalso explain some of the irritant mucous membraneand respiratory symptoms experienced by Area Kemployees. However, there were employees whoserespiratory symptoms clearly continued even afterthey were removed from Area K, and this pattern ofsymptom persistence cannot be explained by thetime-limited isocyanate/solvent exposure scenariodescribed above. It is unclear as to why Area Kemployees would continue to experience symptomsin the absence of any verifiable continuous chemicalexposure. Therefore, the available medical evidencedoes suggest, but cannot verify with certainty, thepossibility of workplace isocyanate and/or solventexposure as a cause of the health problems beingreported by Area K employees.

Prior to the implementation of engineering controlsand changes in work practices, the following threemigration pathways potentially existed from theproduction area on the first floor to Area K on thesecond floor. The first, and most likely route ofentrainment was from the paint spray boothmechanical room into Area K. Entrainment ofisocyanate-containing paints into Area K would havebeen a feasible mechanism allowing for low-levelairborne exposure to the paints over a specified timeperiod. This theory is strengthened by the fact that asignificant number of Area K employees, whosecubicles resided closest to the mechanical room,experienced more numerous and severe symptomswhich occurred very early in the course of thechemical exposure time frame. Secondly, there was

an open catwalk leading from the first floorproduction area into the mechanical room above.Therefore, any chemicals used for cleaning parts, etc.in this area, could have migrated into Area K. Athird potential route of entrainment was from theAHU located on the mezzanine level of theproduction area. Because the AHU is under negativepressure, it draws in air from the surrounding areas.Any chemical being used in this area could then besupplied to Area K through the supply ductwork. ALMAS management representative reported thatparts had been cleaned in this area in the past beforethe core-clean room was designated for this use.

In response to the health complaints in Area K,LMAS initiated a number of actions to controlemissions and migration from the production area toArea K. These general improvements to theworkplace environment included modifications tothe existing ventilation system, such as increasingthe amount of supply air received by Area K, as wellas limiting the use of chemicals in the productionarea to the core-clean room. Other improvementsfocused on preventing the migration of contaminantsfrom the first floor to Area K. The mechanical roomwas renovated, including moving the exhaust fansfor the paint spray booth to the roof, removing thedoors of the mechanical room leading into Area Kand replacing them with sheetrock, and closing offaccess from the catwalk to the mechanical room.The release of tracer gas in the paint spray boothsuggests that these measures have successfullyaddressed the concerns of migration from themechanical room into Area K. It should be notedthat isocyanate paints are no longer being used inBuilding L-11. In addition to the paint spray booth,LMAS has limited the use of MEK to the core-cleanroom. As shown from tracer gas released in the core-clean room, migration from this room or its exhaustsinto Area K does not appear likely. Air sampling forMEK and MIBK immediately outside of this roomhas indicated no detectable amounts of these agents.Tracer gas release around the AHU served twopurposes. First, it was determined that Area K isundergoing approximately four ACH, which isconsistent with a recent test and balancing reportdescribing the ventilation system serving this area.The fact that tracer gas was entrained into the AHUand supplied to Area K indicates that any chemicals,contaminants, or odors generated in this area couldpotentially expose individuals in Area K. Additionally, LMAS hired an outside contractor(who specializes in asbestos abatement) to clean allsurfaces in Area K in preparation for moving


1. NIOSH [1992]. Recommendations foroccupational safety and health: compendium ofpolicy documents and statements. Cincinnati,OH: U.S. Department of Health and HumanServices, Public Health Service, Centers forDisease Control and Prevention, National Institutefor Occupational Safety and Health, DHHS(NIOSH) Publication No. 92-100.

2. ACGIH [1999]. 1999 TLVs® and BEIs®.Cincinnati, OH: American Conference ofGovernmental Industrial Hygienists.

3. Code of Federal Regulations [1997]. 29 CFR1910.1000. Washington, DC: U.S. GovernmentPrinting Office, Federal Register.

4. Public Law 91 – 596 Occupational safety andHealth Act of 1970, Sec. 5.(a)(1).

5. Woods G [1987]. The ICI PolyurethanesBook. New York, NY: ICI Polyurethanes andJohn Wiley & Sons. Inc.

6. NIOSH [1978]. Criteria for a recommendedstandard: occupational exposure to diisocyanates.DHEW (NIOSH) Publication No. 78-215.Cincinnati, OH: U.S. Dept. of Health, Education,and Welfare, Public Health Service, Center forDisease Control, NIOSH.

7. NIOSH [1990]. Pocket guide to chemicalhazards. DHHS (NIOSH) Publication No. 90-117.Cincinnati, OH: U.S. Dept. of Health and HumanServices, Public Health Service, Centers forDisease Control, NIOSH.

employees back into this office space. According toa representative from the LMAS industrial hygienegroup, the contractors wet-wiped the walls, ceilings,and office furniture, and vacuumed the carpetingwith a high-efficiancy particulate air filtered vacuum.LMAS has also continued to monitor for airbornesolvents in the production area on the first floor.

RECOMMENDATIONS1. Employees who are currently experiencingrespiratory or other symptoms should continue tofollow up with the occupational physician and/orspecialty physician provider.

2. Employees’ treating physicians should beinformed of both LMAS’s and NIOSH’senvironmental findings, to assist them in evaluatingthe work-related nature of their symptoms.

3. The AHU serving Area K should be isolated fromthe production area. This can be accomplished byeither moving it to the roof of the building orenclosing it.

4. Area K should be maintained under positivepressure at all times to prevent contaminantmigration from chemical use areas into the officearea.

5. An IEQ Management Plan should beimplemented for Building L-11. An IEQ manager oradministrator with clearly defined responsibilities,authority, and resources should be selected. Thisindividual should have a good understanding of thebuilding’s structure and function, and should be ableto effectively communicate with occupants. Theelements of a good plan include the following:

• Proper operation and maintenance of HVACequipment.

• Overseeing the activities of occupants andcontractors that affect IEQ (e.g., housekeeping, pestcontrol, maintenance).

• Maintaining and ensuring effective and timelycommunication with occupants regarding IEQ.

• Educating building occupants and contractorsabout their responsibilities in relation to IEQ.

• Pro-active identification and management ofprojects that may affect IEQ (e.g., redecoration,renovation, relocation of personnel, etc.).

The NIOSH/Environmental Protection Agency(EPA) Building Air Quality Guidance Documentshould be consulted for details on developing andimplementing IEQ management plans.51

REFERENCES


8. NIOSH [1986]. Occupational respiratorydiseases. DHHS (NIOSH) Publication No. 86-102. Cincinnati, OH: U.S. Dept. of Health andHuman Services, Public Health Service, Centersfor Disease Control, NIOSH.

9. Levy BS, Wegman DH (editors) [1988].Occupational Health: Recognizing andPreventing Work-Related Diseases. SecondEdition. Boston/Toronto: Little, Brown andCompany.

10. Porter CV, Higgins RL, Scheel LD [1975]. Aretrospective study of clinical, physiologic, andimmunologic changes in workers exposed totoluene diisocyanate. American IndustrialHygiene Association Journal 36: 159-168.

11. Chan Yeung M, Lam S [1986]. Occupationalasthma. American Review of Respiratory Disease133: 686-703.

12. NIOSH [1981]. Technical report: respiratoryand immunologic evaluation of isocyanateexposure in a new manufacturing plant. DHHS(NIOSH) Publication No. 81-125. Cincinnati,OH: U.S. Dept. of Health and Human Services,Public Health Service, Centers for DiseaseControl, NIOSH.

13. McKay RT, Brooks SM [1981]. Toluenediisocyanate (TDI): biochemical and physiologicstudies. American Review of Respiratory Disease123: 132.

14. Harries M, Burge S, Samson M, Taylor A,Pepys J [1979]. Isocyanate asthma: respiratorysymptoms due to 1,5-naphthylene di-isocyanate.Thorax 34: 762-766.

15. Woolrich PF [1982]. Toxicology, industrialhygiene and medical control of TDI, MDI, andPMPPI. American Industrial Hygiene AssociationJournal 43: 89-98.

16. Mobay Corporation [1983]. Health & safetyinformation for MDI, diphenylmethanediisocyanate, monomeric, polymeric, modified.Pittsburgh, PA: Mobay Corporation.

17. Berlin L, Hjortsberg U, Wass U [1981]. Life-threatening pulmonary reaction to car paintcontaining a prepolymerized isocyanate.Scandinavian Journal of Work, Environment andHealth 7: 310-312.

18. Zammit-Tabona M, Sherkin M, Kijek K,Chan H, Chan-Yeung M [1983]. Asthma causedby diphenylmethane diisocyanate in foundryworkers. American Review of RespiratoryDisease 128: 226-230.

19. Chang KC, Karol MH [1984].Diphenylmethane diisocyanate (MDI)-inducedasthma: evaluation of immunologic responses andapplication of an animal model of isocyanatesensitivity. Clinical Allergy 14: 329-339.

20. Seguin P, Allard A, Cartier A, Malo JL[1987]. Prevalence of occupational asthma inspray painters exposed to several types ofisocyanates, including polymethylene polyphenylisocyanate. Journal of Occupational Medicine29: 340-344.

21. Nielsen J, Sungo C, Winroth G, Hallberg T,Skerfving S [1985]. Systemic reactions associatedwith polyisocyanate exposure. ScandinavianJournal of Work, Environment and Health 11: 51-54.

22. Alexandersson R, Gustafsson P, HedenstiernaG, Rosen G [1986]. Exposure to naphthalene-diisocyanate in a rubber plant: symptoms and lungfunction. Archives of Environmental Health 41:85-89.

23. Mapp CE, Chiesura-Corona P, DeMarzo N,Fabbri L [1988]. Persistent asthma due toisocyanates. American Review of RespiratoryDisease 137: 1326-1329.

24. Liss GM, Bernstein DI, Moller DR,Gallagher JS, Stephenson RL, Bernstein IL[1988]. Pulmonary and immunologic evaluationof foundry workers exposed to methylene


diphenyldiisocyanate (MDI). Journal of Allergyand Clinical Immunology 82: 55-61.

25. Keskinen H, Tupasela O, Tiikkainen U,Nordman H [1988]. Experiences of specific IgEin asthma due to diisocyanates. Clinical Allergy18: 597-604.

26. Cartier A, Grammar L, Malo JL, Lagier F,Ghezzo H, Harris K, Patterson R [1989]. Specificserum antibodies against isocyanates: associationwith occupational asthma. Journal of Allergy andClinical Immunology 84: 507-514.

27. Mobay Corporation [1991]. Hexamethylenediisocyanate based polyisocyanates, health andsafety information. Pittsburgh, PA: MobayCorporation.

28. Vandenplas O, Cartier A, Lesage J, PerraultG, Grammar LC, Malo JL [1992]. Occupationalasthma caused by a prepolymer but not themonomer of toluene diisocyanate (TDI). Journalof Allergy and Clinical immunology 89: 1183-1188.

29. Vandenplas O, Cartier A, Lesage J, CloutierY, Perrault G, Grammar LC, Shaughnessy MA,Malo JL [1992]. Prepolymers of hexamethylenediisocyanate as a cause of occupational asthma.Journal of Allergy and Clinical Immunology 91:850-861.

30. Baur X, Marek W, Ammon J, Czuppon AB,Marczynski B, Raulf-Heimsoth M, Roemmelt H,Fruhmann G [1994]. Respiratory and otherhazards of isocyanates. International Archives ofOccupational and Environmental Health 66: 141-152.

31. Weill H [1979]. Epidemiologic andmedical-legal aspects of occupational asthma.The Journal of Allergy and Clinical Immunology64: 662-664.

32. Adams WGF [1975]. Long-term effects onthe health of men engaged in the manufacture oftolylene diisocyanate. British Journal ofIndustrial Medicine 32: 72-78.

33. White WG, Sugden E, Morris MJ, Zapata E[1980]. Isocyanate-induced asthma in a carfactory. Lancet i: 756-760.

34. Karol MH, Hauth BA, Riley EJ, Magreni CM[1981]. Dermal contact with toluene diisocyanate(TDI) produces respiratory tract hypersensitivityin guinea pigs. Toxicology and AppliedPharmacology 58: 221-230.

35. Erjefalt I, Persson CGA [1992]. Increasedsensitivity to toluene diisocyanate (TDI) inairways previously exposed to low doses of TDI.Clinical and Experimental Allergy 22: 854-862.

36. Rattray NJ, Bothman PA, Hext PM,Woodcock DR, Fielding I, Dearman RJ, KimberI [1994]. Induction of respiratory hypersensitivityto diphenylmethane-4,4'-diisocyanate (MDI) inguinea pigs. Influence of route of exposure.Toxicology 88: 15-30.

37. Bickis U [1994]. Investigation of dermallyinduced airway hyperreactivity to toluenediisocyanate in guinea pigs. Ph.D. Dissertation,Department of Pharmacology and Toxicology,Queens University, Kingston, Ontario, Canada.

38. Baur X, Dewair M, Rommelt H [1984].Acute airway obstruction followed byhypersensitivity pneumonitis in an isocyanate(MDI) worker. Journal of Occupational Medicine26: 285-287.

39. Yoshizawa Y, Ohtsuka M, Noguchi K,Uchida Y, Suko M, Hasegawa S [1989].Hypersensitivity pneumonitis induced by toluenediisocyanate: sequelae of continuous exposure.Annals of Internal Medicine 110: 31-34.

40. Selden AI, Belin L, Wass U [1989].Isocyanate exposure and hypersensitivitypneumonitis - report of a probable case andprevalence of specific immunoglobulin Gantibodies among exposed individuals.Scandinavian Journal of Work, Environment andHealth 15: 234-237.


41. Vanderplas O, Malo JL, Dugas M, Cartier A,Desjardins A, Levesque J, Shaughnessy MA,Grammar LC [1993]. Hypersensitivitypneumonitis-like reaction among workers exposedto diphenylmethane diisocyanate (MDI).American Review of Respiratory Disease 147:338-346.

42. NTP [1986]. NTP technical report on thetoxicology and carcinogenesis studies ofcommercial grade 2,4(80%)- and 2,6(20%)-toluene diisocyanate (CAS No. 26471-62-5) inF344/N rats and B6C3F1 mice (gavage studies).NTP TR 328, NIH Publication No. 88-2584.Research Triangle Park, NC: U.S. Dept. of Healthand Human Services, Public Health Service,National Institutes of Health, National ToxicologyProgram.

43. Andersen M, Binderup ML, Kiel P, Larsen H,Maxild J [1980]. Mutagenic action of isocyanatesused in the production of polyurethanes.Scandinavian Journal of Work, Environment andHealth 6:221-226.

44. NIOSH [1989]. Current intelligence bulletin53: toluene diisocyanate (TDI) andtoluenediamine (TDA), evidence ofcarcinogenicity. DHHS (NIOSH) Publication No.90-101. Cincinnati, Ohio: U.S. Dept. of Healthand Human Services, Public Health Service,Centers for Disease Control, NIOSH.

45. Proctor NH, Hughes JP, Fischman ML[1991]. Chemical hazards of the workplace. 3rd

ed. New York, NY: Van Nostrand Reinhold.

46. Ellenhorn MJ, Barceloux DG [1988].Medical toxicology: diagnosis and treatment ofhuman poisoning. New York, NY: Elsevier, pp1000-1001.

47. Dyro FM [1978]. Methyl ethyl ketonepolyneuropathy in shoe factory workers. ClinToxicol 13:371-376.

48. NIOSH [1978]. Criteria for a recommendedstandard: occupational exposure to ketones.Cincinnati, OH: U.S. Department of Health,Education, and Welfare, Public Health Service,Center for Disease Control, National Institute forOccupational Safety and Health, DHEW (NIOSH)Publication No. 78-173.

49. NTP [1991]. Sixth annual report oncarcinogens: 1991 summary. Research TrianglePark, NC: U.S. Department of Health and HumanServices, National Toxicology Program.

50. NIOSH [1976]. Criteria for a recommendedstandard: occupational exposure to isopropylalcohol. Cincinnati, OH: U.S. Department ofHealth, Education, and Welfare, Public HealthService, Center for Disease Control, NationalInstitute for Occupational Safety and Health,DHEW (NIOSH) Publication No. 76-142.

51. NIOSH/EPA [1991]. Building air quality: aguide for building owners and facility managers.Cincinnati, OH: U.S. Department of Health andHuman Services, Public Health Service, Centersfor Disease Control, National Institute forOccupational Safety and Health, DHHS (NIOSH)Publication No 91-114.


0.00E+005.00E-031.00E-021.50E-022.00E-022.50E-023.00E-02

12:42

:56

12:45

:53

12:48

:36

12:51

:31

12:54

:15

12:57

:00

12:59

:45

13:03

:00

13:05

:42Sulfu

r Hex

aflu

orid

e (p

pm)

0.00E+00

5.00E-03

1.00E-02

1.50E-02

2.00E-02

2.50E-02

3.00E-02

13:08

:28

13:10

:16

13:12

:24

13:14

:13

13:16

:03

13:17

:52

13:19

:43

13:21

:43

13:23

:32

13:25

:21

13:27

:10

13:28

:58

Sulfu

r Hex

aflu

orid

e (p

pm)

Figure 1. Background Concentrations of Sulfur Hexafluoride in Area K.

Figure 2. Concentrations of Sulfur Hexafluoride in Area K During Release in Paint Booth.


0.00E+00

5.00E-03

1.00E-02

1.50E-02

2.00E-02

2.50E-02

3.00E-02

13:31

:20

13:33

:09

13:34

:58

13:36

:46

13:38

:35

13:40

:24

13:42

:33

13:44

:22

Sulfu

r Hex

aflu

orid

e (p

pm)

0.00E+002.00E+004.00E+006.00E+008.00E+001.00E+011.20E+011.40E+011.60E+011.80E+01

13:45

:17

13:48

:03

13:51

:00

13:53

:44

13:56

:27

13:59

:10

14:02

:24

14:05

:07

14:07

:52

Sulfu

r Hex

aflu

orid

e (p

pm)

Figure 3. Concentrations of Sulfur Hexafluoride in Area K During Release in Core Room.

Figure 4. Concentrations of Sulfur Hexafluoride in Bag Sample From Core Room.


Figure 5. Concentrations of Sulfur Hexafluoride in Area K During Release by AHU.

Figure 6. Curve Fit Concentration of Sulfur Hexafluoride During Release by AHU.

0.00E+001.00E-022.00E-023.00E-024.00E-025.00E-026.00E-027.00E-028.00E-029.00E-021.00E-01

14:09

:41

14:12

:44

14:15

:28

14:18

:13

14:21

:09

14:23

:54

14:26

:36

14:29

:21

14:32

:35

14:35

:20

14:38

:04

14:41

:07

14:43

:51

14:46

:36

14:49

:21

Sulfu

r Hex

aflu

orid

e (p

pm)

-3.4

-3.2

-3-2

.8-2

.6

14:00:00 14:10:00 14:20:00 14:30:00 14:40:00 14:50:00 15:00:00

Time

Ln (

Sul

fur

Hex

aflu

orid

e) measured values

curve fit

For Information on Other

Occupational Safety and Health Concerns

Call NIOSH at:1–800–35–NIOSH (356–4674)or visit the NIOSH Web site at:

www.cdc.gov/niosh

!!!!Delivering on the Nation’s promise:

Safety and health at work for all peoplethrough research and prevention

HHE #: 98-0347-2758

SIC Code: 381 (Search, Detection, Navigation,Guidance, Aeronautical, and Nautical Sytems,Instruments, and Equipment

Keywords: Indoor Environmental Quality, IndoorAir Quality, IEQ, IAQ, Ventilation, Tracer Gas,Sulfur Hexafluoride, Composites, Diisocyanate-Containing Paints, Methyl Ethyl Ketone, MEK,Methyl Ethyl Isobutyl Ketone, MIBK, Isoproponal.

Toxicity Determination: Negative Positive Medical

Positive IHPositive Both

Undetermined