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Pesticide Action Network Aotearoa New Zealand

Co-ordinator: Dr Meriel Watts PO Box 296, Ostend, Waiheke Island Auckland 1971, New Zealand

Ph/fax 64-9-372-2034; 021-1807830 merielwatts@xtra.co.nz

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Submission to: Environmental Protection Authority Te Mana Rauhii Taiao

Subject: Reassessment of organophosphate and carbamate insecticides

From: Pesticide Action Network Aotearoa New Zealand (PAN ANZ)

Contact: Dr Meriel Watts

Date: January 22nd, 2013 I wish to be heard at a public meeting 1. DECISIONS SOUGHT 1.1 SUPPORT EPA proposed decision: Bendiocarb - revoke approvals with 6-month phase-out Benomyl - revoke approvals with 6-month phase-out Carbofuran - revoke approvals with 6-month phase-out Carbosulfan - revoke approvals with 6-month phase-out Dichlofenthion - revoke approvals with 6-month phase-out Ethion - revoke approvals with 6-month phase-out Famphur - revoke approvals with 6-month phase-out Isazofos - revoke approvals with 6-month phase-out Omethoate - revoke approvals with 6-month phase-out Phoxim - revoke approvals with 6-month phase-out Pyrazophos - revoke approvals with 6-month phase-out 1.2 SUPPORT proposed phase-out, but OPPOSE EPA phase-out period (NB: EPA proposed phase-out in brackets; PAN proposed phase-out after colon) Diazinon (10 yrs): requested phase out - home use and granules in 1 mth; other high bird risk uses in 1 yr; all other uses 3 yrs Dimethoate (3yrs): requested phase out - outdoor uses in 18 mths; all other uses 3 yrs Fenitrothion (3 yrs): requested phase out - all uses 18 mths Methamidophos (5 yrs): requested phase out - all uses 18 mths Phorate (3 yrs): requested phase out - all uses in 6 mths

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Prothiophos (10 yrs): requested phase out - all uses 18 mths, except grape vines 3 yrs Terbufos (3 yrs): requested phase out - all uses 1 yr 1.3 OPPOSE EPA proposal to retain approvals, and request phase-out: Acephate: requested phase out - home use 1 mth; citrus and indoor biosecurity 3 yrs; all other uses 18 mths Carbaryl: requested phase out - home use 1 mth; all other uses 18 mths Chlorpyrifos: requested phase-out - home use 1 mth; granules 1 mth; all other uses 18 mths Chlorpyrifos-methyl: requested phase out -1 yr Methomyl (EPA proposes18 mths outdoors; retain indoors): requested phase out - outdoor in 1 yr; indoors in 3 yrs Pirimicarb: requested phase out - uses with risks to birds 1yr; all other uses 3 yrs. 1.4 Support some retained use Dichlorvos (EPA proposes phase-out outdoor uses in 18 mths; retain indoor uses, biosecurity strips). PAN ANZ requests:

i) phase out: home use in 1 mth; outdoor uses in 1 yr; indoor uses in 3 yrs;

ii) retain biosecurity strips Fenamiphos (EPA proposes phase-out in 5 yrs). PAN ANZ requests: i) phase out: high bird risk uses in 1 yr; all other uses 3yrs

ii) retain for emergency indoor biosecurity

Maldison/malathion:

i) phase out: home use 1 mth; all other uses 3 yrs ii) retain for biosecurity baits

Pirimiphos-methyl:

i) phase-out: outdoor uses in 1 yr ii) retain for empty grain silos and indoor biosecurity

Oxamyl:

i) phase-out: outdoor uses in 3 yrs ii) retain for glasshouse use only.

1.4 Reasons for seeking this decision: These pesticides are all highly hazardous pesticides that pose significant risks to human health and the environment (especially birds and bees), and for which safer alternatives, including biopesticides, biological controls, and sustainable management practices, are available and proven effective. The OPCs are particularly hazardous to young children, and it is notable that 42% of OPC poisoning cases in New Zealand between 2006-2010 were children aged 1-10 years (p 23 Consultation report).

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2. GENERAL COMMENTS

1. It is impossible for PAN ANZ to adequately provide technical information on 30 pesticides and alternatives to these at one time to back our proposed decisions. We believe that assessing so many chemicals at once is not appropriate: quite apart from the huge burden this places on non-profit organisations with non-paid ‘staff’, in PAN ANZ’s view the chemicals and their alternatives have not been properly assessed by EPA. In fact it is stated on page 22 of the APP201045 Consultation report that “EPA staff are aware that there are more recent studies which it has been unable to incorporate into its assessment because of the timing and number of substances in this Application”. That is tantamount to confessing that the chemicals have not been properly assessed, and this is an unacceptable situation.

2. As a result of our resource limitations only chlorpyrifos has been fully addressed in this submission – refer Annexes A and B – as it is judged to be one of the worst problems, and a chemical warranting global phase-out. Other OPCs are addressed only in a limited way to back up our view that they need to be phased out much more quickly than currently proposed by EPA.

Human health effects and exposure

3. We are concerned about the ADI values used by EPA as the sole basis for determining the safety or otherwise of the OPCs. For example, the California EPA has concluded that “there is now evidence that chlorpyrifos directly targets events that are specific to the developing brain and that are not related to inhibition of cholinesterase, including: inhibition of DNA synthesis, impairment of cell acquisition and differentiation, interactions with neurotrophic factors, interruption of cell signalling cascades, and alteration in synaptic function”; and established a child-specific reference dose (chRfD) of only 0.0001 mg/kg/day (CAL EPA 2010), 30-fold lower than the ADI of 0.003 mg/kg/day used by NZ EPA – “based on cholinesterase inhibitions in dogs and rats and supporting information on cognitive deficiencies in rats”. That indicates that the NZ EPA’s evaluation of the risk from chlorpyrifos exposure is not protective of children or the developing foetus. It should be noted that the APVMA (2009) dietary risk assessment showed that their chronic dietary exposure was 55% of their ADI, and acute dietary exposure for children reached 55% of their RfD. Given that the Cal EPA has set a child reference dose 30-fold lower that the Australian RfD, the residue pattern in Australia at least poses significant risk to children; in the absence of such an analysis in NZ, a similar risk to children must be assumed.

4. The EPA assessment appears to have been based solely on acute toxicity arising from acetylcholinesterase inhibition, and has ignored neurodevelopmental effects, long-term neurological effects and conditions, mutagenicity, carcinogenicity, immune toxicity, endocrine disrupting effects, reproductive toxicity, diabetes, and obesity. EPA justifies their approach by claiming that other overseas jurisdictions regulate OPs on the basis of neurological effects resulting from acetylcholinesterase inhibition, but that is

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not the complete truth: for example EU banned dichlorvos because of concerns about genotoxicity and carcinogenicity; US EPA has identified a number of OPs as possible or probable carcinogens.

5. When these chronic effects are included in the assessment, there is a vastly different risk profile for a number of the OPCs in terms of human health risk. For example, chlorpyrifos moves from being one of the OPCs with the lowest risk to one with the highest risk. As chronic ecotoxicity and environmental fate data are missing, this cannot be called a reassessment – it is really only a screening based on acute exposure.

6. All of the OPCs should be considered as posing unacceptable risk to humans. There are numerous studies showing that on-going occupational exposure to OPCs has detrimental effects, including neurological, endocrine and carcinogenic effects. For example: i) a recent meta-analysis (Ross et al 2012) of 16 “well-designed” studies found

a significant and consistent association between on-going low-level occupational exposure to OPs and impaired neurobehavioural function, primarily with cognitive function such as psychomotor speed, executive function, visuospatial ability, working and visual memory. It included greenhouse workers, farm workers and fruit tree sprayers. Only 3 of 6 studies found no difference between exposed and control subjects, and all 3 were methodologically flawed. This is the first time there has been a meta-analysis of the literature on on-going low-level occupational exposure to OPs. The authors hoped that this study would be taken into account by governments performing reviews of low-level exposure to OPs.

ii) A longitudinal study of male floriculture workers in Mexico correlated OP exposure with hormonal impacts, including increased serum levels of follicle-stimulating hormone and prolactin, and decreased testosterone (Aguilar-Garduño et al 2012).

iii) An earlier longitudinal study of floriculture workers in Mexico found OP exposure associated with alterations in thyroid hormones, including increased TSH and T4 and decreased T3 serum levels (Lacasaña et al 2010).

iv) A prospective study of pregnant women in the Rio Negro province of Argentina where OPs (particularly chlorpyrifos, dimethoate, azinphos methyl and phosmet) are used intensively for 6 months of the year, concluded that OP exposure ‘very significantly’ (by 55%) increased cortisol levels in the first trimester of pregnancy when that coincided with the spraying period, and that this increase may lead to impaired foetal growth and postnatal development (Cecchi et al 2012).

v) A case-control study, involving 2,348 incident lymphoma cases and 2,462 controls in 6 European countries, found a significantly increased risk (odds ratio 2.7) of chronic lymphocytic leukaemia with occupational exposure to OPs (Cocco et al 2012).

vi) People that have been exposed to acute or chronic levels of OP compounds exhibit long-term alterations in neuropsychological performance that mainly affect cognitive processes, such as speed of processing, visual attention, visuoperceptual abilities, memory impairment and problem solving (Moreno et al 2008).

vii) Low doses of OPs that do not inhibit acetylcholinesterase have also been associated with neurological dysfunction, including clinically significant

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extrapyramidal symptoms, anxiety, depression (Salvi et al 2003).

7. A number of studies show that low-level neonatal exposure to OPs can lead to mis-programming of metabolism, appetite and endocrine status leading to obesity, type-2 diabetes, and metabolic disease (Newbold et al 2007; Lassiter & Brimijoin 2008; La Merrill & Birnbaum 2011; Slotkin 2011). OP exposure has been shown repeatedly to be associated with hyperglycaemia in animal models (Montgomery et al 2008; Rezg et al 2010); and to increase the risk of obesity in both laboratory studies and epidemiological studies (Rezg et al 2010).

8. For many of the OPs, exposure to even low levels during prenatal and early childhood developmental periods can have a profound effect on neurodevelopment of the child, producing effects that in some cases last into adulthood. This includes chlorpyrifos and diazinon. OPs can cross the placenta, and exposure of pregnant women results in exposure of the developing foetus, as evidenced by contamination of meconium with chlorpyrifos, diazinon, and malathion (Barr et al 2007; Ostrea et al 2009). Chlorpyrifos, diazinon, malathion, and terbufos have also been found in umbilical cord blood (Wickerham et al 2012); dichlorvos, malathion, phorate, profenofos and terbufos in neonate plasma (Whyatt et al 2003); and chlorpyrifos, chlorpyrifos-methyl, diazinon, dichlorvos, dimethoate, and malathion in breast milk (Gandhi & Snedeker 1999; Cal EPA 2008; Srivastava et al 2011; Weldon et al 2011; Sanghi et al 2003).

9. Genetic polymorphisms for the detoxifying enzyme paraoxonase (PON 1) render some people much more susceptible to OPs than other people, and at much greater risk of developing ill health following exposure. For example, as a result of PON 1 variations, the range for chlorpyrifos sensitivity can be as much as 35-fold among mothers and 65-fold among newborns; and newborns can be 164 times more vulnerable than adults to OPs (Furlong et al 2006). Manthripragada et al (2010) found increased risk of Parkinson’s disease when exposed to diazinon or chlorpyrifos, and the risk increases for those carrying the PON1-55 variation. Has the occurrence of these polymorphisms in the New Zealand population been taken into account?

10. ERMA’s exposure assessment for bystanders most likely has not included exposure via house dust, a route that is of particular importance for children. This assumption is based on EPA’s failure to include this route of exposure in previous assessments. Numerous studies in the USA show the ubiquitous nature of organophosphate contamination of children and their homes in areas where the OPs are used:

i) Diazinon is commonly detected in the urine of US farmworkers’ children (Arcury et al 2007; Curwin et al 2007).

ii) In a pilot study in California, Bradman et al (1997) found diazinon and chlorpyrifos on the hands of farmworkers’ children.

iii) In the US state of Washington, OP metabolites have been detected in 47 percent of the urine samples of young children living in pesticide applicators’ households compared with 27 percent of samples from children in non-

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applicator households, and at levels four times higher in the applicators’ children. The younger the child the higher the level of contamination even within the same family (Loewenherz et al 1997).

iv) In another study chlorpyrifos was measured in the house dust of all homes tested; but concentrations were highest for applicator homes, followed by farm-worker homes, followed by non-agricultural homes. Chlorpyrifos was found on the hands of 11 percent of the agricultural children (Fenske et al 2002).

v) In Salinas Valley, California, chlorpyrifos and diazinon were detected in up to 90 percent of dust samples in farmworker houses (Bradman et al 2007).

vi) In another study in California, chlorpyrifos and diazinon were found in carpet dust in over 90 percent of rural households, with carbaryl in 84 percent, and phosmet less frequently (Gunier et al 2011).

vii) A study of apple and pear orchard workers in Washington State, USA, and their families found metabolites of OPs in 93 percent of the children, with similar frequency of detection in house dust and vehicles (Coronado et al 2006).

viii) Ambient community air monitoring data from agricultural regions of California showed that short-term chlorpyrifos exposure estimates exceeded the Acute Reference Dose for 50 percent of children; and non-cancer risks were higher for children than adults (Lee et al 2002).

ix) One study in the US state of Washington found that pesticide contamination of dust in vehicles used by farmworkers to get to and from work was even greater than in their homes. Malathion, phosmet, chlorpyrifos and diazinon were found in houses and vehicles (Curl et al 2002).

Uses

11. It seems that EPA has relied on sector assessments of needs for their (EPA’s) determination of whether the pesticides are necessary or not, without adequate independent analysis of this information. For example, the consultation report APP20145 (page 28) states that 100% of onion growers use chlorpyrifos. This is clearly nonsense for New Zealand has a number of certified organic onion growers, including this author, who do not use chlorpyrifos, or other OPs or carbamates, or other synthetic chemical insecticides. The vast array of needs put forward by the industry sectors should be regarded with a degree of scepticism. For example, the pipfruit sector has said it uses/needs chlorpyrifos, diazinon, dimethoate, Maldison/malathion, and prothiophos to control 21 different pests, yet pipfruit scientist Jim Walker (New Zealand Institute of Plant and Food Research), in his presentation to the 2012 OECD seminar on IPM in Queenstown, stated that no OPs are used in the pipfruit sector in New Zealand anymore, and haven’t been used since 2010. It appears the lists provided by the sectors may be a ‘wish list’, a ‘just in case list’ or a ‘lets keep it registered list’, and does not truly reflect actual usage or needs. The sector lists contain 121 crop/pest uses for chlorpyrifos including 13 for pipfruit, which are clearly outdated, and others for such vague things as ‘chewing pests’. PAN ANZ has provided, in Annex B, safer available alternatives for all these uses.

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12. Additionally, the information on critical uses in the Consultation Report is inconsistent: Table 2 contains different critical uses to those in the following text descriptions of each OPC. Many of the so-called critical uses in Table 2 mention only the generic crop sector, e.g. ornamentals, and not the pest. These critical uses have been ignored because it is impossible to find alternatives for unknown pests on unknown plants; critical uses contained in the text have been addressed.

13. Many of the pests for which growers have claimed they need OPCs can be controlled effectively by biological controls such as pathogens, predators and parasitoids, together with other nonchemical techniques such as mating disruption and pheromone traps. Many of the growers seem to be unaware of these techniques or not prepared to try them. Removing the crutch of highly ecotoxic OPCs will assist them to make the change to more sustainable pest management practices.

Benefits

14. In terms of benefits to society and communities, EPA refers (p 34-35, Consultation Report) to concern expressed by growers about what to grow and where to live if their use of OPCs is restricted. This cost would disappear if they were provided with information on alternatives. Removal of OPCs would have the effect of guiding growers to the use of safer alternatives, which should be seen as a benefit to society and communities. There is no evidence at all that removal of OPCs and their replacement with alternatives would lead to lower crop yield, or the inability to produce a specific crop, let alone change the makeup and vibrancy of local communities as suggested. Indeed it is more likely that a change to alternatives would lead to increased vibrancy of communities as less damage to health of users, their families, and the environment could be anticipated. Similarly, home gardeners are perfectly able to produce the full range of crops and ornamentals that they currently produce, without the use of OPCs, and they are likely to enjoy improvements to their health and well-being and that of their families by ceasing such use and replacing OPCs with nonchemical alternatives, especially organic ones. This author has been, for decades, a highly successful home gardener providing an abundance of a vegetables, fruit, and flowers without every having recourse to an insecticide, other than certified organic fish emulsion for black aphids on leeks and chives.

International obligations

15. In terms of international obligations, the EPA should be aware of the likelihood of chlorpyrifos being nominated to the POPS Review Committee of the Stockholm Convention, for assessment as a POP warranting global phase out. This nomination is expected to occur in time to be considered by next POPs Review Committee meeting in October 2013. Further information can be provided on request.

Ecological risks

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16. All OPCs with high bee toxicity should be phased out rapidly, as the EPA’s assumption that controls (i.e. restricted application times) will be effective in preventing risk to bees cannot be replied on. There is no compliance monitoring of such application times. EPA acknowledges that all OPCS are very toxic to terrestrial invertebrates such as bees.

17. As stated above, EPA has acknowledged that all OPCs are very toxic to terrestrial invertebrates, – this includes beneficial insects that act as valuable biological controls for pests if they are not obliterated by OPCs. But EPA has failed to acknowledge the risk of OPCs to biological controls, which are essential to the maintenance of the balanced agro-ecosystem that lies at the heart of modern, environmentally sustainable pest management. Most of the OPCs pose high risks to predators and parasitoids. They also needlessly destroy myriads of other harmless invertebrates, many of then indigenous. Airblast spraying and aerial spraying in particular give rise to a high risk of agroecological disruption and destruction of birds and invertebrates beneficial to the wider environment.

18. All outdoor uses of OPCs that create risks for birds should be rapidly phased out. EPA acknowledges risk to birds from many of the OPCs, yet fails to acknowledge the worth of birds in our ecosystem or even that on animal welfare grounds they should not be poisoned. It is unacceptable for EPA to recommend a 10-year phase-out period for diazinon when at the same time it acknowledges that the majority of uses of diazinon pose high risk to birds and describes poisoning incidents.

Controls and phase out

19. PAN ANZ agrees with ERMA that all users of OPCs be required to be approved handlers, and that all home garden uses are phased out. In our view this should be in 1 month, with home gardeners notified through media including gardening magazines, garden centres, and other outlets selling pesticides. Provision should be made for collecting unused product from gardeners.

20. Further PAN ANZ submits that aerial application of all OPCs should be phased out in 1 month because of ecological risks, as well as risks to bystanders.

21. PAN ANZ cannot agree with EPA that 3 years is short-term and 5 years is medium term with regards to phase-out time. We see 5 years as long term, 18 mths to 3 years as medium term, and 1-12 months as short term.

22. The approval for chlorpyrifos-methyl should be revoked. The products in which chlorpyrifos-methyl is used are not identified, nor is their destination. However, given that it is not used in New Zealand but residues are constantly found in grain products in the Total Diet Surveys, it seems that New Zealand’s exported chemical is finding its way back home in our food.

23. PAN ANZ would like to see the complete phase-out of all OPCs. However, recognising the importance of biosecurity tools, we propose retaining dichlorvos and malathion for biosecurity traps and baits only; and fenamiphos and pirimiphos-methyl for emergency indoor biosecurity use

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only. Fenamiphos and pirimiphos-methyl have been chosen because, of the OPCs currently used for this purpose according to EPA’s consultation document, they are the only ones without mutagenic, carcinogenic and/or endocrine disrupting properties. Oxamyl or phorate could be considered instead.

Recommendation

24. Lastly, PAN ANZ suggests that EPA, in making its decision on the OPCs, makes recommendations on the provision of information to growers on how to foster and release beneficial insects such as parasitoids and predators, and how to make use of pathogens, mating disruption, pheromone traps and other nonchemical methods of pest management that do not create risks for humans or the environment, but which will greatly ease pest pressure for farmers moving off OPC use.

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3. SPECIFIC PESTICIDES 3.1 Acephate Decision sought: phase-out home use in 1 month; phase-out all other use in 18 months, with the exception of citrus and indoor biosecurity uses which should be phased out in 3 years. All proposed controls, and the addition of R-7 Aerial application prohibited, should apply in the interim. Reasons: carcinogenicity, endocrine disruption, high toxicity to bees; risks to humans, birds, bees, biological controls and other non-target insects, and aquatic organisms. Acephate is a possible carcinogen – US EPA Group C for liver adenomas and carcinomas (NPIC). It is an EU designated endocrine disruptor1 and a Tier 1 chemical for endocrine disruptor testing in USA (NPIC). It causes hyperglycaemia, adrenal cortex hyperactivity, increased serum corticosterone and aldosterone levels, increased corticotropin releasing factor expression and release, and decreased serotonin levels (NPIC). It is a neurotoxicant (IUPAC). In 2002 the European Commission withdrew authorisation of acephate for use in plant protection because of concerns about acute consumer exposure and non-target organisms, in particular non-target arthropods, birds and mammals, as well as aquatic organisms (EC 2002). NZ EPA identified medium risk to birds. The only critical use identified was for citrus flower moth on Yen Ben lemons. If mating disruption is not proving sufficiently effective, further research should be carried out to improve its efficiency. Lures and traps are commercially available from Etec Crop Solutions2, so it seems likely they are proving effective for some growers at least. Since citrus flower moth is a Lepidoptera, Bacillus thuringiensis should be effective against it, as should azadirachtin, and Beauvaria bassiana.3 3.2 Carbaryl Decision sought: phase out home use in 1 month; phase-out all other uses in 18 months. All proposed controls, and the addition of R-7 Aerial application prohibited, should apply in the interim. Reasons: carcinogenicity, endocrine disruption, high bee toxicity; risks to humans, birds, biological controls and other non-target insects, and aquatic organisms. Carbaryl is classified by US EPA as likely to be a carcinogen for humans based on malignant vascular neoplasms in female mice (NPIC). It is an EU carcinogen (IUPAC), and an EU

1 EU Regulation 1272/2008/EC 2 http://www.elliottchemicals.co.nz/products/pest57.html 3 http://www.plantwise.org/?dsid=43910&loadmodule=plantwisedatasheet&page=4270&site=234

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endocrine disruptor4. It causes reduced sperm motility and count and increased abnormal sperm in rats (NPIC). The Agricultural Health epidemiological study in the US found an increased odds ratio of 4.11 for melanoma (Weichenthal et al 2010). A population-based case-control study in Canada found an increased odds ratio of 1.89 for multiple myeloma (Pahwa et al 2012). A case-control study in Canada found an odds ratio of 1.54 for prostate cancer (Band et al 2011). Exposure to carbaryl has been linked to childhood brain cancer (Zahm & Ward 1998). Elevated risks of non-Hodgkin’s lymphoma were found amongst men occupational exposed to carbaryl in the USA (Cantor et al 1992). In 2006 the European Commission (EC 2006) revoked approval for carbaryl for plant protection because of: • the toxicity of breakdown products • potential carcinogenic properties of the active substance • high long-term risk for insectivorous birds • high acute risk to herbivorous mammals • high acute and long-term risk to aquatic organisms • high risk for beneficial arthropods. No critical uses were identified by EPA.

3.3 Chlorpyrifos Decision sought: phase out use of granules in 1 month; phase out home uses in 1 month; phase out all other uses within 18 months. All proposed controls, and the addition of R-7 Aerial application prohibited, should apply in the interim. Reasons: potential POP, undergoes long-range transport and is a common pollutant in Arctic regions, measured also in the Southern Alps; potent developmental neurotoxin, endocrine disruptor; evidence of genotoxicity, mutagenicity, carcinogenicity, immune toxicity, teratogenicity, Parkinson’s disease, diabetic risk; high bee toxicity, high aquatic toxicity; risks to humans especially children, bees, birds, biological controls and other non-target insects, aquatic organisms, Arctic animals and people, Antarctic animals. Chlorpyrifos residues are found in meconium (Barr et al 2007; Ostrea et al 2009), umbilical cord blood (Wickerham et al 2012), and breast milk (Weldon et al 2011). Chlorpyrifos meets the criteria for a Persistent Organic Pollutant and is likely to be nominated to the Stockholm Convention’s POPs review committee in 2013 for assessment for global phase-out. As well as its widespread occurrence in Arctic media resulting from long range transport (refer Annex A), chlorpyrifos is also subject to regional transport, and has been measured in air in the Southern Alps, presumed to have originated from uses in Canterbury, and detected on 25% of sampling days, at levels of up to 12 pg/m3 (Lavin et al 2012). Chlorpyrifos was 1 of the 4 most frequently detected pesticides, the others being dieldrin, chlordane and endosulfan, all now banned.

4 EU Regulation 1272/2008/EC

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Chlorpyrifos is still registered in the EU, but its reassessment, currently underway, has been brought forward because of concerns about developmental neurotoxicity.5 It has also identified high risk to birds and small herbivorous mammals, and concerns about aquatic organisms and non-target arthropods (EPA Application doc). The EPA’s conclusion that risks are negligible failed to take into account the wealth of information on developmental neurotoxic effects at low levels of exposure. EPA did not identify any critical uses, and in fact concluded that most uses confer a low level of benefit. Alternatives are available for all uses – refer Annex 2. PAN ANZ does not agreed with EPA’s view that chlorpyrifos has a high level of economic benefit simply because its use is widespread. All those uses can be replaced with safer alternatives, therefore the level of economic benefit is low. EPA identified high risk to birds especially through use of granules. This use should be phased out immediately; all home uses should be phased out immediately because of the developmental neurotoxic effects. Refer Annex A for full assessment of chlorpyrifos, and Annex B for alternatives to uses identified in sector reports.

3.4 Diazinon Decision sought: phase-out granules in 1 month; phase-out home use in 1 month; phase out all other uses with high risks to birds in 1 year; all remaining uses in 3 years. All proposed controls, and the addition of R-7 Aerial application prohibited, should apply in the interim. Reasons: endocrine disruptor, developmental neurotoxin, cancer, high bee toxicity; risks to humans, birds, biological controls and other non-target insects, fish, aquatic invertebrates. EPA stated that the majority of uses carry high risk to birds. Diazinon is an EU endocrine disruptor6. It is a neurotoxicant, respiratory tract irritant, skin irritant and eye Irritant (IUPAC). Foetal exposure occurs following maternal exposure: residues have been found in meconium (Barr et al 2007; Ostrea et al 2009) and umbilical cord blood (Huen et al 2012; Wickerham et al 2012). It has also been found in breast milk (Cal EPA 2008).

Numerous studies have linked exposure to organophosphates with various forms of childhood cancer. Case-control studies have linked it to childhood brain cancer (Zahm & Ward 1998). Case control studies have found increased risk of childhood cancers from exposure in home gardening (Davis et al 1993); and non-Hodgkin’s lymphoma with occupational exposure in at least 3 studies (Cantor et al 1992; Waddell et al 2001; De Roos et al 2003). In a prospective cohort study of 4,961 licensed pesticide applicators in the USA who reported using diazinon, 301 incident cancer cases were diagnosed during the follow-up period, compared with 968 cases among 18,145 participants who reported no use. Increased risks for lung cancer and leukaemia were observed (Freeman et al 2005). It has

5 http://www.pan-europe.info/News/PR/121009.html 6 EU Regulation 1272/2008/EC

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been found to be mutagenic in mouse lymphocyte cells (McGregor et al 1988), and genotoxic in human cells (Tisch et al 2002).

Diazinon alters oestrogen-regulated gene expression in MCF-7 human breast cancer cells, disrupting their ability to repair DNA damage (Mankame et al 2006), and it may contribute to breast cancer risk by this mechanism. Diazinon is a developmental neurotoxin. Exposure impairs foetal growth in humans (Whyatt et al 2004). Doses of diazinon given to newborn rats at levels below those that tigger changes to acetylcholinesterase were sufficient to cause changes in the developing brain: the effect was on emotional responsiveness and cognitive function with changes in the developing brain that correspond to neurodevelopmental delays (Slotkin et al 2008a). Diazinon interferes with sexual differentiation of the brain, narrowing or eliminating many of the normal sex differences in behavioural and/or neurochemical parameters (Slotkin et al 2008b). Prenatal exposure of mice to diazinon caused transcriptional changes in gene expression associated with Parkinson’s disease (Slotkin & Seidler 2011). Manthripragada et al (2010) found increased risk of Parkinson’s disease with exposure to diazinon (odds ratio 1.55, increasing to 2.24 for those carrying the PON1-55 genetic variation). Diazinon caused developmental immunotoxicity in rats (Holladay & Smialowicz 2000). Neonatal exposure of both male and female rats to diazinon resulted in diabetes-like metabolic dysfunction in adult rats (Adigun et al 2010). It is moderately to highly toxic to fish, and has resulted in fish kills overseas, very highly toxic to aquatic invertebrates, very highly toxic to birds, and highly toxic to bees and beneficial insects (NPIC). The EPA acknowledges in its application document that diazinon is responsible for numerous bird deaths of waterfowl after treatment for grass grub, including an incident as recently as April 2012. The EU revoked approval for diazinon in 2006 (EC 2006) because of concerns with regard to: • operator exposure although a high degree of personal protective equipment is used • workers and bystanders • consumer exposure • acute risk to insectivorous birds • long-term risk to insectivorous mammals • high toxicity to aquatic organisms. EC (2006) also noted the presence of very toxic impurities, which were not analysed in the their toxicological and ecotoxicological risk assessment – did NZ EPA analyse them, or include them in their risk assessments? Critical uses identified by NZ EPA are for apple leaf curling midge, and for grass grub. It is hard to imagine that apple leaf curling midge is a critical use, as according to the presentation made to the OECD seminar on IPM in Queenstown, Nov 2012, by pipfruit scientist Jim Walker (New Zealand Institute for Plant and Food Research), OPs have not been used on apples since 2010. There are other less hazardous chemicals registered in

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New Zealand for this midge; for example spirotetramat (Movento). Neem granules are available for grass grub and porina control, as is neem oil. Deepak (a blend of eucalyptus and tea tree oils) may be useful on sports and ornamental turf.7 Biological controls for grass grub include the bacterium Serratia entomophila.8 Additionally a biopesticide based on the bacterium Yersinia entomophaga, developed by AgResearch, is in the process of being registered.9

3.5 Dichlorvos Decision sought: phase-out home uses in 1 month; phase-out all uses except biosecurity strips in 1 year; retain biosecurity strips until less harmful alternative is found. All proposed controls should apply in the interim, and in addition notification of neighbours, and buffer zones. Reasons: high acute toxicity (fatal if inhaled, swallowed or absorbed through the skin -IUPAC), carcinogenicity, diabetes, high bee toxicity; risks to humans, birds, bees, biological controls and other non-target insects, aquatic organisms. Dichlorvos is classified by the EU as R26 very toxic by inhalation, an IARC possible carcinogen (2b), a US EPA possible carcinogen but probable by oral route of exposure, causing forestomach tumours, leukaemias, pancreatic acinar adenomas and mammary gland tumours in adult rodents (US EPA 2007). The IUPAC Footprint database lists it as a known mutagen. It has been found to be mutagenic in a number of studies, including in human cells (e.g. Aquilina et al 1984), and Chinese hamster ovarian cells (e.g. Oshiro et al 1991). Epidemiological studies have indicated increased risk of childhood leukaemia (Zahm & Ward 1998), non-Hodgkin’s lymphoma amongst men occupationally exposed (Cantor et al 1992), multiple myeloma (Brown et al 1993) and childhood brain cancer (Davis et al 1993) from exposure to dichlorvos. A number of laboratory studies have shown elevated rates of mammary tumours in rodents. It has been found in breast milk in Taiwan (Gandhi & Snedeker 1999). Dichlorvos has been shown to disrupt glucose homeostasis in male rats (Sarin & Gill 1999). Applicators exposed to dichlorvos had increased odds of diabetes and the odds increased with increasing cumulative days of use (Montgomery et al 2008). In the Agricultural Health Study, USA, Engel et al (2005) found slightly increased risk of breast cancer associated with husbands’ and women’s own use of dichlorvos in Iowa. There is also evidence dichlorvos may be an endocrine disruptor: in a study in China, male rats were exposed to a mixture of the OPs dichlorvos, dimethoate and malathion before mating with females, who were subsequently exposed to the same pesticides during gestation and lactation. The offspring, when sexually mature, had abnormal levels of progestin, estradiol, testosterone, and luteinizing hormone. Females had enlarged uteruses and males enlarged testes and epididymis, and there was a reduction in rates of pregnancy and live births (Yu et al 2011).

7 http://www.greenlink.co.nz/lawnguru-news/article/grass-grub-prevention 8 http://www.teara.govt.nz/en/insect-pests-of-crops-pasture-and-forestry/4/2; http://www.teara.govt.nz/en/agricultural-and-horticultural-research/9/2 9 http://www.agresearch.co.nz/news/pages/news-item.aspx?News-id=12-11-23-01

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The European Union phased it out in 2006, citing concerns about uncertainties of genotoxicity and carcinogenicity (EC 2006). No critical uses were identified other than for biosecurity strips. 3.6 Dimethoate Decision sought: phase-out all outdoor uses in 18 months; phase-out all other uses in 3 years. All proposed controls, and the addition of R-7 Aerial application prohibited, should apply in the interim. Reasons: carcinogenicity, endocrine disruption, high bee toxicity; risks to humans, birds, bees, biological controls and other non-target insects, aquatic organisms. Dimethoate is a US EPA possible carcinogen, and EU endocrine disruptor10. It disrupts steroidogenesis in Leydig cells and may impair reproductive function (Walsh et al 2000), and affects the thyroid preventing the release of thyroid hormone and the conversion of T4 to T3 (Colborn 2004). It has immunotoxic effects, for example in female mice (Aly & el-Gendy 2000). It is teratogenic in chickens, producing abnormal development of brain, heart, neural tube and somites (Alhifi et al 2008). Dimethoate has been found in breast milk (Srivastava et al 2011). In a study in China, male rats were exposed to a mixture of dichlorvos, dimethoate and malathion before mating with females, who were subsequently exposed to the same pesticides during gestation and lactation. The offspring, when sexually mature, had abnormal levels of progestin, estradiol, testosterone, and luteinizing hormone. Females had enlarged uteruses and males enlarged testes and epididymis, and there was a reduction in rates of pregnancy and live births (Yu et al 2011). No critical uses were identified, except aphid control in fodder and forage. There are a number of biological control options available in New Zealand for aphids, including Aphidius colemani, Aphidoletes aphidimyza, Orius vicinus, best utilized in conjunction with Integrated Pest Management techniques.

3.7 Fenamiphos Decision sought: phase-out all uses with high risk to birds in 1 year; all other uses in 3 years. All proposed controls should apply in the interim. Reasons: high acute toxicity; highly toxic to bees; high risk to birds; risk to humans, bees, biological controls and other non-target insects, aquatic organisms; high potential for groundwater contamination (metabolite). Not approved in USA, Canada; used only in drip irrigation in Europe.

10 EU Regulation 1272/2008/EC

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‘Critical uses’ – potatoes, carrots, parsnip, turf - carrot rust fly and Argentine stem weevil, nematodes. There are a number of cultural practices that can dramatically reduce the burden of carrot rust fly, including crop rotation, crop hygiene, timing of plantings, mulching, floating crop covers, interplanting, etc. Biological controls include predatory ground beetles.11 The parasitic wasp Microctonus hyperodae is a biological control for Argentine stem weevil.12 The biological control Hyper-Mite™ (a predator) is said to be useful in controlling nematodes (http://www.bioforce.net.nz/products/Hyper-Mite.html).

3.8 Fenitrothion Decision sought: phase out all uses in 18 mths. Controls in the interim should include R-7 Aerial application prohibited, buffer zones, and notification of neighbours. Reasons: endocrine disruptor, highly toxic to bees; risk to humans, birds, bees, biological controls and other non-target insects, aquatic organisms. EU endocrine disruptor13. It is anti-androgenic (Orton et al 2011). It has been banned in the EU because of unacceptable risk to operators and workers, consumers, and aquatic and terrestrial organisms; used only in bait stations in the US (EPA Consultation document). ‘Critical’ uses: late stage porina control in arable, pasture, forage and fodder crops. Late stage porina can be controlled with azadirachtin/neem.14

3.9 Maldison / malathion Decision sought: phase out home uses in 1 month; phase out all other uses in 3 years, except biosecurity baits. All proposed controls, and the addition of R-7 Aerial application prohibited, should apply in the interim. Reasons: carcinogenicity, endocrine disruption, immune toxicity, high bee toxicity; risk to humans, bees, birds, biological controls and other non-target insects, aquatic organisms. US EPA possible carcinogen, EU endocrine disruptor. Both malathion (Giri et al 2002) and its metabolite malaoxon (Blasiak et al 1999) have has been shown to be genotoxic in human cells, as well as causing chromosomal aberrations in mouse bone marrow cells (Amer & Fahmy 2004). US EPA (2000) reported liver tumours. In a subsequent study (Cabello et al 2001) it caused mammary tumours in rats. It increased

11 http://www.organicfarm.org.nz/wp-content/uploads/2010/02/Canterbury-Regional-Workshop-07-Pest-Management.pdf 12 http://www.trc.govt.nz/assets/Publications/information-sheets-and-newsletters/land-management-information-sheets/09argentinestemweevil2.pdf 13 EU Regulation 1272/2008/EC 14 http://www.greenlink.co.nz/lawnguru-news/article/grass-grub-prevention

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cell proliferation of terminal end buds of the mammary gland of rats, followed by formation of mammary tumours in 24 percent of cases. These effects were associated with a reduction in acetylcholinesterase activity, and the authors concluded that malathion induces changes in the epithelium of the mammary gland stimulating the process of carcinogenesis, and this effect occurs as a result of increasing cholinergic stimulation (Cabello et al 2001). Malathion increases PCNA and induces mutant p53 protein expression of MCF-7 breast cancer cells, thus inducing the progression of breast cancer cells (Cabello et al 2003). Exposure to malathion has also been linked to non-Hodgkin’s lymphoma in Canada (McDuffie et al 2001), and the USA (Cantor et al 1992). Mills & Yang (2005) found increased risk of breast cancer associated with exposure to malathion in a case-control study of breast cancer in Hispanic agricultural workers in California, involving 128 breast cancer cases newly diagnosed in 1988–2001 and 640 cancer-free controls. Koutros et al (2012) found a significant association between exposure to malathion and aggressive prostate cancer (risk ratio 1.43). There is also evidence malathion may be an endocrine disruptor: in a study in China, male rats were exposed to a mixture of the OPs dichlorvos, dimethoate and malathion before mating with females, who were subsequently exposed to the same pesticides during gestation and lactation. The offspring, when sexually mature, had abnormal levels of progestin, estradiol, testosterone, and luteinizing hormone. Females had enlarged uteruses and males enlarged testes and epididymis, and there was a reduction in rates of pregnancy and live births (Yu et al 2011). Malathion adversely effects thyroid (Colborn 2004).

Maternal exposure of pregnant women during the second trimester to malathion from aerial

spraying for Mediterranean fruit fly in the San Francisco area is associated with gastrointestinal

anomalies in newborns (Thomas et al 1992).

Malathion is found in meconium (Barr et al 2007; Ostrea et al 2009), umbilical cord blood (Wickerham et al 2012); neonate plasma (Whyatt et al 2003); and in breast milk (Sanghi et al 2003; NPIC). According to Finkelstein et al (2010) malathion was banned in Israel in 2009. It had been mainly used for controlling Mediterranean fruit fly and this use was replaced with spinosad and sterile male release, as part of Israel’s policy of replacing highly toxic substances with less toxic ones (personal communication with the author of the paper, Professor Finkelstein of the Shaare Zedek Medical Center). Critical uses: crickets in kumara and pasture; important for greenhouse thrips on citrus. There are a variety of biological controls for crickets, including Metarhizium anisopliae (Milner & Rowland 1998), Steinernema carpocapsae, S. feltiae, Heterrohabditis indica or H. basteriophora (Mahar et al 2012) and the parasitic fly Ormia ochracea (Thomson et al 2012). It is not known if any of these are currently available in New Zealand, or if there are other available biological controls that could be used instead. Thrips can be controlled by a wide variety of means, including Amblyseius cucumeris, Orius vicinus, azadirachtin/neem, silicon dioxide, polysaccharides (Agri-50NF), mineral oil, Eco-oil®, and taufluvalinate.

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3.10 Methamidophos Decision sought: phase out home uses in 1 month; phase out all uses in 18 months. All proposed controls, and the addition of R-7 Aerial application prohibited, should apply in the interim. Reasons: high acute toxicity, mutagenic, reproductive and developmental toxin; highly toxic to bees; risks to humans, bees, birds, biological controls and other nontarget insects, aquatic organisms. It is classified by the EU as R26 very toxic by inhalation. It is not approved in US, EU, Australia, Canada, China. It has been banned in Brazil, reportedly because the National Sanitary Surveillance Agency (ANVISA) has characterized it as being neurotoxic, immunotoxic and endocrine disrupting.15 No critical uses identified.

3.11 Methomyl Decision sought: phase out home uses in 1 month; phase out all outdoor uses in 1 year; phase out for greenhouse crops in 3 years. All proposed controls, and the addition of R-7 Aerial application prohibited, should apply in the interim. Reasons: high acute toxicity, endocrine disruption, highly toxic to bees; risks to humans, birds, bees, biological controls and other nontarget insects, aquatic organisms.

EU endocrine disruptor. In male rats it significantly decreased fertility, weight of testes, and

accessory male sexual glands, serum testosterone, and sperm mobility and count, and increased abnormal sperm (Shalaby et al 2010). Maternal residence near the use of methomyl is associated with neural tube defects (Rull et al 2006). No critical uses identified. 3.12 Oxamyl Decision sought: phase out home uses in 1 month; phase out all outdoor uses in 3 years; retain for greenhouse crops. All proposed controls should apply in the interim. Reasons: high acute toxicity, high bee toxicity; risk to birds, bees, biological controls and other nontarget insects, aquatic organisms.

15 http://www.farmchemicalsinternational.com/news/?storyid=2925&style=1; http://news.agropages.com/News/NewsDetail---3390.htm; http://www.agrow.com/markets/southamerica/Brazil-bans-methamidophos-308823?autnRef=/contentstore/agrow/codex/f4a86e68-22ec-11e0-92f3-cf1dfcf723f1.xml

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Very toxic by inhalation (EU R26). ‘Critical’ uses: carrot rust fly. There are a number of cultural practices that can dramatically reduce the burden of carrot rust fly, including crop rotation, crop hygiene, timing of plantings, mulching, floating crop covers, interplanting, etc. Biological controls include predatory ground beetles.16

3.13 Phorate Decision sought: phase out home uses in 1 month; phase out all uses in 6 months. R-7 Aerial application prohibited, should apply in the interim. Reasons: high acute toxicity; highly toxic to bees; high risk for birds, bees, biological controls and other nontarget insects, aquatic organisms. EPA has identified high risks for birds from all uses. Not approved in EU, Canada. No critical uses identified.

3.14 Pirimicarb Decision sought: phase out home uses in 1 month; phase out all uses with risk to birds in 1 year; all other uses in 3 years. All proposed controls, and the addition of R-7 Aerial application prohibited, should apply in the interim. Reasons: carcinogenicity, persistence; risks to humans, birds, aquatic organisms. US EPA probably human carcinogen. EU identified concerns about haematological effects, anaemia, and lung tumours in mice. Very persistent in sediment, with only limited degradation. 17 Not approved in USA and Canada; use on wheat only in EU. No critical uses identified.

3.15 Pirimiphos-methyl Decision sought: phase out all outdoor uses in 1 year; retain for empty grain silos and emergency indoor biosecurity uses. All proposed controls, and the addition of R-7 Aerial application prohibited, should apply in the interim.

16 http://www.organicfarm.org.nz/wp-content/uploads/2010/02/Canterbury-Regional-Workshop-07-Pest-Management.pdf 17 http://www.efsa.europa.eu/de/scdocs/doc/43r.pdf

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Reasons: highly toxic to bees; risk to bees, biological controls and other nontarget insects birds, aquatic organisms. It is not approved in Canada, and approved only for empty cereal stores in the EU, and buildings and stored grain in Australia. Critical uses: Grain silos.

3.16 Prothiofos Decision sought: restrict to use on grapes for 3 years; phase-out all other uses in 18 mths. All proposed controls should apply in the interim. Reasons: risks to operators, re-entry workers, bystanders, birds, aquatic organisms; high Kow indicating high potential for bioaccumulation. Not approved in EU, USA or Canada. ‘Critical’ uses: mealy bug in Nth Island grape vines. Biological controls for mealy bug in New Zealand vineyards include the parasitoids Tetracnemoidea breviconis, Coccophagus gurneyi and Anagyrus fusciventris.18 3.17 Terbufos Decision sought: phase out all uses in 1 year. Controls in the interim should include R-7 Aerial application prohibited. Reasons: very high acute toxicity; risks to birds, biological controls and other nontarget insects. Not approved in EU, Canada.

4. Concluding remarks All OPCs pose unacceptable risks to birds, bees, beneficial insects and other non-target insects, and many also poses risks to aquatic organisms. Additionally, many are carcinogenic, endocrine disruptors, and/or neurodevelopmental neurotoxins. Many carry additional risk to humans. There are nonchemical and less hazardous chemical options available for most if not all uses. For this reason all home garden use and aerial spraying should cease immediately; all outdoor uses cease as soon as possible; and indoor uses be phased out rapidly except where some biosecurity uses need to be retained.

18 http://www.skeltons.co.nz/files/docs/grapevine%20intelligence%20july%2009%20web%203.pdf

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