Comment submitted by L. Parks

Loretta Parks 26 Berkley Dr. Downingtown, PA 10335 April 7, 2008 Environmental Protection Agency 1200 Pennsylvania Ave. Washington DC 20460-0001 RE: Docket ID: EPA-HQ-OPP-2007-0674 To Whom It May Concern: I am writing in response to EPA’s call for comments for the proposed tolerance actions for 2, 4-D, Bensulide, DCPA, Desmedipham, Dimethoate, Fenamiphos, Phorate, Sethoxydim, Terbufos, and Tetrachlorvinphos. My research and comments are directed towards the proposed actions for dimethoate. As a professional in the public health field and concerned citizen, I’ve found the research data demonstrating the harmful effects of dimethoate to be quite disturbing. I fully support EPA’s proposed action to revoke certain tolerance levels for dimethoate and establish tolerance level for animal forage products. Thank you for your consideration. Under Federal Registrar Docket: EPA-HQ-OPP-2007-0674, the EPA has proposed revoking the tolerance levels for combined dimethoate residuals on apples, cabbage, collards, grapes, lentils, seeds, spinach and leaf lettuce. Additionally, the EPA is seeking to revise the combined dimethoate residual levels for alfalfa, corn, grain, forage products and turnip tops to 2.0ppm. Dimethoate has been registered as a general use insecticide with the EPA since 1956. Based on several evaluations conducted by the Environmental Protection Agency, Food and Agriculture Organization, and World Health Organization the tolerance levels for dimethoate residuals have been drastically reduced and banned on particular food products over the years. Scientific research has clearly demonstrated several adverse human health effects and ecological threats associated with the usage of dimethoate including mutagenic, teratogenic, and possible carcinogenic effects in humans. Dimethoate is also highly toxic in the environment, harming terrestrial animals and aquatic ecosystems. Upon reviewing the scientific data, I’ve concluded that dimethoate presents an immense hazard to humans and the environment. Based on my research outlined in this paper, it’s essential that we reduce the usage of dimethoate to protect public health. Therefore, I fully support EPA’s proposal to revoke the usage of dimethoate on particular food products and establish a new residual limit of 2.0ppm for animal feed crops. Background and Environmental Fate Dimethoate is an organophosphate insecticide utilized to kill mites, insects, houseflies, and botflies on livestock. The Environmental Protection Agency has listed dimethoate as a Toxicity Class II, for general use. It is applied using a variety of methods including: aerosol spray, dust, emulsifiable concentrate, ULV concentrates formulation, and aerial spraying. One of the major concerns associated with dimethoate is the degradation of the product and its formation of metabolites in the environment and animals. The metabolites can potentially be toxic to mammals and aquatic species. In various root plant and fruit studies analyzed by the FAO and WHO, they found that dimethoate breaks down within one day and forms an oxygen analogue known as omethoate. Omethoate is highly persistent in the environment and degrades as a much slower rate than dimethoate. The half life for omethoate is approximately 9 days. Although omethoate is considerably more toxic than Dimethoate with an LD50 of 25 mg/kg of body weight in rats, the metabolite residual levels are extremely low in the environment. Dimethoate has been found to rapidly degrade within the first 7 days; however, low levels of the pesticide have been detected in products for up to 35 days. Based on the low metabolite levels and toxicity data for dimethoate, the FAO and WHO concluded that residual levels should be measured as a combination of both dimethoate and its metabolites. Toxicological Effects Toxicological data for dimethoate clearly demonstrates that it presents a considerable risk to human health including mutagenic, teratogenic and possible carcinogenic effects. Although some of the health effects data is limited, there is enough research to substantiate the health hazards associated with dimethoate. Over the years research has concluded that dimethoate is non-carcinogenic, including the 1976 U.S. National Cancer Institute Study. Additional studies and the revaluation of existing research have prompted scientists and public health officials to reconsider their initial conclusion. The U.S. National Cancer Institute Study conducted in 1976 identified an increase in neoplastic and non-neoplastic lesions in mice orally fed dimethoate, but concluded there was no biological significance. Dr. Reuber (1982), along with other researchers have reviewed this study and discovered faults in the study design and conclusions. The first design flaw was the dose feeding levels for mice, the levels were extremely high with the lowest dose set at 250 ppm. The second flaw was limiting the histological sectioning of the liver to a single section; a minimum of four different sectional sites should have been examined. The development of lesions predominantly among male mice was considered to be statistically insignificant; however, many of the mice did not survive the full length of the study due to the high feeding doses so it’s difficult to assess whether those mice would have demonstrated the same effects. Further research has shown that dimethoate drastically reduces enzyme activity and promotes tumor growth, signifying that it is oncogenic and may be a possible human carcinogen. A study conducted by Sayim (2007) found significant changes in the liver and enzyme activity. Wistar albino rats were divided into three groups receiving oral doses of dimethoate ranging from 2mg/kg, 8 mg/kg and 20 mg/kg. Examination of the liver confirmed a decrease in weight, reduction in cholinesterase enzyme activity, degenerative changes in the liver, tissue inflammation and enlarged veins, along with the development of lesions. The study concluded that dimethoate may be extremely hazardous to non-target organisms, including humans. A second study examined by Reuber (1982) demonstrated possible carcinogenic effects in Wistar rats administered dimethoate for over a year. Dimethoate was administered by gavage or intramuscular at doses of 5 mg/kg, 15 mg/kg, and 30 mg/kg two times per week. The rats demonstrated a significant decrease in their lifespan and almost one third of the population displayed an increase in benign and malignant neoplasms. Based on the studies presented and additional available research, it is highly probably that dimethoate is a human carcinogen. Research confirming the reproductive and teratogenic effects of dimethoate in animal studies is quite concerning, especially since the side effects are so severe. Workers exposed to high doses of dimethoate and pregnant women are at the greatest risk. The Oregon State University toxicological database maintains extensive research data regarding the birth defects associated with exposure to dimethoate through drinking water. These defects include bone deformation, runting, physical disfigurement and overall growth and survival rates in both rodent and cat studies. In 2004, Alhifi and fellow researchers conducted a chicken embryo study examining the teratogenic effects associated with dimethoate. The pesticide was injected into embryo air sac at dosages of 2.5 ppm, 5ppm and 40ppm. The embryos were harvested after 48 hours to determine the effects. A second study group was exposed to a daily dose of dimethoate at 5ppm to examine acetylcholinesterase enzyme activity. Based on the study results complications were seen with the positioning and malformation of the heart at doses of 40ppm, brain development anomalies were detected at all three dose levels, and neural tube defects were seen at 40ppm. The repeated exposure to 5ppm of Dimethoate for two weeks demonstrated significant inhibition of AChE activity at 40%. Additional reproductive research by El-Aswad et al. (2007) assessed the reproductive toxicity of dimethoate in male mice. Significant adverse effects were seen in mice fed 15 mg/kg/day and 28 mg/kg/day of dimethoate for twenty days. During a reproductive evaluation the mice demonstrated a statistically significant decrease in the number of implantation sites and live fetuses, there was also a large decrease in the percentage of motile sperm. The histological examination showed a decrease in AChE levels, a reduction in brain and muscle activities, and testicular lesions. Both studies emphasize the high risk associated with exposure to dimethoate for occupational workers and pregnant women, providing further justification to reduce the usage of dimethoate on food products. Populations at Risk for Exposure The application of dimethoate to large crop fields may result in a high level of exposure for the pesticide applicator and local communities. Exposure can occur through ingestion, dermal exposure, or inhalation. Dimethoate is considered to be moderately toxic to humans with acute and chronic effects. Symptoms of exposure include: numbness, headaches, dizziness, tremors, blurred vision, respiratory depression, slow heartbeat, impaired memory and concentration, unconsciousness, convulsions, and fatality. Symptoms have been seen with dose levels as low as 28 to 30mg/kg. Accidental exposures are fairly common for local communities in close proximity to growing fields due to pesticide drift. Frequently farmers will use spray applicators or aerial spray to treat large growing fields; according to Cox (1995) The Office of Technology Assessment estimates that approximately 40% of the chemical leaves the target area during an aerial spray. A prime example of pesticide drift was the 1999 case at Dixieland School in California, school children were exposed to dimethoate by an aerial application completed over a mile away. The California EPA reported that children experienced acute toxicity symptoms and test results confirmed pesticide residuals were present on the school equipment and children’s clothing. By reducing the number of crops being treated with dimethoate and decreasing the amount of applied product, we will see a reduction in accidental exposures for workers and local communities. The exposure rate for children to pesticides is very alarming. Children maintain a high dietary intake of fresh fruits and vegetables and have a relatively small body mass increasing their exposure to pesticides. A study by Curl et al. (2003) on the organophosphorus pesticide exposure of preschool age children concluded that children consuming a conventional diet (non-organic) maintained a much higher pesticide metabolite level than children following organic diets. Some of these doses actually exceeded EPA’s chronic reference dose based on urine testing. Approximately 76-100% of dimethoate is absorbed into the gastro intestinal tract when consumed orally, and a majority of it is excreted within 24 hours based on human studies. Benomran et al. (2007) examined the distribution of dimethoate in the body after a fatal organophosphate intoxication and found that the distribution of the pesticide was not only in the blood but it had traveled to the brain, liver, kidneys and a high level of accumulation was found in the skeletal muscles. The accumulation of dimethoate in skeletal muscles and quick travel time to the brain may have a significant impact on the neurological development of small children since they are exposed to higher doses of pesticides. A significant number of animal studies have identified neurological effects associated with dimethoate exposure; however, the actual effects on children are still unknown and require additional research. Effects on Feed Crops and Animal Byproducts The usage of Dimethoate on animal feed crops seems to have little to no effect on animal byproducts, based on the few research studies available. Cattle metabolize the pesticide very rapidly and excrete it through their urine. Dimethoate has been detected at low levels in crops such as alfalfa, wheat, and maize. Based on a pesticide residual study for alfalfa conducted by Holland et al. (1963), dimethoate was found to persist at 0.35ppm for fourteen days after treatment at the rate of 1 pound per acre. In a cattle feeding study, dimethoate was fed to Jersey cow at the rates of 0.28 mg/kg and 0.56 mg/kg of body weight over a 14 day period. Out of 56 milk samples the concentration of dimethoate was found to be less than 5 to 10 parts per billion. Based on the research it was concluded that application rates of 1 pound per acre of dimethoate yielded no contamination or adverse effects to dairy cows. The 1984 WHO and FAO assessment of a cattle feeding study, found the residual levels of dimethoate in the fat and tissues of cattle were 3 mg/kg three hours after biopsy, but continued to drop to levels below 0.1mg/kg after 14 days. Approximately 90 percent of the oral dose is eliminated in cattle after 24 hours. The feeding study was based on a dosage of 10 mg/kg of body weight and almost a majority of the dimethoate was excreted. Based on the study results EPA’s proposed tolerance levels of 2ppm for animal forage products would be safe and maintain little to no pesticide residual in cattle byproducts. Ecological Effects Pesticide pollution is regarded as a large source of contamination for surface waters, especially due to surface runoff from rainfall, non-point source pollution, and pesticide drift. Insecticides are highly toxic to aquatic fauna. Schulz (2004) identified the results of a Canadian risk reduction program in Ontario and concluded that the only way to reduce risk is to reduce the use of high-risk pesticides on fruits and vegetables. Ecological toxicity data for dimethoate has deemed it highly toxic in aquatic environments due to its solubility in water and likeliness to leach through the soil. An organophosphate study reviewed by Schulz (2004) detected levels of dimethoate and other pesticides in drainage ditches utilized for fruit and vegetable crops. Additional studies have detected dimethoate and other organophosphates in streams and rivers with repeated fish kill. According to toxicological data presented by Oregon State University (1996) the half life in soil for dimethoate is approximately 4-16 days and the half life in water is 8 days. Unfortunately by the time dimethoate biodegrades the damage is already done. It has also been found to be highly toxic to other forms of wildlife including: birds, honeybees and livestock in high doses. The only way to protect our wildlife and environment is to reduce the usage of toxic pesticides. Conclusion The data presented in this paper substantiates the risks and health hazards associated with the use of dimethoate. Dimethoate is extremely harmful to public health and poses a number of side effects including: mutagenic, teratogenic, and possible carcinogenic effects in humans. Pregnant women, children and pesticide applicators are often at the greatest risk for exposure due to dietary practices and accidental inhalation from the application of pesticides. Pesticide drifts can also affect local communities. Dimethoate is highly toxic in the environment, damaging aquatic ecosystems and harming wildlife. By revoking the tolerance levels for combined dimethoate residuals on apples, cabbage, collards, grapes, lentils, seeds, spinach and leaf lettuce we will be protecting both public health and environmental health. Understandably, it continues to be necessary for farmers to treat large crop fields of alfalfa, corn and wheat to prevent damage and loss due to pests. Using integrated pest management techniques and applying chemicals as a last resort is the best approach to pest management. Research studies have shown that the application of dimethoate to cattle feed crops has very little effect on animal byproducts, because it is rapidly metabolized by the animals. EPA’s proposed tolerance level of 2.0ppm for animal forage crops will present no adverse effects and should be considered safe. I fully support EPA’s proposal to revoke the tolerance levels for combined dimethoate residuals on apples, cabbage, collards, grapes, lentils, seeds, spinach and leaf lettuce. I also agree with their proposed tolerance level of 2ppm for dimethoate residuals on animal feed crops. References 1. El-Aswad, A. T, Ahmed, F. , & Shaaban, N.(2007). Assessment of reproductive toxicity of orally administered technical dimethoate in male mice. Science Direct , 232-238. 2. Alhifi, M., Khan, M., Algoshai, H., & Ghole, V. (2004). Teratogenic Effect of Dimethoate on Chick Embryos. International Medical Journal , 1-10. 3. California EPA. (1999). Enforcement Letter 2001-051, Attachment. Retrieved March 17, 2008, from California Environmental Protection Agency: http://www.cdpr.ca.gov/docs/county/cacltrs/penfltrs/penf2001/2001atch/attach51.ht m 4. Cox, C. (1995). Pesticide Drift: INDISCRIMINATELY FROM THE SKIES. Journal of Pesticide Reform , 1-6. 5. Cunningham., M., & Matthews, H. (1995). Cell proliferation as a determining factor for the carcinogenicity of chemicals: studies with mutagenic carcinogens and mutagenic noncarcinogens. Toxicology Letters 82/83 , 9-14. 6. Curl, C., Elgethun, K., & Fenske, R.(2003). Orangophosphorus Pesticide Exposure of Urban and Suburban Preschool Children with Organic and Conventional Diets. Environmental Health Perspectives , 377-382. 7. Food and Agriculture Organization of United Nations and World Health Organization. (1984, October). Pesticide Residues in Food: Dimethoate. Retrieved March 14, 2008, from International Program on Chemical Safety: http://www.inchem.org/documents/jmpr/jmpmono/v84pr19.htm 8. Hardee, D., Keenan, G., Gyrisco, G., & Lisk, D. (1963). Effects of Feeding Low Levels of Dimethoate on Milk and on Whole Blood Cholinesterase Activity of Dairy Cattle. American Dairy Science Association , 510-512. 9. Oregon State University. (1996, June). Dimethoate. Retrieved March 15, 2008, from Extension Toxicology Network: http://extoxnet.orst.edu/pips/dimethoa.htm 10. World Health Organization (1989). Environmental Health Criteria: Dimethoate. 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