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CHLORPYRIFOS/DURSBAN Organophosphates were first developed in Germany during World War II by the I.G. Farben Company, which developed them as nerve gas agents in warfare. Chlorpyrifos is closely related chemically to these chemical warfare agents developed under the Third Reich and are in the same chemical family. Organophosphate pesticides are potent neurotoxins, which can cause long term, persisting neurologic and neurotoxic damage to humans. The first report of chemical injury associated with Dursban exposure was in 1966, fairly soon after chlorpyrifos was introduced to the market. A review of 114 cases three years after exposure showed chemical injuries present in 22 or 19%. An additional 18 or 16% developed other persistent chronic health problems following exposure to Dursban including seven with persistent headaches, six with visual disturbances, and five with increased nervousness. Because Tabershaw and Cooper, the authors of this study, were frequent consultants to industry and widely published, and this article appeared in the mostly widely read occupational journal of its day, industry should have been aware of this work (Tabershaw, I.R. and Cooper, W.C. "Sequelae of acute organic phosphate pesticide poisoning." Journal of Occupational Medicine 8:5-20, 1966). The National Pesticide Telecommunications Network has received 158 incoming phone calls on their pesticide hotline indicating the development of chemical injury in persons exposed to Dursban. Indeed, chlorpyrifos ranks first as a cause of heightened sensitivity to chemicals in data collected by the National Pesticide Telecommunications Network and ranks second in the precipitation of peripheral neuropathy. Other organophosphates were also involved with 104 suspect cases attributed to diazinon exposure and 51 cases attributed to malathion. DowElanco for years withheld information from the government, which should have been reported by law indicating chronic health effects following Dursban (Dow's brand of chlorpyrifos) exposure. This data has been reviewed by Albert Donnay and Jeanette Sherman, both scientists well known to me and with scientific integrity and skills that I respect. Chemical injury was the second most common disturbance reported to DowElanco following Dursban exposure with 35 affected people. A total of 239 individuals reported adverse health affects following exposure to chlorpyrifos. In contrast, 2,4-D, the Agent Orange herbicide, had only one case of chemical injury, and other pesticides had either no cases or one case each. This relatively low incidence of chemical injury after overexposure to other pesticides is clear indication of a physiologic rather than a psychologic factor, since the public would have no way of knowing that chlorpyrifos is disproportional toxic compared to many other pesticides. In the Donnay/Sherman analysis of the Dow data concerning which organ systems were involved with chronic health effects during the years 1984 to 1994, 24 other cases which were coded by DowElanco as "odor" involved virtually the same organ systems being chronically affected as the category chemical sensitivity/intolerance. I feel that these were also chemically intolerant patients mis-classified. Further, the category of "other" also involves essentially the same organ systems as the odor and chemical sensitivity/intolerance categories and indicates the presence of chronic illness in the intestinal tract, respiratory tract, and nervous system. Other adverse health effect claims from chlorpyrifos made to Dow in the decade of 1984 to 1985 include claims of neurotoxicity (22 cases) and respiratory toxicity (20 cases), both effects seen in chemically sensitive patients. This indicates that DowElanco, as in the 1980's, had knowledge of chronic Chlorpyrifos/Dursban Page 2 of 4 illness including odor intolerance and chemical sensitivity following exposure to Dursban. This is in addition to the manufacturer's duty to have reviewed the literature and the availability of the Tabershaw and Cooper report described above. Dr. Sherman's own 1995 publication of her patients discusses 57 people poisoned by Dursban, of whom 37% developed multiple chemical sensitivity. Miller's 1995 study showed that individuals poisoned by organophosphate pesticides, including 19 poisoned by chlorpyrifos, developed chemical sensitivity. Rosenthal described long-standing chemical sensitivity accompanied by chronic illness induced in an attorney following chlorpyrifos use in his house as a termiticide. Cases of pesticide poisoning from chlorpyrifos (Dursban) have been increasing in the United States. Many of these cases are office workers. Dursban has been evaluated by the U.S. EPA as the 8th most common cause of hospitalizations from pesticide poisoning. Immune changes can also occur from exposure to chlorpyrifos. These have been found by physicians such as Gunnar Heuser, Elaine Panitz, Jack Thrasher and Jeanette Sherman. Immune alterations associated with Dursban exposure has also been documented in the medical literature consisting of immune activation and the formation of autoantibodies (increased autoimmune tendency). Indoor use of Dursban causes an increase in the indoor air concentration. Chlorpyrifos also causes specific neuropathy-related abnormalities in the lymphocytes (neuropathy target esterase). Dursban has been found to be toxic to the bone marrow, causing chromosomal alterations. An infant crawling on a treated surface of Dursban can absorb up to 90% of the minimum effect level. Skin contact with adults may cause less serious aggravation, but can obviously be problematic from the many case reports listed above and below. High exposures can occur with broadcast application as well as with foggers. Even crack and crevice treatment can exceed the levels recommended by the National Academy of Sciences. Persistent long-term symptoms have been reported from Dursban in the Journal of Pesticide Reform. A family poisoned by Dursban had symptoms persisting for many months, according to the Texas Center for Rural Study. An unusual pattern of birth defects has been reported by Sherman in 1995 in children whose mothers were exposed during pregnancy to chlorpyrifos (Dursban) or other organophosphate pesticides. Permanent eye abnormalities in children have also been reported, including damage to the retina, reduced peripheral vision and impaired visual acuity. Organophosphates interfere with the function of the nervous system by interfering with nerve transmitters, including muscarinic, nicotine, and brain nerve transmitters. Muscarinic nerve receptors, which are located in organs such as the heart, endocrine glands, blood vessels, and other smooth muscle organs have altered function resulting in symptoms such as wheezing, nausea, abdominal cramps, visual disturbance, and even vomiting. Nicotinic nerve receptors are located in the nerves of skeletal muscles and the ganglia of the autonomic nervous system and interference with their function causes symptoms such as muscle twitching and cramping, fatigue, weakness, rapid or irregular heart rate, and changes in blood pressure. Delayed effects can occur as well following acute or repeated chronic exposures. These can involve the peripheral nerves resulting in impaired balance and increased weakness. Chlorpyrifos/Dursban Page 3 of 4 The nerves controlling the intestinal and urinary tract can be interfered with causing reduced control of bladder and bowel function. Neurotransmitters in the brain can also be affected by organophosphate compounds resulting in symptoms such as confusion, tremors, poor coordination, sleep disturbance, weakness, anxiety, impaired coordination, mood alterations, etc. Persistent neurobehavioral alterations in brain function can also result. There are also reports in the literature for both humans and animals of disturbances of porphyrin metabolism, which can be persistent following exposure to organophosphates. Other changes with organophosphates includes increased susceptibility to infectious diseases, possibly because of disturbances of immune function, impaired liver function, loss of vigor (fatigue) and acceleration of the aging process as well as loss or decline in potency and libido. Both chlorpyrifos and diazinon have been associated with alterations in brain function in humans consistent with the general description for organophosphates above. An epidemiologic study with a control group showed increased immune activation (CD 26), reduced cell division (nitogeneses) and increased autoimmunity (autoantibodies) with organophosphate exposure to chlorpyifos. Chlorpyrifos has induced more cases of chemical/brain injury with neural sensitization among patients than all other pesticides on the market put together. The only pesticide which has caused more cases of chemical injury among Dr. Ziem’s patients than chlorpyrifos is chlordane, which has been removed from the market due to its toxicity. Chronic health effects from such agents have been reported for decades. Dr. Ziem personally reported neurologic, respiratory and other health damage from chlorpyrifos to Dow representatives in sworn testimony in 1991. References: 1. 2. Tabershaw, I.R., Cooper, W.C. "Sequelae of acute organic phosphate pesticide poisoning." J Occup Med 8:5-20, 1966. Sherman, J. "Chlorpyrifos (Dursban)-associated birth defects: a proposed syndrome, report of four cases, and discussion of the toxicology." Int J Ac Med Tox, 4:417-31, 1995. 3. Sherman, J. "Organophosphate pesticides/neurological and respiratory toxicity," Health 11:33-39, 1995. Toxicology and Industrial 4. Miller, C.S. and Mitzel, H.C. "Chemical sensitivity attributed to pesticide exposures vs remodeling," Archiv Environ Health 50:119-129, 1995. 5. Rosenthal, N.E. and Cameron, C.L. Psychiatry 148:1416, 1991. 6. The United Stated Environmental Protection Agency, Chlorpyrifos Science Chapters, June 1989. U.S. EPA Document: 0002-EPAO-89-006. 7. California Morbidity Weekly Report, April 11, 1980. 8. Pattern, B. Journal of Allergy and Clinical Immunology, 1977. No. 597-603, 1986. 9. Broughton, A. Chronic health effects and immunologic alternations associated with pesticides. Toxicology, 4:59-71, 1990. "Exaggerated sensitivity to an organophosphate pesticide," Amer J 10. Anderson, D. Environmental Science and Technology, 22:717-720, 1988. 11. Lotti, M. Inhibition of lymphocytic neuropathy target esterase predicts the development organophosphate-induced delayed polyneuropathy. Archives of Toxicology, 59:176-179, 1986. of 12. Amer, S. Cytogenetic effects of pesticides: I induction of micronuclei in mouth bone marrow by the insecticide Dursban. Mutation Research, 101:247-255, 1982. Chlorpyrifos/Dursban Page 4 of 4 13. Berteau, P. Insecticide absorption from indoor surfaces. Biological Monitoring for Pesticide Exposure, American Chemical Society, Washington, DC, Chapter 24, 1987. 14. Vaccaro, J. Risks associated with exposure to chlorpyrifos and chlorpyrifos formulation components. Chapter 25. Pesticides in Urban Environments: Fate and Significance, American Chemical Society, 1993. 15. Aiuto, L. Life-threatening organophosphate-induced delayed polyneuropathy in a child after accidental chlorpyrifos ingestion. Journal of Pediatrics, 22:658-660, 1993. 16. O'Brien, M. Chlorpyrifos. Journal of Pesticide Reform, 8:42-44, 1989. 17. Poisoning our Homes: Exposure to Pesticides Through Indoor Pest Extermination in Texas, Texas Center for Rural Studies, Austin, Texas, 1987. 18. Stalberg, E. Effect of occupational exposure to organophosphorus insecticides on neuromuscular function. Scandinavian Journal of Work Environment and Health, 4:255-261, 1978. 19. Rosenstock, L. Chronic central nervous system effects of acute organophosphate pesticide intoxication. Lancet, 338:223-227, 1991. 20. Savage, B. Chronic neurological sequelae of an acute organophosphate pesticide poisoning. Archiv Environ Health, 43:38-45, 1988. 21. Senanayake, N. Neurotoxic effects of organophosphorus insecticides: intermediate syndrome. New England Journal of Medicine, 316:761-763, 1987. 22. JD Thrasher etal, "Part Title", Archiv Environ Health 57:181-187, 2002. 23. MB Abou-Donia, “Organophosphorus ester-induced chronic neurotoxicity”, Archives of Environmental Health, Vol 58:8 484-497, Aug. 2003.