2,4-D Beyond Pesticides Rating: Toxic Adding to public concern over dioxin and nitrosamine contamination in 2,4-dichlorophenoxy acetic acid (2,4-D), several recent studies show that this pesticide can cause lymphatic cancer in exposed humans. 2,4-D is the most widely used herbicide in the non-agricultural sector with 23-27 million pounds used annually (U.S. EPA 1999). All 2,4-D products are required to carry the DANGER signal word on the label indicating its EPA toxicity rating of I, the highest of four categories. The U.S. Environmental Protection Agency (EPA) has not fully evaluated 2,4-D’s effects on human health and the environment. Carcinogenicity The findings on carcinogenicity add to the already incriminating body of evidence on 2,4-D, including a manufacturers’ study submitted to EPA in June 1986, indicating the herbicide, which is widely used in agriculture, forestry and urban settings, can cause rare brain tumors (astrocytomas) in rats. These studies indicate a need for closer examination of other commonly used phenoxies such as dichlorprop, mecoprop (MCPP), MCPA and 2,4,5-T (banned in the U.S.). A 1988 National Cancer Institute (NCI) study, conducted by Drs. Sheila Hoar and Aaron Blair, examined all cases of diagnosed cancer among Kansas farmers between 1976 and 1982. According to the study, farmers who were exposed to 2,4-D for 20 or more days per year had a sixfold higher risk of developing non-Hodkin’s lymphoma than non-farmers, while farmers who mixed or spread the herbicide had an eightfold higher risk of developing the tumor. Significantly, the researchers noted that farmers who took precautions to minimize their exposure were at lesser risk (Hoar-Zahm 1988). Dr. Hoar also published a 1990 study of Nebraska farmers which demonstrates a 50% increase in non-Hodgkin’s lymphoma for growers who handle 2,4-D. The linkage between 2,4-D exposure and non-Hodgkin’s lymphoma has also been documented in Sweden, Canada, Nebraska and Washington (Zahm 1990). Furthermore, a 1991 NCI study found that dogs whose owners’ lawns were treated with 2,4-D four or more times per year were twice as likely to contract canine malignant lymphoma than dogs whose owners did not use the herbicide. Malignant lymphoma in dogs is considered very similar to non-Hodgkin’s lymphoma in humans (Hayes 1991). In addition to these studies, a bioassay conducted by the Food and Drug Administration found increased incidences of lymph sarcoma (malignant tumors) in both male and female rats, breast tumors in female rats and reticulum cell sarcoma (malignant blood cell tumors) in male rats exposed to 2,4-D. The latter were also found in mice exposed to the iso-octyl salt of 2,4-dichlorophenol, major breakdown product, to be a cancer promoter. Even with all the mounting evidence, EPA has listed 2,4-D as a Group D chemical for its carcinogenic potential. Chemicals in the classification category represents chemicals with inadequate human and animal evidence of carcinogenicity or for which no data are available (U.S. EPA 2000). Toxicity According to EPA, 2,4-D is irritating to the eyes, skin and mucous membrane and since it is easily absorbed dermally or by inhalation, can injure liver, kidney, muscle and brain tissues. Acute symptoms of exposure include: chest and abdominal pain, vomiting, dizziness and muscle twitching, tenderness or stiffness (U.S. EPA 1982). Studies in rats have demonstrated that 2,4-D can migrate into nervous tissue and concentrate in certain areas of the brain. Not too surprisingly, behavioral changes have also been observed in treated rats (Evangelista de Duffard 1990). In humans, seemingly minor dermal exposures have bee known to cause peripheral neuropathy (irreversible loss of feeling in the extremities). Depression, lethargy and coma have also been documented in animals and humans. 2,4-D is also a mutagen. In laboratory tests it has mutagenic effects on human lymphocytes and human fibroblasts. Genotoxicity has even been documented in plants. Reproductive toxicity has been observed in animals at high dose levels. Exposure resulted in fetuses with abdominal cavity bleeding, increased mortality and inhibition of DNA synthesis in the testes (ETN 1996). A study of male farmers also demonstrated reduced sperm counts and sperm abnormalities in 2,4-D exposed farmers, and abnormalities were still apparent even one year after exposure. 2,4-D is slightly toxic to wildfowl (mallards, pheasants, quail and pigeons), while some formulations are highly toxic to fish. Moderate doses of the chemical fed to honeybees caused severe impairment of blood production. Contaminants Industry reports show that amine salt formulations of 2,4-D may become contaminated during synthesis with up to several hundred parts per billion of nitrosamines, known to be potent carcinogens. Several forms of dioxin have been identified in 2,4-D, including 2,3,7,8-tetrachlorodibenzo-p-diozin (also known as TCDD, the most toxic of the dioxin family, at levels greater than one part per billion); 1,3,7,9 and 1,3,6,8-TCDD; 2,7-dichlorodibenzo-p-dioxin; and 1,2,4- and 1,3,7-trichlorodioxins. The dioxins can cause cancer, birth defects, reproductive effects, liver damage and chloracne. Other contaminants include 1,3,6,8-tetrachloroxanthone (TCX) and 2,4-dichlorophenol. Environmental Fate A systemic herbicide, 2,4-D is easily absorbed by foliage and translocated throughout the treated plant, which dies in 7-14 days. Phenoxy acid herbicides like 2,4-D mimic the action of natural plant growth regulators known as auxins, causing treated plants to literally grow themselves to death. In soil, 2,4-D residues usually dissipate within a month, primarily due to microbial degradation). 2,4-D is known to leach from soils low in clay or organic content and in cool, dry, nutrient-poor soils. Under these conditions, residues may persists for several months. References: Barnes, G. 1991. “2,4-D.” Journal of Pesticide Reform 11(3): 21-25. Eugene, OR. CA Department of Health Services. 1980. 2,4-D: Evaluation of the human health effects. Berkeley, CA. Casey, P., et al. 1984. “Severe mental retardation and multiple congenital anomalies of uncertain cause after extreme parental exposure to 2,4-D.” Journal of Pediatrics 104:313-314. Chernoff, N., et al. 1990. “Effects of chemically induced maternal toxicity on prenatal development in the rat.” Teratology 42:651-658. Cochrane, W., et al. 1981. “Determination of chlorinated dibenzo-p-dioxin contaminants in 2,4D products by gas chromatography-mass spectrometric techniques.” Journal of Chromatography 217:289-299. “2,4-D produces rare brain tumor in male rats, EPA officials note.” Pesticide & Toxic Chemical News June 25, 1986. Duffard, R., et al. 1990. “Biochemical alterations in skeletal muscle induced by 2,4-dichlorophenoxyacetic butyl ester during chick embryonic development.” Biochemical Pharmacology 40(11): 2433-2440. Evangelista de Duffard, A.M., C. Orta and R. Duffard. 1990. “Behavioral changes in rats fed a diet containing 2,4-dichlorophenoxyacetic butyl ester.” Neurotoxicology 11: 563-572. Extension Toxicology Network (ETN). 1996. Pesticide Information Profile for 2,4-D. pmep.cce.cornell.edu/…/extox…/24d-captan/24d-ext.html. Goldstein, N., et al. 1959. “Peripheral neuropathy after exposure to an ester of dichlorophenoxyacetic butyl ester.” Neurotoxicology 11:563-572. Hagenmeier, H. 1986. “Determination of 2,3,7,8-tetrachlorodibenzo-p-dioxin in commercial chlorophenols and related products.” Journal of the American Medical Association 171(10): 1306-1308. Hardell, L., et al. 1988. “The association between soft tissue sarcomas and exposure to phenoxyacetic acids: A new case-referent study.” Cancer 62: 652-656. Hayes, H.M., et al. 1991. “Case-control study of canine malignant lymphoma: positive association with dog owner’s use of 2,4-dichlorophenoxyacetic acid herbicides.” Journal of the National Cancer Institute 83(17): 1226-1231. Hindle, R., et al. 1987. “Determination of N-nitroso-dimethylamine levels in some Canadian 2,4-D amine formulations.” Journal of the Association of Analytical Chemistry 70(1): 49-51. Hoar, S., et al. 1986. “Agricultural herbicide use and risk of lymphoma and soft tissue sarcoma.” Journal of the American Medical Association 256: 1141-47. Hoar-Zahm, S., et al. 1988. “A case-control study of non-Hodgkin’s lymphoma and agricultural factors in eastern Nebraska.” (abstract). “Jury charges Dow $1.5 million for 2,4-D caused death of forest worker.” Journal of Pesticide Reform 7 (4): 30. Krumel, K. and R. Arnold. 1978. “A study of the formation and removal of impurities ion the process for 2,4-D.” R&D Report. Dow Chemical, USA. Kumari, T. and K. Vaidyanath. 1989. “Testing of genotoxic effects of 2,4-dichlorophenoxyacetic acid (2,4-D) using multiple genetic assay systems of plants.” Mutation Research 226: 235-238. Lerda, D. and R. Rizzi. 1990. “Study of reproductive function in person occupationally exposed to 2,4-dichlorophenoxyacetic acid (2,4-D).” Mutation Research 262-47-50. Morgan, D. 1982. Recognition and Management of Pesticide Programs. U.S. EPA. Office of Pesticide Programs. Washington, DC. Municipality of Metropolitan Seatlle. 1980. “Literature reviews of four selected herbicides: 2,4D, dichlobenil, diquat and endothall.” Seattle, WA. Mustonen, R., et al. 1989. ”Effects of commercial chlorophenolate, 2,3,7,8-TCDD, and pure phenoxyacetic acids on hepatic peroxisome proliferation, xenobiotic metabolism and sister chromatid exchange in the rat.” Archives of Toxicology 63:203-208. Mustonen, R., et al. 1986. “Effects of phenoxyacetic acids on the induction of chromosome aberrations in vitro and in vivo.” Mutagenesis 1(4):241-245. PBI/Gordon. 1982. Report to EPA: Analysis for N-nitroso compounds in four 2,4-D amine salt formulations. Washington, DC. Persson, B., et al. 1989. “Malignant lymphoma and occupational exposure.” Br. J. Ind. Med. 46:516-520. U.S. Department of Agriculture. 1988. Managing Competing and Unwanted Vegetation: Final Environmental Impact Statement Appendices D & H. Forest Service, Pacific Northwest Region. November. U.S. EPA. 2000. List of Chemicals Evaluated for Carcinogenic Potential. Office of Pesticide Programs. Washington, DC. U.S. EPA. 1999. Pesticides Industry Sales & Usage: 1996 and 1997 Market Estimates. Office of Pesticide Programs. Washington, DC. epa.gov/oppbead1/pestsales/97pestsales/index.htm U.S. EPA. 1986. Compilation of reviews by independent scientists (D.P. Morgan, L.F. Burmeister, B. Macmahon, & M.S. Linet) of Hoar, S., et al., 1986. Hazard Evaluation Division, Office of Pesticide Programs. Washington, DC. U.S. EPA. 1985. Draft health advisory: 2,4-D. Office of Drinking Water. Washington, DC. U.S. EPA. 1982. 2,4-D Fact Sheet. Office of Pesticide Programs. Washington, DC. U.S. EPA. 1981. Memorandum: Analysis for di- and tetra-chloronated dibenzo-p-dioxins in 2,4-D, from R. Harless to Mike Dellarco. Office of Toxic Substances. Washington, DC. As cited in Banes, 1991. Weisenburger, D. 1990. “Environmental epidemiology of non-Hodgkin’s lymphoma in eastern Nebraska.” American Journal of Industrial Medicine 18:303-305. Wigle, D., et al. 1990. “Mortality study of Canadian farm operators: non-Hodgkin’s lymphoma mortality and agricultural practices in Saskatchewan.” Journal of the National Cancer Institute 82(7): 575-582. Woods, J. 1989. “Non-Hodgkin’s lymphoma among phenoxy herbicide-exposed farm workers in western Washington state.” Chemosphere 18(1-6): 401-406. Ylitalo, P., et al. 1990. “Increase in the acute toxicity and brain concentrations of chlorophenoxyacetic acids by probenecid in rats.” General Pharmacology 21(5): 811-814. Zahm, S.H., et al. 1990. “A case-control study of non-Hodgkin’s lymphoma and the herbicide 2,4-dichlorophenoxyacetic acid (2,4-D) in Eastern Nebraska.” Epidemiology 1(5): 349-356.
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