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2,4-D 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.
http://pmep.cce.cornell.edu/profiles/extoxnet/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. http://www.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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