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• DDT was banned by an EPA administrator who ignored the decision of his own administrative law judge.
• Extensive hearings on DDT before an EPA administrative law judge occurred during 1971-1972. The EPA hearing examiner, Judge Edmund Sweeney, concluded that "DDT is not a carcinogenic hazard to man... DDT is not a mutagenic or teratogenic hazard to man... The use of DDT under the regulations involved here do not have a deleterious effect on freshwater fish, estuarine organisms, wild birds or other wildlife."
[Sweeney, EM. 1972. EPA Hearing Examiner's recommendations and findings concerning DDT hearings, April 25, 1972 (40 CFR 164.32, 113 pages). Summarized in Barrons (May 1, 1972) and Oregonian (April 26, 1972)]
• Overruling the EPA hearing examiner, EPA administrator Ruckelshaus banned DDT in 1972. Ruckelshaus never attended a single hour of the seven months of EPA hearings on DDT. Ruckelshaus' aides reported he did not even read the transcript of the EPA hearings on DDT.
[Santa Ana Register, April 25, 1972]
• After reversing the EPA hearing examiner's decision, Ruckelshaus refused to release materials upon which his ban was based. Ruckelshaus rebuffed USDA efforts to obtain those materials through the Freedom of Information Act, claiming that they were just "internal memos." Scientists were therefore prevented from refuting the false allegations in the Ruckelshaus' "Opinion and Order on DDT."
Feeding primates more than 33,000 times the average daily human exposure to DDT (as estimated in 1969 and 1972) was "inconclusive with respect to a carcinogenic effect of DDT in nonhuman primates."
[J Cancer Res Clin Oncol 1999;125(3-4):219-25]
In congressional testimony, Charles Wurster, a biologist for the Environmental Defense Fund, noted the abundance of birds during the DDT years, referring to "increasing numbers of pheasants, quail, doves, turkeys and other game species."
[Wurster, C.F. 1969 Congressional Record S4599, May 5, 1969]
The Audubon Society's annual bird census in 1960 reported that at least 26 kinds of birds became more numerous during 1941 - 1960.
[See Anon. 1942. The 42nd annual Christmas bird census." Audubon Magazine 44;1-75 (Jan/Feb 1942), and Cruicjshank, AD (editor) 1961. The 61st annual Christmas bird census. Audubon Field Notes 15(2); 84-300]
Statistical analysis of the Audubon data bore out the perceived increases.
[White-Stevens, R. 1972. Statistical analyses of Audubon Christmas bird censuses. Letter to New York Times, August 15, 1972]
The white-tailed kite, a raptor, was "in very real danger of complete extirpation in the U.S." in 1935, but "by the 1960's, a very great population increase and range expansion had become apparent in California and the breeding range had extended through the Central American countries."
[Eisenmann, E. 1971. Range expansion and population increase of the White-tailed kite. American Birds 25(3):529-535]
Great increases inmost kinds of hawks during the DDT years were reported by the Hawk Mountain Sanctuary Association (Hawk Mountain, Pennsylvania).
[Taylor, JW. Summaries of Hawk Mountain migrations of raptors, 1934 to 1970. In Hawk Mountain Sanctuary Association Newsletters]
National forest studies from Wisconsin and Michigan reported an increase in nesting osprey productivity from 11 young in 1965 to 74 young in 1970.
[U.S. Forest Service, Milwaukee. 1970. Annual report on osprey status in national forests in Wisconsin and Michigan]
Many experiments on caged-birds demonstrate that DDT and its metabolites (DDD and DDE) do not cause serious egg shell thinning, even at levels many hundreds of times greater than wild birds would ever accumulate.
[Cecil, HC et al. 1971. Poultry Science 50: 656-659 (No effects of DDT or DDE, if adequate calcium is in diet); Chang, ES & ELR Stokstad. 1975. Poultry Science 54: 3-10 1975. (No effects of DDT on shells); Edwards, JG. 1971. Chem Eng News p. 6 & 59 (August 16, 1971) (Summary of egg shell- thinning and refutations presented revealing all data); Hazeltine, WE. 1974. Statement and affidavit, EPA Hearings on Tussock Moth Control, Portland Oregon, p. 9 (January 14, 1974); Jeffries, DJ. 1969. J Wildlife Management 32: 441-456 (Shells 7 percent thicker after two years on DDT diet); Robson, WA et al. 1976. Poultry Science 55:2222- 2227; Scott, ML et al. 1975. Poultry Science 54: 350-368 (Egg production, hatchability and shell quality depend on calcium, and are not effected by DDT and its metabolites); Spears, G & P. Waibel. 1972. Minn. Science 28(3):4-5; Tucker, RK & HA Haegele. 1970. Bull Environ Contam. Toxicol 5:191-194 (Neither egg weight nor shell thickness affected by 300 parts per million DDT in daily diet);Edwards, JG. 1973. Statement and affidavit, U.S. Senate Committee on Agriculture, 24 pages, October 24, 1973; Poult Sci 1979 Nov;58(6):1432-49 ("There was no correlation between concentrations of pesticides and egg shell thinning] .")
After 15 years of heavy and widespread usage of DDT, Audubon Society ornithologists counted 25 percent more eagles per observer in 1960 than during the pre-DDT 1941 bird census.
[Marvin, PH. 1964 Birds on the rise. Bull Entomol Soc Amer 10(3):184-186; Wurster, CF. 1969 Congressional Record S4599, May 5, 1969; Anon. 1942. The 42nd Annual Christmas Bird Census. Audubon Magazine 44:1-75 (Jan/Feb 1942; Cruickshank, AD (Editor). 1961. The 61st Annual Christmas Bird Census. Audubon Field Notes 15(2):84-300; White-Stevens, R.. 1972. Statistical analyses of Audubon Christmas Bird censuses. Letter to New York Times, August 15, 1972]
"When U.S. Environmental Protection Agency chief William Ruckelshaus was about to announce his decision to ban DDT in June 1972, he confided to a friend, "There is no scientific basis for banning this chemical --- this is a political decision."" The 'friend' was never identified however. In a commentary the magazine concluded (page 56): "The EPA and environmentalists must be held accountable for their crime: There was not a single human death from DDT usage; there have been untold thousands of deaths and millions of disease-stricken persons as a result of the DDT banning."
The original method of DDT synthesis involves reacting one mol of chloral with two mols of chlorobenzene in the presence of sulfuric acid. Although different condensing agents can be used, practically all other processes are modifications of the original method.
Today, indoor DDT spraying to control malaria in Africa is supported by the World Health Organization; the Global Fund to Fight AIDS, Tuberculosis and Malaria; and the United States Agency for International Development.
Originally posted by Resurrectio
reply to post by punctual
Ok, source something saying it has negative effects on humans or animals.
DDT as a Cause of Cat Deaths
Bigart concedes that some cats were killed after huts were sprayed with DDT, but also states that experts believe the explosion in the rat population was more likely due to a combination of favorable factors such as moisture, climate, availability of food “and, chiefly, the Government’s failure to insure adequate supplies of rat poison.”
Similar to the events in Vietnam, there are several other renditions of the cat story from other locales. The situation of this sort that arose closest to the probable site of a cat drop was briefly described in an annual report on conditions in North Borneo (Colony of North Borneo 1959) in which the author remarks: “Field rats were a greater menace than usual, partly as a result of antimalarial spraying which accidentally killed many cats”. This report does not specifically state which insecticide was used but does mention that zinc phoshide was used to kill the rats. Another story of this sort describes a situation in which it was conjectured that insecticide spraying caused the death of cats in Bolivia. This was determined during an investigation of an outbreak of Bolivian hemorrhagic fever (a rodent-borne disease) that was “due to invasion of houses by rodents” (Johnson 1965; Garcia et al. 1979). Furthermore, in a text on malaria, Robert Desowitz, mentioned that cats died in villages in Thailand after homes were sprayed with DDT resulting in an increase in the rat population (Desowitz 1991). Desowitz further commented that there were “numerous reports of village cats dying within one week after malaria-control teams sprayed DDT onto household walls”.
Cat deaths as a result of DDT spraying were also reported in Oaxaca, Mexico (Anonymous 1977) where the exterminators were called los matagatos, “the cat killers”, because “the cats lick the DDT residue off their paws and die of a disease of the nervous system”. Furthermore, Michael Colbourne (1962), who worked for the WHO during the 1950’s, conceded that malaria eradication campaigns in the western Pacific caused the death of some “domestic animals”, although he states, “such killings can be reduced, but not wholly prevented, by adequate precautions.” This remark was one of the few made by a WHO representative on the unintentional deaths of cats via indoor residual spraying of DDT during the height of the eradication program. In 1969, Anthony Brown of the WHO prepared an address to members of a convention on the biological impacts of pesticides in the environment during which he stated, “DDT as applied has not caused any side-effects among domestic animals.” Despite this claim, only several years later, Brown conceded that there were undocumented cases of cats dying from contact with DDT in Bolivia and Sabah “because of their habit of continually cleaning themselves by licking.
These sources confirm that cats died as a result of DDT spraying during malaria eradication programs. However, evidence points to the cause of cat deaths as being related to their propensity for licking their fur and that this trait provided a means for ingesting a lethal dose of DDT obtained directly from contact with the DDT residue clinging to sprayed floors and walls.
Nonmalarial infant deaths and DDT use for malaria control.
Although dichlorodiphenyl trichloroethane (DDT) is being banned worldwide, countries in sub-Saharan Africa have sought exemptions for malaria control. Few studies show illness in children from the use of DDT, and the possibility of risks to them from DDT use has been minimized. However, plausible if inconclusive studies associate DDT with more preterm births and shorter duration of lactation, which raise the possibility that DDT does indeed have such toxicity. Assuming that these associations are causal, we estimated the increase in infant deaths that might result from DDT spraying. The estimated increases are of the same order of magnitude as the decreases from effective malaria control. Unintended consequences of DDT use need to be part of the discussion of modern vector control policy.
DDT and breast cancer in young women
Women exposed to relatively high levels of DDT prior to mid-adolescence are 5 times more likely to develop breast cancer later in life than women with lower exposures. But exposure after adolescence does not increase risk.
This conclusion comes from a prospective study of young women's blood that was collected between 1959 and 1967 and stored by freezing, combined with an analysis of their current medical records. The median time to diagnosis of breast cancer after the sample was taken of 17 years.
Many US women who were heavily exposed to DDT in childhood have not yet reached the age of 50. According to the scientists who conducted the study, "the public health significance of DDT exposure in early life may be large.