For definition of Groups, see Preamble Evaluation.
VOL.: 53 (1991) (p. 179)
Technical-grade DDT is a complex mixture of para,para'-DDT, its isomers and related compounds. It has been used since 1943 as a nonsystemic insecticide with a broad spectrum of activities. DDT has been used extensively for the control of vectors of malaria, typhus, yellow fever and sleeping sickness, and also on food crops. Its use is banned in some countries and has been restricted since the 1970s in many others to the control of vector-borne diseases.
DDT has been formulated in almost every conceivable form, including granules and powders, solutions, concentrates, aerosols and others, alone and in combination with other insecticides.
DDT is ubiquitous in the environment. It is highly persistent and has been found extensively in foods, soils and sediments. Residual levels in human tissues have been declining slowly with the decreasing use of DDT worldwide.
Exposure may occur during its production and application and as a result of persistent residual levels in surface water and sediments, and in foods.
Slight excess risks for lung cancer were observed among workers at two DDT producing facilities in the USA. A nested case-control study in one of these investigations found a slight deficit of respiratory cancer. No other cancer occurred in sufficient numbers for analysis. In a prospective cohort study in which exposures were estimated on the basis of serum levels of DDT, the risk for lung cancer rose with increasing concentration but was based on small numbers.
Several investigators have compared serum or tissue levels of DDT and/or DDE among individuals with and without cancer, with inconsistent results.
Results from case-control studies of soft-tissue sarcoma do not point to an association.
An elevated risk for non-Hodgkin's lymphoma in relation to potential exposure to DDT was found in a study from Washington State in the USA, but not for other agricultural exposures. An elevated risk for malignant lymphomas was also found in a case-control study in northern Sweden, with adjustment for exposure to herbicides. The only study available found no association between exposure to DDT and primary liver cancer. In the USA, a slight increase in the risk for leukaemia occurred among farmers who reported use of DDT and many other agricultural exposures. The relative risks for leukaemia rose with frequency of use of DDT on animals.
Epidemiological data on cancer risks associated with exposure to DDT are suggestive, but limitations in the assessments of exposure in the studies and the finding of small and inconsistent excesses complicate an evaluation. The slight excesses of respiratory cancer seen among cohorts exposed to DDT are based on differences of five or fewer cases between exposed and unexposed groups. In case-control studies of lymphatic and haematopoietic cancers, exposure to agricultural pesticides other than DDT resulted in excesses as large as or larger than those associated with exposure to DDT. In most of the case-control studies, adjustment was not made for the potential influence of other exposures.
The cohort and case-control studies that have become available since the last evaluation was made in 1987 (see IARC, 1987) add to some extent to the concern about DDT. Most of these investigations were not specifically designed to evaluate the effects of DDT; consequently, the findings for DDT were not reported as fully as would have been desirable.
DDT has been tested adequately for carcinogenicity by oral administration in mice, rats and hamsters, and by subcutaneous administration in mice. Following oral administration to mice, it caused liver-cell tumours, including carcinomas, in animals of each sex and hepatoblastomas in males. In one study, the incidence of lung carcinomas was increased, and in three studies the incidence of malignant lymphomas was increased; the incidence of lymphoma was decreased in two studies. The incidence of liver tumours was increased in mice following subcutaneous injection of DDT. Oral administration of DDT to rats increased the incidence of liver tumours in female rats in one study and in male rats in two studies. In two studies in which DDT was administered orally to hamsters at concentrations similar to or higher than those found to cause liver tumours in mice and rats, some increase in the incidence of adrenocortical adenomas was observed.
A metabolite of DDT, para,para'-DDE, has been tested for carcinogenicity by oral administration in mice and hamsters. A second metabolite, TDE, was tested by oral administration in mice and rats. TDE increased the incidence of liver tumours in male mice and of lung tumours in animals of each sex in one of the two studies in mice. An increase in the number of thyroid tumours was observed in one study in male rats. DDE produced a high incidence of liver tumours in male and female mice in two studies. An increased incidence of neoplastic liver nodules was observed in one study in male and female hamsters.
The liver is the target organ for the chronic toxicity of DDT. This compound induced liver microsomal enzymes in rodents and primates and increased the frequency of enzyme-positive foci in rat liver.
DDT impaired reproduction and/or development in mice, rats, rabbits, dogs and avian species.
In one study, higher DDT levels were noted in the serum of women who had delivered prematurely than in those who had had a normal delivery. Studies of spontaneous abortion, gestational period and newborn status showed no clear association with body levels of DDT.
In one study, increased frequencies of chromatid-type but not chromosome-type aberrations were observed in peripheral lymphocytes of workers with increased plasma levels of DDT. No data were available on the genetic and related effects of metabolites of DDT in humans.
DDT reduced gap-junctional areas in rat liver cells in vivo and inhibited gap-junctional intercellular communication in rodent and human cell systems. Conflicting data were obtained with regard to some genetic endpoints. In most studies, DDT did not induce genotoxic effects in rodent or human cell systems nor was it mutagenic to fungi or bacteria.
para,para'-DDE weakly induced chromosomal aberrations in cultured rodent cells and caused mutation in mammalian cells and insects, but not bacteria. para,para'-DDE inhibited gap-junctional intercellular communication in cultured rodent cells.
In most studies, para,para'-TDE did not induce genetic effects in short-term tests in vitro. It inhibited gap-junctional intercellular communication in cultured rodent cells.
There is no evidence that ortho,para'-TDE induced genetic effects in short-term tests in vitro on the basis of the few studies available.
There is inadequate evidence in humans for the carcinogenicity of DDT.
There is sufficient evidence in experimental animals for the carcinogenicity of DDT.
DDT is possibly carcinogenic to humans (Group 2B).
For definition of the italicized terms, see Preamble Evaluation.
Previous evaluations: Vol. 5 (1974) (p. 83); Suppl. 7 (1987) (p. 186)
Synonyms for para,para'-DDT
Synonyms for ortho,para'-DDT
Synonyms for para,para'-TDE
Synonyms for ortho,para'-TDE
Synonyms for para,para'-DDE
Last updated: 20 November 1997
See Also: Toxicological Abbreviations