The effect of long‐term exposure to DDT on CF‐1 mice

Abstract

CF-I minimal inbred mice were given technical DDT mixed into the diet atThe main reasons for the concern regarding the potential hazard for human health represented by DDT are based on (a) its ubiquity, (b) its persistence in the environment, (c) its capacity to accumulate in living organisms, including man, and its capacity to accumulate in the foetus and in mothers' milk and (d) the experimental evidence of its ability to increase tumour incidence in laboratory animals.The experimental evidence of the carcinogenicity of DDT is based on five published reports. Fitzhugh and Nelson (1947) reported the occurrence of hepatic cell tumours in four of 156 Osborne Mendel rats receiving DDT (81.8% pp isomer and 18.2% op isomer) in the diet at levels of 200-800 ppm, while 1 1 other rats were described as showing nodular adenomatoid hyperplasia of the liver. All 15 rats survived over 18 months and the age distribution for rats with liver tumours corresponded to that in untreated controls. Hepatomas occurred in about 1% of the untreated controls. KemCny and Tarjan (1966) reported in a preliminary paper that the administration of DDT (crystalline pp'DDT) at levels of 2.8 and 3.0 ppm in the diet to BALB/c mice for five consecutive generations resulted in a progressively increased incidence of tumours from the second generation onwards. Tarjan and KemCny (1969) published a final report on this experiment, from which it appeared that the total incidence of tumours was higher in the DDT-treated groups of all five generations than in the control group. The most frequent tumour types were leukaemia, reticulum-cell sarcoma, carcinoma of the lungs and haemangioendothelioma. A transgeneration cumulative effect, resulting in a progressive increase in tumour incidence from the second generation onwards, was not substantiated in this report (Terracini and Tarjan, 1970).Halver ( 1967) reported the occurrence of hepatomas in rainbow trout fed a diet of 18 or 75 ppm DDT. Innes et al. (1969) reported the occurrence of hepatomas in mice of two strains following the continuous administration of DDT for 80 weeks. DDT (pp'DDT) was given

Induction of cell proliferation, micronuclei and hyperdiploidy/polyploidy in the mammary cells of DDT- and DMBA-treated pubertal rats

“…It should be noted, however, that the doses of o,p 0 -DDT used in the present study were significantly higher than those administered with the technical grade DDT. Exposure to technical grade DDT at doses as low as 0.26 mg DDT/kg/day produced liver tumors in mice [Tomatis et al, 1972;Thorpe and Walker, 1973]. Increases in pulmonary adenomas and malignant lymphomas also were seen in mice at doses ranging from 1-32.5 mg/kg/day [Kashyap et al, 1977].…”

Transplacental and combined long‐term effect of DDT in five generations of a‐strain mice

“…However, in the investigation of Tomatis et al (1972) in DDT-treated CF-I mice the most frequent types of tumours were not only lung tumours, but also lymphomas, osteomas and, especially, hepatocellular liver tumours. This difference may depend on the various strains of mice used and on the more prolonged time span of the experiments of Tomatis et al We used mice of strain A, which were very susceptible to lung blastomogenesis.…”

Histogenesis of Hyperplasia and Carcinomas of the Liver Arising around Central Veins in Mice Ingesting Chlorinated Hydrocarbons

“…Similar well-differentiated and moderately well-differentiated carcino mas, such as those described here, were reported in CF1 mice by T omatis et al [21] and Walker et al [22], Similar small carcinomas have been observed in rats ingesting dieldrin and aldrin [4,5]; however, one study using rats was described as being negative [23], The carcinomas also de veloped from hyperplastic parenchymal cells adjacent to central veins. A few moderately well-differentiated carcinomas were described in rats receiving subcutaneous injections of another organochlorine chemical, carbon tetrachloride [13].…”