Storage Levels of Ddt Metabolites in Mouse Tissues following Long Term Exposure to Technical DDT

Tomatis, Lorenzo; Turusov,; Terracini, Benedetto; Day, Nicholas E.; Barthel, W. F.; Charles, R. T.; Collins, G.B.; Boiocchi, Mauro

doi:10.1177/030089167105700603

Cited by 15 publications

(7 citation statements)

References 37 publications

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“…at 4-5 weeks of age. A number of males and females from at least one colony for each dose level of DDT were killed before the 30th week of age to enable evaluations of DDT levels to be carried out in various tissues (Tomatis et al, 1971). These mice have not been considered in the present series.…”

Section: Methodsmentioning

confidence: 99%

The effects of long‐term feeding of DDT to BALB/c mice

Terracini

Testa

Cabral

et al. 1973

Intl Journal of Cancer

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A multigenerational study on the long-term efects of three dose levels of DDT (2, 20 and 250ppm in the diet) and one dose level of N-nitrosodimethylamine ( D M N ) (0.0003 % in the drinking water) was started in 1968. Each treatment was administered to two separate colonies of BALB/c mice. Treatment ofparent mice started at 4-5 weeks of age. The results observed in the first two generations are presented in this report.Survival in males was poor because of fighting. In females, the highest dose level of DDT produced liver-cell tumours in 44% of the parent mice and 74% of the first generation mice, whereas no liver-cell tumours were found in mice given the control diet, or lower dietary concentrations of DDT. Liver cell tumours did not give metastases, but grew after transplantation to syngeneic mice. The ability of DDT to induce liver-cell tumours was identical in both colonies of mice given 250ppm DDT. Malignant lymphomas occurred in about SO % of the mice in all colonies given 0, 2 or 20 ppm DDT. In one of the two colonies given 250ppm DOT, the incidence of malignant lymphomas was 14 %, whereas in the other it was 36 %. The incidence of lung adenomas was not affected by DDT treatment. Tumours at sites other than liver, lymphatic system and lungs were highest in control mice and lowest in mice given 250ppm DDT. However, no linear dose-response was found, and the decrease was more obvious in the parental than in the first generation. A study on the combinations of tumours in mice with more than one tumour and an analysis of litter distribution of liver-cell tumourbearing mice did not reveal any particular trend in the distribution of liver-cell tumours. The quantitative aspects of tumour induction by DDT in BALBIc mice are compared with data from previous studies in mice. DMN consistently produced lung adenomas, liver blood cysts and haemangioendotheliomas.

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Section: Methodsmentioning

confidence: 99%

The effects of long‐term feeding of DDT to BALB/c mice

Terracini

Testa

Cabral

et al. 1973

Intl Journal of Cancer

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“…In the diet to which DDT was added, the concentration varied between +lo% to -20% of the expected values. Further details are given elsewhere (Tomatis et a/., 1971). The food was also examined for the possible presence of aflatoxins at the Tropical Products Institute in London, whose collaboration in gratefully acknowledged.…”

Section: Methodsmentioning

confidence: 99%

“…Details are given elsewhere (Tomatis et al, 1971). All other mice were kept until natural death or killed when moribund.…”

Section: Methodsmentioning

confidence: 99%

“…Two males and two females of the control and of each of the DDT-treated groups were killed at 28 to 29 weeks (P generation) and 16 to 17 weeks of age (F, generation), to carry out the evaluation of DDT levels in various tissues. Details are given elsewhere (Tomatis et al, 1971). All other mice were kept until natural death or killed when moribund.…”

Section: Methodsmentioning

confidence: 99%

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

Tomatis¹,

Turusov²,

Day³

et al. 1972

Intl Journal of Cancer

121

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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

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“…For instance, in the mouse 2 ppm of DDT in the diet will yield, after about 11/2 yr of exposure, a concentration in the fat of 5 to 6 ppm of DDT and its metabolites (10). This is about the same concentration present in the fat of the average U.S. citizen after decades of exposure at an exposure rate of about 0.015 to 0.04 ppm in his diet (11).…”

mentioning

confidence: 99%

Pharmacokinetic and other factors related to mutagenicity testing: quantitative analysis of the testing procedures.

Rall¹

1973

Environ Health Perspect

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Storage Levels of Ddt Metabolites in Mouse Tissues following Long Term Exposure to Technical DDT

Cited by 15 publications

References 37 publications

The effects of long‐term feeding of DDT to BALB/c mice

The effects of long‐term feeding of DDT to BALB/c mice

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

Pharmacokinetic and other factors related to mutagenicity testing: quantitative analysis of the testing procedures.

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