The Induction of Renal Tumours by Feeding Lead Acetate to Rats

Boyland, E.; Dukes, C. E.; Grover, Philip L.; Mitchley, B. C. V.

doi:10.1038/bjc.1962.33

Cited by 143 publications

(37 citation statements)

References 5 publications

(2 reference statements)

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“…The first possibility is dealt with in more detail by Boyland et al (1962). We have only observed that coproporphyrin is produced abundantly under the conditions of our experiment.…”

Section: Determination Of Lead Iron and Coproporphyrinmentioning

confidence: 84%

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The Induction of Renal Tumours by Feeding of Basic Lead Acetate to Rats

Esch¹,

Genderen²,

Vink³

1962

Br J Cancer

109

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SOME years ago we attempted to produce inclusion bodies in the nuclei of kidney cells by feeding rats a diet containing basic lead acetate. Kidney tumours developed in some of the animals which were studied after a long and unintentional delay during which the feeding of basic lead acetate had been continued. Zollinger (1953) had reported on the induction of renal tumours in rats following long-term treatment by weekly injections of lead phosphate. Additional information about these kidney tumours was published by Tonz in 1957.The importance of this carcinogenic effect of lead salts prompted us to do further work. The present report records the results of long-term feeding experiments with rats using two different dosage levels of basic lead acetate in the food. In addition, a virological study was made, based on the assumption that the inclusion bodies observed after treatment with lead salts could be of viral nature and the carcinogenic effect be caused by the activation of a virus. The linking of the carcinogenic effect of lead with its content of radioactive material was also considered. EXPERIMENTALTwo series of feeding experiments were made with an interval of about 6 months, each consisting of a control group and an experimental group of 24-30 rats. In both series about equal numbers of male and female animals were distributed over the control and experimental groups, using litter-mates. The animals were obtained from our own rat colony shortly after weaning. The " Wistar strain " used has been randomly bred for more than 15 years. The animals were housed in wire cages, in groups of five, according to sex and supplied a powdered standard diet consisting of two thirds whole wheat flour, one third whole milk powder with addition of 0-5 per cent sodium chloride and 0-5 per cent calcium carbonate. Food and water were given ad libitum. Twice weekly some vegetables were supplied.The experimental groups received basic lead acetate (crystalline, Merck, Darmstad) mixed into the diet in the following dosages:Group 1 : Control I, diet without addition of basic lead acetate. Group 2: Diet with 0.1 per cent of basic lead acetate. Group 3: Control II, diet without addition of basic lead acetate. Group 4: Diet with 1 per cent of basic lead acetate. The duration of the experiments was 29 months for groups 1 and 2 and 24 months for groups 3 and 4. Moribund animals were killed and at the end of the experiment the remaining animals were also killed and examined.

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“…The first possibility is dealt with in more detail by Boyland et al (1962). We have only observed that coproporphyrin is produced abundantly under the conditions of our experiment.…”

Section: Determination Of Lead Iron and Coproporphyrinmentioning

confidence: 84%

“…Walpole (1957, personal communication) and from Boyland, Dukes, Grover and Mitchley (1962). The spontaneous occurrence of such tumours in our strain of rats is extremely rare (Eker, 1954).…”

Section: Determination Of Lead Iron and Coproporphyrinmentioning

confidence: 92%

The Induction of Renal Tumours by Feeding of Basic Lead Acetate to Rats

Esch¹,

Genderen²,

Vink³

1962

Br J Cancer

109

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“…Such tumors have been produced in experimental animals by near-lethal doses of lead (6,7,8,28,40,44,45,46,51,52,53). There are reports (5,22) describing single cases of renal cancer in long-term smelter workers.…”

Section: Renal Cancermentioning

confidence: 99%

Mortality among employees of lead battery plants and lead-producing plants, 1947-1980.

Cooper¹,

Wong²,

Kheifets³

1985

Scand J Work Environ Health

121

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Mortality among employees of lead battery plants and lead-producing plants, . Scand J Work En viron Health II (1985) 331-345. Two cohorts of male lead workers, 4 519 battery plant workers and 2 300 lead production workers, all of whom had been employed for at least one year during the period I January 1946 through 31 December 1970, were observed for mortality during the 34 years from 1 Januar y 1947 through 31 December 1980. Vital status as of the closing date was determined for 94.7 lifo of the former group and 91.6 lifo of the latter. There were 1 718 deaths in the first cohort and 621 in the second. Mortality from all causes combined was significantly greater than expected in each cohort, the standardized mortality ratio (SMR) being 107 and 113, respectively. Among the battery plant workers the greater than expected mortality rate resulted in large part from a significant number of excess deaths from malignant neoplasms (SMR 113), other hypertensive disease (mainly renal) (SMR 320), chronic nephritis (SMR 222), and a group of ill-defined conditions (SMR 355). Among the lead production workers the pattern was similar, with a significant number of excess deaths from other hypertensive disease (SMR 475), hypertensive heart disease (SMR 203), chronic nephritis (SMR 265), and ill-defined conditions (SMR 214). There was also a significant excess of deaths from external causes (SMR 143). The SMR for total malignancies was 113, but this value was not significantly elevated at the 5 % level. In neither cohort were deaths from cerebrovascular disease in significant excess, the SMR being 93 and 132, respectively. A proport ionate mortality analysis showed that the excess deaths from cerebrovascular diseaseand from hypertensive heart disease among smelter workers were in part due to the high proportion of nonwhites in the smelter populations. The stomach, liver, and lungs were the sites responsible for most excess cancer deaths in both cohorts, but the elevated SMR values were statistically significant only for gastric and lung cancers in battery plant workers. There were no excess deaths from malignancies of the kidney, brain, or Iymphopoeitic system in either cohort. It is impossible to relate the observed mortality to levels of lead exposure; because of meager quantit ative information prior to 1960. It is known that past exposures had been very high. Ethnicity, diet, alcohol, and cigarette smoking could not be ruled out as possibleconfounding etiologic factors for the cancer deaths.

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“…Of 16/20 rats that survived for 320 days or more 15 developed kidney tumours, 14 of which were renal carcinomas. No untreated control group was studied (Boyland et al, 1962).…”

Section: Route and Dosagementioning

confidence: 99%

Evaluation of the carcinogenic risk of chemicals to humans

Hamilton¹

1979

Science of The Total Environment

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The Induction of Renal Tumours by Feeding Lead Acetate to Rats

Cited by 143 publications

References 5 publications

The Induction of Renal Tumours by Feeding of Basic Lead Acetate to Rats

The Induction of Renal Tumours by Feeding of Basic Lead Acetate to Rats

Mortality among employees of lead battery plants and lead-producing plants, 1947-1980.

Evaluation of the carcinogenic risk of chemicals to humans

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