Failure of testosterone or xanthopterin to influence the induction of renal neoplasms by lead in rats

Roe, F. J. C.; Boyland, E.; Dukes, C. E.; Mitchley, B. C. V.

doi:10.1038/bjc.1965.99

Cited by 36 publications

(14 citation statements)

References 5 publications

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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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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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“…Lead has been found in experimental studies in rats, mice, and hamsters to produce renal tumors (63)(64)(65)(66)(67)(68)(69). Dosage was by several routes including oral.…”

Section: Carcinogenicitymentioning

confidence: 99%

The Health Effects of Low Level Exposure to Lead

Needleman¹,

Bellinger²

1981

Annu. Rev. Public Health

145

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“…The induction of renal carcinonia in animals following chronic oral and subcutaneous administration of lead salts is a well-recognized and reproducible phenomenon [Zollinger, 1953;Van Esch et al, 1962;Boyland et al, 1962;Roe et al, 1965;Mao et al, 1967;Zawirska et a], 1968;Van Esch et al, 1960;Oyasu et al, 1970;Ishibe et al, 1970;Ito, 1973 19761. These neoplasms have been associated with administration of various inorganic lead compounds (basic lead acetate, lead carbonate, lead arsenate, lead subacetate, lead acetate, and lead phosphate) for periods of 16 to 29 months in several animal species.…”

Section: Introductionmentioning

confidence: 99%

Occupational lead exposure, nephropathy, and renal cancer

Baker

Goyer

Fowler

et al. 1980

American J Industrial Med

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A 48-year-old lead worker was found to have a cystic renal carcinoma during an evaluation of his occupational lead poisoning. Clinical studies showed elevated blood lead levels, impaired urinary concentrating ability, and reduced creatinine clearance. Histologic and electron microscopic studies showed this cystic tumor to be similar to renal carcinomas observed in animals with prolonged lead exposure. Lead content of the tumor was elevated (2.49 micrograms/gm) in comparison with adjacent renal tissue and with normal adult levels. In light of previous animal studies, this case adds increased evidence to the concern over the carcinogenic potential of prolonged lead exposure.

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Failure of testosterone or xanthopterin to influence the induction of renal neoplasms by lead in rats

Cited by 36 publications

References 5 publications

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

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

The Health Effects of Low Level Exposure to Lead

Occupational lead exposure, nephropathy, and renal cancer

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