Carcinogenicity of lead

The information available regarding the association of occupational exposure to lead with increased cancer risk is generally limited in its usefulness because the actual compound(s) of lead, the route(s) of exposure, and level(s) of lead to which the workers were exposed were often not reported. Furthermore, potential for exposure to other chemicals including arsenic, cadmium, and antimony occurred, particularly in lead smelters, and smoking was a possible confounder (Cooper 1976 IARC 1987). These studies, therefore, are not sufficient to determine the carcinogenicity of lead in humans, and the following discussion is restricted to the most comprehensive of these studies. 

Cancer. The information available on the carcinogenicity of lead in occupationally exposed humans is limited in its usefulness because the lead compound(s), the route(s) of exposure, and the levels of exposure were not always reported. Furthermore, concurrent exposure to other chemical (including arsenic, particularly in lead smelters) and confounding variables, such as smoking, were often not evaluated. Therefore, the data currently available do not support an assessment of the potential carcinogenic risk of lead in humans. 

According to EPA (IRIS 1999), the available human epidemiological studies lack quantitative exposure data for lead and for possible confounding exposures (e.g., arsenic, smoking). Cancer excesses in the lung and stomach of lead-exposed workers that are reported are relatively small, dose-response relationships are not demonstrated neither is there consistency in the site of cancers reported. EPA (IRIS 1999) concluded that the human data are inadequate to refute or demonstrate the potential carcinogenicity of lead exposure. 

The International Agency for Research on Cancer (IARC 1987) concluded that the evidence for carcinogenicity of lead and inorganic lead compounds was inadequate in humans and sufficient in animals. IARC (1987) classified lead and inorganic lead compounds in IARC Group 2B, possible human carcinogen. The Department of Health and Human Services (DHHS) has determined that lead acetate and phosphate may reasonably be anticipated to be carcinogens based on sufficient evidence from animal studies, but inadequate evidence from human studies (NTP 1994). 

EPA. 1989b. Evaluation of the potential carcinogenicity of lead compounds In support of reportable quantity adjustments pursuant to CERCLA Section 102, external review draft. March 1989 EPA/600/889/045A, NTIS PB89-181366/AS. 

GoyerR. 1992. Nephrotoxicity and carcinogenicity of lead. In Beck, BD. Symposium overview an update on exposure and effects of lead. Fundam Appl Toxicol 18 1-16. 

The lARC has concluded that there is sufficient evidence in experimental animals and in humans for the carcinogenicity of lead chromate. ... 

U.S. Environmental Protection Agency, Evaluation of the Potential Carcinogenicity of Lead and Lead Compounds, Office of Health and Environmental Assessment, EPA/600/8-89/045A., Washington, DC, 1989. 

Landrigan PJ, Boeeetta P and Apostoli P (2000) The reproductive toxicity and carcinogenicity of lead a critical review. Am J Ind Med 38 231-243. 

Lead acetate and lead subacetate caused kidney and brain tumors, while lead phosphate caused kidney tumors in rodents following oral or parenteral administration (lARC 1987). However, the doses were high and caused gross morphological changes in the kidney. lARC (1987) concluded that there was sufficient evidence in experimental animals for the carcinogenicity of lead. 

The carcinogenicity of lead was evaluated at a recent lARC conference held in Garg-nano, Italy (Landrigan etal. 2000). An update of the previously reported epidemiological meta-analysis by Fu and Boffetta... 

Landrigan, P. J., P. Boffetta, and P. Apostoli. 2000. The Reproductive Toxicity and Carcinogenicity of Lead A Critical Review. American Journal of Industrial Medicine 38 231-243. 

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