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detailed data on lead exposure levels and from potential confounding exposures to cadmium, arsenic,
and tobacco smoke.
In an epidemiologic study of 7,121 deceased California plumbers and pipefitters, Cantor et al. (1986)
found increased cancer incidence for all neoplasms and for cancers of several sites including the
respiratory system, kidney, and stomach. In addition to lead, these workers were exposed to
carcinogens such as asbestos and chromium. Since excess mesotheliomas were observed (16
observed, 2 expected), asbestos exposure likely contributed to the observed increase in stomach and
respiratory system cancer. Asbestos, chromium, and cigarette smoking are likely contributors to lung
cancer but are not generally considered causes of kidney cancer.
There are 2 case reports of renal cancer in men occupationally exposed to toxic levels of lead (Baker et
al., 1980; Lilis, 1981). Baker et al. (1980) thought that the histology in the renal tumor in their case
report was similar to that of kidney tumors in lead-exposed animals. Despite the long history of human
lead exposure and the chronic nephropathy induced by lead, the data on lead-induced, human renal
cancer is not definitive.
In regard to induction of cancer in organs other than the kidney, the largest occupational cohort studied
for lead-induced cancer included approximately 6,800 employees of 6 lead smelters and recycling
plants and 10 battery manufacturing plants in the United States (Cooper and Gaffey, 1975; Cooper,
1976; Kang et al., 1980; Cooper, 1981; Cooper et al., 1985; Cooper, 1988). Statistically significant
increases in cancer have been reported for total malignant neoplasms in lead production workers
(Cooper and Gaffey, 1975), total malignant neoplasms and cancers of both the digestive tract and the
respiratory tract in lead production workers and in battery workers (Kang et al., 1980), no sites
(Cooper, 1981; 1988), and total malignancies in the battery workers (Cooper at al., 1985) principally
due to cancers of the respiratory and digestive tracts. In these studies several factors including cigarette
smoking could not be ruled out as confounders.
Ades and Kazantzis (1988) studied 4,293 men at a zinc-lead-cadmium smelter in Great Britain. An
effect of lead exposure on lung cancer was noted but lead exposure was highly correlated with exposure
to arsenic, a known respiratory carcinogen, and no data on cigarette smoking were reported.
Fu and Boffetta (1995) have conducted a meta-analysis of the published studies on cancer and
workplace exposures to inorganic lead compounds. The studies include the 2 case reports, 16 papers
dealing with cohort studies, and 7 papers dealing with case-control studies. The meta-analysis showed
a statistically significant, excess relative risk of cancer overall (RR = 1.11, 95% CI = 1.05-1.17), of
stomach cancer (RR = 1.33, CI = 1.18-1.49), of lung cancer (RR = 1.29, CI = 1.10-1.50), and of
bladder cancer (RR = 1.41, CI = 1.16=1.71). The relative risk for kidney cancer did not reach
statistical significance (RR = 1.19, CI = 0.96-1.48). A separate analysis of studies involving workers
heavily exposed to lead found higher relative risks for stomach cancer (RR = 1.50, CI = 1.23-1.43,
based on 4 studies) and lung cancer (RR = 1.42, CI = 1.29-1.62, based on 4 studies). The metaanalysis
is further indication of a relationship between lead exposure and cancer, but it is limited by the
paucity of information in the various studies on confounders such as cigarette smoking, dietary habits,
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