Comiendo Caca

Report on Carcinogens, Twelfth Edition  (2011)

Lead and Lead Compounds
CAS No. 7439-92-1 (Lead)
No separate CAS No. assigned for lead compounds as a class
Reasonably anticipated to be human carcinogens
First listed in the Eleventh Report on Carcinogens (2004)
Also known as Pb

Introduction
The compounds lead phosphate and lead acetate were first listed in
the Second Annual Report onCarcinogens in 1981 as reasonably anticipated to be human carcinogens based on sufficient evidence of
carcinogenicity in experimental animals. The listing of lead and lead
compounds supersedes the previous listing of lead phosphate and
lead acetate in the Report on Carcinogens and applies to lead and
all lead compounds.

Carcinogenicity
Lead and lead compounds are reasonably anticipated tobe human
carcinogens based on limited evidence of carcinogenicity from studies in humans and sufficient evidence of carcinogenicity from studies
in experimental animals.
Cancer Studies in Humans
Lead exposure has been associated with increased risk of lung, stomach, and urinary-bladder cancer in diverse human populations (Fu
and Boffetta 1995, Steenland and Boffetta 2000, NTP 2003). Thestrongest epidemiological evidence is for lung and stomach cancer,
which are consistently but weakly associated with occupations and
industries entailing lead exposure and with indices of individual lead
exposure, including job history and biological monitoring of occupationally exposed and general populations. However, most studies of
lead exposure and cancer reviewed had limitations, includingpoor
exposure assessment and failure to control for confounding by other
factors that could increase the risk of cancer (such as lifestyle factors
and concurrent occupational exposure to other carcinogens), and did
not demonstrate relationships between the level or duration of exposure and the magnitude of cancer risk. The crude exposure measures
used in most studies, such as treating wholeplants or occupations
as having uniform exposure, may have limited the magnitude of risk
estimates, most of which were modest. Evidence from epidemiological studies therefore is compatible with small increases in the risk
of lung or stomach cancer; however, this evidence must be weighed
against the potential for confounding by factors such as smoking, diet,
or coexposure to arsenic.
CancerStudies in Experimental Animals
Lead compounds caused tumors in several species of experimental animals, at several different tissue sites, and by several different
routes of exposure. Carcinogenicity was observed in studies with
inorganic lead compounds, both soluble (lead acetate and lead subacetate) and insoluble (lead phosphate, lead chromate), and with tetraethyl lead (an organic leadcompound). Lead caused cancer in rats
and/or mice exposed orally, by injection, or perinatally (via the placenta or lactation). Benign and malignant kidney tumors (adenoma,
carcinoma, and adenocarcinoma) were most frequently associated
with lead exposure, and tumors of the brain, hematopoietic system,
and lung were reported in some studies (IARC 1980, 1987).
Lead subacetate administered in the dietcaused benign and malignant kidney tumors (adenoma and carcinoma or adenocarcinoma)
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Table of Contents: http://ntp.niehs.nih.gov/go/roc12
in mice and rats of both sexes and brain tumors (glioma) in rats,
and its administration by intraperitoneal injection caused benign
lung tumors (adenoma) in mice. Lead acetate administered in the
diet or drinking water caused benign and malignantkidney tumors
(adenoma and carcinoma) in rats and increased the incidence of
virus-induced lymphocytic leukemia in mice. After pregnant mice
were given lead acetate in the drinking water from gestation day 12
to four weeks postpartum, the offspring showed a dose-related increase in proliferative lesions of the kidneys (including atypical hyperplasia, adenoma, and adenocarcinoma) (Waalkes et...