Arsenic - Toxicology of Metals - page 380

drinking water and Fowler's solution; and from inha-
lation through copper smelting and production and
application of arsenic-containing pesticides. Because
hepatic angiosarcoma is a very rare disease, its associa-
tion with exposures to inorganic arsenic does not seem
likely to be a matter of chance.
Long-term exposure to inorganic arsenic through
ingestion and inhalation has been associated with the
development of hepatocellular carcinoma. The expo-
sure of ingested arsenic was from high-arsenic arte-
sian well water and arsenic-contaminated grape wine,
and that of inhaled arsenic was from copper smelting
(Chen et al ., 1997b). Ecological studies have shown a
dose-response relationship between ingested inorganic
arsenic from drinking water and risk of hepatocellu-
lar carcinoma among residents in the endemic area of
arseniasis in southwestern Taiwan (Chen and Wang,
1990; Chen et al ., 1988a).

and nervous systems. Ingested inorganic arsenic
through drinking high-arsenic artesian well water has
been found to be signifi cantly associated with mortal-
ity from prostate cancer in a dose-response relation-
ship (Chen and Wang, 1990; Chen et al ., 1988ab). There
were no reports on the association between inhaled
inorganic arsenic and prostate cancer.
A signifi cant ecological correlation between the
arsenic content in drinking water and the mortality
from cancer of the nasal cavity was reported recently
(Chen and Wang, 1990). Although perforation of the
nasal septum has been documented among smelter
workers exposed to high levels of inorganic arsenic
(WHO, 1981), there were no other reports on the asso-
ciation between nasal cavity cancer risk and exposure
to arsenic through inhalation or ingestion.

7.5.6 Lifetime Cancer Risk Induced by Arsenic

As shown in Table 6, the lifetime risk of develop-
ing cancers of the skin, lung, bladder, liver, and kid-
ney have been estimated on the basis of Armitage-Doll
multistage models. The lifetime risk of developing skin
cancer from the ingestion of 1

7.5.5 Other Internal Cancers

Inhaled and ingested inorganic arsenic have been
associated with an increased risk of gastrointestinal
cancers, hematolymphatic malignancies, and malig-
nant neoplasms of the nervous system (Chen et al .,
1997b; IARC, 2004; NRC, 1999; WHO, 1981; 2001).
Excess mortality from cancers of the digestive tract
has been observed among copper smelter workers,
Moselle vintners, and residents in the endemic area of
arseniasis in Taiwan. Workers in copper smelters and
pesticide manufacturing plants were reported to have
an increased mortality from malignant neoplasms of
lymphatic and hematopoietic tissues. Copper smelter
workers also had an increased mortality from malignant
neoplasms of the brain and nervous system.
There were no reports on the association between
exposure to ingested inorganic arsenic and mortality
from malignant neoplasms of the hematolymphatic

g/kg/day inorganic
arsenic was estimated according to the prevalence of
skin cancer among residents in an endemic area of
arseniasis and an unexposed control area (Tseng et al .,
1968). The lifetime risk of developing lung cancer from
1

µ

g/kg/day arsenic through inhalation was based on
the data from copper smelter workers in Anaconda,
Montana (Brown and Chu, 1983; Higgins et al ., 1982;
Lee-Feldstein, 1983), and in Tacoma, Washington
(Enterline and Marsh, 1982).
The lifetime risks of developing cancer of the lung,
liver, bladder, and kidney from 1

µ

g/kg/day inorganic
arsenic through ingestion were based on the mortality
date of residents in the endemic area of arseniasis south-
western Taiwan (Chen et al ., 1992). The lifetime risks of

µ

TABLE 6 Lifetime Risk of Developing Cancers of Skin, Lung, Liver, Bladder, and Kidney
Caused by 1 mg/kg/day Inorganic Arsenic Through Ingestion and Inhalation

Cancer Exposure Study Lifetime risk (per 1000)

site type area Reference Male Female

Skin Ingestion Taiwan Tseng et al ., 1968 3.0 2.1

Lung Inhalation Anacoda Higgins et al ., 1982 17.0 —

Lee-Feldstein, 1983 9.8 —

Brown and Chu, 1983 4.6 —

Tacoma Enterline and Marsh, 1980 24.0 —

Ingestion Taiwan Chen et al ., 1992 1.2 1.3

Bladder Ingestion Taiwan Chen et al ., 1992 1.2 1.7

Kidney Ingestion Taiwan Chen et al ., 1992 0.4 0.5

Liver Ingestion Taiwan Chen et al ., 1992 0.4 0.4

Source: US Environmental Protection Agency, 1984; Chen et al ., 1992.