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al. (1988) did not induce lung tumors in male hamsters similarly treated with arsenic trioxide or gallium
arsenide.
Arsenic (V) has also induced tumors in animals. Calcium arsenate injected intratracheally induced lung
adenomas in male hamsters (Pershagen and Bjorklund, 1985) and leukemia and lymphoma were
produced by sodium arsenate by subcutaneous injection in mice (Osswald and Goerttler, 1971).
Among oral studies, only one study reported positive findings. Tumors, including adenocarcinomas of
the skin, lung, and lymph nodes, were noted in mice given Fowler's solution (potassium arsenite), but the
report lacks experimental details necessary for critical assessment (Knoth, 1966; as reviewed in U.S.
EPA, 1984).
Other oral studies reported that arsenite (3 µg arsenic/l in drinking water) reduced the total tumor
incidence in male and female white Charles River CD mice (Kanisawa and Schroeder, 1967), and
enhanced the growth rate of "spontaneous" (common) mammary tumors in female inbred C3H mice
(Schrauzer and Ishmael, 1974; Schrauzer et al., 1978).
IV.
DERIVATION OF CANCER POTENCY
Basis for Cancer Potency
Inhalation
The International Agency for Research on Cancer (IARC) evaluated arsenic in 1980 and classified
"arsenic and arsenic compounds" in Group 1, which includes the "chemicals and groups of chemicals
(which) are causally associated with cancer in humans." Ingestion of arsenic is associated with cancer at
sites different from those associated with arsenic inhalation: ingestion is associated with skin cancer,
while inhalation results in lung neoplasms.
In contrast, arsenic has not conclusively produced carcinogenesis in animals. Arsenic produces tumors
in animals, but these tumors are rarely malignant. The few reports of carcinogenic effects of arsenic
compounds in animals are seriously flawed. The hypothesis that arsenic may act as a tumor promoter
has been tested but not proven in animals.
CDHS (1990) used human data for its cancer risk assessment of arsenic because (1) these data
showed a strong, consistent association with increased respiratory cancer in epidemiologic studies, (2)
quantitative exposure measurements were made in several of these studies, and (3) clear dose-response
relationships were observed. No risk assessment has been conducted using animal data because the
cancer bioassays using relevant routes of exposure have been negative and because no adequate
inhalation bioassay has been published.
The quantitative cancer risk assessment for arsenic considered data from the occupational mortality
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