Arsenic - Toxicology of Metals - page 385

arsenic in drinking water of 3 g/L, the lifetime risk

estimates for bladder and lung cancer combined are
approximately 4 and 10 per 10,000 using the Taiwan
or U.S. background rates of these cancers, respectively.
The U.S. EPA has not yet calculated a unit risk value or
slope factor for arsenic-induced internal tumors.
Some data on dose-response relationships for res-
piratory cancer have been given by Pinto et al . (1977).
They found an almost linear increase in respiratory
cancer with an increasing “exposure index.” From
the data, it can be estimated that exposure to airborne
arsenic of about 50

µ signifi cantly increased in a concentration-related fash-

ion in the low (SMR = 213.0), medium (SMR = 312.1), and
high (SMR = 340.9) arsenic exposure groups, which had
mean estimated time-weighted average arsenic expo-
sure of 0.213, 0.564, and 1.487 mg/m 3 , respectively.
Respiratory cancer mortality was signifi cantly
increased (SMR = 285) on the basis of 302 observed
respiratory cancer deaths between 1938 and 1977 in a
cohort of 8045 white male workers employed for at least
1 year at the Anaconda smelter (Lee-Feldstein, 1986).
Analysis of a subset of the Anaconda cohort ( n = 1800,
including all 277 employees with heavy arsenic expo-
sure) that included information on smoking and other
occupational exposures showed that lung cancer mor-
tality increased with increasing time-weighted average
arsenic exposure, with a small nonsignifi cant increase
in the low group (SMR = 138) exposed to 0.05 mg/m 3
and signifi cant increases in the medium (SMR = 303),
high (SMR = 375), and very high (SMR = 704) groups
exposed to 0.3, 2.75, and 5.0 mg/m 3 , respectively.
Lubin et al . (2000) reweighed the exposure concentra-
tion on the basis of duration and time of exposure and
reevaluated the effects of exposure. Relative risks for
respiratory cancer increased with increasing duration.
SMRs were signifi cantly elevated after exposure to
0.58 mg/m 3 (SMR = 3.01, 95% CI = 2.0-4.6) or 11.3 mg/
m 3 (SMR = 3.68; 95% CI = 2.1-6.4) for 10 or more years,
and after exposure to 0.29 mg/m 3 (SMR = 1.86, 95%
CI = 1.2-2.9) for 25 or more years.
On the basis of the dose-response relationships
between arsenic exposure and excess lung cancer
mortality in workers at the Anaconda smelter and the
ASARCO smelter, the U.S. EPA (2005) has derived a
unit risk estimate (the excess of lung cancer associ-
ated with lifetime exposure to 1

g/m 3 for more than 25 years might
increase the risk for developing respiratory cancer
nearly threefold.
The data must be interpreted with caution because
of the possible infl uence-complicating factors. As for
workers engaged in production of insecticides such
as lead arsenate, calcium arsenate, copper acetoarsen-
ite, and magnesium arsenite, a positive dose-response
relationship between the degree of arsenic exposure
and lung cancer was indicated (Blejer and Wager, 1976;
Ott et al ., 1974). The ratio of observed to expected res-
piratory cancer deaths ranged from 0.6 in the lowest
exposure category to 7.0 in the highest. However, this
dose-response relationship in regard to lung cancer
should be reevaluated after epidemiological adjust-
ment of the smoking histories of the workers.
Jarup et al . (1989) reported signifi cantly increased
lung cancer mortality (SMR = 372, 95% confi dence
interval [CI] = 304-450) based on 106 lung cancer
deaths in a cohort of 3916 male workers employed for
at least 3 months between 1928 and 1967 at the Ron-
skar smelter and followed for mortality through 1981.
Workers were separated into low, medium, and high
arsenic exposure groups, with mean time-weighted
average exposure estimates of 0.05, 0.2, and 0.4 mg/m 3 ,
respectively. Lung cancer mortality was signifi cantly
increased in all three exposure groups in a concentra-
tion-related fashion (SMR = 201, 353, and 480, respec-
tively). A nested case-control analysis of 102 lung
cancer cases and 190 controls from the cohort showed
that lung cancer risk increased with increasing arsenic
exposure in nonsmokers, light smokers, and heavy
smokers (Jarup and Pershagen, 1991).
Enterline and Marsh (1982) reported a signifi cant
increase in respiratory cancer mortality (SMR = 189.4)
based on 104 observed respiratory cancer deaths and
only 54.9 expected over the years 1941-1976 in a cohort
of 2802 male workers employed for at least 1 year
between 1940 and 1964 at the ASARCO smelter. Enter-
line et al . (1987) reanalyzed these data using improved
exposure estimates that incorporated historical meas-
urements of arsenic in the ambient and personal breath-
ing zone of workers. Respiratory cancer mortality was

µ

µ g inhaled inorganic

arsenic/m 3 ) of 4.3 × 10 −3 per ( µ g/m 3 ).

9 DIAGNOSIS, TREATMENT, AND
PROGNOSIS

When specifi c exposures have occurred, poison
control centers and medical toxicologists should be
consulted for medical advice. There are several medical
toxicology texts that provide specifi c information about
clinical treatment after exposures to arsenic (Ellenhorn,
1997; Goldfrank et al ., 1998; Tintinalli et al., 1996).

9.1 Acute Poisoning
9.1.1 Inhalation Diagnosis

Acute intoxication caused by inhalation of arsenic
is unusual except in the case of arsine (see Section 10),