Chemistry Reference
In-Depth Information
the nasopharynx against an expected 0.2, with a risk
ratio of 10; however, heavy exposure to nickel had
also occurred. In a follow-up and an extension of the
study in the nickel-cadmium battery workers, many of
whom had been heavily exposed to both cadmium and
nickel, in a subgroup exposed for more than 15 years,
there were now 3 deaths from prostatic cancer with
1.6 expected and 3 deaths from lung cancer where 2.5
had been expected from Swedish male mortality rates.
Thus, the small, no signifi cant excess mortality from
prostatic cancer in this cohort has been maintained
(Andersson
et al.
, 1984). In a further analysis of the
total cohort, the standardized mortality ratio for both
prostatic and lung cancer increased with increasing
dose and latency but did not attain statistical signifi -
cance (Elinder
et al.
, 1985).
In copper-cadmium alloy workers in Britain, again
with heavy past exposure exceeding 1 mg Cd/m
3
, a
total of 7 cases of lung cancer was observed compared
with 3.9 expected in men exposed for more than 10
years (Holden, 1980). Among vicinity workers not
directly involved in cadmium processes, 8 cases of pro-
static cancer were observed compared with 3 expected,
although only 3 of these 8 had had more than 15 years'
exposure (Holden, 1980). With no evidence of a dose-
response relationship, their association with past
cadmium exposure might be questioned. No new evi-
dence of any relation between occupational exposure
to cadmium oxide dust and cancer of the prostate was
found in a mortality study of more than 3000 nickel-
cadmium battery workers in Britain, which included
the 4 cases previously observed by Kipling and
Waterhouse (1967). There was some indication of an
increased risk from cancers of the respiratory system,
because 89 deaths were observed, whereas only 70.2
were expected, although exposure to welding fumes
and nickel hydroxide was considered an important
confounding factor (Sorahan and Waterhouse, 1983).
In an extended follow-up study of the cohort
described by Lemen
et al.
(1976), mortality experience
has been investigated through 5 additional years and
the cohort extended to include white men with at least
6 months' employment in a production area (Thun
et al.
, 1985). Since 1925, the plant had refi ned cadmium
and a number of other trace metals from “baghouse”
dust, a by-product of lead smelting. Previously, the
plant had functioned as an arsenic smelter and ini-
tially as a lead smelter. Exposure to cadmium had been
heavy; more than 80% of the workers measured had a
mean urine cadmium concentration of at least 20
In addition, the study showed a signifi cant dose-
response relationship between lung cancer mortality
and cumulative exposure to cadmium (Stayner
et al.
,
1992a; 1992b). No further deaths from prostatic cancer
have been reported since the earlier study, thus weak-
ening the original observation by Lemen
et al.
(1976)
of a possible association between prostatic cancer and
cadmium exposure. With regard to lung cancer, Thun
et al.
(1985) made certain assumptions from which they
concluded that the two confounding factors, smoking
cigarettes and past arsenic exposure, were unlikely
to account for the observed excess lung cancer risk.
However, arsenic exposures after 1926 may have been
higher than estimated, and no account was taken of
the possible combined effect of smoking cigarettes and
arsenic exposure (Pershagen
et al.
, 1981).
To investigate mortality on a scale larger than avail-
able in earlier studies, the mortality of almost 7000
cadmium-exposed male workers from 17 cadmium
processing plants in England, born before 1940 and
exposed to cadmium for more than 1 year between
1942 and 1970, was examined initially until the end
of 1979 (Armstrong and Kazantzis, 1983), followed up
for an initial 5-year period from 1980-1984 (Kazantzis
et al.
, 1988), and for a second 5-year period to the end
of 1989 (Kazantzis
et al.
, 1992). Jobs were assessed for
each year as involving high, medium, or low exposure
to cadmium. The years at risk of the study population
were divided into three groups, “ever high” (minimum
of 1 year), “ever medium” (minimum of 1 year), and
“always low.” Signifi cant excess lung cancer mortality
was observed in both the 5-year and the total study
periods. The SMR increased with intensity of expo-
sure in both the 5-year and the total study periods,
being signifi cantly raised in the “ever high” exposure
groups. The increased risk was most marked in men
fi rst employed before 1940 with long exposure and
a long period of follow-up. However, in attributing
this apparent dose-response relationship to cadmium,
account has to be taken of multiple confounding fac-
tors, including arsenic, in the study population (Ades
and Kazantzis, 1988). No increased risk from prostatic
cancer was observed in the overall cohort, with one
case in the “ever high” exposure group where one was
expected.
In a systematic review of studies since the IARC
(1993) classifi cation of cadmium as a human carcino-
gen, several cohorts of cadmium workers have been
updated with additional data available regarding envi-
ronmental exposure to cadmium and cancer risk (IARC,
1993). A lower relative risk of lung cancer in occupa-
tional groups exposed to cadmium in the absence of
arsenic and nickel is indicated in some studies. No
evidence was found that nonmalignant respiratory
g/l.
Mortality from lung cancer was signifi cantly greater
among the workers employed for 2 years or more than
would have been expected from US white male rates,
with 20 observed deaths where 11.43 were expected.
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