Chromium
exists in several valence states, the most stable being trivalent,
hexavalent and metallic chromium (valence state 0). Chromium in other
valence states is apparently important mechanistically, but information
on the toxicity of such compounds is practically non-existent.
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Metallic chromium and trivalent chromium
The
toxicity and fate of chromium species in the body varies with its
valence state: trivalent chromium, as well as metallic chromium, seem
to be relatively innocuous. Although several epidemiological studies
have been carried out with the intention of uncovering even long-term
effects due to these chromium species, no study convincingly shows
any health effects (5,8,15).
Also, in experimental studies, notably on carcinogenicity in experimental
animals, as well on mutagenicity in vitro and in vivo systems, these
chromium species are not active.
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Hexavalent chromium
Hexavalent
chromium species are potent sensitisers of the skin. They also induce
sensitisation of the respiratory tract (although the phenomenon is
not very frequent), they induce mutations in vitro and in vivo and
they cause cancer in experimental animals and in humans (4,5,8,10).
Within the large group of hexavalent chromium compounds, the physico-chemical
characteristics show a wide variation. Notably, the water solubilities
of different hexavalent species - and consequently their fate in the
human body - have distinct characteristics. Also, the carcinogenicity
of different hexavalent chromium compounds differs markedly. Strontium
chromate is apparently more carcinogenic by far than any other chromium
compound and calcium and zinc chromates are also relatively potent.
These chromates are all relatively insoluble in water. Different lead
chromates have been studied rather extensively and are apparently
carcinogenic but have a low potency. Barium chromate, which has not
been equally well studied, shows no convincing evidence of carcinogenicity.
Lead and barium chromates are practically insoluble in water. Of the
readily water-soluble alkali chromates, evidence of carcinogenicity
exists for chromium trioxide (chromic acid) and sodium dichromate.
This evidence is limited and the carcinogenic potency of these compounds
in the experimental settings used is low.
In epidemiological studies on cancer in humans, clearly and consistently
elevated lung cancer risks have been observed in chromate production
(exposure mainly to trivalent and water-soluble hexavalent chromium
compounds), in chromate pigment production (exposure mainly to water-soluble
and water-insoluble chromates) and also in chromium plating using
chromic acid.
•
Health effects among workers in chromium plating
Effects
on nasal mucosa and skin
Exposure to chromic acid (like other hexavalent chromium compounds)
may induce nasal irritation, which in its extreme form may lead to
nasal perforation(2,7,11,13,19).
The information on exposure levels and durations that cause these
different nasal problems is very scanty. Lindberg and Hedenstierna(14)
reported nasal irritation in chrome platers exposed to chromic acid
mist at concentrations >1 µg/m3
and a high frequency of nasal perforations among workers exposed to
peak concentrations >20 µg/m3. Rather
similar results were reported by Lin and co-workers(I3).
Scar formation was estimated to appear in the nasal septum at cumulative
exposure of 0.4 - 1 mg/m3 months
(i.e. exposure to, for example, 40 - 100 µg/m3
for 10 months or 4 - 10 µg/m3 for
100 months), while nasal septum perforations started to appear after
an exposure of 1 - 3 mg/m3 months.
Although chromic acid is acutely irritating, it seems that the risk
of nasal ulceration increases with the time of exposure(19).
In the two British cohort studies(23,25),
four cases of nasal cancer were reported among chromium platers. In
one of the studies, where three cases were observed, this reached
statistical significance. Because of these findings, and because of
the known carcinogenicity of hexavalent chromium compounds in general,
possible pre-cancerous lesions in the nasal mucosa have also been
investigated among chrome platers. No increase in the frequency of
micronuclei - as an indication of genotoxic action - was observed
in exfoliated cells of the nose. In the same study, a positive finding
was observed among ethylene oxide exposed workers(20).
On the other hand, squamous cell metaplasia and cellular atypia were
observed in cells brushed from the nasal mucosa(2).
Chromic acid is irritating to the skin, and induces skin ulceration,
which may lead to "chrome holes" and scar formation(12,19,28).
It has been proposed that chromic acid exposure leads to skin ulcers
only when there is a pre-existing cut, abrasion or other defect in
the protective epidermis(28).
Both sensitisation and irritation may be behind a contact dermatitis
in a chrome plater. The latter mechanism seems to be involved more
often(12).
Cancer of the lung
Suspicion of an increased risk of cancer among chrome plating workers
was raised in a small study performed on decorative chrome platers
in the UK(27).
Forty-nine lung cancer deaths were observed, while only 35 were expected.
Based on studies published in the 1980s and earlier, the International
Agency for Research on Cancer concluded in 1990 that there is sufficient
evidence of carcinogenicity of chromium VI compounds as encountered
in (the chromate production, chromate pigment production and) chromium
plating industries. This conclusion was based mainly on five studies.
The largest of these was a mortality analysis of the population investigated
in the previously cited UK study(27).
It reported(23) a 1.5-fold mortality
from lung cancer among chrome bath workers. No association was observed
between lung cancer mortality and work with nickel baths.
In another study from the UK(18),
the mortality from lung cancer among chromium platers from Yorkshire
was 1.4-fold in comparison to manual workers from other industries
in the same geographic area.
In a small Japanese study(16,26),
an increased risk of lung cancer was observed among platers. When
the cohort of platers was divided into chrome platers and other platers,
the excess was larger among the chrome platers - but did not reach
statistical significance for either subgroup.
In a study in the US, a doubling of lung cancer mortality was observed
among workers in a die-casting facility that also performed nickel
and chromium electroplating. However, the workers had also been exposed
to nickel and polycyclic aromatic hydrocarbons, both of which increase
the risk of lung cancer(21).
Finally, in a small cohort of Italian chrome platers, the risk of
lung cancer was three-fold over the expected and the lung cancer risk
was only observed among hard chrome platers, whose exposure to chromic
acid was higher than that of the decorative chrome platers(3).
Two of the above studies have recently been updated, and form the
most reliable basis for the assessment of the carcinogenicity of chromic
acid mist in humans. They also give indications on the potency of
this exposure in cancer induction(22,24,25).
In the follow-up to the largest-studied chromium plater cohort in
England(22),
the mortality experience of 2,689 men and women was investigated between
the years 1946 and 1995. Altogether 69 lung cancer cases and 621 deaths
from other causes were observed. In both women and men, lung cancer
excess was observed among chrome bath workers, but not among other
chrome-exposed workers. The magnitude of the risk increased with the
time of work at chrome baths, and was about 4-fold among those working
longer than 5 years (relative risk, 3.88, 95% confidence interval,
1.68 to 8.74). As in all studies on lung cancer, smoking is a potential
confounding factor, especially since no information was available
on the smoking habits of this cohort.
However, the magnitude of the risk is such that it cannot be explained
by smoking: risks greater than 1.5-fold cannot be attributed to smoking
differences alone. In addition, the fact that the lung cancer risk
was related to the duration of work at the chrome baths, makes smoking
a very unlikely factor for explaining the finding of increased cancer
risk with chromate exposure. Another potential cause for the excess
lung cancer could be exposure to nickel compounds, which have also
been shown to cause lung and nasal cancer at exposure levels encountered
in nickel refining(1,9).
However, the mortality from lung cancer was not elevated for those
platers in the studied factory, who had exposure to nickel, but not
to chromium(17).
In a follow-up of the workers in 54 chromium plating plants in Yorkshire,
England(25),
the lung cancer mortality between 1972-1997 was studied in reference
to their working histories before 1972. For 85% of the members of
this cohort, smoking habits were known; the results could thus be
corrected for this potentially important confounding factor. However,
the effect of smoking correction was very minor. The overall lung
cancer risk among the chrome platers was 1.9-fold over the expected
figures (SMR 185, 95% CI 141-238).
Carcinogenic potency of chromic acid mist
The information on how strong a carcinogen chromic acid mist is, is
quite limited.
Exposure has not generally been quantitatively assessed. Instead,
surrogates such as time at work have been used. No laboratory animal
studies are available, where the exposure is qualitatively similar
to chromium plating operations.
Limited quantitative information on exposure to chromic acid was only
available in the previously mentioned study carried out in a large
chromium-plating plant in England(22,24),
based on data collected by the company from the year 1973 onwards,
the working levels of chromic acid mist exposure were "almost always
below 50 µg/m3 CrO3
(about 25 µg/m3 Cr VI)" and "earlier
conditions were, in general, certainly worse".
If it is assumed that all lung cancer risk in this cohort was due
to exposure to chromic acid mist, and that the working-time average
exposure was 100 µg Cr VI/m3, then it could
be very roughly calculated that for 1,000 workers exposed for the
duration of their working life to 50 µg Cr VI/m3,
there would be 310 excess lung cancer deaths.
If, however, the true exposure in the studied cohort had been 1,000
µg Cr VI/m3 (i.e. the exposures before 1973
had been very high indeed), the similarly calculated excess lung cancer
number would be 40.
Furthermore, on the assumption that, rather than all lung cancers
being induced by chromic acid, 2/3 of them were in fact induced by
other factors such as smoking, the corresponding predicted number
of lung cancer cases per 1,000 workers exposed for their working life
to 50 µg Cr VI/m3 would be 130 and
14(24).
Thus, predicted cancer risk in the worst case scenario is a catastrophe
and even the lowest estimate means a significant increase in the lung
cancer risk.
Other respiratory diseases
Some studies have reported an elevated occurrence of respiratory symptoms
and of decreased pulmonary function among chrome platers(11,14,19).
No clear-cut picture emerges from the mortality from non-malignant
respiratory diseases in the cohort studies (on lung cancer). Bronchial
asthma is a rare disease after exposure to hexavalent chromium compounds
and cases have been reported also among chromium platers(19).
•
Prevention of exposure and control of chromic acid mist
The
most effective prevention of exposure is replacement of hexavalent
chromium with trivalent, which has been shown to be feasible in decorative
chrome finishing.
With tightening environmental and health requirements and improved
technology, such substitution is now a very viable alternative.
Safer Chromium Finishing, published by the Metal Finishing Association
(UK) provides further information(6).
Where such a change to the process is not possible (i.e. leads to
lower quality products) it is necessary to achieve adequate control
of chromic acid mist by other means.
With some operations the emission of chromic acid mist can be controlled
by total enclosure of the process. Where this is not reasonably practicable,
it is necessary to achieve adequate control by providing efficient
exhaust ventilation and/or by treating the electrolyte (plating solution)
with a mist suppressant to limit the emission of mist into the workplace
atmosphere.
Even when the process can be completely enclosed, extract ventilation
should still be provided at the enclosure. The extraction should be
sufficient to ensure that there is movement of air into the enclosure
when any access points in the enclosure are opened for purposes of
process control, so preventing emission of chromic acid mist into
the workroom atmosphere.
•
Conclusions
Workers
in chromium electroplating, where (hexavalent) chromic acid is used,
are at risk of developing lung cancer. It is likely that there is
also a low risk of nasal cancer.
Hexavalent chromium is genotoxic, and although it is not clear that
this is the mechanism of carcinogenesis - or the sole such mechanism
- it is prudent to keep the exposure as low as is possible using best
available technology.
Exposure to chromic acid at levels that are in compliance with the
prevailing occupational exposure standards in many countries, that
is, 50 µg Cr VI/m3, are likely to carry a substantial
- albeit unlikely, an epidemiologically detectable - lung cancer risk.
Whether there is also a risk of other lung diseases is not clear.
Exposure to chromic acid causes irritation, erosion, and ulceration
of nasal mucosa. Serious irritative effects have been observed at
exposure levels of approximately 10 µg/m3.
Chromic acid exposure induces contact dermatitis and, especially when
the skin has pre-existing mechanical trauma, chrome ulcer. In experimental
animals, chromic acid is a strong sensitiser, and chromium-induced
respiratory and dermal sensitisation have been - infrequently - reported
among chromium platers.
Where possible, trivalent rather than hexavalent chromium should be
used in electroplating. Where this is not technically viable, workers
should be effectively protected against exposure, primarily using
closed electroplating systems.
•
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