revised final - Agency for Toxic Substances and Disease Registry ...

MERCURY
2. HEALTH EFFECTS
control subjects. However, these data should also be interpreted with caution since age has an influence on
aneuploidy, and in this study, there was a general trend toward a higher incidence of aneuploidy in the older
exposed workers (ages 36–63 years). It is noteworthy that in a subsequent study performed by these
investigators (Verschaeve et al. 1979), no adverse effects on the structure or number of chromosomes were
demonstrated in 28 subjects exposed to moderate levels of metallic mercury (urinary levels of 50 µg/L).
The authors concluded that the results from their 1976 study, showing an association between increased
chromosomal aberrations and occupational exposure to mercury, may have been affected by factors other
than exposure to mercury compounds.
No increased frequency of structural aberrations was found in 22 workers exposed to mercury vapors; no
information was provided on numerical aberrations (Mabille et al. 1984). The mean duration of exposure
was 4 years, and the mean urinary and blood mercury levels in the exposed group were 117 µg/g creatinine
and 0.031 µg/mL, respectively. More recently, peripheral lymphocytes from 26 male chloralkali workers
exposed to mercury vapors (25–50 µg/m 3 ), for a mean exposure time of 10 years, were analyzed for
micronucleus induction. The results were compared to results obtained from 26 unexposed subjects
(Barregard et al. 1991). Groups were matched for age (±7 years) and smoking habits; plasma, erythrocyte,
and urine mercury levels were determined. Parallel lymphocyte cultures from each donor group were
incubated in the presence of pokeweed mitogen, which stimulates both B- and T-lymphocytes, and
phytohemagglutinin, which primarily activates T-cells. The analysis showed no significant increase in the
frequency or the size of micronuclei in the exposed versus the control group. Nor was there a correlation
between micronuclei induction and plasma, erythrocyte, or urinary levels of mercury. Within the exposed
group, however, there was a significant correlation between micronuclei induction in phytohemagglutininstimulated
lymphocytes and cumulative exposure (whole-blood mercury level over employment time); the
response was independent of age or smoking habits. These results, suggesting a genotoxic effect on
T-lymphocytes, are unusual since there is evidence that B-lymphocytes may be more sensitive indicators of
chemically induced clastogenesis than T-lymphocytes (Högstedt et al. 1988). The authors stated that the
evidence of a genotoxic response confined to T-lymphocytes could have been a random finding but
hypothesized that long-term exposure to mercury may cause an accumulation of cytogenetic effects.
Similarly, there was no correlation between urinary mercury levels (60–245 µg/L) or the duration of
exposure (11–34 years) and increased frequency of structural aberrations and micronuclei in the
lymphocytes of 29 male workers exposed to mercury fulminate (Anwar and Gabal 1991). From the overall
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