Mercury Exposure In Humans

By Author: Sulamita Berrezi
Total Articles: 115
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Skin Mercury produces a symptom complex called acrodynia. Its main features are redness of the lips and pharynx, a strawberry tongue, tooth loss, skin desquamation, and pink or red fingertips, palms, and soles. The eyes are also affected, and photophobia and conjunctivitis are seen. In addition, there is enlargement of the cervical lymph nodes, loss of appetite, joint pain, and, occasionally, vascular thromboses, possibly by the induction of platelet aggregation, which has been shown in in vitro experiments. There is also a neurological component to this symptom complex: irritability, weakness of the proximal muscles, hypotonia, depressed reflexes, apathy, and withdrawal. Kidneys Mercury has been hypothesized to stimulate T lymphocytes to produce a glomerular antibasement membrane antibody, which produces sufficient damage to lead to the proteinuria observed with mercury toxicity. The basis for this theory derives from studies in rats in which mercuric chloride injection produced these antibodies, both as IgG and IgM. There was also an observed increase in CD8þ (suppressor) T cells in the glomeruli. In addition, the rats ...
... developed proximal tubular necrosis. However, it is not clear that this theory is correct because methyl mercury can induce apoptosis, or programmed cell death, of the T lymphocytes, possibly by damaging mitochondria and inducing oxidative stress. Nervous system In the large epidemics of methyl mercury ingestion reported in both Japan and Iraq, infants were reported to have psychomotor retardation, flaccid paralysis, microcephaly, ataxia, choreoathetotic motions of the hands, tonic seizures, and narrowing of the visual fields. Studies of neonatal rats injected with methyl mercuric chloride reported postural and movement changes during the fourth week of life. Mercury exposure in humans can result in deficits in attention and concentration, especially under pressure of time deadlines. One report suggests that this may be due to mercury damage to the posterior cingulate cortex, where these functions are regulated.A toxic effect of mercury on bone marrow would explain the abnormalities in red cell production, immune cell production, and bone formation.Hemolysis of red blood cells resulting from mercury exposure may be at least in part due to peroxidative damage inasmuch as studies on workers chronically exposed to mercury vapors demonstrate a reduction in erythrocyte enzyme activity of glutathione peroxidase.Finally, although the effects of mercury exposure on bone have not been studied in humans, experiments in mice indicate that the administration of an anti-metallothionein antibody and mercury results in decreased biochemical markers of bone formation and decreased bone mineral density. The mechanism for this is unknown, but mercury interference with differentiation of osteogenic precursor cells is postulated.