Contamination of the environment by mercury occurs mainly through industrial waste and through its use as a fungicide on crops. This inorganic or elemental mercury is then methylated to organic mercury by microorganisms and incorporated into the food chain where it biomagnifies. The primary exposure to humans comes from consuming fish with high levels of biomagnified mercury in their tissues.

Elemental, inorganic, and organic mercury are toxic to living organisms. The toxic effects mainly manifest as delays in neurological developmental and mental retardation, but immunologic effects are also seen. The immune effects of mercury are both inhibitory and stimulatory. Mercury decreases antibody titers in rabbits, lowers serum IgG, IgG1, and IgE levels in mice, and reduces the lymphoproliferative response to T cell mitogens in rats (Wild et al. 1997). In humans, inorganic mercury causes an autoimmune response with IgG and complement C3 deposition in the kidney, the presence of antiglomerular basement membrane antibodies, and an increase in anti-DNA antibody titer (U.S. DHHS 1999a; Cardenas et al. 1993). Additionally, T cells are stimulated with increases in CD3+, CD4+ and CD8+ cells. In mice, mercury vapor and mercuric chloride both induced a syndrome similar to the autoimmune response in humans characterized by general stimulation of the immune system, hyperimmunoglobulinemia, anti-nucleolar autoantibodies, and glomerular disease accompanied by vascular immune complex deposits.

Mercury stimulated or suppressed immune responses depending on genetics and susceptibility of the mouse strain. Immune hyperreactivity and autoimmunity were seen in SJL/N mice, but immune responses were suppressed in B6C3Fj mice (U.S. DHHS 1999a). B6C3Fj mice exposed to 2.9 or 14.3 mg Hg/kg/day as mercuric chloride in the drinking water demonstrated a suppression of lymphocyte proliferation to T cell mitogens. When SJL/N mice were exposed to mercuric chloride, antinucleolar antibodies were observed and deposition of granular IgG in the renal mesangium and glomerular blood vessels occurred (U.S. DHHS 1999a).

All forms of mercury transfer across the placenta to the fetus, but methyl mercury transfers to a greater extent than other forms. Mercury actually accumulates in placental tissues, and concentrations 2.25 times higher than in maternal tissues have been reported (Wild et al. 1997). Mercury is also transferred in milk during lactation (Wild et al. 1997). The fetus is more susceptible to mercury exposure than adults with 1/10 the adult toxic dose inducing toxic responses in the fetus. Abnormalities from gestational mercury exposure are dose-dependant and are greatest when exposure occurs in the second trimester. Developmental defects following in utero exposure include fetal death, dystocia, decreased fetal weight, immunologic alterations, skeletal deformities, brain lesions, hydronephrosis, and renal hypoplasia (U.S. DHHS 1999a).

Low-dose placental and lactational exposure to mercury affects thymocyte development and stimulates certain mitogen- or antigen-induced lymphocyte activities. Rat pups indirectly exposed to methyl mercury during gestation and lactation through their dams' drinking water at a dose recognized as safe for adults (5 or 500 mg/L methyl mercury chloride) exhibited depressed NK cytolytic activity and enhanced PWM-stimulated lymphocyte proliferation (Wild et al. 1997). In another study, female mice were exposed to methyl mercury at 0, 0.5, or 5 mg Hg/kg for 10 weeks prior to mating and during gestation and through 10 days of lactation (Thuvander et al. 1996c). The numbers of splenocytes in the pups were increased at day 10 and day 22, and thymocytes were increased at day 22 in the 0.5 mg/Kg-exposed animals. There were increased numbers and altered proportions of the lymphocyte subpopulations within the thymus at both concentrations of mercury. The proliferative response of splenocytes to LPS was increased in the high exposure group as was the antibody response to viral antigen in pups from the 0.5 mg Hg/kg exposure (Thuvander et al. 1996c). The significance of the immune stimulation is not known but may be a sign of induced autoimmunity.

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