High doses of cadmium are immunotoxic, consistently causing decreased levels of immunoglobulin; suppressing phagocytosis, humoral, and CMI responses; and decreasing host resistance (Blakley 1988; Ritz et al. 1998). Inhalation exposure to lower doses of cadmium caused lymphoid hyperplasia and increased monocyte counts, but did not affect serum IgG, IgM, IgA, lymphocyte, neutrophil, or eosinophil cell counts (Kutzman et al. 1986; Karakaya et al. 1994).
There is little information available on the developmental immunotoxic effects of cadmium. Many authors have demonstrated cadmium transfer across the placenta and alterations in development of human and animal fetuses following maternal exposure to cadmium (U.S. DHHS 1999b). Even low-dose exposure to cadmium during gestation and lactation results in fetotoxicity, characterized predominantly by decreased birth weight, neurophysiologic dysfunction, and skeletal deformities (Branski 1985; Kostial et al. 1993; Nagymajtenyi et al. 1997; Desi et al. 1998). Given that cadmium exposure affects adult immune responses, and that cadmium readily crosses the placenta affecting neurophysiologic responses of the offspring, the possibility exists for immunologic deficits in neonates resulting from in utero cadmium exposure. The close association and interrelatedness in function between neurological and immunologic processes makes this possibility even greater. Further studies are warranted to determine what if any changes in immune function are associated with exposure to this heavy metal.
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