There is a progressive increase in the general background level of mercury in our North American environment. Inorganic mercury in the environment can be converted to organic mercurials in the biological food chain and accumulate in food stuffs, principally as methylmercury. Man may directly consume methylmercury as an occupational hazard or may indirectly acquire chronic intoxication as the final predator in the biological food chain. Methylmercury in man, unlike inorganic and some other organic mercurials, is widely distributed in body tissues, producing a different pattern of clinical findings than inorganic or elemental mercury. Methylmercury freely passes through the placental barrier of man and some experimental animals. In addition to the neuronolysis seen in the adult, the fetal brain injury is diffuse. A generalized decrease in size of the brain and other viscera is seen. Beyond this fragmentary evidence little is known about the embryopathic effects of chronic mercury intoxication on the primate. The investigation is designed to uncover deleterious effects on the fetus at the level of human "subclinical" exposure as well as at higher dosage levels. The purpose of this experiment is to determine the threshold level of chronic exposure of pregnant monkeys to methylmercury which produces neruophysiologic deficits in the offspring. Other parameters in the primate such as embryopathic dose range, pathogenesis of the animals, size of brain and viscera and molecular mechanism of injury will be investigated. Although rodents are an excellent experimental animal for determining some features of the above, extension of the studies to primates will yield more information more directly transposable to man. Findings in the rodents will be tested in primates where subtle sensory behavioral and intellectual changes can be tested.
NIH ExPorter
NIH ExPorter