Methylmercury Exposure and Neurotoxicity

Exposure to high levels of methylmercury has produced fatalities and devastating neurological damage among adult survivors. 1 Severe cases of in utero methylmercury poisoning strongly resemble cerebral palsy and are often accompanied by deafness and mental retardation. 1,2 In addition, clinically evident cases of neurological damage have occurred among infants born to mothers whose own symptoms were often only transient paresthesias. Consequently, the fetus is considered much more sensitive to methylmercury exposure than is the adult. See also p 701. Although recognizing clinically evident symptoms is relatively straightforward, determining levels of in utero methylmercury exposures associated with the onset of toxic responses in infants and children is a much more complex problem. In this issue of THE JOURNAL, Davidson et al 3 present findings from a cohort in the Republic of Seychelles that indicate consumption of methylmercury from fish did not produce developmental deficits among children exposed both in utero and postnatally to methylmercury. Developmental status among the Seychellois was assessed by traditional indices of child development (among others, the Woodcock-Johnson Tests of Achievement and the General Cognitive Index of the McCarthy Scales of Children’s Abilities). In the Seychellois cohort, mean maternal hair mercury concentrations during pregnancy were 6.8 ppm (SD, 4.5; range, ,3-26.7 ppm). Davidson et al have responded to the need to evaluate effects of long-term, low-level methylmercury exposures and suggest that the Seychellois data can be used to support efforts to define an upper tolerable level for methylmercury in hair. The most direct comparison with the Seychellois data is the longitudinal assessment of children from a seafood (mostly pilot whales)‐consuming population in the Faroe Islands. 4