Comparison of visual function at adulthood and during aging in monkeys exposed to lead or methylmercury.
Of critical importance is the issue of whether exposure to a neurotoxic agent early in life or over a major portion of the lifespan can result in an age-related accelerated decline in neurological function. There is evidence in humans and animals that exposure to methylmercury may produce delayed neurotoxicity associated with aging. While lead is a ubiquitous pollutant, the potential of long-term lead exposure to accelerate age-related functional decline in nervous system function has apparently not been explored. In the current study, visual function assessed during adulthood was compared to results during aging in monkeys exposed to 500 or 2000 microg/kg/day of lead from birth onward, 50 microg/kg/day of methylmercury from birth to seven years, or 10, 25, or 50 microg/kg/day of methylmercury throughout gestation to four years of age. Spatial contrast sensitivity functions and visual fields were assessed in methylmercury-exposed monkeys, and spatial and temporal contrast sensitivity functions were assessed in monkeys exposed to lead. The frequency and amplitude at peak sensitivity and the high-frequency cut-off were compared at the two assessment periods for the contrast sensitivity functions. Age-related decrements were observed on both spatial and temporal visual function for all parameters. Treatment-related effects were observed in the monkeys exposed to methylmercury in utero and postnatally during the first assessment period but not during aging, whereas lead-exposed monkeys exhibited differences in temporal visual function at the first assessment but not the second. There was no evidence for accelerated decline in contrast sensitivity as a result of exposure to either toxicant. However, four of 10 methylmercury-treated monkeys exhibited slight constriction of visual fields at the second assessment that had not been present earlier. These results extend previous findings of evidence for delayed neurotoxicity in the somatosensory and auditory systems of these methylmercury-exposed groups.
Rice
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Toxicology Research Division, Bureau of Chemical Safety, Food Directorate, Health Protection Branch, Health Canada. rice.deborah@epa.gov
Hayward
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D000375:Aging / Q000502:physiology*; D000465:Algorithms; D000818:Animals; D002138:Calibration; D005260:Female; D000882:Haplorhini; D006801:Humans; D007854:Lead / Q000633:toxicity*; D008297:Male; D008767:Methylmercury Compounds / Q000633:toxicity*; D011601:Psychophysics; D014785:Vision, Ocular / Q000187:drug effects*; D014794:Visual Fields / Q000502:physiology
D008767:Methylmercury Compounds; D007854:Lead