Abstract
Environmental toxicants can modulate endocrine function. Interest has been directed at those chemicals which interact with sex hormone because of their potentially irreversible effects on brain development. Studies on the effects of in utero and lactational exposure to hormone‐modulating pollutants have focused on cognitive function. Study objectives included: a) identification of a combination of behaviours that differentiate between boys and girls; and b) determination if early chemical exposure affects variability in sex‐dimorphic behaviours. We utilized an established epidemiologic cohort (New York State Angler Cohort Study) assembled to assess the influence of contaminated sport fish consumption on health in adults and their offspring. Children 5 to 11 years of age were targeted. Using a postal questionnaire survey methodology in which a parent served as the informant, 1,112 of 1,692 households contacted (66%) returned completed questionnaires on 1,415 children (52% male, 48% female). Maternal report confirms both pre‐ and postnatal contaminant exposures: 40% of the mothers consumed sport fish for 1 yr and 28% of their offspring ate contaminated fish. Consumption durations do not differentiate respondents from nonrespondents. A discriminant function based upon gender behaviour scale scores was robust in differentiating boys and girls. Stepwise multiple regression analyses revealed that masculine behaviour increased among boys with age and the number of years of maternal sport fish consumption whereas feminine behaviour increased among girls with the duration of breast‐feeding. Increased age and previous live‐births were associated with more masculine behaviour in the girls. For both sexes, exposure was unrelated to the prevalence of learning problems, non‐right handedness, or behavioural problems. Although this study does not rule out differential gender socialization influences, the findings are consistent with an effect of contaminant exposure on sex‐dimorphic behaviours in humans. This study was in part funded with grants from the National Institute of Environmental Health Sciences, NIH (R03ES08500‐01), the Great Lakes Protection Fund (RM791‐3021), and the Agency for Toxic Substances and Disease Registry (H75/ATH298338).
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