Maternal pesticide exposure from multiple sources and selected congenital anomalies

We explored the relation between various potential sources of maternal peri conceptional pregnancy exposures to pesticides and congenital anomalies in offspring. Data were derived from a case-control study of fetuses and liveb orn infants with orofacial clefts, neural tube defects, conotruncal defects , or limb anomalies, among 1987-1989 California births and fetal deaths. We conducted telephone interviews with mothers of 662 (85% of eligible) orofa cial cleft cases, 265 (84%) neural tube defect cases, 207 (87%) conotruncal defect cases, 165 (84%) limb cases, and 734 (78%) nonmalformed controls. T he odds ratio (OR) estimates did not indicate increased risk for any of the studied anomaly groups among women whose self-reported occupational tasks were considered by an industrial hygienist likely to involve pesticide expo sures. Paternal occupational exposure to pesticides, as reported by the mot her, revealed elevated ORs for only two of the cleft phenotypes {OR = 1.7 [ 95% confidence interval (CI) = 0.9-3.4] for multiple cleft lip with/without cleft palace and OR = 1.6 [95% CI = 0.7-3.4] for multiple cleft palate}. U se of pesticide products for household gardening, by mothers or by professi onal applicators, was associated with ORs greater than or equal to 1.5 for most of the studied anomalies. Use of pesticide products for the control of pests in or around homes was not associated with elevated risks for most o f the studied anomalies, although women who reported that a professional ap plied pesticides to their homes had increased risks for neural tube defect- affected pregnancies [OR = 1.6 (95% CI = 1.1-2.5)] and limb anomalies [OR = 1.6 (95% CI = 1.0-2.7)]. Having a pet cat or dog and treating its fleas wa s not associated with increased anomaly risk. Women who reported living wit hin 0.25 miles of an agricultural crop revealed increased risks for offspri ng with neural tube defects [OR = 1.5 (95%CI = 1.1-2.1)]. For many of the c omparisons, data were sparse, resulting in imprecise effect estimation. Des pite our investigating multiple sources of potential pesticide exposures, w ithout more specific information on chemical and level of exposure, we coul d not adequately discriminate whether the observed effects are valid, wheth er biased exposure reporting contributed to the observed elevated risks, or whether nonspecific measurement of exposure was responsible for many of th e observed estimated risks not being elevated.