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.