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R M Whyatt

Publications and source records attributed to R M Whyatt.

20 records · Page 2Linked to original sources

Developmental effects of exposure to environmental tobacco smoke and material hardship among inner-city children.

Because of the growing concern that exposures to airborne pollutants have adverse effects on fetal growth and early childhood neurodevelopment, and the knowledge that such exposures are more prevalent in disadvantaged populations, we assessed the joint impact of prenatal exposure to environmental tobacco smoke (ETS) and material hardship on the 2-year cognitive development of inner-city children, adjusted for other sociodemographic risks and chemical exposures. The purpose was to evaluate the neurotoxicant effects of ETS among children experiencing different degrees of socioeconomic disadvantage, within a minority population. The sample did not include children exposed to active maternal smoking in the prenatal period. Results showed significant adverse effects of prenatal residential ETS exposure and the level of material hardship on 2-year cognitive development, as well as a significant interaction between material hardship and ETS, such that children with both ETS exposure and material hardship exhibited the greatest cognitive deficit. In addition, children with prenatal ETS exposure were twice as likely to be classified as significantly delayed, as compared with nonexposed children. Postnatal ETS exposure in the first 2 years of life did not contribute independently to the risk of developmental delay, over and above the risk posed by prenatal ETS exposure. The study concluded that prenatal exposure to ETS in the home has a negative impact on 2-year cognitive development, and this effect is exacerbated under conditions of material hardship in this urban minority sample.

Child↗

Exposure misclassification error in studies on prenatal effects of tobacco smoking in pregnancy and the birth weight of children.

Adverse effects of maternal smoking have been mostly identified through epidemiologic investigations that have used questionnaires to assess active and passive smoking. However, unvalidated self-reports of cigarette smoking may bias true estimates of relative risk of smoking-related health outcomes. This report is based on two separate investigations. First, within a molecular epidemiologic study of the relationship between environmental exposures (smoking, air pollution, diet) and developmental impairment, we have compared self-reported tobacco smoke exposure during pregnancy to plasma cotinine measurements in mothers. One hundred and fifty-eight patients from obstetrical wards in Cracow and in Limanowa, Poland were included in the parent study. Biochemically-identified smokers were defined as persons with plasma cotinine levels greater than 25 ng/mL. The data showed that exposure classification based on self-reported smoking status compared with cotinine values was of low sensitivity (52%) but of high specificity (98%). We assessed the effect of this exposure classification error on the association between low birth weight (LBW) and smoking in pregnancy using data from a related epidemiologic study of children's health in Cracow involving 1115 subjects. The odds ratio (OR) estimates for smoking and LBW after adjustment for exposure misclassification error were significantly higher than before adjustment (crude OR = 2.9, corrected OR = 5.1). The estimated attributable fraction (AF(pop)) based on the crude OR amounted to 22%; however, after adjustment it reached 50%. The corresponding values for the attributable fraction in the exposed group (AF(exp)) were 66% and 80%. These results illustrate the value of validating questionnaire responses on smoking during pregnancy against reliable biologic markers.

Adult↗