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http://ehp.niehs.nih.gov/1205921/
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Prenatal Exposure to the Pesticide DDT and Hypertension Diagnosed in Women before Age 50: A Longitudinal Birth Cohort Study
Michele La Merrill,1,2,3 Piera M. Cirillo,4 Mary Beth Terry,5 Nickilou Y. Krigbaum,4 Julie D. Flom,5 and Barbara A. Cohn4
Background: Elevated levels of the pesticide DDT (dichlorodiphenyltrichloroethane) have been positively associated with blood pressure and hypertension in studies among adults. Accumulating epidemiologic and toxicologic evidence suggests that hypertension during adulthood may also be affected by earlier life and possibly the prenatal environment.
Objectives: We assessed whether prenatal exposure to the pesticide DDT increases risk of adult hypertension.
Methods: We examined concentrations of DDT (p,p?- and o,p?-) and its metabolite p,p?-DDE (dichlorodiphenyldichloroethylene) in prenatal serum samples from a subset of women (n = 527) who had participated in the prospective Child Health and Development Studies birth cohort in the San Francisco Bay area while they were pregnant between 1959 and 1967. We surveyed daughters 39?47 years of age by telephone interview from 2005 to 2008 to obtain information on self-reported physician-diagnosed hypertension and use of hypertensive medication. We used multivariable regression analysis of time to hypertension based on the Cox proportional hazards model to estimate relative rates for the association between prenatal DDT exposures and hypertension treated with medication in adulthood, with adjustment for potential confounding by maternal, early-life, and adult exposures.
Results: Prenatal p,p?-DDT exposure was associated with hypertension [adjusted hazard ratio (aHR) = 3.6; 95% CI: 1.8, 7.2 and aHR = 2.5; 95% CI: 1.2, 5.3 for middle and high tertiles of p,p?-DDT relative to the lowest tertile, respectively]. These associations between p,p?-DDT and hypertension were robust to adjustment for independent hypertension risk factors as well as sensitivity analyses.
Conclusions: These findings suggest that the association between DDT exposure and hypertension may have its origins early in development.
Michele La Merrill,1,2,3 Piera M. Cirillo,4 Mary Beth Terry,5 Nickilou Y. Krigbaum,4 Julie D. Flom,5 and Barbara A. Cohn4
Background: Elevated levels of the pesticide DDT (dichlorodiphenyltrichloroethane) have been positively associated with blood pressure and hypertension in studies among adults. Accumulating epidemiologic and toxicologic evidence suggests that hypertension during adulthood may also be affected by earlier life and possibly the prenatal environment.
Objectives: We assessed whether prenatal exposure to the pesticide DDT increases risk of adult hypertension.
Methods: We examined concentrations of DDT (p,p?- and o,p?-) and its metabolite p,p?-DDE (dichlorodiphenyldichloroethylene) in prenatal serum samples from a subset of women (n = 527) who had participated in the prospective Child Health and Development Studies birth cohort in the San Francisco Bay area while they were pregnant between 1959 and 1967. We surveyed daughters 39?47 years of age by telephone interview from 2005 to 2008 to obtain information on self-reported physician-diagnosed hypertension and use of hypertensive medication. We used multivariable regression analysis of time to hypertension based on the Cox proportional hazards model to estimate relative rates for the association between prenatal DDT exposures and hypertension treated with medication in adulthood, with adjustment for potential confounding by maternal, early-life, and adult exposures.
Results: Prenatal p,p?-DDT exposure was associated with hypertension [adjusted hazard ratio (aHR) = 3.6; 95% CI: 1.8, 7.2 and aHR = 2.5; 95% CI: 1.2, 5.3 for middle and high tertiles of p,p?-DDT relative to the lowest tertile, respectively]. These associations between p,p?-DDT and hypertension were robust to adjustment for independent hypertension risk factors as well as sensitivity analyses.
Conclusions: These findings suggest that the association between DDT exposure and hypertension may have its origins early in development.