Recent data suggest that prenatal exposure to p,p'-DDE may reduce height and increase body mass index (BMI) in childhood, thus potentially raising the risk of adult health problems. The association between prenatal DDE exposure and growth was evaluated in 788 boys from Chiapas, an area of Mexico where DDT was recently used. The median DDE levels in maternal serum at birth (2002)(2003) were 2.7 μg/g lipid. 2,633 measurements of height (cm) and weight (kg) were obtained in [2004][2005]. The median age of the children during follow-up was 18 months (quartiles 14 and 22 months). Height and body mass index (kg/m 2 ) were age-standardized and expressed as standard deviation scores (SDS). Multivariate random-effect models for longitudinal data were fitted and predicted height and BMI SDS were estimated from the adjusted models. Overall, associations between prenatal DDE level and height or BMI SDS at any given age were not observed. For example, the predicted values showed that children with the highest exposure (DDE: >9.00 μg/g) compared to those least exposed (DDE: < 3.01 μg/g) grew similarly and they had a BMI SDS similar to the referent group. The results do not support the prior findings of an association of DDE exposure with childhood height or BMI.

Background Prenatal exposure to 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (p,p′-DDE), the major breakdown product of DDT, has been associated with recurrent lower respiratory tract infections (LRTI) in infants. However, epidemiological investigations are limited. Objective To assess the association of prenatal exposure to p,p′-DDE and p,p′-DDT with the occurrence of LRTI in boys from Chiapas, a highly exposed area of Mexico. Methods We analyzed data from 747 singleton boys whose prenatal exposure to p,p′-DDE and p,p′-DDT was determined in maternal serum drawn at delivery (2002–2003). LRTI (i.e., pneumonia, bronchiolitis, and other illness of the bronchi) experienced by the children were reported by their mothers during in-person interviews. The median age of the children when they were last seen was 21.4 months (quartiles 19.1 and 25.3 months). Results Median exposure to p,p′-DDE in this population was higher (2.7 μg/g lipid) than recent U.S. levels (0.20 μg/g). There were 0.19 episodes of LRTI per child-year. After adjusting for potential confounders, children in the highest category of p,p′-DDE (>9.00 μg/g) exposure compared to those in the lowest (≤3.00 μg/g) had an adjusted incidence rate ratio (aIRR) of LRTI of 0.77 (95% confidence interval [CI], 0.41–1.46). The corresponding aIRR for p,p′-DDT (≥2.00 μg/g compared to ≤0.25 μg/g) was 0.65 (95% CI: 0.30–1.39). Conclusion An association of prenatal exposure to p,p′-DDE and p,p′-DDT with LRTI during childhood was not supported in this population with relatively high levels of exposure.

Our results did not confirm the relationship of serum levels of PUFA omega-3 and omega-6/omega-3 ratio with depressive symptoms; the negative correlation of serum ALA with depressive symptoms remains to be confirmed in prospective studies.

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