DDE, a Degradation Product of DDT, and Duration of Lactation in a Highly Exposed Area of Mexico

Abstract

Higher levels of 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (DDE), the major degradation product of 1,1,1-trichloro-2,2-bis(4-chlorophenyl)ethane (DDT), have been related to shorter duration of breast-feeding in previous studies. If DDE truly shortens lactation, this has public health importance regarding infant mortality and the use of DDT for malaria control. Our aim was to assess the relationship of maternal DDE concentrations with length of subsequent lactation. We conducted a relatively large study in a highly exposed area of Mexico. We followed 784 mother–son pairs to determine length of lactation. DDE and DDT were measured in maternal serum obtained within a day of delivery. We fit proportional hazard models with and without stratifying by previous breast-feeding, because an association of DDE with duration of lactation among those who breast-fed previously could be attributed to a noncausal mechanism. Compared with those with DDE concentrations ≤ 3.00 μg/g, the adjusted hazard ratios of weaning according to DDE category were, for concentrations 3.01–6.00 μg/g, 1.27 [95% confidence interval (CI), 1.04–1.55]; for concentrations 6.01–9.00 μg/g, 1.23 (95% CI, 0.92–1.63); and for concentrations > 9.00 μg/g, 1.17 (95% CI, 0.92–1.49). The corresponding ratios for women who previously breast-fed were 1.40 (95% CI, 1.06–1.87); 1.91 (95% CI, 1.24–2.93); and 1.76 (95% CI, 1.22–2.53). Those for women who had not breast-fed previously were 1.14 (95% CI, 0.86–1.52); 0.90 (95% CI, 0.61–1.31); and 0.91 (95% CI, 0.66–1.26). Data from our relatively large study in a highly exposed area of Mexico did not support the hypothesis that exposure to DDE shortens length of lactation. The association seen in women who previously breast-fed was likely attributed to a noncausal mechanism. Nonetheless, whether DDT has other important adverse effects on humans is still an open question.