BACKGROUND:

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.

OBJECTIVE:

Our aim was to assess the relationship of maternal DDE concentrations with length of subsequent lactation.

METHODS:

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.

RESULTS:

Compared with those with DDE concentrations < or = 3.00 microg/g, the adjusted hazard ratios of weaning according to DDE category were, for concentrations 3.01-6.00 microg/g, 1.27 [95% confidence interval (CI), 1.04-1.55]; for concentrations 6.01-9.00 microg/g, 1.23 (95% CI, 0.92-1.63); and for concentrations > 9.00 microg/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).

CONCLUSIONS:

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.