| DDE, a Degradation Product of DDT, and
Duration of Lactation in a Highly Exposed Area of Mexico Lea A. Cupul-Uicab,1,2 Beth C.
Gladen,3,* Mauricio Hernández-Ávila,1,4
Jean-Philippe Weber,5 and Matthew P. Longnecker2 1Center
for Population Health Research, Instituto Nacional de Salud
Pública, Cuernavaca, Morelos, México; 2Epidemiology
Branch, and 3Biostatistics Branch, National Institute of
Environmental Health Sciences, National Institutes of Health,
Department of Health and Human Services, Research Triangle
Park, North Carolina, USA; 4Subsecretaría de Promoción y
Prevención de la Salud. Ministry of Health,
México City, Mexico; 5Centre de Toxicology,
Institut National de Santé Publique du Québec, Québec,
QC, Canada Abstract
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 ≤ 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) . 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. Key words: breast-feeding, DDE, DDT, infant, lactation. Environ Health Perspect 116:179–183 (2008) . doi:10.1289/ehp.10550 available via http://dx.doi.org/ [Online 22 November 2007]
Address correspondence to M.P. Longnecker, National Institute of Environmental Health Sciences, MD A3-05, PO Box 12233, Research Triangle Park, North Carolina 27709 USA. Telephone: (919) 541-5118. Fax: (919) 541-2511. E-mail: longnec1@niehs.nih.gov *Currently retired, Cary, NC, USA. We thank the field work team in Tapachula, Chiapas, México, for their valuable support during data collection. This study was supported in part by a contract from the National Institute of Environmental Health Sciences (NIEHS) , National Institutes of Health (NIH) (N01-ES-15467) , in part by the Intramural Research Program of the NIEHS, NIH, and in part by the Instituto Nacional de Salud Pública. The authors declare they have no competing financial interests. Received 12 June 2007 ; accepted 21 November 2007.
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