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Breakthroughs in Andrology |
From the * Centre de Recherche en Biologie de la
Reproduction, Département des Sciences Animales, Université
Laval, Québec City, Québec, Canada;
Environmental Health, School of Health Systems
& Public Health, University of Pretoria, Pretoria, South Africa;
Centro de Investigación en Salud
Poblacional, Instituto Nacional de Salud Pública, Cuernavaca Morelos,
México; Unité de Recherche en
Santé Publique, Centre de Recherche du Centre Hospitalier de
l'Université Laval-Centre Hospitalier Universitaire de Québec,
Université Laval et Direction de la Toxicologie Humaine-Institut de la
Recherche en Santé Publique du Québec, Sainte Foy,
Québec, Canada; || Unité de Recherche
en Génétique Humaine et Moléculaire, Services de
Biochimie Médicale et de Génétique de Laboratoire, Centre
Hospitalier Universitaire de Québec, Pavillon St-François
d'Assise, Québec, City, Québec, Canada; and the ¶
Departmento de Biología de la
Reproducción, Instituto Nacional de Nutrición, México DF,
México.
| Correspondence to: Dr Janice L. Bailey, Centre de Recherche en Biologie de la Reproduction, Département des Sciences Animales, Université Laval, Québec City, Québec, Canada, G1K 7P4 (e-mail: janice.bailey{at}crbr.ulaval.ca). |
In response to mounting concerns about the endocrine-disrupting influence
of environmental chemicals on human health, this epidemiological study was
initiated to test the hypothesis that nonoccupational exposure to the
estrogenic pesticide 1,1,1-trichloro-2,2-bis(chlorodiphenyl)ethane (DDT)
affects male reproductive parameters. One hundred and sixteen men aged 27
years (SD = 8.2) living in malaria endemic-areas in Chiapas (Mexico), where
DDT was sprayed until 2000, participated in a cross-sectional study. Semen
analyses were conducted according to World Health Organization methods and a
quality control program was followed. DDT exposure was defined as the level of
blood plasma p,p'-dichlorodiphenyl dichloroethylene (DDE), the
major metabolite of DDT. The p,p'-DDE concentration adjusted
for total lipids was 100 times higher than that reported for nonexposed
populations at 45 plus or minus 32 µg/g (mean ± SD). Crude
regression analysis showed that several sperm motion parameters, including the
percentage of motile sperm, decreased with higher p,p'-DDE
concentrations (ß = -8.38; P = .05 for squared motility), and
the percentage of sperm with morphological tail defects increased with higher
plasma p,p'-DDE concentration (ß = 0.003; P =
.017). Insufficient sperm chromatin condensation was observed in 46.6% of
participants, and the most severe category of incomplete DNA condensation was
also positively correlated with p,p'-DDE concentration
(r = .223; P = .044). Therefore, nonoccupational exposure to
DDT, as assessed by plasma p,p'-DDE concentrations, is
associated with poorer semen parameters in men, indicating adverse effects on
testicular function and/or the regulation of reproductive hormones.
Previously, a causal role of environmental toxicants in human male infertility
has been lacking because observed effects have been the result of unusually
high exposures, either occupationally or as a result of industrial accidents,
resulting in unprecedented controversy (reviewed by Cheek & McLachlan,
Environmental hormones and the male reproductive system. J Androl.
1998;19:5). This is the first epidemiological study demonstrating effects
after nonoccupational exposures to DDT. Based on these findings, the effect of
DDT on male reproductive health should not be ignored.
Key words: Pesticide, organochlorine, spermatozoa, sperm motility, sperm morphology, chromatin
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