Exposure to 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (DDT) in relation to bone mineral density and rate of bone loss in menopausal women.

The organochlorine pesticide 2,2-bis(p-chlorophenyl)-1,1,1,-trichloroethane (DDT) and its metabolite 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (DDE) are examples of an environmental contaminant that may have hormonal properties. Bone metabolism is both estrogen- and androgen-dependent. Exposures to various environmental endocrine disrupters can affect bone metabolism in animals, but there are no published data concerning the effect of DDE exposure on bone metabolism in humans. We hypothesized that high levels of DDE would be associated with lower bone density in peri- and postmenopausal women than in premenopausal women. Study subjects were drawn from the cohort of women who had participated in the Mount Sinai Medical Center Longitudinal Normative Bone Density Study (1984-1987). We used serum samples obtained at study entry to measure DDE levels in 103 (50 black, 53 white) women (mean age = 54.5 y [standard deviation = 5 y]). Measurements of bone mineral density at the lumbar spine and radius were made at 6-mo intervals during a 2-y period. DDE concentrations were significantly (p < .001) higher in blacks (13.9 ng/ml) than in whites (8.4 ng/ml), but there was no correlation between DDE concentration and bone density at the spine (mean levels = 1.065 g/cm2 and 1.043 g/cm2 in the lowest and highest quartiles, respectively, of DDE [trend p value = .85]) or at the radius (mean levels = 0.658 g/cm and 0.664 g/cm in the lowest and highest quartiles, respectively, of DDE [trend p value = .34]). Longitudinal analyses revealed no correlation between DDE and the rate of bone loss at either bone site. Similar results were seen in race-stratified analyses, as well as in analyses in which we controlled for lactation history and other potential confounders. We found little evidence that chronic low-level DDT exposure is associated with bone density in peri- and postmenopausal women.