Background: Urinary metabolites of several nonpersistent insecticides have been measured in a high percentage of men in the general population, suggesting widespread environmental exposures to these compounds. The present study explored the association of urinary concentrations of 3,5,6-trichloro-2-pyridinol (TCPY), a metabolite of chlorpyrifos and chlorpyrifos-methyl, and 1-naphthol (1N), a metabolite of carbaryl and naphthalene, with serum reproductive hormone levels in adult men.
Methods: Subjects (n = 268) were the male partners in couples presenting to a Massachusetts infertility clinic in years 2000 through 2003. TCPY and 1N were measured in a spot urine sample from each subject and adjusted for dilution using specific gravity. Reproductive hormones (follicle-stimulating hormone, leuteinizing hormone, inhibin B, testosterone, and sex hormone-binding globulin) were measured in serum collected from subjects during the same clinic visit.
Results: Multiple linear regression models showed an inverse association between TCPY and testosterone concentration. An interquartile range (IQR) increase in TCPY was associated with a decline of 25 ng/dL (95% confidence interval = −40 to −10) in testosterone concentration. The association appeared to be dose-dependent when exposure was divided into quintiles. The highest TCPY quintile was associated with a testosterone decline of 83 ng/dL (−128 to −39) compared with the lowest TCPY quintile. We also found inverse associations between TCPY and free androgen index and between 1N and testosterone, and suggestive inverse associations between TCPY and leuteinizing hormone and between 1N and free androgen index.
Conclusion: In adult men, TCPY and 1N were associated with reduced testosterone levels. On a population level, these reductions are of potential public health importance because of widespread exposure to these nonpersistent insecticides.
From the Departments of *Environmental Health and †Biostatistics, Harvard School of Public Health, Boston, Massachusetts; and the ‡Centers for Disease Control and Prevention, Atlanta, Georgia.
Submitted 15 March 2005; accepted 10 August 2005.
Supported by grants ES09718 and ES00002 from the National Institute of Environmental Health Sciences (NIEHS), National Institutes of Health (NIH). Dr. Meeker was supported by NIH training grant T32 ES07069.
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Correspondence: Russ Hauser, Harvard School of Public Health, Department of Environmental Health, Occupational Health Program, Building 1, Room 1405, 665 Huntington Avenue, Boston, MA 02115. E-mail: firstname.lastname@example.org.