TOTAL SERUM TESTOSTERONE AND GONADOTROPINS IN WORKERS EXPOSED TO DIOXIN

Human reproductive endocrine data may be an important source of epidem iologic information in regard to the toxic potential of 2,3,7,8-tetrac hlorodibenzo-p-dioxin (dioxin). The association of serum dioxin with t otal serum testosterone, luteinizing hormone, and follicle-stimulating hormone was examined in 248 chemical production workers from New Jers ey and Missouri plants and 231 nonexposed neighborhood referents who p articipated in a medical evaluation in 1987. In linear regression anal yses, current serum dioxin was positively and significantly related to luteinizing hormone and follicle-stimulating hormone and inversely re lated to total testosterone after adjustment for potential confounders (p < 0.05). These trends were also apparent in logistic regression an alyses, in which the authors examined the odds ratios of high luteiniz ing hormone (>28 IU/liter), high follicle-stimulating hormone (>31 IU/ liter), and low testosterone (<10.4 nmol/liter) by serum dioxin quarti les. There was a greater prevalence of high luteinizing hormone among workers in the second (odds ratio (OR) = 1.9, 95% confidence interval (Cl) 0.7-5.5), third (OR = 2.5, 95% Cl 0.9-7.3), and fourth (OR = 1.9, 95% Cl 0.7-5.0) quartiles of serum dioxin compared with referents. Fo r follicle-stimulating hormone, the authors observed a greater prevale nce of high follicle-stimulating hormone among workers in the fourth q uartile (OR = 2.0, 95% Cl 0.7-5.6) compared with referents. Similarly, the prevalence of low testosterone was two to four times greater amon g workers in the second (OR = 3.9, 95% Cl 1.3-11.3), third (OR = 2.7, 95% Cl 0.9-8.2), and fourth quartiles (OR = 2.1, 95% Cl 0.8-5.8) than among referents. The trends observed in these data offer human evidenc e of alterations in male reproductive hormone levels associated with d ioxin exposure. The results support the animal literature in which dio xin-related effects have been observed on the hypothalamic-pituitary-L eydig-cell axis and on testosterone synthesis.