Reproductive hormone profile among pesticide factory workers

Serum follicle-stimulating hormone (FSH), luteinizing hormone (LH), and tes tosterone levels, as well as urinary levels of FSH, LH, and E1C, a metaboli te of testosterone, were measured to investigate the adverse reproductive e ffects of organophosphate pesticides among Chinese factory workers who were occupationally exposed to ethylparathion and methamidophos. Thirty-four ex posed workers were randomly chosen and recruited from a large pesticide fac tory, and 44 unexposed workers were selected from a nearby textile factory. A quantitative pesticide exposure assessment was performed among a subset of the exposed and unexposed workers. Information on potential confounders was collected in an interview. A single blood sample was collected at the e nd of a work shift, when each subject also donated a semen sample. Three fi rst-voided urine samples were collected from each worker on 3 consecutive d ays. Urinary p-nitrophenol level at 1 hour after the work shift correlated with serum (r = 0.71, P < 0.01) and urinary (r = 0.51, P = 0.04) FSH levels . Stratifying by the subjects' exposure status, we found a significant nega tive correlation among the exposed group between urinary FSH level and sper m count (r = -0.61, P < 0.01) and between urinary FSH level and sperm conce ntration (r = -0.53, P = 0.03). Pesticide exposure alone was significantly associated with serum LH level (beta [coefficient of exposure effect] = 0.7 9; 95% confidence interval [CI] = 0.42, 1.16) but not with serum FSH or tes tosterone or with any urinary hormone levels. With adjustment for age, rota ting shift work, current cigarette smoking, and current alcohol consumption , exposure significantly increased the serum LH level by 1.1 mIU/mL (95% CI = 0.34, 1.82). Meanwhile, the serum FSH level was slightly elevated (beta [coefficient of exposure effect] = 1.38; 95% CI = -0.09, 2.85) and the seru m testosterone level was decreased (beta = -55.13; 95% CI = -147.24, 37) wi th increased pesticide exposure. Age and rotating shift work appeared to ac t as confounders. We conclude the organophosphate pesticides have a small e ffect on male reproductive hormones, suggestive of a secondary hormonal dis turbance after testicular damage.