Paraoxonase polymorphism and its effect on male reproductive outcomes among Chinese pesticide factory workers

Background Sei um paraoxonase has been associated with the metabolism of or ganophosphate pesticides in humans. Molecular analysis of the human paraoxo nase gene (PON1) has revealed that Arg(192) homozygotes have a greater deto xifying capability than Gln(192) homozygotes. We examined the effects of PO N1 genotypes on male reproductive outcomes and its interaction with exposur e to organophosphate pesticides. Methods We studied 60 Chinese pesticide-factory workers and 89 textile-fact ory workers who were unexposed to pesticides. The respective allele frequen cies of Arg(192) and Gln(192) were 0.62 and 0.38. Pesticide exposure among 36 exposed subjects and 12 unexposed subjects, regardless of gender was ass essed by personal measurement of pesticide residues over an entire 8-hr shi ft and measurement of urinary p-nitrophenol level over a 24-hr period. We a nalyzed semen and hormone data collected from male subjects. Results When the three PON1 genotypes were analyzed separately, a gene dose effect was not detected, We used rite unexposed Arg(192) homo/heterozygote s as the reference group, and re-analyzed the data. Exposed Arg(192) homo/h eterozygotes had significantly lower sperm count (chi(2) = 9.01, P < 0.01) and lower percentage of sperm with normal morphology (chi(2) = 4.18, P < 0. 05) than the reference group. Both unexposed Gln(192) homozygotes (chi(2) = 4.90 P < 0.05) and exposed Arg(192) homo/heterozygotes (chi(2) = 10.00, P < 0.01) showed significantly lower sperm concentrations than the reference group. In addition, exposed Arg(192) homo/heterozygotes had significantly h igher serum LH levels (chi(2) = 7.94, P < 0.01) than the reference group. Conclusions Because of a small sample size, our findings are highly prelimi nary: Nevertheless, it calls for further investigation of the interaction b etween the PON1 genotype and organophosphate pesticide exposure on male rep roductive outcomes. Am. J. Ind. Med. 36:379-387, 1999. (C) 1999 Wiley-Liss, Inc.