Testicular function among carbaryl‐exposed employees

Abstract

A cohort of 101 male carbaryl production workers with at least 1 yr experience in the carbaryl area was selected from employment records. Of these individuals, 47 provided satifactory semen samples for analysis; 36 of the 47 provided blood for hormone assay. There were no major age or employment-status differences between those who agreed to participate and those who did not. In the absence of sufficiently detailed industrial hygiene exposure data, a subjective exposure classification was developed. No apparent relationships were found between sperm count and exposure category or years worked in classifications based on carbaryl exposure. Also, no relationship was found between fathering children and exposure to carbaryl. When the sperm-count distribution of the carbaryl-exposed workers was compared with a distribution of sperm counts representing a nonexposed (control) population, no overall differences were observed that could be related to carbaryl exposure. There was a small excess in the number of sperm counts less than 20 million per milliliter among the carbaryl-exposed men, but the excess was not significant at alpha = 0.05.

Pesticide Exposure and Health Related Issues in Male and Female Reproductive System

“…Tomenson et al (1999) conducted a longitudinal study and found no evidence that sperm and serum hormones levels were related to molinate exposure (thiocarbamate herbicide). Whorton et al (1979) found no apparent effects on sperm count in workers exposed to carbaryl, but three subsequent relative studies indicated contrary results. Table 2a.…”

Evidence that mammalian sex ratios at birth are partially controlled by parental hormone levels around the time of conception

“…It had originally been reported that DBCP lowers men's sperm counts (Whorton et al 1977), and for this reason, to the author's knowledge it was then banned in many countries, no further data have been published on its effect on offspring sex ratios. It has also been reported that exposure to DBCP causes increases in men's luteinizing hormone (LH) and folliclestimulating hormone levels, while leaving their testosterone levels unchanged (Whorton et al 1979). The author suggests that this hormone profile is responsible for the female excess among the offspring of these men.…”

Review: Environmental endocrine disruptors of testicular function

“…The net biologic effect of oestradiol in the testis appears to be inhibition of androgen production, either by limiting development and growth of the Leydig cell population or through direct action in the Leydig cell (95). However, oestradiol is now considered as a survival factor for germ cells (99,100), and it appears that a balanced ratio between testosterone and oestradiol is critical to normal spermatogenesis (1). In a study (101) conducted on subjects attending a Massachusetts infertility clinic from years 2000-2003, it was reported that 3,5,6-trichloro-2-pyridinol, the major urinary metabolite of chlorpyrifos and chlorpyrifos-methyl, may be associated with altered oestradiol levels in adult men.…”