Reproductive toxicity

A number of studies have demonstrated reproductive toxicity for glycol ethers in animals, both males and females (reviewed in Hardin, 1983; Paustenbach, 1988; IPCS, 1990; ECETOC, 1995). In an assessment of developmental risks from occupational exposure to glycol ethers in the semiconductor industry, Paustenbach (1988) concluded that employees should not be at risk of adverse developmental, reproductive and other effects provided that the airborne concentrations of these chemicals were maintained below safety limits and that dermal exposure was minimal.

Testicular changes

There is limited information in humans and much of the available data are inconclusive. Exposed workers have been shown to have an increased prevalence of oligospermia and azoospermia compared to controls (Welch et al., 1988). A study of workers exposed to EGME possibly showed a smaller testicular size in 6 exposed subjects compared to 9 controls (Cook et al., 1982). A study of semen quality in workers concluded that exposure to EGEE may have an effect on sperm counts, but not on other parameters of morphology and function. The average sperm count per ejaculate was significantly lower in workers than in the controls when other factors were taken into account. However, the mean sperm concentration of the two groups did not differ. Also, no effect of exposure to EGEE was detected in semen volume, sperm viability, motility, velocity, morphology or testicular volume (Ratcliffe et al., 1989).

A study comparing male patients diagnosed as infertile or subfertile attending a clinic for reproductive disorders, found ethoxyacetic acid in the urine of 39 patients and 6 controls. Methoxyacetic acid was found in 1 patient and 2 controls. Urinary concentrations of ethoxyacetic acid did not correlate with various measures of sperm quality (Veulemans et al., 1993).

Studies in animals have demonstrated degenerative changes in germinal epithelium (Miller et al., 1981; Foster et al., 1983), testicular atrophy (Beattie et al., 1984; Grant et al., 1985; Horimoto et al., 2000) and decreased sperm count and motion (Horimoto et al., 2000). These changes are usually reversible, but very high doses may prevent complete recovery (Foster et al., 1983). Testicular changes are characterised by degeneration and depletion of the primary spermatocyte population at the pachytene stage of the meiotic prophase and in division (Foster et al., 1983; Moss et al., 1985).

Fetotoxicity/embryotoxicity and teratogenicity

Potential exposure to mixtures containing glycol ethers have been associated with an increased risk of subfertility and spontaneous abortion among female workers (Pastides et al., 1988; Correa et al., 1996). A dose-response effect with subfertility and spontaneous abortion has been demonstrated. Among the spouses of exposed male workers there was no increased risk of spontaneous abortion (Correa et al., 1996). In another study of female workers there was an increased risk of miscarriage in workers using glycol ethers (Pastides et al., 1988).

There is limited information on the reproductive effects of the glycol ether acetates. A woman exposed to EGMEA during both pregnancies gave birth to two boys with hypospadia (failure of closure of the urethral groove) and bifid scrotum. The first boy also had micropenis. Dermal absorption was thought to be important in this case (Bolt and Golka, 1990).

Animal studies have shown malformations involving numerous organ systems (Nagano et al., 1981; Hanley et al., 1984; Horton et al., 1985), an increased incidence of resorptions (Hanley et al., 1984; Horton et al., 1985) and decreased fetal weight (Nagano et al., 1981; Doe et al., 1983; Hanley et al., 1984; Horton et al., 1985). Teratogenic effects appear to be similar among the species tested, but there is variation in susceptibility, with rabbits being the most susceptible (Hanley et al., 1984). Prolongation of gestation has also been observed (Hardin, 1983).

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