Exposure in the Workplace and from Industrial Accidents

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Exposure to a variety of chlorinated and brominated pesticides, organic solvents, and other probable EDCs in occupational settings and in communities exposed as a result of industrial accidents have been shown to alter male reproductive function. Findings in occupationally exposed cohorts are summarized

Table 6. Adverse male endpoint in relation to occupational exposure to EDCs

Exposure

Endpoints

References

Dibromochloropropane

Azoospermia and oligospermia

[15, 101, 102, 259]

(DBCP)

Decreased motility and morphology

Elevated FSH and LH

Deficit of male births

[103, 104,260]

Ethylene dibromide (EDB)

Decreased sperm counts

[16, 102, 105,106]

Chlordecone (kepone)

Oligospermia, decreased sperm motility

[17, 109]

Perchloroethylene (PCE)

Dose-related morphological changes

[110]

Carbaryl

Impaired semen quality

[107,108]

Ethylene glycol ethers (EGE)

Decreased sperm counts

[111, 112, 113]

Decreased fertility

TCDD (dioxin)

Reduced serum testosterone, increased LH

[261]

Deficit of male births

[262]

p-Nitrophenol (PNP)

Decreased sperm concentration

[263]

Decreased percent motile sperm

Increased serum LH

[264]

4,4'-Diaminostilbene-

Reduced serum testosterone

[117]

2,2'-disulfonic acid (DAS)

Impotence

[116]

Ethinyl estradiol

Gynecomastia, impotence

[265]

in Table 6. A dramatic example of an occupational exposure to a male reproductive toxicant was reported in 1977. Whorton and Meyer [100] found a history of infertility in male workers strongly linked to the manufacture of the ne-matocide dibromochloropropane (DBCP). This finding was confirmed and exposure-dependent effects on sperm counts, LH and FSH, and impaired sperm motility and morphology documented [100]. Similar findings were reported in DBCP-exposed occupational cohorts in Israel [101] and Hawaii [102]. More recently, a decreased sex ratio has been reported in offspring of exposed workers who recovered sufficient sperm function to conceive [103,104].

Other chlorinated pesticides, including ethylene dibromide [16,102,105,106], carbaryl [107,108], and chlordecone [17,109] have been shown to impair semen quality among cohorts exposed occupationally. Organic solvents including per-chlorethylene [110] and ethylene glycol ethers (EGE), a class of organic solvents widely used in semiconductor manufacture, shipyard paints, and other industrial uses, have been shown to be spermatotoxic in several occupational settings [111 -113]. These solvents have also been shown to increase time to pregnancy [114].

Occupational exposure to polyvinyl chloride (PVC), but not other plastics, has been associated with increased risk of testicular cancer. In a case control study including 148 cases, the odds ratio for PVC exposure was 6.6 (95% CI 1.4-32). The association was strongest in men without a history of cryptorchidism, and was limited to seminomas [115].

The stilbene derivative 4,4'-diaminostilbene-2,2'disulfonic acid (DAS) is produced in the manufacture of whitening agents and laundry detergents and is structurally similar to diethylstilbestrol. A study in 1981 -1983 of 39 DAS workers reported low testosterone in 37% of men tested, as well as impotence [116]. A follow-up study found significantly reduced testosterone (both total and free) in both current and former DAS-exposed workers compared to unexposed controls [117]. Thus, it is clear that at the high levels present in the work place, a variety of EDCs have the capacity to alter significantly male reproductive function.

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