Environmental and Occupational Hazards and Male infertility

Environmental and Occupational Hazards and Male infertility

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Environmental agents can adversely affect germ cell development at many different stages from proliferating spermatogonia to mature spermatozoa.Although they have been shown to affect male reproductive function in animals, large difference in reproductive function between species limit extrapolation to human. Human data are often conflicting.

Possible different toxic effects include cell death, sublethal cell damage or genetic change. Cell dying within the epithelium may do so by necrosis or apoptosis (or programmed cell death). Recent evidence suggest that apoptosis is the major mechanism of action of some testicular toxins or adverse physiological conditions such as gonadotropins deprivation. Nonlethal germ cell damage will be repaired or leave permanent effect on structure or function of mature spermatozoa, including possibility of genetic defects.

Occupational exposure to sex steroids such as estrogens, can exert negative biofeedback on FSH secretion and result in decreased sperm production, sexual dysfunction, gynecomastia and hypogonadotropic hypogonadism, and potentially to cryptorchidism and testicular cancer). Prenatal exposure to estrogens could potentially inhibit fetal gonadotropins secretion and reduce Sertoli cell proliferation. Several compounds are known to have antiandrogenic activity (9,10-Dihydrophenanthrene, Linuron, Vincozolin, DDT/DDE, and Flutamide)

Direct testicular toxicity may potentially affect separate cell types within testis with subsequent affect on spermatogenesis and steroidogenesis in general. No specific human Sertoli cell toxins have yet been established. Iionizing radiation and alkylating agents ( e.g. nitrogen mustard, vincristine, procarbazine, prednisone) were found to have most profiund toxicity to human germ cells . The most sensitive cells are spermatogonia. Nonproliferating spermatogonia A0 , if destructed, leads to irreversible spermatogenic damage, while proliferating spermatogonia can be replaced from stem cell reserves.

Although persistent mutation in stem cells DNA can lead to persistent genetic changes in sperm, such chromosome defects did not translated to excess congenital malformation or carcinogenesis among offsprings of male cancer treatment survivors.

Adrenolytic drugs such as guanethidine or methoxamine lead to stasis of sperm in the epididymis. Gossipol affects epididymal epithelium and interfere with epididymal fluid excretion. 



Possible Effects


Low sperm count, motility, morphology

Ionizing Radiation


Nonionizing radiation


Electromagnetic fields


Low sperm count and motility(temporary)

Low sperm count and motility


Lead ,Mercury, Cadmium, Boron


Sperm morphology, count, motility, semen volume



Synthetic (Diethylstilbestrol)

Dietary( lignans, mycoestrogens , phytoestrogens )

 Hormone levels

Gynecomastia, libido, impotence

Low sperm count


Dibromochlorpropane , Ethylene dibromide, Chlordecone

 Sperm morphology, count, motility

Hormonal imbalance


Carbon disulfide, Glycol ethers 

 Sperm morphology, count, impotence

Hormonal imbalance


Effect of ionizing radiation:

Dose (cGy)




Little effect



Azoospermia (20-60%) 

6-8 months


Azoospermia (50-80%)

8-14 months



12-24 months



>24 months