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. 

 

Exposure

Possible Effects

Heat

Low sperm count, motility, morphology

Ionizing Radiation

Azoospermia

Nonionizing radiation

Microwaves

Electromagnetic fields

 

Low sperm count and motility(temporary)

Low sperm count and motility

Metals 

Lead ,Mercury, Cadmium, Boron

 

Sperm morphology, count, motility, semen volume

 

Estrogens

Synthetic (Diethylstilbestrol)

Dietary( lignans, mycoestrogens , phytoestrogens )

 Hormone levels

Gynecomastia, libido, impotence

Low sperm count

Pesticides

Dibromochlorpropane , Ethylene dibromide, Chlordecone

 Sperm morphology, count, motility

Hormonal imbalance

Solvents 

Carbon disulfide, Glycol ethers 

 Sperm morphology, count, impotence

Hormonal imbalance

 

Effect of ionizing radiation:

Dose (cGy)

Effect

Reversibility

15-20

Little effect

-

20-50

Azoospermia (20-60%) 

6-8 months

50-100

Azoospermia (50-80%)

8-14 months

100-200

Azoospermia(90-100%)

12-24 months

>200

Azoospermia(100%)

>24 months