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Research

Men's Reproductive Health Risks

Threats to men's fertility and reproductive health include disease, cancer and exposure to toxins.

Network: Spring 1998, Vol. 18, No. 3

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Dangers to men's reproductive health come in several varieties. Some -- namely, sexually transmitted diseases (STDs) -- are preventable. However, when means of prevention are unknown, unavailable, unused or fail, STDs can pose a threat not only to a man's fertility and health but to those of his sexual partner.

Other threats, such as environmental toxins that may affect men's offspring or reduce sperm count and thus reduce fertility, have not been consistently identified. Yet, if they do exist and can be pinpointed, they may prove to be avoidable.

Still other reproductive system conditions, such as prostate and testicular cancer, may or may not be preventable, but pose no risk to others.

In the AIDS era, greater attention has been focused on STDs as primary reproductive health threats. "Before the era of incurable and often fatal viral STDs, STDs did not concern men very much since the 'traditional' diseases often were asymptomatic or produced symptoms that could be treated with antibiotics, with no apparent lasting sequelae for men," says Dr. Willard Cates Jr., FHI's president and an expert on STDs. "But some of these STDs affected men indirectly; by infecting their partners, these men often impaired the fertility of the women who would have borne their children."

Now, however, it is known that such STDs can reduce men's fertility as well. Infections can block the vas deferens or cause epididymitis, inflammation of the tubes through which sperm move from the testes to the vas. Sexually transmitted organisms -- particularly Neisseria gonorrhoeae or Chlamydia trachomatis -- are the most common cause of epididymitis in heterosexual men under the age of 35. When the tubes transporting sperm from both testes are infected, incidence of infertility may approach 40 percent.1

That infertility affects men, as well as women, often is unknown or forgotten. Women, particularly in developing countries, may be blamed and even divorced based on the belief that they are solely responsible for not bearing children. But men were either the sole cause or a contributing factor to infertility in more than half of 5,800 infertile couples studied by the World Health Organization (WHO) between 1979 and 1984. This multicenter WHO study concluded that male causes accounted for between 8 to 22 percent of infertility worldwide; both male and female causes accounted for between 21 to 38 percent; and female causes accounted for between 25 to 37 percent.2

Infertility in developing countries is widespread, but often preventable. Infertility can be caused by infectious and parasitic diseases. It also often results from poor health care practices such as unhygienic or inappropriate obstetric and gynecologic practices for women, or vascular injuries due to poorly performed hernia repairs in men.3 STDs, however, are the leading preventable cause of infertility. In the WHO study of 5,800 couples from 25 countries throughout the developed and developing world, African couples were more likely than other couples to have a history of STDs and infertility diagnoses suggestive of previous genital infections.

Family risks

The reproductive health status and behavior of men play a critical role in maintaining the health of women and children. Men having unsafe sex outside of marriage may become infected and share their infection with their wives.

The physiology of a woman's reproductive tract means that her risk of being infected with STDs, especially HIV, by an infected man is much greater than that of a man's being infected by a woman. Once a woman is infected, the couple's unborn children also may be affected. An infected women can transmit various STDs to her fetus, newborn or infant through the placenta, during vaginal delivery or via breastfeeding.

In both men and women, sexually transmitted pathogens can lead to cancer. Almost all cancers of the anus, penis, cervix, vagina and vulva are now thought to be caused by sexually acquired human papilloma virus (HPV).

"In the STD prevention area, men are crucial because the main method we have for prevention is the male condom, which requires the male partner's cooperation to use," says Dr. Cates. "When used consistently and correctly, latex male condoms give substantial protection against both bacterial and viral STDs, including HIV. Fortunately, condom use in younger populations seems to be going up."

In collaboration with the Komfo Anokye Teaching Hospital in Kumasi, Ghana, FHI conducted a study of contraceptive use at an STD clinic in Kumasi. Half (47 percent) of 108 sexually active men in the study reported that they used condoms all or most of the time. Among condom users, 16 percent reported using them solely for STD prevention and 66 percent reported using them both for contraception and STD prevention. The most common reason given by men for not using condoms was desired pregnancy (20 percent). In this study, the vast majority of men (89 percent) reported that they had no problems obtaining condoms.4

Even the female condom, which has not been adequately studied as a protection measure for viral STDs but may protect against some bacterial STDs, requires a degree of male cooperation. In addition, some men object to the use of spermicides, which protect against some bacterial STDs.

Environmental threats

Various environmental factors have been studied as possible causes of male infertility. Chronic exposure to high levels of arsenic in drinking water in one area of Mexico, for example, is believed to contribute to male infertility.5 High levels of aflatoxins, the result of fungi contaminating stored agricultural crops, also have been suspected of reducing male fertility. Aflatoxins were present in 40 percent of semen samples from an infertile group of Nigerian men, compared with 8 percent of semen samples from a group of fertile men.6

The question of whether men's occupational exposure to toxins poses risks to their offspring remains a "relatively understudied area in which few epidemiologists or laboratory researchers work and where there has been no resolution of conflicting data," says Dr. Andy Olshan, associate professor in the department of epidemiology at the University of North Carolina, Chapel Hill, NC, USA.

There is epidemiological evidence suggesting an association between paternal exposure to certain toxins and adverse outcomes in offspring -- including miscarriage, birth defects and childhood cancers -- but it is limited. "Geneticists tend to feel that the probability of toxin-induced mutations of sperm leading to a birth defect in offspring is very low," says Dr. Olshan. "But more solid research looking at a variety of toxic exposures in the laboratory and field is needed, if only to close out the issue."

Similarly, research is not conclusive regarding theories that sperm counts may be declining among men worldwide.

In 1992, researchers from the University of Copenhagen reported that the average sperm count had declined about 50 percent (from 113 million to 66 million per milliliter) over the last half-century.7 This review has been criticized for ignoring marked geographical and temporal variations in sperm count, as well as sampling bias. Some investigators point out that, in specific places, sperm counts have been constant for decades or are rising;8 still others maintain that reliable data on the issue simply do not exist. However, evidence of low or declining sperm counts in certain parts of the world remains of interest since such regional variations may reflect nutritional, socioeconomic or environmental influences.9

Based on animal data, various researchers have suggested the possibility that hormone-like compounds, such as pesticides, might be capable of triggering a fall in sperm counts and other reproductive system impairments in humans. However, any threat to human reproductive health remains unproved.

In recent years, widespread concern has arisen that diethylstilbestrol (DES), an estrogen-like synthetic agent that was prescribed between the late 1940s and early 1970s in the USA to prevent pregnancy complications, might induce infertility among these women's children. DES, believed to have been used by pregnant women in some developing countries, is known to cause a rare cancer of the vagina and cervix in young women whose mothers received DES during pregnancy, as well as increasing the daughters' risk of infertility, miscarriage, preterm delivery and fetal or infant death of their children.

Although the largest, most carefully conducted study of adult men exposed in utero to DES did not measure sperm counts, it showed no impairment of fertility or sexual function among these men.10 Sons of women who took DES while pregnant, however, are more likely than unexposed men to have testicular abnormalities at birth, including undescended testicles. This condition, if not corrected in early childhood, has been linked to a greatly increased risk of testicular cancer. Whether prenatal exposure to DES directly increases the risk of testicular cancer is unknown.

Prostate cancer

In recent years, the subject of cancer of the prostate -- the diminutive, walnut-sized gland located deep in a man's lower abdomen -- has generated vigorous debate. As yet, there is little medical consensus about prostate cancer's etiology, recommendations for screening, or usefulness of early detection and treatment.

The incidence rates for prostate cancer, which is rare before age 50, have been particularly high in the developed areas of the world, such as North America, Europe, Australia and New Zealand. These high incidence rates may, in part, reflect better cancer detection strategies.

In most developing countries, there are no guidelines for prostate cancer screening and "very, very few prostate cancer screening programs exist," says Dr. Sanka Ranarayanan of WHO's International Agency for Research on Cancer, based in Lyon, France. "In developing countries with very limited health care resources, money is allocated to more pressing problems. Also, it is not yet clear that screening is really beneficial."

Incidence rates of prostate cancer are related to race. In the United States, the 1994 incidence of the cancer among African American men (234.4 new cases per 100,000 men) was significantly higher than that for white American men (135.3 per 100,000 men).11 Elevated rates of prostate cancer have been observed in Temperate and Tropical South America (especially Brazil) where substantial numbers of people of African descent reside. Among African countries, those with higher incidences of prostate cancer also have relatively higher per capita incomes and life expectancies.12

Dietary and environmental factors might contribute to risk, as well. Asian immigrants to the west coast of the United States have had higher prostate cancer incidence rates than those who remained in Asia, with incidence rates for second generation Asian immigrants nearing the average rate for Caucasian Americans.13 Various studies have suggested that a high-fat diet might accelerate the rate of growth of established prostate tumors. The American Cancer Society recommends that men limit intake of high-fat foods from animal sources and eat five or more servings of fruits and vegetables each day. Vitamin E may reduce the risk, according to a recent study among more than 29,000 men in Finland. About half of the men took 50 mg of vitamin E daily, and this group experienced 32 percent fewer cases of prostate cancer than among men who did not take Vitamin E supplements. Foods rich in vitamin E include vegetable oils, particularly those from safflower, sunflower and cotton seeds; wheat germ and whole grains; and whole nuts, such as almonds.14

Questions remain about whether vasectomy increases prostate cancer risks. A possible association between vasectomy and increased risk of prostate cancer was suggested in 1990, but the researchers later discounted their own findings. Since 1990, several studies have looked at a possible link between vasectomy and prostate cancer. However, a plausible biological mechanism for the association has yet to be identified, study results have been inconsistent, and reported elevations in risk have been small.15

In 1993, a National Institutes of Health (NIH) panel in the United States stated that providers should continue offering and performing vasectomy. The panel recommended that further research be conducted to clarify any possible risk, but "nothing essential has changed in regard to this issue since 1993," notes Dr. Pamela Schwingl of FHI, an epidemiologist who has studied the relationship.

Whether vasectomy increases the risk of prostate cancer in developing countries is the subject of an on-going study coordinated by WHO involving 1,200 men in China, Nepal and the Republic of Korea. FHI is collaborating with researchers at the Korean site. FHI is also collaborating with researchers at the University of Otago in New Zealand on a similar study begun in 1997.

Results of a recent study of more than 1,000 men in Mumbai (Bombay), India suggested an association between vasectomy and prostate cancer, particularly among men who underwent vasectomy at least 20 years before cancer diagnosis or who were at least 40 years old when they had a vasectomy.16 Another study involving about 750 men from 12 cities in China, a country where both the use of vasectomy and the incidence of prostate cancer are increasing, suggested that vasectomized Chinese men may be at increased risk for prostate cancer.17

Another risk for men is testicular cancer, which is relatively rare, and is almost always curable if found early. It can be treated with surgery, radiation therapy, chemotherapy, surveillance, or a combination of these therapies.

No one really knows what causes testicular cancer, but accumulated data have convincingly demonstrated that vasectomy does not elevate the risk of testicular cancer. A Danish study in which 73,917 vasectomized men were identified from hospital and pathology registers between 1977 and 1989 demonstrated no increased risk of testicular cancer in the group.18 This data is supported by results from the United Kingdom Testicular Cancer Study Group.19

Notably, testicular cancer is more common in white men than in men of other races. Incidence rates in Switzerland and Denmark -- approximately eight new cases per 100,000 men per year -- are among the world's highest.

-- Kim Best

References

  1. Berger RE. Acute epididymitis. Sexually Transmitted Diseases. Ed. Holmes KK, Mårdh P-A, Sparling PF, et al. New York: McGraw-Hill, Inc., 1990.
  2. Cates W, Farley TMM, Rowe PJ. Worldwide patterns of infertility: is Africa different? Lancet 1985;2(8455):596-98.
  3. Kuku SF, Osegbe DN. Oligo/azoospermia in Nigeria. Arch Androl 1989;22(3):233-38.
  4. Adu-Sarkodie Y, Steiner MJ, Attufuah JD. Contraceptive use at an STD clinic in Kumasi, Ghana. Unpublished paper. Family Health International, 1998.
  5. Leke RJ, Oduma JA, Bassol-Mayagoitia S, et al. Regional and geographical variations in infertility: effects of environmental, cultural, and socioeconomic factors. Environ Health Perspect 1993;
  6. 101(Suppl 2):73-80.
  7. Ibeh IN, Uraih N, Ogonar JI. Dietary exposure to aflatoxin in human male infertility in Benin City, Nigeria. Int J Fert Menopausal Stud 1994;39(4):208-14.
  8. Carlsen E, Giwercman A, Keiding N, et al. Evidence for decreasing quality of semen during past 50 years. BMJ 1992;305(6854):609-13.
  9. Fisch H, Goluboff ET, Olson JH, et al. Semen analyses in 1,283 men from the United States over a 25-year period: no decline in quality. Fertil Steril 1996;65(5):1009-14.
  10. Swan SH, Elkin EP, Fenster L. Have sperm densities declined? A reanalysis of global trend data. Environ Health Perspect 1997;105(11):1228-32.
  11. Wilcox AJ, Baird DD, Weinberg CR, et al. Fertility in men exposed prenatally to diethylstilbestrol. N Engl J Med 1995;332(21):1411-16.
  12. Recent trends in prostate cancer incidence and mortality, November 21, 1997. National Cancer Institute. (http://cancernet.nci.nih.gov).
  13. Kehinde EO. The geography of prostate cancer and its treatment in Africa. Cancer Surveys 1995;23:281-86.
  14. Whelan P. Are we promoting stress and anxiety? BMJ 1997;315(7121):1549-50.
  15. Heinonen OP, Albanes D, Virtamo J, et al. Prostate cancer and supplementation with alpha-tocopherol and beta-carotene: incidence and mortality in a controlled trial. J Natl Cancer Inst 1998;90(6):40-46.
  16. Mettlin C, Natarajan N, Huben R. Vasectomy and prostate cancer risk. Am J Epidemiol 1990;132(6):1056-61; Schwingl PJ, Guess HA. Vasectomy and cancer: an update. Gynaecol Forum 1996;1(1):24-28.
  17. Platz EA, Yeole BB, Cho E, et al. Vasectomy and prostate cancer: a case-control study in India. Int J Epidemiol 1997;26(5):933-38.
  18. Hsing AW, Wang RT, Gu FL, et al. Vasectomy and prostate cancer risk in China. Cancer Epidemiol Biomarkers Prev 1994;3(4):285-88.
  19. Møller H, Knudsen LB, Lynge E. Risk of testicular cancer after vasectomy: cohort study of over 73 000 men. Br Med J 1994;309(6950):295-99.
  20. United Kingdom Testicular Cancer Group. Aetiology of testicular cancer: association with congenital abnormalities, age at puberty, infertility, and exercise. BMJ 1994;308(6941):1393-99.
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