Smoking and Ferility

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Tobacco smoking is widely recognized today as a health hazard and a major cause of preventable mortality. Many studies have shown that women who smoke take longer to conceive, or have difficulty maintaining pregnancy. Population studies show links between cigarette smoking and reduced fertility, earlier mean age of menopause, impaired oocyte (unfertilized egg cell) function and viability, and depleted ovarian reserves – apparently because certain components in cigarette smoke interact, directly or indirectly, with the gamete cells (eggs and sperm) to disrupt their normal function.

Yet despite a decrease in the incidence of smoking in the general population, the percentage of female smokers has increased dramatically (Health Canada 2003). What is even more troubling is the incidence of smoking among young women. Two years ago, a survey of high school students in south-western Ontario revealed that 36.2% of teenage girls smoke (Cohen et al. 2003). A study from the United Kingdom in the late 1990s reported that, at the age of 15, 33% of girls were regular smokers (Augood et al. 1998).

At McMaster University, in co-operation with the Centre for Reproductive Care, we are conducting research into the toxic effects of cigarette smoking and fertility outcomes. This research is particularly important since the largest group of new smokers in Canada is women in their teenage years.

Data from our study of active and passive smokers, compared with non-smokers, revealed that the reproductive consequences of passive smoke exposure were as great as if the woman herself smoked (Neal et al. 2004). This is not surprising, since most of the toxic substances generated by smoking emanate from the smouldering end of the cigarette (Lodovici et al. 2004). But although there is evidence that environmental smoke exposure reduces fertility in women, the mechanism that causes this is still unknown. Several studies have shown that smoking can result in a reduced response to ovarian stimulation, fewer unfertilized egg cells produced, poor fertilization rates, lower implantation and increased miscarriage – all of which ultimately contribute to an overall reduction in pregnancy rates.

Couples who smoke also have less success when they resort to assisted reproductive technologies to solve fertility problems. This might be the result of adverse effects of the constituents of cigarette smoke. Cotinine, the metabolite of nicotine, and cadmium, a heavy metal, have been detected in the follicular fluid of women who smoke (Zenzes, 2000; Younglai et al., 2002). More recently we have shown that benzo-[a]-pyrene (BaP), a polycyclic aromatic hydrocarbon (PAH) constituent of cigarette smoke, reaches the follicular fluid in the ovaries of women exposed to either passive or active smoke (Neal et al. 2004). In addition, concentrations of estradiol (the most potent of the natural estrogens) in follicular fluid and serum are lower in smokers than in non-smokers. This suggests that smoking alters a woman’s crucial steroid metabolism. making the endometrial cells that line the uterus less prepared to receive the embryo. What this means for the smoker is that pregnancy itself may be harder to achieve – and maintain.. Other research shows that active smoking leads to chemical stresses that could be toxic in the oocyte and companion granulosa cells (Paszkowski et al. 2002). There is also evidence of earlier onset of menopause by two to four years in women who smoke, compared to non-smokers (El-Nemr et al. 1998).

The link between cigarette smoking and decreased fertility and earlier age at menopause is well established. Preliminary data from my laboratory (based on animal studies) have shown that cigarette smoke exposure depletes the pool of reserve follicles in the ovary. Taken together these data strongly support the conclusion that cigarette smoking is hazardous to reproductive health and is a modifiable factor known to be involved in impaired fertility. 

About the Authors: Michael S. Neal is an embryologist at the McMaster University Centre for Reproductive Care and is pursuing doctoral training under the direction of Dr. Warren Foster. He was recently honoured with the Serono LIFE Award and RT WEAVER Obstetrics & Gynecology Research Day Best Basic Science Paper Award in recognition of his work in establishing an innovative follicle culture assay to study ovarian function in vitro. Dr. Warren Foster obtained his Ph.D. at McMaster University, where he worked on reproductive endocrinology. In 1990 he joined the staff of Health Canada and was named Head of the Reproductive Toxicology Section in 1992. Dr. Foster was Associate Director/Director of Research at the Center for Women’s Health, Cedars-Sinai Medical Center in Los Angeles (1999) before returning to Canada in 2001 to join the faculty of McMaster University as Associate Professor and Director of the Reproductive Biology Division in the Department of Obstetrics and Gynaecology. Dr. Foster’s research interests are focused on developing a better understanding of the link between environment (dietary and man-made chemicals) and infertility.

Augood C, Duckitt K, Templeton AA. (1998) Smoking and female infertility: a systematic review and meta-analysis. Hum Reprod 13: 1532-1539.

Cohen B, Evers S, Manske S, Bercovitz K, Edward HG. (2003) Smoking, physical activity and breakfast consumption among secondary school students in a southwestern Ontario community. Can J Public Health 94: 41-44.

El-Nemr A, Al-Shawaf T, Sabatini L, Wilson C, Lower AM, Grudzinskas JG. (1998) Effect of smoking on ovarian reserve and ovarian stimulation in in-vitro fertilization and embryo transfer.

Health Canada (2003) Canadian Tobacco Use Monitoring Survey. http://www.hc-hc.gc.ca/hecshesc/tobacco/research/ctums/2003/supplementary_annual_2003.html

Lodovici M, Akpan V, Evangelisti C, Dolara P. (2004) Sidestream tobacco smoke as the main predictor of exposure to polycyclic aromatic hydrocarbons. J App Tox 24: 277-281.

Neal MS, Hughes EG, Holloway AC, Foster WG. (2005) Sidestream smoking is equally as damaging as mainstream smoking on IVF outcomes. Hum Reprod (submitted).

Neal MS, Zhu J, Stampfli MR, Holloway AC, Foster WG. (2004) Mechanism of cigarette smoke toxicant (benzo-[a]-pyrene induced impairment of folliculogenesis in vitro. Canadian Fertility and Andrology Society (CFAS) Jasper, AB. Poster # FP36.

Paszkowski T, Clarke RN, Hornstein MD. (2002) Smoking induces oxidative stress inside the Graffian follicle. Hum Reprod 17: 921-925.

Younglai EV, Foster WG, Hughes EG, Trim K, Jarrell JF. (2002) Levels of environmental contaminants in human follicular fluid, serum and seminal plasma of couples undergoing in vitro fertilization. Arch Environ Contam Toxicol 43: 121-126.

Zenzes MT. (2000) Smoking and reproduction: gene damage to human gametes and embryos. Hum Reprod Update 6: 122-131.