The effect of passive smoke-exposure on fertility

Although tobacco smoking is a widely recognized health hazard and a major cause of preventable mortality, smoking remains prevalent in our society. Approximately 30% of women and 35% of men of reproductive age smoke. But more importantly, the incidence of smoking is increasing among adolescents and specifically teenage girls. Environmental tobacco smoke (ETS), or passive smoke, is a significant source of exposure to a large number of substances known to be hazardous to human health. Recently, substantial harmful effects of cigarette smoke on the ability to become pregnant have become apparent. The deleterious effect of passive smoke exposure is similar to active smoking with respect to fertility. Women who smoke take longer to achieve a natural pregnancy, require more hormonal stimulation during IVF treatment with reduced success, and reach menopause earlier than their non-smoking counterparts. Toxicants found in passive smoke have been isolated at higher levels in the serum and follicular fluid of women exposed to ETS compared to non-smokers implying that cigarette smoke may act as an ovarian toxicant as one mechanism to disrupt fertility. However, the male contribution to infertility cannot be excluded. The paternal effect on infertility is largely dependant on sperm function. The effect of cotinine, for example, has been shown to alter sperm function, and may be an underlying mechanism of impaired fertility. Paternal smoking is associated with sperm with a higher incidence of DNA abnormalities that may account for higher implantation failures and miscarriage rates. Both the female and male gamete are sensitive to toxic exposure(s) and slight alterations to either the sperm or oocyte may be lethal at the peri-implantation stage of embryo development leading to sub-fertility. Passive smoke exposure may induce toxic effects and compromise fertility through several direct or indirect mechanisms. © 2011 by Nova Science Publishers, Inc. All rights reserved.