Most patients know not to smoke, don’t they? Maybe so, but that doesn’t mean that they (and their partners) don’t smoke, or that they tell the truth to their doc, or that they aren’t exposed to significant amounts of secondhand smoke.
Approximately 30% of reproductive age women and 35% of reproductive age men in the United States smoke cigarettes, as do an increasing percentage of adolescent and teenage girls. This is despite costly and long-standing national campaigns to limit their use.
Given the high prevalence of smoking and the documented variety of deleterious health effects, C. Everette Koop, MD, the former U.S. Surgeon General had appropriately labeled smoking “the chief single avoidable cause of death in our society and the single most important health issue of our time.” Specifically addressing the adverse effects of smoking on reproductive health in the introduction to a Seminars in Reproductive Medicine issue devoted to a review of the this subject , Dr. Koop summarized the available data in stark terms: “Women who smoke have decreased fertility. The risk of spontaneous abortion is higher for pregnant women who smoke… Babies born to smokers weigh, on average, 200 grams less than babies born to comparable women who do not smoke, with low birth weight being an important predictor of infant mortality”
In addition to smokers who inhale the toxic, carcinogenic and mutagenic substances known to be prevalent in cigarette smoke, many nonsmokers are regularly exposed by inhalation of “sidestream” smoke from burning cigarettes and / or from “passive” smoke exhaled by smokers. A recent study documented cotinine, a major metabolite of nicotine, to be found in dose dependent concentrations relative to the number of cigarettes smoked in 100% of the follicular fluids of infertility patients undergoing in vitro fertilization oocyte retrieval. One hundred percent (100%) of women known to be exposed to passive smoke in the home also had follicular fluid cotinine detected, albeit at lower concentrations. What was as alarming was that 84% of women reporting themselves as non-smokers and with a non-smoking partner also had detectable levels of cotinine in their follicular fluids. These women were exposed environmentally, with all but one working outside the home. As the authors, who had previously reported the ovarian toxin heavy metal cadmium in the follicular fluid of smoking infertile patients, state regarding these women, “this constitutes an unsolicited hazard to their health and is an argument for smoke free public areas and workplaces.”
A number of comprehensive reviews of the literature have been published summarizing the cumulative data supporting an association between cigarette smoking and diminished female fecundity. The impact of cigarette smoking on early spontaneous abortion has been an important addition to these reviews on fertility, with the increase in pregnancy loss and ectopic pregnancies attributable to smoking adding to the overall adverse reproductive impact of this habit. It has led Joffe to describe smoking as the foremost reproductive poison of the 20th Century – and, might we add, perhaps the 21st.
Augood estimates that up to 13% of female infertility is caused by cigarette smoking.
The available biologic, experimental and epidemiological data support a substantial increase in female infertility attributable to cigarette smoking. Stopping smoking in many women not already in earlier menopause and not permanently effected with tubal factor infertility returns the potential for fertility. Ex-smokers have fecundity similar to that of women who have never smoked, often when they quit even within a year of starting to try to conceive. The adverse effects of sidestream and passive smoking are notable and add to the urgency of addressing not only those who smoke in campaigns aimed at prevention of infertility, but those with whom they live and work or share the environment.
Those couples already suffering from infertility need to know that continuing to smoke adversely effects the success of therapy. In particular regarding Assisted Reproductive Technology (e.g. in vitro fertilization therapy), ovarian reserve, ovarian response to stimulation, the number of oocytes retrieved and fertilized, and the pregnancy rates are reduced in smokers compared to non-smokers.
The pregnancy rate in in vitro fertilization treatment cycles was thus reduced in smokers by 34%. The deleterious effect of smoking becomes more detectable in older women undergoing therapy. The percentage of women experiencing conception delay for over 12 months was 54% higher for smokers compared to non-smokers. Exposure to passive smoke further increased the odds against a woman conceiving within 6 months. Smoking by the mother, the father, or other exposure to tobacco smoke were all associated with a longer time to conception.
This information may help those seeking to conceive and carry a healthy full-term infant to do so by imploring them to stop, especially those already having difficulty conceiving or maintaining a pregnancy. And for those not currently seeking to conceive but with wishes and dreams for the future, if they are in need of yet one more health risk to add to the panoply of reasons to discontinue their habit or never start, this information and data may be most useful in the prevention of infertility.
The good news is the ready availability of evidence-based Smoking Cessation Guideline materials for health care professionals and the public, including beneficial brief interventions designed for the busy doctor’s office. First developed in 1996, the Guideline is updated regularly.
ACOG also has material at www.acog.org/departments/dept_web.cfm?recno=13.
And the American Cancer Society has Great American Smokeout aids at www.cancer.org.