Ashok Agarwal, Ph.D. and Anthony J. Thomas, Jr., M.D.

Cigarette smoking is a serious health and social problem throughout the world. Up to 40% of men and women of reproductive age in the United States utilize nicotine via smoking on a daily basis. Epidemiological studies have shown decreased fecundity in smoking couples versus non-smoking couples. The impact of cigarette smoking on male fertility remains controversial. Most smokers have never been evaluated with respect to the toxicity effect on spermatozoa. The subject of possible detrimental effects of cigarette smoking on reproductive performance and specifically on semen parameters is of great interest but the currently available data is inconclusive.

A recent prospective study in our male infertility unit investigated semen quality, levels of seminal oxidative stress (OS) and sperm DNA damage among infertile men with a history of smoking. Information on smoking habit (number of cigarettes per day and number of years of smoking) was obtained from 48 infertile men at the time of clinical examination. Semen samples were examined according to the World Health Organization (WHO) criteria. Seminal leukocytes were examined by Endtz test. Basal levels of reactive oxygen species (ROS) were determined in washed sperm suspensions by a chemiluminescence assay and results expressed as X 106 counted photons per minute (cpm)/ 20 X106 sperm. Total non-enzymatic antioxidant capacity (TAC) was measured in seminal plasma by an enhanced chemiluminescence assay and results expressed as trolox equivalents. A composite value of ROS-TAC score was calculated as an index for OS. Sperm nuclear DNA damage was assessed by sperm chromatin structure assay (SCSA) to determine the percentage of cells outside the main population (% COMP(t) with abnormal chromatin structure.

Smoking resulted in a 48% increase in seminal leukocyte counts (p < 0.0001), 107% increase in ROS levels (P = 0.0003) and 11% decrease in ROS-TAC score (P = 0.002). We found no significant differences in sperm concentration, motility, morphology or DNA damage in infertile smoker compared to non-smokers. There was a strong correlation between cigarette smoking, increased seminal leukocytic counts and OS. Metabolites from smoke may cause a sub-clinical inflammation within the male reproductive tract with a consequent recruitment of leukocytes. Activation of these leukocytes results in an oxidative burst and OS. Smoking-related OS may explain reduced sperm fertilizing capacity and increased oxidative damage to sperm DNA among male smokers. The argument against smoking holds true for anyone wishing to conceive, however, it is particularly true for individuals having infertility problems. These results are important when counseling patients as to the harmful effects of smoking on their fertility potential.

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