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Invited review
Lifestyle factors and male infertility: an evidence-based review

Jaime Mendiola
,
Alberto M. Torres-Cantero
,
Ashok Agarwal

Arch Med Sci 2009; 5, 1A: S3–S12
Online publish date: 2009/06/10
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- Lifestyle factors.pdf  [0.14 MB]
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Introduction
There is a mounting evidence that human semen quality and fecundity have been declining during the last decades, at least across large sections of the United States and Europe [1-10]. However, those changes may not have occurred homogeneously [11, 12]. Geographical variations in semen quality support the idea that specific factors, present in some areas but not in others, may be responsible for the decline in semen quality [13-16]. Environmental pollutants, occupational exposures and lifestyle have been explored as possible contributors to those changes [17, 18]. Malfunction of the male reproductive system seems to be a good sensitive marker of environmental hazards (Figure 1) [19].
In this article we review the current evidence on the association between the main occupational and lifestyle exposures and male infertility.
Lifestyle factors
Special attention has been devoted in the scientific literature to factors that are well established as health risks, such as smoking, alcohol and obesity. Other factors also being considered in the literature include drug use, genital heat stress, psychological stress and cellular phones. These factors have received much less attention, and the evidence of their impact on semen quality and male fertility is still inconclusive.
Smoking
Cigarette smoke is a known somatic carcinogen and cell mutagen. Considerable evidence also exists that smoking adversely affect male reproductive health, although the impact of cigarette smoking on male fertility has been a highly controversial issue. Some early studies did not find an association between smoking and sperm quality [20] or sperm DNA damage [21] while another only found effects on sperm volume [22]. However, methodological issues, especially the complexity in adjusting for confounding factors, may underlie some of these negative findings.
The harmful effects of cigarette smoking on human male fertility are now clear [23]. Tobacco effects can be observed at both microscopic and molecular levels. Microscopically, sperm concentration, motility and morphology are affected [24-31]. At the molecular level, an increased risk of sperm aneuploidy [32, 33], higher levels of seminal oxidative stress [34], alteration of sperm plasma membrane phospholipids asymmetry [35] and sperm DNA fragmentation [36, 37] have been documented. Furthermore, maternal smoking during pregnancy may have an adverse and irreversible effect on semen quality in male descendants [38], in addition to its association with a higher risk of birth defects and childhood cancers in the offspring [39].
Alcohol
Alcoholism has been long associated with reproductive health disturbances such as impotence or testicular atrophy [40]. Spermatogenesis seems to deteriorate progressively with increasing levels of alcohol intake [41]. Chronic alcohol consumption has a detrimental effect on male reproductive hormones and on semen quality [42]. A case-control study conducted in Japan showed that alcohol intake was significantly more common in infertile men than in controls [43]. Alcohol exposure in vitro induces reduction of sperm motility and morphology, and the response is dose-related [44]. Moreover, the risk for XY sperm aneuploidy is greater in alcohol drinkers compared to nondrinkers (RR=1.38, 95% CI: 1.2-1.6) [33]. However, whether all alcoholic beverages have similar adverse effects on semen quality, or whether there is a safe threshold for alcohol intake is unknown.
An additional concern is the possible synergistic effect of concurrent toxic habits on male reproduction. A synergistic effect of alcohol and smoking consumption on sperm parameters has been described, but further research is needed to explore other associations with other lifestyle and occupational or environmental exposures [45, 46].
Obesity
A common observation in the Western world is the increased average body mass index (BMI) in the general population that has resulted in an increased prevalence of obesity. Several studies have associated lower World Health Organization (WHO) semen parameters with obesity [47, 48]. In a follow-up study of couples enrolled in the Agricultural Health Study in the United States, Sallmén et al. found, after adjustment for potential confounders, that male BMI was associated with infertility (defined as no pregnancy after 12 months of unprotected intercourse) [49]. They found a dose-response relationship between infertility and male BMI, and that association was similar for older or younger men. Other authors have found that semen parameters (mainly sperm counts, motility or sperm DNA integrity) and/or reproductive hormones (testosterone, inhibin B, estradiol) are affected in men with BMIs above or below normal levels [50-55].
Maternal BMI also may have an effect on the future semen parameters of the male offspring, although the issue is far from being elucidated. In a follow-up study Ramlau-Hansen et al. found an inverse dose-response between maternal BMI and the son’s inhibin B hormone [56]. In addition, point estimates of sperm concentration, semen volume, percent motile sperm, testosterone and FSH suggested impaired semen quality in sons of overweight mothers, although the values did not reach statistical significance. The study may have lacked sufficient power to detect real differences, and the evidence remains inconclusive.
Recreational drug use
Very few articles explore the effects of recreational cocaine or cannabis use on semen quality and the male reproductive system, and our knowledge is still very preliminary. In 1990, Bracken et al. assessed the association of cocaine use with sperm concentration, motility and morphology [57]. After adjustment for potential confounders, cocaine use for five or more years was more common in men with low sperm motility, low concentration or large proportion of abnormal forms; while cocaine use within the previous two years was twice as frequent in men with oligozoospermia. Authors concluded that given the high prevalence of cocaine use in their male population, the history of cocaine use should be ascertained during diagnostic interviews. Whan et al. investigated the effects of delta-9-tetrahydrocannabinol (Delta [9]-THC) on human sperm function in vitro, showing reduced sperm progressive motility and acrosome reaction [58]. Recently, Badawy et al. investigated the effects of Delta [9]-THC and Delta [8]-THC on sperm mitochondrial O2 consumption (respiration), showing that these compounds are potent inhibitors of mitochondrial O2 consumption in human sperm [59]. Overall, these studies emphasize the potential adverse effects of recreational drugs on male fertility although more observational studies are needed.
Genital heat stress
Normal sperm production depends on an optimal testicular temperature maintained below body temperature (typically between 34-35°C) [60]. Several experimental studies have shown that heat exposure may reduce semen quality [61-63]. In male llamas (Lama glama) moderate increases in temperature alter spermatogenesis and all sperm parameters, while showing on histological analysis a higher destruction of tubules and a lower spermatogonial proliferation rate [64]. In humans, occupational activities that require sedentary postures increase scrotal temperature [65-67]. In observational studies, individuals involved in activities that increase scrotal temperature have been found to have poor sperm morphology [68]. Other activities such as sitting over a heated floor [69] or recreational exposure to wet heat (Jacuzzi or hot baths) also result in impaired semen quality [70]. However, these effects may be reversible once the exposure to heat is ended.
The association between type of underwear and increased scrotal temperature also has been studied. Jung et al. found that scrotal temperature in volunteers wearing wool trousers and shirts fitted to body size was significantly higher for tight vs. loose-fitting clothing [71]. However, whether that temperature increase results in reduced semen quality remains to be studied. Finally, nocturnal scrotal cooling in infertile men with a history of testicular maldescent and oligozoospermia seems to have a positive effect on improving semen quality after eight weeks, suggesting that nocturnal scrotal cooling might be a therapeutic option in some patients [72].
Psychological stress
The impact of male psychological stress on semen quality is an area of great interest in which further research is needed, especially population-based studies. At the molecular level, the mechanisms of stress-related semen quality alterations have not been fully elucidated. Eskiocak et al. showed that some seminal antioxidant contents (glutathione and free sulphydryl), as well as motility and morphologically normal spermatozoa decrease in healthy subjects undergoing examination stress [73]. A few prospective studies in the general population have shown a small or nonexistent effect of the psychological stress of daily life on semen quality [74, 75]. In couples attending fertility clinics, Zorn et al. found a weak association between psychological factors and impaired semen quality [76]. In males involved in IVF procedures, the quality of the semen sample obtained on the day of egg retrieval was significantly worse than the quality of the first sample analyzed in the same patients. The decline in semen quality in the second sample was attributed to the psychological stress involved in that clinical process [77, 78].
Cellular telephone use
Concerns are escalating about the possible adverse effects of cell phones on human health and the male reproductive system. A few observational studies have shown that prolonged use of cell phones may have negative effects on sperm parameters like sperm count, motility, viability and normal morphology [79-81]. The impact of radiofrequency electromagnetic waves on semen quality still needs further investigation, including research in animal and in vitro models to better understand the mechanisms that are involved in this particular exposure [82-85].
Occupational and environmental factors
Endocrine disruptor compounds (EDCs) such as some polychlorinated biphenyls (PCBs) [86-88], organochlorine compounds (pesticides) [89, 90] or phthalate esters (PEs) [91], several heavy metals such as lead and cadmium [92-94] and several air pollutants [polycyclic aromatic hydrocarbons (PAHs), dioxins] [95, 96] have been shown to compromise reproductive male function (Table I).
Alteration of the male reproductive system may result from gonadal endocrine disruption [97, 98] or by direct damage to the spermatogenesis process (Figure 1) [92, 99]. Not surprisingly, occupational activities involving exposure to some of those specific chemicals and toxins are associated with infertility [93, 99-109]. Although literature relating the effect of specific substances on semen quality is expanding, the relationship between environmental chemical exposure and male infertility is not always available. Several studies have compared semen parameters and occupational exposure in male partners of infertile couples attending fertility clinics [93, 101, 110, 111]. An association has been found between welding and reduced semen quality (sperm count and motility) [93, 110]. In other case-control studies, infertile men had more frequent exposure to organic solvents [108, 109, 111], electromagnetic fields (engineering technicians, etc.) and heavy metals than did normozoospermic controls [93, 109, 112]. Recently, studies have suggested that environmental toxins alter sperm DNA integrity [113, 114]. DNA fragmentation may be an excellent marker of exposure to reproductive toxicants and a diagnostic tool for potential male infertility [115-117].
Endocrine disruptor compounds
Endocrine disruptor compounds (EDCs) cause testicular dysgenesis syndrome (TDS) and disturb meiosis in developmental germinal cells [6, 118]. Sharpe and Skakkebaek have suggested that the male reproductive system is most vulnerable to estrogenic agents during the critical period of cell differentiation and organ development in fetal and neonatal life [118]. In this period, the testes are structurally organized, establishing Sertoli cell and spermatogonia numbers to support spermatogenesis that will be initiated at puberty. Endogenous hormones have a vital role in fetal life and ensuring future fertility. The maintenance of tightly regulated estrogen levels is therefore essential for its completion [97, 118]. Exposure to the wrong hormones (male fetus exposed to female hormones) or inadequate amounts of the correct hormones could affect the reproductive system by resulting in fertility problems in adulthood [119, 120]. Moreover, due to their chemical composition, EDSs are able to cross a blood-tissue barrier in the testis, suggesting that intratubular germ cells also may be directly exposed [121, 122].
Dietary soy foods also have estrogenic activity and may affect semen quality. In animal models, genistein crosses the rat placenta and can reach significant levels in fetal brains [121]. In a recent observational study, Chavarro et al. after controlling for potential confounders found an inverse association between soy food intake and sperm concentration that was more pronounced in the high end of the distribution (90th and 75th percentile of intake) and among overweight and obese men [123].
Pesticides are another important source of EDCs. Juhler et al. investigated the hypothesis that farmers with high intakes of organically grown commodities would have good semen quality due to their expected lower levels of pesticide exposure [124]. An independent analysis of 40 groups of pesticides found no effects on semen quality. However, the analysis did not take into account the synergistic effect that pesticides in combination may exert on the reproductive system [125, 126].
A recent work published by the Nordic Cryptorchidism Study Group studied the human association between maternal exposure to 27 groups of pesticides and cryptorchidism among male children. In a nested case-control study within a prospective birth cohort, researchers compared 62 milk samples from mothers of cryptorchid boys and 68 from mothers of healthy ones. No significant differences were found for any individual chemical. However, combined statistical analysis of the eight most abundant and persistent pesticides showed that pesticide levels in breast milk were significantly higher in boys with cryptorchidism [127]. This finding has given rise to speculation that male reproductive anomalies (hypospadias, cryptorchidism) [128] and the global fall in sperm quality [1] might be attributed to the marked increased of EDCs in our water and diet [129].
In a recent review about the sensitivity of children to sex steroids and the possible impact of exogenous estrogens, Aksglaede et al. concluded that children are extremely sensitive to estradiol before puberty and may respond with increased growth and/or breast development even at serum levels below the current detection limits, and that those changes in hormone levels during fetal and prepubertal development may have severe (probably nonreversible) effects in adult life [130]. The authors concluded, therefore, that a cautionary approach should be taken to avoid unnecessary exposure of fetuses and children to exogenous sex steroids and endocrine disruptors, even at very low levels. That caution includes food intake, as possible adverse effects on human health may result from consumption of meat from hormone-treated animals [131].
A recent study published by Swan et al. suggests that maternal consumption of xenobiotics (anabolic steroids) from beef may damage testicular development in utero in the offspring and adversely affect reproductive capacity of the males [132]. Sons of “high beef consumers” (>7 beef meals/week) had sperm concentrations 24.3% lower than those found in sons whose mothers ate less beef [132, 133]. The general population is exposed to many potential endocrine disruptors concurrently. Studies, both in vivo and in vitro, have shown that the action of estrogenic compounds is additive [134, 135], but little is known about the possible synergistic or additive effects of these compounds in humans [136].
Heavy metals
Exposure to metals (mainly lead and cadmium) has been long associated with low sperm motility and density, increased morphological anomalies and male infertility [95, 137]. Males employed in metal industries had a decreased fertility when compared with other workers as shown by delayed pregnancy and reduced semen quality [92, 115, 138-144]. Akinloye et al. analyzed the serum and seminal plasma concentrations of cadmium (Cd) in 60 infertile males and 40 normozoospermic subjects [143]. Seminal plasma Cd levels were significantly higher than serum levels in all subjects. A statistically significant inverse correlation was observed between serum Cd levels and all biophysical semen parameters except sperm volume. Naha et al. studied the blood and semen lead level concentration among battery and paint factory workers [144]. Their results included oligozoospermia and increased percentage of sperm DNA haploids, suggesting a diminution of sperm cell production after occupational lead exposure. Additionally, sperm velocity and forward progressive motility were reduced with a high percentage of stationary motile spermatozoa, suggesting retarded sperm activity among the exposed workers. Finally, an increased incidence of teratozoospermia is associated with high blood and semen lead levels.
Telisman et al. conducted a study that compared semen quality of 98 subjects with light to moderate occupational exposure to lead (Pb) to that of 51 men with no occupational exposure. They concluded that even moderate exposures to Pb (blood Pb <400 µg/l) and cadmium (blood Cd <10 µg/l) significantly reduced human semen quality without conclusive evidence of a parallel impairment of the male reproductive endocrine function [145].
Moreover, other reports also have found that blood lead concentration in the general population is negatively correlated with semen quality [94, 145, 146]. Recently Telisman et al. reported reproductive toxicity of low-level lead exposure in men with no occupational exposure to metals [147]. In this study, a significant association was found between blood lead (BPb) and reproductive parameters such as immature sperm concentration, percentage of pathologic sperm, wide sperm, round and short sperm, serum levels of testosterone and estradiol, and a decrease in seminal plasma zinc and serum prolactin (P<0.05).
These reproductive effects were observed at low-level lead exposures (median BPb 49 µg/l, range 11-149 µg/l in the 240 subjects) that are similar to those of the general population worldwide. However, other articles have been less conclusive in finding adverse effects of lead or cadmium exposure on semen quality or decreased fertility [148-151]. With regards to other possible metals affecting fertility; recently, Meeker et al. [152] assessed relationships between environmental exposure to multiple metals (arsenic, cadmium, chromium, copper, lead, manganese, mercury, molybdenum, selenium and zinc) and human semen quality. The associations involving molybdenum were the most consistent. They found a dose-dependent relationship between molybdenum and declining sperm concentration and morphology in adjusted analyses. These findings are consistent with animal data, but more mechanistic studies are needed.
Occupational and environmental pollutants Several solvents may affect human seminal quality [17, 107] proportional to the amount and duration of exposure [108, 109]. Semen quality in workers exposed occupationally to hydrocarbons like toluene, benzene and xylene present anomalies in viscosity, liquefaction capacity, sperm count, sperm motility and the proportion of sperm with normal morphology compared with unexposed males [153-155]. An association also has been observed between exposure to styrene in boat-building factory workers [156], PAH in coke- oven workers [157], and episodic air pollution with an increasing fragmentation of the DNA sperm [158], as well as altered WHO seminal parameters in young men [159]. Dioxin exposure also is associated with impaired male fertility.
Recently, Mocarelli et al. [96] investigated the reproductive hormones and sperm quality in males exposed to the accidental dioxin leak in Seveso, Italy in 1976. Three groups of males exposed at infancy/prepuberty, puberty and adulthood, respectively were compared with 184 healthy males. Men exposed in infancy/prepuberty (mean age at exposure: 6.2 years) showed reductions in sperm concentration, progressive motility, total motile sperm count and estradiol and an increase in FSH. The other two groups with later exposure (mean age at exposure 13.2 years and 21.5 years of age, respectively) did not have decreased semen parameters. The study suggests that exposure to dioxins in infancy, even at relatively low concentrations, may permanently reduce semen quality.
Conclusions
A growing body of literature shows that a wide variety of substances adversely affects semen quality and may impair human fertility. However, the evidence for adverse effects on fertility is incomplete, and our knowledge is still fairly limited.
Although our knowledge is expanding related to the single effect of individual products, the reality is more complex. Single exposure does not occur, and very few studies address the consequences for semen quality and male infertility of simultaneous, complex exposure to compounds such as food additives, toxicants, contaminants, outdoor and indoor air pollutants, endocrine disruptors and hazardous substances. A clear side effect of that lack of information is that we may be underestimating the consequences of exposing the population to a wide variety of products because we are missing the larger, broader picture of complex exposures.
Finally, study design does not always facilitate the interpretation of the results. To be useful, studies must be designed in a way that confounding factors can be controlled. Ideally this would include all variables that are known to affect semen quality such as lifestyle, occupational and environmental exposures, and exposure would be tracked along the main developmental stages of the male’s life span.
References
1. Carlsen E, Giwercman A, Keiding N, Skakkebaek NE. Evidence for decreasing quality of semen during the past 50 years. BMJ 1992; 305: 609-13.
2. Irvine S, Cawood E, Richardson D, MacDonald E, Aitken J. Evidence of deteriorating semen quality in the United Kingdom: birth cohort study in 577 men in Scotland over 11 years. BMJ 1996; 312: 467-71.
3. Swan SH, Elkin EP, Fenster L. Have sperm densities declined? A reanalysis of global trend data. Environ Health Perspect 1997; 105: 1228-32.
4. Swan SH, Elkin EP, Fenster L. The question of declining sperm density revisited: an analysis of 101 studies published 1934-1996. Environ Health Perspect 2000; 108: 961-6.
5. Aitken RJ, Koopman P, Lewis SE. Seeds of concern. Nature 2004; 432: 48-52.
6. Skakkebøk NE, Rajpert-De Meyts E, Main KM. Testicular dysgenesis syndrome: an increasingly common developmental disorder with environmental aspects. Hum Reprod 2001; 16: 972-8.
7. Skakkebøk NE, Jørgensen N, Main KM, et al. Is human fecundity declining? Int J Androl 2006; 29: 2-11.
8. Jørgensen N, Asklund C, Carlsen E, et al. Coordinated European investigations of semen quality: results from studies of Scandinavian young men is a matter of concern. Int J Androl 2006; 29: 54-61.
9. Hauser R. The environment and male fertility: recent research on emerging chemicals and semen quality. Semin Reprod Med 2006; 24: 156-67.
10. Swan SH. Does our environment affect our fertility? Some examples to help reframe the question. Semin Reprod Med 2006; 24: 142-6.
11. Fisch H, Goluboff ET, Olson JH, Feldshuh J, Broder SJ, Barad DH. Semen analyses in 1,283 men from the United States over a 25-year period: no decline in quality. Fertil Steril 1996; 65: 1009-14.
12. Paulsen CA, Berman NG, Wang C. Data from men in greater Seattle area reveals no downward trend in semen quality: further evidence that deterioration of semen quality is not geographically uniform. Fertil Steril 1996; 65: 1015-20.
13. Fisch H, Goluboff ET. Geographic variations in sperm counts: a potential cause of bias in studies of semen quality. Fertil Steril 1996; 65: 1044-6.
14. Fisch H, Ikeguchi EF, Goluboff ET. Worldwide variations in sperm counts. Urology 1996; 48: 909-11.
15. Jørgensen N, Andersen AG, Eustache F, et al. Regional differences in semen quality in Europe. Hum Reprod 2001; 16: 1012-9.
16. Swan SH, Brazil C, Drobnis EZ, et al. Geographic differences in semen quality of fertile U.S. males. Environ Health Perspect 2003; 111: 414-20.
17. Tielemans E, Burdorf A, te Velde ER, et al. Occupationally related exposures and reduced semen quality: a case-control study. Fertil Steril 1999; 71: 690-6.
18. Homan GF, Davies M, Norman R. The impact of lifestyle factors on reproductive performance in the general population and those undergoing infertility treatments: a review. Hum Reprod Update 2007; 13: 209-23.
19. Bonde JP, Giwercman A, Ernst E. Identifying environmental risk to male reproductive function by occupational sperm studies: logistics and design options. Occup Environ Med 1996; 53: 511-9.
20. Vogt HJ, Heller WD, Borelli S. Sperm quality of healthy smokers, ex-smokers, and never-smokers. Fertil Steril 1986; 45: 106-10.
21. Sergerie M, Ouhilal S, Bissonnette F, Brodeur J, Bleau G. Lack of association between smoking and DNA fragmentation in the spermatozoa of normal men. Hum Reprod 2000; 15: 1314-21.
22. Pasqualotto FF, Sobreiro BP, Hallak J, Pasqualotto EB, Lucon AM. Cigarette smoking is related to a decrease in semen volume in a population of fertile men. BJU Int 2006; 97: 324-6.
23. Vine MF. Smoking and male reproduction: a review. Int J Androl 1996; 19: 323-37.
24. Vine MF, Tse CK, Hu P, Truong KY. Cigarette smoking and semen quality. Fertil Steril 1996; 65: 835-42.
25. Zhang JP, Meng QY, Wang Q, Zhang LJ, Mao YL, Sun ZX. Effect of smoking on semen quality of infertile men in Shandong, China. Asian J Androl 2000; 2: 143-6.
26. Wang SL, Wang XR, Chia SE, et al. A study on occupational exposure to petrochemicals and smoking on seminal quality. J Androl 2001; 22: 73-8.
27. Künzle R, Mueller MD, Hänggi W, Birkhäuser MH, Drescher H, Bersinger NA. Semen quality of male smokers and nonsmokers in infertile couples. Fertil Steril 2003; 79: 287-91.
28. Storgaard L, Bonde JP, Ernst E, et al. Does smoking during pregnancy affect sons’ sperm counts? Epidemiology 2003; 14: 278-86.
29. Jensen TK, Jo/rgensen N, Punab M, et al. Association of in utero exposure to maternal smoking with reduced semen quality and testis size in adulthood: a cross-sectional study of 1,770 young men from the general population in five European countries. Am J Epidemiol 2004; 159: 49-58.
30. Said TM, Ranga G, Agarwal A. Relationship between semen quality and tobacco chewing in men undergoing infertility evaluation. Fertil Steril 2005; 84: 649-53.
31. Ramlau-Hansen CH, Thulstrup AM, Aggerholm AS, Jensen MS, Toft G, Bonde JP. Is smoking a risk factor for decreased semen quality? A cross-sectional analysis. Hum Reprod 2007; 22: 188-96.
32. Shi Q, Ko E, Barclay L, Hoang T, Rademaker A, Martin R. Cigarette smoking and aneuploidy in human sperm. Mol Reprod Dev 2001; 59: 417-21.
33. Robbins WA, Elashoff DA, Xun L, et al. Effect of lifestyle exposures on sperm aneuploidy. Cytogenet Genome Res 2005; 111: 371-7.
34. Saleh RA, Agarwal A, Sharma RK, Nelson DR, Thomas AJ Jr. Effect of cigarette smoking on levels of seminal oxidative stress in infertile men: a prospective study. Fertil Steril 2002; 78: 491-9.
35. Belcheva A, Ivanova-Kicheva M, Tzvetkova P, Marinov M. Effects of cigarette smoking on sperm plasma membrane integrity and DNA fragmentation. Int J Androl 2004; 27: 296-300.
36. Potts RJ, Newbury CJ, Smith G, Notarianni LJ, Jefferies TM. Sperm chromatin damage associated with male smoking. Mutat Res 1999; 423: 103-11.
37. Sepaniak S, Forges T, Gerard H, Foliguet B, Bene MC, Monnier-Barbarino P. The influence of cigarette smoking on human sperm quality and DNA fragmentation. Toxicology 2006; 223: 54-60.
38. Ramlau-Hansen CH, Thulstrup AM, Storgaard L, Toft G, Olsen J, Bonde JP. Is prenatal exposure to tobacco smoking a cause of poor semen quality? A follow-up study. Am J Epidemiol 2007; 165: 1372-9.
39. Sorahan T, Prior P, Lancashire RJ, et al. Childhood cancer and parental use of tobacco: deaths from 1971 to 1976. Br J Cancer 1997; 76: 1525-31.
40. Boyden TW, Pamenter RW. Effects of ethanol on the male hypothalamic-pituitary-gonadal axis. Endocr Rev 1983; 4: 389-95.
41. Pajarinen J, Karhunen PJ, Savolainen V, Lalu K, Penttilä A, Laippala P. Moderate alcohol consumption and disorders of human spermatogenesis. Alcohol Clin Exp Res 1996; 20: 332-7.
42. Muthusami KR, Chinnaswamy P. Effect of chronic alcoholism on male fertility hormones and semen quality. Fertil Steril 2005; 84: 919-24.
43. Tsujimura A, Matsumiya K, Takahashi T, et al. Effect of lifestyle factors on infertility in men. Arch Androl 2004; 50: 15-7.
44. Donnelly GP, McClure N, Kennedy MS, Lewis SE. Direct effect of alcohol on the motility and morphology of human spermatozoa. Andrologia 1999; 31: 43-7. 45. Martini AC, Molina RI, Estofán D, Senestrari D, Fiol de Cuneo M, Ruiz RD. Effects of alcohol and cigarette consumption on human seminal quality. Fertil Steril 2004; 82: 374-7. 46. Kalyani R, Basavaraj PB, Kumar ML. Factors influencing quality of semen: a two year prospective study. Indian J Pathol Microbiol 2007; 50: 890-5.
47. Magnusdottir EV, Thorsteinsson T, Thorsteinsdottir S, Heimisdottir M, Olafsdottir K. Persistent organochlorines, sedentary occupation, obesity and human male subfertility. Hum Reprod 2005; 20: 208-15.
48. Nguyen RH, Wilcox AJ, Skjaerven R, Baird DD. Men’s body mass index and infertility. Hum Reprod 2007; 22: 2488-93.
49. Sallmén M, Sandler DP, Hoppin JA, Blair A, Baird DD. Reduced fertility among overweight and obese men. Epidemiology 2006; 17: 520-3.
50. Jensen TK, Andersson AM, Jo/rgensen N, et al. Body mass index in relation to semen quality and reproductive hormones among 1,558 Danish men. Fertil Steril 2004; 82: 863-70.
51. Koloszár S, Fejes I, Závaczki Z, Daru J, Szöllosi J, Pál A. Effect of body weight on sperm concentration in normozoospermic males. Arch Androl 2005; 51: 299-304.
52. Fejes I, Koloszár S, Závaczki Z, Daru J, Szöllösi J, Pál A. Effect of body weight on testosterone/estradiol ratio in oligozoospermic patients. Arch Androl 2006; 52: 97-102.
53. Kort HI, Massey JB, Elsner CW, et al. Impact of body mass index values on sperm quantity and quality. J Androl 2006; 27: 450-2.
54. Aggerholm AS, Thulstrup AM, Toft G, Ramlau-Hansen CH, Bonde JP. Is overweight a risk factor for reduced semen quality and altered serum sex hormone profile? Fertil Steril 2008; 90: 619-26.
55. Hammoud AO, Wilde N, Gibson M, Parks A, Carrell DT, Meikle AW. Male obesity and alteration in sperm parameters. Fertil Steril 2008; Epub ahead of print.
56. Ramlau-Hansen CH, Nohr EA, Thulstrup AM, Bonde JP, Storgaard L, Olsen J. Is maternal obesity related to semen quality in the male offspring? A pilot study. Hum Reprod 2007; 22: 2758-62.
57. Bracken MB, Eskenazi B, Sachse K, McSharry JE, Hellenbrand K, Leo-Summers L. Association of cocaine use with sperm concentration, motility, and morphology. Fertil Steril 1990; 53: 315-22.
58. Whan LB, West MC, McClure N, Lewis SE. Effects of delta-9-tetrahydrocannabinol, the primary psychoactive cannabinoid in marijuana, on human sperm function in vitro. Fertil Steril 2006; 85: 653-60.
59. Badawy ZS, Chohan KR, Whyte DA, Penefsky HS, Brown OM, Souid AK. Cannabinoids inhibit the respiration of human sperm. Fertil Steril 2008 Epub ahead of print.
60. Thonneau P, Bujan L, Multigner L, Mieusset R. Occupational heat exposure and male fertility: a review. Hum Reprod 1998; 13: 2122-5.
61. Hjollund NH, Storgaard L, Ernst E, Bonde JP, Olsen J. The relation between daily activities and scrotal temperature. Reprod Toxicol 2002; 16: 209-14.
62. Hjollund NH, Storgaard L, Ernst E, Bonde JP, Olsen J. Impact of diurnal scrotal temperature on semen quality. Reprod Toxicol 2002; 16: 215-21.
63. Jung A, Schuppe HC. Influence of genital heat stress on semen quality in humans. Andrologia 2007; 39: 203-15.
64. Schwalm A, Gauly M, Erhardt G, Bergmann M. Changes in testicular histology and sperm quality in llamas [Lama glama], following exposure to high ambient temperature. Theriogenology 2007; 67: 1316-23.
65. Bujan L, Daudin M, Charlet JP, Thonneau P, Mieusset R. Increase in scrotal temperature in car drivers. Hum Reprod 2000; 15: 1355-7.
66. Sheynkin Y, Jung M, Yoo P, Schulsinger D, Komaroff E. Increase in scrotal temperature in laptop computer users. Hum Reprod 2005; 20: 452-5.
67. Jung A, Strauss P, Lindner HJ, Schuppe HC. Influence of heating car seats on scrotal temperature. Fertil Steril 2008; 90: 335-9.
68. Figa`-Talamanca I, Cini C, Varricchio GC, et al. Effects of prolonged autovehicle driving on male reproduction function: a study among taxi drivers. Am J Ind Med 1996; 30: 750-8.
69. Song GS, Seo JT. Changes in the scrotal temperature of subjects in a sedentary posture over a heated floor. Int J Androl 2006; 29: 446-57.
70. Shefi S, Tarapore PE, Walsh TJ, Croughan M, Turek PJ. Wet heat exposure: a potentially reversible cause of low semen quality in infertile men. Int Braz J Urol 2007; 33: 50-6.
71. Jung A, Leonhardt F, Schill WB, Schuppe HC. Influence of the type of undertrousers and physical activity on scrotal temperature. Hum Reprod 2005; 20: 1022-7.
72. Jung A, Schill WB, Schuppe HC. Improvement of semen quality by nocturnal scrotal cooling in oligozoospermic men with a history of testicular maldescent. Int J Androl 2005; 28: 93-8.
73. Eskiocak S, Gozen AS, Yapar SB, Tavas F, Kilic AS, Eskiocak M. Glutathione and free sulphydryl content of seminal plasma in healthy medical students during and after exam stress. Hum Reprod 2005; 20: 2595-600.
74. Hjollund NH, Bonde JP, Henriksen TB, Giwercman A, Olsen J; The Danish First Pregnancy Planner Study Team. Reproductive effects of male psychologic stress. Epidemiology 2004; 15: 21-7.
75. Fenster L, Katz DF, Wyrobek AJ, et al. Effects of psychological stress on human semen quality. J Androl 1997; 18: 194-202.
76. Zorn B, Auger J, Velikonja V, Kolbezen M, Meden-Vrtovec H. Psychological factors in male partners of infertile couples: relationship with semen quality and early miscarriage. Int J Androl 2008; 31: 557-64.
77. Clarke RN, Klock SC, Geoghegan A, Travassos DE. Relationship between psychological stress and semen quality among in-vitro fertilization patients. Hum Reprod 1999; 14: 753-8.
78. Ragni G, Caccamo A. Negative effect of stress of in vitro fertilization program on quality of semen. Acta Eur Fertil 1992; 23: 21-3.
79. Fejes I, Závaczki Z, Szöllosi J, et al. Is there a relationship between cell phone use and semen quality? Arch Androl 2005; 51: 385-93.
80. Wdowiak A, Wdowiak L, Wiktor H. Evaluation of the effect of using mobile phones on male fertility. Ann Agric Environ Med 2007; 14: 169-72.
81. Agarwal A, Deepinder F, Sharma RK, Ranga G, Li J. Effect of cell phone usage on semen analysis in men attending infertility clinic: an observational study. Fertil Steril 2008; 89: 124-8.
82. Aitken RJ, Bennetts LE, Sawyer D, Wiklendt AM, King BV. Impact of radio frequency electromagnetic radiation on DNA integrity in the male germline. Int J Androl 2005; 28: 171-9.
83. Erogul O, Oztas E, Yildirim I, et al. Effects of electromagnetic radiation from a cellular phone on human sperm motility: an in vitro study. Arch Med Res 2006; 37: 840-3.
84. Yan JG, Agresti M, Bruce T, Yan YH, Granlund A, Matloub HS. Effects of cellular phone emissions on sperm motility in rats. Fertil Steril 2007; 88: 957-64.
85. Deepinder F, Makker K, Agarwal A. Cell phones and male infertility: dissecting the relationship. Reprod Biomed Online 2007; 15: 266-70.
86. Rozati R, Reddy PP, Reddanna P, Mujtaba R. Role of environmental estrogens in the deterioration of male factor fertility. Fertil Steril 2002; 78: 1187-94.
87. Spanò M, Toft G, Hagmar L, et al.; INUENDO. Exposure to PCB and p,p´-DDE in European and Inuit populations: impact on human sperm chromatin integrity. Hum Reprod 2005; 20: 3488-99.
88. Toft G, Rignell-Hydbom A, Tyrkiel E, et al. Semen quality and exposure to persistent organochlorine pollutants. Epidemiology 2006; 17: 450-8.
89. Swan SH. Semen quality in fertile US men in relation to geographical area and pesticide exposure. Int J Androl 2005; 29: 62-8.
90. Carreńo J, Rivas A, Granada A, et al. Exposure of young men to organochlorine pesticides in Southern Spain. Environ Res 2007; 103: 55-61.
91. Duty SM, Silva MJ, Barr DB, et al. Phthalate exposure and human semen parameters. Epidemiology 2003; 14: 269-77.
92. Robins TG, Bornman MS, Ehrlich RI, et al. Semen quality and fertility of men employed in a South African lead acid battery plant. Am J Ind Med 1997; 32: 369-76.
93. Irgens A, Krüger K, Ulstein M. The effect of male occupational exposure in infertile couples in Norway. J Occup Environ Med 1999; 41: 1116-20.
94. Benoff S, Jacob A, Hurley IR. Male infertility and environmental exposure to lead and cadmium. Hum Reprod Update 2000; 6: 107-21.
95. Srám RJ, Benes I, Binková B, et al. Teplice program – the impact of air pollution on human health. Environ Health Perspect 1996; 104 (Suppl 4): 699-714.
96. Mocarelli P, Gerthoux PM, Patterson DG Jr, et al. Dioxin exposure, from infancy through puberty, produces endocrine disruption and affects human semen quality. Environ Health Perspect 2008; 116: 70-7.
97. Skakkebaek NE, Rajpert-De Meyts E, Main KM. Testicular dysgenesis syndrome: an increasingly common developmental disorder with environmental aspects. Hum Reprod 2001; 16: 972-8.
98. Sharpe RM, Irvine DS. How strong is the evidence of a link between environmental chemicals and adverse effects on human reproductive health? BMJ 2004; 328: 447-51.
99. Wyrobek AJ, Schrader SM, Perreault SD, et al. Assessment of reproductive disorders and birth defects in communities near hazardous chemical sites. III Guidelines for field studies of male reproductive disorders. Reprod Toxicol 1997; 11: 243-59.
100. Alexander BH, Checkoway H, Faustman EM, van Netten C, Muller CH, Ewers TG. Contrasting associations of blood and semen lead concentrations with semen quality among lead smelter workers. Am J Ind Med 1998; 34: 464-9.
101. Bigelow PL, Jarrell J, Young MR, Keefe TJ, Love EJ. Association of semen quality and occupational factors: comparison of case-control analysis and analysis of continuous variables. Fertil Steril 1998; 69: 11-8.
102. Viskum S, Rabjerg L, Jo/rgensen PJ, Grandjean P. Improvement in semen quality associated with decreasing occupational lead exposure. Am J Ind Med 1999; 35: 257-63.
103. Sallmen M, Lindbohm ML, Nurminen M. Paternal exposure to lead and infertility. Epidemiology 2000; 11: 148-52.
104. Figà-Talamanca I, Traina ME, Urbani E. Occupational exposures to metals, solvents and pesticides: recent evidence on male reproductive effects and biological markers. Occup Med (Lond) 2001; 51: 174-88.
105. Sheiner EK, Sheiner E, Hammel RD, Potashnik G, Carel R. Effect of occupational exposures on male fertility: literature review. Ind Health 2003; 41: 55-62.
106. Chang HY, Shih TS, Guo YL, Tsai CY, Hsu PC. Sperm function in workers exposed to N,N-dimethylformamide in the synthetic leather industry. Fertil Steril 2004; 81: 1589-94.
107. Jensen TK, Bonde JP, Joffe M. The influence of occupational exposure on male reproductive function. Occup Med (Lond) 2006; 56: 544-53.
108. Cherry N, Moore H, McNamee R, et al.; participating centres of Chaps-UK. Occupation and male infertility: glycol ethers and other exposures. Occup Environ Med 2008; 65: 708-14.
109. Mendiola J, Torres-Cantero AM, Moreno-Grau JM, et al. Exposure to environmental toxins in males seeking infertility treatment: a case-controlled study. Reprod Biomed Online 2008; 16: 842-50.
110. Bonde JP. The risk of male subfecundity attributable to welding of metals. Studies of semen quality, infertility, fertility, adverse pregnancy outcome and childhood malignancy. Int J Androl 1993; 16 (Suppl 1): 1-29.
111. Cherry N, Labrèche F, Collins J, Tulandi T. Occupational exposure to solvents and male infertility. Occup Environ Med 2001; 58: 635-40.
112. Chia SE, Tay SK. Occupational risk for male infertility: a case-control study of 218 infertile men and 227 fertile men. J Occup Environ Med 2001; 43: 946-51.
113. Stronati A, Manicardi GC, Cecati M, et al. Relationships between sperm DNA fragmentation, sperm apoptotic markers and serum levels of CB-153 and p,p´-DDE in European and Inuit populations. Reproduction 2006; 132: 949-58.
114. Aitken RJ, De Luliis GN. Origins and consequences of DNA damage in male germ cells. Reprod Biomed Online 2007; 14: 727-33.
115. Evenson DP, Wixon R. Environmental toxicants cause sperm DNA fragmentation as detected by the Sperm Chromatin Structure Assay (SCSA). Toxicol Appl Pharmacol 2005; 207 (2 Suppl): 532-7.
116. Ozmen B, Caglar GS, Koster F, Schopper B, Diedrich K, Al-Hasani S. Relationship between sperm DNA damage, induced acrosome reaction and viability in ICSI patients. Reprod Biomed Online 2007; 15: 208-14.
117. Meeker JD, Barr DB, Hauser R. Human semen quality and sperm DNA damage in relation to urinary metabolites of pyrethroid insecticides. Hum Reprod 2008; 23: 1932-40.
118. Sharpe RM, Skakkebaek NE. Are estrogens involved in falling sperm counts and disorders of the male reproductive tract? Lancet 1993; 341: 1392-5.
119. Toppari J, Larsen JC, Christiansen P, et al. Male reproductive health and environmental xenoestrogens. Environ Health Perspect 1996; 104 Suppl 4: 741-803.
120. Sharpe RM, Franks S. Environment, lifestyle and infertility- an inter-generational issue. Nat Cell Biol 2002; 4 Suppl: s33-40.
121. Doerge DR, Churchwell MI, Chang HC, Newbold RR, Delclos KB. Placental transfer of the soy isoflavone genistein following dietary and gavage administration to Sprague Dawley rats. Reprod Toxicol 2001; 15: 105-10.
122. West MC, Anderson L, McClure N, Lewis SE. Dietary oestrogens and male fertility potential. Hum Fertil 2005; 8: 197-207.
123. Chavarro JE, Toth TL, Sadio SM, Hauser R. Soy food and isoflavone intake in relation to semen quality parameters among men from an infertility clinic. Hum Reprod 2008; 23: 2584-90.
124. Juhler RK, Larsen SB, Meyer O, et al. Human semen quality in relation to dietary pesticide exposure and organic diet. Arch Environ Contam Toxicol 1999; 37: 415-23.
125. Kortenkamp A. Low dose mixture effects of endocrine disrupters: implications for risk assessment and epidemiology. Int J Androl 2008; 31: 233-40.
126. Kortenkamp A, Faust M, Scholze M, Backhaus T. Low-level exposure to multiple chemicals: reason for human health concerns? Environ Health Perspect 2007; 115 Suppl 1: 106-14.
127. Damgaard IN, Skakkebaek, Toppari J, et al.; Nordic Cryptorchidism Study Group. Persistent pesticides in human breast milk and cryptorchidism. Environ Health Perspect 2006; 114: 1133-8.
128. Toppari J, Kaleva M, Virtanen HE. Trends in the incidence of cryptorchidism and hypospadias, and methodological limitations of registry-based data. Hum Reprod Update 2001; 7: 282-6.
129. O’Donnell L, Robertson KM, Jones ME, Simpson ER. Estrogens and spermatogenesis. Endocr Rev 2001; 22: 289-318.
130. Aksglaede L, Juul A, Leffers H, Skakkebaek NE, Andersson AM. The sensitivity of the child to sex steroids: possible empact of exogenous estrogens. Hum Reprod Update 2006; 12: 341-9.
131. Andersson AM, Skakkebaek NE. Exposure to exogenous estrogens in food: possible impact on human development and health. Eur J Endocrinol 1999; 140: 477-85.
132. Swan SH, Liu F, Overstreet JW, Brazil C, Skakkebaek NE. Semen quality of fertile US males in relation to their mothers’ beef consumption during pregnancy. Hum Reprod 2007; 22: 1497-502.
133. vom Saal FS. Could hormone residues be involved? Hum Reprod 2007; 22: 1503-5.
134. Rajapakse N, Silva E, Kortenkamp A. Combining xenoestrogens at levels below individual no-observed-effect concentrations dramatically enhances steroid hormone action. Environ Health Perspect 2002; 110: 917-21.
135. Tinwell H, Ashby J. Sensitivity of the immature rat uterotrophic assay to mixtures of estrogens. Environ Health Perspect 2004; 112: 575-82.
136. Toppari J, Skakkebaek NE. Sexual differentiation and environmental endocrine disrupters. Baillieres Clin Endocrinol Metab 1998; 12: 143-56.
137. Umeyama T, Ishikawa H, Takeshima H, Yoshii S, Koiso K. A comparative study of seminal plasma trace elements in fertile and infertile men. Fertil Steril 1986; 46: 494-9.
138. Xuezhi J, Youxin L, Yilan W. Studies of lead exposure on reproductive system: a review of work in China. Biomed Environ Sci 1992; 5: 266-75.
139. Gennart JP, Buchet JP, Roels H, Ghyselen P, Ceulemans E, Lauwerys R. Fertility of male workers exposed to cadmium, lead or manganese. Am J Epidemiol 1992; 135: 1208-19.
140. Chia SE, Chan OY, Sam CT, Heng BH. Blood cadmium levels in non-occupationally exposed adult subjects in Singapore. Sci Total Environ 1994; 145: 119-23.
141. Spinelli A, Figa-Talamanca, Osborn J. Time to pregnancy and occupation in a group of Italian women. Int J Epidemiol 1997; 26: 601-9.
142. Danadevi K, Rozati R, Reddy PP, Grover P. Semen quality of Indian welders occupationally exposed to nickel and chromium. Reprod Toxicol 2003; 17: 451-6.
143. Akinloye O, Arowojolu AO, Shittu OB, Anetor JI. Cadmium toxicity: a possible cause of male infertility in Nigeria. Reprod Biol 2006; 6: 17-30.
144. Naha N, Chowdhury AR. Inorganic lead exposure in battery and paint factory: effect on human sperm structure and functional activity. J UOEH 2006; 28: 157-71.
145. Telisman S, Cvitković P, Jurasović J, Pizent A, Gavella M, Rocić B. Semen quality and reproductive endocrine function in relation to biomarkers of lead, cadmium, zinc and copper in men. Environ Health Perspect 2000; 108: 45-53.
146. Benoff S, Hurley IR, Millan C, Napolitano B, Centola GM. Seminal lead concentrations negatively affect outcomes of artificial insemination. Fertil Steril 2003; 80: 517-25.
147. Telisman S, Colak B, Pizent A, Jurasović J, Cvitković P. Reproductive toxicity of low-level lead exposure in men. Environ Res 2007; 105: 256-66.
148. Coste J, Mandereau L, Pessione F, et al. Lead-exposed workman and fertility: a cohort study on 354 subjects. Eur J Epidemiol 1991; 7: 154-8.
149. Abou-Shakra FR, Ward NI, Everard DM. The role of trace elements in male infertility. Fertil Steril 1989; 52: 307-10.
150. Hovatta O, Venäläinen ER, Kuusimäki L, Heikkilä J, Hirvi T, Reima I. Aluminium, lead and cadmium concentrations in seminal plasma and spermatozoa, and semen quality in Finnish men. Hum Reprod 1998; 13: 115-9.
151. Inhorn MC, King L, Nriagu JO, et al. Occupational and environmental exposures to heavy metals: risk factors for male infertility in Lebanon? Reprod Toxicol 2008; 25: 203-12.
152. Meeker JD, Rossano MG, Protas B, et al. Cadmium, Lead and Other Metals in Relation to Semen Quality: Human Evidence for Molybdenum as a Male Reproductive Toxicant. Environ Health Perspect 2008; In press.
153. Xiao G, Pan C, Cai Y, Lin H, Fu Z. Effect of benzene, toluene, xylene on the semen quality of exposed workers. Chin Med J 1999; 112: 709-12.
154. De Celis R, Feria-Velasco A, González-Unzaga M, Torres-Calleja J, Pedrón-Nuevo N. Semen quality of workers occupationally exposed to hydrocarbons. Fertil Steril 2000; 73: 221-8.
155. De Rosa M, Zarrilli S, Paesano L, et al. Traffic pollutants affect fertility in men. Hum Reprod 2003; 18: 1055-61.
156. Migliore L, Naccarati A, Zanello A, Scarpato R, Bramanti L, Mariani M. Assessment of sperm DNA integrity in workers exposed to styrene. Hum Reprod 2002; 17: 2912-8.
157. Hsu PC, Chen IY, Pan CH, et al. Sperm DNA damage correlates with polycyclic aromatic hydrocarbons biomarker in coke-oven workers. Int Arch Occup Environ Health 2006; 79: 349-56.
158. Rubes J, Selevan SG, Evenson DP, et al. Episodic air pollution is associated with increased DNA fragmentation in human sperm without other changes in semen quality. Hum Reprod 2005; 20: 2776-83.
159. Selevan SG, Borkovec L, Slott VL, et al. Semen quality and reproductive health of young Czech men exposed to seasonal air pollution. Environ Health Perspect 2000; 108: 887-94.
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