Effect of current tobacco consumption on the male reproductive hormone profile
Introduction
Despite numerous campaigns to reduce the consumption of tobacco, smoking is still highly prevalent in Mexico. According to the 2011 National Addiction Survey, in Mexico 31.4% of men between ages 12 and 65 are active smokers, and 30.9% are former smokers (ENA, 2011). The number of deaths ascribable to smoking is 25,383, of which 16,418 correspond to the male sex (Valdés-Salgado et al., 2005).
Previous studies have reported adverse effects of active smoking on the male reproductive function. Authors have found that smoking in men is associated to morphological alterations of spermatozoa (Ozgur et al., 2005), as well as reduction of sperm density and motility (Sofikitis et al., 1995, Zinaman et al., 2000), of semen volume (Pasqualotto et al., 2006), and of fertility (Sépaniak et al., 2006). Although the underlying mechanisms have not been determined, some of these effects could be mediated by the action of tobacco on the male hormone profile (Vogt et al., 1986). Experimental studies have shown that nicotine stimulates the nicotinic acetylcholine receptors in the neurons of the mesolimbic system, thereby increasing dopamine release (Di Chiara, 2000, Watkins et al., 2000). This may affect the release of gonadotropins (FSH and LH) and of prolactin within the anterior hypophysis (Funabashi et al., 2005, Fuxe et al., 1989), as well as alter the feedback mechanism of the hypothalamus-hypophysis-gonads, and may have an impact on testosterone and inhibin B production or secretion in the testes. However, to date, research assessing the association between tobacco smoke exposure and male hormone profile has shown inconsistent results (Kapoor and Jones, 2005, Vine, 1996).
Because many studies assessing the effect of smoking on the male hormone profile have been carried out on men who resort to clinics due to infertility problems, the possibilities of generalizing their results are limited. On the other hand, the fact that most studies do not measure the complete profile—only few of them measure inhibin B, prolactin and estradiol—is equally an obstacle for a comprehensive interpretation of the results.
The present study assesses the effect of active exposure to tobacco smoke on the male hormone profile of 136 healthy men employed in the flower industry in two states (Morelos and Mexico) of the Mexican Republic, who are also exposed to organophosphate (OP) and organochlorine (OC) pesticides, which also act as endocrine disruptors in humans (Blanco-Muñoz et al., 2010).
Section snippets
Study population
The methodology employed in this study has been published before in full detail (López-Flores et al., 2009). Briefly, during the July–October period, in 2004, a cross-sectional study was carried out in a population of men working in the production of flowers and ornamental plants in the states of Morelos and Mexico. These men performed different activities (from administrative tasks to pesticide application). The workers were identified through employee records from 45 companies, most of which
Results
At the time of the interview, 29 men (21.32%) reported never to have smoked; 40 (29.41%) were former smokers, and 67 (49.26%) were current smokers; 55 of these smoked less than five cigarettes/day, and 12 smoked between 5 and 12 cigarettes/day.
Regarding hormonal profile, most workers had hormonal values within reference range (WHO, 1999), however except for prolactin, there were individuals who were outside this range: 5.1% for FSH, 7.4% for LH, 5.9% for testosterone, 5.1 for inhibin B and 0.7%
Discussion
We found a positive association between current smoking and serum LH, testosterone and prolactin concentrations, regardless of the flower growers’ age, BMI, alcohol consumption and other environmental or occupational exposures (secondhand smoke exposure, p,p′-DDE and DAP concentrations) that might potentially confound the results. These results were significant, although the reported number of cigarettes was relatively low, since only 12 of the 67 current smokers reported smoking equal or more
Acknowledgments
The authors thank the participants of this study. We also thank Susana Bassol, Mariano E. Cebrián, Rosa María García Hernández and Cecilia Hernández for his help in laboratory analysis.
Funding. This study was supported by the Consejo Nacional de Ciencia y Tecnología of Mexico, CONACYT (National Council of Science and Technology), Project Number: SALUD-2002-C01-7574 and by the Fondo Sectorial de Investigación para la Educación SEP-CONACYT, Project Number: 49793. The founding source had no
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Present address of Dr. Marina Lacasaña and Dr. Clemente Aguilar-Garduño: Escuela Andaluza de Salud Pública (EASP) (Andalusian School of Public Health); Campus Universitario de la Cartuja; c/Cuesta del Observatorio 4, CP: 18180 Granada, Spain.
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CIBER Epidemiología y Salud Pública (CIBER of Epidemiology and Public Health), Granada, Spain.