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Review – Andrology

The Link Between Cigarette Smoking and Erectile Dysfunction: A Systematic Review

By: Paolo Verzea , Markus Margreiterb, Katherine Espositoc, Piero Montorsid and John Mulhalle

EU Focus, Volume 1 Issue 1, November 2015, Pages 39-46

Published online: 13 November 2015

Keywords: Smoking, Erectile dysfunction, Cardiovascular risk, Nicotine, Impotence

Abstract Full Text Full Text PDF (347 KB) Patient Summary

Abstract

Context

Cigarette smoking is an established risk factor for erectile dysfunction (ED). To what extent smoking affects erectile function, however, remains debated.

Objective

To integrate the available evidence regarding the impact of smoking status and smoking exposure on prevalence, severity, and progression in patients with ED.

Evidence acquisition

A systematic search of the literature was conducted using the Medline, Embase, and Scopus databases limited to articles published in English between January 1998 and October 2014. We selected 13 articles according to predefined inclusion criteria and the Preferred Reporting Items for Systematic Reviews and Meta-analysis.

Evidence synthesis

Most of the studies demonstrated an association between smoking and ED. Evidence was also found supporting the beneficial effect of smoking cessation on the restoration of erectile function. We noted marked heterogeneity in patient populations and smoking categorizations across studies, precluding conduct of a meta-analysis. Considerable evidence exists to support the hypothesis/theory that smoking-related ED is mainly associated with endothelial impairment, reduction in nitric oxide availability, and imbalance between oxidative and antioxidative reactions increasing oxidative stress. Passive secondhand cigarette smoking, especially with a long-term exposure, can also have a negative impact on erectile function.

Conclusions

Smoking is strongly associated with ED. Endothelial dysfunction together with increased oxidative stress represent major pathophysiologic mechanisms, and smoking cessation may mitigate this effect.

Patient summary

Current smoking is significantly associated with erectile dysfunction, and smoking cessation has a beneficial effect on the restoration of erectile function.

Take Home Message

We reviewed and summarized the scientific evidence supporting the link between smoking and erectile dysfunction. We found that strong correlations between these two conditions exist. Passive secondhand smoking can cause erectile impairment, and smoking cessation has a beneficial effect for the restoration of erectile function.

Keywords: Smoking, Erectile dysfunction, Cardiovascular risk, Nicotine, Impotence.

1. Introduction

Erectile dysfunction (ED) is defined as the recurrent or consistent inability to obtain and/or maintain a penile erection sufficient for satisfactory sexual performance [1]. The incidence of ED increases with age, reaching 20–40% in men aged 60–69 yr and 50–100% in men in their 70s and 80s, depending on the heterogeneity of ED definition in different studies [2]. Smoking, one of the world's greatest public health problems, is also postulated to be related to an increased risk of ED in some epidemiological studies. Although a clear causal relationship exists between cigarette smoking and ED, the influence of smoking on ED severity, progression, and treatment success and the influence of smoking cessation on the restoration of normal erectile function is less clear [3].

The aim of this review was to critically analyze the relationship between ED and smoking by addressing the epidemiological and pathophysiologic aspects on which this link is founded. We focused on the clinically relevant aspects of this association, trying to clarify whether a dose–response relationship exists and to what extent smoking cessation affects normalization of erectile function.

2. Evidence acquisition

A systematic literature review was performed in October 2014 using Medline, Embase, and Scopus databases. The search strategy included the terms smok*, tobacco, cig*, erectile dysfunction, ED, erectile function, impotence, occurrence, progression, and response. We limited our search to prospective trials and major preclinical and retrospective studies published in English between January 1998 and October 2014. Meeting abstracts, editorials, and commentaries were excluded. In addition, cited references from selected articles and from review articles retrieved in our search were used to identify manuscripts that were not included in the previous search. The articles that provided the highest level of evidence were selected with the consensus of all the authors. We identified 4214 articles from electronic databases after the exclusion of duplicates. Of these, most were excluded after the first screening based on titles and abstracts because they were not relevant or did not fulfill the inclusion criteria. After evaluating the full texts of 110 remaining articles that seemed to be relevant for this review, we finally included 13 studies (Fig. 1).

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Fig. 1

Flowchart of study selection.

2.1. Data extraction

Data from all selected studies were extracted and tabulated by one author (M.M.) and corroborated by a second author (P.V.). The p values were recorded for relationship of smoking with end points, and statistical significance was defined as p < 0.05. If p values were not available, 95% confidence intervals (CIs) were recorded. Wherever available, hazard ratios or odds ratios (ORs) were also recorded. In cases in which multiple statistical tests were used to assess an association, results of the most rigorous test were reported (eg, a multivariable analysis adjusting for standard clinical and pathologic characteristics was preferred over a univariable analysis).

2.2. Quality of the selected studies

We assessed the methodological quality of all included studies. Each individual study was given a summary rating of good (low risk of bias), fair, or poor (high risk of bias). The rating was based on the following components: methods for selecting the participants/groups of the study, methods used for randomization, comparability, and assessment of the outcome or exposure. The rating for each study therefore addressed both study design and intervention characteristics. All included studies were rated as good or fair.

2.3. Smoking strata and clinical end point definitions

For a reported association of smoking with an outcome, we recognized two possible general stratifications of the participants: smoking status and smoking exposure. The following categories of smoking status were reported in included studies: nonsmokers or never smokers (a negligible number of lifetime cigarettes smoked), smokers (a non-negligible number of lifetime cigarettes smoked), former smokers (stopped smoking prior to diagnosis), and current smokers (smoked at the time of diagnosis). In studies including a quitter category, former smokers stopped smoking ≥1 yr before diagnosis, and quitters stopped smoking between 1 yr before and 3 mo after diagnosis.

3. Evidence synthesis

3.1. Association between erectile dysfunction and smoking

3.1.1. Epidemiological evidence

The Massachusetts Male Aging Study that evaluated ED in men aged 40–70 yr with a self-administered questionnaire first reported that cigarette smoking at baseline almost doubled the likelihood of moderate or complete ED at up to 10 yr of follow-up. Former smokers, compared with never smokers, were not at increased risk of ED [4], but there was no information on dose response based on the number of cigarettes smoked. An earlier study of Vietnam-era veterans, aged 31–49 yr, found that a higher percentage of smokers than nonsmokers reported ED problems. However, neither number of years of smoking nor number of cigarettes smoked per day were significant predictors of ED in current smokers in this study [5].

In 2005 Gades et al investigated a population-based cohort extrapolated from the Olmsted County Study of Urinary Symptoms and Health Status Among Men showing an association between smoking and ED. Although these cross-sectional data did not prove cause and effect, a dose–response relationship was reported. The association may be of greater magnitude in the younger age group in whom other traditional causes of ED are not as prevalent compared with the older age group [3].

Another observational cross-sectional study conducted in Italy showed that current smokers of ≥10 cigarettes per day (OR: 1.4; 95% CI, 1.2–1.5; p < 0.0001) and former smokers (OR: 1.3; 95% CI, 1.2–1.5; p < 0.0001) presented a higher risk of developing ED when compared with nonsmokers [6] and [7].

Millett et al examined factors associated with ED in a large representative sample of 8367 Australian men aged 16–59 yr. Compared with nonsmokers, the adjusted ORs for ED in this cohort were 1.24 (95% CI, 1.01–1.52; p = 0.04) for those smoking <20 cigarettes per day and 1.39 (95% CI, 1.05–1.83; p = 0.02) for those smoking >20 cigarettes per day, after adjusting for other confounding factors [8].

He et al examined the association between cigarette smoking and risk of ED among 7684 Chinese men aged 35–74 yr without clinical vascular disease. The OR of ED was 1.41 (95% CI, 1.09–1.81) for cigarette smokers compared with never smokers [9].

Chew et al explored the relationship between cigarette smoking, ED, and cardiovascular disease (CVD) using data from a population-based cross-sectional study of 1580 participants. Compared with never smokers, the odds of ED, adjusted for age, age squared, and CVD, were significantly higher among current smokers (OR2 = 1.40; 95% CI, 1.02–1.92) and ever smokers (OR: 1.57; 95% CI, 1.02–2.42). Similarly, the adjusted odds of severe ED were significantly higher among former smokers. Compared with never smokers without CVD, the age-adjusted odds of ED among former smokers and ever smokers without CVD were about 1.6. Interestingly, this study shows that the relationship between smoking and ED is independent of that between smoking and CVD [10].

More recently, Wu et al reported data of a population-based study among noninstitutionalized Chinese men aged 17–88 yr (Fangchenggang Area Male Health Examination Survey) where ED was assessed by using the international Index of Erectile Function erectile function domain score. After adjusting for age, alcohol drinking, physical activity, hypertension, diabetes, dyslipidemia, and obesity, smokers who smoked >20 cigarettes per day had a significantly increased risk of ED than never smokers (OR2: 1.23; 95% CI, 1.03–1.49; p = 0.02). After further adjustment for education, the risk of ED was still significantly higher in men smoking >23 yr than never smokers (OR: 1.60; 95% CI, 1.22–2.09; p = 0.001) [11].

Table 1 provides a detailed overview of the characteristics, outcomes, and covariates of studies assessing the risk of smoking for ED.

Table 1

Characteristics, outcomes, and covariates of studies assessing the risk of smoking for erectile dysfunction

StudySample size, nAge range, yrClassification standard of smokingCategoryOR (95% CI)Adjustment for covariates
Gades et al, 2005 [3]132940–79Cigarettes per day, no.01Age and the occurrence of hypertension, diabetes, or coronary heart disease
<201.63 (0.72–3.67)
≥201.64 (0.82–3.27)
Austoni et al, 2005 [6]16 724NACigarettes per day, no.01Age, marital status, education, body mass index, alcohol drinking, physical activity, diabetes, cardiovascular disease, hypercholesterolemia
1–101.00 (0.90–1.20)
≥101.40 (1.20–1.50)
Duration of smoking, yr01
<101.2 (0.80–1.60)
10–201.6 (1.20–2.00)
>201.6 (1.30–2.00)
Mirone et al, 2002 [7]2010>19Cigarettes per day, no.01Age and education
≤101.60 (1.00–2.40
>101.60 (1.10–2.50)
Duration of smoking, yr01
≤201.20 (0.80–1.90)
>201.60 (1.10–2.40)
Millett et al, 2006 [8]836716–59Cigarettes per day, no.01Age, education, presence of cardiovascular disease and diabetes, current alcohol consumption, and employment
≤201.24 (1.01–1.52)
>201.39 (1.05–1.83)
He et al, 2007 [9]476335–74Cigarettes per day, no.01Age, education, alcohol consumption, physical inactivity, diabetes, hypertension, overweight, and hypercholesterolemia
1–101.27 (0.91–1.77)
11–201.45 (1.08–1.95)
>201.65 (1.08–2.50)
Chew et al, 2009 [10]1580>21Cigarettes per day, no.01Age, square of age, and cardiovascular disease
1–101.30 (0.69–2.44)
11–201.69 (0.79–3.64)
>201.57 (0.74–3.34)
Wu et al, 2012 [11]268620–79Cigarettes per day, no.01Age, alcohol drinking, physical activity, hypertension, diabetes, dyslipidemia, obesity, and education
<201.16 (0.95–1.43)
≥201.18 (0.98–1.43)
Duration of smoking, yr<111.18 (0.89–1.56)
11–170.95 (0.74–1.21)
17–231.07 (0.84–1.36)
≥231.60 (1.22–2.09)
Bortolotti et al, 2001 [22]967020–70Cigarettes per day, no.<151Age, education, type of diabetes, and metabolic control
15–241.20 (1.10–1.40)
≥251.40 (1.30–1.70)
Duration of smoking, yr<101
10–201.40 (1.10–1.90)
>201.70 (1.30–2.30)

CI = confidence interval; NA = not available; OR = odds ratio.

3.1.2. Pathophysiologic evidence

Considerable evidence supports the concept that smoking-related ED is mainly associated with endothelial impairment and reduction in nitric oxide (NO) availability. Smoking provokes different detrimental effects on the endothelial cells, based on architectural and functional changes that include decreased endothelial nitric oxide synthase (eNOS) activity, impaired endothelium-dependent vasorelaxation, increased expression of cell adhesion molecules and transendothelial migration of monocyte-like cells, reduced response to vascular endothelial growth factor, and impaired regulation of important thrombotic factors [12] and [13]. Furthermore, a connection between cigarette smoking and the oxidative damage to endothelial cells caused by superoxide and other reactive oxygen species (ROS) is well established. The dynamic balance between oxidative and antioxidative reactions is heavily impaired by smoking, and the final result is a net increase of oxidative stress that contributes to the loss of cavernosal integrity [14]. Numerous preclinical studies showed the role of specific compounds of cigarette smoke in increasing superoxide generation by both endothelial and smooth muscle cells, impairing acetylcholine-induced relaxation of arteries, increasing messenger RNA expression of proinflammatory cytokines such as interleukin (IL)-1β, IL-6, and tumor necrosis factor-α. All these detrimental effects are prevented by inhibiting nicotinamide adenine dinucleotide phosphate oxidase or by using antioxidant agents [15].

To date, less robust evidence exists regarding the effects of smoking on neuronal nitric oxide synthase–mediated penile erection and on inducible nitric oxide (iNOS) activity and expression [13].

From a clinical standpoint, numerous studies have shown that smoking exposure leads to impaired arterial flow to the penis or acute vasospasm of the penile arteries. For instance, the relative risk of developing atherosclerosis in the penis and subsequent ED is 1.31 for each 10 pack-years smoked [16], and 86% of smokers have an abnormal penile vascular evaluation [17]. Furthermore, penile rigidity during nocturnal erection inversely correlates with the number of cigarettes smoked per day [18].

Pathophysiologic biochemical and clinical mechanisms involved in the causal relationship between smoking and erectile dysfunction are outlined in Figure 2.

gr2

Fig. 2

Pathophysiologic biochemical and clinical mechanisms involved in the causal relationship between smoking and erectile dysfunction.

eNOS = endothelial nitric oxide synthase; IL = interleukin; iNOS = inducible nitric oxide synthase; mRNA = messenger RNA; nNOS = neuronal nitric oxide synthase; TNF = tumor necrosis factor.

3.2. Erectile dysfunction and smoking: dose–response relationship

3.2.1. Smoking quantity

In the most recent dose–response meta-analysis, Cao et al evaluated the association of quantity and duration of smoking with ED [19]. One cohort study and nine cross-sectional studies were included in the meta-analysis (50 360 participants and 12 218 cases with ED). The authors found the risk for an increment of 10 cigarettes smoked per day and 10 yr of smoking was increased by 14% and 15%, respectively. The summary OR of ED for an increase of 10 cigarettes smoked per day was 1.14 (95% CI, 1.09–1.18), with moderate heterogeneity (p = 0.061; I2 = 44.7%). For an increment of 10 yr of smoking, the combined ORs of ED was 1.15 (95% CI, 1.10–1.19), without substantial heterogeneity (p = 0.522; I2 = 0.0%). No evidence of a curve linear association was observed between smoking and risk of ED. However, most of the studies were cross sectional, and the methods used to diagnose ED were different across the included studies. In a study by He et al, there was a statistically significant dose–response relationship between smoking and the risk of ED (p = 0.005). Multivariate-adjusted ORs of ED were 1.27 (95% CI, 0.91–1.77), 1.45 (95% CI, 1.08–1.95), and 1.65 (95% CI, 1.08–2.50) for those who smoked 1–10, 11–20, and >20 cigarettes per day, respectively, compared with never smokers [9].

A Canadian study by Polsky et al found that men with ED were twice as likely to be former smokers (OR: 2.2; 95% CI, 1.2–3.9), and cumulative smoking in pack-years suggests a dose–response pattern with the risk of ED [20].

Parazzini et al performed a cross-sectional study to analyze the prevalence and risk factors for ED in Italy. In comparison with never smokers, the OR of ED was 1.7 (95% CI, 1.2–2.4) for current smokers and 1.6 (95% CI, 1.1–2.3) for former smokers and increased with duration of the habit [21].

Evaluating smoking as a risk factor for ED in 9670 men with diabetes, Bortolotti et al found the ORs of ED in comparison with never smokers was 1.4 (95% CI, 1.3–1.6) for smokers and 1.5 (95% CI, 1.3–1.6) for former smokers. Duration and intensity of the smoking habit was associated with an increased risk of ED. Among former smokers, the risk of ED significantly decreased, with an increase in the number of years since the patient quit smoking [22]. Austoni et al evaluated 16 724 subjects and showed a dose and duration–response effect of smoking on ED. ORs of ED for current smokers were 1.1 (95% CI, 0.7–1.6), 1.7 (95% CI, 1.2–2.3), and 1.6 (95% CI, 1.3–2.0) for <10 yr, 10–20 yr, and >20 yr, respectively, compared with never smokers. Also, former smokers had a duration–response effect of smoking on ED with ORs of 1.0 (95% CI, 0.6–1.7), 1.2 (95% CI, 0.8–1.8), and 2.0 (95% CI, 1.3–2.0) for <10 yr, 10–20 yr, and >20 yr, respectively, compared with never smokers [6].

3.3. The role of passive smoking on erectile dysfunction

Evidence exists that secondhand (passive) smoking increases the risk of heart disease (by approximately 30%) and adversely affects vascular function. Despite the fact that the dose of smoke delivered to active smokers is ≥100 times than that delivered to a passive smoker, the relative risk of CVD for active smokers is 1.78 compared with 1.31 for passive smokers. In many cases, the effects of even brief (minutes to hours) passive smoking are nearly as large as those from chronic active smoking. Passive smoking leads to 68–86% of the risk of light smoking, depending on the level of secondhand smoke exposure [23]. To date very few data regarding the role of passive smoking on ED development are available. A recent report addressing this issue derives from the Boston Area Community Health survey. This study demonstrated that, although the association between passive smoking and ED is not statistically significant, the magnitude of the effect of passive smoking is comparable with 10–19 pack-years of smoking exposure [24]. Previously published data from the Massachusetts Male Aging Study also showed that men exposed to passive smoking double the risk of developing ED over a 9-yr follow-up period [4].

Bivalacqua et al recently determined the effect of passive cigarette smoke on erectile function in vivo, molecular mechanisms involved in penile vascular function, and erectile function and penile molecular signaling in the presence of phosphodiesterase type 5 inhibitor therapy. The results of their study showed that short-term exposure to secondhand smoke impairs erectile function through excessive penile ROS, signaling an iNOS activity. Decreased penile constitutive NOS activity may be attributable to the decreased eNOS activity resulting from increased oxidative stress. Sildenafil therapy restored NOS activity and decreased ROS signaling, resulting in improved erectile function [25].

Overall, these results suggest that, although the increased risk in ED with passive smoking is small, long-term chronic exposure to passive smoking may have adverse effects on erectile function.

3.4. Smoking cessation and erectile function recovery

Only a few studies have investigated the effects of quitting smoking on erectile function. Guay et al were the first to measure nocturnal penile tumescence and rigidity using the RigiScan portable home monitor in 10 male smokers. All patients had smoked for at least 30 pack-years and were smoking ≥1 pack of cigarettes per day. Two nights were monitored: For the first night, the patients had not stopped smoking; for the second night, the patients had stopped smoking for 24 h. In addition, four men were monitored after cessation of smoking and wearing nicotine patches for 1 mo. Rigidity activity units and tumescence activity units were recorded. Results showed significant improvement 24 h after smoking cessation for both of these indices. More interestingly, the results relative to the four men who were assessed 1 mo later while adhering to a daily 21-mg nicotine transdermal patch regimen indicated a trend for continued improvement [26]. Similarly, Sighinolfi et al showed a significant improvement in penile blood flow 24–36 h after smoking discontinuation in a sample of 20 heavy smokers affected with ED [27]. In a prospective comparative study conducted on 118 former smokers and 163 current smokers, Pourmand et al assessed whether stopping smoking can improve ED in smokers. After 1 yr of follow-up, the ED status improved in ≥25% of former smokers but in none of the current smokers; 2.5% of former smokers and 6.8% of current smokers had a deterioration in ED. Former smokers had a significantly better ED status after the follow-up (p = 0.009). Among former smokers, patients with advanced ED and those who were older had less improvement [28].

More recently, the association between smoking cessation and an improvement in men's sexual health was demonstrated in another prospective study. Participants were aged 23–60 yr, smoked at least 15 cigarettes per day for a minimum of 5 consecutive years, had no self-reported sexual dysfunction before smoking onset, and received an 8-wk nicotine transdermal patch treatment. Study results showed that successful quitters, compared with unsuccessful quitters, presented significantly greater penile tumescence at follow-up (4 wk after nicotine patch discontinuation), but there were no differences at midtreatment (while using a high-dose nicotine patch). The overall pattern of results was similar to previous studies showing that smoking cessation leads to significant improvements in penile blood flow, as well as rigidity and tumescence. Interestingly, results suggested for the first time that cessation-induced improvements in sexual health were attributable primarily to nicotine elimination (as evidenced by between-group differences in physiologic outcome measures at follow-up when successful quitters were nicotine and smoke free), rather than tobacco smoke discontinuation alone [29]. As reported in the study from Chew et al, among former smokers, the age-adjusted odds of ED were significantly higher 6–10 yr following cessation of smoking than <5 or >10 yr. These patterns of ED in former smokers suggest that there may be a latent interval between active smoking and symptomatic ED, involving a process initially triggered by smoking [10]. Table 2 presents a detailed overview of the characteristics, outcomes, and covariates of studies assessing the risk of smoking cessation and erectile function recovery.

Table 2

Characteristics, outcomes, and covariates of studies assessing the risk of smoking cessation and erectile function recovery

StudySample size, nAge range, yrFollow-upMeasurementsOutcomes
Guay et al, 1998 [26]1032–6224 h, 1 moNPT and PTSignificant improvement for both indices
Sighinolfi et al, 2007 [27]2031–4824 h, 36 hPD50% PSV and 60% EDV improvement
Pourmand et al, 2004 [28]28130–601 yrIIEF-525% improvement in IIEF-5
Harte et al, 2012 [29]6523–604 wkIIEF and PT75% improvement in IIEF and >30% change in PT

EDV = end-diastolic velocity; IIEF = International Index of Erectile Function; NPT = nocturnal penile tumescence; PD = penile Doppler; PSV = peak systolic velocity; PT = penile tumescence.

4. Conclusions

Smoking negatively affects erectile function, and current knowledge most strongly suggests that smoking increases the risk of ED occurrence showing a dose–response correlation with the number of years of smoking and cigarettes smoked. Considerable evidence supports the concept that smoking-related ED is mainly associated with endothelial impairment, reduction in NO availability, and an imbalance between oxidative and antioxidative reactions increasing oxidative stress. Although several studies have demonstrated that smoking cessation significantly enhances indices of sexual health including long-term male smokers and irrespective of baseline erectile impairment, the current evidence base lacks prospective evaluation of this relationship. Passive secondhand cigarette smoking, especially with long-term exposure, can also have a negative impact on erectile function. Further investigation into the impact of smoking on various demographic and clinical subgroups of ED patients (eg, by age or comorbidities) is needed.


Author contributions: Paolo Verze had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.

Study concept and design: Verze, Margreiter, Esposito, Montorsi, Mulhall.

Acquisition of data: Verze, Margreiter.

Analysis and interpretation of data: Verze, Margreiter.

Drafting of the manuscript: Verze, Margreiter.

Critical revision of the manuscript for important intellectual content: Mulhall.

Statistical analysis: Mulhall.

Obtaining funding: None.

Administrative, technical, or material support: None.

Supervision: Verze, Margreiter, Esposito, Montorsi, Mulhall.

Other (specify): None.

Financial disclosures: Paolo Verze certifies that all conflicts of interest, including specific financial interests and relationships and affiliations relevant to the subject matter or materials discussed in the manuscript (eg, employment/affiliation, grants or funding, consultancies, honoraria, stock ownership or options, expert testimony, royalties, or patents filed, received, or pending), are the following: None.

Funding/Support and role of the sponsor: None.

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Footnotes

a Department of Urology, University Federico II of Naples, Naples, Italy

b Department of Urology, Medical University Vienna, General Hospital, Vienna, Austria

c Department of Geriatrics and Metabolic Diseases, Second University of Naples, Naples, Italy

d Department of Clinical Sciences and Community Health, University of Milan, Centro Cardiologico Monzino, IRCCS, Milan, Italy

e Division of Urology, Sexual and Reproductive Medicine Program, Memorial Sloan-Kettering Cancer Center, New York, NY, USA

Corresponding author. Department of Urology, University Federico II of Naples, Naples, Italy. Tel. +39 081 746 2520; Fax: +39 081 7464311.

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