Prospective study of effect of switching from cigarettes to pipes or cigars on mortality from three smoking related diseases.

OBJECTIVE: To estimate the extent to which cigarette smokers who switch to cigars or pipes alter their risk of dying of three-smoking related diseases-lung cancer, ischaemic heart disease, and chronic obstructive lung disease. DESIGN: A prospective study of 21520 men aged 35-64 years when recruited in 1975-82 with detailed history of smoking and measurement of carboxyhaemoglobin. MAIN OUTCOME MEASURES: Notification of deaths (to 1993) classified by cause. RESULTS: Pipe and cigar smokers who had switched from cigarettes over 20 years before entry to the study smoked less tobacco than cigarette smokers (8.1 g/day v 20 g/day), but they had the same consumption as pipe and cigar smokers who had never smoked cigarettes (8.1 g) and had higher carboxyhaemoglobin saturations (1.2% v 1.0%, P < 0.001), indicating that they inhaled tobacco smoke to a greater extent. They had a 51% higher risk of dying of the three smoking related diseases than pipe or cigar smokers who had never smoked cigarettes (relative risk 1.51; 95% confidence interval 0.96 to 2.38), a 68% higher risk than lifelong non-smokers (1.68; 1.16 to 2.45), a 57% higher risk than former cigarette smokers who gave up smoking over 20 years before entry (1.57; 1.04 to 2.38), and a 46% lower risk than continuing cigarette smokers (0.54; 0.38 to 0.77). CONCLUSION: Cigarette smokers who have difficulty in giving up smoking altogether are better off changing to cigars or pipes than continuing to smoke cigarettes. Much of the effect is due to the reduction in the quantity of tobacco smoked, and some is due to inhaling less. Men who switch do not, however, achieve the lower risk of pipe and cigar smokers who have never smoked cigarettes. All pipe and cigar smokers have a greater risk of lung cancer than lifelong non-smokers or former smokers.     

Environmental tobacco smoke and tobacco related mortality in a prospective study of Californians, 1960-98

Objective To measure the relation between environmental tobacco smoke, as estimated by smoking in spouses, and long term mortality from tobacco related disease.Design Prospective cohort study covering 39 years.Setting Adult population of California, United States.Participants 118 094 adults enrolled in late 1959 in the American Cancer Society cancer prevention study (CPS I), who were followed until 1998. Particular focus is on the 35 561 never smokers who had a spouse in the study with known smoking habits.Main outcome measures Relative risks and 95% confidence intervals for deaths from coronary heart disease, lung cancer, and chronic obstructive pulmonary disease related to smoking in spouses and active cigarette smoking.Results For participants followed from 1960 until 1998 the age adjusted relative risk (95% confidence interval) for never smokers married to ever smokers compared with never smokers married to never smokers was 0.94 (0.85 to 1.05) for coronary heart disease, 0.75 (0.42 to 1.35) for lung cancer, and 1.27 (0.78 to 2.08) for chronic obstructive pulmonary disease among 9619 men, and 1.01 (0.94 to 1.08), 0.99 (0.72 to 1.37), and 1.13 (0.80 to 1.58), respectively, among 25 942 women. No significant associations were found for current or former exposure to environmental tobacco smoke before or after adjusting for seven confounders and before or after excluding participants with pre-existing disease. No significant associations were found during the shorter follow up periods of 1960-5, 1966-72, 1973-85, and 1973-98.Conclusions The results do not support a causal relation between environmental tobacco smoke and tobacco related mortality, although they do not rule out a small effect. The association between exposure to environmental tobacco smoke and coronary heart disease and lung cancer may be considerably weaker than generally believed.     

The effect of cigarette smoke on adherence of respiratory pathogens to buccal epithelial cells

Smoking is associated with an increased risk of respiratory tract infection in adults. In children, exposure to cigarette smoke is a risk factor for respiratory tract infection and bacterial meningitis: Active smoking and passive exposure to cigarette smoke is also associated with carriage of some potentially pathogenic species of bacteria in both adults and children. The aims of the study were to determine the effect of active smoking on: (1) bacterial binding to epithelial cells; (2) expression of host cell antigens that act as receptors for some species; and (3) the effects of passive exposure to water-soluble components of cigarette smoke on bacterial binding. Flow cytometry was used to assess binding to buccal epithelial cells of the following species labelled with fluorescein isothiocyanate: Neisseria meningitidis, Neisseria lactamica, Streptococcus pneumoniae, Bordetella pertussis, Haemophilus influenzae, Moraxella catarrhalis, Staphylococcus aureus. Flow cytometry was also used to assess expression of host cell antigens which have been identified as bacterial receptors. For each species, binding to cells of smokers was significantly higher than to cells of non-smokers; however, expression of host cell antigens was similar on epithelial cells of both groups. Non-dilute cigarette smoke extract reduced binding of bacteria to epithelial cells, but dilutions between 1 in 10 and 1 in 320 enhanced binding. We conclude that smokers might be more densely colonised by a variety of potentially pathogenic bacteria. The enhanced bacterial binding to epithelial cells of smokers is not related to enhanced expression of host cell antigens that can act as receptors for some species, but possibly to components in the smoke that alter charge or other properties of the epithelial cell surface. Passive coating of mucosal surfaces with components of cigarette smoke might enhance binding of potentially pathogenic bacteria.     

Passive cigarette smoking increases isoprostane formation

Passive smoking has been demonstrated to exert a variety of deleterious effects eventually resulting in vascular damage. Isoprostanes, a reliable marker of in vivo oxidation injury, have been shown to increase in active cigarette smoking. Data for passive smoking are lacking. We were examining the isoprostane 8-epi-PGF2alpha in 12 smokers and non-smokers exposed daily to passive cigarette smoke for 12 days. Plasma samples stored at liquid nitrogen from people having been examined earlier were used. Prevalues of 8-epi-PGF2alpha are higher in cigarette smokers. Exposure to passive smoking causes a significant increase in 8-epi-PGF2alpha in non-smokers, while in smokers there is only a trendwise increase. After repeated passive smoke exposure, 8-epi-PGF2alpha in non-smokers approaches the respective values of smokers. There is a significant correlation of 8-epi-PGF2alpha to the thromboxane (plasma, serum, conversion from exogenous precursor, 11-dehydro-TXB2) parameters (MDA, HHT- conversion) examined in these patients before. The findings document a significant temporary increase in in vivo oxidation injury due to passive smoke favouring development and/or progression of vascular disease.     

Estimation of urinary cotinine cut-off points distinguishing non-smokers, passive and active smokers

An objective assessment of exposure to tobacco smoke may be accomplished by means of examining particular biomarkers in body fluids. The most common biomarker of tobacco smoke exposure is urinary, or serum, cotinine. In order to distinguish non-smokers from passive smokers and passive smokers from active smokers, it is necessary to estimate cotinine cut-off points. The objective of this article was to apply statistical distribution of urinary cotinine concentration to estimate cut-off points distinguishing the three above-mentioned groups. The examined group consisted of 327 volunteers (187 women and 140 men) who were ethnically homogenous inhabitants of the same urban agglomeration (Sosnowiec, Poland). The values which enabled differentiation of the examined population into groups and subgroups were as follows: 50 µg l^-1 (differentiation of non-smokers from passive smokers), 170 µg l^-1 (to divide the group of passive smokers into two subgroups: minimally and highly exposed to environmental tobacco smoke), 550 µg l^-1 (differentiation of passive smokers from active smokers), and 2100 µg l^-1 (to divide group of active smokers into two subgroups: minimally and highly exposed to tobacco smoke). The results suggest that statistical distribution of urinary cotinine concentration is useful for estimating urinary cotinine cut-off points and for assessing the smoking status of persons exposed to tobacco smoke.     

Demographic characteristics of cigarette smokers in the United States.

This research uses a multivariate log-linear examination of a national data set to analyze the combined influences of ethnicity, age, and sex on cigarette smoking status, not only for smokers but for former smokers and current nonsmokers as well. In general, we find that demographic differences in smoking vary across several dimensions. For instance, compared to females, males are more likely to smoke and to smoke heavily. The differences between male and female cessation rates vary with ethnicity; also, males and females tend to have different ratios of former smokers to light, moderate, and heavy smokers. Mexican-Americans who smoke generally smoke small quantities of cigarettes. And Blacks are as likely as other groups not to smoke at all, and less likely than Anglos to smoke heavily. This article discusses potential future mortality effects, intervention strategies, and directions for future research.     

The Support for Smoke Free Policy and How It Is Influenced by Tolerance to Smoking – Experience of a Developing Country

This cross sectional survey was conducted to determine the support in making Penang UNESCO World Heritage Site (GTWHS) smoke free and to determine the influence of tolerance towards smoking on this support. This is the first phase in making Penang, Malaysia a smoke free state. A multistage sampling process was done to select a sample of respondents to represent the population of GTWHS. Attitude towards smoking was assessed using tolerance as a proxy. A total of 3,268 members of the community participated in the survey. A big majority (n = 2969; 90.9%) of the respondents supported the initiative. Support was lowest among the owners and residents/tenants, higher age groups, the Chinese, men, respondents who had poor knowledge of the places gazetted as smoke free, and respondents with poor knowledge of the health effects on smokers and on passive smokers. The odds (both adjusted and unadjusted) of not supporting the initiative was high among those tolerant to smoking in public areas. Tolerance towards smoking was associated with 80.3% risk of non-support in the respondents who were tolerant to smoking and a 57.2% risk in the population. Health promotion and education concerning the harm of tobacco smoke in Malaysia, which has mainly targeted smokers, must change. Health education concerning the risks of second hand smoke must also be given to non-smokers and efforts should be made to denormalize smoking.     

Disordered microbial communities in the upper respiratory tract of cigarette smokers

Cigarette smokers have an increased risk of infectious diseases involving the respiratory tract. Some effects of smoking on specific respiratory tract bacteria have been described, but the consequences for global airway microbial community composition have not been determined. Here, we used culture-independent high-density sequencing to analyze the microbiota from the right and left nasopharynx and oropharynx of 29 smoking and 33 nonsmoking healthy asymptomatic adults to assess microbial composition and effects of cigarette smoking. Bacterial communities were profiled using 454 pyrosequencing of 16S sequence tags (803,391 total reads), aligned to 16S rRNA databases, and communities compared using the UniFrac distance metric. A Random Forest machine-learning algorithm was used to predict smoking status and identify taxa that best distinguished between smokers and nonsmokers. Community composition was primarily determined by airway site, with individuals exhibiting minimal side-of-body or temporal variation. Within airway habitats, microbiota from smokers were significantly more diverse than nonsmokers and clustered separately. The distributions of several genera were systematically altered by smoking in both the oro- and nasopharynx, and there was an enrichment of anaerobic lineages associated with periodontal disease in the oropharynx. These results indicate that distinct regions of the human upper respiratory tract contain characteristic microbial communities that exhibit disordered patterns in cigarette smokers, both in individual components and global structure, which may contribute to the prevalence of respiratory tract complications in this population.     

Estimation of urinary cotinine cut-off points distinguishing non-smokers,passive and active smokers

Abstract

An objective assessment of exposure to tobacco smoke may be accomplished by means of examining particular biomarkers in body fluids. The most common biomarker of tobacco smoke exposure is urinary, or serum, cotinine. In order to distinguish non-smokers from passive smokers and passive smokers from active smokers, it is necessary to estimate cotinine cut-off points. The objective of this article was to apply statistical distribution of urinary cotinine concentration to estimate cut-off points distinguishing the three above-mentioned groups. The examined group consisted of 327 volunteers (187 women and 140 men) who were ethnically homogenous inhabitants of the same urban agglomeration (Sosnowiec, Poland). The values which enabled differentiation of the examined population into groups and subgroups were as follows: 50 µg l^?1 (differentiation of non-smokers from passive smokers), 170 µg l^?1 (to divide the group of passive smokers into two subgroups: minimally and highly exposed to environmental tobacco smoke), 550 µg l^?1 (differentiation of passive smokers from active smokers), and 2100 µg l^?1 (to divide group of active smokers into two subgroups: minimally and highly exposed to tobacco smoke). The results suggest that statistical distribution of urinary cotinine concentration is useful for estimating urinary cotinine cut-off points and for assessing the smoking status of persons exposed to tobacco smoke.     

Metabolic effects of cigarette smoking.

The inverse relationship between cigarette smoking and body weight, a potent obstacle to stopping smoking, may be due in part to effects of smoking on increasing whole body metabolism. Studies examining chronic and acute metabolic effects of smoking, as well as its constituent nicotine, are reviewed. Evidence suggests the absence of a chronic effect; most studies indicate that smokers and nonsmokers have similar resting metabolic rates (RMR) and that RMR declines very little after smoking cessation. Although an acute effect due to smoking is apparent, its magnitude is inconsistent across studies, possibly because of variability in smoke exposure or nicotine intake. In smokers at rest, the acute effect of smoking (and nicotine intake) appears to be significant but small (less than 10% of RMR) and transient (less than or equal to 30 min). However, the specific situations in which smokers tend to smoke may mediate the magnitude of this effect, inasmuch as smoking during casual physical activity may enhance it while smoking after eating may reduce it. Sympathoadrenal activation by nicotine appears to be primarily responsible for the metabolic effect of smoking, but possible contributions from nonnicotine constituents of tobacco smoke and behavioral effects of inhaling may also be important. Improved understanding of these metabolic effects may lead to better prediction and control of weight gain after smoking cessation, thus increasing the likelihood of maintaining abstinence.     

Smoking and leanness: evidence for change in Finland.

Many studies have shown smokers to weigh less than non-smokers, which is plausible given the metabolic effects of cigarette smoke. The interrelation between smoking and relative body weight and its change over time were analysed by using data from Finnish population based surveys from 1982 and 1987. Among both men and women the inverse association between smoking and body mass index was clearly weakened between 1982 and 1987. In 1987 among men aged 25-44 smoking was positively related to body mass index. Moreover, the relation between smoking and waist to hip girth ratio was positive in both sexes at all ages. Years of smoking was nevertheless confirmed as a significant inverse predictor of relative weight. A cluster of unfavourable health habits, including high consumption of alcohol and saturated fats, especially emerged among younger smokers. This may have been due to different selection of smokers in Finland, where smoking increasingly seems to be a form of deviant or risk taking behaviour. It is concluded that at a population level the metabolic effects of smoking seem to be increasingly overridden by several other unfavourable health behaviours of smokers.     

Harmful health effects of cigarette smoking

This is a comprehensive review on the harmful health effects of cigarette smoking. Tobacco smoking is a reprehensible habit that has spread all over the world as an epidemic. It reduces the life expectancy among smokers. It increases overall medical costs and contributes to the loss of productivity during the life span. Smoking has been shown to be linked with various neurological, cardiovascular, and pulmonary diseases. Cigarette smoke not only affects the smokers but also contributes to the health problems of the non-smokers. Exposure to environmental tobacco smoke contributes to health problems in children and is a significant risk factor for asthma. Cigarette smoke contains several carcinogens that alter biochemical defense systems leading to lung cancer.     

Genotoxicity of environmental tobacco smoke: a review

Environmental tobacco smoke (ETS), or second-hand smoke, is a widespread contaminant of indoor air in environments where smoking is not prohibited. It is a significant source of exposure to a large number of substances known to be hazardous to human health. Numerous expert panels have concluded that there is sufficient evidence to classify involuntary smoking (or passive smoking) as carcinogenic to humans. According to the recent evaluation by the International Agency for Research on Cancer, involuntary smoking causes lung cancer in never-smokers with an excess risk in the order of 20% for women and 30% for men. The present paper reviews studies on genotoxicity and related endpoints carried out on ETS since the mid-1980s. The evidence from in vitro studies demonstrates induction of DNA strand breaks, formation of DNA adducts, mutagenicity in bacterial assays and cytogenetic effects. In vivo experiments in rodents have shown that exposure to tobacco smoke, whole-body exposure to mainstream smoke (MS), sidestream smoke (SS), or their mixture, causes DNA single strand breaks, aromatic adducts and oxidative damage to DNA, chromosome aberrations and micronuclei. Genotoxicity of transplacental exposure to ETS has also been reported. Review of human biomarker studies conducted among non-smokers with involuntary exposure to tobacco smoke indicates presence of DNA adducts, urinary metabolites of carcinogens, urinary mutagenicity, SCEs and hypoxanthine-guanine phosphoribosyltransferase (HPRT) gene mutations (in newborns exposed through involuntary smoking of the mother). Studies on human lung cancer from smokers and never-smokers involuntarily exposed to tobacco smoke suggest occurrence of similar kinds of genetic alterations in both groups. In conclusion, these overwhelming data are compatible with the current knowledge on the mechanisms of carcinogenesis of tobacco-related cancers, occurring not only in smokers but with a high biological plausibility also in involuntary smokers.     

A Rat Model of Cigarette Smoke Abuse Liability

We sought to develop a rat model of cigarette smoke exposure (CSE) that created cotinine serum levels comparable to those of smokers and induced conditioned place preference (CPP) suggestive of cigarette smoke abuse liability. Rats were exposed to sidestream cigarette smoke delivered semicontinuously for 2 periods of 20 (group S20), 40 (group S40), or 60 (group S60) min daily for 12 wk. Serum cotinine concentration in blood samples was determined at 1 and 20 h after CSE. A biased (black versus white chamber) CPP paradigm was used. In the high CSE group (group S60), serum cotinine at 1 h (250 to 300 ng/mL) was comparable to average cotinine levels reported for addicted smokers (around 300 ng/mL). Cotinine levels at 20 h after CSE were higher than the smoker–nonsmoker cut-off value (greater than 14 ng/mL) in all smoking groups, with the S60 group having the highest levels. All rats preferred the black chamber to the white chamber during the preexposure CPP test. The time spent in the white chamber was increased compared with 0-wk values in group S40 at 8 wk, group S60 at 4 and 8 wk, and the control group at 4 and 8 wk but not at 12 wk; however, the shift in CPP was significantly higher at 8 wk in group S60 compared with other groups. In conclusion, interrupted 2-h daily CSE for 8 wk induced serum cotinine levels in rats comparable to those of smokers and induced CPP suggestive of cigarette smoke abuse liability.Abbreviations: CPP, conditioned place preference; CSE, cigarette smoke exposureThe devastating consequences of smoking on health have been studied extensively in numerous clinical and animal studies over time. This chronic habit leads to dependence on tobacco smoke, with nicotine, a main active ingredient of tobacco products, being recognized as the basic addictive substance.³²The known health benefits of smoking cessation motivate smokers to quit tobacco use. However, unaided efforts usually are unsuccessful, resulting in smoking relapse. The fight against nicotine addiction may be undermined by potential weight gain after smoking cessation, potentially discouraging those attempting to quit smoking and contributing to relapse. During the past few years, research has been focused on 2 main areas of interest toward this direction: understanding the underlying biologic mechanisms related to nicotine addiction to effectively design therapeutic strategies to support those who wish to quit smoking and investigating the hormonal and molecular mechanisms responsible for weight gain after smoking cessation.So far, animal models used to study the consequences of smoking cessation involved the administration of nicotine as a sole agent until addiction was achieved.²³ However, nicotine-administration models do not completely represent the toxic and addictive effects of cigarette smoke, given that smoke contains more than 4000 chemicals whose actions or coactions have not been thoroughly evaluated yet.¹ Cigarette smoke exposure (CSE) animal models have been used in studies investigating the metabolic changes conferred by smoking^10-12 but not in those after its cessation. In toxicity studies, animals are exposed to tobacco smoke for various periods, which depend on the side effect under investigation.^18,25,27 Smoke exposure timetables usually do not involve weekends for practical reasons, and addiction of animals to tobacco smoke is not assessed in current models.In our opinion, an ideal animal model of cigarette smoke abuse liability suitable for the study of smoking cessation resembles the clinical situation in terms of chronic daily inhalation of cigarette smoke sufficient to attain blood nicotine levels comparable to those of smokers and in cessation of the CSE period after achieving tobacco smoke abuse liability. In the present project, we sought to establish such a model in rats by defining the daily timetable of CSE to induce serum levels of cotinine, nicotine''s major proximate metabolite, comparable to those of smokers and by determining the minimum total CSE period required to induce abuse liability to cigarette smoke. We assessed the CSE period by using a biased conditioned place preference (CPP) paradigm.⁸     

Smokers’ Decision Making: More than Mere Risk Taking

The fact that smoking is bad for people’s health has become common knowledge, yet a substantial amount of people still smoke. Previous studies that sought to better understand this phenomenon have found that smoking is associated with the tendency to take risk in other areas of life as well. The current paper explores factors that may underlie this tendency. An experimental analysis shows that smokers are more easily tempted by immediate high rewards compared to nonsmokers. Thus the salience of risky alternatives that produce large rewards most of the time can direct smokers to make bad choices even in an abstract situation such as the Iowa Gambling Task. These findings suggest that the risk taking behavior associated with smoking is not related to the mere pursuit of rewards but rather reflects a tendency to yield to immediate temptation.     

Reducing harm from tobacco smoke exposure during pregnancy

In addition to the health risks that maternal tobacco smoke exposure in pregnancy poses to women, this is a cause of substantial fetal morbidity and mortality. In pregnancy, maternal tobacco smoke exposure can arise because women either smoke or are passively exposed to environmental tobacco smoke as a consequence of other's smoking. This article discusses the scope for clinicians to help reduce both types of tobacco smoke exposure in pregnancy, with a specific focus on available and effective interventions for smoking cessation by pregnant women. Behavioral support with smoking cessation is the only intervention that has been proven to encourage smoking cessation in pregnancy and reduces smoking rates in late pregnancy by 6 to 7%. There are physiological reasons to suspect that nicotine replacement therapy (NRT) will be less or (in)effective for smoking cessation in pregnancy when compared with its use by nonpregnant smokers. However, there are also strong theoretical reasons to suspect that NRT is likely to be safer than continued smoking in pregnancy. Consequently, this article reviews evidence for the safety and effectiveness of NRT when used for smoking cessation in pregnancy and recommendations concerning the use of NRT in pregnancy are presented.     

Carbon monoxide yield of cigarettes and its relation to cardiorespiratory disease.

Estimates of the carbon monoxide yield of their cigarettes have been obtained for 4910 smokers (68% of all smokers) in the Whitehall study of men aged 40 to 64. In the 10 years after examination 635 men died. When men smoking cigarettes with high carbon monoxide yield were compared with those smoking cigarettes with a low yield, and after adjusting for age, employment grade, amount smoked, and tar yield, the risk of death was 32% lower for coronary heart disease, 49% higher for lung cancer, and 10% lower for total mortality; these differences were not statistically significant. Among men who said that they inhaled the risk of fatal coronary heart disease was 51% lower in the high carbon monoxide group (p less than 0.01), while the risk of lung cancer was 75% higher. These results provide no evidence that a smoker can reduce his risk of death by smoking a brand with a low carbon monoxide yield; he might even increase it. The complex interactions between characteristics of the smoker, smoking behaviour, constituents of tobacco smoke, and health are again demonstrated.     

Population burden of lung cancer due to environmental tobacco smoke

The population burden of lung cancer due to environmental tobacco smoke is significant because a large fraction of the population is exposed. The risks are, of course, lower than those to smokers themselves; but smoking is self-inflicted, passive smoking is involuntary. Making various assumptions, the proportion of lung cancer cases among non-smokers that could reasonably be attributed to environmental tobacco smoke can be calculated to be about 20–30% in western countries. Thus, non-smokers in the society could benefit considerably from diminishing exposures to other people's smoke.     

Mortality in relation to smoking: 22 years' observations on female British doctors.

A total of 6194 female doctors who in 1951 replied to a questionnaire about their smoking habits were followed up prospectively for 22 years. During that time 1094 died. Ischaemic heart disease, lung cancer, and chronic obstructive lung disease were all significantly (p < 0.001) related to smoking, though the absolute excess risks were lower than in male doctors smoking equivalent amounts. Female smokers born before the first world war were less likely to describe themselves as inhalers or as having started to smoke while young than were female smokers who were born later. In these respects this younger group resembled male smokers, and as they move into their 60s and 70s their absolute risk of lung disease and relative risk of ischaemic heart disease will probably come to resemble the risks for men smoking the same numbers of cigarettes. These findings show only that cigarette smoking causes lung cancer, chronic obstructive lung disease, and heart disease in women as in men. Whether the proportional increase in mortality from these diseases is as great in women as in men might be estimated directly from new case-control studies on men and women born since 1920.     

Genotoxicity of cigarette smoking in maternal and newborn lymphocytes

Tobacco smoke contains a large number of substances known to induce DNA damage and to be hazardous to human health. Several reviews and meta-analyses have reported an association between maternal or paternal smoking habits and genetic-related diseases, such as cancer, in children. The aim of the present study was to evaluate the level of DNA damage in lymphocytes of active- and passive-smoking mothers and in their newborns, using the comet assay. A total of 40 active smokers, 40 passive smokers, and 40 non-smokers, and their respective newborns, were evaluated. The active smokers presented a statistically significant increase of DNA damage when compared to the non-smokers and passive-smokers. No significant difference was observed between passive and non-smoking women. Similar results were detected in newborns. Those born to active-smoking mothers presented higher levels of DNA damage than those from passive- and non-smoking mothers. Additionally, no significant difference was detected between newborns from non-smoking and passive-smoking mothers. Also, no statistically significant difference in DNA damage was observed between mothers and their respective newborns, and a positive correlation in the level of DNA damage was detected between them. Logistic regression analyses showed positive associations between DNA damage, spontaneous abortion and smoking status. In conclusion, our data indicate that tobacco exposure during pregnancy has genotoxic effects for both mother and child, and it can be considered an important risk factor for childhood cancer or other genetic-related diseases.