Estimation of smoke dosage and mortality of non-smokers from environmental tobacco smoke

This paper shows how biochemical markers can be used to estimate smoke intake from passive smoking to complement epidemiological studies on the health risks and mortality to non-smokers. Using data from slow nicotine infusions given over 1 h, we estimated that the nicotine intake from passive smoking averages about 0.014 mg/h among urban non-smokers leading their usual daily lives. This compares with 0.23 mg/h in a smoke-filled public house, 0.36 mg/h during maximum exposure in an unventilated room, and 1.0 to 1.4 mg nicotine per cigarette taken in by active smokers. Data from several studies on urinary nicotine concentrations and those of cotinine in blood, urine and saliva were collated. The results show that the concentrations in non-smokers averaged about 0.7% (for nicotine) and 0.6% (for cotinine) of the levels found in smokers. From this we estimate that the mortality from passive smoking is about 1000 non-smokers per year in Britain and about 4000 per year in the United States, assuming that the relation of dose to risk is linear.     

Environmental tobacco smoke exposure among smokers and non-smokers receiving outpatient substance abuse treatment

Introduction

Environmental Tobacco Smoke (ETS) has been linked to numerous health problems. While research has demonstrated high prevalence of tobacco use among individuals receiving treatment for substance use disorders (SUDs), no studies have examined ETS among individuals receiving treatment for SUDs, paying specific attention to non-smokers who may be at risk for high exposure to ETS.

Methods

Participants (N = 261) enrolled in outpatient substance abuse treatment completed a survey, in which 14 items were used to quantify ETS exposure and smoking policies across several environments.

Results

Among smokers, 85% reported that their significant others also smoked as compared to 15% among non-smokers (χ² = 6.624, p < .05). A logistic regression examined the characteristics that predicted smoking in the home. The overall model was significant, (χ² = 36.046, p < .0005) with variables that independently predicted smoking in the home included having less than a high school diploma, being female, and living with a smoker. Income, age, and living with children were not found to be significant. Overall, 42% white collar workers 26% of service workers and 30% of blue collar workers reported no exposure to ETS. Sixty-seven percent of smokers strongly agreed or agreed that the hazards of secondhand smoke have been clearly demonstrated versus 58% of non-smokers.

Conclusions

Smokers and non-smokers enrolled in outpatient substance abuse treatment are frequently exposed to ETS at home, work, and in social settings. The dangers of ETS should be addressed among this population through education, smoke-free policies, and cessation resources, with help from their treatment facility.     

Mainstream and environmental tobacco smoke

Environmental tobacco smoke (ETS) is derived from cigarette smoldering and active smoker exhalation. Its composition displays broad quantitative differences and redistributions between gas and respirable suspended particulate (RSP) phases when compared with the mainstream smoke (MSS) that smokers puff. This is because of different generation conditions and because ETS is diluted and ages vastly more than MSS. Such differences prevent a direct comparison of MSS and ETS and their biologic activities. However, even assuming similarities on an equal mass basis, ETS-RSP inhaled doses are estimated to be between 10,000- and 100,000-fold less than estimated average MSS-RSP doses for active smokers. Differences in effective gas phase doses are expected to be of similar magnitude. Thus the average person exposed to ETS would retain an annual dose analogous to the active MSS smoking of considerably less than one cigarette dispersed over a 1-year period. By contrast, consistent epidemiologic data indicate that active smoking of some 4-5 cigarettes per day may not be associated with a significantly increased risk of lung cancer. Similar indications also obtain for cardiovascular and respiratory diseases. Since average doses of ETS to nonsmoking subjects in epidemiologic studies are several thousand times less than this reported intake level, the marginal relative risks of lung cancer and other diseases attributed to ETS in some epidemiologic studies are likely to be statistical artifacts, derived from unaccounted confounders and unavoidable bias.     

Differences in platelet serotonin transporter sites between African-American tobacco smokers and non-smokers

Rationale. The serotonin transporter (5HTT) regulates the magnitude and duration of serotonergic neurotransmission. Although nicotine and other constituents of tobacco smoke may influence serotonin turnover among animals, few studies have examined whether smoking is associated with alteration in 5HTT in humans. Objective. We investigated whether tobacco smokers and non-smokers differed in platelet tritiated paroxetine binding, a measure of 5HTT sites, and whether severity of nicotine dependence (ND) was related to 5HTT measures. Methods. Tritiated paroxetine binding sites on platelets were assayed in 26 African-American smokers and 30 non-smokers. Severity of smoking was assessed using the Fagerstrom Test for Nicotine Dependence (FTND). Relationships between FTND scores and maximum number of transporter sites (B_max) and affinity constant (K_d) of paroxetine binding were determined. Results. B_max values showed a significant negative correlation with FTND scores (rho=−0.28, P<0.01). Notably, smokers with higher ND had significantly lower B_max compared to those with lower ND and non-smokers; the latter two groups did not differ in B_max (F=3.92, P<0.05). Smokers scored higher on impulsivity than non-smokers, however, behavioral variables did not influence the relationship of smoking with B_max. Age, gender and K_d values were not associated with smoking or B_max. Conclusions. Smoking, in particular higher nicotine dependence, appears to be correlated with decreased density of platelet 5HTT sites in African-Americans. The nature of the relationship and whether similar changes occur in the brain merit further investigation. Electronic Publication     

Misclassification of environmental tobacco smoke exposure: its potential influence on studies of environmental tobacco smoke and lung cancer

The effects of selection, confounding, misclassification and bias must be eliminated from case-control studies of 'passive smoking' and lung cancer before a meaningful interpretation can be made. Misclassification includes the misclassification of the subject's non-smoking status, of the disease status or of the spouse's smoking habits. This paper shows that inflation of the amount smoked by the husbands of female lung cancer cases may have accounted for the apparent 'dose-response' relationships in 3 widely referenced case-control studies.     

The contribution of low tar cigarettes to environmental tobacco smoke

A series of low tar cigarettes (LTC) were smoked and the quantities of condensable mainstream (inhaled) and sidestream (between puffs) smoke compounds were determined and compared to those produced by a high tar, nonfilter cigarette. It was found that the LTC produced large quantities of sidestream smoke condensates, about equal to the high tar cigarette, and contained very high levels of toxic or cocarcinogenic phenols. On an equal weight basis, the LTC emitted more of these hazardous compounds into sidestream and environmental tobacco smoke. Higher smoke yields of a flavor additive and a sugar degradation product indicated addition of such compounds during the manufacture of LTC. It was concluded that, compared to a high tar cigarette, smoking LTC may be better for the smoker, but not for the nearby nonsmoker. Information should be developed to allow smokers to choose LTC that produce lower levels of hazardous compounds in their environmentally emitted sidestream smoke.     

Oxidative stress in smokers and non-smokers

Oxidative stress plays an important role in the pathogenesis of some diseases such as lung cancer, chronic obstructive pulmonary disease, and atheroscleorosis. Smoking may enhance oxidative stress not only through the production of reactive oxygen radicals in smoke but also through weakening of the antioxidant defense systems. In this study, we investigated the effects of smoking on lipid peroxidation and paraoxonase activity in a healthy population. The study consisted of (n = 30) smokers and (n = 30) nonsmokers. The age of the population which is studied was 44.74 +/- 10.59 yr. The levels of serum malondialdehyde (MDA) and paraoxonase (PON1) activities were measured by the modified Buege method and the Eckerson method, respectively. Student's t-test was used to analyze the data. The serum MDA levels were significantly higher (p < .05) and serum PON1 activities were significantly lower (p < .001) in smokers than in nonsmokers. Thus, increased levels of serum MDA and decreased PON1 activities may be important in determining the oxidant/antioxidant imbalance in smokers.     

Urinary hydroxyproline excretion in smokers, non-smokers and passive smokers

The hydroxyproline/creatinine ratio in urine was investigated in 200 cigarette smokers, 199 pipe and/or cigar smokers and 24 non-smokers. For cigarette smokers a statistically significant positive correlation is found between this ratio and daily cigarette consumption, COHb, serum cotinine and nicotine excretion in urine. This smoking-related increase in the hydroxyproline/creatinine ratio is, for the most part or completely, due to the fact that creatinine urine concentrations inversely correlate with the smoke uptake variables. Neither pipe and/or cigar smoking nor passive smoke exposure of non-smokers seem to affect the hydroxyproline/creatinine ratio. A seasonal influence is found in these studies as well as in two experiments with limited numbers of subjects: the hydroxyproline/creatinine ratio is higher in winter than in summer for both smokers and non-smokers. Our data do not favour the idea that measuring hydroxyproline/creatinine ratios in urine is an accurate method of investigating early effects of smoking, passive smoking and air pollution in man.     

Effects of environmental tobacco smoke on respiratory symptoms and pulmonary function

The aim of this study was to examine the effects of environmental tobacco smoke (ETS) on pulmonary function and respiratory symptoms. During periodic medical examination, 392 French nonsmokers responded to an interviewer-administered questionnaire. Then spirometry was performed to assess pulmonary function. All of the subjects were carefully examined by two occupational physicians. ETS exposure at the workplace was more common than this exposure at home (20% vs. 5%). ETS exposure was significantly associated with forced vital capacity (FVC; -3.16%; 95% CI: -5.67 to -0.64) and forced expiratory volume in 1s (FEV1; -2.90%; 95% CI: -5.59 to -0.23). Abnormal FVC results were significantly increased in exposed subgroup [odds ratio = 2.71 (95% CI: 1.09 to 6.75)]. We did not find any significant dose-response relationship between ETS exposure and lung function results. The effects of ETS exposure on respiratory symptoms and diseases (asthma, wheezing, chronic bronchitis, and dyspnea) were not significant. Thus, this study showed that there was a significant inverse association between exposure to ETS and pulmonary function. Even pulmonary function results inferior to the lower limit of normal may be possible. A stricter legislation against ETS is proposed.     

German Environmental Survey IV: Children's exposure to environmental tobacco smoke

Different aspects of the environmental tobacco smoke (ETS) exposure of children in Germany have been investigated in the German Environmental Survey for Children (GerES IV). The field work of GerES IV was conducted from 2003 to 2006 using questionnaires, indoor air monitoring and human biomonitoring.     

Environmental tobacco smoke and cancer of sites other than the lung in adult non-smokers.

Evidence from epidemiological studies relating environmental tobacco smoke (ETS) exposure to risk of cancer of sites other than the lung in adult non-smokers is reviewed. Problems common to many studies include small sample size, inadequate control of potential confounding, failure to consider the possibility of misclassification of smoking status, reliance on death certificate diagnosis, use of proxy respondents and the possibility of recall bias. A number of the studies have other obvious weaknesses. Publication bias is known to be a problem, with two very large prospective studies having reported only very limited results. For cancers of the digestive system, bladder and brain, there is little evidence of an association with ETS exposure. Some studies have reported a relationship with cancer of the breast, cervix or nasopharynx, but the overall evidence for these sites is inconsistent and inconclusive, as is that for total cancer incidence. All three studies of nasosinus cancer have reported a statistically significant association with ETS exposure, but they are small, control poorly for potential confounding and have other weaknesses. Taken as a whole, the epidemiological evidence provides little support for the view that ETS causes cancer of any of the sites considered.     

Occupational exposure to environmental tobacco smoke: a study in Lisbon restaurants

Environmental tobacco smoke (ETS), also referred to as secondhand smoke (SHS), is a major threat to public health and is increasingly recognized as an occupational hazard to workers in the hospitality industry. Therefore, several countries have implemented smoke-free regulations at hospitality industry sites. In Portugal, since 2008, legislation partially banned smoking in restaurants and bars but until now no data have been made available on levels of indoor ETS pollution/exposure at these locations. The aim of this study was to examine the occupational exposure to ETS/SHS in several restaurants in Lisbon, measured by indoor fine particles (PM(2.5)) and urinary cotinine concentration in workers, after the partial smoking ban in Portugal. Results showed that the PM(2.5) median level in smoking designated areas was 253 μg/m3, eightfold higher than levels recorded in canteens or outdoor. The nonsmoking rooms of mixed restaurants exhibited PM(2.5) median level of 88 μg/m3, which is higher than all smoke-free locations studied, approximately threefold greater than those found in canteens. Importantly, urinary cotinine concentrations were significantly higher in nonsmoker employees working in those smoking designated areas, confirming exposure to ETS. The proportion of smokers in those rooms was found to be significantly positively correlated with nonsmoker urinary cotinine and indoor PM(2.5) levels, establishing that both markers were occupational-ETS derived. The use of reinforced ventilation systems seemed not to be sufficient to decrease the observed ETS pollution/exposure in those smoking locations. Taken together, these findings demonstrate that the partial restrictions on smoking in Portuguese venues failed to provide adequate protection to their employees, irrespective of protective measures used. Therefore, a smoke-free legislation protecting individuals from exposure to ETS/SHS in all public places and workplaces is urgently needed in Portugal.     

Effects of exposure to environmental tobacco smoke on a human tracheobronchial epithelial cell line

BEAS-2B cells, a human bronchial epithelial line immortalized by viral transformation, were exposed to sidestream tobacco smoke (STS) as a surrogate for environmental tobacco smoke (ETS) under biphasic culture conditions where the apical portion of the cells was in direct contact with the gas phase. Dose-dependent cytotoxicity was observed. In addition, induction of an as yet uncharacterized protein of molecular weight 45 000 was associated with exposure to STS. This protein might be part of a protective response of exposed cells, which do not show a classical heat shock response when exposed to STS. We conclude that STS and ETS can be directly cytotoxic to human airway epithelial cells in biphasic culture at concentrations not unreasonable for smoky indoor atmospheres. The model system described in this paper should be useful for studying the detailed mechanisms of cytotoxicity of, and protection from, ETS exposure in the human cells most directly exposed to ETS in vivo.     

Urinary mutagenicity after controlled exposure to environmental tobacco smoke (ETS)

20 non-smokers on a defined diet low in polycyclic aromatic hydrocarbons (PAH) were exposed to environmental tobacco smoke (ETS) in an unventilated room for 8 h. The urinary mutagenicity in the 24-h urine samples as tested with the Salmonella (TA98) microsome assay did not significantly increase after exposure to either 10 ppm CO or 20-25 ppm CO. We conclude that exposure of non-smokers to ETS does not lead to an increase in their urinary mutagenicity, provided the exposure conditions are within a realistic range.     

A critical look at N-nitrosamines in environmental tobacco smoke

The amounts of cigarette smoke carcinogens released into the environment as sidestream smoke (SS) constituents are generally twice as high as the levels of the carcinogens that are inhaled as mainstream smoke (MS). However, certain carcinogens in undiluted SS, such as nitrosamines, exceed MS levels up to 50 times. Regardless of the fact that SS is usually substantially diluted before being inhaled, its constituents can be determined in environmental tobacco smoke (ETS) by modern analytical methods and levels of exposure of involuntary smokers can be assessed by the use of specific markers. Currently, the uptake of ETS by nonsmokers is determined by measuring nicotine and its metabolite cotinine in saliva, serum and/or urine. In on-going studies, we are now exploring the determination of the two highly carcinogenic nicotine-derived nitrosamines N'-nitrosonornicotine (NNN) and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), respectively of their metabolites, in physiological fluids of smokers and nonsmokers.     

Measures of impulsivity in cigarette smokers and non-smokers

Rationale: Drug users are thought to be more ”impulsive” than non-users. Objectives: This study examined whether regular smokers are more impulsive than never smokers using personality and behavioral measures of impulsivity. Methods: Twenty regular smokers (≥15 cigarettes/day) and 20 never smokers were recruited. Participants completed five personality questionnaires to assess impulsivity: Adjective Checklist, Barratt’s Impulsivity Scale, the Tridimensional Personality Questionnaire, Eysenck’s Personality Questionnaire, and the Sensation-Seeking Scale. Participants also performed three behavioral choice tasks designed to assess impulsivity. In the delay task, participants chose between small, immediate and large, delayed monetary rewards. Impulsivity was defined as a relative preference for the small, immediate alternative. In the probability task, participants chose between small, certain and large, uncertain monetary rewards. Impulsivity was defined as a relative preference for the large but more risky alternative. In the work task, participants chose between small monetary rewards obtained by performing a negligible amount of work and a larger amount of money requiring more work. Impulsivity was defined as a relative preference for the smaller, easier alternative. Results: On the personality questionnaires, smokers had statistically higher impulsivity scores on most scales. On the behavioral choice tasks, smokers chose small, immediate money over large, delayed money more frequently, signifying greater levels of impulsivity. There were no differences between the groups’ choices on the other tasks. Correlations between questionnaire and task data were small, as were correlations between data from each task. Conclusions: Together, these results indicate that the smokers were more impulsive than never smokers. Received: 2 December 1998 / Final version: 1 April 1999     

Psychosocial differences between smokers and non-smokers during pregnancy

Despite the well-established adverse birth and childhood health outcomes associated with maternal smoking, smoking rates among pregnant women remain high. Psychosocial health attributes, including anxiety, depression, perceived stress, self-efficacy, and personality characteristics, have especially important roles in smoking behavior. Understanding who smokes during pregnancy and what factors influence this behavior choice may be key to improving the effectiveness of smoking cessation intervention programs. We use data from a prospective cohort study of pregnant women to understand the psychosocial health profiles of women who choose to smoke during pregnancy compared to the profiles of women who do not smoke or successfully quit smoking during pregnancy. Multinomial logistic regression analyses on 1518 non-Hispanic black and non-Hispanic white women assessed the association between smoking status and psychosocial health while controlling for demographic characteristics. Higher levels of perceived stress, depression, neuroticism, negative paternal support, and perceived racism among non-Hispanic blacks were associated with higher odds of being a smoker than a non-smoker (p < 0.05). Higher levels of self-efficacy, extraversion, agreeableness, conscientiousness, interpersonal support, positive paternal support, and perceived social standing were associated with lower odds of being a smoker than a non-smoker (p < 0.05). Our analysis indicates that women who smoked during pregnancy experienced a more negative constellation of psychosocial adversities than women who did not smoke. Given the psychosocial needs and personality profiles experienced by smokers, more attention to the psychosocial strengths and weaknesses of these women may allow for more tailored smoking cessation programs, enhancing both the short- and long-term effectiveness of such interventions.     

Hydroxy-phenanthrenes in the urine of non-smokers and smokers

Urinary hydroxy-phenanthrene (HO-PHE) excretion in non-smokers exposed to environmental tobacco smoke (ETS) is not increased. There is no significant difference in HO-PHE excretion between smokers (S) and non-smokers (NS), though excretion seems to be slightly elevated in smokers. A diet rich in polycyclic aromatic hydrocarbons leads to a rise in urinary HO-PHE excretion as compared to a diet low in polycyclic aromatic hydrocarbons (PAH), coming close to significance. HO-PHE excretion is not correlated with the mutagenic activity in urine.