Role Of Environmental Tobacco Smoke Research Articles

Smoking habits and osteoporosis in community-dwelling men subjected to dual-X-ray absorptiometry: a cross-sectional study

BackgroundActive and Environmental Tobacco Smoke (ETS) are a global cause of death. Osteoporosis (Op) is the most common metabolic bone disorder worldwide, impacting on mortality and disability, with high health and welfare costs. Active smoking is a known risk factor for Op, but there is few information regarding Op and ETS in men.PurposeThe study aim is to evaluate the association between smoking habits and Op in community-dwelling men that have been subjected to Dual-X-ray Absorptiometry and completed a questionnaire about their own and cohabiter’s smoking habits.MethodsWe performed a cross-sectional study based on administrative data. This study is part of the SIMON protocol. The binary logistic regression analysis was used to estimate the role of ETS on the risk of Op, adjusting for age, body mass index (BMI), type 2 diabetes mellitus (T2DM) and eGFR.ResultsFour hundred sixteen men were selected and, based on questionnaire replies, 167 were classified as current smokers (CS), 93 as passive smokers (PS) and 156 as never smokers (NS). NS showed a lower prevalence of past fragility fracture, radiological features of osteoporosis and hypovitaminosis D compared to PS and CS (p < 0.05). NS showed a lower prevalence of Op compared to PS and CS, also after correction for age, BMI, T2DM and eGFR (p < 0.05).ConclusionThe study results demonstrate that PS and CS have a higher risk of Op, fragility fractures and vitamin D deficiency compared to NS.

Environmental Tobacco Smoke And Risk Of Breast Cancer

Introduction. Even though it is well understood that tobacco smoking has substantial and adverse effects on human health, the role of environmental tobacco smoke (ETS) on breast cancer (BC) remains unclear. This study aimed to examine the association between ETS exposure at home and the risk of BC. Methods. A hospital-based case-control study was carried out in 585 cases and 1170 controls. Information on ETS at home and other possible risk factors was collected via a structured questionnaire. Logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs) for BC by exposure to ETS. All statistical tests were two-sided. Results. Women, who never smoked actively but had ever experienced exposure to ETS at home in life had a 2-fold increased risk of BC compared with non-smokers without exposure to ETS at home (OR = 2.11 95% CI = 1.63-2.74, p &lt; 0.001), after adjustment for age, education, marital status, family history on breast cancer, number of given births, estrogen-active period, hormone therapy during menopause, alcohol use, body mass index, diabetes mellitus, and thyroid diseases. However, the association between BC risk and exposure to ETS in ex-smokers or current smokers was not defined (OR = 0.98 95% CI = 0.48-2.0, p = 0.954 and OR = 1.06 95% CI = 0.53-2.14, p = 0.86, respectively). Conclusion. The data obtained show increased risk of breast cancer in never smoked women exposed to environmental tobacco smoke at home in their life.

Systematic literature review assessing tobacco smoke exposure as a risk factor for serious respiratory syncytial virus disease among infants and young children.

BackgroundThe role of environmental tobacco smoke (ETS) exposure as a risk factor for serious respiratory syncytial virus (RSV) disease among infants and young children has not been clearly established. This systematic review was conducted to explore the association between ETS exposure and serious RSV disease in children younger than 5 years, including infants and young children with elevated risk for serious RSV disease.MethodsA systematic review of English-language studies using the PubMed and EMBASE databases (1990–2009) was performed to retrieve studies that evaluated ETS as a potential risk factor for serious RSV illness. Studies assessing risk factors associated with hospitalization, emergency department visit, or physician visit due to RSV (based on laboratory confirmation of RSV or clinical diagnosis of RSV) in children under the age of 5 years were included.ResultsThe literature search identified 30 relevant articles, categorized by laboratory confirmation of RSV infection (n = 14), clinical diagnosis of RSV disease (n = 8), and assessment of RSV disease severity (n = 8). Across these three categories of studies, at least 1 type of ETS exposure was associated with statistically significant increases in risk in multivariate or bivariate analysis, as follows: 12 of 14 studies on risk of hospitalization or ED visit for laboratory-confirmed RSV infection; 6 of 8 studies of RSV disease based on clinical diagnosis; and 5 of the 8 studies assessing severity of RSV as shown by hospitalization rates or degree of hypoxia. Also, 7 of the 30 studies focused on populations of premature infants, and the majority (5 studies) found a significant association between ETS exposure and RSV risk in the multivariate or bivariate analyses.ConclusionWe found ample evidence that ETS exposure places infants and young children at increased risk of hospitalization for RSV-attributable lower respiratory tract infection and increases the severity of illness among hospitalized children. Additional evidence is needed regarding the association of ETS exposure and outpatient RSV lower respiratory tract illness. Challenges and potential pitfalls of assessing ETS exposure in children are discussed.

Psychophysiological reactivity to environmental tobacco smoke on smokers and non-smokers

Environmental tobacco smoke (ETS) is an air pollutant with a relevant impact on public health. In addition, ETS is a significant stimulus that may elicit different responses depending on previous experience and current status regarding smoking. Exposure to cigarette cues has been shown to be a reliable method for inducing subjective and physiological responses. However, the role of ETS as a stimulus has not received, to date, enough attention in the research literature. This study aimed to analyse both the autonomic and subjective responses of smokers and non-smokers to exposure to ETS. To that end, 41 non-smokers and 57 smokers were exposed to ETS, in a controlled laboratory setting. We measured the subjective perception of smoke, unpleasantness, heart rate and skin conductance to compare the reactions of smokers and non-smokers to ETS. Additionally, subjective tobacco craving after exposure was assessed for current smokers. We found different psychophysiological responses to ETS exposure for smokers and non-smokers. Smokers showed a generalised increase in autonomic activity, significantly greater than that of non-smokers. In addition, heart rate increase during exposure to ETS was positively correlated with subjective craving. Our data suggested that ETS was an important stimulus and acted as a relevant cue for smokers; it induced both psychophysiological reactions and subjective craving. Hence, this kind of stimulus within the cue-reactivity research paradigm may be useful for studying the effect of ETS on smokers' reactions, craving, quitting attempts, or relapse probabilities.

Parental smoking, nasal resistance and rhinitis in children

To determine whether parent-reported perennial rhinitis or objectively measured nasal resistance is more common in children from smoking families. To assess tonsillar size, nasopharyngeal airway and upper airway surgery frequency in children with smoking and non-smoking parents. Ninety-five children (age 3-6 years, median 68 months) participated in this prospective cross-sectional clinical study. History of nasal symptoms was obtained, and all underwent an ear-nose-throat examination, anterior rhinomanometry and a lateral cephalogram. Regular smoking by either parent and their child's snoring was inquired about with a parental questionnaire. We compared children with a parental smoker and children without a parental smoker in the family. Smoking in the family led to increased risk for perennial rhinitis in the children up to 2.76-fold (aOR, 95%CI 1.00-7.67), but with no difference in nasal resistance between children from smoking and non-smoking households. Neither tonsillar size, nasopharyngeal airway nor upper airway surgery was associated with parental smoking. Parental smoking is associated with symptoms of perennial rhinitis in children. The possible role of environmental tobacco smoke should be taken into account in parent counselling and in evaluation of children being treated for symptoms of rhinitis and nasal obstruction.

Environmental Tobacco Smoke and Bladder Cancer Risk in Never Smokers of Los Angeles County

Cigarette smoking is a major risk factor for bladder cancer and a prominent point source of 4-aminobiphenyl (4-ABP), a recognized human bladder carcinogen. 4-ABP-hemoglobin (Hb) adducts are established biomarkers of 4-ABP exposure in humans. The role of environmental tobacco smoke (ETS) in the etiology of bladder cancer is largely unknown. As part of a large population-based bladder cancer study in Los Angeles County, California, lifetime exposure to ETS was ascertained for 148 cases and 292 control subjects who had never used any tobacco products over their lifetime. 4-ABP-Hb adducts were quantitatively measured on 230 control subjects. Female lifelong nonsmokers living with two or more smokers during childhood were significantly related to risk of bladder cancer [odds ratio (OR), 3.08; 95% confidence interval (95% CI), 1.16-8.22]. During adulthood, approximately 2-fold risks were seen among women living with a spouse/domestic partner who smoked for > or =10 years or having a coworker who smoked in an indoor environment for > or =10 years. When all sources of ETS exposure were combined, a statistically significant, dose-dependent association (P for trend = 0.03) was noted in women, with the OR for the highest category of ETS exposure being 5.48 (95% CI, 1.06-28.36). Levels of 4-ABP-Hb adducts varied by ETS exposure status among female control subjects. Mean level was lowest in women never exposed to ETS (16.4 pg/g Hb) and highest in those with current ETS exposure (23.6 pg/g Hb). ETS exposure was associated with neither bladder cancer risk nor 4-ABP-Hb adduct levels in male lifelong nonsmokers. In conclusion, ETS is a risk factor for bladder cancer in women who were lifelong nonusers of any tobacco products.

The role of environmental tobacco smoke in the origins and progression of asthma

Exposure to environmental tobacco smoke (ETS) is a major source of indoor air pollution and causes adverse effects on the respiratory health of individuals with asthma. At least one third of children and adults with asthma are exposed to ETS on a regular basis. There is convincing evidence for a causal relationship between exposure to ETS and development of asthma in children and in nonsmoking adults. Exposure to ETS also worsens asthma control in children and nonsmoking adults who have established asthma. The mechanism by which ETS causes these harmful effects is not established but may involve genetic predisposition, impairment of lung development, and altered lung inflammatory responses. Workplace smoking restrictions and reduced smoking in the home may lower the prevalence of asthma, improve asthma control, and reduce the use of medical services in both children and adults who are exposed to ETS.

Long term environmental tobacco smoke activates nuclear transcription factor-kappa B, activator protein-1, and stress responsive kinases in mouse brain

Environmental tobacco smoke (ETS) is a key mediator of several diseases. Tobacco smoke contains a mixture of over 4700 chemical components many of which are toxic and have been implicated in the etiology of oxidative stress related diseases such as chronic obstructive pulmonary disease, Parkinson's disease, asthma, cancer and cardiovascular disease. However, the mechanism of action of cigarette smoke in the onset of these diseases is still largely unknown. Previous studies have revealed that the free radicals generated by cigarette smoke may contribute to many of these chronic health problems and this study sought to address the role of environmental tobacco smoke in oxidative stress related damage in different regions of the mouse brain. In this study, male mice were exposed for 7 h/day, 7 days/week, for 6 months. Our results show that tobacco smoke led to increased generation of reactive oxygen species with an increase in NF-κB activation. Gel shift analysis also revealed the elevated level of the oxidative stress sensitive proinflammatory nuclear transcription factor-kappa B and activator protein-1 in different regions of the brain of cigarette smoke exposed mice. Tobacco smoke led to activation of COX-2 in all the regions of the brain. Activation of mitogen activated protein kinase and c-Jun N-terminal kinase were also observed in various regions of brain of ETS exposed mice. Overall our results indicate that exposure to long-term cigarette smoke induces oxidative stress leading to activation of stress induced kinases and activation of proinflammatory transcription factors.

Environmental Tobacco Smoke and Risk of Adult Leukemia

The role of environmental tobacco smoke (ETS) in the causation of lung and breast cancer has been repeatedly evaluated over recent years. In contrast, its impact on the risk of adult leukemia has received little attention. We used the lifetime residential and occupational ETS exposure histories from a population-based sample of 1068 incident and histologically confirmed adult leukemia cases and 5039 population controls age 20 to 74 years to evaluate the relationship between ETS exposure and adult leukemia risk among nonsmokers in Canada. The duration of exposure and smoker-years index were used as indices of ETS exposure. We restricted our analysis to the 266 case and 1326 control subjects who reported being lifetime nonsmokers and provided residential ETS exposure history for at least 75% of their lifetime. No association was found for most leukemia subtypes, and in particular for acute myeloid leukemia. In contrast, the risk for chronic lymphocytic leukemia was clearly associated with ETS exposure, with an adjusted odds ratio of 2.3 (95% confidence interval = 1.2-4.5) for more than 83 smoker-years of residential exposure and 2.4 (1.3-4.3) for more than 72 smoker-years of occupational exposure. There was a dose-response relationship for chronic lymphocytic leukemia with both indices of exposure. Risk was not higher with recent exposure, using time-window-exposure analyses. Regular long-term ETS exposure may be a risk factor for chronic lymphocytic leukemia.

The role of environmental tobacco smoke in genetic susceptibility to asthma.

The increase in asthma prevalence over the past 50 years suggests that exposures to environmental risk factors have also increased during this time. Environmental tobacco smoke is one of the most common indoor air pollutants and has been associated in epidemiologic studies with airway and allergic phenotypes in exposed individuals. However, symptoms occur in only some individuals, suggesting that individual genotypes determine sensitivity to environmental tobacco smoke exposure. In this review, we summarize studies evaluating the relationship between genotype, environmental tobacco smoke exposure and risk for asthma and related phenotypes. Using either candidate gene or genome-wide approaches, a number of studies have examined interactions between genotypes at specific loci or genome regions and environmental tobacco smoke exposure and risk for asthma or asthma-associated phenotypes. These studies implicate variation in the genes encoding the alpha(2)-adrenergic receptor, interleukin-10, glutathione S-transferase M1, interleukin-1 beta and interleukin-1 receptor antagonist, matrix metalloproteinases 1 and 12, interleukin-4 receptor alpha-chain, alpha(1)-antitrypsin, and microsomal epoxide hydrolase, as well as unknown genes on chromosomes 1p, 5q and 17p as contributing toward susceptibility in smoking exposed individuals. Considering environmental tobacco smoke exposure in genetic studies may help to identify more homogeneous subsets of patients that share a common disease etiology. By stratifying samples by environmental tobacco smoke exposure, associations or linkages with specific polymorphisms or chromosomal region may be revealed, as illustrated in the studies discussed in this review.

Association between exposure to environmental tobacco smoke and the development of acute coronary syndromes: the CARDIO2000 case–control study

Objective: To investigate the association between environmental tobacco smoke (ETS) exposure (at least 30 minutes a day) and the risk of developing acute coronary syndromes (ACS). Design and setting: The...

Secondhand Smoke Induces Allergic Sensitization in Mice

Purpose of the Study. Although there is evidence that environmental tobacco smoke (ETS) can exacerbate allergic responses, the role of ETS in primary allergic sensitization remains unclear. The objective of this study was to examine the influence of ETS on allergic sensitization in a mouse model.Study Population. Female BALB/c and C57BL/6 mice.Methods. The investigators exposed mice to either ovalbumin (OVA), saline, ETS, or OVA + ETS by nebulization. Total IgE and OVA-specific immunoglobulin E (IgE), IgG1 and IgG2a were quantified for each of the 4 exposure groups. Mice were reexposed to nebulized OVA 30 days after the initial exposure and cytokine levels in bronchoalveolar lavage (BAL) fluid were measured. Interleukin (IL)-2, IL-4, IL-5, IFN-γ and granulocyte-macrophage colony-stimulating factor (GM-CSF) were measured to look for evidence of Th1 or Th2 skewed immune responses. Two strains of mice were studied, BALB/c, a high IgE producer, and C57BL/6, a low IgE producer.Results. An allergic antibody response, as measured by total IgE and OVA-specific IgE and IgG1, was present in C57BL/6 mice exposed to OVA + ETS, but was not detectable in those exposed to saline, OVA alone, or ETS alone. The results were statistically significant. The allergic antibody response in the BALB/c mice was also most pronounced in the group exposed to OVA + ETS. As this strain more readily produces IgE, there was detectable total IgE as well as OVA-specific IgE and IgG1 in the group exposed to OVA alone, but levels of OVA-specific IgE and IgG1 were statistically significantly higher in the OVA + ETS group. BAL fluid was examined for eosinophilia after rechallenge with OVA in C57BL/6 mice. The OVA + ETS group had marked eosonophilia while the saline, OVA and ETS groups had no eosinophils. Cytokines were also quantified in BAL fluid. IFN-γ, a Th1-associated cytokine, was decreased in OVA + ETS mice as compared with the OVA-exposed group (P < .01), while IL-5, a Th2-associated cytokine, was increased as compared with the OVA-exposed group (P < .05).Conclusion. ETS exposure appears to facilitate the primary allergic response in mice as measured by allergic antibody response and BAL cytokine response and eosinophilia.Reviewers’ Comments. Although some evidence has been published regarding ETS and its role in exacerbating allergic responses, this is the first study demonstrating a significant role for ETS in primary allergic sensitization in mice. Future studies will no doubt address the applicability of these findings to humans.

Tobacco hypersensitivity and environmental tobacco smoke exposure in a pediatric population

Skin testing and RAST have verified the existence of tobacco-specific IgE. However, published studies report conflicting results concerning the clinical significance of tobacco IgE. Previous studies have not focused on the role of environmental tobacco smoke (ETS) as it relates to tobacco hypersensitivity (TH) in nonsmoking children. We used nonsmoking pediatric patients to investigate the relationship between ETS and TH. Children, ages 4 to 10 years, were prospectively enrolled. ETS exposure and smoke-triggered symptoms were recorded by questionnaire and physician history. Patients were given a skin test (ST) with a panel of aeroallergens plus tobacco extract. A ST reaction to at least one aeroallergen classified a patient as atopic; a ST reaction to tobacco classified a patient as TH. We enrolled 170 patients, mean age 7.2 years. We found 58 (34%) patients reported routine exposure to ETS and 78 (46%) patients reported ETS-induced symptoms. We found 121 (71%) atopic patients and 61 (36%) TH patients. TH was more common in atopic patients (P < .0001) and those routinely exposed to ETS (P < .05). However, TH failed to predict ETS-induced symptoms in either atopic or non-atopic patients (PPV = 0.40, NPV = 0.69). We evaluated the clinical significance of TH in a nonsmoking patient population related to ETS exposure. We concluded that although TH is statistically related to atopy and ETS exposure, the low predictive values of skin testing for TH limit its clinical usefulness.

Epidemiology of tobacco carcinogenesis.

Tobacco smoking is a worldwide epidemic. Tobacco smoke is an established human carcinogen that contains more than 50 carcinogens, among the most potent of which are polycyclic aromatic hydrocarbons (PAHs) and tobacco- specific nitrosamines (TSNs). Over the last 40 years, the level of tar and nicotine in cigarettes has decreased, along with the level of PAHs, but the level of TSNs has increased. Also, decreases in nicotine content can lead to an attendant increase in smoking in order for an individual to maintain his or her blood nicotine levels. Several factors determine the biologically effective dose of carcinogens, including the number of cigarettes smoked per day, type of cigarette, smoking topography, carcinogen metabolism, and DNA repair. Many studies have shown a relationship between tobacco smoke exposure, carcinogen-DNA adduct formation, tumor specific mutations (eg, p53 mutational spectra), and cancer risk. Genetically determined host capacity can influence these outcomes and the risk for tobacco addiction. Current areas of interest include determining whether women are indeed at greater risk of lung cancer compared with men, and if blacks are at higher risk than women. Also, newer methods can probably clarify the role of environmental tobacco smoke in carcinogenesis.

Environmental tobacco smoke: Association with cardiovascular function at rest and during stress

Chronic exposure to environmental tobacco smoke (ETS) contributes to cardiovascular disease morbidity and mortality, and ETS alters cardiovascular performance during exercise stress. However, no study has examined whether those with ETS exposure have altered cardiovascular functioning during psychological stress, relative to those with no substantial ETS exposure. Seventy-eight healthy, nonsmoking adult men with either high levels of current ETS exposure at home and work or no current or significant lifetime ETS exposure were tested in a stress reactivity protocol. Blood pressure and heart rate were monitored during rest and during two psychological stressors. Those with high ETS exposure had significantly elevated heart rate and blood pressure at baseline, relative to those with no exposure. The groups did not differ on their cardiovascular stress responses. These data suggest that chronic ETS exposure is associated with altered cardiovascular functioning at rest, but not during stress. Results are discussed with regard to the role of ETS on the development of heart disease among nonsmokers.

Urinary mutagenicity and thioethers in nonsmokers: Role of environmental tobacco smoke (ETS) and diet

The urinary excretion of mutagens and thiothers was investigated in a controlled diet study and in two field studies. A diet containing charcoal-broiled meat and other items rich in mutagenic compounds increased the urinary mutagenicity as assessed in Salmonella typhimurium strain TA98 with metabolic activation ∼ 46-fold compared to a diet low in mutagens. The excretion of thiothers after ingestion of the diet rich in mutagens also increased significantly when compared to the diet low in mutagens. The increase was associated with the content of preformed thiothers in the diet. In the first field study with 21 nonsmokers, urinary mutagenicity as assessed in Salmonella typhimurium strain TA98 and excretion of thiothers showed no relation to either the self-reported exposure to environmental tobacco smoke (ETS) or to serum cotinine concentrations used as an objective marker for ETS exposure. In the second field study, urinary mutagenicity was determined with a tobacco-smoke sensitive Salmonella typhimurium strain YG1024 with metabolic activation. No correlation was found between the mutagenic activity in urine and ETS exposure duration, nicotine on the personal sampler, cotinine in saliva and cotinine in urine. Our results suggest that real-life ETS exposure does not measurably increase either urinary mutagen or urinary thioether excretion. Furthermore, diet seems to be the most important source for both urinary mutagen and thioether excretion in nonsmokers.

Chronic obstructive pulmonary disease in lifelong nonsmokers: results from NHANES.

The prevalence of chronic obstructive pulmonary disease was evaluated in 12,980 lifelong nonsmoking adults who participated in one of three National US Health and Nutrition Examination Surveys. Also evaluated were the relationships between chronic obstructive pulmonary disease and age, sex, ethnicity, education, income, and certain environmental and occupational factors. Overall, 4% of men and 5% of women reported physician-diagnosed chronic obstructive pulmonary disease. Prevalence increased with age and with decreasing household income, was higher in Whites than in non-Whites, and was particularly high in Hispanic women. Further research is needed to explain the excess risk for chronic obstructive pulmonary disease in economically disadvantaged nonsmokers, and to assess the role of environmental tobacco smoke in nonsmokers' risk for the disease.

Relationship of environmental tobacco smoke to otitis media in young children

Otitis media (OM) continues to be a major health problem of children in the United States. The role of environmental tobacco smoke (ETS) as a predisposing factor has not been completely discerned. This study and discussion is an investigation and review of the influence of passive cigarette smoking on OM in children, and its effect on the practice of otolaryngology within the pediatric population. A prospective study of 175 children with recurrent OM and requiring tympanostomy tubes (case group) was compared to an age-matched group of 175 children (controls) to determine the role passive cigarette smoking has on the incidence of this disease. The results revealed that the case group more commonly had exposure to ETS (P = .04). Prospective follow-up of the case group revealed no significant difference in the clinical course of the children who were exposed to ETS and those who were not.

How much does Environmental Tobacco Smoke Contribute to the Building Symptom Index?

Environmental tobacco smoke (ETS) has been identified as one of the factors associated with the symptoms of the sick building syndrome (SBS). We investigated the role of ETS in an office building during the phased introduction of a smoking ban. Over a two-year period we measured symptoms using a validated questionnaire, environmental nicotine levels and salivary cotinine as a biological marker of nicotine absorption in a stratified systemic sample of 375 office employees (91% response rate). In addition, 26 persons from a non-smoking office were studied as a control group. This report describes the findings derived from a cross-sectional analysis of the initial baseline data. Amongst the validated nonsmokers, symptoms increased with increasing nicotine exposure from ETS (r= 0.165 p < 0. 01), supporting the role of ETS in the SBS. Smokers reported significantly fewer symptoms than non-smokers, as has been found before, but were exposed to higher levels of airborne nicotine as expected. We suggest that this factor, along with the misclassification of smoking status, may have obscured an association between ETS exposure and the SBS in previous studies. An analysis of the findings after implementation of the smoking ban should provide further information on how much of the SBS is attributable to ETS in this study population.

Environmental tobacco smoke and otitis media.

Environmental tobacco smoke (secondhand smoke) is a health hazard experienced by one half to two thirds of the nation's children younger than 5 years of age. Although the role of environmental tobacco smoke in the genesis of pulmonary disease in children has been increasingly recognized, somewhat less attention has been paid to the role of environmental tobacco smoke in the development of childhood otitis. This presentation will review current data regarding environmental tobacco smoke, with a particular emphasis on its effects on the ears and eustachian tube. Current American Academy of Otolaryngology-Head and Neck Surgery Foundation, Inc. education efforts will also be discussed.