Effects Of Environmental Tobacco Smoke Exposure Research Articles

Association of environmental tobacco smoke exposure with metabolic syndrome: A longitudinal Cohort Study of 71,055 never smokers

Background and aimsEffects of environmental tobacco smoke (ETS) exposure and a change in ETS exposure status on metabolic syndrome (MetS) remain unknown. Thus, the aim of this study was to evaluate the effect of ETS exposure on MetS in self-reported and cotinine-validated never smokers. Methods and resultsFrom a large longitudinal cohort study, 71,055 cotinine-validated never smokers without MetS at baseline were included. These participants were divided into four groups (no, new, former, and continuous ETS exposure groups) based on their ETS exposure status at baseline and follow-up. The association between ETS exposure and MetS was assessed using multivariable Cox hazard regression analyses.During a median follow-up of 33 months, 15.0 cases/10,000 person-years (PY) developed MetS. Incidence rates per 10,000 PY of MetS in no, new, former, and continuous ETS exposure groups were 14.0, 18.5, 16.5, and 19.0, respectively. In multivariable Cox hazard regression analyses, the new and continuous ETS exposure groups showed increased risk of MetS compared to the no ETS exposure group (hazard ratio [95% confidence interval]: 1.35 [1.16, 1.56], p-value < 0.001 for the new ETS exposure group and 1.19 [1.06, 1.34], p-value = 0.004 for the continuous ETS exposure group). However, the former ETS exposure group did not show an increased risk of MetS (0.96 [0.88, 1.05], p-value = 0.36). ConclusionThis study showed that ETS exposure and changes in ETS exposure status over approximately three years could modify the risk of MetS, suggesting that avoidance of ETS may not increase the risk of incidence of MetS.

Sex-Specific Association between Environmental Tobacco Smoke Exposure and Asthma Severity among Adults with Current Asthma.

Background: Tobacco smoke has been associated with negative health outcomes, including those with chronic respiratory illnesses, such as asthma. This study aimed to assess the relationship between exposure to environmental tobacco smoke (ETS), as well as tobacco use (cigarette and electronic cigarettes), on asthma severity among adults with current asthma, with stratification by sex to understand potential biological sex differences. Methods: The study population consisted of Californian adults 18 years or older with self-reported physician/health care diagnosis of asthma and still having current asthma from 2020 California Health Interview Survey. All descriptive statistics and analyses were sex-stratified and survey-weighted. Crosstabulations were used to understand the association between asthma attack and ETS or firsthand smoke exposure, while binary logistic regression models were used to assess the effect of ETS exposure, current smoking status, and control variables on asthma attack in the past 12 months, with a sub-analysis among non-smoking adults with asthma. Results: Among the primary variable of interest, 35% of males and 30% of females reported ETS exposure in the past 12 months, while 13% of males and 6% of females reported being a current smoker. Past year asthma attack was reported among 43% and 55% of males and females, respectively. Among males, after adjusting for all control variables, asthma attack was significantly higher among those with ETS exposure (OR: 1.75, 95% CI: 1.01–3.02) and among current smokers (OR: 3.82, 95% CI: 1.49, 9.81). Male non-smokers with ETS exposure had a 109% higher odds of asthma attack, compared to non-exposure individuals. Conclusion: Using a population-based survey, our results highlight the ongoing burden of tobacco use and exposure particularly among males with current asthma, further corroborate the literature on the relationship between tobacco and asthma, and highlight putative sex-specific outcomes.

Environmental Tobacco Smoke Exposure and Brain Functioning Associated with Smoking Cue-Reactivity and Inhibitory Control in Nonsmoking Adolescents

Introduction: Despite its well-established negative effects, environmental tobacco smoke (ETS) exposure remains highly prevalent worldwide. ETS exposure is associated with a wide range of physical and mental health-related problems among youth, including an increased likelihood to develop nicotine dependence. Up till now, neurocognitive effects of ETS exposure are largely unknown, while such effects could explain the role of ETS exposure in the development of nicotine dependence. Therefore, this preregistered study investigated the role of current ETS exposure in brain functioning associated with smoking cue-reactivity and inhibitory control. Method: Concurrent with functional magnetic resonance imaging, nonsmoking adolescents aged 14–18 years (N = 51) performed a smoking cue-reactivity task, assessing brain functioning to smoking cues, and a Go/NoGo task measuring inhibitory control. ETS exposure was measured using a self-report questionnaire and biochemically verified. Results: No significant associations were observed between current ETS exposure and brain functioning associated with smoking cue-reactivity and inhibitory control. Conclusion: These findings suggest that low-to-moderate levels of current ETS exposure are not associated with increased salience of smoking cues or deficits in inhibitory control in nonsmoking adolescents. Longitudinal research is needed to further clarify the exact effect of lifetime ETS exposure on brain functioning, as well as research focusing on the effects of higher levels of ETS exposure.

Environmental tobacco smoke (ETS) and hyperlipidemia modified by perceived work stress.

BackgroundAccumulating evidence has shown that exposure to environmental tobacco smoke (ETS) is associated with cardiovascular diseases (CVDs) However, few studies have assessed both exposure to ETS and high-perceived work stress on hyperlipidemia. The aim of the present study is to assess the interaction effect of ETS exposure and high-perceived work stress on the risk of hyperlipidemia.MethodsA total of 11,875 middle-aged civil servants from 647 registered institutions employed by the Taiwan government were randomly selected using multistage stratified cluster sampling based on proportional probabilistic sampling. Each participant anonymously and independently filled out a web-based questionnaire and informed consent.ResultsThe prevalence of hyperlipidemia in middle-aged civil servants diagnosed by physicians was 11.5% for men and 6.1% for women. Hyperlipidemia was significantly associated with smoking, alcohol consumption, betel nut chewing, weight gain and perceived work stress. In both the obesity and smoking groups, there were consistent interaction effects of ETS exposure and perceived work stress on hyperlipidemia for middle-aged civil servants. Non-obese and non-smoking groups were more at risk for hyperlipidemia from exposure to both ETS and high-perceived work stress.ConclusionThere is an interaction effect of ETS exposure and high-perceived work stress on hyperlipidemia, regardless of obesity and smoking. It is crucial to immediately reduce ETS exposure and stressful work by enforcing smoke-free policies and reducing pressure for civil servants.

Correlation of environmental tobacco smoke to gingival pigmentation and salivary alpha amylase in young adults.

Objective:Passive smoking leads to melanin pigmentation on gingiva. However, documentation of gingival pigmentation and salivary amylase activity in passive smokers relative to the duration of exposure to environmental tobacco smoke (ETS), is incomplete and requires further investigation. Thus, this study aimed to assess effects of ETS exposure on gingival pigmentation in young adults. In addition, to correlate a number of years of exposure to an extent, the intensity of gingival pigmentation and salivary amylase activity.Materials and Methods:A total of 200 nonsmokers aged 18–35 years with a positive history of ETS exposure were recruited for the study. Duration and source of ETS were assessed using a questionnaire. Gingival pigmentation was assessed using gingival pigmentation index for the extent and Dummett oral pigmentation index for intensity. The skin color of all patients was also assessed. Pearson Chi-square test and one-way ANOVA was used to statistically analyze the data.Results:Number of years of exposure to passive smoking was highly significant to the extent and intensity of gingival pigmentation (P < 0.001). ETS from home environment was highly significant to the intensity of pigmentation. Environmental sources of ETS contributed to pigmentation as the majority of patients reported exposure from vehicles and workplace. The salivary amylase levels were inversely proportional to the duration of exposure to ETS.Conclusion:Within limitations of this cross-sectional observational study, it was concluded that there was a strong correlation between ETS exposure and gingival pigmentation. Duration of exposure was significant to an extent, the intensity of pigmentation and salivary amylase activity.

Environmental Tobacco Smoke and Atrial Fibrillation: The REasons for Geographic And Racial Differences in Stroke (REGARDS) Study.

This study examines the association between environmental tobacco smoke (ETS) exposure and atrial fibrillation (AF). We examined the cross-sectional association between ETS exposure and AF in 12,021 participants (mean age: 65 ± 9.9 years; 60% women; 40% blacks) from the REasons for Geographic And Racial Differences in Stroke study who self-identified as never smokers between 2003 and 2007. A total of 2503 (21%) participants reported ETS exposure. In a multivariate logistic regression model adjusted for sociodemographics and potential confounders, ETS exposure was significantly associated with AF (odds ratio = 1.27, 95% confidence interval = 1.08, 1.50). Our findings suggest that the harmful effects of ETS exposure extend to sustained arrhythmias such as AF.

Exposure of Neonatal Mice to Tobacco Smoke Disturbs Synaptic Proteins and Spatial Learning and Memory from Late Infancy to Early Adulthood.

Exposure to environmental tobacco smoke (ETS) in the early postnatal period has been associated with several diseases; however, little is known about the brain effects of ETS exposure during this critical developmental period or the long-term consequences of this exposure. This study investigated the effects of the early postnatal ETS exposure on both reference and working memory, synaptic proteins and BDNF from late infancy to early adulthood (P3-P73). BALB/c mice were exposed to ETS generated from 3R4F reference research cigarettes (0.73 mg of nicotine/cigarette) from P3 to P14. Spatial reference and working memory were evaluated in the Morris water maze during infancy (P20-P29), adolescence (P37-P42) and adulthood (P67-P72). Synapsin, synaptophysin, PSD95 and brain-derived neurotrophic factor (BDNF) were assessed at P15, P35 and P65 by immunohistochemistry and immunoblotting. Mice that were exposed to ETS during the early postnatal period showed poorer performance in the spatial reference memory task. Specifically, the ETS-exposed mice exhibited a significantly reduced time and distance traveled in the target quadrant and in the platform location area than the controls at all ages evaluated. In the spatial working memory task, ETS disrupted the maintenance but not the acquisition of the critical spatial information in both infancy and adolescence. ETS also induced changes in synaptic components, including decreases in synapsin, synaptophysin, PSD95 and BDNF levels in the hippocampus. Exposure to ETS in the early postnatal period disrupts both spatial reference and working memory; these results may be related to changes in synaptogenesis in the hippocampus. Importantly, most of these effects were not reversed even after a long exposure-free period.

Influence of maternal environmental tobacco smoke exposure assessed by hair nicotine levels on birth weight.

While the perinatal outcomes of active maternal smoking are well documented, results of the effects of environmental tobacco smoke (ETS) exposure during pregnancy are inconsistent. We aimed to examine the effect of ETS exposure, assessed by maternal hair nicotine levels at 35th week of gestation, on birth weight and the risk of small for gestational age (SGA) and low birth weight (LBW). A total of 871 non-smoking healthy pregnant women were recruited by one Korean hospital between 1 October 2006 and 31 July 2007. Hair samples were collected and anthropometric questionnaires administered at 35th week of gestation. The primary outcome was birth weight and secondary outcomes were the risk of babies being SGA and LBW. Log-transformed hair nicotine concentrations were inversely related with birth weight after adjusting for confounding variables (β=-0.077, p=0.037). After stratifying hair nicotine levels by tertiles (T1, low [0.0-0.28 ng/mg]; T2, medium [0.29-0.62 ng/mg]; and T3, high [0.63-5.99 ng/mg]), the mean birth weight in each groups were 3,342 g (T1) 3,296 g (T2) and 3,290 g (T3), respectively. However the difference between groups was not statistically significant by analysis of co-variance (ANCOVA) adjusting for covariates (p=0.062). In logistic regression analysis, the risk of SGA was higher in the T3 (OR=1.59, 95%CI 1.05-2.42) than in the reference group (T1), after controlling for confounding variables. The risk of low birth weight (<2,500 g, LBW) was not significantly higher (OR=1.44, 95%CI 0.95-2.19), but the risk of babies being below 3,000g birth weight was increased in the T3 group (OR=1.53, 95%CI 1.00-2.36) compared with that in the T1 group. Maternal ETS exposure during pregnancy was inversely related with birth weight. The risk of SGA increased in the highest ETS exposure group compared with in the low exposure group. To prevent ETS exposure during pregnancy, more comprehensive tobacco control policies are needed.

Environment Tobacco Smoke Exposure Affect Childhood Atopic Dermatitis Modified By TNF-α and TLR4 Polymorphisms

Although environmental tobacco smoke (ETS) exposure was associated with asthma, the effect of ETS exposure on the atopic dermatitis (AD) is unclear. TNF-α and TLR4 genetic polymorphisms interact with air pollutants and modify the development of allergic disease. We investigated the gene-environmental interaction between ETS exposure and TNF-α/TLR4 on the development of AD in children.

Australian and New Zealand Indigenous mothers' report respect for smoking bans in homes.

There is limited data about the reasons behind residential rules to reduce environmental tobacco smoke (ETS) exposure or the establishment or enforcement of such rules in Indigenous populations. We aimed to gain an understanding of smokefree rules around Australian and New Zealand (NZ) Indigenous infants. This was a qualitative study nested within a randomised controlled trial that aimed to test the efficacy of a family-centred tobacco control programme about environmental tobacco smoke (ETS) to improve the respiratory health of Indigenous infants in Australia and New Zealand. Qualitative semi-structured interviews were conducted with 26 Indigenous mothers of infants in Australia (n=7) and NZ (n=19). We asked about the presence of smokefree rules, who set the rules, how the rules were set and enforced, and presence of smokefree rules in participants' wider social circle. Interviews were audiotaped, transcribed, and inductively analysed to identify key themes. Sixty-nine percent of mothers had partners, 77% smoked and all reported some presence of smokefree rules for house and car. Three main themes were identified: strategies to minimise exposure to ETS, establishing smokefree rules in homes and cars, and, adherence and enforcement of smokefree rules. Several strategies were identified to limit children's exposure to ETS, including rules to limit exposure to third-hand smoke. Mothers extended their smokefree rules to apply to other people's houses or cars, and reported that their family and social circles also had smokefree rules. The main reason for having smokefree rules was for the health of their children. Rules were most commonly set by the mother, often jointly with their partner. Few mothers reported challenges or problems with other people adhering to the smokefree rules. Women tried very hard to, and believed that they were effective in, protecting their children from the harmful effects of ETS exposure. In this context, health professionals need to emphasise smoking cessation in parents, so that children are maximally protected from ETS exposure.

Environmental tobacco smoke in the early postnatal period induces impairment in brain myelination.

Environmental tobacco smoke (ETS) is associated with high morbidity and mortality, mainly in children. However, few studies focus on the brain development effects of ETS exposure. Myelination mainly occurs in the early years of life in humans and the first three postnatal weeks in rodents and is sensitive to xenobiotics exposure. This study investigated the effects of early postnatal ETS exposure on myelination. BALB/c mice were exposed to ETS generated from 3R4F reference research cigarettes from the third to the fourteenth days of life. The myelination of nerve fibers in the optic nerve by morphometric analysis and the levels of Olig1 and myelin basic protein (MBP) were evaluated in the cerebellum, diencephalon, telencephalon, and brainstem in infancy, adolescence, and adulthood. Infant mice exposed to ETS showed a decrease in the percentage of myelinated fibers in the optic nerve, compared with controls. ETS induced a decrease in Olig1 protein levels in the cerebellum and brainstem and an increase in MBP levels in the cerebellum at infant. It was also found a decrease in MBP levels in the telencephalon and brainstem at adolescence and in the cerebellum and diencephalon at adulthood. The present study demonstrates that exposure to ETS, in a critical phase of development, affects the percentage of myelinated fibers and myelin-specific proteins in infant mice. Although we did not observe differences in the morphological analysis in adolescence and adulthood, there was a decrease in MBP levels in distinctive brain regions suggesting a delayed effect in adolescence and adulthood.

Awareness of an obstetric population about environmental tobacco smoking

Background and Objectives:The reported rate of women's smoking is typically low. However, many pregnant women are exposed to environmental tobacco smoke (ETS), which could affect their own health and the health of their growing fetus. The aim of this study was to estimate the magnitude of the problem of exposure to ETS and assess the awareness of postpartum women to ETS and its possible effects.Designs and Settings:This was a cross-sectional study conducted on 1182 postpartum women at a university hospital in Riyadh, Saudi Arabia, between 1st January and 30th June, 2012.Materials and Methods:A structured questionnaire was used for data collection. Factors associated with the level of understanding of the possible effects of ETS exposure were analyzed.Results:The majority of the participating women knew that exposure to ETS had adverse effects on maternal and fetal health (>80%), but their knowledge of the specific effects on fetal health was limited. The level of mothers’ education was found to be associated with better knowledge of effects on mother and fetal health (P < 0.01).Conclusion:This study revealed that pregnant women in our sample had limited knowledge of the specific effects of ETS on fetal health. This shortcoming in knowledge needs to be addressed by improving health.

Return on Investment of an Asthma Education Program

McQuaid EL, Garro A, Seifer R, et al. Integrating asthma education and smoking cessation for parents: financial return on investment. Pediatr Pulmonol. 2012; 47(10): 950– 955; doi: 10.1002/ppul.22559Investigators from Brown University and the University of California, Berkeley sought to determine the financial return on investment (ROI) of the Parents of Asthmatics Quit Smoking (PAQS) program. PAQS is a program for caregivers who are smokers and have a child with asthma. As part of the program, nurses provide asthma education and smoking cessation counseling in 3 home visits. Investigators calculated the ROI by analyzing claims data 12 months pre-enrollment and post-completion of the intervention in a subsample of PAQS participants who were on a Medicaid managed care plan. Total billable costs (TBC) were determined by summing the costs of short-acting β-agonists, controller medications, emergency department (ED) visits, hospitalizations, and outpatient visits for asthma. The cost of delivering the PAQS intervention was calculated by summing direct expenditures, start-up costs, and elements of overhead. The primary outcome was ROI, calculated as ([TBC pre-PAQS – TBC post-PAQS] – Intervention Costs) / Intervention Costs, for the total sample and for 3 subgroups (children <6 years old, children 6-18 years old, and children with moderate to severe persistent asthma).The analysis included 224 PAQS participant children. The cost of the PAQS intervention in this sample was $34,481. Postintervention, there was a significant increase in mean annual fills for β-agonist and controller medications and a corresponding increase in medication costs per participant. However, there was also a significant decrease in health care utilization including emergency room visits, hospitalizations, and outpatient visits postintervention. The ROI for the total sample was –21.8%. However, for children <6 years old it was 106.9%, and for children with moderate to severe persistent asthma, it was 6.9%. The ROI was –150.3% for children 6 to 18 years old.The authors conclude that while the overall ROI of PAQS was negative, PAQS yielded a highly positive ROI for children <6 years old.Adverse effects of tobacco smoke exposure on children’s health have been well documented.1 There has been a steady increase in the number of studies showing an association of environmental tobacco smoke (ETS) exposure and asthma. As a result, the Expert Panel Report-3 (EPR-3) 2007 Asthma Guidelines, citing this supporting evidence,2 published a longer statement regarding education on smoking cessation compared to EPR-2 (1997, revised in 2002).3 EPR-3 recommends assessing ETS exposure in the household and referring parents and caretakers who smoke to smoking cessation programs.A study prior to PAQS showed that reduced ETS exposure to asthmatic children in an urban setting was associated with a decrease in asthma-related exacerbations.4 Consequently, there has been substantial effort to develop effective asthma education and smoking cessation programs. A home-based educational program model is costly compared to the standard education given at patient encounters, yet these programs offer the benefit of reaching out to caregivers who may have limited access for follow-up. A recent Cochrane review, however, concluded that home-based educational programs are not more effective than standard educational programs given at medical visits.5 Furthermore, another Cochrane review concluded that there is inconclusive evidence that smoking cessation programs for caregivers are effective.6This study lends support to a combined smoking cessation and asthma program in a home-based setting, especially for children under 6 years old. Younger patients utilize more health care, so stand to benefit more. It is also possible parents of young children are more motivated. A recent study found caregivers of younger children seemed to be more receptive to an asthma education program and more likely to complete the intervention.7 Perhaps early intervention with parents of young children should be our focus: it is cost-beneficial and can help curtail the detrimental effects of ETS exposure on asthma severity long-term.The ROI analysis in this study is an elegant way to assess a program such as PAQS; we need more studies like this. However, the positive results (limited as they are) seem more related to asthma management education than counseling on smoking cessation.

Asthma severity, polymorphisms in 20p13 and their interaction with tobacco smoke exposure

We investigated the association between genetic variation in chromosomal region 20p13-p12 (ADAM33 and flanking genes ATRN, GFRA4, SIGLEC1 and HSPA12B) and asthma. Amongst asthmatics, we then investigated the association between genetic variants and asthma severity. We evaluated the effect of environmental tobacco smoke (ETS) exposure in the context of genetic variants. In a case-control study, we recruited 423 asthmatic children and 414 non-asthmatic controls (age 5-18yr). Amongst asthmatics, we measured lung function and extracted data on hospitalisation for asthma exacerbation from medical records. Early-life ETS exposure was assessed by questionnaire. We included 85 single-nucleotide polymorphisms (SNPs) in the analysis. Seventeen SNPs were significantly associated with asthma; one (rs41534847 in ADAM33) remained significant after correction for multiple testing. Thirty-six SNPs were significantly associated with lung function, of which 15 (six ARTN, three ADAM33, five SIGLEC1 and one HSPA12B) remained significant after correction. We observed a significant interaction between 23 SNPs and early-life ETS exposure in relation to lung function measures. For example, for rs512625 in ADAM33, there was significant interaction with ETS exposure in relation to hospitalisations (p(int) =0.02) and lung function (p(int) =0.03); G-allele homozygotes had a 9.15-fold [95% CI 2.28-36.89] higher risk of being hospitalized and had significantly poorer lung function if exposed to ETS, with no effect of ETS exposure amongst A-allele carriers. We demonstrated several novel significant interactions between polymorphisms in 20p13-p12 and early-life ETS exposure with asthma presence and, amongst asthmatics, a significant association with the severity of their disease.

Household Environmental Tobacco Smoke Exposure and Respiratory Health in School Age Children

SUMMARY In the recent years the exposure to environmental tobacco smoke (ETS) has been an important public health hazard, especially in Serbia, a country with too many smokers. A common component of tobacco smoke is particulate matter less than 10μm in aerodynamic diameter (PM10), which is considered to be the most dangerous air pollutant for health. The aim of this paper was to investigate the association between respiratory symptoms and illnesses in schoolchildren in relation to their environmental tobacco smoke exposure. We conducted an epidemiological study that included 708 participants (49.15 % male) aged 11-14 years from Niš, Serbia. The children were surveyed by original structured questionnaire, based on the instrument developed for similar investigations. Data about the prevalence of respiratory symptoms in the last 12-month period of life and lifetime prevalence of respiratory illnesses were obtained. The questionnaire also included items about other indoor environmental determinants. Tobacco smoke was the most prevalent source of indoor air pollution at children’s home (60.73%). We found a significant association between ETS exposure and increased prevalence of dyspnea, wheezing, bronchitis and asthma among children. It is necessary to inform parents in Serbia on the health effects of ETS exposure during childhood and to encourage them to change smoking habits in order to protect their children from ETS exposure at home.

Exposure of Rats to Environmental Tobacco Smoke during Cerebellar Development Alters Behavior and Perturbs Mitochondrial Energetics

Background: Environmental tobacco smoke (ETS) exposure is linked to developmental deficits and disorders with known cerebellar involvement. However, direct biological effects and underlying neurochemical mechanisms remain unclear.Objectives: We sought to identify and evaluate underlying neurochemical change in the rat cerebellum with ETS exposure during critical period development.Methods: We exposed rats to daily ETS (300, 100, and 0 µg/m3 total suspended particulate) from postnatal day 8 (PD8) to PD23 and then assayed the response at the behavioral, neuroproteomic, and cellular levels.Results: Postnatal ETS exposure induced heightened locomotor response in a novel environment on par initially with amphetamine stimulation. The cerebellar mitochondrial subproteome was significantly perturbed in the ETS-exposed rats. Findings revealed a dose-dependent up-regulation of aerobic processes through the modification and increased translocation of Hk1 to the mitochondrion with corresponding heightened ATP synthase expression. ETS exposure also induced a dose-dependent increase in total Dnm1l mitochondrial fission factor; although more active membrane-bound Dnm1l was found at the lower dose. Dnm1l activation was associated with greater mitochondrial staining, particularly in the molecular layer, which was independent of stress-induced Bcl-2 family dynamics. Further, electron microscopy associated Dnm1l-mediated mitochondrial fission with increased biogenesis, rather than fragmentation.Conclusions: The critical postnatal period of cerebellar development is vulnerable to the effects of ETS exposure, resulting in altered behavior. The biological effect of ETS is underlain in part by a Dnm1l-mediated mitochondrial energetic response at a time of normally tight control. These findings represent a novel mechanism by which environmental exposure can impact neurodevelopment and function.

Association of maternal diabetes and child asthma

Perinatal programming is an emerging theory for the fetal origins of chronic disease. Maternal asthma and environmental tobacco smoke (ETS) are two of the best-known triggers for the perinatal programming of asthma, while the potential role of maternal diabetes has not been widely studied. To determine if maternal diabetes is associated with child asthma, and if so, whether it modifies the effects of ETS exposure and maternal asthma. We studied 3,574 Canadian children, aged 7-8 years, enrolled in a population-based birth cohort. Standardized questionnaires were completed by the children's parents, and data were analyzed by multivariable logistic regression. Asthma was reported in 442 children (12.4%). Compared to those without asthma, asthmatic children were more likely to have mothers (P = 0.003), but not fathers (P = 0.89), with diabetes. Among children without maternal history of diabetes, the likelihood of child asthma was 1.4-fold higher in those exposed to ETS (adjusted odds ratio, 1.40; 95% confidence interval, 1.13-1.73), and 3.6-fold higher in those with maternal asthma (3.59; 2.71-4.76). Among children born to diabetic mothers, these risks were amplified to 5.7-fold (5.68; 1.18-27.37) and 11.3-fold (11.30; 2.26-56.38), respectively. In the absence of maternal asthma or ETS, maternal diabetes was not associated with child asthma (0.65, 0.16-2.56). Our findings suggest that maternal diabetes may contribute to the perinatal programming of child asthma by amplifying the detrimental effects of ETS exposure and maternal asthma.

Maternal diabetes amplifies the influence of maternal asthma and smoke exposure on the development of asthma in offspring

Background Perinatal programming is an emerging theory for the fetal origins of chronic disease. Maternal asthma and environmental tobacco smoke (ETS) are two of the bestknown triggers for the perinatal programming of asthma, while the potential role of maternal diabetes has not been widely studied. The goal of this study was to determine if maternal diabetes contributes to the perinatal programming of asthma, and if so, whether its effect is additive or synergistic with respect to ETS exposure and maternal asthma. Methods We studied 3,574 Canadian children, aged 7-8 yr, enrolled in a population-based birth cohort. Standardized questionnaires were completed by the children’s parents, and data were analyzed by multivariate logistic regression. Results Asthma was reported in 442 children (12.4%). Asthmatic children were more likely to have mothers, but not fathers, with diabetes. In children without maternal history of diabetes, ETS exposure increased the risk of child asthma by 1.4-fold (adjusted odds ratio, 1.40; 95% confidence interval, 1.13-1.73), while maternal asthma increased risk by 3.6-fold (3.59; 2.71-4.76). In children born to diabetic mothers, these effects were amplified to 5.7-fold (5.68; 1.18-27.37) and 11.3-fold (11.30; 2.2656.38), respectively. There was no independent effect of maternal diabetes after adjusting for maternal asthma and ETS exposure (OR 0.65, 95%CI 0.16-2.56). Conclusions Maternal diabetes contributes to the perinatal programming of child asthma by amplifying the detrimental effects of ETS exposure and maternal asthma.

Environmental tobacco smoke exposure increases Mycobacterium tuberculosis infection risk in children.

Data on the association between exposure to environmental tobacco smoke (ETS) and Mycobacterium tuberculosis infection in children are limited. To examine the dose-response effect of ETS exposure on the risk of M. tuberculosis infection in children in a high tuberculosis (TB) burden setting. This cross-sectional study included healthy South African children from impoverished urban communities. Data were collected on household ETS and M. tuberculosis exposure, demographics, socio-economic and anthropometric data, M. tuberculosis infection, human immunodeficiency virus and TB disease status. Among 196 children (median age 6.8 years, range 0.3-15.9), 97 (49.5%) were M. tuberculosis - i nfected (tuberculin skin test [TST] ≥ 10 mm) and 128 (65.3%) reported ETS exposure; of these, 81/128 (63.3%) were exposed to ≥ 2 household smokers. The presence of ≥ 2 household smokers was associated with M. tuberculosis infection in univariate analysis, irrespective of TST cut-off point. In analysis adjusting for M. tuberculosis exposure, socio-economic status, age and previous TB treatment, ETS exposure remained associated with M. tuberculosis infection. In univariate and multivariate analysis, pack-years of exposure were associated with risk of TB infection. Exposure to ETS is associated with M. tuberculosis infection in children after adjustment for multiple variables, with a dose-response relationship between the degree of ETS exposure and risk of infection. Public health interventions to reduce exposure to tobacco smoke among children in high TB burden settings are urgently needed.

Laryngeal cancer and passive smoking: the neglected factor?

In the present paper we investigate the relationship of environmental tobacco smoke (ETS) exposure to laryngeal cancer. 209 patients who were diagnosed with laryngeal cancer from 2000 to 2009 at the University Hospital of Patras, Western Greece, were reviewed with regard to patient age, disease stage at presentation, tumor differentiation, tobacco product use, alcohol consumption, occupation, and ETS exposure in the working environment. Pearson Chi-square method was used to determine the effect of ETS exposure on cancer stage, TNM classification and tumor differentiation in the dichotomized population (exposed vs. not exposed) and in groups of low, medium and high ETS exposure. ETS exposure in the working environment was found to significantly affect overall disease stage and T stage (p < 0.01) both in the dichotomic analysis and the group analysis. Minor significance was also noted for N stage (p = 0.047) in the exposure group analysis. Our data suggest that occupational ETS exposure presents a contributing risk factor for laryngeal cancer that requires further research to determine its significance.