Related Articles

Objective

Associations between single-nucleotide polymorphisms in the β2-adrenergic receptor gene and asthma and wheeze have been inconsistent. Recent studies indicated that tobacco smoke affects β2-adrenergic receptor gene expression and associations of β2-adrenergic receptor gene variants with asthma in adults. We aimed to investigate the joint effects of in utero and childhood secondhand tobacco smoke exposure and 2 well-characterized functional single-nucleotide polymorphisms (Arg16Gly and Glu27Gln) of β2-adrenergic receptor gene on asthma and wheezing in 3128 non-Hispanic and Hispanic white children of the Children's Health Study.

Methods

We fitted logistic regression models to estimate odds ratios and 95% confidence intervals for the independent and joint effects of these single-nucleotide polymorphisms and in utero and secondhand tobacco smoke exposure on asthma and wheeze outcomes.

Results

Exposures to in utero maternal smoking and secondhand tobacco smoke were associated with wheezing. Children who were homozygous for the Arg16 allele and were exposed to maternal smoking in utero were at a threefold increased risk for lifetime wheeze compared with children who were unexposed and had at least 1 Gly16 allele. We found similar joint effects of secondhand tobacco smoke and Arg16Gly with wheezing. The risk for lifetime, current, and nocturnal wheeze increased with the number of smokers at home among Arg16 homozygous children. The results were consistent in 2 cohorts of children recruited in 1993 and 1996. Diplotype-based analyses were consistent with the single-nucleotide polymorphism–specific results. No associations were found for Glu27Gln.

Conclusions

Both in utero and childhood exposure to tobacco smoke were associated with an increased risk for wheeze in children, and the risks were greater for children with the Arg16Arg genotype or 2 copies of the Arg16–Gln27 diplotype. Exposures to smoking need to be taken into account when evaluating the effects of β2-adrenergic receptor gene variants on respiratory health outcomes.

We hypothesized that the joint effect of genetic propensity to asthma and exposure to environmental tobacco smoke on the risk of childhood asthma is greater than expected on the basis of their independent effects. We performed a population-based 4-year cohort study of 2,531 children born in Oslo, Norway. We collected information on the child's health and environmental exposures at birth and when the child was 6, 12, 18, and 24 months and 4 years of age. The outcomes of interest were bronchial obstruction during the first 2 years and asthma at the age of 4 years. Parental atopy was defined as a history of maternal or paternal asthma or hay fever. Exposure to environmental tobacco smoke was defined on the basis of questionnaire information on household smokers at birth. In logistic regression analysis adjusting for confounding, parental atopy alone increased the risk of bronchial obstruction [odds ratio 1.62; 95% confidence interval (CI) 1.10-2.40] and asthma (1.66; 95% CI, 1.08-2.54). In children without parental atopy, there was little effect of exposure to environmental tobacco smoke on bronchial obstruction (1.29; 95% CI, 0.88-1.89) and asthma (0.84; 95% CI, 0.53-1.34). The presence of parental atopy and exposure had a substantial effect both on bronchial obstruction (2.88; 95% CI, 1.91-4.32) and asthma (2.68; 95% CI, 1.70-4.22). The results are consistent with the hypothesized joint effect of parental atopy and exposure to environmental tobacco smoke. This phenomenon--denoted as effect modification of environmental exposure by genetic constitution, or gene by environment interaction--suggests that some genetic markers could indicate susceptibility to environmental factors.

Background

Although studies show that maternal smoking during pregnancy increases the risks of respiratory outcomes in childhood, evidence concerning the effects of household environmental tobacco smoke (ETS) exposure remains inconsistent.

Methods

We conducted a population-based study comprised of 5,019 seventh and eighth-grade children in 14 Taiwanese communities. Questionnaire responses by parents were used to ascertain children's exposure and disease status. Logistic regression models were fitted to estimate the effects of ETS exposures on the prevalence of asthma, wheeze, and bronchitic symptoms.

Results

The lifetime prevalence of wheeze was 11.6% and physician-diagnosed asthma was 7.5% in our population. After adjustment for potential confounders, in utero exposure showed the strongest effect on all respiratory outcomes. Current household ETS exposure was significantly associated with increased prevalence of active asthma, ever wheeze, wheeze with nighttime awakening, and bronchitis. Maternal smoking was associated with the increased prevalence of a wide range of wheeze subcategories, serious asthma, and chronic cough, but paternal smoking had no significant effects. Although maternal smoking alone and paternal smoking alone were not independently associated with respiratory outcomes, joint exposure appeared to increase the effects. Furthermore, joint exposure to parental smoking showed a significant effect on early-onset asthma (OR, 2.01; 95% CI, 1.00-4.02), but did not show a significant effect on late-onset asthma (OR, 1.17; 95% CI, 0.36-3.87).

Conclusion

We concluded that prenatal and household ETS exposure had significant adverse effects on respiratory health in Taiwanese children.

Background

Polymorphisms in the proinflammatory cytokine genes tumor necrosis factor-α (TNF) and lymphotoxin-α (LTA, also called TNF-β) have been associated with asthma and atopy in some studies. Parental smoking is a consistent risk factor for childhood asthma. Secondhand smoke and ozone both stimulate TNF production.

Objectives

Our goal was to investigate whether genetic variation in TNF and LTA is associated with asthma and atopy and whether the association is modified by parental smoking in a Mexican population with high ozone exposure.

Methods

We genotyped six tagging single nucleotide polymorphisms (SNPs) in TNF and LTA, including functional variants, in 596 nuclear families consisting of asthmatics 4–17 years of age and their parents in Mexico City. Atopy was determined by skin prick tests.

Results

The A allele of the TNF-308 SNP was associated with increased risk of asthma [relative risk (RR) = 1.54; 95% confidence interval (CI), 1.04–2.28], especially among children of non-smoking parents (RR = 2.06; 95% CI, 1.19–3.55; p for interaction = 0.09). Similarly, the A allele of the TNF-238 SNP was associated with increased asthma risk among children of nonsmoking parents (RR = 2.21; 95% CI, 1.14–4.30; p for interaction = 0.01). LTA SNPs were not associated with asthma. Haplotype analyses reflected the single SNP findings in magnitude and direction. TNF and LTA SNPs were not associated with the degree of atopy.

Conclusions

Our results suggest that genetic variation in TNF may contribute to childhood asthma and that associations may be modified by parental smoking.

BACKGROUND—An increase in the prevalence of obesity and asthma over recent decades has been reported in affluent societies. Both overweight and obesity have been shown to be inversely related to having been breastfed, which is also a potential protective factor against childhood atopic diseases. The aim of this analysis was to explore the relation of body mass index (BMI) to asthma and atopy in a large representative sample of the United States population.
METHODS—Children aged 4-17 years were included in the NHANES III survey. Prevalences of atopic diseases and potential confounding factors such as exposure to environmental tobacco smoke, birth weight, breast feeding, and household size were assessed using structured interviews with parents. Height and weight were measured, and BMI was calculated as kg/m2 and transformed into Z scores. Children underwent skin prick tests for atopy to a battery of food and inhalant allergens.
RESULTS—The prevalence of asthma (8.7% v 9.3% v 10.3% v 14.9%, p=0.0001) and atopy (48.6% v 50.5% v 53.0% v 53.2%, p=0.05) rose significantly with increasing quartiles of BMI. After adjustment for confounders, a significant positive association between BMI and asthma remained (adjusted OR 1.77, 95% confidence interval 1.44 to 2.19 between the highest and lowest quartiles of BMI), whereas no independent relation between BMI and atopy was evident. No effect modification by sex or ethnic group was seen.
CONCLUSIONS—The effects of increased BMI on asthma may be mediated by mechanical properties of the respiratory system associated with obesity or by upregulation of inflammatory mechanisms rather than by allergic eosinophilic inflammation of the airway epithelium.



Rationale: Although involuntary exposure to maternal smoking during the in utero period and to secondhand smoke are associated with occurrence of childhood asthma, few studies have investigated the role of active cigarette smoking on asthma onset during adolescence.

Objectives: To determine whether regular smoking is associated with the new onset of asthma during adolescence.

Methods: We conducted a prospective cohort study among 2,609 children with no lifetime history of asthma or wheezing who were recruited from fourth- and seventh-grade classrooms and followed annually in schools in 12 southern California communities. Regular smoking was defined as smoking at least seven cigarettes per day on average over the week before and 300 cigarettes in the year before each annual interview. Incident asthma was defined using new cases of physician-diagnosed asthma.

Measurements and Main Results: Regular smoking was associated with increased risk of new-onset asthma. Children who reported smoking 300 or more cigarettes per year had a relative risk (RR) of 3.9 (95% confidence interval [95% CI], 1.7–8.5) for new-onset asthma compared with nonsmokers. The increased risk from regular smoking was greater in nonallergic than in allergic children. Regular smokers who were exposed to maternal smoking during gestation had the largest risk from active smoking (RR, 8.8; 95% CI, 3.2–24.0).

Conclusions: Regular smoking increased risk for asthma among adolescents, especially for nonallergic adolescents and those exposed to maternal smoking during the in utero period.

Objectives

To estimate the prevalence of tobacco consumption and secondhand smoke (SHS) exposure in private cars, commercial vehicles and taxis in the city of Barcelona in Spain.

Design setting and participants

We carried out an observational cross-sectional study in 2011. We selected a systematic sample of 2442 private cars, commercial vehicles and taxis on 40 public roads regulated by traffic lights in all 10 districts of Barcelona. We calculated the prevalence rates and 95% CIs of smoking and SHS exposure in cars, and the corresponding ORs adjusting for the potential confounding variables.

Results

The prevalence of tobacco consumption was 5.5% (95% CI 4.6% to 6.4%) and was greater for commercial vehicles (9.8%; 95% CI 7.1% to 12.5%). The prevalence of SHS exposure was 5.2% (95% CI 3.8% to 6.6%) and 2.2% (95% CI 0.5% to 3.9%) of passengers under 14 years of age were exposed to SHS in vehicles.

Conclusions

This study highlights the need to promote public health measures aimed at reducing tobacco consumption in vehicles, especially in the presence of children, as well as enforcement of the current Spanish law against smoking in commercial vehicles and taxis.

Article summary

Article focus

Tobacco consumption and secondhand smoke (SHS) exposure in vehicles should be targeted because of the high concentrations of SHS due to the confined environment.

Tobacco consumption while driving can also increase the risk of traffic accidents due to driver distraction.

Few studies have used direct observation to examine the consumption of tobacco and SHS exposure in vehicles.

Key messages

Reducing smoking in vehicles in the presence of children must be prioritised.

Smoking laws should be enforced in commercial vehicles and taxis.

Smoking in vehicles should be recognised by legislation as a distraction.

Strengths and limitations of this study

The main limitation of this study is the inherent observer bias, especially as regards variables such as age, where physical appearance can result in misclassification by the observer.

Obtaining a truly random and representative sample of vehicles in circulation in a city is difficult.

This observational study avoids the information bias generated by the use of self-reported questionnaires.

A pilot study found that direct observational studies are useful for monitoring smoking by motor vehicle drivers.

Background

Studies on the associations between smoking and allergic diseases have mostly focused on asthma. Epidemiological studies in adults on the effects of smoking on allergic diseases other than asthma, such as eczema and rhinoconjunctivitis, have been limited, and the information that is available has been inconsistent. The aim of this study was to investigate the association between smoking status and environmental tobacco smoke (ETS) exposure and the prevalence of allergic diseases.

Methods

Study subjects were 1743 pregnant Japanese women. The definitions of wheeze and asthma were based on criteria from the European Community Respiratory Health Survey whereas those of eczema and rhinoconjunctivitis were based on criteria from the International Study of Asthma and Allergies in Childhood. Adjustment was made for age; region of residence; family history of asthma, atopic eczema, and allergic rhinitis; household income; and education.

Results

Compared with never smoking, current smoking and ≥ 4 pack-years of smoking were independently positively associated with the prevalence of wheeze. There were no associations between smoking status and the prevalence of asthma, eczema, or rhinoconjunctivitis. When subjects who had never smoked were classified into four categories based on the source of ETS exposure (never, only at home, only at work, and both), exposure occurring both at home and at work was independently associated with an increased prevalence of two outcomes: wheeze and rhinoconjunctivitis. No relationships were observed between exposure to ETS and the prevalence of asthma or eczema.

Conclusions

Our results provide evidence that current smoking and ETS exposure may increase the likelihood of wheeze. The possibility of a positive association between ETS exposure and rhinoconjunctivitis was also suggested.

BACKGROUND:

The effects of in utero tobacco smoke exposure on childhood respiratory health have been investigated, and outcomes have been inconsistent.

OBJECTIVE:

To determine if in utero tobacco smoke exposure is associated with childhood persistent asthma in Mexican, Puerto Rican, and black children.

PATIENTS AND METHODS:

There were 295 Mexican, Puerto Rican, and black asthmatic children, aged 8 to 16 years, who underwent spirometry, and clinical data were collected from the parents during a standardized interview. The effect of in utero tobacco smoke exposure on the development of persistent asthma and related clinical outcomes was evaluated by logistic regression.

RESULTS:

Children with persistent asthma had a higher odds of exposure to in utero tobacco smoke, but not current tobacco smoke, than did children with intermittent asthma (odds ratio [OR]: 3.57; P = .029). Tobacco smoke exposure from parents in the first 2 years of life did not alter this association. Furthermore, there were higher odds of in utero tobacco smoke exposure in children experiencing nocturnal symptoms (OR: 2.77; P = .048), daily asthma symptoms (OR: 2.73; P = .046), and emergency department visits (OR: 3.85; P = .015) within the year.

CONCLUSIONS:

Exposure to tobacco smoke in utero was significantly associated with persistent asthma among Mexican, Puerto Rican, and black children compared with those with intermittent asthma. These results suggest that smoking cessation during pregnancy may lead to a decrease in the incidence of persistent asthma in these populations.

Summary

Maternal smoking during pregnancy is associated with increased risk of childhood overweight body mass index (BMI). Less is known about the association between prenatal secondhand tobacco smoke (SHS) exposure and childhood BMI. We followed 292 mother-child dyads from early pregnancy to 3 years of age. Prenatal tobacco smoke exposure during pregnancy was quantified using self-report and serum cotinine biomarkers. We used linear mixed models to estimate the association between tobacco smoke exposure and BMI at birth, 4 weeks, and 1, 2, and 3 years. During pregnancy, 15% of women reported SHS exposure and 12% reported active smoking, but 51% of women had cotinine levels consistent with SHS exposure and 10% had cotinine concentrations indicative of active smoking. After adjustment for confounders, children born to active smokers had higher BMI at 2 and 3 years of age (self-report or serum cotinine), compared to unexposed children. Children born to women with prenatal serum cotinine concentrations indicative of SHS exposure had higher BMI at 2 (Mean Difference [MD]:0.3; 95% confidence interval [CI]:−0.1, 0.7) and 3 (MD:0.4; [0, 0.8]) years compared to unexposed children. Using self-reported prenatal exposure resulted in non-differential exposure misclassification of SHS exposures that attenuated the association between SHS exposure and BMI compared to serum cotinine concentrations. These findings suggest active and secondhand prenatal tobacco smoke exposure may be related to an important public health problem in childhood and later life. In addition, accurate quantification of prenatal secondhand tobacco smoke exposures is essential to obtaining valid estimates.

Parental, particularly maternal, smoking increases the risk of childhood allergic asthma and infection. Similarly, in a murine allergic asthma model, prenatal plus early postnatal exposure to secondhand cigarette smoke (SS) exacerbates airway hyperreactivity and Th2 responses in the lung. However, the mechanism and contribution of prenatal versus early postnatal SS exposure on allergic asthma remains unresolved. To identify the effects of prenatal and/or early postnatal SS on allergic asthma, BALB/c dams and their offspring were exposed gestationally and/or 8–10 weeks post-birth to filtered air or SS. Prenatal, but not postnatal SS strongly increased methacholine and allergen (Aspergillus)-induced airway resistance, Th2-cytokines levels and atopy, and activated the Th2 polarizing pathway GATA3/Lck/ERK1/2/STAT6. Either prenatal and/or early postnatal SS downregulated the Th1-specific transcription factor T-bet and, surprisingly, in spite of high levels of IL-4/IL-13, dramatically blocked the allergen-induced mucous cell metaplasia, airway mucus formation, and the expression of mucus-related genes/proteins: Muc5ac, GABAA-receptors, and SPDEF. Given that SS/nicotine exposure of normal adult mice promotes mucus formation, the results suggest that fetal and neonatal lung are highly sensitive to cigarette smoke. Thus, while the gestational SS promotes Th2 polarization/allergic asthma, it may also impair and/or delay the development of fetal and neonatal lung, affecting mucociliary clearance and Th1 responses. Together, this may explain the increased susceptibility of children from smoking parents to allergic asthma and childhood respiratory infections.

Introduction:

Secondhand smoke (SHS) causes significant disease and death. A person’s home represents a prominent source of SHS, and the potential for exposure is elevated among those who live in close proximity to smokers in multiunit housing (MUH). This study assessed the prevalence and predictors of SHS exposure and smoke-free policy support among MUH residents.

Methods:

Data were obtained from 5,936 MUH residents who participated in the New York State Adult Tobacco Survey between May 2007 and May 2009. Bivariate analyses were used to assess the prevalence of smoke-free home policies, SHS incursions, and support for smoke-free policies. Logistic regression was used to identify predictors of these measures while adjusting for gender, age, ethnicity, education, region, children in household, and housing type.

Results:

A total of 73.1% of respondents reported a personal smoke-free home policy in their home. Among these individuals, 46.2% indicated that SHS has ever entered their home in the past year, while 9.2% reported daily incursions. Overall, a majority of respondents (55.6%) support a policy that bans smoking in all areas of their building, including residential units; support was significantly higher among ethnic minorities and individuals who reside with children.

Discussion:

Nearly half of New York MUH residents with a smoke-free home policy have experienced a SHS incursion in their home. Since a majority of MUH residents support smoke-free policies and nearly three quarters already prohibit smoking in their home, opportunities exist for initiatives to promote smoke-free building policies.

Background

Exposure to secondhand smoke during adulthood has detrimental health effects, including increased lung cancer risk. Compared with adults, children may be more susceptible to secondhand smoke. This susceptibility may be exacerbated by alterations in inherited genetic variants of innate immunity genes. We hypothesized a positive association between childhood secondhand smoke exposure and lung cancer risk that would be modified by genetic polymorphisms in the mannose binding lectin-2 (MBL2) gene resulting in well-known functional changes in innate immunity.

Methods

Childhood secondhand smoke exposure and lung cancer risk was assessed among men and women in the ongoing National Cancer Institute-Maryland Lung Cancer (NCI-MD) study, which included 624 cases and 348 controls. Secondhand smoke history was collected via in-person interviews. DNA was used for genotyping the MBL2 gene. To replicate, we used an independent case-control study from Mayo Clinic consisting of 461 never smokers, made up of 172 cases and 289 controls. All statistical tests were two-sided.

Results

In the NCI-MD study, secondhand smoke exposure during childhood was associated with increased lung cancer risk among never smokers [odds ratio (OR), 2.25; 95% confidence interval (95% CI), 1.04-4.90]. This was confirmed in the Mayo study (OR, 1.47; 95% CI, 1.00-2.15). A functional MBL2 haplotype associated with high circulating levels of MBL and increased MBL2 activity was associated with increased lung cancer risk among those exposed to childhood secondhand smoke in both the NCI-MD and Mayo studies (OR, 2.52; 95% CI, 1.13-5.60, and OR, 2.78; 95% CI, 1.18-3.85, respectively).

Conclusions

Secondhand smoke exposure during childhood is associated with increased lung cancer risk among never smokers, particularly among those possessing a haplotype corresponding to a known overactive complement pathway of the innate immune system.

Airway hyperreactivity (AHR), lung inflammation, and atopy are clinical signs of allergic asthma. Gestational exposure to cigarette smoke (CS) markedly increases the risk for childhood allergic asthma. Muscarinic receptors regulate airway smooth muscle tone, and asthmatics exhibit increased AHR to muscarinic agonists. We have previously reported that in a murine model of bronchopulmonary aspergillosis maternal exposure to mainstream CS increases AHR after acute intratracheal administration of Aspergillus fumigatus extract (Af). However, the mechanism by which gestational CS induces allergic asthma is unclear. We now show for the first time that, compared to controls, mice exposed prenatally to secondhand CS exhibit increased lung inflammation (predominant infiltration by eosinophils and polymorphs), atopy, and airway resistance, and produce proinflammatory cytokines (IL-4, IL-5, IL-6, and IL-13, but not IL-2 or IFN-γ). These changes, which occur only after an allergen (Af) treatment, are correlated with marked upregulated lung expression of M1, M2, and M3 muscarinic receptors and phosphodiesterase-4D5 (PDE4D5) isozyme. Interestingly, the PDE4-selective inhibitor rolipram attenuates the increase in AHR, muscarinic receptors, and PDE4D5, but fails to downregulate lung inflammation, Th2 cytokines, or serum IgE levels. Thus, the fetus is extraordinarily sensitive to CS, inducing allergic asthma after postnatal exposure to allergens. While the increased AHR might reflect increased PDE4D5 and muscarinic receptor expression, the mechanisms underlying atopy and lung inflammation are unrelated to the PDE4 activity. Thus, PDE4 inhibitors might ease AHR, but are unlikely to attenuate lung inflammation and atopy associated with childhood allergic asthma.

Background

Dietary fat exerts numerous complex effects on proinflammatory and immunologic pathways. Several epidemiological studies have examined the relationships between intake of fatty acids and/or foods high in fat and allergic rhinitis, but have provided conflicting findings. The current cross-sectional study investigated such relationships in Japan.

Methods

Study subjects were 1745 pregnant women. The definition of rhinoconjunctivitis was based on criteria from the International Study of Asthma and Allergies in Childhood. Information on dietary factors was collected using a validated self-administered diet history questionnaire. Adjustment was made for age; gestation; region of residence; number of older siblings; number of children; smoking; secondhand smoke exposure at home and at work; family history of asthma, atopic eczema, and allergic rhinitis; household income; education; and body mass index.

Results

The prevalence of rhinoconjunctivitis in the past 12 months was 25.9%. Higher meat intake was significantly associated with an increased prevalence of rhinoconjunctivitis: the adjusted odds ratio between extreme quartiles was 1.71 (95% confidence interval: 1.25-2.35, P for trend = 0.002). No measurable association was found between fish intake and rhinoconjunctivitis. Intake of total fat, saturated fatty acids, monounsaturated fatty acids, n-3 polyunsaturated fatty acids, α-linolenic acid, eicosapentaenoic acid, docosahexaenoic acid, n-6 polyunsaturated fatty acids, linoleic acid, arachidonic acid, and cholesterol and the ratio of n-3 to n-6 polyunsaturated fatty acid intake were not evidently related to the prevalence of rhinoconjunctivitis.

Conclusions

The current results suggest that meat intake may be positively associated with the prevalence of rhinoconjunctivitis in young adult Japanese women.

Background

Secondhand smoke exposure (SHSe) is perhaps one of the most important toxic exposures in childhood. However, epidemiological studies on the relation between SHSe and dental caries are limited and have yielded inconsistent results. The present cross-sectional study examined the potential association between SHSe at home and the prevalence of dental caries in children.

Methods

Subjects were 20,703 schoolchildren aged 6 to 15 years in Okinawa, Japan. Information on SHSe at home and potential confounding factors was obtained through questionnaires. Data on dental caries were obtained from school records. Children were classified as having decayed and/or filled teeth (DFT) if a dentist diagnosed these conditions. Additionally, we analyzed decayed teeth (DT) and filled teeth (FT) separately. Adjustment was made for sex, age, region of residence, toothbrushing frequency, use of fluoride, sugar intake, and paternal and maternal educational level.

Results

The prevalence of DFT was 82.0%. Compared with never smoking in the household, former and current household smoking were independently associated with an increased prevalence of DFT (adjusted prevalence ratios [95% confidence intervals] for former household smoking and current light and heavy household smoking were 1.03 [1.00-1.05], 1.04 [1.02-1.05], and 1.04 [1.03-1.06], respectively); when analyzed separately there was an increased prevalence of DT (adjusted prevalence ratios [95% confidence intervals] for former household smoking and current light and heavy household smoking were 1.06 [1.02-1.11], 1.10 [1.06-1.13], and 1.10 [1.07-1.14], respectively) but not FT. A statistically significant dose-response relationship between cumulative smoking in the household and the prevalence of DFT and DT (P for trend < 0.0001), but not FT, was observed. In an analysis of 2 subgroups, subjects who had at least 1 deciduous tooth and subjects who had at least 1 permanent tooth, household smoking exposure was associated with an increased prevalence of DFT and DT not only in those with deciduous but also those with permanent dentition.

Conclusion

Our findings suggested that household smoking might be associated with an increased prevalence of dental caries in children.

Introduction

Secondhand smoke is a major cause of morbidity and mortality. It has been associated with serious health problems in both children and adults. Efforts to reduce exposure to secondhand smoke in Nebraska have included programs to prevent tobacco use among young people and campaigns for smoke-free workplaces and homes. Despite these interventions, young people continue to be exposed to secondhand smoke at an unacceptably high rate. The objective of this study was to examine the extent to which Nebraska public middle and high school students were exposed to secondhand smoke in 2002 and 2006, to evaluate factors associated with this exposure, and to propose interventions.

Methods

The Nebraska Youth Tobacco Survey was administered in 2002 and 2006 to a representative sample of students from public middle and high schools. All students who chose to participate completed an anonymous, self-administered survey that included questions on demographics, tobacco use, tobacco-related knowledge and attitudes, and exposure to secondhand smoke. Data were weighted to account for nonresponses at both student and school levels and to ensure generalizability of the estimates for public school students in Nebraska according to their grade, sex, and race/ethnicity. This study analyzed a subset of responses on secondhand smoke exposure, which was defined as being in a room or vehicle during the previous 7 days with someone who was smoking cigarettes.

Results

Secondhand smoke exposure in a room, a vehicle, or both declined significantly among all students from 2002 (69.0%) to 2006 (61.3%). In both 2002 and 2006, students were significantly more likely to be exposed to secondhand smoke in a room than in a vehicle (64.4% vs 48.2% in 2002 and 56.9% vs 40.2% in 2006). Among racial and ethnic groups, only white students experienced a significant decline in exposure from 2002 (70.0%) to 2006 (61.4%). Girls were significantly more likely to be exposed to secondhand smoke in 2006 than were boys, and only boys experienced a significant overall decline in exposure from 2002 (69.3%) to 2006 (57.7%). Smoking behaviors and attitudes continued to influence secondhand smoke exposure from 2002 to 2006, although students experienced significant declines whether they were smokers or nonsmokers, and whether they lived with a smoker or not. Those with close friends who smoked and those who did not perceive secondhand smoke as harmful, however, did not benefit.

Conclusion

These data indicate reductions in exposure to secondhand smoke among Nebraska's middle and high school students, but exposure remains a problem, particularly in rooms. Adoption of a comprehensive statewide smoke-free policy will contribute to significantly reduced exposure to secondhand smoke among young people in public places, but other measures to address exposure in the home and private vehicles are needed or should be strengthened. These include physician counseling based on behavioral change theory to encourage cessation and home-based no-smoking rules, in addition to interventions that target minorities, who are disproportionately affected by secondhand smoke exposure. Evaluation of existing measures, such as programs to prevent tobacco use among young people and campaigns to collect pledges for smoke-free homes, will be required to determine their effectiveness in reducing exposure to secondhand smoke among youth in Nebraska.

Background

Environmental tobacco smoke is a leading environmental asthma trigger and has been linked to the development of asthma in children and adults. Smoking cessation and reduced exposure to secondhand tobacco smoke are key components of asthma management. We describe a partnership involving two state agencies and 14 health plans; the goal of the partnership was to decrease smoking and exposure to environmental tobacco smoke among Medicaid-insured Oregonians with asthma.

Context

Oregon's asthma rate is higher than that of the national population, and approximately one third of Oregonians with asthma smoke. The Health Promotion and Chronic Disease Prevention Program (HPCDP) in the Oregon Department of Human Services has collaborated with the Office of Medical Assistance Programs (OMAP) to promote preventive care at the population level.

Methods

Two HPCDP programs — the Oregon Asthma Program and the Oregon Tobacco Prevention and Education Program — worked with OMAP to launch the statewide Asthma–Tobacco Integration Project in 2003. A primary focus of the project is the development of partnerships among health plans, health care providers, and large health care organizations to integrate asthma management and smoking control through systems innovations and provider education. OMAP and its participating health plans also decided to focus cessation efforts on its members with chronic diseases. In addition, HPCDP has collaborated with OMAP to distribute educational tools and information about tobacco's impact on asthma morbidity to Oregon's health care providers who serve low-income Oregonians.

Consequences

The partnership between OMAP and HPCDP program staff members has allowed them to discuss problems, leverage resources, and obtain support for many public health initiatives. In addition, OMAP–HPCDP collaboration on educational workshops and outreach to health care providers has helped convince quality improvement specialists and administrators about the importance of addressing smoking among patients with asthma. The Asthma–Tobacco Integration Project has also led to formative research aimed at increasing community involvement in promoting tobacco-free environments.

Interpretation

Collaboration between HPCDP and OMAP has been an important factor in Oregon's successful smoking cessation efforts in general and in recent efforts to address tobacco use among Oregonians with asthma.

Background

The objective of this study was to assess the correlation between childhood asthma and potential risk factors, especially exposure to indoor allergens, in a Native American population.

Methods

A case-control study of St. Regis Mohawk tribe children ages 2–14 years, 25 diagnosed with asthma and 25 controls was conducted. Exposure was assessed based on a personal interview and measurement of mite and cat allergens (Der p 1, Fel d 1) in indoor dust.

Results

A non-significant increased risk of childhood asthma was associated with self-reported family history of asthma, childhood environmental tobacco smoke exposure, and air pollution. There was a significant protective effect of breastfeeding against current asthma in children less than 14 years (5.2 fold lower risk). About 80% of dust mite and 15% of cat allergen samples were above the threshold values for sensitization of 2 and 1 μg/g, respectively. The association between current asthma and exposure to dust mite and cat allergens was positive but not statistically significant.

Conclusion

This research identified several potential indoor and outdoor risk factors for asthma in Mohawks homes, of which avoidance may reduce or delay the development of asthma in susceptible individuals.

Objective

To examine the tactics the tobacco industry in Germany used to avoid regulation of secondhand smoke exposure and to maintain the acceptance of public smoking.

Methods

Systematic search of tobacco industry documents available on the internet between June 2003 and August 2004.

Results

In West Germany, policymakers were, as early as the mid 1970s, well aware of the fact that secondhand smoke endangers non‐smokers. One might have assumed that Germany, an international leader in environmental protection, would have led in protecting her citizens against secondhand smoke pollution. The tobacco manufacturers in Germany, however, represented by the national manufacturing organisation “Verband” (Verband der Cigarettenindustrie), contained and neutralised the early debate about the danger of secondhand smoke. This success was achieved by carefully planned collaboration with selected scientists, health professionals and policymakers, along with a sophisticated public relations programme.

Conclusions

The strategies of the tobacco industry have been largely successful in inhibiting the regulation of secondhand smoke in Germany. Policymakers, health professionals, the media and the general public should be aware of this industry involvement and should take appropriate steps to close the gap between what is known and what is done about the health effects of secondhand smoke.

Background

Implementation of smoke free policies has potentially substantial effects on health by reducing secondhand smoke exposure. However little is known about whether the introduction of anti-smoking legislation translates into decreased secondhand smoke exposure. We examined whether smoking bans impact rates of secondhand smoke exposure in public places and rates of complete workplace smoking restriction.

Methods

Canadian Community Health Survey was used to obtain secondhand smoking exposure rates in 15 Ontario municipalities. Data analysis included descriptive summaries and 95% confidence intervals were calculated and compared across groups

Results

Across all studied municipalities, secondhand smoke exposure in public places decreased by 4.7% and workplace exposure decreased by 2.3% between the 2003 and 2005 survey years. The only jurisdiction to implement a full ban from no previous ban was also the only setting that experienced significant decreases in both individual exposure to secondhand smoke in a public place (-17.3%, 95% CI -22.8, -11.8) and workplace exposure (-18.1%, 95% CI -24.9, -11.3). Exposures in vehicles and homes declined in almost all settings over time.

Conclusions

Implementation of a full smoking ban was associated with the largest decreases in secondhand smoke exposure while partial bans and changes in existing bans had inconsistent effects. In addition to decreasing exposure in public places as would be expected from legislation, bans may have additional benefits by decreasing rates of current smokers and decreasing exposures to secondhand smoke in private settings.

The Syracuse AUDIT (Assessment of Urban Dwellings for Indoor Toxics) project is a birth cohort study of wheezing in the first year of life in a low-income urban setting. Such studies are important because of the documented serious risks to children's health and the lack of attention and published work on asthma development and intervention in communities of this size. We studied 103 infants of mothers with asthma, living predominantly in inner-city households. Our study combines measurements of a large panel of indoor environmental agents, in-home infant assessments, and review of all prenatal and postnatal medical records through the first year of life. We found multiple environmental pollution sources and potential health risks in study homes including high infant exposure to tobacco smoke. The prevalence of maternal smoking during pregnancy was 54%; postnatal environmental tobacco smoke (ETS) exposure was nearly 90%. The majority (73%) of homes showed signs of dampness. Participants' lives were complicated by poverty, unemployment and single-parenthood. Thirty-three percent of fathers were not involved with their children, and 62% of subjects moved at least once during the study period. These socioeconomic issues had an impact on project implementation and led to modification of study eligibility criteria. Extensive outreach, follow up, and relationship-building were required in order to recruit and retain families and resulted in considerable work overload for study staff. Our experiences implementing the project will inform further studies on this and other similar populations. Future reports on this cohort will address the role of multiple environmental variables and their effects on wheezing outcome during the first year of life.

BACKGROUND—Exposure to environmental tobacco smoke (ETS) during childhood and in utero exposure to maternal smoking are associated with adverse effects on lung growth and development.
METHODS—A study was undertaken of the associations between maternal smoking during pregnancy, exposure to ETS, and pulmonary function in 3357 school children residing in 12 Southern California communities. Current and past exposure to household ETS and exposure to maternal smoking in utero were assessed by a self-administered questionnaire completed by parents of 4th, 7th, and 10th grade students in 1993.Standard linear regression techniques were used to estimate the effects of in utero and ETS exposure on lung function, adjusting for age, sex, race, Hispanic ethnicity, height, weight, asthma, personal smoking, and selected household characteristics.
RESULTS—In utero exposure to maternal smoking was associated with reduced peak expiratory flow rate (PEFR) (-3.0%, 95% CI -4.4 to -1.4), mean mid expiratory flow (MMEF) (-4.6%, 95% CI -7.0 to -2.3), and forced expiratory flow (FEF75) (-6.2%, 95% CI -9.1 to -3.1), but not forced expiratory volume in one second (FEV1). Adjusting for household ETS exposure did not substantially change these estimates. The reductions in flows associated with in utero exposure did not significantly vary with sex, race, grade, income, parental education, or personal smoking. Exposure to two or more current household smokers was associated with reduced MMEF (-4.1%, 95% CI -7.6 to -0.4) and FEF75 (-4.4%, 95% CI -9.0 to 0.4). Current or past maternal smoking was associated with reductions in PEFR and MMEF; however, after adjustment for in utero exposure, deficits in MMEF and FEF75 associated with all measurements of ETS were substantially reduced and were not statistically significant.
CONCLUSIONS—In utero exposure to maternal smoking is independently associated with decreased lung function in children of school age, especially for small airway flows.



Management of asthma requires attention to environmental exposures both indoors and outdoors. Americans spend most of their time indoors, where they have a greater ability to modify their environment. The indoor environment contains both pollutants (eg, particulate matter, nitrogen dioxide, secondhand smoke, and ozone) and allergens from furred pets, dust mites, cockroaches, rodents, and molds. Indoor particulate matter consists of particles generated from indoor sources such as cooking and cleaning activities, and particles that penetrate from the outdoors. Nitrogen dioxide sources include gas stoves, furnaces, and fireplaces. Indoor particulate matter and nitrogen dioxide are linked to asthma morbidity. The indoor ozone concentration is mainly influenced by the outdoor ozone concentration. The health effects of indoor ozone exposure have not been well studied. In contrast, there is substantial evidence of detrimental health effects from secondhand smoke. Guideline recommendations are not specific for optimizing indoor air quality. The 2007 National Asthma Education and Prevention Program asthma guidelines recommend eliminating indoor smoking and improving the ventilation. Though the guidelines state that there is insufficient evidence to recommend air cleaners, air cleaners and reducing activities that generate indoor pollutants may be sound practical approaches for improving the health of individuals with asthma. The guidelines are more specific about allergen avoidance; they recommend identifying allergens to which the individual is immunoglobin E sensitized and employing a multifaceted, comprehensive strategy to reduce exposure. Outdoor air pollutants that impact asthma include particulate matter, ozone, nitrogen dioxide, and sulfur dioxide, and guidelines recommend that individuals with asthma avoid exertion outdoors when these pollutants are elevated. Outdoor allergens include tree, grass, and weed pollens, which vary in concentration by season. Recommendations to reduce exposure include staying indoors, keeping windows and doors closed, using air conditioning and perhaps high-efficiency particulate arrestor (HEPA) air filters, and thorough daily washing to remove allergens from one’s person.

While chronic exposure to secondhand smoke has been well recognized as a cause of heart disease in nonsmokers, there has been recent speculation about the potential acute cardiovascular effects of transient exposure to secondhand smoke among nonsmokers; in particular, the possibility that such exposure could increase the risk of acute myocardial infarction even in an otherwise healthy nonsmoker. This paper reviews the claims being made by a number of anti-smoking and public health groups regarding the acute cardiovascular effects of secondhand smoke exposure among otherwise healthy adults, analyzes the validity of these claims based on a review of the scientific evidence, and discusses the implications of the findings for tobacco control and public health practice. Based on the analysis, it appears that a large number of anti-smoking organizations are making inaccurate claims that a single, acute, transient exposure to secondhand smoke can cause severe and even fatal cardiovascular events in healthy nonsmokers. The dissemination of inaccurate information by anti-smoking groups to the public in support of smoking bans is unfortunate because it may harm the tobacco control movement by undermining its credibility, reputation, and effectiveness. Disseminating inaccurate information also represents a violation of basic ethical principles that are a core value of public health practice that cannot and should not be sacrificed, even for a noble end such as protecting nonsmokers from secondhand smoke exposure. How the tobacco control movement responds to this crisis of credibility will go a long way towards determining the future effectiveness of the movement and its ability to continue to save lives and protect the public's health.