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.
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.
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.
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.
β-2 adrenergic receptor; prenatal exposure; secondhand-smoke exposure; asthma; wheeze
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.
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.
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.
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).
We concluded that prenatal and household ETS exposure had significant adverse effects on respiratory health in Taiwanese children.
One of the mechanisms supposed to explain the increasing prevalence of asthma, among children in particular, is the use of antibiotics because they may modify natural microbial exposure and development of the immune system in early childhood. The aim of this study is to investigate the association between the use of various classes of antibiotics (penicillin, cephalosporin and macrolide derivatives) in early childhood and the medical diagnosis of asthma or wheezing reported by mothers over the follow-up after adjustment for potential confounders and respiratory infections. In a population-based sample of 5-year-olds, a part of the ongoing birth cohort study, the standardized interviews on health outcomes, potential confounders (child’s gender, maternal atopy, parity, prenatal and postnatal environmental tobacco smoke) and the use of antibiotics were gathered from mothers of 310 children. While the overall use of antibiotics during the early childhood was insignificantly associated with asthma (adjusted OR = 1.65, 95%CI: 0.93 – 2.93), the risk estimates were significant both for macrolide antibiotics (adjusted OR=2.14, 95%CI: 1.16–3.95) and cephalosporins (OR=1.98, 95%CI: 1.14–3.37). The significant excess in IRR (incident risk ratio) of wheezing episodes was related only to the use of macrolide antibiotics (adjusted IRR=1.91, 95%CI: 1.12–3.27). The use of other classes of antibiotics was found not to be associated with the medical diagnosis of asthma or wheezing episodes recorded in the study period. Conclusion: as early childhood use of broad spectrum antibiotics is associated with an increased risk of developing asthma in 5-year-olds, it may be hypothesized that the antibiotic- related suppression of allergic inflammatory responses in the course of treatment may later lead to greater than before atopic immune response in Th2 children or an impairment of Th1 immune responses in early childhood.
antibiotics; asthma; childhood; wheezing; Th1 immune responses; allergic reactions
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.
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.
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.
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.
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.
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.
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.
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.
Our results suggest that genetic variation in TNF may contribute to childhood asthma and that associations may be modified by parental smoking.
allergy; asthma; atopy; environmental tobacco smoke; genetic predisposition to disease; lymphotoxin-α (LTA); ozone; secondhand smoke; single nucleotide polymorphism (SNP); tumor necrosis factor-α (TNF)
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
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.
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.
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.
The effects of in utero tobacco smoke exposure on childhood respiratory health have been investigated, and outcomes have been inconsistent.
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.
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.
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.
asthma; tobacco; Latino; African American; pregnancy
Background: Some countries have recently extended smoke-free policies to particular outdoor settings; however, there is controversy regarding whether this is scientifically and ethically justifiable.
Objectives: The objective of the present study was to review research on secondhand smoke (SHS) exposure in outdoor settings.
Data sources: We conducted different searches in PubMed for the period prior to September 2012. We checked the references of the identified papers, and conducted a similar search in Google Scholar.
Study selection: Our search terms included combinations of “secondhand smoke,” “environmental tobacco smoke,” “passive smoking” OR “tobacco smoke pollution” AND “outdoors” AND “PM” (particulate matter), “PM2.5” (PM with diameter ≤ 2.5 µm), “respirable suspended particles,” “particulate matter,” “nicotine,” “CO” (carbon monoxide), “cotinine,” “marker,” “biomarker” OR “airborne marker.” In total, 18 articles and reports met the inclusion criteria.
Results: Almost all studies used PM2.5 concentration as an SHS marker. Mean PM2.5 concentrations reported for outdoor smoking areas when smokers were present ranged from 8.32 to 124 µg/m3 at hospitality venues, and 4.60 to 17.80 µg/m3 at other locations. Mean PM2.5 concentrations in smoke-free indoor settings near outdoor smoking areas ranged from 4 to 120.51 µg/m3. SHS levels increased when smokers were present, and outdoor and indoor SHS levels were related. Most studies reported a positive association between SHS measures and smoker density, enclosure of outdoor locations, wind conditions, and proximity to smokers.
Conclusions: The available evidence indicates high SHS levels at some outdoor smoking areas and at adjacent smoke-free indoor areas. Further research and standardization of methodology is needed to determine whether smoke-free legislation should be extended to outdoor settings.
exposure markers; outdoor tobacco smoke; particulate matter; passive smoking; secondhand smoke; smoking ban; tobacco smoke pollution
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.
Environmental (secondhand) tobacco smoke; airways hyperreactivity; allergic asthma; Th2 polarization; airway mucus
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.
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.
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.
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.
Asthma; Cross-sectional studies; Eczema; Environmental tobacco smoke; Smoking; Wheeze; Rhinoconjunctivitis
Although an inverse relationship between number of siblings and likelihood of allergic disorders has been shown in many epidemiological studies, the biological mechanism underlying this phenomenon has not yet been identified. There is no epidemiological research regarding the sibling effect on allergic disorders in Japanese adults. The current cross-sectional study examined the relationship between number of siblings and prevalence of allergic disorders among adult women in Japan.
Subjects were 1745 pregnant women. This study was based on questionnaire data. 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, pack-years of smoking, secondhand smoke exposure at home and at work, family history of asthma, atopic eczema, and allergic rhinitis, household income, and education.
The prevalence values of wheeze, asthma, eczema, and rhinoconjunctivitis in the past 12 months were 10.4%, 5.5%, 13.0%, and 25.9%, respectively. A significant inverse exposure-response relationship was observed between the number of older siblings and rhinoconjunctivitis, but not wheeze, asthma, or eczema (P for trend = 0.03); however, the adjusted odds ratio (OR) for having 2 or more older siblings was not significant although the adjusted OR for having 1 older sibling was statistically significant (adjusted OR = 0.71 [95% CI: 0.56-0.91]). Number of total siblings and number of younger siblings were not related to wheeze, asthma, eczema, or rhinoconjunctivitis.
This study found a significant inverse relationship between the number of older siblings and the prevalence of rhinoconjunctivitis among pregnant Japanese women. Our findings are likely to support the intrauterine programming hypothesis; however, we could not rule out the hygiene hypothesis.
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.
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.
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.
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.
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.
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.
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.
Our findings suggested that household smoking might be associated with an increased prevalence of dental caries in children.
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.
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
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.
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.
Although tobacco smoke is an established risk factor for adult cancer, studies of the association between parental smoking and childhood cancer have produced inconsistent results. To investigate the transgenerational relationship between pre-natal and post-natal tobacco smoke exposure from the grandmother’s pregnancies until after the post-natal period and childhood cancer.
Exposure to tobacco smoke was recorded for three generations. Data were collected through personal interviews using the paediatric environmental history, and were compared among 128 children with cancer and 128 matched controls. The contingency tables and a logistic multivariable regression model were used to control for possible confounding factors.
Smoke exposure during oogenesis (maternal grandmother smokers) – odds ratio (OR) 2.2 (95% confidence interval (CI) 1.1–4.9) – and during the mother’ pregnancies – OR 1.8 (95% CI 1.1–3.3) – were significantly associated with an increased risk of childhood cancer.
Tobacco smoke exposure during the grandmother’s and mother’s pregnancies increase the risk of cancer in the descendants. The results suggest that the biological plausibility of the association between parental smoking and paediatric cancer can be explained by the large latency period of paediatric carcinogenesis.
case-control studies; childhood cancer; tobacco smoke pollution
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.
Body Mass Index; Children; Cotinine; Growth; Prenatal; Tobacco Smoke
Secondhand smoke or environmental tobacco smoke is a combination of smoke from a burning cigarette and exhaled smoke from a smoker. This substance is an involuntarily inhaled mix of compounds that causes or contributes to a wide range of adverse health effects, including cancer, cardiovascular diseases, respiratory infections, adverse reproductive effects, and asthma. This paper presents findings from Global Youth Tobacco Surveys (GYTS) conducted in 132 countries between 1999 and 2005. GYTS data indicate that a large proportion of students in every World Health Organization Region are exposed to secondhand smoke at home (43.9%) and in public places (55.8%), and many have parents (46.5%) or best friends who smoke (17.9%). GYTS data have shown widespread and strong support among students for bans on smoking in public areas all over the world (76.1%). Countries should engage this positive public health attitude among youth to promote and enforce policies for smoke‐free public places and workplaces, including restaurants and bars.
secondhand smoke; youth; school; surveillance
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.
asthma; epidemiology; smoking
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.
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.
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).
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.
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.
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.
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.
The current results suggest that meat intake may be positively associated with the prevalence of rhinoconjunctivitis in young adult Japanese women.
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.
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.
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.
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.
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.
Among people with asthma, the clinical impact and relative contribution of maternal smoking during pregnancy (in utero smoking) and current secondhand smoke exposure on asthma control is poorly documented, and there is a paucity of research involving minority populations.
To examine the association between poor asthma control and in utero smoking and current secondhand smoke exposure among Latino and Black children with asthma.
Case-only analysis of 2 multi-center case-control studies conducted from 2008–2010 using similar protocols. We recruited 2,481 Latinos and Blacks with asthma (ages 8–17) from the mainland United States and Puerto Rico. Ordinal logistic regression was used to estimate the effect of in utero smoking and current secondhand smoke exposures on National Heart Lung and Blood Institute-defined asthma control.
Poor asthma control among children 8–17 years of age was independently associated with in utero smoking (odds ratio; 95% confidence interval = 1.5; 1.1–2.0). In utero smoking via the mother was also associated with secondary asthma outcomes, including early onset asthma (1.7; 1.1–2.4), daytime symptoms (1.6; 1.1–2.1), and asthma-related limitation of activities (1.6; 1.2–2.2).
Maternal smoking while in utero is associated with poor asthma control in Black and Latino subjects assessed at 8–17 years of age.
Secondhand smoke; prenatal exposure delayed effects; asthma; health status disparities
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.
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.
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.
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.