PMCC PMCC

Search tips
Search criteria

Advanced
Results 1-25 (851727)

Clipboard (0)
None

Related Articles

1.  Preterm Birth and Childhood Wheezing Disorders: A Systematic Review and Meta-Analysis 
PLoS Medicine  2014;11(1):e1001596.
In a systematic review and meta-analysis, Jasper Been and colleagues investigate the association between preterm birth and the development of wheezing disorders in childhood.
Please see later in the article for the Editors' Summary
Background
Accumulating evidence implicates early life factors in the aetiology of non-communicable diseases, including asthma/wheezing disorders. We undertook a systematic review investigating risks of asthma/wheezing disorders in children born preterm, including the increasing numbers who, as a result of advances in neonatal care, now survive very preterm birth.
Methods and Findings
Two reviewers independently searched seven online databases for contemporaneous (1 January 1995–23 September 2013) epidemiological studies investigating the association between preterm birth and asthma/wheezing disorders. Additional studies were identified through reference and citation searches, and contacting international experts. Quality appraisal was undertaken using the Effective Public Health Practice Project instrument. We pooled unadjusted and adjusted effect estimates using random-effects meta-analysis, investigated “dose–response” associations, and undertook subgroup, sensitivity, and meta-regression analyses to assess the robustness of associations.
We identified 42 eligible studies from six continents. Twelve were excluded for population overlap, leaving 30 unique studies involving 1,543,639 children. Preterm birth was associated with an increased risk of wheezing disorders in unadjusted (13.7% versus 8.3%; odds ratio [OR] 1.71, 95% CI 1.57–1.87; 26 studies including 1,500,916 children) and adjusted analyses (OR 1.46, 95% CI 1.29–1.65; 17 studies including 874,710 children). The risk was particularly high among children born very preterm (<32 wk gestation; unadjusted: OR 3.00, 95% CI 2.61–3.44; adjusted: OR 2.81, 95% CI 2.55–3.12). Findings were most pronounced for studies with low risk of bias and were consistent across sensitivity analyses. The estimated population-attributable risk of preterm birth for childhood wheezing disorders was ≥3.1%.
Key limitations related to the paucity of data from low- and middle-income countries, and risk of residual confounding.
Conclusions
There is compelling evidence that preterm birth—particularly very preterm birth—increases the risk of asthma. Given the projected global increases in children surviving preterm births, research now needs to focus on understanding underlying mechanisms, and then to translate these insights into the development of preventive interventions.
Review Registration
PROSPERO CRD42013004965
Please see later in the article for the Editors' Summary
Editors' Summary
Background
Most pregnancies last around 40 weeks, but worldwide, more than 11% of babies are born before 37 weeks of gestation (the period during which a baby develops in its mother's womb). Preterm birth is a major cause of infant death—more than 1 million babies die annually from preterm birth complications—and the number of preterm births is increasing globally. Multiple pregnancies, infections, and chronic (long-term) maternal conditions such as diabetes can all cause premature birth, but the cause of many preterm births is unknown. The most obvious immediate complication that is associated with preterm birth is respiratory distress syndrome. This breathing problem, which is more common in early preterm babies than in near-term babies, occurs because the lungs of premature babies are structurally immature and lack pulmonary surfactant, a unique mixture of lipids and proteins that coats the inner lining of the lungs and helps to prevent the collapse of the small air sacs in the lungs that absorb oxygen from the air. Consequently, preterm babies often need help with their breathing and oxygen supplementation.
Why Was This Study Done?
Improvements in the management of prematurity mean that more preterm babies survive today than in the past. However, accumulating evidence suggests that early life events are involved in the subsequent development of non-communicable diseases (non-infectious chronic diseases). Given the increasing burden of preterm birth, a better understanding of the long-term effects of preterm birth is essential. Here, the researchers investigate the risks of asthma and wheezing disorders in children who are born preterm by undertaking a systematic review (a study that uses predefined criteria to identify all the research on a given topic) and a meta-analysis (a statistical method for combining the results of several studies). Asthma is a chronic condition that is caused by inflammation of the airways. In people with asthma, the airways can react very strongly to allergens such as animal fur and to irritants such as cigarette smoke. Exercise, cold air, and infections can also trigger asthma attacks, which can sometimes be fatal. The symptoms of asthma include wheezing (a high-pitched whistling sound during breathing), coughing, chest tightness, and shortness of breath. Asthma cannot be cured, but drugs can relieve its symptoms and prevent acute asthma attacks.
What Did the Researchers Do and Find?
The researchers identified 30 studies undertaken between 1995 and the present (a time span chosen to allow for recent changes in the management of prematurity) that investigated the association between preterm birth and asthma/wheezing disorders in more than 1.5 million children. Across the studies, 13.7% of preterm babies developed asthma/wheezing disorders during childhood, compared to only 8.3% of babies born at term. Thus, the risk of preterm babies developing asthma or a wheezing disorder during childhood was 1.71 times higher than the risk of term babies developing these conditions (an unadjusted odds ratio [OR] of 1.71). In analyses that allowed for confounding factors—other factors that affect the risk of developing asthma/wheezing disorders such as maternal smoking—the risk of preterm babies developing asthma or a wheezing disorder during childhood was 1.46 times higher than that of babies born at term (an adjusted OR of 1.46). Notably, compared to children born at term, children born very early (before 32 weeks of gestation) had about three times the risk of developing asthma/wheezing disorders in unadjusted and adjusted analyses. Finally, the population-attributable risk of preterm birth for childhood wheezing disorders was more than 3.1%. That is, if no preterm births had occurred, there would have been more than a 3.1% reduction in childhood wheezing disorders.
What Do These Findings Mean?
These findings strongly suggest that preterm birth increases the risk of asthma and wheezing disorders during childhood and that the risk of asthma/wheezing disorders increases as the degree of prematurity increases. The accuracy of these findings may be affected, however, by residual confounding. That is, preterm children may share other, unknown characteristics that increase their risk of developing asthma/wheezing disorders. Moreover, the generalizability of these findings is limited by the lack of data from low- and middle-income countries. However, given the projected global increases in children surviving preterm births, these findings highlight the need to undertake research into the mechanisms underlying the association between preterm birth and asthma/wheezing disorders and the need to develop appropriate preventative and therapeutic measures.
Additional Information
Please access these websites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.1001596.
The March of Dimes, a nonprofit organization for pregnancy and baby health, provides information on preterm birth (in English and Spanish)
Nemours, another nonprofit organization for child health, also provides information (in English and Spanish) on premature babies and on asthma (including personal stories)
The UK National Health Service Choices website provides information about premature labor and birth and a real story about having a preterm baby; it provides information about asthma in children (including real stories)
The MedlinePlus Encyclopedia has pages on preterm birth, asthma, asthma in children, and wheezing (in English and Spanish); MedlinePlus provides links to further information on premature birth, asthma, and asthma in children (in English and Spanish)
doi:10.1371/journal.pmed.1001596
PMCID: PMC3904844  PMID: 24492409
2.  The impact of secondhand smoke on asthma control among Black and Latino children 
Background
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.
Objectives
To examine the association between poor asthma control and in utero smoking and current secondhand smoke exposure among Latino and Black children with asthma.
Methods
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.
Results
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).
Conclusions
Maternal smoking while in utero is associated with poor asthma control in Black and Latino subjects assessed at 8–17 years of age.
doi:10.1016/j.jaci.2012.03.017
PMCID: PMC3367092  PMID: 22552109
Secondhand smoke; prenatal exposure delayed effects; asthma; health status disparities
3.  Active or Passive Exposure to Tobacco Smoking and Allergic Rhinitis, Allergic Dermatitis, and Food Allergy in Adults and Children: A Systematic Review and Meta-Analysis 
PLoS Medicine  2014;11(3):e1001611.
In a systematic review and meta-analysis, Bahi Takkouche and colleagues examine the associations between exposure to tobacco smoke and allergic disorders in children and adults.
Please see later in the article for the Editors' Summary
Background
Allergic rhinitis, allergic dermatitis, and food allergy are extremely common diseases, especially among children, and are frequently associated to each other and to asthma. Smoking is a potential risk factor for these conditions, but so far, results from individual studies have been conflicting. The objective of this study was to examine the evidence for an association between active smoking (AS) or passive exposure to secondhand smoke and allergic conditions.
Methods and Findings
We retrieved studies published in any language up to June 30th, 2013 by systematically searching Medline, Embase, the five regional bibliographic databases of the World Health Organization, and ISI-Proceedings databases, by manually examining the references of the original articles and reviews retrieved, and by establishing personal contact with clinical researchers. We included cohort, case-control, and cross-sectional studies reporting odds ratio (OR) or relative risk (RR) estimates and confidence intervals of smoking and allergic conditions, first among the general population and then among children.
We retrieved 97 studies on allergic rhinitis, 91 on allergic dermatitis, and eight on food allergy published in 139 different articles. When all studies were analyzed together (showing random effects model results and pooled ORs expressed as RR), allergic rhinitis was not associated with active smoking (pooled RR, 1.02 [95% CI 0.92–1.15]), but was associated with passive smoking (pooled RR 1.10 [95% CI 1.06–1.15]). Allergic dermatitis was associated with both active (pooled RR, 1.21 [95% CI 1.14–1.29]) and passive smoking (pooled RR, 1.07 [95% CI 1.03–1.12]). In children and adolescent, allergic rhinitis was associated with active (pooled RR, 1.40 (95% CI 1.24–1.59) and passive smoking (pooled RR, 1.09 [95% CI 1.04–1.14]). Allergic dermatitis was associated with active (pooled RR, 1.36 [95% CI 1.17–1.46]) and passive smoking (pooled RR, 1.06 [95% CI 1.01–1.11]). Food allergy was associated with SHS (1.43 [1.12–1.83]) when cohort studies only were examined, but not when all studies were combined.
The findings are limited by the potential for confounding and bias given that most of the individual studies used a cross-sectional design. Furthermore, the studies showed a high degree of heterogeneity and the exposure and outcome measures were assessed by self-report, which may increase the potential for misclassification.
Conclusions
We observed very modest associations between smoking and some allergic diseases among adults. Among children and adolescents, both active and passive exposure to SHS were associated with a modest increased risk for allergic diseases, and passive smoking was associated with an increased risk for food allergy. Additional studies with detailed measurement of exposure and better case definition are needed to further explore the role of smoking in allergic diseases.
Please see later in the article for the Editors' Summary
Editors' Summary
Background
The immune system protects the human body from viruses, bacteria, and other pathogens. Whenever a pathogen enters the body, immune system cells called T lymphocytes recognize specific molecules on its surface and release chemical messengers that recruit and activate other types of immune cells, which then attack the pathogen. Sometimes, however, the immune system responds to harmless materials (for example, pollen; scientists call these materials allergens) and triggers an allergic disease such as allergic rhinitis (inflammation of the inside of the nose; hay fever is a type of allergic rhinitis), allergic dermatitis (also known as eczema, a disease characterized by dry, itchy patches on the skin), and food allergy. Recent studies suggest that all these allergic (atopic) diseases are part of a continuous state called the “atopic march” in which individuals develop allergic diseases in a specific sequence that starts with allergic dermatitis during infancy, and progresses to food allergy, allergic rhinitis, and finally asthma (inflammation of the airways).
Why Was This Study Done?
Allergic diseases are extremely common, particularly in children. Allergic rhinitis alone affects 10%–30% of the world's population and up to 40% of children in some countries. Moreover, allergic diseases are becoming increasingly common. Allergic diseases affect the quality of life of patients and are financially costly to both patients and health systems. It is important, therefore, to identify the factors that cause or potentiate their development. One potential risk factor for allergic diseases is active or passive exposure to tobacco smoke. In some countries up to 80% of children are exposed to second-hand smoke so, from a public health point of view, it would be useful to know whether exposure to tobacco smoke is associated with the development of allergic diseases. Here, the researchers undertake a systematic review (a study that uses predefined criteria to identify all the research on a given topic) and a meta-analysis (a statistical approach for combining the results of several studies) to investigate this issue.
What Did the Researchers Do and Find?
The researchers identified 196 observational studies (investigations that observe outcomes in populations without trying to affect these outcomes in any way) that examined the association between smoke exposure and allergic rhinitis, allergic dermatitis, or food allergy. When all studies were analyzed together, allergic rhinitis was not associated with active smoking but was slightly associated with exposure to second-hand smoke. Specifically, compared to people not exposed to second-hand smoke, the pooled relative risk (RR) of allergic rhinitis among people exposed to second-hand smoke was 1.10 (an RR of greater than 1 indicates an increased risk of disease development in an exposed population compared to an unexposed population). Allergic dermatitis was associated with both active smoking (RR = 1.21) and exposure to second-hand smoke (RR = 1.07). In the populations of children and adolescents included in the studies, allergic rhinitis was associated with both active smoking and exposure to second-hand smoke (RRs of 1.40 and 1.09, respectively), as was allergic dermatitis (RRs of 1.36 and 1.06, respectively). Finally food allergy was associated with exposure to second-hand smoke (RR = 1.43) when cohort studies (a specific type of observational study) only were examined but not when all the studies were combined.
What Do These Findings Mean?
These findings provide limited evidence for a weak association between smoke exposure and allergic disease in adults but suggest that both active and passive smoking are associated with a modestly increased risk of allergic diseases in children and adolescents. The accuracy of these findings may be affected by the use of questionnaires to assess smoke exposure and allergic disease development in most of the studies in the meta-analysis and by the possibility that individuals exposed to smoke may have shared other characteristics that were actually responsible for their increased risk of allergic diseases. To shed more light on the role of smoking in allergic diseases, additional studies are needed that accurately measure exposure and outcomes. However, the present findings suggest that, in countries where many people smoke, 14% and 13% of allergic rhinitis and allergic dermatitis, respectively, among children may be attributable to active smoking. Thus, the elimination of active smoking among children and adolescents could prevent one in seven cases of allergic rhinitis and one in eight cases of allergic dermatitis in such countries.
Additional Information
Please access these websites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.1001611.
The UK National Health Service Choices website provides information about allergic rhinitis, hay fever (including personal stories), allergic dermatitis (including personal stories), and food allergy (including personal stories)
The US National Institute of Allergy and Infectious Disease provides information about allergic diseases
The UK not-for-profit organization Allergy UK provides information about all aspects of allergic diseases and a description of the atopic march
MedlinePlus encyclopedia has pages on allergic rhinitis and allergic dermatitis (in English and Spanish)
MedlinePlus provides links to further resources about allergies, eczema, and food allergy (in English and Spanish)
doi:10.1371/journal.pmed.1001611
PMCID: PMC3949681  PMID: 24618794
4.  High prevalence of asthma symptoms in Warao Amerindian children in Venezuela is significantly associated with open-fire cooking: a cross-sectional observational study 
Respiratory Research  2013;14(1):76.
Background
The International Study on Asthma and Allergies in Childhood (ISAAC) reported a prevalence of asthma symptoms in 17 centers in nine Latin American countries that was similar to prevalence rates reported in non-tropical countries. It has been proposed that the continuous exposure to infectious diseases in rural populations residing in tropical areas leads to a relatively low prevalence of asthma symptoms. As almost a quarter of Latin American people live in rural tropical areas, the encountered high prevalence of asthma symptoms is remarkable. Wood smoke exposure and environmental tobacco smoke have been identified as possible risk factors for having asthma symptoms.
Methods
We performed a cross-sectional observational study from June 1, 2012 to September 30, 2012 in which we interviewed parents and guardians of Warao Amerindian children from Venezuela. Asthma symptoms were defined according to the ISAAC definition as self-reported wheezing in the last 12 months. The associations between wood smoke exposure and environmental tobacco smoke and the prevalence of asthma symptoms were calculated by means of univariate and multivariable logistic regression analyses.
Results
We included 630 children between two and ten years of age. Asthma symptoms were recorded in 164 of these children (26%). The prevalence of asthma symptoms was associated with the cooking method. Children exposed to the smoke produced by cooking on open wood fires were at higher risk of having asthma symptoms compared to children exposed to cooking with gas (AOR 2.12, 95% CI 1.18 - 3.84). Four percent of the children lived in a household where more than ten cigarettes were smoked per day and they had a higher risk of having asthma symptoms compared to children who were not exposed to cigarette smoke (AOR 2.69, 95% CI 1.11 - 6.48).
Conclusion
Our findings suggest that children living in rural settings in a household where wood is used for cooking or where more than ten cigarettes are smoked daily have a higher risk of having asthma symptoms.
doi:10.1186/1465-9921-14-76
PMCID: PMC3723947  PMID: 23870058
Asthma[Mesh]; Wheeze; Woodsmoke; Tobacco smoke pollution[Mesh]; Smoke[Mesh]; Indigenous children
5.  An animal model of cigarette smoke-induced in utero growth retardation 
Toxicology  2008;246(2-3):193-202.
Maternal/fetal genetic constitution and environmental factors are vital to delivery of a healthy baby. In the United States (US), a low birth weight (LBW) baby is born every minute and a half. LBW, defined as weighing less than 5.5 lbs at birth, affects nearly 1 in 12 infants born in the US with resultant costs for the nation of more than 15 billion dollars annually. Infant birth weight is the single most important factor affecting neonatal mortality. Various environmental and genetic risk factors for LBW have been identified. Several risks are preventable, such as cigarette smoking during pregnancy. Over one million babies are exposed prenatally to cigarette smoke accounting for over 20% of the LBW incidence in the US. Cigarette smoke exposure in utero results in a variety of adverse developmental outcomes with intrauterine growth restriction and infant LBW being the most well documented. However, the mechanisms underlying the causes of LBW remain poorly understood. The purpose of this study was: (1) to establish an animal model of cigarette smoke-induced in utero growth retardation and LBW using physiologically relevant inhalation exposure conditions which simulate “active” and “passive” tobacco smoke exposures, and (2) to determine whether particular stages of development are more susceptible than others to the adverse effects of in utero smoke exposure on embryo/fetal growth. Pregnant C57BL/6J mice were exposed to cigarette smoke during three periods of gestation: pre-/peri-implantation (gestational days [gds] 1−5), post-implantation (gds 6−18), and throughout gestation (gds 1−17). Reproductive and fetal outcomes were assessed on gd 18.5. Exposure of dams to mainstream/sidestream cigarette smoke, simulating “active” maternal smoking, resulted in decreases in fetal weight and crown–rump length when exposed throughout gestation (gds 1−17). Similar results were seen when dams were exposed only during the first 5 days of gestation (pre-/peri-implantation period gds 1−5). Exposure of dams from the post-implantation period through gestation (gds 6−18) did not result in reduced fetal weight, although a significant reduction in crown–rump length remained evident. Interestingly, maternal sidestream smoke exposure, simulating exposure to environmental tobacco smoke (ETS), during the pre-/peri-implantation period of development also produced significant decreases in fetal weight and crown–rump length. Collectively, results from the present study confirm an association between prenatal exposure to either “active” or “passive” cigarette smoke and in utero growth retardation. The data also identify a period of susceptibility to in utero cigarette smoke exposure-induced growth retardation and LBW during pre-/peri-implantation embryonic development.
doi:10.1016/j.tox.2008.01.014
PMCID: PMC2746649  PMID: 18316152
Embryo; Fetus; Pre-implantation; Cigarette smoke; Tobacco; Low birth weight
6.  Impact of active and passive smoking as risk factors for asthma and COPD in women presenting to primary care in Syria: first report by the WHO-GARD survey group 
Background
The burden of chronic respiratory disease (CRD) is alarming. International studies suggest that women with CRD are undersurveyed and underdiagnosed by physicians worldwide. It is unclear what the prevalence of CRD is in the general population of Syria, particularly among women, since there has never been a survey on CRD in this nation. The purpose of this study was to investigate the impact of different patterns of smoking on CRD in women.
Materials and methods
We extracted data on smoking patterns and outcome in women from the Global Alliance Against Chronic Respiratory Diseases survey. Using spirometric measurements before and after the use of inhaled bronchodilators, we tracked the frequency of CRD in females active and passive narghile or cigarette smokers presenting to primary care. We administered the questionnaire to 788 randomly selected females seen during 1 week in the fiscal year 2009–2010 in 22 primary care centers in six different regions of Syria. Inclusion criteria were age >6 years, presenting for any medical complaint. In this cross-sectional study, three groups of female subjects were evaluated: active smokers of cigarettes, active smokers of narghiles, and passive smokers of either cigarettes or narghiles. These three groups were compared to a control group of female subjects not exposed to active or passive smoking.
Results
Exposure to active cigarette smoke but not narghile smoke was associated with doctor-diagnosed chronic obstructive pulmonary disease (COPD). However, neither cigarette nor narghile active smoking was associated with increased incidence of spirometrically diagnosed COPD. Paradoxically, exposure to passive smoking of either cigarettes or narghiles resulted in association with airway obstruction, defined as forced expiratory volume in 1 second (FEV1)/forced vital capacity (FVC) < 70% according to the Global initiative for chronic Obstructive Lung Disease criteria; association with FEV1 < 80% predicted, evidencing moderate to severe GOLD spirometric grade, and doctor-diagnosed COPD. Physicians tend to underdiagnose COPD in women who present to primary care clinics. Whereas around 15% of enrolled women had evidence of COPD with FEV1/FVC < 70% after bronchodilators, only 4.8% were physician-diagnosed. Asthma did not appear to be a significant spirometric finding in these female subjects, although around 11% had physician-diagnosed asthma. One limitation is FEV1/FVC < 70% could have also resulted from uncontrolled asthma. The same limitation has been reported by the Proyecto Latinoamericano de Investigacion en Obstruccion Pulmonar (PLATINO) study.
Conclusion
Contrary to popular belief in developing countries, women exposed to tobacco smoke, whether active or passive, and whether by cigarettes or narghiles, like men are at increased risk for the development of COPD, although cultural habits and taboos may decrease the risk of active smoking in some women.
Recommendations
These findings will be considered for country and region strategy for noncommunicable diseases, to overcome underdiagnosis of CRD in women, fight widespread female cigarette and narghile smoking, and promote behavioral research in this field.
doi:10.2147/COPD.S50551
PMCID: PMC3794890  PMID: 24124359
passive smoking; women; COPD; asthma; narghile; water pipe; behavior
7.  Effects of In Utero and Childhood Tobacco Smoke Exposure and β2-Adrenergic Receptor Genotype on Childhood Asthma and Wheezing 
Pediatrics  2008;122(1):e107-e114.
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.
doi:10.1542/peds.2007-3370
PMCID: PMC2748980  PMID: 18558635
β-2 adrenergic receptor; prenatal exposure; secondhand-smoke exposure; asthma; wheeze
8.  Incidence of asthma in Swedish teenagers: relation to sex and smoking habits. 
Thorax  1995;50(3):260-264.
BACKGROUND--The prevalence of asthma and the use of asthma drugs is increasing worldwide. Studies of the incidence of asthma are few but are of interest in finding factors associated with onset of the disease. A study was performed to estimate the incidence of asthma and its relation to sex and to tobacco smoking between the ages of 16 and 19 years, and to compare the incidence of asthma with the proportion of individuals receiving a prescription of an asthma drug for the first time during one year. METHODS--A questionnaire was sent in 1990 to all 3627 individuals born in 1974 living in the county of Jämtland and Gästrikland, the southern part of the county of Gävleborg in central Sweden. Individuals reporting airways disease or obstructive symptoms were investigated with a further interview and lung function tests. The cross sectional questionnaire study was repeated in 1993. The incidence of asthma was calculated in the 2308 individuals who answered the questionnaire in both surveys and who were found not to have asthma in 1990. RESULTS--The yearly incidence of asthma defined from self reported disease, physician diagnosed asthma, drug use, or asthma associated symptoms was between 0.8% and 1.3%, depending on the criteria used. All criteria used resulted in a higher incidence in female subjects. Female sex was a risk factor for asthma when standardised for smoking, and smoking was also a risk factor for asthma when standardised for sex to all but two of the criteria used. In all the criteria the increased risk of asthma combined with smoking was greater in female subjects. CONCLUSION--The yearly incidence of asthma was about 1% between the ages of 16 and 19 years. Smoking and female sex were found to be risk factors for asthma. The incidence of asthma was close to the incidence of new drug use for asthma.
PMCID: PMC1021189  PMID: 7660339
9.  Association of Secondhand Smoke Exposure with Pediatric Invasive Bacterial Disease and Bacterial Carriage: A Systematic Review and Meta-analysis 
PLoS Medicine  2010;7(12):e1000374.
Majid Ezzati and colleagues report the findings of a systematic review and meta-analysis that probes the association between environmental exposure to secondhand smoke and the epidemiology of pediatric invasive bacterial disease.
Background
A number of epidemiologic studies have observed an association between secondhand smoke (SHS) exposure and pediatric invasive bacterial disease (IBD) but the evidence has not been systematically reviewed. We carried out a systematic review and meta-analysis of SHS exposure and two outcomes, IBD and pharyngeal carriage of bacteria, for Neisseria meningitidis (N. meningitidis), Haemophilus influenzae type B (Hib), and Streptococcus pneumoniae (S. pneumoniae).
Methods and Findings
Two independent reviewers searched Medline, EMBASE, and selected other databases, and screened articles for inclusion and exclusion criteria. We identified 30 case-control studies on SHS and IBD, and 12 cross-sectional studies on SHS and bacterial carriage. Weighted summary odd ratios (ORs) were calculated for each outcome and for studies with specific design and quality characteristics. Tests for heterogeneity and publication bias were performed. Compared with those unexposed to SHS, summary OR for SHS exposure was 2.02 (95% confidence interval [CI] 1.52–2.69) for invasive meningococcal disease, 1.21 (95% CI 0.69–2.14) for invasive pneumococcal disease, and 1.22 (95% CI 0.93–1.62) for invasive Hib disease. For pharyngeal carriage, summary OR was 1.68 (95% CI, 1.19–2.36) for N. meningitidis, 1.66 (95% CI 1.33–2.07) for S. pneumoniae, and 0.96 (95% CI 0.48–1.95) for Hib. The association between SHS exposure and invasive meningococcal and Hib diseases was consistent regardless of outcome definitions, age groups, study designs, and publication year. The effect estimates were larger in studies among children younger than 6 years of age for all three IBDs, and in studies with the more rigorous laboratory-confirmed diagnosis for invasive meningococcal disease (summary OR 3.24; 95% CI 1.72–6.13).
Conclusions
When considered together with evidence from direct smoking and biological mechanisms, our systematic review and meta-analysis indicates that SHS exposure may be associated with invasive meningococcal disease. The epidemiologic evidence is currently insufficient to show an association between SHS and invasive Hib disease or pneumococcal disease. Because the burden of IBD is highest in developing countries where SHS is increasing, there is a need for high-quality studies to confirm these results, and for interventions to reduce exposure of children to SHS.
Please see later in the article for the Editors' Summary
Editors' Summary
Background
The deleterious health effects of smoking on smokers are well established, but smoking also seriously damages the health of nonsmokers. Secondhand smoke (SHS), which is released by burning cigarettes and exhaled by smokers, contains hundreds of toxic chemicals that increase the risk of adults developing lung cancer and heart disease. Children, however, are particularly vulnerable to the effects of SHS exposure (also known as passive smoking) because they are still developing physically. In addition, children have little control over their indoor environment and thus can be heavily exposed to SHS. Exposure to SHS increases the risk of ear infections, asthma, respiratory symptoms (coughing, sneezing, and breathlessness), and lung infections such as pneumonia and bronchitis in young children and the risk of sudden infant death syndrome during the first year of life.
Why Was This Study Done?
Several studies have also shown an association between SHS exposure (which damages the lining of the mouth, throat, and lungs and decreases immune defenses) and potentially fatal invasive bacterial disease (IBD) in children. In IBD, bacteria invade the body and grow in normally sterile sites such as the blood (bacteremia) and the covering of the brain (meningitis). Three organisms are mainly responsible for IBD in children—Streptococcus pneumoniae, Haemophilus influenzae type B (Hib), and Neisseria meningitidis. In 2000, S. pneumonia (pneumococcal disease) alone killed nearly one million children. Here, the researchers undertake a systematic review and meta-analysis of the association between SHS exposure in children and two outcomes—IBD and the presence of IBD-causing organisms in the nose and throat (bacterial carriage). A systematic review uses predefined criteria to identify all the research on a given topic; meta-analysis is a statistical method that combines the results of several studies. By combining data, it is possible to get a clearer view of the causes of a disease than is possible from individual studies.
What Did the Researchers Do and Find?
The researchers identified 30 case-control studies that compared the occurrence of IBD over time in children exposed to SHS with its occurrence in children not exposed to SHS. They also identified 12 cross-sectional studies that measured bacterial carriage at a single time point in children exposed and not exposed to SHS. The researchers used the data from these studies to calculate a “summary odds ratio” (OR) for each outcome—a measure of how SHS exposure affected the likelihood of each outcome. Compared with children unexposed to SHS, exposure to SHS doubled the likelihood of invasive meningococcal disease (a summary OR for SHS exposure of 2.02). Summary ORs for invasive pneumococcal disease and Hib diseases were 1.21 and 1.22, respectively. However, these small increases in the risk of developing these IBDs were not statistically significant unlike the increase in the risk of developing meningococcal disease. That is, they might have occurred by chance. For bacterial carriage, summary ORs for SHS exposure were 1.68 for N. meningitidis, 1.66 for S. pneumonia (both these ORs were statistically significant), and 0.96 for Hib (a nonsignificant decrease in risk).
What Do These Findings Mean?
These findings indicate that SHS exposure is significantly associated with invasive meningococcal disease among children. However, the evidence that SHS exposure is associated with invasive pneumococcal and Hib disease is only suggestive. These findings also indicate that exposure to SHS is associated with an increased carriage of N. meningitidis and S. pneumoniae. The accuracy and generalizability of these findings is limited by the small number of studies identified, by the lack of studies from developing countries where SHS exposure is increasing and the burden of IBD is high, and by large variations between the studies in how SHS exposure was measured and IBD diagnosed. Nevertheless, they suggest that, by reducing children's exposure to SHS (by, for example, persuading parents not to smoke at home), the illness and death caused by IBDs among children could be greatly reduced. Such a reduction would be particularly welcome in developing countries where vaccination against IBDs is low.
Additional Information
Please access these Web sites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.1000374.
The US Centers for Disease Control and Prevention provides information on secondhand smoke, on children and secondhand smoke exposure, on meningitis, and on Hib infection
The US Environmental Protection Agency also provides information on the health effects of exposure to secondhand smoke (in English and Spanish) and a leaflet (also in English and Spanish) entitled Secondhand Tobacco Smoke and the Health of Your Family
The US Office of the Surgeon General provides information on the health consequences of involuntary exposure to tobacco smoke
The World Health Organization provides a range of information on the global tobacco epidemic
The World Health Organization has information on meningococcal disease (in English only) and on Hib (in several languages)
The US National Foundation for Infectious Diseases provides a fact sheet on pneumococcal disease
doi:10.1371/journal.pmed.1000374
PMCID: PMC2998445  PMID: 21151890
10.  Parental smoking during pregnancy and risk of overweight and obesity in the daughter 
Objective
Emerging evidence suggests that prenatal exposures may affect long-term health outcomes. In utero exposure to smoking is associated with an increased risk of overweight and obesity in children and adolescents. However, few studies have examined how prenatal exposure to parental smoking influences risk of obesity in adulthood and whether these associations are independent of childhood and adolescent adiposity. The aim of the current study was to investigate whether prenatal exposure to parental smoking influences body size in adulthood and whether any association may be mediated by childhood and adolescent body size.
Methods
We investigated the association between parental smoking during pregnancy and risk of overweight and obesity in adulthood and at age 18, and adiposity during childhood among 35,370 participants in the Nurses’ Health Study II. Data on smoking during pregnancy and socioeconomic variables were provided by the mothers, and anthropometric data and adult risk factors were reported by participants.
Results
After adjustment for socioeconomic and behavioral variables, maternal smoking during pregnancy was associated with adiposity at ages 5–10, age 18, and during adulthood. For age 18 overweight the ORs (95% CIs) for 1–14, 15–24, and 25+cigarettes/day were 1.13 (1.18–1.50), 1.40 (1.20–1.64), and 1.15 (0.79–1.69) and for obesity were 1.41 (1.14–1.75), 1.69 (1.31–2.18), and 2.36 (1.44–3.86). The corresponding ORs (95% CIs) for obesity in adulthood were 1.26 (1.16–1.37), 1.46 (1.30–1.63), and 1.43 (1.10–1.86). Risk of adiposity was not increased among daughters whose mothers stopped smoking during the first trimester (OR [95% CI] for overweight (1.03 [95% CI 0.90–1.17] and obesity (1.12 [95% CI 0.97–1.30]). Women whose fathers smoked during pregnancy were also at increased risk of overweight and obesity in adulthood with covariate-adjusted ORs (95% CIs) for obesity of 1.19 (1.11–1.29) for 1–14 cigarettes/day, 1.27 (1.18–1.37) for 15–24 cigarettes/day, and 1.40 (1.27–1.54) for 25+ cigarettes/day compared to fathers who did not smoke (ptrend<0.0001). Paternal smoking during pregnancy was also associated with an increased risk of obesity at age 18 among those whose fathers smoked 15 or more cigarettes/day but was not associated with childhood body size.
Conclusions
Maternal smoking during pregnancy was associated in a dose-response manner with overweight and obesity in the daughter through adolescence and adult life. Smoking cessation during the first trimester appears to mitigate this excess risk.
Paternal smoking was also associated with risk of overweight and obesity of the adult daughter and this association persisted after adjustment for maternal smoking.
doi:10.1038/ijo.2013.101
PMCID: PMC3795801  PMID: 23736356
pregnancy; prenatal programming; cigarette smoking; obesity
11.  Transforming Growth Factor-β1 C-509T Polymorphism, Oxidant Stress, and Early-Onset Childhood Asthma 
Rationale: Transforming growth factor (TGF)-β1 is involved in airway inflammation and remodeling, two key processes in asthma pathogenesis. Tobacco smoke and traffic emissions induce airway inflammation and modulate TGF-β1 gene expression. We hypothesized that the effects of functional TGF-β1 variants on asthma occurrence vary by these exposures.
Objectives: We tested these hypotheses among 3,023 children who participated in the Children's Health Study.
Methods: Tagging single-nucleotide polymorphisms rs4803457 C>T and C-509T (a functional promoter polymorphism) accounted for 94% of the haplotype diversity of the upstream region. Exposure to maternal smoking in utero was based on smoking by biological mother during pregnancy. Residential distance from nearest freeway was calculated based on residential address at study entry.
Measurements and Main Results: Children with the −509TT genotype had a 1.8-fold increased risk of early persistent asthma (95% confidence interval [CI], 1.11–2.95). This association varied marginally significantly by in utero exposure to maternal smoking. Compared with children with the −509CC/CT genotype with no in utero exposure to maternal smoking, those with the −509TT genotype with such exposure had a 3.4-fold increased risk of early persistent asthma (95% CI, 1.46–7.80; interaction, P = 0.11). The association between TGF-β1 C-509T and lifetime asthma varied by residential proximity to freeways (interaction P = 0.02). Children with the −509TT genotype living within 500 m of a freeway had over three-fold increased lifetime asthma risk (95% CI, 1.29–7.44) compared with children with CC/CT genotype living > 1500 m from a freeway.
Conclusions: Children with the TGF-β1 −509TT genotype are at increased risk of asthma when they are exposed to maternal smoking in utero or to traffic-related emissions.
doi:10.1164/rccm.200704-561OC
PMCID: PMC2176104  PMID: 17673695
maternal smoking; traffic; asthma; genetics; gene–environment interaction; association study
12.  A Longitudinal Study of Medicaid Coverage for Tobacco Dependence Treatments in Massachusetts and Associated Decreases in Hospitalizations for Cardiovascular Disease 
PLoS Medicine  2010;7(12):e1000375.
Thomas Land and colleagues show that among Massachusetts Medicaid subscribers, use of a comprehensive tobacco cessation pharmacotherapy benefit was followed by a substantial decrease in claims for hospitalizations for acute myocardial infarction and acute coronary heart disease.
Background
Insurance coverage of tobacco cessation medications increases their use and reduces smoking prevalence in a population. However, uncertainty about the impact of this coverage on health care utilization and costs is a barrier to the broader adoption of this policy, especially by publicly funded state Medicaid insurance programs. Whether a publicly funded tobacco cessation benefit leads to decreased medical claims for tobacco-related diseases has not been studied. We examined the experience of Massachusetts, whose Medicaid program adopted comprehensive coverage of tobacco cessation medications in July 2006. Over 75,000 Medicaid subscribers used the benefit in the first 2.5 years. On the basis of earlier secondary survey work, it was estimated that smoking prevalence declined among subscribers by 10% during this period.
Methods and Findings
Using claims data, we compared the probability of hospitalization prior to use of the tobacco cessation pharmacotherapy benefit with the probability of hospitalization after benefit use among Massachusetts Medicaid beneficiaries, adjusting for demographics, comorbidities, seasonality, influenza cases, and the implementation of the statewide smoke-free air law using generalized estimating equations. Statistically significant annualized declines of 46% (95% confidence interval 2%–70%) and 49% (95% confidence interval 6%–72%) were observed in hospital admissions for acute myocardial infarction and other acute coronary heart disease diagnoses, respectively. There were no significant decreases in hospitalizations rates for respiratory diagnoses or seven other diagnostic groups evaluated.
Conclusions
Among Massachusetts Medicaid subscribers, use of a comprehensive tobacco cessation pharmacotherapy benefit was associated with a significant decrease in claims for hospitalizations for acute myocardial infarction and acute coronary heart disease, but no significant change in hospital claims for other diagnoses. For low-income smokers, removing the barriers to the use of smoking cessation pharmacotherapy has the potential to decrease short-term utilization of hospital services.
Please see later in the article for the Editors' Summary
Editors' Summary
Background
Smoking is the leading preventable cause of death in the world. Globally, it is responsible for one in ten deaths among adults. In developed countries, the death toll is even higher—in the USA and the UK, for example, one in five deaths are caused by cigarette smoking. In the USA alone, where a fifth of adults smoke, smoking accounts for more than 400,000 deaths every year; globally, smoking causes 5 million deaths per year. On average, smokers die 14 years earlier than nonsmokers, and half of all long-term smokers will die prematurely because of a smoking-related disease. These diseases include lung cancer, other types of cancer, heart disease, stroke, and lung diseases such as chronic airway obstruction, bronchitis, and emphysema. And, for every smoker who dies from one of these smoking-related diseases, another 20 will develop at least one serious disease because of their addiction to tobacco.
Why Was This Study Done?
About half of US smokers try to quit each year but most of these attempts fail. Many experts believe that counseling and/or treatment with tobacco cessation medications such as nicotine replacement products help smokers to quit. In the USA, where health care is paid for through private or state health insurance, there is some evidence that insurance coverage of tobacco cessation medications increases their use and reduces smoking prevalence. However, smoking cessation treatment is poorly covered by US health insurance programs, largely because of uncertainty about the impact of such coverage on health care costs. It is unknown, for example, whether the introduction of publicly funded tobacco cessation benefits decreases claims for treatment for tobacco-related diseases. In this longitudinal study (a study that follows a group of individuals over a period of time), the researchers ask whether the adoption of comprehensive coverage of tobacco cessation medications by the Massachusetts Medicaid program (MassHealth) in July 2006 has affected claims for treatment for tobacco-related diseases. During its first two and half years, more than 75,000 MassHealth subscribers used the tobacco cessation medication benefit and smoking prevalence among subscribers declined by approximately 10% (38.3% to 28.8%).
What Did the Researchers Do and Find?
The researchers used MassHealth claims data and a statistical method called generalized estimating equations to compare the probability of hospitalization prior to the use of tobacco cessation medication benefit with the probability of hospitalization after benefit use among MassHealth subscribers. After adjusting for other factors that might have affected hospitalization such as influenza outbreaks and the implementation of the Massachusetts Smoke-Free Workplace Law in July 2004, there was a statistically significant annualized decline in hospital admissions for heart attack of 46% after use of the tobacco cessation medication benefit. That is, the calculated annual rate of admissions for heart attacks was 46% lower after use of the benefit than before among MassHealth beneficiaries. There was also a 49% annualized decline in admissions for coronary atherosclerosis, another smoking-related heart disease. There were no significant changes in hospitalization rates for lung diseases (including asthma, pneumonia, and chronic airway obstruction) or for seven other diagnostic groups.
What Do These Findings Mean?
These findings show that, among MassHealth subscribers, the use of a tobacco cessation medication benefit was followed by a significant decrease in claims for hospitalization for heart attack and for coronary atherosclerosis but not for other diseases. It does not, however, show that the reduced claims for hospitalization were associated with a reduction in smoking because smoking cessation was not recorded by MassHealth. Furthermore, it is possible that the people who used the tobacco cessation medication benefit shared other characteristics that reduced their chances of hospitalization for heart disease. For example, people using tobacco cessation medication might have been more likely to adhere to prescription schedules for medications such as statins that would also reduce their risk of heart disease. Finally, these findings might be unique to Massachusetts, so similar studies need to be undertaken in other states. Nevertheless, the results of this study suggest that, for low-income smokers, removing financial barriers to the use of smoking cessation medications has the potential to produce short-term decreases in the use of hospital services that will, hopefully, outweigh the costs of comprehensive tobacco cessation medication benefits.
Additional Information
Please access these Web sites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.1000375.
The US Centers for Disease Control and Prevention Office on Smoking and Health has information on all aspects of smoking and health, including advice on how to quit
The UK National Health Service Choices Web site provides advice about quitting smoking; more advice on quitting is provided by Smokefree
The American Heart Association provides information on heart disease, including advice on how to quit smoking (in several languages)
Information about MassHealth is available, including information on smoking and tobacco use prevention
doi:10.1371/journal.pmed.1000375
PMCID: PMC3000429  PMID: 21170313
13.  “Efforts to Reprioritise the Agenda” in China: British American Tobacco's Efforts to Influence Public Policy on Secondhand Smoke in China 
PLoS Medicine  2008;5(12):e251.
Background
Each year, 540 million Chinese are exposed to secondhand smoke (SHS), resulting in more than 100,000 deaths. Smoke-free policies have been demonstrated to decrease overall cigarette consumption, encourage smokers to quit, and protect the health of nonsmokers. However, restrictions on smoking in China remain limited and ineffective. Internal tobacco industry documents show that transnational tobacco companies (TTCs) have pursued a multifaceted strategy for undermining the adoption of restrictions on smoking in many countries.
Methods and Findings
To understand company activities in China related to SHS, we analyzed British American Tobacco's (BAT's) internal corporate documents produced in response to litigation against the major cigarette manufacturers to understand company activities in China related to SHS. BAT has carried out an extensive strategy to undermine the health policy agenda on SHS in China by attempting to divert public attention from SHS issues towards liver disease prevention, pushing the so-called “resocialisation of smoking” accommodation principles, and providing “training” for industry, public officials, and the media based on BAT's corporate agenda that SHS is an insignificant contributor to the larger issue of air pollution.
Conclusions
The public health community in China should be aware of the tactics previously used by TTCs, including efforts by the tobacco industry to co-opt prominent Chinese benevolent organizations, when seeking to enact stronger restrictions on smoking in public places.
Monique Muggli and colleagues study British American Tobacco (BAT) internal documents and find that from the mid 1990s BAT pursued a strategy aimed at influencing the public debate on secondhand smoke in China.
Editors' Summary
Background.
Each year, about one million people die in China from tobacco-caused diseases, including cancer, heart disease, and lung disease. Although most of these deaths occur among smokers—300 million people smoke in China, accounting for one-third of the global “consumption” of cigarettes—more than 100,000 deaths from tobacco-related causes occur annually among the 540 million Chinese people who are exposed to secondhand smoke. Tobacco smoke contains 4,000 known chemicals, 69 of which are known or probable carcinogens, and, when it is produced in enclosed spaces, both smokers and nonsmokers are exposed to its harmful effects. The only effective way to reduce tobacco smoke exposure indoors to acceptable levels is to implement 100% smoke-free environments—ventilation, filtration, and the provision of segregated areas for smokers and nonsmokers are insufficient. Importantly, as well as protecting nonsmokers from secondhand smoke, the implementation of smoke-free public places also reduces the number of cigarettes smoked among continuing smokers, increases the likelihood of smokers quitting, and reduces the chances of young people taking up smoking.
Why Was This Study Done?
Article 8 of the World Health Organization's Framework Convention on Tobacco Control (FCTC; an international public-health treaty that seeks to reduce tobacco-caused death and disease) calls on countries party to the treaty to protect their citizens from secondhand smoke exposure. China became a party to the FCTC in 2005 but restrictions on smoking in public places in China remain limited and ineffective. Previous analyses of internal tobacco industry documents have revealed that transnational tobacco companies (TTCs) have used a multifaceted approach to undermine the adoption of restrictions on smoking in many countries. TTCs have been shown to influence media coverage of secondhand smoke issues and to promote ineffective ventilation and separate smoking and nonsmoking areas in restaurants, bars, and hotels (so-called “resocalization of smoking” accommodation principles) with the aim of undermining smoke-free legislation. In addition, TTCs have created organizations interested in non-tobacco-related diseases to draw attention away from the public-health implications of secondhand smoke. In this study, the researchers ask whether TTCs have used a similar approach to undermine the adoption of restrictions on smoking in China, one of the most coveted cigarette markets in the world by the major TTCs.
What Did the Researchers Do and Find?
The researchers analyzed internal corporate documents produced by British American Tobacco (BAT; the predominant TTC in China) in response to litigation against major cigarette manufacturers stored in document depositories in Minnesota, USA and Guildford, UK. Among these documents, they found evidence that BAT had attempted to divert attention from secondhand smoke issues toward liver disease prevention by funding the Beijing Liver Foundation (BFL) from its inception in 1997 until at least 2002 (the most recent year that BAT's corporate records are available for public review). The researchers also found evidence that BAT had promoted “resocialization of smoking” accommodation principles as a “route to avoid smoking bans” and pushed ventilation and air filtration in airports and in establishments serving food and drink. Finally, the researchers found evidence that BAT had sought to “present the message that ‘tobacco smoke is just one of the sources of air polution [sic] and a very insignificant one compared with other pollutants'” through presentations given to the Chinese tobacco industry and media seminars aimed at Chinese journalists.
What Do These Findings Mean?
These findings indicate that, beginning in the mid 1990s and continuing until at least 2002, BAT has followed an intensive, multi-pronged strategy designed to undermine the health policy agenda on secondhand smoke in China. Given their findings, the researchers suggest that BFL and other charitable organizations in China must be wary of accepting tobacco money and that measures must be taken to improve the transparency and accountability of these and other public organizations. To meet FCTC obligations under Article 5.3 (industry interference), policy makers in China, they suggest, must be made aware of how BAT and other TTCs have repeatedly sought to influence health policy in China by focusing attention toward the adoption of ineffective air filtration and ventilation systems in hospitality venues rather than the implementation of 100% smoke-free environments. Finally, Chinese policy makers and the media need to be better informed about BAT's long-standing attempts to communicate misleading messages to them about the health effects of secondhand smoke.
Additional Information.
Please access these Web sites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.0050251.
The World Health Organization's Regional Office for the Western Pacific provides smoking statistics for China and other countries in the region
The World Health Organization provides information on the health problems associated with secondhand smoke, about its Tobacco Free Initiative (available in several languages), and about the Framework Convention on Tobacco Control (also available in several languages)
MedlinePlus provides links to information about the dangers of secondhand smoke (available in English and Spanish)
The UK National Health Service Smokefree Web site provides information about the advantages of giving up smoking, how to give up smoking, and the dangers associated with secondhand smoke
British American Tobacco documents stored in the Minnesota and Guildford Depositories, including those analyzed in this study, can be searched through the British American Tobacco Documents Archive
doi:10.1371/journal.pmed.0050251
PMCID: PMC2605899  PMID: 19108603
14.  IL13 gene polymorphisms modify the effect of exposure to tobacco smoke on persistent wheeze and asthma in childhood, a longitudinal study 
Respiratory Research  2008;9(1):2.
Background
Tobacco smoke and genetic susceptibility are risk factors for asthma and wheezing. The aim of this study was to investigate whether there is a combined effect of interleukin-13 gene (IL13) polymorphisms and tobacco smoke on persistent childhood wheezing and asthma.
Methods
In the Isle of Wight birth cohort (UK, 1989–1999), five IL13 single nucleotide polymorphisms (SNPs): rs1800925 (-1112C/T), rs2066960, rs1295686, rs20541 (R130Q) and rs1295685 were genotyped. Parents were asked whether their children had wheezed in the last 12 months at ages 1, 2, 4 and 10 years. Children who reported wheeze in the first 4 years of life and also had wheezing at age 10 were classified as early-onset persistent wheeze phenotype; non-wheezers never wheezed up to age 10. Persistent asthma was defined as having a diagnosis of asthma both during the first four years of life and at age 10. Logistic regression methods were used to analyze data on 791 children with complete information. Potential confounders were gender, birth weight, duration of breast feeding, and household cat or dog present during pregnancy.
Results
Maternal smoking during pregnancy was associated with early-onset persistent wheeze (OR 2.93, p < 0.0001); polymorphisms in IL13 were not (OR 1.15, p = 0.60 for the common haplotype pair). However, the effect of maternal smoking during pregnancy was stronger in children with the common IL13 haplotype pair compared to those without it (OR 5.58 and OR 1.29, respectively; p for interaction = 0.014). Single SNP analysis revealed a similar statistical significance for rs20541 (p for interaction = 0.02). Comparable results were observed for persistent childhood asthma (p for interaction = 0.03).
Conclusion
This is the first report that shows a combined effect of in utero exposure to smoking and IL13 on asthma phenotypes in childhood. The results emphasize that genetic studies need to take environmental exposures into account, since they may explain contradictory findings.
doi:10.1186/1465-9921-9-2
PMCID: PMC2265286  PMID: 18186920
15.  Early-life environmental risk factors for asthma: findings from the Children's Health Study. 
Environmental Health Perspectives  2004;112(6):760-765.
Early-life experiences and environmental exposures have been associated with childhood asthma. To investigate further whether the timing of such experiences and exposures is associated with the occurrence of asthma by 5 years of age, we conducted a prevalence case-control study nested within the Children's Health Study, a population-based study of > 4,000 school-aged children in 12 southern California communities. Cases were defined as physician-diagnosed asthma by age 5, and controls were asthma-free at study entry, frequency-matched on age, sex, and community of residence and countermatched on in utero exposure to maternal smoking. Telephone interviews were conducted with mothers to collect additional exposure and asthma histories. Conditional logistic regression models were fitted to estimate odds ratios (ORs) and 95% confidence intervals (CIs). Asthma diagnosis before 5 years of age was associated with exposures in the first year of life to wood or oil smoke, soot, or exhaust (OR = 1.74; 95% CI, 1.02-2.96), cockroaches (OR = 2.03; 95% CI, 1.03-4.02), herbicides (OR = 4.58; 95% CI, 1.36-15.43), pesticides (OR = 2.39; 95% CI, 1.17-4.89), and farm crops, farm dust, or farm animals (OR = 1.88; 95% CI, 1.07-3.28). The ORs for herbicide, pesticide, farm animal, and crops were largest among children with early-onset persistent asthma. The risk of asthma decreased with an increasing number of siblings (ptrend = 0.01). Day care attendance within the first 4 months of life was positively associated with early-onset transient wheezing (OR = 2.42; 95% CI, 1.28-4.59). In conclusion, environmental exposures during the first year of life are associated with childhood asthma risk.
PMCID: PMC1241973  PMID: 15121522
16.  Influence of family income on hospital visits for asthma among Canadian school children 
Thorax  2002;57(6):513-517.
Background: A study was undertaken to investigate the mechanisms by which socioeconomic status may influence asthma morbidity in Canada.
Methods: A total of 2968 schoolchildren aged 5–19 years with reported asthma were divided into three family income ranges. Hospital visits and risk factors for asthma, ascertained by questionnaire, were compared between the three groups.
Results: The mean (SE) annual period prevalence of a hospital visit was 25.0 (3.1)% among schoolchildren with household incomes of less than $20 000 Canadian compared with 16.0 (1.3)% among those with incomes of more than $60 000 (p<0.05). Students with asthma from lower income households were more likely to be younger and exposed to environmental tobacco smoke and cats, and their parents were more likely to have a lower educational attainment and be unmarried (p<0.05). Across all income groups, younger age, lower parental education, having unmarried parents, and regular exposure to environmental tobacco smoke were each associated with an increase in risk of a hospital visit (p<0.05). No increased risk was detected due to sex, having pets, and not taking dust control measures. Although not statistically significant at p<0.05, there may have been an interactive effect between income and susceptibility to environmental tobacco smoke. In the lower income group those children who were regularly exposed to second hand smoke had a 79% higher risk of a hospital visit compared with a 45% higher risk in the higher income group. In a logistic regression model the association between income and hospital visit was no longer significant after adjusting for differences in reported exposure to passive smoking.
Conclusion: Socially disadvantaged Canadian schoolchildren have increased asthma morbidity. Exposure to cigarette smoke appears to be one important explanation for this observation.
doi:10.1136/thorax.57.6.513
PMCID: PMC1746352  PMID: 12037226
17.  Ozone, Oxidant Defense Genes, and Risk of Asthma during Adolescence 
Rationale: Although oxidative stress is a cardinal feature of asthma, the roles of oxidant air pollutants and antioxidant genes heme oxygenase 1 (HMOX-1), catalase (CAT), and manganese superoxide dismutase (MNSOD) in asthma pathogenesis have yet to be determined.
Objectives: We hypothesized that the functional polymorphisms of HMOX-1 ([GT]n repeat), CAT (−262C>T −844C>T), and MNSOD (Ala-9Val) are associated with new-onset asthma, and the effects of these variants vary by exposure to ozone, a potent oxidant air pollutant.
Methods: We assessed this hypothesis in a population-based cohort of non-Hispanic (n = 1,125) and Hispanic white (n = 586) children who resided in 12 California communities and who were followed annually for 8 years to ascertain new-onset asthma.
Measurements and Main Results: Air pollutants were continuously measured in each of the study communities during the 8 years of study follow-up. HMOX-1 “short” alleles (<23 repeats) were associated with a reduced risk for new-onset asthma among non-Hispanic whites (hazard ratio [HR], 0.64; 95% confidence interval [CI], 0.41–0.99). This protective effect was largest in children residing in low-ozone communities (HR, 0.48; 95% CI, 0.25–0.91) (interaction P value = 0.003). Little evidence for an association with HMOX-1 was observed among Hispanic children. In contrast, Hispanic children with a variant of the CAT-262 “T” allele (CT or TT) had an increased risk for asthma (HR, 1.78; P value = 0.01). The effects of these polymorphisms were not modified by personal smoking or secondhand-smoke exposure.
Conclusions: Functional promoter variants in CAT and HMOX-1 showed ethnicity-specific associations with new-onset asthma. Oxidant gene protection was restricted to children living in low-ozone communities.
doi:10.1164/rccm.200706-863OC
PMCID: PMC2258440  PMID: 18048809
asthma; catalase; heme oxygenase-1; MnSOD; oxidative stress; ozone
18.  Parental smoking and adolescent smoking initiation: an intergenerational perspective on tobacco control 
Pediatrics  2009;123(2):e274-e281.
Objective
Adolescence is an important period of risk for the development of lifelong smoking behaviors. Compelling, although inconsistent, evidence suggests a relation between parental smoking and the risk of smoking initiation during adolescence. This study investigates unresolved issues concerning the strength and nature of the association between parent smoking and offspring smoking initiation.
Methods
We enrolled 564 adolescents aged 12-17, along with one of their parents, into the New England Family Study between 2001-2004. Lifetime smoking histories were obtained from parents and their adolescent offspring. Discrete-time survival analysis was used to investigate the influence of parental smoking histories on the risk of adolescent smoking initiation.
Results
Parental smoking was associated with a significantly higher risk of smoking initiation in adolescent offspring (odds ratio=2.81, 95% CI=1.78, 4.41). In addition, the likelihood of offspring smoking initiation increased with the number of smoking parents and the duration of exposure to parental smoking, suggesting a dose-response relation between parental smoking and offspring smoking. Offspring of parents who had quit smoking were no more likely to smoke than offspring of parents who had never smoked. The effects of parental smoking on offspring initiation differed by sex (with a stronger effect of father's smoking on boys than girls), developmental period (with a stronger effect of parental smoking before the adolescent was age 13 than afterwards), and residence of parents (with effects of father's smoking being dependent on living in the same household as the adolescent). Parental smoking was also associated with stronger negative reactions to adolescents' first cigarette, a potential marker of the risk of progression to higher levels of use.
Conclusions
Parental smoking is an important source of vulnerability to smoking initiation among adolescents, and parental smoking cessation might attenuate this vulnerability.
doi:10.1542/peds.2008-2251
PMCID: PMC2632764  PMID: 19171580
Smoking; adolescents; parent-offspring transmission
19.  Characterizing Patterns of Smoking Initiation in Adolescence: Comparison of Methods for Dealing With Missing Data 
Nicotine & Tobacco Research  2011;13(12):1266-1275.
Introduction:
Tobacco use is common and remains one of the leading causes of preventable death in developed countries. Smoking commonly begins in adolescence, and hence, it is important to understand how smoking behavior develops during this period.
Methods:
In a U.K.-based birth cohort, we analyzed repeated measures of smoking frequency in a sample of 7,322 young adolescents. Latent class analysis was used to summarize the data, and the resulting classes of behavior were related to a range of smoking risk factors. Results from a complete case analysis were compared with estimation using full-information maximum likelihood (FIML) and estimation using multiple imputation (MI).
Results:
Fifty-three percent of the sample reported having smoked a whole cigarette by age 16 years. The longitudinal data were summarized by 4 distinct patterns of smoking initiation: nonsmokers (79.7%), experimenters (10.3%), late-onset regular smokers (5.5%), and early-onset regular smokers (4.5%). Social disadvantage, other substance use, conduct problems, and female sex were strongly related to being a regular smoker; however, no risk factors studied showed any strong or consistent association with experimentation. In the complete case sample, smoking prevalence was lower, and in addition, the association between different smoking patterns and covariates was often inconsistent with those obtained through FIML/MI.
Conclusions:
Most young people have experimented with tobacco smoking by age 16 years, and regular smoking is established in a substantial minority characterized by social disadvantage, other substance, use and conduct disorder. Prevention strategies should focus on this subgroup as most children who experiment with tobacco do not progress to regular smoking.
doi:10.1093/ntr/ntr161
PMCID: PMC3223580  PMID: 21994336
20.  Does maternal smoking during pregnancy predict the smoking patterns of young adult offspring? A birth cohort study 
Tobacco Control  2006;15(6):452-457.
Objective
To examine the association between maternal smoking during pregnancy and the development of smoking behaviour patterns among young adult offspring.
Method
Data were from the Mater‐University of Queensland Study of Pregnancy (MUSP), a birth cohort of 7223 mothers and children enrolled in Brisbane, Australia, in 1981. The development of smoking behaviours (early or late onset, or combination of onset and prevalence patterns) among offspring at age 21 years with different patterns of maternal smoking (never smoked, smoked before or after pregnancy but not during pregnancy, or smoked during pregnancy) were compared. Maternal smoking information was derived from the prospectively collected data from the beginning of pregnancy until the child was 14 years of age. Analyses were restricted to the 3058 mothers and children whose smoking status was reported.
Results
The proportion of young adults who smoked regularly, either with early onset or late onset, was greater among those whose mothers had smoked during pregnancy compared with those whose mothers had never smoked. The smoking patterns among those adolescent offspring whose mothers stopped smoking during pregnancy, but who then smoked at other times during the child's life, were similar to those whose mothers had never smoked. This association was robust to adjustment for a variety of potential covariates.
Conclusions
The findings provide some evidence for a direct effect of maternal smoking in utero on the development of smoking behaviour patterns of offspring and provide yet another incentive to persuade pregnant women not to smoke.
doi:10.1136/tc.2006.016790
PMCID: PMC2563674  PMID: 17130374
21.  Individual and Social Influences on Progression to Daily Smoking During Adolescence 
Pediatrics  2009;124(3):895-902.
Objectives
To identify individual and social predictors of progression to daily smoking by the end of high school among youth who initiated less than daily smoking by eighth grade.
Methods
The analysis sample of 270 adolescent smokers was taken from the longitudinal community panel of the Raising Healthy Children project. Data used in this study were taken from annual interviews between grades 7 and 12. Daily smoking was defined as having smoked at least one cigarette per day in the past 30 days at the time of each interview. Discrete-time survival analysis was used to assess the overall and unique associations between hazard of progression to daily smoking and time-varying measures of potential individual, family, peer, and school predictors.
Results
. A total of 58% (n = 156) of the analysis sample made the transition to daily smoking by grade 12. The likelihood of onset of daily smoking among those who had not yet onset was smallest in grade 9 (.12) and greatest at grade 12 (.25). Youth depression, prosocial belief, and antisocial behavior had overall associations with risk of smoking escalation. In addition, parental and peer cigarette use, family management, academic achievement, and school commitment had significant univariate associations with smoking progression. After adjusting for gender, low-income status, and other potential predictors, youth antisocial behavior and parental and peer smoking predicted greater likelihood of escalation to daily smoking, while parental use of positive family management predicted lower likelihood of escalation.
Conclusions
. This study supports preventing escalation in adolescent smoking through targeting risk factors of parent and peer smoking and involvement in other forms of antisocial behavior and working with parents to improve their use of positive family management practices.
doi:10.1542/peds.2008-2015
PMCID: PMC2891669  PMID: 19706575
progression; daily smoking; smoking prevention; smoking predictors; family management
22.  Prospective study of asthma in relation to smoking habits among 14,729 adults. 
Thorax  1988;43(7):534-539.
The prevalence and incidence of asthma in relation to cigarette smoking habits was studied in a population of 14,729 Finnish adult men and women who participated in a postal health survey in 1975. Of those invited to participate in a new survey in 1981, 89.7% replied. Asthma was diagnosed on the basis of self reporting of asthma diagnosed by a physician and by record linkage to a national register of hospital admissions to all general and tuberculosis hospitals during 1972 and 1983. The prevalence of diagnosed asthma in 1975 was significantly higher among male smokers than among male non-smokers (relative risk (RR) = 1.73); no significant difference was observed for women (RR = 1.33). People with asthma were slightly but not significantly more likely to stop smoking during the six year follow up period (RR = 1.23). The incidence of asthma among those who had neither reported asthma in 1975 nor been admitted to hospital for asthma before the 1975 questionnaire study was not significantly higher among smokers than among non-smokers during follow up. Although possible mechanisms exist to explain how smoking could have a role in the aetiology of asthma, this study suggests that smoking is not a strong risk factor for asthma.
PMCID: PMC461360  PMID: 3269222
23.  Association Between Trauma Exposure and Smoking in a Population-Based Sample of Young Adults 
Purpose
To evaluate the relationship between smoking and trauma exposure in a population-based, longitudinal sample. Contrary to current smoking trends in the general population, recent findings indicate continued high smoking rates in trauma-exposed samples.
Methods
A nationally representative sample of 15,197 adolescents was followed from 1995 (mean age=15.6) to 2002 (mean age=22) as part of 3 waves of The National Longitudinal Study of Adolescent Health (Add Health). We examined the relation between self-reported trauma exposure and smoking behaviors (lifetime regular, current regular), nicotine dependence (Fagerström Test of Nicotine Dependence (FTND)), number of cigarettes per day, and age of onset of regular smoking.
Results
Controlling for demographics and depressive symptoms, exposure to traumatic events yielded a significant increase in the odds of lifetime regular smoking. Nicotine dependence and cigarettes smoked per day was also significantly related to exposure to Childhood Physical and Sexual Abuse. Decreased age of regular smoking onset was seen for those reporting Childhood Physical Abuse and Childhood Sexual Abuse.
Conclusions
Exposure to traumatic life events during childhood and young adulthood increases the risk of smoking, highlighting the need to prevent and treat tobacco use in this vulnerable population.
doi:10.1016/j.jadohealth.2007.08.029
PMCID: PMC2675188  PMID: 18295135
Traumatic Stress; Smoking; Nicotine Dependence; Adolescent; Depression
24.  Changes in Exposure to Secondhand Smoke Among Youth in Nebraska, 2002–2006 
Preventing Chronic Disease  2008;5(3):A84.
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.
PMCID: PMC2483572  PMID: 18558034
25.  The Global Youth Tobacco Survey: 2001–2002 in Riyadh region, the Kingdom of Saudi Arabia 
Background
Tobacco use is a major public health problem, and its prevalence is globally increasing, especially among children and adolescents.
Objective
The Global Youth Tobacco Survey aimed to explore the epidemiological trends and risk factors of tobacco smoking among intermediate school boys in Riyadh region of the Kingdom of Saudi Arabia.
Method
A two-stage cluster sample design was used to produce a representative sample of male students from selected schools. The participants (n = 1830) self recorded their responses on the Global Youth Tobacco Survey questionnaire.
Results
Lifetime prevalence of cigarette smoking was 35%, while 13% of students currently used other tobacco products. About 16% of students currently smoked at home, and 84% of students bought cigarettes without any refusal from storekeepers. Thirty-one percent and 39% of students were exposed to secondhand tobacco smoke inside and outside the house, respectively, which was definitely or probably harmful to health as opined by 87% of participants, and 74% voiced to ban smoking from public places. Among current smokers, 69% intended (without attempt) to quit and 63% attempted (but failed) to quit during the past year. Almost an equal number of students saw antismoking and prosmoking media messages in the last month, and 28% of students were offered free cigarettes by a tobacco company representative. In schools, more than 50% of students were taught about the dangers of cigarette smoking in the last year. Smoking by parents, older brothers, and close friends, watching prosmoking cigarette advertisements, free offer of cigarettes by tobacco company representatives, perception of smoking being not harmful, and continuing smoking which can be easily quit significantly increased the odds of smoking by students.
Conclusion
The common use of tobacco in school populations needs to be addressed by, among other tobacco control measures, a strict ban on cigarette selling to minors and intensive regular tobacco control campaigns involving health and religious messages.
Video abstract
doi:10.2147/SAR.S23626
PMCID: PMC3846322  PMID: 24474857
tobacco use; secondhand tobacco smoke; environmental tobacco smoke; intermediate school boys; Global Youth Tobacco Survey; Saudi Arabia

Results 1-25 (851727)