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 association of air pollution with the prevalence of chronic lower respiratory tract symptoms among children with a history of asthma or related symptoms was examined in a cross-sectional study. Parents of a total of 3,676 fourth, seventh, and tenth graders from classrooms in 12 communities in Southern California completed questionnaires that characterized the children's histories of respiratory illness and associated risk factors. The prevalences of bronchitis, chronic phlegm, and chronic cough were investigated among children with a history of asthma, wheeze without diagnosed asthma, and neither wheeze nor asthma. Average ambient annual exposure to ozone, particulate matter (PM(10) and PM(2.5); [less than/equal to] 10 microm and < 2.5 microm in aerodynamic diameter, respectively), acid vapor, and nitrogen dioxide (NO(2)) was estimated from monitoring stations in each community. Positive associations between air pollution and bronchitis and phlegm were observed only among children with asthma. As PM(10) increased across communities, there was a corresponding increase in the risk per interquartile range of bronchitis [odds ratio (OR) 1.4/19 microg/m(3); 95% confidence interval (CI), 1.1-1.8). Increased prevalence of phlegm was significantly associated with increasing exposure to all ambient pollutants except ozone. The strongest association was for NO(2), based on relative risk per interquartile range in the 12 communities (OR 2.7/24 ppb; CI, 1.4-5.3). The results suggest that children with a prior diagnosis of asthma are more likely to develop persistent lower respiratory tract symptoms when exposed to air pollution in Southern California.
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.
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.
A substantial number of adolescents are current and regular cigarette smokers, and there is a need to better understand factors that contribute to smoking behavior during these years. Sensation seeking (SS) is one factor that has consistently been associated with smoking, but less is known about mechanisms that may explain this relationship.
The present study tested the hypothesis that high school students high in SS would report heavier cigarette smoking and that this relationship would be mediated by negative affect and by perceptions about the risks of smoking. Students (n = 1,688) participated in an annual survey of substance use and related attitudes and characteristics.
As expected, higher SS was associated with greater levels of past 30-day (odds ratio [OR] = 1.46, p = .004) and lifetime (OR = 1.37, p = .004) smoking, particularly for males. Multiple mediation models indicated that effect of SS on both 30-day (combined indirect effect z = 5.38, p < .001) and lifetime (z = 6.14, p < .001) smoking was mediated by both negative affect and risk perception.
These findings suggest a need for increasing the sensation value of anti-tobacco messages to increase their efficacy for high SS youth. High SS youth may also benefit from prevention efforts designed to teach healthy ways of coping with negative affect.
Although specific pesticides have been associated with wheeze in farmers, little is known about pesticides and asthma. We used data from 19,704 male farmers in the Agricultural Health Study to evaluate lifetime use of 48 pesticides and prevalent adult-onset asthma, defined as doctor-diagnosed asthma after age 20. We categorized asthma cases as allergic (N=127) and non-allergic (N=314) based on their history of eczema or hayfever. We used polytomous logistic regression controlling for age, state, smoking, and body mass to assess pesticide associations.
High pesticide exposure events were associated with a doubling of both allergic and non-allergic asthma. For ever use, 12 individual pesticides were associated with allergic asthma and four with non-allergic asthma. For allergic asthma, coumaphos (odds ratio (OR) =2.34, 95% Confidence Interval (CI) =1.49,3.70), heptachlor (OR=2.01, 95%CI=1.30,3.11), parathion (OR=2.05, 95%CI=1.21,3.46), 80/20 mix (carbon tetrachloride/carbon disulfide) (OR=2.15, 95%CI=1.23,3.76) and ethylene dibromide (OR=2.07, 95%CI=1.02,4.20), all had odds ratios greater than 2.0 and significant exposure-response trends. For non-allergic asthma, DDT had the strongest association (OR=1.41, 95%CI=1.09,1.84) but with little evidence of increasing asthma with increasing use. Current animal handling and farm activities did not confound these results. We saw little evidence that allergy alone was driving these associations.
Pesticides may be an overlooked contributor to asthma risk among farmers.
allergy; farming; occupational exposure; pesticides; respiratory disease
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.
Traffic-related air pollution has been associated with adverse cardiorespiratory effects, including increased asthma prevalence. However, there has been little study of effects of traffic exposure at school on new-onset asthma.
We evaluated the relationship of new-onset asthma with traffic-related pollution near homes and schools.
Parent-reported physician diagnosis of new-onset asthma (n = 120) was identified during 3 years of follow-up of a cohort of 2,497 kindergarten and first-grade children who were asthma- and wheezing-free at study entry into the Southern California Children’s Health Study. We assessed traffic-related pollution exposure based on a line source dispersion model of traffic volume, distance from home and school, and local meteorology. Regional ambient ozone, nitrogen dioxide (NO2), and particulate matter were measured continuously at one central site monitor in each of 13 study communities. Hazard ratios (HRs) for new-onset asthma were scaled to the range of ambient central site pollutants and to the residential interquartile range for each traffic exposure metric.
Asthma risk increased with modeled traffic-related pollution exposure from roadways near homes [HR 1.51; 95% confidence interval (CI), 1.25–1.82] and near schools (HR 1.45; 95% CI, 1.06–1.98). Ambient NO2 measured at a central site in each community was also associated with increased risk (HR 2.18; 95% CI, 1.18–4.01). In models with both NO2 and modeled traffic exposures, there were independent associations of asthma with traffic-related pollution at school and home, whereas the estimate for NO2 was attenuated (HR 1.37; 95% CI, 0.69–2.71).
Traffic-related pollution exposure at school and homes may both contribute to the development of asthma.
air pollution; asthma; child; epidemiology; vehicular traffic
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.
The question of whether air pollution contributes to asthma onset remains unresolved.
In this study, we assessed the association between asthma onset in children and traffic-related air pollution.
We selected a sample of 217 children from participants in the Southern California Children’s Health Study, a prospective cohort designed to investigate associations between air pollution and respiratory health in children 10–18 years of age. Individual covariates and new asthma incidence (30 cases) were reported annually through questionnaires during 8 years of follow-up. Children had nitrogen dioxide monitors placed outside their home for 2 weeks in the summer and 2 weeks in the fall–winter season as a marker of traffic-related air pollution. We used multilevel Cox models to test the associations between asthma and air pollution.
In models controlling for confounders, incident asthma was positively associated with traffic pollution, with a hazard ratio (HR) of 1.29 [95% confidence interval (CI), 1.07–1.56] across the average within-community interquartile range of 6.2 ppb in annual residential NO2. Using the total interquartile range for all measurements of 28.9 ppb increased the HR to 3.25 (95% CI, 1.35–7.85).
In this cohort, markers of traffic-related air pollution were associated with the onset of asthma. The risks observed suggest that air pollution exposure contributes to new-onset asthma.
air pollution; asthma onset; children; nitrogen dioxide
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.
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.
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.
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.
Traumatic Stress; Smoking; Nicotine Dependence; Adolescent; Depression
Rationale: The potential role of physical activity in preventing asthma exacerbations is unknown.
Objectives: To investigate the longitudinal association between regular physical activity and asthma exacerbations.
Methods: A total of 2,818 women with asthma from a large U.S. cohort (the Nurses' Health Study) were monitored from 1998 to 2000. Physical activity was self-reported at baseline, using a validated questionnaire, and categorized in quintiles. Exacerbations during follow-up were defined as a self-report of asthma-related hospitalization, emergency department visit, or urgent office visit. Baseline information about severity of asthma, treatment, previous exacerbations, sociodemographic factors, smoking, and other potential confounders was obtained.
Measurements and Main Results: Participants had a mean age of 63 years, and 71% had mild-to-moderate persistent asthma. About half of the women were ever-smokers (48% former, 6% current), and median physical activity was 10 MET·hours/week (equivalent to walking at a brisk pace for 20 minutes three times per week). Risk of exacerbations during follow-up decreased with increasing level of physical activity. In a multivariate logistic regression model, the higher level of physical activity, the lower risk of admission (odds ratio 0.85, 0.81, 0.78, and 0.76, for the 2nd, 3rd, 4th, and 5th quintiles compared with the 1st quintile, P for trend = 0.05). There were no relevant differences on stratifying by age group, smoking status, body mass index, baseline use of inhaled corticosteroids, or previous exacerbations.
Conclusions: Regular physical activity was associated with reduced risk of exacerbations in women with asthma in this longitudinal study.
motor activity; exercise; asthma; epidemiology
environmental tobacco smoke (ETS) during childhood and in utero
exposure to maternal smoking are associated with adverse effects on
lung growth and development.
METHODS—A study was
undertaken of the associations between maternal smoking during
pregnancy, exposure to ETS, and pulmonary function in 3357 school
children residing in 12 Southern California communities. Current and
past exposure to household ETS and exposure to maternal smoking in
utero were assessed by a self-administered questionnaire completed by
parents of 4th, 7th, and 10th grade students in 1993.Standard linear
regression techniques were used to estimate the effects of in utero and
ETS exposure on lung function, adjusting for age, sex, race, Hispanic
ethnicity, height, weight, asthma, personal smoking, and selected
exposure to maternal smoking was associated with reduced peak
expiratory flow rate (PEFR) (-3.0%, 95% CI -4.4 to -1.4), mean mid
expiratory flow (MMEF) (-4.6%, 95% CI -7.0 to -2.3), and forced
expiratory flow (FEF75) (-6.2%, 95% CI -9.1 to -3.1),
but not forced expiratory volume in one second (FEV1). Adjusting for household ETS exposure did not substantially change these
estimates. The reductions in flows associated with in utero exposure
did not significantly vary with sex, race, grade, income, parental
education, or personal smoking. Exposure to two or more current
household smokers was associated with reduced MMEF (-4.1%, 95% CI
-7.6 to -0.4) and FEF75 (-4.4%, 95% CI -9.0 to 0.4).
Current or past maternal smoking was associated with reductions in PEFR and MMEF; however, after adjustment for in utero exposure, deficits in
MMEF and FEF75 associated with all measurements of ETS were substantially reduced and were not statistically significant.
exposure to maternal smoking is independently associated with decreased
lung function in children of school age, especially for small airway flows.
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
Little is known about the association between cigarette smoking and asthma severity. We assessed smoking as a determinant of disease severity and control in a cohort of clinic-referred allergic subjects who developed new onset asthma.
Allergic rhinitis subjects with no asthma (n = 371) were followed-up for 10 years and routinely examined for asthma diagnosis. In those who developed asthma (n = 152), clinical severity and levels of asthma control were determined. Among these subjects, 74 (48.7%) were current smokers, 17 (11.2%) former smokers, and 61 (40.1%) never smokers.
When comparing current or past smokers to never smokers they had a higher risk of severe asthma in the univariate analysis, which became non-significant in the multivariate analysis. On the other hand, the categories of pack-years were significantly related to severe asthma in a dose response relationship in both the univariate and multivariate analysis: compared to 0 pack years, those who smoked 1-10 pack-years had an OR(95% CI) of 1.47(0.46-4.68), those who smoked 11-20 pack-years had an OR of 2.85(1.09-7.46) and those who smoked more than 20 pack-years had an OR of 5.59(1.44-21.67) to develop more severe asthma. Smokers with asthma were also more likely to have uncontrolled disease. A significant dose-response relationship was observed for pack-years and uncontrolled asthma. Compared to 0 pack years, those who smoked 1-10 pack-years had an OR of 5.51(1.73-17.54) and those who smoked more than 10 pack-years had an OR of 13.38(4.57-39.19) to have uncontrolled asthma.
The current findings support the hypothesis that cigarette smoking is an important predictor of asthma severity and poor asthma control.
To investigate the relative contribution of genetic and environmental factors on smoking trajectory membership and to test whether individual smoking trajectories represent phenotypic thresholds of increasing genetic risk along a common genetic liability dimension.
Prospective study of a birth cohort of female like-sex twin pairs.
Participants completed diagnostic interview surveys 4 times from adolescence (average age 16) through young adulthood (average age 25).
Female twins who had smoked ≥100 cigarettes lifetime (n=1466 regular smokers).
Number of cigarettes smoked per day during the heaviest period of smoking (2 waves) or during the past 12 months (2 waves).
A 4-trajectory class solution provided the best fit to cigarette consumption data and was characterized by Low (n=564, 38.47%), Moderate (n=366, 24.97%), and High level smokers (n=197, 13.44%), and smokers who increased their smoking from adolescence to young adulthood (n=339, 23.12%). The best genetic model fit was a 3-category model that comprised the Low, a combined Increasing + Moderate, and High trajectories. This trajectory categorization was heritable (72.7%) with no evidence for significant contribution from shared environmental factors.
The way that smoking patterns develop in adolescence has a high level of heritability.
smoking trajectories; twins; heritability
Background: While smoke-free restaurant laws are intended to protect the public from secondhand smoke exposure, they may also discourage smoking among adolescents. There is no evidence from longitudinal studies to test this hypothesis.
Objective: To examine the effect of local restaurant smoking regulations on progression to established smoking among adolescents.
Design, setting, and subjects: A cohort of 2623 Massachusetts youths, ages 12–17 years at baseline, was interviewed via random digit dial telephone survey in 2001–2002 and followed up two years later. A generalised estimating equations (GEE) logistic regression analysis was used and controlled for potential individual, household, and town level confounding factors.
Main outcome measure: Progression to established smoking during the two year follow up period (defined as having smoked 100 or more cigarettes in one's life).
Results: Compared to youths living in towns with weak regulations, those living in towns with strong regulations (complete restaurant smoking bans) had less than half the odds of progression to established smoking (odds ratio (OR) 0.39, 95% confidence interval (CI) 0.24 to 0.66). The association was stronger for youths in towns with strong regulations in effect for two or more years (OR 0.11, 95% CI 0.03 to 0.37), although it was still present for those in towns with strong regulations in effect for less than two years (OR 0.55, 95% CI 0.33 to 0.90). No relationship was found between living in a town with a medium restaurant smoking regulation (restriction of smoking to enclosed, separately ventilated areas) and rates of progression to established smoking.
Conclusions: Local restaurant smoking bans may be an effective intervention to prevent youth smoking.
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.
Embryo; Fetus; Pre-implantation; Cigarette smoke; Tobacco; Low birth weight
Studies have demonstrated that clinical- and research-based definitions of who a smoker is and what constitutes smoking often differ from adolescent-derived definitions, which can be problematic for effective intervention and prevention efforts. We investigated how adolescents define different smoker types (nonsmoker, smoker, regular smoker, addicted smoker, heavy smoker, experimental smoker, casual smoker, and social smoker) using multiple indicators of smoking behaviors, including frequency, amount, place, and length of time cigarette smoking, and whether differences exist by smoking experience.
Quantitative and qualitative methods were used to analyze data from a cohort of adolescents (N = 372) in northern California.
We found differences in how adolescents characterized smoker types based on their own smoking experience. Ever-smokers tended to have a greater flexibility in determining what constituted nonsmoking and heavy smoking, while never-smokers had much narrower definitions. Results also indicated that adolescents may mistakenly associate nicotine addiction with a high frequency and amount of cigarette use as 74.3% characterized an addicted smoker as having smoked for a few years or more. In addition, there was a considerable amount of overlap in definitions between different smoker types, particularly among the smoker–regular smoker, addicted smoker–heavy smoker, and casual smoker–social smoker pairs.
Health communication strategies for youth smoking prevention need to address the wide variability and overlap in how adolescents define different smoker types. Greater attention should be directed to understanding the nuances of how adolescents define smoking in order to maximize the effectiveness of youth-centered smoking prevention and cessation messages.
To examine the association between cigarette smoke exposure and depression among Korean adolescents using the seventh Korea Youth Risk Behavior Web-based Survey (KYRBWS).
A nationally representative sample of middle and high school students across South Korea.
75 643 eligible participants across the country.
Primary outcome measures
Current smoking, secondhand smoke exposure and depression.
Data were analysed from a nationally representative survey of 75 643 participants (37 873 men and 37 770 women). Data were gathered on extensive information including current smoking, secondhand smoke exposure and depression in adolescence. Multiple logistic regression analysis was used to estimate the association between current smoking, secondhand smoke exposure and depression in Korean adolescents.
Among those who had never smoked, secondhand smoke exposure was positively associated with depression in male and female adolescents in a dose–response relation (OR 1.27, OR 1.52 in males; OR 1.25, OR 1.72 in females). Similar associations were observed among currently smoking men and women in a dose–response manner (OR 1.29, OR 1.55 in males; OR 1.22, OR 1.41 in females). These significant trends were consistently observed even after adjustments.
We suggested that current smoking and secondhand smoke exposure were positively associated with depression in male and female adolescents. Efforts to encourage no smoking and no secondhand smoke exposure will be established for adolescents.
Epidemiology; Public Health; Preventive Medicine; Mental Health
Background: Although many children with asthma may have a remission as they grow and other children who did not have asthma may develop asthma in adult life, knowledge about the factors that influence the onset and prognosis of asthma during adolescence and young adulthood is very limited.
Methods: A cohort of 8–10 year old children (n=718) living in Belmont, New South Wales, Australia were surveyed six times at 2 yearly intervals from 1982 to 1992, and then again 5 years later in 1997. From this cohort, 498 subjects had between three and seven assessments and were included in the analysis. Atopy, airway hyperresponsiveness (AHR), and wheeze in the last 12 months were measured at each survey. Late onset, remission, and persistence were defined based on characteristics at the initial survey and the changes in characteristics at the follow up surveys.
Results: The proportion of subjects with late onset atopy (13.7%) and wheeze (12.4%) was greater than the proportion with remission of atopy (3.2%) and wheeze (5.6%). Having atopy at age 8–12 years (OR 2.8, 95% CI 1.5 to 5.1) and having a parental history of asthma (OR 2.0, 95% CI 1.02 to 4.13) were significant risk factors for the onset of wheeze. Having AHR at age 8–12 years was a significant risk factor for the persistence of wheeze (OR 4.3, 95% CI 1.3 to 15.0). Female sex (OR 1.9, 95% CI 1.01 to 3.60) was a significant risk factor for late onset AHR whereas male sex (OR 1.9, 95% CI 1.1 to 2.8) was a significant risk factor for late onset atopy.
Conclusions: The onset of AHR is uncommon during adolescence, but the risk of acquiring atopy and recent wheeze for the first time continues during this period. Atopy, particularly present at the age of 8–10 years, predicts the subsequent onset of wheeze.
Prior studies have demonstrated that both nicotine administration and cigarette smoking lead to dopamine (DA) release in the ventral striatum/nucleus accumbens. In tobacco-dependent individuals, smoking denicotinized cigarettes leads to reduced craving, but less pleasure, than smoking regular cigarettes. Using denicotinized cigarettes and 11C-raclopride positron emission tomography (PET) scanning, we sought to determine if nicotine is necessary for smoking-induced DA release. Sixty-two tobacco-dependent smokers underwent 11C-raclopride PET scanning, during which they smoked either a regular or denicotinized cigarette (double-blind). Change in 11C-raclopride binding potential (BP) in the ventral striatum from before to after smoking was determined as an indirect measure of DA release. Cigarette craving, anxiety, and mood were monitored during scanning. Smoking a regular cigarette resulted in a significantly greater mean reduction in ventral striatal 11C-raclopride BP than smoking a denicotinized cigarette. Although both groups had reductions in craving and anxiety with smoking, the regular cigarette group had a greater improvement in mood. For the total group, change in BP correlated inversely with change in mood, indicating that greater smoking-induced DA release was associated with more smoking-related mood improvement. Thus, nicotine delivered through cigarette smoking appears to be important for ventral striatal DA release. Study findings also suggest that mood improvement from smoking is specifically related to ventral striatal DA release.
dopamine; nicotine; tobacco; ventral striatum; positron emission tomography; 11C-raclopride
To examine the dimensionality of sensations experienced during initial tobacco smoking.
Thirteen secondary schools located in British Columbia, Canada.
Data from 1187 adolescents who responded ‘yes’ to the question: ‘Have you ever tried cigarette smoking, even one or two puffs?’.
Participants answered questions about their demographic characteristics, tobacco smoking history and sensations experienced during their initial smoking episodes.
The sensations appear to represent the following three separate but modestly correlated dimensions: a pleasant dimension defined by feeling good and relaxed; an unpleasant dimension defined by coughing, feeling sick and nervous; and a ‘buzz’ dimension defined by feeling high and dizzy. The three factors made statistically significant contributions to the prediction of transition to regular smoking (defined as having smoked at least 100 cigarettes in one's life-time) after adjusting for age, sex and age at first puff.
The results suggest that three relatively distinct physiological systems appear to explain the relationship between initial smoking sensations and probability of becoming a regular smoker. Researchers examining sensations experienced during initial tobacco smoking episodes should consider using a three-dimensional profile of symptoms composed of pleasant, unpleasant and buzz dimensions.
adolescent; factor analysis; initial sensations; tobacco smoking
Rationale: Factors predicting the development of wheeze may differ between sexes and between childhood and adolescence. Methods: A New Zealand birth cohort of 1,037 children was followed to age 26. For this analysis, those reporting recurrent wheezing at two or more assessments were classified as “wheezers.” We examined risk factors for development of wheeze before age 10 (childhood) and subsequently (adolescent-onset) for males and for females separately using Cox regression modeling. Results: Males more often developed childhood wheeze (p = 0.002) and females adolescent-onset wheeze (p < 0.001). Maternal atopy (asthma or hay fever) was a risk factor for childhood wheeze in both sexes (hazard ratio [HR], 1.48, p < 0.05 for males; HR, 2.37, p < 0.001 for females). Paternal atopy also influenced childhood wheeze, significantly for males (HR, 1.72; p = 0.01), and similarly but not significantly for females (HR, 1.70; p = 0.08). For adolescent-onset wheeze, neither maternal (HR, 1.41; p = 0.19) nor paternal history (HR, 0.73; p = 0.42) was a risk factor in males, but maternal history (HR, 2.08; p < 0.01) was a significant risk factor for females. When both age ranges were combined, providing greater power for analysis, paternal history was a stronger risk factor for wheeze in females (HR, 1.62; p = 0.02) than in males (HR, 1.35; p = 0.12). Conclusion: The influence of parental atopy on the development for wheeze differs between males and females and between childhood- and adolescent-onset wheeze.
age of onset; asthma; parental history; risk factors; sex
The association between smoking and asthma or wheeze has been extensively studied in cross sectional studies, but evidence from large prospective cohort studies on the incidence of asthma during adolescence is scarce.
We report data from a cohort study in two German cities, Dresden and Munich. The study population (n = 2936) was first studied in 1995/6 at age 9–11 years as part of phase II of the International Study of Asthma and Allergies in Childhood (ISAAC II) and followed up in 2002/3. At baseline the parents completed a questionnaire and children underwent clinical examination and blood sampling. At follow up the young adults completed questionnaires on respiratory health, living, and exposure conditions. Incidence risk ratios (IRR) were calculated and adjusted for potential confounders using a modified Poisson regression approach.
The adjusted IRR for incident wheeze for active smokers compared with non‐smokers was 2.30 (95% confidence interval (CI) 1.88 to 2.82). The adjusted IRR was slightly higher for incident wheeze without a cold (2.76, 95% CI 1.99 to 3.84) and the incidence of diagnosed asthma (2.56, 95% CI 1.55 to 4.21). Analysis of duration and intensity of active smoking indicated dose dependent associations. Stratified analyses showed that the risk of incident wheeze without a cold in atopic smokers increased with decreasing plasma α1‐antitrypsin levels at baseline (1.64, 95% CI 1.22 to 2.20 per interquartile range).
Active smoking is an important risk factor for the incidence of asthma during adolescence. Relatively lower plasma levels of α1‐antitrypsin, although well above currently accepted thresholds, may increase susceptibility to respiratory disease among atopic smokers.
asthma; incidence; smoking; adolescence; α1‐antitrypsin