Exposure to man-made combustion products, including secondhand tobacco smoke, maternal smoking during pregnancy, and near-roadway air pollution (NRAP), have been associated with increased body mass index and obesity in children and have been shown to result in excess weight gain in animal models. Potential mechanisms include pro-inflammatory central nervous system effects of airborne particles on appetite control, resulting in increased caloric intake, or changes in basal metabolism due to effects on mitochondria and brown adipose tissue. Combustion-derived polyaromatic hydrocarbons have also been linked to altered lipid metabolism, epigenetic effects on PPARγ expression, particle-induced estrogenic effects, and alterations in the distribution of visceral fat. Emerging evidence that a broad spectrum of environmental chemicals have “obesogenic” properties and alter the metabolic profile of adipose tissue challenges the prevailing model that the childhood obesity epidemic is explained solely by increased caloric density of food and decreased physical activity. Research on environmental obesogens could identify novel targets for intervention and yield public health benefits, since NRAP and SHS exposure are both common in populations most at-risk for development of obesity.
Near-Roadway Air pollution; Built Environment
Exposure to ambient air pollutants increases risk for adverse cardiovascular health outcomes in adults. We aimed to evaluate the contribution of prenatal air pollutant exposure to cardiovascular health, which has not been thoroughly evaluated. The Testing Responses on Youth (TROY) study consists of 768 college students recruited from the University of Southern California in 2007–2009. Participants attended one study visit during which blood pressure, heart rate and carotid artery arterial stiffness (CAS) and carotid artery intima-media thickness (CIMT) were assessed. Prenatal residential addresses were geocoded and used to assign prenatal and postnatal air pollutant exposure estimates using the U.S. Environmental Protection Agency’s Air Quality System (AQS) database. The associations between CAS, CIMT and air pollutants were assessed using linear regression analysis. Prenatal PM10 and PM2.5 exposures were associated with increased CAS. For example, a 2 SD increase in prenatal PM2.5 was associated with CAS indices, including a 5% increase (β = 1.05, 95% CI 1.00–1.10) in carotid stiffness index beta, a 5% increase (β = 1.05, 95% CI 1.01–1.10) in Young’s elastic modulus and a 5% decrease (β = 0.95, 95% CI 0.91–0.99) in distensibility. Mutually adjusted models of pre- and postnatal PM2.5 further suggested the prenatal exposure was most relevant exposure period for CAS. No associations were observed for CIMT. In conclusion, prenatal exposure to elevated air pollutants may increase carotid arterial stiffness in a young adult population of college students. Efforts aimed at limiting prenatal exposures are important public health goals.
Several studies have estimated the burden of coronary heart disease (CHD) mortality from ambient regional particulate matter ≤ 2.5 μm (PM2.5). The burden of near-roadway air pollution (NRAP) generally has not been examined, despite evidence of a causal link with CHD.
We investigated the CHD burden from NRAP and compared it with the PM2.5 burden in the California South Coast Air Basin for 2008 and under a compact urban growth greenhouse gas reduction scenario for 2035.
We estimated the population attributable fraction and number of CHD events attributable to residential traffic density, proximity to a major road, elemental carbon (EC), and PM2.5 compared with the expected disease burden if the population were exposed to background levels of air pollution.
In 2008, an estimated 1,300 CHD deaths (6.8% of the total) were attributable to traffic density, 430 deaths (2.4%) to residential proximity to a major road, and 690 (3.7%) to EC. There were 1,900 deaths (10.4%) attributable to PM2.5. Although reduced exposures in 2035 should result in smaller fractions of CHD attributable to traffic density, EC, and PM2.5, the numbers of estimated deaths attributable to each of these exposures are anticipated to increase to 2,500, 900, and 2,900, respectively, due to population aging. A similar pattern of increasing NRAP-attributable CHD hospitalizations was estimated to occur between 2008 and 2035.
These results suggest that a large burden of preventable CHD mortality is attributable to NRAP and is likely to increase even with decreasing exposure by 2035 due to vulnerability of an aging population. Greenhouse gas reduction strategies developed to mitigate climate change offer unexploited opportunities for air pollution health co-benefits.
Ghosh R, Lurmann F, Perez L, Penfold B, Brandt S, Wilson J, Milet M, Künzli N, McConnell R. 2016. Near-roadway air pollution and coronary heart disease: burden of disease and potential impact of a greenhouse gas reduction strategy in Southern California. Environ Health Perspect 124:193–200; http://dx.doi.org/10.1289/ehp.1408865
Epidemiological studies have demonstrated associations of chronic respiratory disease with near-roadway pollutant exposure, effects that were independent of those of regional air pollutants. However, there has been limited study of the potential mechanisms for near-roadway effects. Therefore, we examined the in vitro effect of respirable particulate matter (PM) collected adjacent to a major Los Angeles freeway and at an urban background location. PM was collected on filters during two consecutive 15-day periods. Oxidative stress and inflammatory response (intracellular reactive oxygen species [ROS], IL-1β, IL-6, IL-8, and TNF-α) to PM aqueous extract was assessed in THP-1 cells, a model for evaluating monocyte/macrophage lineage cell responses. The near-roadway PM induced statistically significantly higher levels of IL-6, IL-8, and TNF-α (P < 0.01) and a near significant increase in IL-1β (P = 0.06) but did not induce ROS activity (P = 0.17). The contrast between urban background and near-roadway PM-induced inflammatory cytokines was similar in magnitude to that corresponding to temporal differences between the two collection periods. PM-induced proinflammatory protein expression was attenuated by antioxidant pretreatment, and PM stimulation enhanced the activity of protein kinases, including extracellular signal-regulated kinase and c-Jun N-terminal kinase. Pretreatment of THP-1 cells with kinase inhibitors reduced PM-induced proinflammatory mediator expression. The proinflammatory response was also reduced by pretreatment with polymyxin B, suggesting a role for endotoxin. However, the patterns of PM-induced protein kinase response and the attenuation of inflammatory responses by antioxidant or polymyxin B pretreatment did not vary between near-roadway and urban background locations. We conclude that near-roadway PM produced greater inflammatory response than urban background PM, a finding consistent with emerging epidemiologic findings, but these differences were not explained by PM endotoxin content or by MAPK pathways. Nevertheless, THP-1 cells may be a model for the development of biologically relevant metrics of long-term spatial variation in exposure for study of chronic disease.
traffic-related air pollution; oxidative stress; inflammation; exposure assessment; epidemiology
We examined the impact of parental psychological stress on body mass index (BMI) in pre-adolescent children over four years of follow-up.
We included 4,078 children aged 5–10 years (90% were between 5.5 and 7.5 years) at study entry (2002–2003) into the Children's Health Study, a prospective cohort study in southern California. A multi-level linear model simultaneously examined the effect of parental stress at study entry on the attained BMI at age 10 and the slope of change across annual measures of BMI during follow-up, controlled for the child's age and sex. Body mass index was calculated based on objective measurements of height and weight by trained technicians following a standardized procedure.
A two standard deviation increase in parental stress at study entry was associated with an increase in predicted BMI attained by age 10 of 0.287 kg/m2 (95% confidence interval 0.016-0.558; a 2% increase at this age for a participant of average attained BMI). The same increase in parental stress was also associated with an increased trajectory of weight gain over follow-up, with the slope of change in BMI increased by 0.054 kg/m2 (95% confidence interval 0.007-0.100; a 7% increase in the slope of change for a participant of average BMI trajectory).
We prospectively demonstrated a small effect of parental stress on BMI at age 10 and weight gain earlier in life than reported previously. Interventions to address the burden of childhood obesity should address the role of parental stress in children.
Parental stress; psychological stress; obesity; weight gain; pre-adolescents; children; prospective cohort
Emerging evidence suggests that near-roadway air pollution (NRP) exposure causes childhood asthma. Associated costs are not well documented.
We estimated the cost of childhood asthma attributable to residential NRP exposure and regional ozone (O3) and nitrogen dioxide (NO2) in Los Angeles County. We developed a novel approach to apportion the costs between these exposures under different pollution scenarios.
We integrated results from a study of willingness to pay to reduce the burden of asthma with studies of health care utilization and charges to estimate the costs of an asthma case and exacerbation. We applied those costs to the number of asthma cases and exacerbations due to regional pollution in 2007 and to hypothetical scenarios of a 20% reduction in regional pollution in combination with a 20% reduction or increase in the proportion of the total population living within 75m of a major roadway.
Cost of air pollution-related asthma in Los Angeles County in 2007 was $441 million for O3 and $202 million for NO2 in 2010 dollars. Cost of routine care (care in absence of exacerbation) accounted for 18% of the combined NRP and O3 cost and 39% of the combined NRP and NO2 cost—costs not recognized in previous analyses. NRP-attributable asthma accounted for 43% (O3) to 51% (NO2) of the total annual cost of exacerbations and routine care associated with pollution. Hypothetical scenarios showed that costs from increased NRP exposure may offset savings from reduced regional pollution.
Our model disaggregates the costs of regional pollution and NRP exposure and illustrates how they might vary under alternative exposure scenarios. The cost of air pollution is a substantial burden on families and an economic loss for society.
air pollution; asthma; cost of illness; urban growth; vehicle emissions; willingness to pay
Associations between exposure to smoke during wild-fire events and respiratory symptoms are well documented, but the role of airway size remains unclear. We conducted this analysis to assess whether small airway size modifies these relationships.
We analyzed data from 465 nonasthmatic 16- to 19-year-old participants in the Children’s Health Study. Following an outbreak of wildfires in 2003, each student completed a questionnaire about smoke exposure, dry and wet cough, wheezing, and eye symptoms. We used log-binomial regression to evaluate associations between smoke exposure and fire-related health symptoms, and to assess modification of the associations by airway size. As a marker of airway size, we used the ratio of maximum midexpiratory flow to forced vital capacity.
Forty percent (186 of 465) of this population (including students from 11 of 12 surveyed communities) reported the odor of wildfire smoke at home. We observed increased respiratory and eye symptoms with increasing frequency of wildfire smoke exposure. Associations between smoke exposure and having any of 4 respiratory symptoms were stronger in the lowest quartile of the lung function ratio (eg, fire smoke 6+ days: prevalence ratio: 3.8; 95% confidence interval (CI = 2.0 –7.2), compared with the remaining quartiles (fire smoke 6+ days: prevalence ratio = 2.0; 1.2–3.2). Analysis of individual symptoms suggests that this interaction may be strongest for effects on wheezing.
Small airways may serve as a marker of susceptibility to effects of wildfire smoke. Future studies should investigate the role of airway size for more common exposures and should include persons with asthma.
Prior studies have reported adverse effects of either regional or near-roadway air pollution (NRAP) on lung function. However, there has been little study of the joint effects of these exposures.
To assess the joint effects of NRAP and regional pollutants on childhood lung function in the Children’s Health Study.
Lung function was measured on 1,811 children from eight Southern Californian communities. NRAP exposure was assessed based on (1) residential distance to the nearest freeway or major road and (2) estimated near-roadway contributions to residential nitrogen dioxide (NO2), nitric oxide (NO), and total nitrogen oxides (NOx). Exposure to regional ozone (O3), NO2, particulate matter with aerodynamic diameter less than 10 μm (PM10) and 2.5 μm (PM2.5) was measured continuously at community monitors.
A 17.9 ppb (two standard deviation) increase in near-roadway NOx was associated with deficits of 1.6% in FVC (p=0.005) and 1.1% in FEV1 (p=0.048). Effects were observed in all communities and were similar for NO2 and NO. Residential proximity to a freeway was associated with a reduction in FVC. Lung function deficits of 2–3% were associated with regional PM10 and PM2.5 (FVC and FEV1) and with O3 (FEV1), but not NO2, across the range of exposure between communities. Associations with regional pollution and NRAP were independent in models adjusted for each. Effects of NRAP were not modified by regional pollutant concentrations.
Results indicate that NRAP and regional air pollution have independent adverse effects on childhood lung function.
traffic; lung function; air pollution; children; land-use regression
Global positioning system (GPS) technology is increasingly used to assess geographically varying exposure in population studies. However, there has been limited evaluation of accuracy and completeness of personal GPS data. The ability of a GPS data logger to assess location of children during usual activity was evaluated. Data collected for 4 days from 17 children wearing GPS loggers, recorded every 15 s, were evaluated for completeness by time of day during weekend and weekdays, and for accuracy during nighttime at home. Percentage of possible GPS-recorded points and of 5-min intervals with at least one recorded location were examined. Mean percentage of total possible 15-s interval locations recorded daily was less than 30%. Across participants, the GPS loggers recorded 1–47% of total possible location points on weekends and 1–55% on weekdays. More complete data were measured during travel to school (average 91%). The percentage of daily 5-min intervals with recorded data was as high as 53%. At least one location was recorded during 69% of 5-min intervals before school (0630–0800 h), 62% during school (0800–1400 h) and 56% after school (1400–1700 h). During night time (0000–0600 h), on average, location was recorded for less than 25% of 5-min intervals and accuracy was poor. The large proportion of missing data limits the usefulness of GPS logging instruments for population studies. They have potential utility for assessing on-road travel time and route. GPS technology has limitations, and lessons learned from this evaluation can be generalized to the use of GPS in other research settings.
global positioning systems; accuracy; epidemiology; children
Recent research suggests the burden of childhood asthma attributable to air pollution has been underestimated in traditional risk assessments, and there are no estimates of these associated costs. We estimated the yearly childhood asthma-related costs attributable to air pollution for Riverside and Long Beach, California, including: 1) the indirect and direct costs of health care utilization due to asthma exacerbations linked to traffic-related pollution (TRP); and 2) the costs of health care for asthma cases attributable to local TRP exposure.
We estimated these costs using estimates from peer-reviewed literature and the authors' analysis of surveys (Medical Expenditure Panel Survey, California Health Interview Survey, National Household Travel Survey, and Health Care Utilization Project).
A lower-bound estimate of the asthma burden attributable to air pollution was $18 million yearly. Asthma cases attributable to TRP exposure accounted for almost half of this cost. The cost of bronchitic episodes was a major proportion of both the annual cost of asthma cases attributable to TRP and of pollution-linked exacerbations.
Traditional risk assessment methods underestimate both the burden of disease and cost of asthma associated with air pollution, and these costs are borne disproportionately by communities with higher than average TRP.
asthma burden; vehicle emissions; air pollution; children; burden of disease; economic costs
Air quality has emerged as a key determinant of important health outcomes in children and adults. This study aims to identify factors that influence local, within-community air quality, and to build a model for traffic-related air pollution (TRP).We utilized concentrations of NO2, NO, and total oxides of nitrogen (NOx), which were measured at 942 locations in 12 southern California communities. For each location, population density, elevation, land-use, and several indicators of traffic were calculated. A spatial random effects model was used to study the relationship of these predictors to each TRP.Variation in TRP was strongly correlated with traffic on nearby freeways and other major roads, and also with population density and elevation. After accounting for traffic, categories of land-use were not associated with the pollutants. Traffic had a larger relative impact in small urban (low regional pollution) communities than in large urban (high regional pollution) communities. For example, our best fitting model explained 70% of the variation in NOx in large urban areas and 76% in small urban areas. Compared with living at least 1,500m from a freeway, living within 250m of a freeway was associated with up to a 41% increase in TRP in a large urban area, and up to a 75% increase in small urban areas.Thus, traffic strongly affects local air quality in large and small urban areas, which has implications for exposure assessment and estimation of health risks.
traffic-related air pollution; nitrogen oxides; exposure assessment; traffic; land-use; spatial random effects
The relationship between asthma and socioeconomic status remains unclear. We investigated how neighborhood, school and community social environments were associated with incident asthma in Southern California school children.
New onset asthma was measured over three years of follow-up in the Children’s Health Study cohort. Multilevel random effects models assessed associations between social environments and asthma, adjusted for individual risk factors. Subjects resided in 274 neighborhoods and attended one of 45 schools in 13 communities. Neighborhoods and communities were characterized by measures of deprivation, income inequality and racial segregation. Communities were further described by crime rates. Information on schools included whether a school received funding related to the Title 1 No Child Left Behind program, which aims to reduce academic underachievement in disadvantaged populations.
Increased risk for asthma was observed in subjects attending schools receiving Title I funds compared to those from schools without funding (adjusted hazard ratio 1.71, 95% CI 1.14–2.58), and residing in communities with higher rates of larceny crime (adjusted hazard ratio 2.02, 95% CI 1.08–3.02 across the range of 1827 incidents per 100,000 population).
Risk for asthma was higher in areas of low socioeconomic status, possibly due to unmeasured risk factors or chronic stress.
asthma; multilevel models; socio-economic; air pollution
Few previous studies examined the impact of prenatal air pollution exposures on fetal development based on ultrasound measures during pregnancy.
In a prospective birth cohort of more than 500 women followed during 1993-1996 in Los Angeles, California, we examined how air pollution impacts fetal growth during pregnancy. Exposure to traffic related air pollution was estimated using CALINE4 air dispersion modeling for nitrogen oxides (NOx) and a land use regression (LUR) model for nitrogen monoxide (NO), nitrogen dioxide (NO2) and NOx. Exposures to carbon monoxide (CO), NO2, ozone (O3) and particles <10 μm in aerodynamic diameter (PM10) were estimated using government monitoring data. We employed a linear mixed effects model to estimate changes in fetal size at approximately 19, 29 and 37 weeks gestation based on ultrasound.
Exposure to traffic-derived air pollution during 29 to 37 weeks was negatively associated with biparietal diameter at 37 weeks gestation. For each interquartile range (IQR) increase in LUR-based estimates of NO, NO2 and NOx, or freeway CALINE4 NOx we estimated a reduction in biparietal diameter of 0.2-0.3 mm. For women residing within 5 km of a monitoring station, we estimated biparietal diameter reductions of 0.9-1.0 mm per IQR increase in CO and NO2. Effect estimates were robust to adjustment for a number of potential confounders. We did not observe consistent patterns for other growth endpoints we examined.
Prenatal exposure to traffic-derived pollution was negatively associated with fetal head size measured as biparietal diameter in late pregnancy.
ambient air pollution; fetal growth; pregnancy; traffic-related air pollution; ultrasound measurements
Emerging evidence indicates that near-roadway pollution (NRP) in ambient air has adverse health effects. However, specific components of the NRP mixture responsible for these effects have not been established. A major limitation for health studies is the lack of exposure models that estimate NRP components observed in epidemiological studies over fine spatial scale of tens to hundreds of meters. In this study, exposure models were developed for fine-scale variation in biologically relevant elemental carbon (EC). Measurements of particulate matter (PM) and EC less than 2.5 μm in aerodynamic diameter (EC2.5) and of PM and EC of nanoscale size less than 0.2 μm were made at up to 29 locations in each of eight Southern California Children's Health Study communities. Regression-based prediction models were developed using a guided forward selection process to identify traffic variables and other pollutant sources, community physical characteristics and land use as predictors of PM and EC variation in each community. A combined eight-community model including only CALINE4 near-roadway dispersion-estimated vehicular emissions accounting for distance, distance-weighted traffic volume, and meteorology, explained 51% of the EC0.2 variability. Community-specific models identified additional predictors in some communities; however, in most communities the correlation between predicted concentrations from the eight-community model and observed concentrations stratified by community were similar to those for the community-specific models. EC2.5 could be predicted as well as EC0.2. EC2.5 estimated from CALINE4 and population density explained 53% of the within-community variation. Exposure prediction was further improved after accounting for between-community heterogeneity of CALINE4 effects associated with average distance to Pacific Ocean shoreline (to 61% for EC0.2) and for regional NOx pollution (to 57% for EC2.5). PM fine spatial scale variation was poorly predicted in both size fractions. In conclusion, models of exposure that include traffic measures such as CALINE4 can provide useful estimates for EC0.2 and EC2.5 on a spatial scale appropriate for health studies of NRP in selected Southern California communities.
Childhood body mass index (BMI) and obesity prevalence have been associated with exposure to secondhand smoke (SHS), maternal smoking during pregnancy, and vehicular air pollution. There has been little previous study of joint BMI effects of air pollution and tobacco smoke exposure.
Information on exposure to SHS and maternal smoking during pregnancy was collected on 3,318 participants at enrollment into the Southern California Children’s Health Study. At study entry at average age of 10 years, residential near-roadway pollution exposure (NRP) was estimated based on a line source dispersion model accounting for traffic volume, proximity, and meteorology. Lifetime exposure to tobacco smoke was assessed by parent questionnaire. Associations with subsequent BMI growth trajectory based on annual measurements and attained BMI at 18 years of age were assessed using a multilevel modeling strategy.
Maternal smoking during pregnancy was associated with estimated BMI growth over 8-year follow-up (0.72 kg/m2 higher; 95% CI: 0.14, 1.31) and attained BMI (1.14 kg/m2 higher; 95% CI: 0.66, 1.62). SHS exposure before enrollment was positively associated with BMI growth (0.81 kg/m2 higher; 95% CI: 0.36, 1.27) and attained BMI (1.23 kg/m2 higher; 95% CI: 0.86, 1.61). Growth and attained BMI increased with more smokers in the home. Compared with children without a history of SHS and NRP below the median, attained BMI was 0.80 kg/m2 higher (95% CI: 0.27, 1.32) with exposure to high NRP without SHS; 0.85 kg/m2 higher (95% CI: 0.43, 1.28) with low NRP and a history of SHS; and 2.15 kg/m2 higher (95% CI: 1.52, 2.77) with high NRP and a history of SHS (interaction p-value 0.007). These results suggest a synergistic effect.
Our findings strengthen emerging evidence that exposure to tobacco smoke and NRP contribute to development of childhood obesity and suggest that combined exposures may have synergistic effects.
McConnell R, Shen E, Gilliland FD, Jerrett M, Wolch J, Chang CC, Lurmann F, Berhane K. 2015. A longitudinal cohort study of body mass index and childhood exposure to secondhand tobacco smoke and air pollution: the Southern California Children’s Health Study. Environ Health Perspect 123:360–366; http://dx.doi.org/10.1289/ehp.1307031
The objective of the research was to assess how proximity to parks and recreational resources affects the development of childhood obesity through a longitudinal study. Data were collected on 3173 children aged 9–10 from 12 communities in Southern California in 1993 and 1996. Children were followed for eight years to collect longitudinal information, including objectively measured body mass index (BMI). Multilevel growth curve models were used to assess associations between attained BMI growth at age 18 and numerous environmental variables, including park space and recreational program access. For park acres within a 500 meter distance of children’s homes, there were significant inverse associations with attained BMI at age 18. Effect sizes were larger for boys than for girls. Recreation programs within a 10 km buffer of children’s homes were significantly and inversely associated with achieved levels in BMI at age 18, with effect sizes for boys also larger than those for girls. We conclude that children with better access to park and recreational resources are less likely to experience significant increases in attained BMI.
obesity; built environment; parks and recreation; GIS; multilevel growth curve models
Few studies have evaluated multiple levels of influence simultaneously on whether children walk to school. A large cohort of 4,338 subjects from ten communities was used to identify the determinants of walking through (1) a one-level logistic regression model for individual-level variables and (2) a two-level mixed regression model for individual and school-level variables. Walking rates were positively associated with home-to-school proximity, greater age, and living in neighborhoods characterized by lower traffic density. Greater land use mix around the home was, however, associated with lower rates of walking. Rates of walking to school were also higher amongst recipients of the Free and Reduced Price Meals Program and attendees of schools with higher percentage of English language learners. Designing schools in the same neighborhood as residential districts should be an essential urban planning strategy to reduce walking distance to school. Policy interventions are needed to encourage children from higher socioeconomic status families to participate in active travel to school and to develop walking infrastructures and other measures that protect disadvantaged children.
walking to school; Children's Health Study; multilevel analysis; landscape metrics; Los Angeles
The objective of this study is to examine the relationship between measured traffic density near the homes of children and attained body mass index (BMI) over an eight-year follow up.
Children aged 9–10 years were enrolled across multiple communities in Southern California in 1993 and 1996 (n = 3318). Children were followed until age 18 or high school graduation to collect longitudinal information, including annual height and weight measurements. Multilevel growth curve models were used to assess the association between BMI levels at age 18 and traffic around the home.
For traffic within 150 m around the child’s home, there were significant positive associations with attained BMI for both sexes at age 18. With the 300 m traffic buffer, associations for both male and female growth in BMI were positive, but significantly elevated only in females. These associations persisted even after controlling for numerous potential confounding variables.
This analysis yields the first evidence of significant effects from traffic density on BMI levels at age 18 in a large cohort of children. Traffic is a pervasive exposure in most cities, and our results identify traffic as a major risk factor for the development of obesity in children.
Traffic; built environment; children; overweight and obesity; geographic information systems; multilevel models; cohort study
Psychological stress is often associated with poor health-related outcomes. One potential biomarker for chronic stress, hair cortisol, is minimally invasive compared to other cortisol collection techniques. This pilot study examined the relationships between hair cortisol and self-reported perceived stress, stressful life events, depressive symptoms, and dispositional optimism among adolescents.
This cross-sectional study comprised of a convenience sample of 27 adolescents (age: M=14.96, SD=1.63) recruited from a Southern California after-school program. Along with demographic and hair characteristics (e.g., hair color, type, etc.), participants completed the Perceived Stress Scale, Stressful Life Events checklist, CES-D (depressive symptoms), and Life Orientation Test (optimism). Hair cortisol was measured by analyzing hair samples approximately 1 cm from the scalp representing one month of cortisol exposure.
Hair cortisol had a significant inverse association with dispositional optimism (r=−0.44, p<0.05). Hair cortisol was not significantly associated with self-reported perceived stress, stressful life events, or depressive symptoms.
Assessment of hair cortisol may prove beneficial as an objective measure in research examining chronic stress-related outcomes among adolescents. Resiliency or protective dispositions, such as optimism, merit attention in relation to this biomarker.
Hair cortisol; Stress; Stressful life events; Dispositional optimism; Adolescents
Spatial variation in childhood asthma and a recent increase in prevalence indicate that environmental factors play a significant role in the etiology of this important disease. Socioeconomic position (SEP) has been associated inversely and positively with childhood asthma. These contradictory results indicate a need for systematic research about SEP and asthma. Pathways have been suggested for effects of SEP on asthma at both the individual and community level. We examined the relationship of prevalent asthma to community-level indicators of SEP among 5762 children in 12 Southern California, using a multilevel random effects model. Estimates of community-level SEP were derived by summarizing census block group-level data using a novel method of weighting by the proportion of the block groups included in a community-specific bounding rectangle that contained 95% of local study subjects. Community characteristics included measures of male unemployment, household income, low education (i.e. no high school diploma), and poverty. There was a consistent inverse association between male unemployment and asthma across the inter-quartile range of community unemployment rates, indicating that asthma rates increase as community SEP increases. The results were robust to individual-level confounding, methods for summarizing census block group data to the community level, scale of analysis (i.e. community-level vs. neighborhood-level) and the modeling algorithm. The positive association between SEP and prevalent childhood asthma might be explained by differential access to medical care that remains unmeasured, by the hygiene hypothesis (e.g. lower SES may associate with higher protective exposures to endotoxin in early life), or by SEP acting as a proxy for unmeasured neighborhood characteristics.
USA; neighborhood; childhood asthma; multi-level modeling; socioeconomic position; contextual factors
This study examined associations of asthma with school commuting time.
Time on likely school commute route was used as a proxy for on-road air pollution exposure among 4741 elementary school children at enrollment into the Children's Health Study. Lifetime asthma and severe wheeze (including multiple attacks, nocturnal or with shortness of breath) were reported by parents.
In asthmatic children, severe wheeze was associated with commuting time (odds ratio (OR) 1.54 across the 9-minute 5%-95% exposure distribution; 95% confidence interval (CI) 1.01,2.36). The association was stronger in analysis restricted to asthmatic children with commuting times five minutes or longer (OR 1.97; 95% CI 1.02,3.77). No significant associations were observed with asthma prevalence.
Among asthmatics, severe wheeze was associated with relatively short school commuting times. Further investigation of effects of on-road pollutant exposure is warranted.
air pollution; asthma; child; epidemiology; traffic; commuting
Biologically plausible mechanisms link traffic-related air pollution to metabolic disorders and potentially to obesity. Here we sought to determine whether traffic density and traffic-related air pollution were positively associated with growth in body mass index (BMI = kg/m2) in children aged 5–11 years.
Participants were drawn from a prospective cohort of children who lived in 13 communities across Southern California (N = 4550). Children were enrolled while attending kindergarten and first grade and followed for 4 years, with height and weight measured annually. Dispersion models were used to estimate exposure to traffic-related air pollution. Multilevel models were used to estimate and test traffic density and traffic pollution related to BMI growth. Data were collected between 2002–2010 and analyzed in 2011–12.
Traffic pollution was positively associated with growth in BMI and was robust to adjustment for many confounders. The effect size in the adjusted model indicated about a 13.6% increase in annual BMI growth when comparing the lowest to the highest tenth percentile of air pollution exposure, which resulted in an increase of nearly 0.4 BMI units on attained BMI at age 10. Traffic density also had a positive association with BMI growth, but this effect was less robust in multivariate models.
Traffic pollution was positively associated with growth in BMI in children aged 5–11 years. Traffic pollution may be controlled via emission restrictions; changes in land use that promote jobs-housing balance and use of public transit and hence reduce vehicle miles traveled; promotion of zero emissions vehicles; transit and car-sharing programs; or by limiting high pollution traffic, such as diesel trucks, from residential areas or places where children play outdoors, such as schools and parks. These measures may have beneficial effects in terms of reduced obesity formation in children.
Childhood obesity; Air pollution; Traffic; California