Exposure to ambient air pollutants increases risk for cardiovascular health outcomes in adults. The contribution of childhood air pollutant exposure to cardiovascular health has not been thoroughly evaluated.
Methods and results
The Testing Responses on Youth study consists of 861 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 intima-media thickness (CIMT) were assessed. Self-administered questionnaires collected information about health and socio-demographic characteristics and a 12-hr fasting blood sample was drawn for lipid and biomarker analyses. Residential addresses were geocoded and used to assign cumulative air pollutant exposure estimates based on data derived from the U.S. Environmental Protection Agency’s Air Quality System (AQS) database. The associations between CIMT and air pollutants were assessed using linear regression analysis. Mean CIMT was 603 μm (± 54 SD). A 2 standard deviation (SD) increase in childhood (aged 0–5 years) or elementary school (aged 6–12) O3 exposure was associated with a 7.8 μm (95% CI −0.3, 15.9) or 10.1 μm (95% CI 1.8, 18.5) higher CIMT, respectively. Lifetime exposure to O3 showed similar but non-significant associations. No associations were observed for PM2.5, PM10 or NO2 although adjustment for these pollutants strengthened the childhood O3 associations.
Childhood exposure to O3 may be a novel risk factor for CIMT in a healthy population of college students. Regulation of air pollutants and efforts that focus on limiting childhood exposures continue to be important public health goals.
atherosclerosis; cardiovascular diseases; carotid arteries; epidemiology; pediatrics
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
Inducible nitric oxide synthase (iNOS, encoded by NOS2) is the major enzyme for nitric oxide synthesis in airways. As such, measurement of exhaled nitric oxide (FeNO) provides an in vivo assessment of iNOS activity. Short-term exposure to air pollution, haplotypes and DNA methylation in NOS2 promoter have been associated independently with iNOS expression and/or FeNO.
We aimed to examine the effects of ambient air pollutants, NOS2 promoter haplotypes and NOS2 promoter methylation on FeNO level in children.
We selected 940 participants in the Children’s Health Study who provided buccal samples and had undergone FeNO measurement on the same day. DNA methylation was measured using a bisulfite-polymerase chain reaction Pyrosequencing assay. Seven single nucleotide polymorphisms captured the haplotype diversity in the NOS2 promoter. Average particulate matter with aerodynamic diameter ≤2.5μm and ≤10μm (PM2.5 and PM10), ozone and nitrogen dioxide levels 7 days before FeNO measurement were estimated based on air pollution data obtained at central monitoring sites.
We found interrelated effects of PM2.5, NOS2 promoter haplotypes and iNOS methylation on FeNO. Elevated 7-day average PM2.5 exposure was associated with lower iNOS methylation (P=.01). NOS2 promoter haplotypes were globally associated with NOS2 promoter methylation (P=6.2 × 10−8). There was interaction among one common promoter haplotype, iNOS methylation level and PM2.5 exposure on FeNO (Pinteraction=.00007).
Promoter variants in NOS2 and short term PM2.5 exposure affect iNOS methylation. This is one of the first studies showing contributions of genetic and epigenetic variations in air pollution mediated phenotype expression.
air pollution; biomarker; DNA methylation; epigenetics; genetics; gene-environment interaction; nitrosative stress
T cells mediate the inflammatory responses observed in asthma among genetically susceptible individuals and have been suspected to be prone to epigenetic regulation. However, these relationships are not well established from past clinical studies that have had limited capacity to control for the effects of variable genetic predisposition and early environmental exposures. Relying on a cohort of monozygotic twins discordant for asthma we sought to determine if epigenetic modifications in T cells were associated with current asthma and explored whether such modifications were associated with second hand smoke exposures. Our study was conducted in a monozygotic twin cohort of adult twin pairs (n = 21) all discordant for asthma. Regulatory T cell (Treg) and effector T cell (Teff) subsets were assessed for levels of cellular function, protein expression, gene expression and CpG methylation within Forkhead box P3 (FOXP3) and interferon gamma-γ (IFNγ) loci. Comparisons by asthma and current report of exposure to second hand smoke were made. Treg from asthmatic discordant twins demonstrated decreased FOXP3 protein expression and impaired Treg function that was associated with increased levels of CpG methylation within the FOXP3 locus when compared to their non-asthmatic twin partner. In parallel, Teff from discordant asthmatic twins demonstrated increased methylation of the IFNγ locus, decreased IFNγ expression and reduced Teff function when compared to Teff from the non-asthmatic twin. Finally, report of current exposure to second hand smoke was associated with modifications in both Treg and Teff at the transcriptional level among asthmatics. The results of the current study provide evidence for differential function of T cell subsets in monozygotic twins discordant for asthma that are regulated by changes in DNA methylation. Our preliminary data suggest exposure to second hand smoke may augment the modified T cell responses associated with asthma.
Background: The emerging consensus that exposure to near-roadway traffic-related pollution causes asthma has implications for compact urban development policies designed to reduce driving and greenhouse gases.
Objectives: We estimated the current burden of childhood asthma-related disease attributable to near-roadway and regional air pollution in Los Angeles County (LAC) and the potential health impact of regional pollution reduction associated with changes in population along major traffic corridors.
Methods: The burden of asthma attributable to the dual effects of near-roadway and regional air pollution was estimated, using nitrogen dioxide and ozone as markers of urban combustion-related and secondary oxidant pollution, respectively. We also estimated the impact of alternative scenarios that assumed a 20% reduction in regional pollution in combination with a 3.6% reduction or 3.6% increase in the proportion of the total population living near major roads, a proxy for near-roadway exposure.
Results: We estimated that 27,100 cases of childhood asthma (8% of total) in LAC were at least partly attributable to pollution associated with residential location within 75 m of a major road. As a result, a substantial proportion of asthma-related morbidity is a consequence of near-roadway pollution, even if symptoms are triggered by other factors. Benefits resulting from a 20% regional pollution reduction varied markedly depending on the associated change in near-roadway proximity.
Conclusions: Our findings suggest that there are large and previously unappreciated public health consequences of air pollution in LAC and probably in other metropolitan areas with dense traffic corridors. To maximize health benefits, compact urban development strategies should be coupled with policies to reduce near-roadway pollution exposure.
air pollution; asthma; burden of disease; children; compact urban growth; risk assessment; vehicle emissions
Rationale: Emerging evidence indicates that psychosocial stress enhances the effect of traffic exposure on the development of asthma.
Objectives: We hypothesized that psychosocial stress would also modify the effect of traffic exposure on lung function deficits.
Methods: We studied 1,399 participants in the Southern California Children's Health Study undergoing lung function testing (mean age, 11.2 yr). We used hierarchical mixed models to assess the joint effect of traffic-related air pollution and stress on lung function.
Measurements and Main Results: Psychosocial stress in each child's household was assessed based on parental response to the perceived stress scale (range, 0–16) at study entry. Exposures to nitric oxide, nitrogen dioxide, and total oxides of nitrogen (NOx), surrogates of the traffic-related pollution mixture, were estimated at schools and residences based on a land-use regression model. Among children from high-stress households (parental perceived stress scale >4) deficits in FEV1 of 4.5 (95% confidence interval, −6.5 to −2.4) and of 2.8% (−5.7 to 0.3) were associated with each 21.8 ppb increase in NOx at homes and schools, respectively. These pollutant effects were significantly larger in the high-stress compared with lower-stress households (interaction P value 0.007 and 0.05 for residential and school NOx, respectively). No significant NOx effects were observed in children from low-stress households. A similar pattern of association was observed for FVC. The observed associations for FEV1 and FVC remained after adjusting for sociodemographic factors and after restricting the analysis to children who do not have asthma.
Conclusions: A high-stress home environment is associated with increased susceptibility to lung function effects of air pollution both at home and at school.
parental stress; traffic exposure; lung function; children
Two recent case-control studies in Italy reported that long-term exposure to particulate air pollution or living near major traffic roads was associated with an increased risk of deep vein thrombosis (DVT). No prospective evidence exists about long-term traffic-related air pollution and incident venous thromboembolism (VTE).
To examine the association between long-term traffic exposure and incident VTE in a population-based prospective cohort study.
We studied 13,143 middle-aged men and women in the Atherosclerosis Risk in Communities Study without history of DVT or pulmonary embolus (PE) at baseline examination (1987-1989). Geographical Information System (GIS)-mapped traffic density and distance to major roads in the four study communities served as measures of traffic exposure. We examined the association between traffic exposure and incident VTE using proportional hazards regression models.
405 subjects developed VTE through 2005. Traffic density was not significantly associated with VTE. Relative to those in the lowest quartile of traffic density, the adjusted hazard ratios across increasing quartiles were 1.18 (95%CI 0.88-1.57), 0.99 (95%CI 0.74-1.34) and 1.14 (95%CI 0.86-1.51) (p for trend across quartiles = 0.64). For residents living within 150 meters of major roads compared to subjects living further away, the adjusted hazard ratio was 1.16 (95%CI 0.95-1.42, p=0.14).
This first prospective study in the general population does not support an association between air pollution exposure or traffic proximity and risk of DVT. More data may be needed to clarify whether traffic or air pollution influences the risk of VTE.
traffic exposure; VTE; air pollution; cohort
Little is known about environmental causes and contributing factors for autism. Basic science and epidemiologic research suggest that oxidative stress and inflammation may play a role in disease development. Traffic-related air pollution, a common exposure with established effects on these pathways, contains substances found to have adverse prenatal effects.
We examined the association between autism and proximity of residence to freeways and major roadways during pregnancy and near the time of delivery, as a surrogate for air pollution exposure.
Data were from 304 autism cases and 259 typically developing controls enrolled in the Childhood Autism Risks from Genetics and the Environment (CHARGE) study. The mother’s address recorded on the birth certificate and trimester-specific addresses derived from a residential history obtained by questionnaire were geocoded, and measures of distance to freeways and major roads were calculated using ArcGIS software. Logistic regression models compared residential proximity to freeways and major roads for autism cases and typically developing controls.
Adjusting for sociodemographic factors and maternal smoking, maternal residence at the time of delivery was more likely be near a freeway (≤ 309 m) for cases than for controls [odds ratio (OR) = 1.86; 95% confidence interval (CI), 1.04–3.45]. Autism was also associated with residential proximity to a freeway during the third trimester (OR = 2.22; CI, 1.16–4.42). After adjustment for socioeconomic and sociodemographic characteristics, these associations were unchanged. Living near other major roads at birth was not associated with autism.
Living near a freeway was associated with autism. Examination of associations with measured air pollutants is needed.
autism; epidemiology; gene-environment interaction; roadway proximity; traffic emissions
Traffic exposure is a major contributor to ambient air pollution for people living close to busy roads. The relationship between traffic exposure and lung function remains inconclusive in adults.
A cross‐sectional study was conducted to investigate the association between traffic exposure and lung function in the Atherosclerosis Risk in Communities (ARIC) study, a community based cohort of 15 792 middle aged men and women. Traffic density and distance to major roads were used as measures of traffic exposure.
After controlling for potential confounders including demographic factors, personal and neighbourhood level socioeconomic characteristics, cigarette smoking and background air pollution, higher traffic density was significantly associated with lower forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) in women. Relative to the lowest quartile of traffic density, the adjusted differences across increasing quartiles were 5.1, −15.4 and −21.5 ml for FEV1 (p value of linear trend across the quartiles = 0.041) and 1.2, −23.4 and −34.8 ml for FVC (p trend = 0.010). Using distance from major roads as a simpler index of traffic related air pollution exposure, the FEV1 was −15.7 ml (95% CI −34.4 to 2.9) lower and the FVC was −24.2 ml (95% CI −46.2 to −2.3) lower for women living within 150 m compared with subjects living further away. There was no significant effect of traffic density or distance to major roads on lung function in men. The FEV1/FVC ratio was not significantly associated with traffic exposure in either men or women.
This is the largest published study of traffic exposure and pulmonary function in adults to date. These results add to growing evidence that chronic exposure to traffic related air pollution may adversely affect respiratory health.
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
Diverse environmental exposures, studied separately, have been linked to health outcomes in adult asthma, but integrated multi-factorial effects have not been modeled. We sought to evaluate the contribution of combined social and physical environmental exposures to adult asthma lung function and disease severity.
Data on 176 subjects with asthma and/or rhinitis were collected via telephone interviews for sociodemographic factors and asthma severity (scored on a 0-28 point range). Dust, indoor air quality, antigen-specific IgE antibodies, and lung function (percent predicted FEV1) were assessed through home visits. Neighborhood socioeconomic status, proximity to traffic, land use, and ambient air quality data were linked to the individual-level data via residential geocoding. Multiple linear regression separately tested the explanatory power of five groups of environmental factors for the outcomes, percent predicted FEV1 and asthma severity. Final models retained all variables statistically associated (p < 0.20) with each of the two outcomes.
Mean FEV1 was 85.0 ± 18.6%; mean asthma severity score was 6.9 ± 5.6. Of 29 variables screened, 13 were retained in the final model of FEV1 (R2 = 0.30; p < 0.001) and 15 for severity (R2 = 0.16; p < 0.001), including factors from each of the five groups. Adding FEV1 as an independent variable to the severity model further increased its explanatory power (R2 = 0.25).
Multivariate models covering a range of individual and environmental factors explained nearly a third of FEV1 variability and, taking into account lung function, one quarter of variability in asthma severity. These data support an integrated approach to modeling adult asthma outcomes, including both the physical and the social environment.
Exposure to traffic has been associated with asthma outcomes in children, but its effect on asthma in adults has not been well studied.
To test the hypothesis that lung function and health status are associated with traffic exposures.
We measured forced expiratory volume in 1 second (FEV1) % predicted, general health status using the Physical Component Scale of the Short Form (SF-12 PCS) and quality of life (QoL) using the Marks Asthma Quality of Life questionnaire in a cohort of adults with asthma or rhinitis (n=176; 145 with asthma). We assessed exposures to traffic by geo-coding subjects’ residential addresses and assigning distance to roadways. Associations between distance to nearest roadway and distance to nearest major roadway and FEV1 % predicted or SF-12 PCS were studied using linear regression.
FEV1 % predicted was positively associated with distance from nearest roadway (p=0.01) and major roadway (p=0.02). SF-12 PCS and QoL were not significantly associated with either traffic variable. Adjustment for income, smoking, and obesity did not substantively change the associations of the traffic variables with FEV1 % predicted (p=0.04 for nearest roadway and p=0.02 for nearest major roadway) and did not cause associations with either SF-12 PCS or OoL to become significant
Traffic exposure was associated with decreased lung function in adults with asthma.
asthma; traffic; heavy-duty vehicles; lung function; health status
For people living close to busy roads, traffic is a major source of air pollution. Few prospective data have been published on the effects of long-term exposure to traffic on the incidence of coronary heart disease (CHD).
In this article, we examined the association between long-term traffic exposure and incidence of fatal and nonfatal CHD in a population-based prospective cohort study.
We studied 13,309 middle-age men and women in the Atherosclerosis Risk in Communities study, without previous CHD at enrollment, from 1987 to 1989 in four U.S. communities. Geographic information system–mapped traffic density and distance to major roads served as measures of traffic exposure. We examined the association between traffic exposure and incident CHD using proportional hazards regression models, with adjustment for background air pollution and a wide range of individual cardiovascular risk factors.
Over an average of 13 years of follow-up, 976 subjects developed CHD. Relative to those in the lowest quartile of traffic density, the adjusted hazard ratio (HR) in the highest quartile was 1.32 [95% confidence interval (CI), 1.06–1.65; p-value for trend across quartiles = 0.042]. When we treated traffic density as a continuous variable, the adjusted HR per one unit increase of log-transformed density was 1.03 (95% CI, 1.01–1.05; p = 0.006). For residents living within 300 m of major roads compared with those living farther away, the adjusted HR was 1.12 (95% CI, 0.95–1.32; p = 0.189). We found little evidence of effect modification for sex, smoking status, obesity, low-density lipoprotein cholesterol level, hypertension, age, or education.
Higher long-term exposure to traffic is associated with incidence of CHD, independent of other risk factors. These prospective data support an effect of traffic-related air pollution on the development of CHD in middle-age persons.
air pollution; coronary disease; traffic
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
Asthma is the most important chronic disease of childhood. The U.S. Environmental Protection Agency has concluded that children with asthma continue to be susceptible to ozone-associated adverse effects on their disease.
This study was designed to evaluate time trends in associations between declining warm-season O3 concentrations and hospitalization for asthma in children.
We undertook an ecologic study of hospital discharges for asthma during the high O3 seasons in California’s South Coast Air Basin (SoCAB) in children who ranged in age from birth to 19 years from 1983 to 2000. We used standard association and causal statistical analysis methods. Hospital discharge data were obtained from the State of California; air pollution data were obtained from the California Air Resources Board, and demographic data from the 1980, 1990, and 2000 U.S. Census. SoCAB was divided into 195 spatial grids, and quarterly average O3, sulfurdioxide, particulate matter with aerodynamic diameter ≤ 10 μm, nitrogen dioxide, and carbon monoxide were assigned to each unit for 3-month periods along with demographic variables.
O3 was the only pollutant associated with increased hospital admissions over the study period. Inclusion of a variety of demographic and weather variables accounted for all of the non-O3 temporal changes in hospitalizations. We found a time-independent, constant effect of ambient levels of O3 and quarterly hospital discharge rates for asthma. We estimate that the average effect of a 10-ppb mean increase in any given mean quarterly 1-hr maximum O3 over the 18-year median of 87.7 ppb was a 4.6% increase in the same quarterly outcome.
Our data indicate that at current levels of O3 experienced in Southern California, O3 contributes to an increased risk of hospitalization for children with asthma.
air pollution; asthma; children; epidemiology; ozone
Traffic exposure is a major contributor to ambient air pollution for people living close to busy roads. The relationship between traffic exposure and lung function remains inconclusive in adults.
We conducted a cross-sectional study to investigate the association between traffic exposure and lung function in the Atherosclerosis Risk in Communities (ARIC) study, a community-based cohort of 15,792 middle-aged men and women. Traffic density and distance to major roads were used as measures of traffic exposure.
After controlling for potential confounders including demographic factors, personal and neighborhood level socioeconomic characteristics, cigarette smoking, and background air pollution, higher traffic density was significantly associated with lower forced expiratory volume at 1s (FEV1) and forced vital capacity (FVC) in females. Relative to the lowest quartile of traffic density, the adjusted differences across increasing quartiles were 5.1, −15.4 and −21.5ml for FEV1 (p value of linear trend across the quartiles =0.041), and 1.2, −23.4 and −34.8ml for FVC (p trend =0.010). Using distance from major roads as a simpler index of traffic related air pollution exposure, the FEV1 was −15.7ml (95%CI −34.4ml, 2.9ml) lower and the FVC was −24.2ml (95%CI −46.2ml, −2.3ml) lower for women living within 150 meters compared to subjects living further away. We did not find a significant effect of traffic density or distance to major roads on lung function among men. The FEV1/FVC ratio was not significantly associated with traffic exposure in either gender.
This is the largest published study of traffic exposure and pulmonary function in adults to date. These results add to growing evidence that chronic exposure to traffic-related air pollution may adversely affect respiratory health.
air pollution; traffic; pulmonary function; FEV1; FVC
Rationale: In late October 2003, Southern California wildfires burned more than 3,000 km2. The wildfires produced heavy smoke that affected several communities participating in the University of Southern California Children's Health Study (CHS).
Objectives: To study the acute effects of fire smoke on the health of CHS participants.
Methods: A questionnaire was used to assess smoke exposure and occurrence of symptoms among CHS high-school students (n = 873; age, 17–18 yr) and elementary-school children (n = 5,551; age, 6–7 yr), in a total of 16 communities. Estimates of particulate matter (PM10) concentrations during the 5 d with the highest fire activity were used to characterize community smoke level.
Main Results: All symptoms (nose, eyes, and throat irritations; cough; bronchitis; cold; wheezing; asthma attacks), medication usage, and physician visits were associated with individually reported exposure differences within communities. Risks increased monotonically with the number of reported smoky days. For most outcomes, reporting rates between communities were also associated with the fire-related PM10 levels. Associations tended to be strongest among those without asthma. Individuals with asthma were more likely to take preventive action, such as wearing masks or staying indoors during the fire.
Conclusions: Exposure to wildfire smoke was associated with increased eye and respiratory symptoms, medication use, and physician visits.
air pollution; asthma; sore throat; wheezing
Although numerous epidemiologic studies now use models of intraurban exposure, there has been little systematic evaluation of the performance of different models.
In this present article we proposed a modeling framework for assessing exposure model performance and the role of spatial autocorrelation in the estimation of health effects.
We obtained data from an exposure measurement substudy of subjects from the Southern California Children’s Health Study. We examined how the addition of spatial correlations to a previously described unified exposure and health outcome modeling framework affects estimates of exposure–response relationships using the substudy data. The methods proposed build upon the previous work, which developed measurement–error techniques to estimate long-term nitrogen dioxide exposure and its effect on lung function in children. In this present article, we further develop these methods by introducing between- and within-community spatial autocorrelation error terms to evaluate effects of air pollution on forced vital capacity. The analytical methods developed are set in a Bayesian framework where multistage models are fitted jointly, properly incorporating parameter estimation uncertainty at all levels of the modeling process.
Results suggest that the inclusion of residual spatial error terms improves the prediction of adverse health effects. These findings also demonstrate how residual spatial error may be used as a diagnostic for comparing exposure model performance.
air pollution; Bayesian analysis; lung function; measurement error; spatial exposure models
Experimental data suggest that asthma exacerbation by ambient air pollutants is enhanced by exposure to endotoxin and allergens; however, there is little supporting epidemiologic evidence.
We evaluated whether the association of exposure to air pollution with annual prevalence of chronic cough, phlegm production, or bronchitis was modified by dog and cat ownership (indicators of allergen and endotoxin exposure). The study population consisted of 475 Southern California children with asthma from a longitudinal cohort of participants in the Children’s Health Study. We estimated average annual ambient exposure to nitrogen dioxide, ozone, particulate matter < 10, 2.5, and 10–2.5 μm in aerodynamic diameter (PM10, PM2.5, and PM10–2.5, respectively), elemental and organic carbon, and acid vapor from monitoring stations in each of the 12 study communities. Multivariate models were used to examine the effect of yearly variation of each pollutant. Effects were scaled to the variability that is common for each pollutant in representative communities in Southern California.
Among children owning a dog, there were strong associations between bronchitic symptoms and all pollutants examined. Odds ratios ranged from 1.30 per 4.2 μg/m3 for PM10–2.5 [95% confidence interval (CI), 0.91–1.87) to 1.91 per 1.2 μg/m3 for organic carbon (95% CI, 1.34–2.71). Effects were somewhat larger among children who owned both a cat and dog. There were no effects or small effects with wide CIs among children without a dog and among children who owned only a cat.
Our results suggest that dog ownership, a source of residential exposure to endotoxin, may worsen the relationship between air pollution and respiratory symptoms in asthmatic children.
air pollution; asthma; cats; child; dogs; endotoxin; epidemiology; indoor allergens; particulate matter
Results from studies of traffic and childhood asthma have been inconsistent, but there has been little systematic evaluation of susceptible subgroups. In this study, we examined the relationship of local traffic-related exposure and asthma and wheeze in southern California school children (5–7 years of age). Lifetime history of doctor-diagnosed asthma and prevalent asthma and wheeze were evaluated by questionnaire. Parental history of asthma and child’s history of allergic symptoms, sex, and early-life exposure (residence at the same home since 2 years of age) were examined as susceptibility factors. Residential exposure was assessed by proximity to a major road and by modeling exposure to local traffic-related pollutants. Residence within 75 m of a major road was associated with an increased risk of lifetime asthma [odds ratio (OR) = 1.29; 95% confidence interval (CI), 1.01–1.86], prevalent asthma (OR = 1.50; 95% CI, 1.16–1.95), and wheeze (OR = 1.40; 95% CI, 1.09–1.78). Susceptibility increased in long-term residents with no parental history of asthma for lifetime asthma (OR = 1.85; 95% CI, 1.11–3.09), prevalent asthma (OR = 2.46; 95% CI, 0.48–4.09), and recent wheeze (OR = 2.74; 95% CI, 1.71–4.39). The higher risk of asthma near a major road decreased to background rates at 150–200 m from the road. In children with a parental history of asthma and in children moving to the residence after 2 years of age, there was no increased risk associated with exposure. Effect of residential proximity to roadways was also larger in girls. A similar pattern of effects was observed with traffic-modeled exposure. These results indicate that residence near a major road is associated with asthma. The reason for larger effects in those with no parental history of asthma merits further investigation.
air pollution; asthma; child; epidemiology; traffic
We examined whether ischemic heart disease (IHD) hospital admissions were associated with air pollutants in those with and without secondary diagnoses of arrhythmia (ARR) or congestive heart failure (CHF). We assessed the occurrence of increased vulnerability among persons with these conditions to daily variations in ozone, carbon monoxide, nitrogen dioxide, or particulate matter less than or equal to 10 micro m in aerodynamic diameter (PM10). The study population consisted of members of a large health maintenance organization residing in the South Coast Air Basin of California from 1988 to 1995. After adjustment for day of week, study year, and smoothing splines for day of study, temperature, and relative humidity, CO and NO2 were both associated with admissions with the greatest effects for CO. A 1-ppm increase in 8-hr average CO was associated with a 3.60% [95% confidence interval (CI), 1.62-5.63%] increase in same-day IHD admissions in persons with a secondary diagnosis of CHF, a 2.99% (95% CI, 1.80-4.19%) increase in persons with a secondary diagnosis of ARR, and a 1.62% (95% CI, 0.65-2.59%) increase in IHD admissions in persons without either secondary diagnosis. Air pollution was most strongly associated with myocardial infarction hospital admissions. The vulnerability of the secondary CHF subgroup may be due to a greater prevalence of myocardial infarction primary diagnoses and not the modifying effect of CHF. This study suggests that people with IHD and accompanying CHF and/or ARR constitute a sensitive subgroup in relation to the effects of criteria ambient air pollutants associated with motor vehicle combustion.