With the increase of motor vehicles, ambient air pollution related to traffic exhaust has become an important environmental issue in China. Because of their fast growth and development, children are more susceptible to ambient air pollution exposure. Many chemicals from traffic exhaust, such as carbon monoxide, nitrogen dioxide, and lead, have been reported to show adverse effects on neurobehavioral functions. Several studies in China have suggested that traffic exhaust might affect neurobehavioral functions of adults who have occupational traffic exhaust exposure. However, few data have been reported on the effects on neurobehavioral function in children.
The objective of this study was to explore the association between traffic-related air pollution exposure and its effects on neurobehavioral function in children.
This field study was conducted in Quanzhou, China, where two primary schools were chosen based on traffic density and monitoring data of ambient air pollutants. School A was located in a clear area and school B in a polluted area. We monitored NO2 and particulate matter with aerodynamic diameter ≤ 10 μm as indicators for traffic-related air pollution on the campuses and in classrooms for 2 consecutive days in May 2005. The children from second grade (8–9 years of age) and third grade (9–10 years of age) of the two schools (n = 928) participated in a questionnaire survey and manual-assisted neurobehavioral testing. We selected 282 third-grade children (school A, 136; school B, 146) to participate in computer-assisted neurobehavioral testing. We conducted the fieldwork between May and June 2005. We used data from 861 participants (school A, 431; school B, 430) with manual neurobehavioral testing and from all participants with computerized testing for data analyses.
Media concentrations of NO2 in school A and school B campus were 7 μg/m3 and 36 μg/m3, respectively (p < 0.05). The ordinal logistic regression analyses showed that, after controlling the potential confounding factors, participants living in the polluted area showed poor performance on all testing; differences in results for six of nine tests (66.7%) achieved statistical significance: Visual Simple Reaction Time with preferred hand and with nonpreferred hand, Continuous Performance, Digit Symbol, Pursuit Aiming, and Sign Register.
We found a significant relationship between chronic low-level traffic-related air pollution exposure and neurobehavioral function in exposed children. More studies are needed to explore the effects of traffic exhaust on neurobehavioral function and development.
air pollution; children; health effects; neurobehavioral functions; traffic-related air pollution
Land use regression (LUR) has emerged as an effective means of estimating exposure to air pollution in epidemiological studies. We created the first LUR models of nitric oxide (NO), nitrogen dioxide (NO2) and nitrogen oxides (NOx) for the complex megalopolis of Los Angeles (LA), California. Two-hundred and one sampling sites (the largest sampling design to date for LUR estimation) for two seasons were selected using a location-allocation algorithm that maximized the potential variability in measured pollutant concentrations and represented populations in the health study. Traffic volumes, truck routes and road networks, land use data, satellite-derived vegetation greenness and soil brightness, and truck route slope gradients were used for predicting NOx concentrations. A novel model selection strategy known as “ADDRESS” (A Distance Decay REgression Selection Strategy) was used to select optimized buffer distances for potential predictor variables and maximize model performance.
Final regression models explained 81%, 86% and 85% of the variance in measured NO, NO2 and NOx concentrations, respectively. Cross-validation analyses suggested a prediction accuracy of 87–91%. Remote sensing-derived variables were significantly correlated with NOx concentrations, suggesting these data are useful surrogates for modeling traffic-related pollution when certain land use data are unavailable. Our study also demonstrated that reactive pollutants such as NO and NO2 could have high spatial extents of influence (e.g., > 5000 m from expressway) and high background concentrations in certain geographic areas. This paper represents the first attempt to model traffic-related air pollutants at a fine scale within such a complex and large urban region.
Nitrogen oxides; Air pollution; Traffic; Land use regression; GIS; Remote sensing; Los Angeles
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
Epidemiologic studies associate childhood exposure to traffic-related air pollution with increased respiratory infections and asthmatic and allergic symptoms. The strongest associations between traffic exposure and negative health impacts are observed in individuals with respiratory inflammation. We hypothesized that interactions between nitric oxide (NO), increased during lung inflammatory responses, and reactive oxygen species (ROS), increased as a consequence of traffic exposure ─ played a key role in the increased susceptibility of these at-risk populations to traffic emissions.
Diesel exhaust particles (DEP) were used as surrogates for traffic particles. Murine lung epithelial (LA-4) cells and BALB/c mice were treated with a cytokine mixture (cytomix: TNFα, IL-1β, and IFNγ) to induce a generic inflammatory state. Cells were exposed to saline or DEP (25 μg/cm2) and examined for differential effects on
redox balance and cytotoxicity. Likewise, mice undergoing nose-only inhalation exposure to air or DEP
(2 mg/m3 × 4 h/d × 2 d) were assessed for differential effects on lung inflammation, injury, antioxidant levels,
and phagocyte ROS production.
Cytomix treatment significantly increased LA-4 cell NO production though iNOS activation. Cytomix +
DEP-exposed cells incurred the greatest intracellular ROS production, with commensurate cytotoxicity, as these cells were unable to maintain redox balance. By contrast, saline + DEP-exposed cells were able to mount effective antioxidant responses. DEP effects were mediated by: (1) increased ROS including superoxide anion (O2˙-), related to increased xanthine dehydrogenase expression and reduced cytosolic superoxide dismutase activity; and (2) increased peroxynitrite generation related to interaction of O2˙- with cytokine-induced NO. Effects were partially reduced by superoxide dismutase (SOD) supplementation or by blocking iNOS induction. In mice, cytomix +
DEP-exposure resulted in greater ROS production in lung phagocytes. Phagocyte and epithelial effects were, by and large, prevented by treatment with FeTMPyP, which accelerates peroxynitrite catalysis.
During inflammation, due to interactions of NO and O2˙-, DEP-exposure was associated with nitrosative stress in surface epithelial cells and resident lung phagocytes. As these cell types work in concert to provide protection against inhaled pathogens and allergens, dysfunction would predispose to development of respiratory infection and allergy. Results provide a mechanism by which individuals with pre-existing respiratory inflammation are at increased risk for exposure to traffic-dominated urban air pollution.
Traffic; Diesel; Particles; Epithelial cells; Phagocytes; Nitric oxide; Peroxynitrite; Redox balance
Land-use regression (LUR) models have been developed to estimate spatial distributions of traffic-related pollutants. Several studies have examined spatial autocorrelation among residuals in LUR models, but few utilized spatial residual information in model prediction, or examined the impact of modeling methods, monitoring site selection, or traffic data quality on LUR performance. This study aims to improve spatial models for traffic-related pollutants using generalized additive models (GAM) combined with cokriging of spatial residuals. Specifically, we developed spatial models for nitrogen dioxide (NO2) and nitrogen oxides (NOx) concentrations in Southern California separately for two seasons (summer and winter) based on over 240 sampling locations. Pollutant concentrations were disaggregated into three components: local means, spatial residuals, and normal random residuals. Local means were modeled by GAM. Spatial residuals were cokriged with global residuals at nearby sampling locations that were spatially auto-correlated. We compared this two-stage approach with four commonly-used spatial models: universal kriging, multiple linear LUR and GAM with and without a spatial smoothing term. Leave-one-out cross validation was conducted for model validation and comparison purposes. The results show that our GAM plus cokriging models predicted summer and winter NO2 and NOx concentration surfaces well, with cross validation R2 values ranging from 0.88 to 0.92. While local covariates accounted for partial variance of the measured NO2 and NOx concentrations, spatial autocorrelation accounted for about 20% of the variance. Our spatial GAM model improved R2 considerably compared to the other four approaches. Conclusively, our two-stage model captured summer and winter differences in NO2 and NOx spatial distributions in Southern California well. When sampling location selection cannot be optimized for the intended model and fewer covariates are available as predictors for the model, the two-stage model is more robust compared to multiple linear regression models.
Land-use regression; Spatial residuals; Generalized additive model; Cokriging; Traffic air pollution
Background: The fractional concentration of nitric oxide in exhaled air (FeNO) potentially detects airway inflammation related to air pollution exposure. Existing studies have not yet provided conclusive evidence on the association of FeNO with traffic-related pollution (TRP).
Objectives: We evaluated the association of FeNO with residential TRP exposure in a large cohort of children.
Methods: We related FeNO measured on 2,143 children (ages 7–11 years) who participated in the Southern California Children’s Health Study (CHS) to five classes of metrics of residential TRP: distances to freeways and major roads; length of all and local roads within circular buffers around the home; traffic densities within buffers; annual average line source dispersion modeled nitrogen oxides (NOx) from freeways and nonfreeway roads; and predicted annual average nitrogen oxide, nitrogen dioxide, and NOx from a model based on intracommunity sampling in the CHS.
Results: In children with asthma, length of roads was positively associated with FeNO, with stronger associations in smaller buffers [46.7%; 95% confidence interval (CI), 14.3–88.4], 12.4% (95% CI, –8.8 to 38.4), and 4.1% (95% CI, –14.6 to 26.8) higher FeNO for 100-, 300-, and 1,000-m increases in the length of all roads in 50-, 100-, and 200-m buffers, respectively. Other TRP metrics were not significantly associated with FeNO, even though the study design was powered to detect exposures explaining as little as 0.4% of the variation in natural log-transformed FeNO (R2 = 0.004).
Conclusion: Length of road was the only indicator of residential TRP exposure associated with airway inflammation in children with asthma, as measured by FeNO.
air pollution; airway inflammation; children’s respiratory health; exhaled nitric oxide; traffic
Preeclampsia is a major complication of pregnancy that can lead to substantial maternal and perinatal morbidity, mortality, and preterm birth. Increasing evidence suggests that air pollution adversely affects pregnancy outcomes. Yet few studies have examined how local traffic-generated emissions affect preeclampsia in addition to preterm birth.
We examined effects of residential exposure to local traffic-generated air pollution on preeclampsia and preterm delivery (PTD).
We identified 81,186 singleton birth records from four hospitals (1997–2006) in Los Angeles and Orange Counties, California (USA). We used a line-source dispersion model (CALINE4) to estimate individual exposure to local traffic-generated nitrogen oxides (NOx) and particulate matter < 2.5 μm in aerodynamic diameter (PM2.5) across the entire pregnancy. We used logistic regression to estimate effects of air pollution exposures on preeclampsia, PTD (gestational age < 37 weeks), moderate PTD (MPTD; gestational age < 35 weeks), and very PTD (VPTD; gestational age < 30 weeks).
We observed elevated risks for preeclampsia and preterm birth from maternal exposure to local traffic-generated NOx and PM2.5. The risk of preeclampsia increased 33% [odds ratio (OR) = 1.33; 95% confidence interval (CI), 1.18–1.49] and 42% (OR = 1.42; 95% CI, 1.26–1.59) for the highest NOx and PM2.5 exposure quartiles, respectively. The risk of VPTD increased 128% (OR = 2.28; 95% CI, 2.15–2.42) and 81% (OR = 1.81; 95% CI, 1.71–1.92) for women in the highest NOx and PM2.5 exposure quartiles, respectively.
Exposure to local traffic-generated air pollution during pregnancy increases the risk of preeclampsia and preterm birth in Southern California women. These results provide further evidence that air pollution is associated with adverse reproductive outcomes.
air pollution; nitrogen oxides; particulate matter; preeclampsia; pregnancy outcome; preterm birth; vehicle emission
Living near traffic has been associated with asthma and other respiratory symptoms. Most studies, however, have been conducted in areas with high background levels of ambient air pollution, making it challenging to isolate an independent effect of traffic. Additionally, most investigations have used surrogates of exposure, and few have measured traffic pollutants directly as part of the study.
We conducted a cross-sectional study of current asthma and other respiratory symptoms in children (n = 1,080) living at varying distances from high-traffic roads in the San Francisco Bay Area, California, a highly urbanized region characterized by good regional air quality due to coastal breezes.
We obtained health information and home environmental factors by parental questionnaire. We assessed exposure with several measures of residential proximity to traffic calculated using geographic information systems, including traffic within a given radius and distance to major roads. We also measured traffic-related pollutants (nitrogen oxides and nitrogen dioxide) for a subset of households to determine how well traffic metrics correlated with measured traffic pollutants.
Using multivariate logistic regression analyses, we found associations between current asthma and residential proximity to traffic. For several traffic metrics, children whose residences were in the highest quintile of exposure had approximately twice the adjusted odds of current asthma (i.e., asthma episode in the preceeding 12 months) compared with children whose residences were within the lowest quintile. The highest risks were among those living within 75 m of a freeway/highway. Most traffic metrics correlated moderately well with actual pollutant measurements.
Our findings provide evidence that even in an area with good regional air quality, proximity to traffic is associated with adverse respiratory health effects in children.
air pollution; asthma; bronchitis; children; respiratory health; traffic
Disproportionate life stress and consequent physiologic alteration (i.e., immune dysregulation) has been proposed as a major pathway linking socioeconomic position, environmental exposures, and health disparities. Asthma, for example, disproportionately affects lower-income urban communities, where air pollution and social stressors may be elevated.
We aimed to examine the role of exposure to violence (ETV), as a chronic stressor, in altering susceptibility to traffic-related air pollution in asthma etiology.
We developed geographic information systems (GIS)–based models to retrospectively estimate residential exposures to traffic-related pollution for 413 children in a community-based pregnancy cohort, recruited in East Boston, Massachusetts, between 1987 and 1993, using monthly nitrogen dioxide measurements for 13 sites over 18 years. We merged pollution estimates with questionnaire data on lifetime ETV and examined the effects of both on childhood asthma etiology.
Correcting for potential confounders, we found an elevated risk of asthma with a 1-SD (4.3 ppb) increase in NO2 exposure solely among children with above-median ETV [odds ratio (OR) = 1.63; 95% confidence interval (CI), 1.14–2.33)]. Among children always living in the same community, with lesser exposure measurement error, this association was magnified (OR = 2.40; 95% CI, 1.48–3.88). Of multiple exposure periods, year-of-diagnosis NO2 was most predictive of asthma outcomes.
We found an association between traffic-related air pollution and asthma solely among urban children exposed to violence. Future studies should consider socially patterned susceptibility, common spatial distributions of social and physical environmental factors, and potential synergies among these. Prospective assessment of physical and social exposures may help determine causal pathways and critical exposure periods.
childhood asthma; exposure to violence (ETV); geographic information systems (GIS); intraurban variability; nitrogen dioxide (NO2); social–environmental synergy; stress
Background: Short-term exposure to air pollution has been associated with changes in blood pressure (BP) and emergency department visits for hypertension, but little is known about the effects of long-term exposure to traffic-related air pollution on BP and hypertension.
Objectives: We studied whether long-term exposure to air pollution is associated with BP and hypertension.
Methods: In 1993–1997, 57,053 participants 50–64 years of age were enrolled in a population-based cohort study. Systolic and diastolic BP (SBP and DBP, respectively) were measured at enrollment. Self-reported incident hypertension during a mean follow-up of 5.3 years was assessed by questionnaire. We used a validated dispersion model to estimate residential long-term nitrogen oxides (NOx), a marker of traffic-related air pollution, for the 1- and 5-year periods prior to enrollment and before a diagnosis of hypertension. We conducted a cross-sectional analysis of associations between air pollution and BP at enrollment with linear regression, adjusting for traffic noise, measured short-term NOx, temperature, relative humidity, and potential lifestyle confounders (n = 44,436). We analyzed incident hypertension with Cox regression, adjusting for traffic noise and potential confounders.
Results: A doubling of NOx exposure during 1- and 5-year periods preceding enrollment was associated with 0.53-mmHg decreases [95% confidence interval (CI): –0.88, –0.19 mmHg] and 0.50-mmHg decreases (95% CI: –0.84, –0.16 mmHg) in SBP, respectively. Long-term exposure also was associated with a lower prevalence of baseline self-reported hypertension (per doubling of 5-year mean NOx: odds ratio = 0.96; 95% CI: 0.91, 1.00), whereas long-term NOx exposure was not associated with incident self-reported hypertension during follow-up.
Conclusions: Long-term exposure to traffic-related air pollution was associated with a slightly lower prevalence of BP at baseline, but was not associated with incident hypertension.
air pollution; blood pressure; hypertension; epidemiology; nitrogen oxide
Previous studies have identified associations between traffic-related air pollution and adverse health effects. Most have used measurements from a few central ambient monitors and/or some measure of traffic as indicators of exposure, disregarding spatial variability and/or factors influencing personal exposure-ambient concentration relationships. This study seeks to utilize publicly available data (i.e., central site monitors, geographic information system (GIS), and property assessment data) and questionnaire responses to predict residential indoor concentrations of traffic-related air pollutants for lower socioeconomic status (SES) urban households.
As part of a prospective birth cohort study in urban Boston, we collected indoor and outdoor 3–4 day samples of nitrogen dioxide (NO2) and fine particulate matter (PM2.5) in 43 low SES residences across multiple seasons from 2003 – 2005. Elemental carbon concentrations were determined via reflectance analysis. Multiple traffic indicators were derived using Massachusetts Highway Department data and traffic counts collected outside sampling homes. Home characteristics and occupant behaviors were collected via a standardized questionnaire. Additional housing information was collected through property tax records, and ambient concentrations were collected from a centrally-located ambient monitor.
The contributions of ambient concentrations, local traffic and indoor sources to indoor concentrations were quantified with regression analyses. PM2.5 was influenced less by local traffic but had significant indoor sources, while EC was associated with traffic and NO2 with both traffic and indoor sources. Comparing models based on covariate selection using p-values or a Bayesian approach yielded similar results, with traffic density within a 50m buffer of a home and distance from a truck route as important contributors to indoor levels of NO2 and EC, respectively. The Bayesian approach also highlighted the uncertanity in the models. We conclude that by utilizing public databases and focused questionnaire data we can identify important predictors of indoor concentrations for multiple air pollutants in a high-risk population.
indoor air; NO2; PM2.5; EC; geographic information system
The prevalence of allergic diseases has increased worldwide, a phenomenon that can be largely attributed to environmental effects. Among environmental factors, air pollution due to traffic is thought to be a major threat to childhood health. Residing near busy roadways is associated with increased asthma hospitalization, decreased lung function, and increased prevalence and severity of wheezing and allergic rhinitis. Recently, prospective cohort studies using more accurate measurements of individual exposure to air pollution have been conducted and have provided definitive evidence of the impact of air pollution on allergic diseases. Particulate matter and ground-level ozone are the most frequent air pollutants that cause harmful effects, and the mechanisms underlying these effects may be related to oxidative stress. The reactive oxidative species produced in response to air pollutants can overwhelm the redox system and damage the cell wall, lipids, proteins, and DNA, leading to airway inflammation and hyper-reactivity. Pollutants may also cause harmful effects via epigenetic mechanisms, which control the expression of genes without changing the DNA sequence itself. These mechanisms are likely to be a target for the prevention of allergies. Further studies are necessary to identify children at risk and understand how these mechanisms regulate gene-environment interactions. This review provides an update of the current understanding on the impact of air pollution on allergic diseases in children and facilitates the integration of issues regarding air pollution and allergies into pediatric practices, with the goal of improving pediatric health.
Air pollution; Asthma; Allergy; Child; Oxidative stress; Epigenetics
Background: Few studies have examined the acute health effects of air pollution exposures experienced while cycling in traffic.
Objectives: We conducted a crossover study to examine the relationship between traffic pollution and acute changes in heart rate variability. We also collected spirometry and exhaled nitric oxide measures.
Methods: Forty-two healthy adults cycled for 1 hr on high- and low-traffic routes as well as indoors. Health measures were collected before cycling and 1–4 hr after the start of cycling. Ultrafine particles (UFPs; ≤ 0.1 μm in aerodynamic diameter), particulate matter ≤ 2.5 μm in aerodynamic diameter (PM2.5), black carbon, and volatile organic compounds were measured along each cycling route, and ambient nitrogen dioxide (NO2) and ozone (O3) levels were recorded from a fixed-site monitor. Mixed-effects models were used to estimate associations between air pollutants and changes in health outcome measures relative to precycling baseline values.
Results: An interquartile range increase in UFP levels (18,200/cm3) was associated with a significant decrease in high-frequency power 4 hr after the start of cycling [β = –224 msec2; 95% confidence interval (CI), –386 to –63 msec2]. Ambient NO2 levels were inversely associated with the standard deviation of normal-to-normal (NN) intervals (β = –10 msec; 95% CI, –20 to –0.34 msec) and positively associated with the ratio of low-frequency to high-frequency power (β = 1.4; 95% CI, 0.35 to 2.5) 2 hr after the start of cycling. We also observed significant inverse associations between ambient O3 levels and the root mean square of successive differences in adjacent NN intervals 3 hr after the start of cycling.
Conclusions: Short-term exposures to traffic pollution may contribute to altered autonomic modulation of the heart in the hours immediately after cycling.
black carbon; cycling; heart rate variability; PM2.5; traffic pollution; ultrafine particles
There is conflicting evidence that traffic-related air pollution is a risk factor for allergic conditions. Few studies have investigated this in adults. In adults, a high proportion of asthma, rhinitis and eczema is triggered by non-allergic factors. We investigated traffic as a risk factor for allergic versus non-allergic asthma and rhinitis, and eczema, in adults.
A questionnaire from 2000 (n = 9319, 18–77 years) provided individual data about disease outcome and self-reported traffic exposure. Additional exposure assessments were obtained using Geographical Informations Systems (GIS). Residential addresses were linked to the national Swedish Road Database and to a pollutant database with modelled annual means of NOx (Nitrogen Oxids).
Living within 100 m from a road with a traffic intensity of >10 cars/min (24 hour mean) was associated with prevalence of current asthma reported to be triggered by allergic factors (OR = 1.83, 95% CI = 1.23–2.72) and with allergic rhinitis (OR = 1.30, 95%CI = (1.05–1.61). No relation was seen with asthma or rhinitis triggered by other factors. Living within 100 m of a road with >10 cars/min was also associated with hand-eczema during the last 12 months (OR = 1.63, 95% CI = 1.19–2.23), but not with allergic eczema or diagnosed hand-eczema. Consistent results were seen using self-reported traffic, but the associations with NOx were less consistent.
Exposure to traffic was associated with a higher prevalence of allergic asthma and allergic rhinitis, but not with asthma or rhinitis triggered by non-allergic factors. This difference was suggested by the overall pattern, but only clear using GIS-measured traffic intensity as a proxy for traffic exposure. An association was also found with hand-eczema during the last 12 months. We suggest that asthma and rhinitis should not be treated as homogenous groups when estimating effects from traffic in adults.
Air pollutants may induce airway inflammation and sensitization due to generation of reactive oxygen species. The genetic background to these mechanisms could be important effect modifiers.
Our goal was to assess interactions between exposure to air pollution and single nucleotide polymorphisms (SNPs) in the β2-adrenergic receptor (ADRB2), glutathione S-transferase P1 (GSTP1), and tumor necrosis factor (TNF) genes for development of childhood allergic disease.
In a birth cohort originally of 4,089 children, we assessed air pollution from local traffic using nitrogen oxides (traffic NOx) as an indicator based on emission databases and dispersion modeling and estimated individual exposure through geocoding of home addresses. We measured peak expiratory flow rates and specific IgE for inhalant and food allergens at 4 years of age, and selected children with asthma symptoms up to 4 years of age (n = 542) and controls (n = 542) for genotyping.
Interaction effects on allergic sensitization were indicated between several GSTP1 SNPs and traffic NOx exposure during the first year of life (pnominal < 0.001–0.06). Children with Ile105Val/Val105Val genotypes were at increased risk of sensitization to any allergen when exposed to elevated levels of traffic NOx (for a difference between the 5th and 95th percentile of exposure: odds ratio = 2.4; 95% confidence interval, 1.0–5.3). In children with TNF-308 GA/AA genotypes, the GSTP1–NOx interaction effect was even more pronounced. We observed no conclusive interaction effects for ADRB2.
The effect of air pollution from traffic on childhood allergy appears to be modified by GSTP1 and TNF variants, supporting a role of genes controlling the antioxidative system and inflammatory response in allergy.
ADRB2; air pollution; allergy; asthma; genetics; GSTP1; interaction; nitrogen oxides; polymorphism; TNF
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
Several studies have found an effect on mortality of between-city contrasts in long-term exposure to air pollution. The effect of within-city contrasts is still poorly understood.
We studied the association between long-term exposure to traffic-related air pollution and mortality in a Dutch cohort.
We used data from an ongoing cohort study on diet and cancer with 120,852 subjects who were followed from 1987 to 1996. Exposure to black smoke (BS), nitrogen dioxide, sulfur dioxide, and particulate matter ≤mu;M2.5), as well as various exposure variables related to traffic, were estimated at the home address. We conducted Cox analyses in the full cohort adjusting for age, sex, smoking, and area-level socioeconomic status.
Traffic intensity on the nearest road was independently associated with mortality. Relative risks (95% confidence intervals) for a 10-μg/m3 increase in BS concentrations (difference between 5th and 95th percentile) were 1.05 (1.00–1.11) for natural cause, 1.04 (0.95–1.13) for cardiovascular, 1.22 (0.99–1.50) for respiratory, 1.03 (0.88–1.20) for lung cancer, and 1.04 (0.97–1.12) for mortality other than cardiovascular, respiratory, or lung cancer. Results were similar for NO2 and PM2.5, but no associations were found for SO2.
Traffic-related air pollution and several traffic exposure variables were associated with mortality in the full cohort. Relative risks were generally small. Associations between natural-cause and respiratory mortality were statistically significant for NO2 and BS. These results add to the evidence that long-term exposure to ambient air pollution is associated with increased mortality.
air pollution; cohort; mortality; traffic
Previous studies reported adverse impacts of traffic-related air pollution exposure on pregnancy outcomes. Yet, little information exists on how effect estimates are impacted by the different exposure assessment methods employed in these studies.
To compare effect estimates for traffic-related air pollution exposure and preeclampsia, preterm birth (gestational age less than 37 weeks), and very preterm birth (gestational age less than 30 weeks) based on four commonly-used exposure assessment methods.
We identified 81,186 singleton births during 1997–2006 at four hospitals in Los Angeles and Orange Counties, California. Exposures were assigned to individual subjects based on residential address at delivery using the nearest ambient monitoring station data [carbon monoxide (CO), nitrogen dioxide (NO2), nitric oxide (NO), nitrogen oxides (NOx), ozone (O3), and particulate matter less than 2.5 (PM2.5) or less than 10 (PM10) μm in aerodynamic diameter], both unadjusted and temporally-adjusted land-use regression (LUR) model estimates (NO, NO2, and NOx), CALINE4 line-source air dispersion model estimates (NOx and PM2.5), and a simple traffic-density measure. We employed unconditional logistic regression to analyze preeclampsia in our birth cohort, while for gestational age-matched risk sets with preterm and very preterm birth we employed conditional logistic regression.
We observed elevated risks for preeclampsia, preterm birth, and very preterm birth from maternal exposures to traffic air pollutants measured at ambient stations (CO, NO, NO2, and NOx) and modeled through CALINE4 (NOx and PM2.5) and LUR (NO2 and NOx). Increased risk of preterm birth and very preterm birth were also positively associated with PM10 and PM2.5 air pollution measured at ambient stations. For LUR-modeled NO2 and NOx exposures, elevated risks for all the outcomes were observed in Los Angeles only – the region for which the LUR models were initially developed. Unadjusted LUR models often produced odds ratios somewhat larger in size than temporally-adjusted models. The size of effect estimates was smaller for exposures based on simpler traffic density measures than the other exposure assessment methods.
We generally confirmed that traffic-related air pollution was associated with adverse reproductive outcomes regardless of the exposure assessment method employed, yet the size of the estimated effect depended on how both temporal and spatial variations were incorporated into exposure assessment. The LUR model was not transferable even between two contiguous areas within the same large metropolitan area in Southern California.
Air monitoring; CALINE4; land-use regression; preeclampsia; preterm birth
Traffic-related particles induce oxidative stress and may exert adverse effects on central nervous system function, which could manifest as cognitive impairment.
We assessed the association between black carbon (BC), a marker of traffic-related air pollution, and cognition in older men.
A total of 680 men (mean ± SD, 71 ± 7 years of age) from the U.S. Department of Veterans Affairs Normative Aging Study completed a battery of seven cognitive tests at least once between 1996 and 2007. We assessed long-term exposure to traffic-related air pollution using a validated spatiotemporal land-use regression model for BC.
The association between BC and cognition was nonlinear, and we log-transformed BC estimates for all analyses [ln(BC)]. In a multivariable-adjusted model, for each doubling in BC on the natural scale, the odds of having a Mini-Mental State Examination (MMSE) score ≤ 25 was 1.3 times higher [95% confidence interval (CI), 1.1 to 1.6]. In a multivariable-adjusted model for global cognitive function, which combined scores from the remaining six tests, a doubling of BC was associated with a 0.054 SD lower test score (95% CI, −0.103 to −0.006), an effect size similar to that observed with a difference in age of 1.9 years in our data. We found no evidence of heterogeneity by cognitive test. In sensitivity analyses adjusting for past lead exposure, the association with MMSE scores was similar (odds ratio = 1.3; 95% CI, 1.1 to 1.7), but the association with global cognition was somewhat attenuated (−0.038 per doubling in BC; 95% CI, −0.089 to 0.012).
Ambient traffic-related air pollution was associated with decreased cognitive function in older men.
aging; black carbon; cognitive dysfunction; epidemiology; particulate matter
Few studies have examined associations of birth outcomes with toxic air pollutants (air toxics) in traffic exhaust. This study included 8,181 term low birth weight (LBW) children and 370,922 term normal-weight children born between January 1, 1995, and December 31, 2006, to women residing within 5 miles (8 km) of an air toxics monitoring station in Los Angeles County, California. Additionally, land-use-based regression (LUR)-modeled estimates of levels of nitric oxide, nitrogen dioxide, and nitrogen oxides were used to assess the influence of small-area variations in traffic pollution. The authors examined associations with term LBW (≥37 weeks’ completed gestation and birth weight <2,500 g) using logistic regression adjusted for maternal age, race/ethnicity, education, parity, infant gestational age, and gestational age squared. Odds of term LBW increased 2%–5% (95% confidence intervals ranged from 1.00 to 1.09) per interquartile-range increase in LUR-modeled estimates and monitoring-based air toxics exposure estimates in the entire pregnancy, the third trimester, and the last month of pregnancy. Models stratified by monitoring station (to investigate air toxics associations based solely on temporal variations) resulted in 2%–5% increased odds per interquartile-range increase in third-trimester benzene, toluene, ethyl benzene, and xylene exposures, with some confidence intervals containing the null value. This analysis highlights the importance of both spatial and temporal contributions to air pollution in epidemiologic birth outcome studies.
air pollution; benzene; fetal growth retardation; hydrocarbons, aromatic; infant, low birth weight; pregnancy
Air pollution is associated with respiratory symptoms, lung function decrements, and hospitalizations. However, there is little information about the influence of air pollution on lung injury.
In this study we investigated acute effects of air pollution on pulmonary function and airway oxidative stress and inflammation in asthmatic children.
We studied 182 children with asthma, 9–14 years of age, for 4 weeks. Daily ambient concentrations of sulfur dioxide, nitrogen dioxide, ozone, and particulate matter ≤ 2.5 μm in aerodynamic diameter (PM2.5) were monitored from two stations. Once a week we measured spirometry and fractional exhaled nitric oxide (FeNO), and determined thiobarbituric acid reactive substances (TBARS) and 8-isoprostane—two oxidative stress markers—and interleukin-6 (IL-6) in breath condensate. We tested associations using mixed-effects regression models, adjusting for confounding variables.
Interquartile-range increases in 3-day average SO2 (5.4 ppb), NO2 (6.8 ppb), and PM2.5 (5.4 μg/m3) were associated with decreases in forced expiratory flow between 25% and 75% of forced vital capacity, with changes being −3.1% [95% confidence interval (CI), −5.8 to −0.3], −2.8% (95% CI, −4.8 to −0.8), and −3.0% (95% CI, −4.7 to −1.2), respectively. SO2, NO2, and PM2.5 were associated with increases in TBARS, with changes being 36.2% (95% CI, 15.7 to 57.2), 21.8% (95% CI, 8.2 to 36.0), and 24.8% (95% CI, 10.8 to 39.4), respectively. Risk estimates appear to be larger in children not taking corticosteroids than in children taking corticosteroids. O3 (5.3 ppb) was not associated with health end points. FeNO, 8-isoprostane, and IL-6 were not associated with air pollutants.
Air pollution may increase airway oxidative stress and decrease small airway function of asthmatic children. Inhaled corticosteroids may reduce oxidative stress and improve airway function.
air pollution; asthma; children; exhaled breath condensate; inflammation; oxidative stress; pulmonary function
Previous research has documented effects of both physical and social environmental exposures on childhood asthma. However, few studies have considered how these two environments might interact to affect asthma.
This study aimed to test interactions between chronic exposure to traffic-related air pollution and chronic family stress in predicting biologic and clinical outcomes in children with asthma.
Children with asthma (n = 73, 9–18 years of age) were interviewed about life stress, and asthma-relevant inflammatory markers [cytokine production, immunoglobulin E (IgE), eosinophil counts] were measured. Parents reported on children’s symptoms. Children completed daily diaries of symptoms and peak expiratory flow rate (PEFR) measures at baseline and 6 months later. Exposure to traffic-related air pollution was assessed using a land use regression model for nitrogen dioxide concentrations.
NO2 by stress interactions were found for interleukin-5 (β for interaction term = −0.31, p = 0.02), IgE (interaction β = −0.29, p = 0.02), and eosinophil counts (interaction β = −0.24, p = 0.04). These interactions showed that higher chronic stress was associated with heightened inflammatory profiles as pollution levels decreased. Longitudinally, NO2 by stress interactions emerged for daily diary symptoms (interaction β = −0.28, p = 0.02), parent-reported symptoms (interaction β = −0.25, p = 0.07), and PEFR (interaction β = 0.30, p = 0.03). These interactions indicated that higher chronic stress was associated with increases over time in symptoms and decreases over time in PEFR as pollution levels decreased.
The physical and social environments interacted in predicting both biologic and clinical outcomes in children with asthma, suggesting that when pollution exposure is more modest, vulnerability to asthma exacerbations may be heightened in children with higher chronic stress.
air pollution; asthma; immune; psychosocial; stress; traffic
To estimate long‐term exposure to traffic‐related air pollutants on an individual basis and to assess adverse health effects using a combination of air pollution measurement data, data from geographical information systems (GIS) and questionnaire data.
40 measurement sites in the city of Munich, Germany were selected at which to collect particulate matter with a 50% cut‐off aerodynamic diameter of 2.5 µm (PM2.5) and to measure PM2.5 absorbance and nitrogen dioxide (NO2). A pool of GIS variables (information about street length, household and population density and land use) was collected for the Munich metropolitan area and was used in multiple linear regression models to predict traffic‐related air pollutants. These models were also applied to the birth addresses of two birth cohorts (German Infant Nutritional Intervention Study (GINI) and Influence of Life‐style factors on the development of the Immune System and Allergies in East and West Germany (LISA)) in the Munich metropolitan area. Associations between air pollution concentrations at birth address and 1‐year and 2‐year incidences of respiratory symptoms were analysed.
The following means for the estimated exposures to PM2.5, PM2.5 absorbance and NO2 were obtained: 12.8 μg/m3, 1.7×10−5 m−1 and 35.3 μg/m3, respectively. Adjusted odds ratios (ORs) for wheezing, cough without infection, dry cough at night, bronchial asthma, bronchitis and respiratory infections indicated positive associations with traffic‐related air pollutants. After controlling for individual confounders, significant associations were found between the pollutant PM2.5 and sneezing, runny/stuffed nose during the first year of life (OR 1.16, 95% confidence interval 1.01 to 1.34) Similar effects were observed for the second year of life. These findings are similar to those from our previous analysis that were restricted to a subcohort in Munich city. The extended study also showed significant effects for sneezing, running/stuffed nose. Additionally, significant associations were found between NO2 and dry cough at night (or bronchitis) during the first year of life. The variable “living close to major roads” (<50 m), which was not analysed for the previous inner city cohort with birth addresses in the city of Munich, turned out to increase the risk of wheezing and asthmatic/spastic/obstructive bronchitis.
Effects on asthma and hay fever are subject to confirmation at older ages, when these outcomes can be more validly assessed.
Vehicle engine exhaust includes ultrafine particles with a large surface area and containing absorbed polycyclic aromatic hydrocarbons, transition metals and other substances. Ultrafine particles and soluble chemicals can be transported from the airways to other organs, such as the liver, kidneys, and brain. Our aim was to investigate whether air pollution from traffic is associated with risk for other cancers than lung cancer.
We followed up 54,304 participants in the Danish Diet Cancer and Health cohort for 20 selected cancers in the Danish Cancer Registry, from enrolment in 1993-1997 until 2006, and traced their residential addresses from 1971 onwards in the Central Population Registry. We used modeled concentration of nitrogen oxides (NOx) and amount of traffic at the residence as indicators of traffic-related air pollution and used Cox models to estimate incidence rate ratios (IRRs) after adjustment for potential confounders.
NOx at the residence was significantly associated with risks for cervical cancer (IRR, 2.45; 95% confidence interval [CI], 1.01;5.93, per 100 μg/m3 NOx) and brain cancer (IRR, 2.28; 95% CI, 1.25;4.19, per 100 μg/m3 NOx).
This hypothesis-generating study indicates that traffic-related air pollution might increase the risks for cervical and brain cancer, which should be tested in future studies.
Studies have shown associations between air pollution or traffic exposure and adverse birth outcomes, such as low birth weight. However, very few studies have examined the effect of traffic emissions on spontaneous abortion (SAB).
The goal of this study was to determine whether residential exposure to vehicular traffic was associated with SAB.
Pregnant women from a prepaid health plan in California were recruited into a prospective cohort study in 1990–1991. Three measures of traffic exposure were constructed for the 4,979 participants using annual average daily traffic (AADT) counts near each residence and distance from residence to major roads. SAB was examined in relation to the traffic exposure measures using logistic regression adjusting for a number of demographic and lifestyle variables.
Of the traffic measures, maximum annual average traffic within 50 m showed the strongest association with SAB, although it was not statistically significant. The adjusted odds ratio (AOR) for the top 90th percentile (AADT greater than 15,199) versus the bottom 75th percentile (AADT = 0–1,089) was 1.18 [95% confidence interval (CI), 0.87–1.60]. However, subgroup analyses showed statistically significant associations for traffic with SAB among African Americans (AOR = 3.11; 95% CI, 1.26–7.66) and nonsmokers (AOR = 1.47; 95% CI, 1.07–2.04).
In this cohort, living within 50 m of a road with AADT of 15,200 or more was significantly associated with SAB among African Americans and nonsmokers. Further research is needed to confirm these results and possibly elucidate the mechanisms responsible for the findings.
air pollution; cohort; geographic information system; pregnancy; spontaneous abortion; vehicular traffic