Background

Evidence suggests that longer-term exposure to air pollutants over years confers higher risks of cardiovascular morbidity and mortality than shorter term exposure. One explanation is that cumulative adverse effects that develop over longer durations lead to the genesis of chronic disease. Preliminary epidemiological and clinical evidence suggest that air pollution may contribute to the development hypertension and type 2 diabetes.

Methods and Results

We used Cox proportional hazards models to assess incidence rate ratios (IRRs) and 95% confidence intervals (CI) for incident hypertension and diabetes associated with exposure to fine particulate matter (PM2.5) and nitrogen oxides (NOx) in a cohort of African American women living in Los Angeles. Pollutant levels were estimated at participant residential addresses with land use regression models (NOx) and interpolation from monitoring station measurements (PM2.5). Over follow-up from 1995-2005, 531 incident cases of hypertension and 183 incident cases of diabetes occurred. When pollutants were analyzed separately, the IRR for hypertension for a 10 μg/m3 increase in PM2.5 was 1.48 (95% CI 0.95-2.31) and the IRR for the interquartile range (12.4 parts per billion) of NOx was 1.14 (95% CI 1.03-1.25). The corresponding IRRs for diabetes were 1.63 (95% CI 0.78-3.44) and 1.25 (95% CI 1.07-1.46). When both pollutants were included in the same model, the IRRs for PM2.5 were attenuated and the IRRs for NOx were essentially unchanged for both outcomes.

Conclusions

Our results suggest that exposure to air pollutants, especially traffic-related pollutants, may increase the risk of type 2 diabetes and possibly of hypertension.

This study examined relationships between greenness exposure and free-living physical activity behavior of children in smart growth and conventionally designed communities. Normalized Difference Vegetation Index (NDVI) was used to quantify children’s (n=208) greenness exposure at 30-second epoch accelerometer and GPS data points. A generalized linear mixed model with a kernel density smoothing term for addressing spatial autocorrelation was fit to analyze residential neighborhood activity data. Excluding activity at home and school-time, an epoch-level analysis found momentary greenness exposure was positively associated with the likelihood of contemporaneous moderate-to-vigorous physical activity (MVPA). This association was stronger for smart growth residents who experienced a 39% increase in odds of MVPA for a 10th to 90th percentile increase in exposure to greenness (OR=1.39, 95% CI 1.36–1.44). A subject-level analysis found children who experienced >20 minutes of daily exposure to greener spaces (>90th percentile) engaged in nearly 5 times the daily rate of MVPA of children with nearly zero daily exposure to greener spaces (95% CI 3.09–7.20).

Background: A better understanding of the adverse health effects of chronic exposure to fine particulate matter (PM2.5) requires accurate estimates of PM2.5 variation at fine spatial scales. Remote sensing has emerged as an important means of estimating PM2.5 exposures, but relatively few studies have compared remote-sensing estimates to those derived from monitor-based data.

Objective: We evaluated and compared the predictive capabilities of remote sensing and geostatistical interpolation.

Methods: We developed a space–time geostatistical kriging model to predict PM2.5 over the continental United States and compared resulting predictions to estimates derived from satellite retrievals.

Results: The kriging estimate was more accurate for locations that were about 100 km from a monitoring station, whereas the remote sensing estimate was more accurate for locations that were > 100 km from a monitoring station. Based on this finding, we developed a hybrid map that combines the kriging and satellite-based PM2.5 estimates.

Conclusions: We found that for most of the populated areas of the continental United States, geostatistical interpolation produced more accurate estimates than remote sensing. The differences between the estimates resulting from the two methods, however, were relatively small. In areas with extensive monitoring networks, the interpolation may provide more accurate estimates, but in the many areas of the world without such monitoring, remote sensing can provide useful exposure estimates that perform nearly as well.

Rationale: Several studies have linked long-term exposure to particulate air pollution with increased cardiopulmonary mortality; only two have also examined incident circulatory disease.

Objectives: To examine associations of individualized long-term exposures to particulate and gaseous air pollution with incident myocardial infarction and stroke, as well as all-cause and cause-specific mortality.

Methods: We estimated long-term residential air pollution exposure for more than 100,000 participants in the California Teachers Study, a prospective cohort of female public school professionals. We linked geocoded residential addresses with inverse distance-weighted monthly pollutant surfaces for two measures of particulate matter and for several gaseous pollutants. We examined associations between exposure to these pollutants and risks of incident myocardial infarction and stroke, and of all-cause and cause-specific mortality, using Cox proportional hazards models.

Measurements and Main Results: We found elevated hazard ratios linking long-term exposure to particulate matter less than 2.5 μm in aerodynamic diameter (PM2.5), scaled to an increment of 10 μg/m3 with mortality from ischemic heart disease (IHD) (1.20; 95% confidence interval [CI], 1.02–1.41) and, particularly among postmenopausal women, incident stroke (1.19; 95% CI, 1.02–1.38). Long-term exposure to particulate matter less than 10 μm in aerodynamic diameter (PM10) was associated with elevated risks for IHD mortality (1.06; 95% CI, 0.99–1.14) and incident stroke (1.06; 95% CI, 1.00–1.13), while exposure to nitrogen oxides was associated with elevated risks for IHD and all cardiovascular mortality.

Conclusions: This study provides evidence linking long-term exposure to PM2.5 and PM10 with increased risks of incident stroke as well as IHD mortality; exposure to nitrogen oxides was also related to death from cardiovascular diseases.

Background: Few cohort studies have evaluated the risk of mortality associated with long-term exposure to fine particulate matter [≤ 2.5 μm in aerodynamic diameter (PM2.5)]. This is the first national-level cohort study to investigate these risks in Canada.

Objective: We investigated the association between long-term exposure to ambient PM2.5 and cardiovascular mortality in nonimmigrant Canadian adults.

Methods: We assigned estimates of exposure to ambient PM2.5 derived from satellite observations to a cohort of 2.1 million Canadian adults who in 1991 were among the 20% of the population mandated to provide detailed census data. We identified deaths occurring between 1991 and 2001 through record linkage. We calculated hazard ratios (HRs) and 95% confidence intervals (CIs) adjusted for available individual-level and contextual covariates using both standard Cox proportional survival models and nested, spatial random-effects survival models.

Results: Using standard Cox models, we calculated HRs of 1.15 (95% CI: 1.13, 1.16) from nonaccidental causes and 1.31 (95% CI: 1.27, 1.35) from ischemic heart disease for each 10-μg/m3 increase in concentrations of PM2.5. Using spatial random-effects models controlling for the same variables, we calculated HRs of 1.10 (95% CI: 1.05, 1.15) and 1.30 (95% CI: 1.18, 1.43), respectively. We found similar associations between nonaccidental mortality and PM2.5 based on satellite-derived estimates and ground-based measurements in a subanalysis of subjects in 11 cities.

Conclusions: In this large national cohort of nonimmigrant Canadians, mortality was associated with long-term exposure to PM2.5. Associations were observed with exposures to PM2.5 at concentrations that were predominantly lower (mean, 8.7 μg/m3; interquartile range, 6.2 μg/m3) than those reported previously.

Background: Numerous studies have linked criteria air pollutants with adverse birth outcomes, but there is less information on the importance of specific emission sources, such as traffic, and air toxics.

Objectives: We used three exposure data sources to examine odds of term low birth weight (LBW) in Los Angeles, California, women when exposed to high levels of traffic-related air pollutants during pregnancy.

Methods: We identified term births during 1 June 2004 to 30 March 2006 to women residing within 5 miles of a South Coast Air Quality Management District (SCAQMD) Multiple Air Toxics Exposure Study (MATES III) monitoring station. Pregnancy period average exposures were estimated for air toxics, including polycyclic aromatic hydrocarbons (PAHs), source-specific particulate matter < 2.5 μm in aerodynamic diameter (PM2.5) based on a chemical mass balance model, criteria air pollutants from government monitoring data, and land use regression (LUR) model estimates of nitric oxide (NO), nitrogen dioxide (NO2) and nitrogen oxides (NOx). Associations between these metrics and odds of term LBW (< 2,500 g) were examined using logistic regression.

Results: Odds of term LBW increased approximately 5% per interquartile range increase in entire pregnancy exposures to several correlated traffic pollutants: LUR measures of NO, NO2, and NOx, elemental carbon, and PM2.5 from diesel and gasoline combustion and paved road dust (geological PM2.5).

Conclusions: These analyses provide additional evidence of the potential impact of traffic-related air pollution on fetal growth. Particles from traffic sources should be a focus of future studies.

Background: Lung cancer and cardiovascular disease (CVD) mortality risks increase with smoking, secondhand smoke (SHS), and exposure to fine particulate matter < 2.5 μm in diameter (PM2.5) from ambient air pollution. Recent research indicates that the exposure–response relationship for CVD is nonlinear, with a steep increase in risk at low exposures and flattening out at higher exposures. Comparable estimates of the exposure–response relationship for lung cancer are required for disease burden estimates and related public health policy assessments.

Objectives: We compared exposure–response relationships of PM2.5 with lung cancer and cardiovascular mortality and considered the implications of the observed differences for efforts to estimate the disease burden of PM2.5.

Methods: Prospective cohort data for 1.2 million adults were collected by the American Cancer Society as part of the Cancer Prevention Study II. We estimated relative risks (RRs) for increments of cigarette smoking, adjusting for various individual risk factors. RRs were plotted against estimated daily dose of PM2.5 from smoking along with comparison estimates for ambient air pollution and SHS.

Results: For lung cancer mortality, excess risk rose nearly linearly, reaching maximum RRs > 40 among long-term heavy smokers. Excess risks for CVD mortality increased steeply at low exposure levels and leveled off at higher exposures, reaching RRs of approximately 2–3 for cigarette smoking.

Conclusions: The exposure–response relationship associated with PM2.5 is qualitatively different for lung cancer versus cardiovascular mortality. At low exposure levels, cardiovascular deaths are projected to account for most of the burden of disease, whereas at high levels of PM2.5, lung cancer becomes proportionately more important.

Background

Numerous studies have associated air pollutant exposures with adverse birth outcomes, but there is still relatively little information to attribute effects to specific emission sources or air toxics. We used three exposure data sources to examine risks of preterm birth in Los Angeles women when exposed to high levels of traffic-related air pollutants - including specific toxics - during pregnancy.

Methods

We identified births during 6/1/04-3/31/06 to women residing within five miles of a Southern California Air Quality Management District (SCAQMD) Multiple Air Toxics Exposure Study (MATES III) monitoring station. We identified preterm cases and, using a risk set approach, matched cases to controls based on gestational age at birth. Pregnancy period exposure averages were estimated for a number of air toxics including polycyclic aromatic hydrocarbons (PAHs), source-specific PM2.5 (fine particulates with aerodynamic diameter less than 2.5 μm) based on a Chemical Mass Balance model, criteria air pollutants based on government monitoring data, and land use regression (LUR) estimates of nitric oxide (NO), nitrogen dioxide (NO2) and nitrogen oxides (NOx). Associations between these metrics and odds of preterm birth were estimated using conditional logistic regression.

Results

Odds of preterm birth increased 6-21% per inter-quartile range increase in entire pregnancy exposures to organic carbon (OC), elemental carbon (EC), benzene, and diesel, biomass burning and ammonium nitrate PM2.5, and 30% per inter-quartile increase in PAHs; these pollutants were positively correlated and clustered together in a factor analysis. Associations with LUR exposure metrics were weaker (3-4% per inter-quartile range increase).

Conclusions

These latest analyses provide additional evidence of traffic-related air pollution's impact on preterm birth for women living in Southern California and indicate PAHs as a pollutant of concern that should be a focus of future studies. Other PAH sources besides traffic were also associated with higher odds of preterm birth, as was ammonium nitrate PM2.5, the latter suggesting potential importance of secondary pollutants. Future studies should focus on accurate modeling of both local and regional spatial and temporal distributions, and incorporation of source information.

Background: Population exposure assessment methods that capture local-scale pollutant variability are needed for large-scale epidemiological studies and surveillance, policy, and regulatory purposes. Currently, such exposure methods are limited.

Methods: We created 2006 national pollutant models for fine particulate matter [PM with aerodynamic diameter ≤ 2.5 μm (PM2.5)], nitrogen dioxide (NO2), benzene, ethylbenzene, and 1,3-butadiene from routinely collected fixed-site monitoring data in Canada. In multiple regression models, we incorporated satellite estimates and geographic predictor variables to capture background and regional pollutant variation and used deterministic gradients to capture local-scale variation. The national NO2 and benzene models are evaluated with independent measurements from previous land use regression models that were conducted in seven Canadian cities. National models are applied to census block-face points, each of which represents the location of approximately 89 individuals, to produce estimates of population exposure.

Results: The national NO2 model explained 73% of the variability in fixed-site monitor concentrations, PM2.5 46%, benzene 62%, ethylbenzene 67%, and 1,3-butadiene 68%. The NO2 model predicted, on average, 43% of the within-city variability in the independent NO2 data compared with 18% when using inverse distance weighting of fixed-site monitoring data. Benzene models performed poorly in predicting within-city benzene variability. Based on our national models, we estimated Canadian ambient annual average population-weighted exposures (in micrograms per cubic meter) of 8.39 for PM2.5, 23.37 for NO2, 1.04 for benzene, 0.63 for ethylbenzene, and 0.09 for 1,3-butadiene.

Conclusions: The national pollutant models created here improve exposure assessment compared with traditional monitor-based approaches by capturing both regional and local-scale pollution variation. Applying national models to routinely collected population location data can extend land use modeling techniques to population exposure assessment and to informing surveillance, policy, and regulation.

Studies in air pollution epidemiology may suffer from some specific forms of confounding and exposure measurement error. This contribution discusses these, mostly in the framework of cohort studies. Evaluation of potential confounding is critical in studies of the health effects of air pollution. The association between long-term exposure to ambient air pollution and mortality has been investigated using cohort studies in which subjects are followed over time with respect to their vital status. In such studies, control for individual-level confounders such as smoking is important, as is control for area-level confounders such as neighborhood socio-economic status. In addition, there may be spatial dependencies in the survival data that need to be addressed. These issues are illustrated using the American Cancer Society Cancer Prevention II cohort. Exposure measurement error is a challenge in epidemiology because inference about health effects can be incorrect when the measured or predicted exposure used in the analysis is different from the underlying true exposure. Air pollution epidemiology rarely if ever uses personal measurements of exposure for reasons of cost and feasibility. Exposure measurement error in air pollution epidemiology comes in various dominant forms, which are different for time-series and cohort studies. The challenges are reviewed and a number of suggested solutions are discussed for both study domains.

BACKGROUND:

Asthma is the most common chronic disease in children.

OBJECTIVES:

To describe the prevalence of asthma and allergic disease in a multiethnic, population-based sample of Toronto (Ontario) school children attending grades 1 and 2.

METHODS:

In 2006, the Toronto Child Health Evaluation Questionnaire (T-CHEQ) used the International Study of Asthma and Allergies in Childhood survey methodology to administer questionnaires to 23,379 Toronto school children attending grades 1 and 2. Modifications were made to the methodology to conform with current privacy legislation and capture the ethnic diversity of the population. Lifetime asthma, wheeze, hay fever and eczema prevalence were defined by parental report. Asthma was considered to be current if the child also reported wheeze or asthma medication use in the previous 12 months.

RESULTS:

A total of 5619 children from 283 randomly sampled public schools participated. Children were five to nine years of age, with a mean age of 6.7 years. The overall prevalence of lifetime asthma was 16.1%, while only 11.3% had current asthma. The reported prevalence of lifetime wheeze was 29.2%, while 14.2% reported wheeze in the past 12 months. Sociodemographic and major health determinant characteristics of the T-CHEQ population were similar to 2001 census data, suggesting a diverse sample that was representative of the urban childhood population.

CONCLUSIONS:

Asthma continues to be a highly prevalent chronic disease in Canadian children. A large proportion of children with reported lifetime asthma, who were five to nine years of age, did not report current asthma symptomatology or medication use.

Background

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.

Objectives

We evaluated the relationship of new-onset asthma with traffic-related pollution near homes and schools.

Methods

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.

Results

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).

Conclusions

Traffic-related pollution exposure at school and homes may both contribute to the development of asthma.

This paper has two aims: (1) to summarize various geographic information science methods; and (2) to provide a review of studies that have employed such methods. Though not meant to be a comprehensive review, this paper explains when certain methods are useful in epidemiological studies and also serves as an overview of the growing field of spatial epidemiology.

Background

Cross-sectional studies suggest an association between exposure to ambient air pollution and atherosclerosis. We investigated the association between outdoor air quality and progression of subclinical atherosclerosis (common carotid artery intima-media thickness, CIMT).

Methodology/Principal Findings

We examined data from five double-blind randomized trials that assessed effects of various treatments on the change in CIMT. The trials were conducted in the Los Angeles area. Spatial models and land-use data were used to estimate the home outdoor mean concentration of particulate matter up to 2.5 micrometer in diameter (PM2.5), and to classify residence by proximity to traffic-related pollution (within 100 m of highways). PM2.5 and traffic proximity were positively associated with CIMT progression. Adjusted coefficients were larger than crude associations, not sensitive to modelling specifications, and statistically significant for highway proximity while of borderline significance for PM2.5 (P = 0.08). Annual CIMT progression among those living within 100 m of a highway was accelerated (5.5 micrometers/yr [95%CI: 0.13–10.79; p = 0.04]) or more than twice the population mean progression. For PM2.5, coefficients were positive as well, reaching statistical significance in the socially disadvantaged; in subjects reporting lipid lowering treatment at baseline; among participants receiving on-trial treatments; and among the pool of four out of the five trials.

Conclusion

Consistent with cross-sectional findings and animal studies, this is the first study to report an association between exposure to air pollution and the progression of atherosclerosis – indicated with CIMT change – in humans. Ostensibly, our results suggest that air pollution may contribute to the acceleration of cardiovascular disease development – the main causes of morbidity and mortality in many countries. However, the heterogeneity of the volunteering populations across the five trials, the limited sample size within trials and other relevant subgroups, and the fact that some key findings reached statistical significance in subgroups rather than the sample precludes generalizations to the general population.

Background

Chronic exposure to traffic-related air pollution (TRAP) may contribute to premature mortality, but few studies to date have addressed this topic.

Objectives

In this study we assessed the association between TRAP and mortality in Toronto, Ontario, Canada.

Methods

We collected nitrogen dioxide samples over two seasons using duplicate two-sided Ogawa passive diffusion samplers at 143 locations across Toronto. We calibrated land use regressions to predict NO2 exposure on a fine scale within Toronto. We used interpolations to predict levels of particulate matter with aerodynamic diameter ≤ 2.5 μm (PM2.5) and ozone levels. We assigned predicted pollution exposures to 2,360 subjects from a respiratory clinic, and abstracted health data on these subjects from medical billings, lung function tests, and diagnoses by pulmonologists. We tracked mortality between 1992 and 2002. We used standard and multilevel Cox proportional hazard models to test associations between air pollution and mortality.

Results

After controlling for age, sex, lung function, obesity, smoking, and neighborhood deprivation, we observed a 17% increase in all-cause mortality and a 40% increase in circulatory mortality from an exposure contrast across the interquartile range of 4 ppb NO2. We observed no significant associations with other pollutants.

Conclusions

Exposure to TRAP was significantly associated with increased all-cause and circulatory mortality in this cohort. A high prevalence of cardiopulmonary disease in the cohort probably limits inference of the findings to populations with a substantial proportion of susceptible individuals.

Background

Variations in air pollution exposure within a community may be associated with asthma prevalence. However, studies conducted to date have produced inconsistent results, possibly due to errors in measurement of the exposures.

Methods

A standardized asthma survey was administered to children in grades one and eight in Hamilton, Canada, in 1994–95 (N ~1467). Exposure to air pollution was estimated in four ways: (1) distance from roadways; (2) interpolated surfaces for ozone, sulfur dioxide, particulate matter and nitrous oxides from seven to nine governmental monitoring stations; (3) a kriged nitrogen dioxide (NO2) surface based on a network of 100 passive NO2 monitors; and (4) a land use regression (LUR) model derived from the same monitoring network. Logistic regressions were used to test associations between asthma and air pollution, controlling for variables including neighbourhood income, dwelling value, state of housing, a deprivation index and smoking.

Results

There were no significant associations between any of the exposure estimates and asthma in the whole population, but large effects were detected the subgroup of children without hayfever (predominately in girls). The most robust effects were observed for the association of asthma without hayfever and NO2LUR OR = 1.86 (95%CI, 1.59–2.16) in all girls and OR = 2.98 (95%CI, 0.98–9.06) for older girls, over an interquartile range increase and controlling for confounders.

Conclusion

Our findings indicate that traffic-related pollutants, such as NO2, are associated with asthma without overt evidence of other atopic disorders among female children living in a medium-sized Canadian city. The effects were sensitive to the method of exposure estimation. More refined exposure models produced the most robust associations.

Background

Long-term human exposure to ambient pollutants can be an important contributing or etiologic factor of many chronic diseases. Spatiotemporal estimation (mapping) of long-term exposure at residential areas based on field observations recorded in the U.S. Environmental Protection Agency’s Air Quality System often suffer from missing data issues due to the scarce monitoring network across space and the inconsistent recording periods at different monitors.

Objective

We developed and compared two upscaling methods: UM1 (data aggregation followed by exposure estimation) and UM2 (exposure estimation followed by data aggregation) for the long-term PM10 (particulate matter with aerodynamic diameter ≤ 10 μm) and ozone exposure estimations and applied them in multiple time scales to estimate PM and ozone exposures for the residential areas of the Health Effects of Air Pollution on Lupus (HEAPL) study.

Method

We used Bayesian maximum entropy (BME) analysis for the two upscaling methods. We performed spatiotemporal cross-validations at multiple time scales by UM1 and UM2 to assess the estimation accuracy across space and time.

Results

Compared with the kriging method, the integration of soft information by the BME method can effectively increase the estimation accuracy for both pollutants. The spatiotemporal distributions of estimation errors from UM1 and UM2 were similar. The cross-validation results indicated that UM2 is generally better than UM1 in exposure estimations at multiple time scales in terms of predictive accuracy and lack of bias. For yearly PM10 estimations, both approaches have comparable performance, but the implementation of UM1 is associated with much lower computation burden.

Conclusion

BME-based upscaling methods UM1 and UM2 can assimilate core and site-specific knowledge bases of different formats for long-term exposure estimation. This study shows that UM1 can perform reasonably well when the aggregation process does not alter the spatiotemporal structure of the original data set; otherwise, UM2 is preferable.

Study objective

Prior studies have shown that children are particularly sensitive to air pollution. This study examined whether children of low socioeconomic status suffered greater exposure to outdoor nitrogen dioxide than more affluent ones, both at their place of residence and at school, in a country with widespread state intervention for social equity.

Design

Local scale data on outdoor nitrogen dioxide obtained from a validated air pollution model were analysed, along with all school children accurately geocoded to their building of residence and school.

Participants

All 29 133 children in grades one through nine (aged 7 to 15 years) residing and attending school in Malmö, Sweden, in 2001.

Main results

Defining the socioeconomic status of children according to the mean income in their residential building, the spatial scan statistic technique allowed the authors to identify eight statistically significant clusters of low socioeconomic status children, all of which were located in the most polluted areas of Malmö. Four clusters of high socioeconomic status children were found, all of them located in the least polluted areas. The neighbourhood socioeconomic status better predicted the nitrogen dioxide exposure of children than the socioeconomic status of their building of residence. Exposure to nitrogen dioxide at the place of residence and school of attendance regularly increased as the socioeconomic status of a child's neighbourhood of residence decreased.

Conclusions

Evidence of environmental injustice was found, even in a country noted for its egalitarian welfare state. Enforcement of environmental regulations may be necessary to achieve a higher level of environmental equity.

Background

The question of whether air pollution contributes to asthma onset remains unresolved.

Objectives

In this study, we assessed the association between asthma onset in children and traffic-related air pollution.

Methods

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.

Results

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).

Conclusions

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.

Background

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.

Objectives

We studied the association between long-term exposure to traffic-related air pollution and mortality in a Dutch cohort.

Methods

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.

Results

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.

Conclusions

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.

Background

Although numerous epidemiologic studies now use models of intraurban exposure, there has been little systematic evaluation of the performance of different models.

Objectives

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.

Methods

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

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.

Objective

To assess whether over-the-counter (OTC) sales of gastrointestinal illness (GI)-related medications are associated with temporal trends of reportable community viral, bacterial and parasitic infections.

Methods

The temporal patterns in weekly and seasonal sales of nonprescription products related to GI were compared with those of reportable viral, bacterial and parasitic infections in a Canadian province.

Results

Temporal patterns of OTC product sales and Norovirus activity were similar, both having highest activity in the winter months. In contrast, GI cases from both bacterial and parasitic agents were highest from late spring through to early fall.

Conclusions

Nonprescription sales of antidiarrheal and antinauseant products are a good predictor of community Norovirus activity. Syndromic surveillance through monitoring of OTC product sales could be useful as an early indicator of the Norovirus season, allowing for appropriate interventions to reduce the number of infections.

Background

The growing interest in the effects of contextual environments on health outcomes has focused attention on the strengths and weaknesses of alternate contextual unit definitions for use in multilevel analysis. The present research examined three methods to define contextual units for a sample of children already enrolled in a respiratory health study. The Inclusive Equal Weights Method (M1) and Inclusive Sample Weighted Method (M2) defined communities using the boundaries of the census blocks that incorporated the residences of the CHS participants, except that the former estimated socio-demographic variables by averaging the census block data within each community, while the latter used weighted proportion of CHS participants per block. The Minimum Bounding Rectangle Method (M3) generated minimum bounding rectangles that included 95% of the CHS participants and produced estimates of census variables using the weighted proportion of each block within these rectangles. GIS was used to map the locations of study participants, define the boundaries of the communities where study participants reside, and compute estimates of socio-demographic variables. The sensitivity of census variable estimates to the choice of community boundaries and weights was assessed using standard tests of significance.

Results

The estimates of contextual variables vary significantly depending on the choice of neighborhood boundaries and weights. The choice of boundaries therefore shapes the community profile and the relationships between its components (variables).

Conclusion

Multilevel analysis concerned with the effects of contextual environments on health requires careful consideration of what constitutes a contextual unit for a given study sample, because the alternate definitions may have differential impact on the results. The three alternative methods used in this research all carry some subjectivity, which is embedded in the decision as to what constitutes the boundaries of the communities. The Minimum Bounding Rectangle was preferred because it focused attention on the most frequently used spaces and it controlled potential aggregation problems. There is a need to further examine the validity of different methods proposed here. Given that no method is likely to capture the full complexity of human-environment interactions, we would need baseline data describing people's daily activity patterns along with expert knowledge of the area to evaluate our neighborhood units.

Background

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.

Methods

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.

Results

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.

Conclusion

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.