Feasibility of assessing public health impacts of air pollution reduction programs on a local scale: New Haven case study

Background

New approaches to link health surveillance data with environmental and population exposure information are needed to examine the health benefits of risk management decisions.

Objective

We examined the feasibility of conducting a local assessment of the public health impacts of cumulative air pollution reduction activities from federal, state, local, and voluntary actions in the City of New Haven, Connecticut (USA).

Methods

Using a hybrid modeling approach that combines regional and local-scale air quality data, we estimated ambient concentrations for multiple air pollutants [e.g., PM_2.5 (particulate matter ≤ 2.5 μm in aerodynamic diameter), NO_x (nitrogen oxides)] for baseline year 2001 and projected emissions for 2010, 2020, and 2030. We assessed the feasibility of detecting health improvements in relation to reductions in air pollution for 26 different pollutant–health outcome linkages using both sample size and exploratory epidemiological simulations to further inform decision-making needs.

Results

Model projections suggested decreases (~ 10–60%) in pollutant concentrations, mainly attributable to decreases in pollutants from local sources between 2001 and 2010. Models indicated considerable spatial variability in the concentrations of most pollutants. Sample size analyses supported the feasibility of identifying linkages between reductions in NO_x and improvements in all-cause mortality, prevalence of asthma in children and adults, and cardiovascular and respiratory hospitalizations.

Conclusion

Substantial reductions in air pollution (e.g., ~ 60% for NO_x) are needed to detect health impacts of environmental actions using traditional epidemiological study designs in small communities like New Haven. In contrast, exploratory epidemiological simulations suggest that it may be possible to demonstrate the health impacts of PM reductions by predicting intraurban pollution gradients within New Haven using coupled models.     

Do the Health Benefits of Cycling Outweigh the Risks?

Background

Although from a societal point of view a modal shift from car to bicycle may have beneficial health effects due to decreased air pollution emissions, decreased greenhouse gas emissions, and increased levels of physical activity, shifts in individual adverse health effects such as higher exposure to air pollution and risk of a traffic accident may prevail.

Objective

We describe whether the health benefits from the increased physical activity of a modal shift for urban commutes outweigh the health risks.

Data sources and extraction

We have summarized the literature for air pollution, traffic accidents, and physical activity using systematic reviews supplemented with recent key studies.

Data synthesis

We quantified the impact on all-cause mortality when 500,000 people would make a transition from car to bicycle for short trips on a daily basis in the Netherlands. We have expressed mortality impacts in life-years gained or lost, using life table calculations. For individuals who shift from car to bicycle, we estimated that beneficial effects of increased physical activity are substantially larger (3–14 months gained) than the potential mortality effect of increased inhaled air pollution doses (0.8–40 days lost) and the increase in traffic accidents (5–9 days lost). Societal benefits are even larger because of a modest reduction in air pollution and greenhouse gas emissions and traffic accidents.

Conclusions

On average, the estimated health benefits of cycling were substantially larger than the risks relative to car driving for individuals shifting their mode of transport.     

Public Health and Air Pollution in Asia (PAPA): a multicity study of short-term effects of air pollution on mortality

Background and objectives

Although the deleterious effects of air pollution from fossil fuel combustion have been demonstrated in many Western nations, fewer studies have been conducted in Asia. The Public Health and Air Pollution in Asia (PAPA) project assessed the effects of short-term exposure to air pollution on daily mortality in Bangkok, Thailand, and in three cities in China: Hong Kong, Shanghai, and Wuhan.

Methods

Poisson regression models incorporating natural spline smoothing functions were used to adjust for seasonality and other time-varying covariates that might confound the association between air pollution and mortality. Effect estimates were determined for each city and then for the cities combined using a random effects method.

Results

In individual cities, associations were detected between most of the pollutants [nitrogen dioxide, sulfur dioxide, particulate matter ≤ 10 μm in aerodynamic diameter (PM₁₀), and ozone] and most health outcomes under study (i.e., all natural-cause, cardiovascular, and respiratory mortality). The city-combined effects of the four pollutants tended to be equal or greater than those identified in studies conducted in Western industrial nations. In addition, residents of Asian cities are likely to have higher exposures to air pollution than those in Western industrial nations because they spend more time outdoors and less time in air conditioning.

Conclusions

Although the social and environmental conditions may be quite different, it is reasonable to apply estimates derived from previous health effect of air pollution studies in the West to Asia.     

Evaluation of the cardiovascular effects of methylmercury exposures: current evidence supports development of a dose-response function for regulatory benefits analysis

Background

The U.S. Environmental Protection Agency (U.S. EPA) has estimated the neurological benefits of reductions in prenatal methylmercury (MeHg) exposure in past assessments of rules controlling mercury (Hg) emissions. A growing body of evidence suggests that MeHg exposure can also lead to increased risks of adverse cardiovascular impacts in exposed populations.

Data extraction

The U.S. EPA assembled the authors of this article to participate in a workshop, where we reviewed the current science concerning cardiovascular health effects of MeHg exposure via fish and seafood consumption and provided recommendations concerning whether cardiovascular health effects should be included in future Hg regulatory impact analyses.

Data synthesis

We found the body of evidence exploring the link between MeHg and acute myocardial infarction (MI) to be sufficiently strong to support its inclusion in future benefits analyses, based both on direct epidemiological evidence of an MeHg–MI link and on MeHg’s association with intermediary impacts that contribute to MI risk. Although additional research in this area would be beneficial to further clarify key characteristics of this relationship and the biological mechanisms that underlie it, we consider the current epidemiological literature sufficiently robust to support the development of a dose–response function.

Conclusions

We recommend the development of a dose–response function relating MeHg exposures with MIs for use in regulatory benefits analyses of future rules targeting Hg air emissions.     

Personal exposures to traffic-related air pollution and acute respiratory health among Bronx schoolchildren with asthma

Background

Previous studies have reported relationships between adverse respiratory health outcomes and residential proximity to traffic pollution, but have not shown this at a personal exposure level.

Objective

We compared, among inner-city children with asthma, the associations of adverse asthma outcome incidences with increased personal exposure to particulate matter mass ≤ 2.5 μm in aerodynamic diameter (PM_2.5) air pollution versus the diesel-related carbonaceous fraction of PM_2.5.

Methods

Daily 24-hr personal samples of PM_2.5, including the elemental carbon (EC) fraction, were collected for 40 fifth-grade children with asthma at four South Bronx schools (10 children per school) during approximately 1 month each. Spirometry and symptom scores were recorded several times daily during weekdays.

Results

We found elevated same-day relative risks of wheeze [1.45; 95% confidence interval (CI), 1.03–2.04)], shortness of breath (1.41; 95% CI, 1.01–1.99), and total symptoms (1.30; 95% CI, 1.04–1.62) with an increase in personal EC, but not with personal PM_2.5 mass. We found increased risk of cough, wheeze, and total symptoms with increased 1-day lag and 2-day average personal and school-site EC. We found no significant associations with school-site PM_2.5 mass or sulfur. The EC effect estimate was robust to addition of gaseous pollutants.

Conclusion

Adverse health associations were strongest with personal measures of EC exposure, suggesting that the diesel “soot” fraction of PM_2.5 is most responsible for pollution-related asthma exacerbations among children living near roadways. Studies that rely on exposure to PM mass may underestimate PM health impacts.     

Meeting report: Estimating the benefits of reducing hazardous air pollutants--summary of 2009 workshop and future considerations

Background

Quantifying the benefits of reducing hazardous air pollutants (HAPs, or air toxics) has been limited by gaps in toxicological data, uncertainties in extrapolating results from high-dose animal experiments to estimate human effects at lower doses, limited ambient and personal exposure monitoring data, and insufficient economic research to support valuation of the health impacts often associated with exposure to individual air toxics.

Objectives

To address some of these issues, the U.S. Environmental Protection Agency held the Workshop on Estimating the Benefits of Reducing Hazardous Air Pollutants (HAPs) in Washington, DC, from 30 April to 1 May 2009.

Discussion

Experts from multiple disciplines discussed how best to move forward on air toxics benefits assessment, with a focus on developing near-term capability to conduct quantitative benefits assessment. Proposed methodologies involved analysis of data-rich pollutants and application of this analysis to other pollutants, using dose–response modeling of animal data for estimating benefits to humans, determining dose-equivalence relationships for different chemicals with similar health effects, and analysis similar to that used for criteria pollutants. Limitations and uncertainties in economic valuation of benefits assessment for HAPS were discussed as well.

Conclusions

These discussions highlighted the complexities in estimating the benefits of reducing air toxics, and participants agreed that alternative methods for benefits assessment of HAPs are needed. Recommendations included clearly defining the key priorities of the Clean Air Act air toxics program to identify the most effective approaches for HAPs benefits analysis, focusing on susceptible and vulnerable populations, and improving dose–response estimation for quantification of benefits.     

Traffic-Related Air Pollution and Perinatal Mortality: A Case–Control Study

Background

Ambient levels of air pollution may affect the health of children, as indicated by studies of infant and perinatal mortality. Scientific evidence has also correlated low birth weight and preterm birth, which are important determinants of perinatal death, with air pollution. However, most of these studies used ambient concentrations measured at monitoring sites, which may not consider differential exposure to pollutants found at elevated concentrations near heavy-traffic roadways.

Objectives

Our goal was to examine the association between traffic-related pollution and perinatal mortality.

Methods

We used the information collected for a case–control study conducted in 14 districts in the City of São Paulo, Brazil, regarding risk factors for perinatal deaths. We geocoded the residential addresses of cases (fetal and early neonatal deaths) and controls (children who survived the 28th day of life) and calculated a distance-weighted traffic density (DWTD) measure considering all roads contained in a buffer surrounding these homes.

Results

Logistic regression revealed a gradient of increasing risk of early neonatal death with higher exposure to traffic-related air pollution. Mothers exposed to the highest quartile of the DWTD compared with those less exposed exhibited approximately 50% increased risk (adjusted odds ratio = 1.47; 95% confidence interval, 0.67–3.19). Associations for fetal mortality were less consistent.

Conclusions

These results suggest that motor vehicle exhaust exposures may be a risk factor for perinatal mortality.     

Association between GIS-Based Exposure to Urban Air Pollution during Pregnancy and Birth Weight in the INMA Sabadell Cohort

Background

There is growing evidence that traffic-related air pollution reduces birth weight. Improving exposure assessment is a key issue to advance in this research area.

Objective

We investigated the effect of prenatal exposure to traffic-related air pollution via geographic information system (GIS) models on birth weight in 570 newborns from the INMA (Environment and Childhood) Sabadell cohort.

Methods

We estimated pregnancy and trimester-specific exposures to nitrogen dioxide and aromatic hydrocarbons [benzene, toluene, ethylbenzene, m/p-xylene, and o-xylene (BTEX)] by using temporally adjusted land-use regression (LUR) models. We built models for NO₂ and BTEX using four and three 1-week measurement campaigns, respectively, at 57 locations. We assessed the relationship between prenatal air pollution exposure and birth weight with linear regression models. We performed sensitivity analyses considering time spent at home and time spent in nonresidential outdoor environments during pregnancy.

Results

In the overall cohort, neither NO₂ nor BTEX exposure was significantly associated with birth weight in any of the exposure periods. When considering only women who spent < 2 hr/day in nonresidential outdoor environments, the estimated reductions in birth weight associated with an interquartile range increase in BTEX exposure levels were 77 g [95% confidence interval (CI), 7–146 g] and 102 g (95% CI, 28–176 g) for exposures during the whole pregnancy and the second trimester, respectively. The effects of NO₂ exposure were less clear in this subset.

Conclusions

The association of BTEX with reduced birth weight underscores the negative role of vehicle exhaust pollutants in reproductive health. Time–activity patterns during pregnancy complement GIS-based models in exposure assessment.     

Healthy Neighborhoods: Walkability and Air Pollution

Background

The built environment may influence health in part through the promotion of physical activity and exposure to pollution. To date, no studies have explored interactions between neighborhood walkability and air pollution exposure.

Methods

We estimated concentrations of nitric oxide (NO), a marker for direct vehicle emissions), and ozone (O₃) and a neighborhood walkability score, for 49,702 (89% of total) postal codes in Vancouver, British Columbia, Canada. NO concentrations were estimated from a land-use regression model, O₃ was estimated from ambient monitoring data; walkability was calculated based on geographic attributes such as land-use mix, street connectivity, and residential density.

Results

All three attributes exhibit an urban–rural gradient, with high walkability and NO concentrations, and low O₃ concentrations, near the city center. Lower-income areas tend to have higher NO concentrations and walkability and lower O₃ concentrations. Higher-income areas tend to have lower pollution (NO and O₃). “Sweet-spot” neighborhoods (low pollution, high walkability) are generally located near but not at the city center and are almost exclusively higher income.

Policy implications

Increased concentration of activities in urban settings yields both health costs and benefits. Our research identifies neighborhoods that do especially well (and especially poorly) for walkability and air pollution exposure. Work is needed to ensure that the poor do not bear an undue burden of urban air pollution and that neighborhoods designed for walking, bicycling, or mass transit do not adversely affect resident’s exposure to air pollution. Analyses presented here could be replicated in other cities and tracked over time to better understand interactions among neighborhood walkability, air pollution exposure, and income level.     

Traffic-Related Air Pollution and Incident Type 2 Diabetes: Results from the SALIA Cohort Study

Background

Cross-sectional and ecological studies indicate that air pollution may be a risk factor for type 2 diabetes, but prospective data are lacking.

Objective

We examined the association between traffic-related air pollution and incident type 2 diabetes.

Design

Between 1985 and 1994, cross-sectional surveys were performed in the highly industrialized Ruhr district (West Germany); a follow-up investigation was conducted in 2006 using data from the Study on the Influence of Air Pollution on Lung, Inflammation and Aging (SALIA) cohort.

Participants

1,775 nondiabetic women who were 54–55 years old at baseline participated in both baseline and follow-up investigations and had complete information available.

Materials and Methods

Using questionnaires, we assessed 16-year incidence (1990–2006) of type 2 diabetes and information about covariates. Complement factor C3c as marker for subclinical inflammation was measured at baseline. Individual exposure to traffic-related particulate matter (PM) and nitrogen dioxide was determined at different spatial scales.

Results

Between 1990 and 2006, 87 (10.5%) new cases of diabetes were reported among the SALIA cohort members. The hazards for diabetes were increased by 15–42% per interquartile range of PM or traffic-related exposure. The associations persisted when different spatial scales were used to assess exposure and remained robust after adjusting for age, body mass index, socioeconomic status, and exposure to several non–traffic-related sources of air pollution. C3c was associated with PM pollution at baseline and was a strong independent predictor of incident diabetes. Exploratory analyses indicated that women with high C3c blood levels were more susceptible for PM-related excess risk of diabetes than were women with low C3c levels.

Conclusions

Traffic-related air pollution is associated with incident type 2 diabetes among elderly women. Subclinical inflammation may be a mechanism linking air pollution with type 2 diabetes.

Relevance to clinical practice

Our study identifies traffic-related air pollution as a novel and potentially modifiable risk factor of type 2 diabetes.     

Maternal exposure to air pollution and birth outcomes

Background

The knowledge about air pollution effects on birth weight, prematurity, and small for gestational age (SGA) in low-exposure areas is insufficient.

Objectives

The aim of this birth cohort study was to investigate whether low-level exposure to air pollution was associated with prematurity and fetal growth and whether there are sex-specific effects.

Method

We combined high-quality registry information on 81,110 births with individually modeled exposure data at residence for nitrogen oxides (NO_x) and proximity to roads with differing traffic density. The data were analyzed by logistic and linear regression with and without potential confounders.

Results

We observed an increased risk for babies being SGA when we compared highest and lowest NO_x quartiles, adjusting for maternal age, smoking, sex, and year of birth. After additional adjustment for maternal country of origin and parity (which were highly intercorrelated), the increase was no longer statistically significant. However, in subgroup analyses when we compared highest and lowest NO_x quartiles we still observed an increased risk for SGA for girls [odds ratio (OR) = 1.12; 95% confidence interval (CI), 1.01–1.24); we also observed increased risk among mothers who had not changed residency during pregnancy (OR = 1.09; 95% CI, 1.01–1.18). The confounders with the greatest impact on SGA were parity and country of origin. Concerning prematurity, the prevalence was lower in the three higher NO_x exposure quartiles compared with the lowest category.

Conclusion

For future studies on air pollution effects on birth outcomes, careful control of confounding is crucial.     

Acute decreases in proteasome pathway activity after inhalation of fresh diesel exhaust or secondary organic aerosol

Background

Epidemiologic studies consistently demonstrate an association between acute cardiopulmonary events and changes in air pollution; however, the mechanisms that underlie these associations are not completely understood. Oxidative stress and inflammation have been suggested to play a role in human responses to air pollution. The proteasome is an intracellular protein degradation system linked to both of these processes and may help mediate air pollution effects.

Objectives

In these studies, we determined whether acute experimental exposure to two different aerosols altered white blood cell (WBC) or red blood cell (RBC) proteasome activity in human subjects. One aerosol was fresh diesel exhaust (DE), and the other freshly generated secondary organic aerosol (SOA).

Methods

Thirty-eight healthy subjects underwent 2-hr resting inhalation exposures to DE and separate exposures to clean air (CA); 26 subjects were exposed to DE, CA, and SOA. CA responses were subtracted from DE or SOA responses, and mixed linear models with F-tests were used to test the effect of exposure to each aerosol on WBC and RBC proteasome activity.

Results

WBC proteasome activity was reduced 8% (p = 0.04) after exposure to either DE or SOA and decreased by 11.5% (p = 0.03) when SOA was analyzed alone. RBCs showed similar 8–10% declines in proteasome activity (p = 0.05 for DE alone).

Conclusions

Air pollution produces oxidative stress and inflammation in many experimental models, including humans. Two experimental aerosols caused rapid declines in proteasome activity in peripheral blood cells, supporting a key role for the proteasome in acute human responses to air pollution.     

Traffic-Related Air Pollution and Dementia Incidence in Northern Sweden: A Longitudinal Study

Background

Exposure to ambient air pollution is suspected to cause cognitive effects, but a prospective cohort is needed to study exposure to air pollution at the home address and the incidence of dementia.

Objectives

We aimed to assess the association between long-term exposure to traffic-related air pollution and dementia incidence in a major city in northern Sweden.

Methods

Data on dementia incidence over a 15-year period were obtained from the longitudinal Betula study. Traffic air pollution exposure was assessed using a land-use regression model with a spatial resolution of 50 m × 50 m. Annual mean nitrogen oxide levels at the residential address of the participants at baseline (the start of follow-up) were used as markers for long-term exposure to air pollution.

Results

Out of 1,806 participants at baseline, 191 were diagnosed with Alzheimer’s disease during follow-up, and 111 were diagnosed with vascular dementia. Participants in the group with the highest exposure were more likely than those in the group with the lowest exposure to be diagnosed with dementia (Alzheimer’s disease or vascular dementia), with a hazard ratio (HR) of 1.43 (95% CI: 0.998, 2.05 for the highest vs. the lowest quartile). The estimates were similar for Alzheimer’s disease (HR 1.38) and vascular dementia (HR 1.47). The HR for dementia associated with the third quartile versus the lowest quartile was 1.48 (95% CI: 1.03, 2.11). A subanalysis that excluded a younger sample that had been retested after only 5 years of follow-up suggested stronger associations with exposure than were present in the full cohort (HR = 1.71; 95% CI: 1.08, 2.73 for the highest vs. the lowest quartile).

Conclusions

If the associations we observed are causal, then air pollution from traffic might be an important risk factor for vascular dementia and Alzheimer’s disease.

Citation

Oudin A, Forsberg B, Nordin Adolfsson A, Lind N, Modig L, Nordin M, Nordin S, Adolfsson R, Nilsson LG. 2016. Traffic-related air pollution and dementia incidence in northern Sweden: a longitudinal study. Environ Health Perspect 124:306–312; http://dx.doi.org/10.1289/ehp.1408322     

Chronic Residential Exposure to Particulate Matter Air Pollution and Systemic Inflammatory Markers

Background

Long-term exposure to urban air pollution may accelerate atherogenesis, but mechanisms are still unclear. The induction of a low-grade systemic inflammatory state is a plausible mechanistic pathway. Objectives: We analyzed the association of residential long-term exposure to particulate matter (PM) and high traffic with systemic inflammatory markers.

Methods

We used baseline data from the German Heinz Nixdorf Recall Study, a population-based, prospective cohort study of 4,814 participants that started in 2000. Fine PM [aerodynamic diameter ≤ 2.5 μm (PM_2.5)] exposure based on a small-scale dispersion and chemistry transport model was assigned to each home address. We calculated distances between residences and major roads. Long-term exposure to air pollution (annual PM_2.5 and distance to high traffic) and concentration of inflammatory markers [high-sensitivity C-reactive protein (hs-CRP) and fibrinogen] on the day of the baseline visit were analyzed with sex-stratified multiple linear regression, controlling for individual-level risk factors.

Results

In the adjusted analysis, a cross-sectional exposure difference of 3.91 μg/m³ in PM_2.5 (interdecile range) was associated with increases in hs-CRP of 23.9% [95% confidence interval (CI), 4.1 to 47.4%] and fibrinogen of 3.9% (95% CI, 0.3 to 7.7%) in men, whereas we found no association in women. Chronic traffic exposure was not associated with inflammatory markers. Short-term exposures to air pollutants and temperature did not influence the results markedly.

Conclusions

Our study indicates that long-term residential exposure to high levels of PM_2.5 is associated with systemic inflammatory markers in men. This might provide a link between air pollution and coronary atherosclerosis.     

Prospective Analysis of Traffic Exposure as a Risk Factor for Incident Coronary Heart Disease: The Atherosclerosis Risk in Communities (ARIC) Study

Background

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).

Objectives

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.

Methods

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.

Results

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.

Conclusion

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.     

Association between Local Traffic-Generated Air Pollution and Preeclampsia and Preterm Delivery in the South Coast Air Basin of California

Background

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.

Objectives

We examined effects of residential exposure to local traffic-generated air pollution on preeclampsia and preterm delivery (PTD).

Methods

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 (NO_x) and particulate matter < 2.5 μm in aerodynamic diameter (PM_2.5) 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).

Results

We observed elevated risks for preeclampsia and preterm birth from maternal exposure to local traffic-generated NO_x and PM_2.5. 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 NO_x and PM_2.5 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 NO_x and PM_2.5 exposure quartiles, respectively.

Conclusion

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.     

Chronic Exposure to Ambient Ozone and Asthma Hospital Admissions among Children

Background

The association between chronic exposure to air pollution and adverse health outcomes has not been well studied.

Objective

This project investigated the impact of chronic exposure to high ozone levels on childhood asthma admissions in New York State.

Methods

We followed a birth cohort born in New York State during 1995–1999 to first asthma admission or until 31 December 2000. We identified births and asthma admissions through the New York State Integrated Child Health Information System and linked these data with ambient ozone data (8-hr maximum) from the New York State Department of Environmental Conservation. We defined chronic ozone exposure using three indicators: mean concentration during the follow-up period, mean concentration during the ozone season, and proportion of follow-up days with ozone levels > 70 ppb. We performed logistic regression analysis to adjust for child’s age, sex, birth weight, and gestational age; maternal race/ethnicity, age, education, insurance status, smoking during pregnancy, and poverty level; and geographic region, temperature, and copollutants.

Results

Asthma admissions were significantly associated with increased ozone levels for all chronic exposure indicators (odds ratios, 1.16–1.68), with a positive dose–response relationship. We found stronger associations among younger children, low sociodemographic groups, and New York City residents as effect modifiers.

Conclusion

Chronic exposure to ambient ozone may increase the risk of asthma admissions among children. Younger children and those in low socioeconomic groups have a greater risk of asthma than do other children at the same ozone level.     

Is There Evidence for Synergy Among Air Pollutants in Causing Health Effects?

Background

Environmental air pollutants are inhaled as complex mixtures, but the long dominant focus of monitoring and research on individual pollutants has provided modest insight into pollutant interactions that may be important to health. Trends toward managing multiple pollutants to maximize aggregate health gains place increasing value on knowing whether the effects of combinations of pollutants are greater than the sum of the effects of individual pollutants (synergy).

Objective

We reviewed selected published literature to determine whether synergistic effects of combinations of pollutants on health outcomes have actually been demonstrated.

Methods and results

We reviewed 36 laboratory studies of combinations of ozone with other pollutants that were reported in the recent U.S. Environmental Protection Agency Ozone Criteria Document. We examined original reports to determine whether the experimental design tested for synergy and whether synergy was demonstrated. Fourteen studies demonstrated synergism, although synergistic, additive, and antagonistic effects were sometimes observed among different outcomes or at different times after exposure.

Conclusions

Synergisms involving O₃ have been demonstrated by laboratory studies of humans and animals. We conclude that the plausibility of synergisms among environmental pollutants has been established, although comparisons are limited, and most involved exposure concentrations much higher than typical of environmental pollutants. Epidemiologic research has limited ability to address the issue explicitly.