Long-term Exposure to PM2.5 and Incidence of Acute Myocardial Infarction

Background: A number of studies have shown associations between chronic exposure to particulate air pollution and increased mortality, particularly from cardiovascular disease, but fewer studies have examined the association between long-term exposure to fine particulate air pollution and specific cardiovascular events, such as acute myocardial infarction (AMI).Objective: We examined how long-term exposure to area particulate matter affects the onset of AMI, and we distinguished between area and local pollutants.Methods: Building on the Worcester Heart Attack Study, an ongoing community-wide investigation examining changes over time in myocardial infarction incidence in greater Worcester, Massachusetts, we conducted a case–control study of 4,467 confirmed cases of AMI diagnosed between 1995 and 2003 and 9,072 matched controls selected from Massachusetts resident lists. We used a prediction model based on satellite aerosol optical depth (AOD) measurements to generate both exposure to particulate matter ≤ 2.5 μm in diameter (PM_2.5) at the area level (10 × 10 km) and the local level (100 m) based on local land use variables. We then examined the association between area and local particulate pollution and occurrence of AMI.Results: An interquartile range (IQR) increase in area PM_2.5 (0.59 μg/m³) was associated with a 16% increase in the odds of AMI (95% CI: 1.04, 1.29). An IQR increase in total PM_2.5 (area + local, 1.05 μg/m³) was weakly associated with a 4% increase in the odds of AMI (95% CI: 0.96, 1.11).Conclusions: Residential exposure to PM_2.5 may best be represented by a combination of area and local PM_2.5, and it is important to consider spatial gradients within a single metropolitan area when examining the relationship between particulate matter exposure and cardiovascular events.     

Residential exposure to traffic-related air pollution and survival after heart failure

BACKGROUND: Although patients with heart failure (HF) have been identified as particularly susceptible to the acute effects of air pollution, the effects of long-term exposure to air pollution on patients with this increasingly prevalent disease are largely unknown. OBJECTIVE: This study was designed to examine the mortality risk associated with residential exposure to traffic-related air pollution among HF patients. METHODS: A total of 1,389 patients hospitalized with acute HF in greater Worcester, Massachusetts, during 2000 were followed for survival through December 2005. We used daily traffic within 100 and 300 m of residence as well as the distance from residence to major roadways and to bus routes as proxies for residential exposure to traffic-related air pollution. We assessed mortality risks for each exposure variable using Cox proportional hazards models adjusted for prognostic factors. RESULTS: After the 5-year follow-up, only 334 (24%) subjects were still alive. An interquartile range increase in daily traffic within 100 m of home was associated with a mortality hazard ratio (HR) of 1.15 [95% confidence interval (CI), 1.05-1.25], whereas for traffic within 300 m this association was 1.09 (95% CI, 1.01-1.19). The mortality risk decreased with increasing distance to bus routes (HR = 0.88; 95% CI, 0.81-0.96) and was larger for those living within 100 m of a major roadway or 50 m of a bus route (HR = 1.30; 95% CI, 1.13-1.49). Adjustment for area-based income and educational level slightly attenuated these associations. CONCLUSIONS: Residential exposure to traffic-related air pollution increases the mortality risk after hospitalization with acute HF. Reducing exposure to traffic-related emissions may improve the long-term prognosis of HF patients.     

Ambient Air Pollution and Depressive Symptoms in Older Adults: Results from the MOBILIZE Boston Study

Background: Exposure to ambient air pollution, particularly from traffic, has been associated with adverse cognitive outcomes, but the association with depressive symptoms remains unclear.Objectives: We investigated the association between exposure to ambient air and traffic pollution and the presence of depressive symptoms among 732 Boston-area adults ≥ 65 years of age (78.1 ± 5.5 years, mean ± SD).Methods: We assessed depressive symptoms during home interviews using the Revised Center for Epidemiological Studies Depression Scale (CESD-R). We estimated residential distance to the nearest major roadway as a marker of long-term exposure to traffic pollution and assessed short-term exposure to ambient fine particulate matter (PM_2.5), sulfates, black carbon (BC), ultrafine particles, and gaseous pollutants, averaged over the 2 weeks preceding each assessment. We used generalized estimating equations to estimate the odds ratio (OR) of a CESD-R score ≥ 16 associated with exposure, adjusting for potential confounders. In sensitivity analyses, we considered CESD-R score as a continuous outcome and mean annual residential BC as an alternate marker of long-term exposure to traffic pollution.Results: We found no evidence of a positive association between depressive symptoms and long-term exposure to traffic pollution or short-term changes in pollutant levels. For example, we found an OR of CESD-R score ≥ 16 of 0.67 (95% CI: 0.46, 0.98) per interquartile range (3.4 μg/m³) increase in PM_2.5 over the 2 weeks preceding assessment.Conclusions: We found no evidence suggesting that ambient air pollution is associated with depressive symptoms among older adults living in a metropolitan area in attainment of current U.S. regulatory standards.Citation: Wang Y, Eliot MN, Koutrakis P, Gryparis A, Schwartz JD, Coull BA, Mittleman MA, Milberg WP, Lipsitz LA, Wellenius GA. 2014. Ambient air pollution and depressive symptoms in older adults: results from the MOBILIZE Boston Study. Environ Health Perspect 122:553–558; http://dx.doi.org/10.1289/ehp.1205909     

Traffic-related air pollution and childhood respiratory symptoms, function and allergies

BACKGROUND: Urban air pollution can trigger asthma symptoms in children, but there is conflicting evidence on effects of long-term exposure on lung function, onset of airway disease and allergic sensitization. METHODS: The spatial distribution of nitrogen oxides from traffic (traffic-NOx) and inhalable particulate matter from traffic (traffic-PM10) in the study area was assessed with emission databases and dispersion modeling. Estimated levels were used to assign first-year exposure levels for children in a prospective birth cohort (n = 4089), by linking to geocoded home addresses. Parents in 4 Swedish municipalities provided questionnaire data on symptoms and exposures when the children were 2 months and 1, 2, and 4-year-old. At 4 years, 73% of the children underwent clinical examination including peak expiratory flow and specific IgE measurements. RESULTS: Exposure to air pollution from traffic during the first year of life was associated with an excess risk of persistent wheezing (odds ratio [OR] for 44 microg/m3 [5th-95th percentile] difference in traffic-NOx = 1.60; 95% confidence interval [CI] = 1.09-2.36). Similar results were found for sensitization (measured as specific IgE) to inhalant allergens, especially pollen (OR for traffic-NOx = 1.67; 95% CI = 1.10-2.53), at the age of 4 years. Traffic-related air pollution exposure during the first year of life was also associated with lower lung function at 4 years of age. Results were similar using traffic-NOx and traffic-PM10 as indicators. CONCLUSIONS: Exposure to moderate levels of locally emitted air pollution from traffic early in life appears to influence the development of airway disease and sensitization in preschool children.     

Traffic air pollution and other risk factors for respiratory illness in schoolchildren in the niger-delta region of Nigeria

Background: Association of childhood respiratory illness with traffic air pollution has been investigated largely in developed but not in developing countries, where pollution levels are often very high.Objectives: In this study we investigated associations between respiratory health and outdoor and indoor air pollution in schoolchildren 7–14 years of age in low socioeconomic status areas in the Niger Delta.Methods: A cross-sectional survey was carried out among 1,397 schoolchildren. Exposure to home outdoor and indoor air pollution was assessed by self-report questionnaire. School air pollution exposures were assessed using traffic counts, distance of schools to major streets, and particulate matter and carbon monoxide measurements, combined using principal components analysis. Hierarchical logistic regression was used to examine associations with reported respiratory health, adjusting for potential confounders.Results: Traffic disturbance at home (i.e., traffic noise and/or fumes evident inside the home vs. none) was associated with wheeze [odds ratio (OR) = 2.16; 95% confidence interval (CI), 1.28–3.64], night cough (OR = 1.37; 95% CI, 1.03–1.82), phlegm (OR = 1.49; 95% CI, 1.09–2.04), and nose symptoms (OR = 1.40; 95% CI, 1.03–1.90), whereas school exposure to a component variable indicating exposure to fine particles was associated with increased phlegm (OR = 1.38; 95% CI, 1.09–1.75). Nonsignificant positive associations were found between cooking with wood/coal (OR = 2.99; 95% CI, 0.88–10.18) or kerosene (OR = 2.83; 95% CI, 0.85–9.44) and phlegm compared with cooking with gas.Conclusion: Traffic pollution is associated with respiratory symptoms in schoolchildren in a deprived area of western Africa. Associations may have been underestimated because of nondifferential misclassification resulting from limitations in exposure measurement.     

Long-term exposure to urban air pollution and myocardial infarction

BACKGROUND: Cohort studies have reported increased risks of cardiopulmonary mortality from long-term air pollution exposure, but the evidence is limited and inconclusive. We studied the association between long-term exposure to source-specific air pollution and myocardial infarction (MI) in a case-control study of first-time MI cases and population controls age 45 to 70 years in Stockholm county in 1992 to 1994. METHODS: Home addresses during several decades were combined with historical emission databases and dispersion models to obtain annual mean levels of pollutants from traffic and heating during 30 years for 1397 cases and 1870 controls. Nitrogen dioxide (NO2), carbon monoxide (CO), and particulate matter with an aerodynamic diameter less than 10 microm (PM10) were used as indicators of traffic emissions and sulfur dioxide (SO2) as an indicator of emissions from residential heating. RESULTS: There was no association between long-term average air pollution exposure and overall MI, but an increased risk of fatal MI was suggested, especially for out-of-hospital death. After adjustment for cardiovascular risk factors, the odds ratio for fatal MI associated with a 5th to 95th percentile difference in 30-year average exposure was 1.51 (95% confidence interval = 0.96-2.16) for NO2, 1.22 (0.98-1.52) for CO, 1.39 (0.94-2.07) for PM10, and 1.24 (0.77-2.02) for SO2. For out-of-hospital death, the odds ratio related to NO2 exposure was 2.17 (1.05-4.51). CONCLUSIONS: This study provides some support for an association between long-term air pollution exposure and fatal cardiovascular disease.     

Long-term exposure to traffic-related air pollution associated with blood pressure and self-reported hypertension in a Danish cohort

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 (NO_x), 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 NO_x, 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 NO_x 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 NO_x: odds ratio = 0.96; 95% CI: 0.91, 1.00), whereas long-term NO_x 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.     

Ambient particulate air pollution and circulating C-reactive protein level: A systematic review and meta-analysis

BackgroundAmbient particulate air pollution is a major threat to the cardiovascular health of people. Inflammation is an important component of the pathophysiological process that links air pollution and cardiovascular disease (CVD). A classical marker of inflammation—C-reactive protein (CRP), has been recognized as an independent predictor of CVD risk. Exposure to ambient particulate matter (PM) may cause systemic inflammatory response but its association with CRP has been inconsistently reported.ObjectivesTo estimate the potential effects of short-term and long-term exposures to ambient particulate air pollution on circulating CRP level based on previous epidemiological studies.MethodsA systematic literature search of PubMed, Web of Science, Embase, and Scopus databases for publications up to January 2018 was conducted for studies reporting the association between ambient PM (PM_2.5 or PM₁₀, or both) and circulating CRP level. We performed a meta-analysis for the associations reported in individual studies using a random-effect model and evaluated the effect modification by major potential modifiers.ResultsThis meta-analysis comprised data from 40 observational studies conducted on 244,681 participants. These included 32 (27 PM_2.5 studies and 13 PM₁₀ studies) and 11 (9 PM_2.5 studies and 5 PM₁₀ studies) studies that investigated the associations of CRP with short-term and long-term exposure to particulate air pollution, respectively. A 10 μg/m³ increase in short-term exposure to PM_2.5 and PM₁₀ was associated with increases of 0.83 % (95% CI: 0.30%, 1.37%) and 0.39% (95% CI: -0.04%, 0.82%) in CRP level, respectively, and a 10 μg/m³ increase in long-term exposure to PM_2.5 and PM₁₀ was associated with much higher increases of 18.01% (95% CI: 5.96%, 30.06%) and 5.61% (95% CI: 0.79%, 10.44%) in CRP level, respectively. The long-term exposure to particulate air pollution was more strongly associated with CRP level than short-term exposure and PM_2.5 had a greater effect on CRP level than PM₁₀.ConclusionExposure to ambient particulate air pollution is associated with elevated circulating CRP level suggesting an activated systemic inflammatory state upon exposure, which may explain the association between particulate air pollution and CVD risk.     

Air pollution and emergency admissions in Boston, MA

STUDY OBJECTIVE: Many studies have shown that ambient particulate air pollution (PM) is associated with increased risk of hospital admissions and deaths for cardiovascular or respiratory causes around the world. In general these have been analysed in association with PM(10) and ozone, whereas PM(2.5) is now the particle measure of greatest health and regulatory concern. And little has been published on associations of hospital admissions and PM components. DESIGN: This study analysed hospital admissions for myocardial infarction (15 578 patients), and pneumonia (24 857 patients) in associations with fine particulate air pollution, black carbon (BC), ozone, nitrogen dioxide (NO(2)), PM not from traffic, and carbon monoxide (CO) in the greater Boston area for the years 1995-1999 using a case-crossover analysis, with control days matched on temperature. MAIN RESULTS: A significant association was found between NO(2) (12.7% change (95% CI: 5.8, 18)), PM(2.5) (8.6% increase (95% CI: 1.2, 15.4)), and BC (8.3% increase (95% CI: 0.2, 15.8)) and the risk of emergency myocardial infarction hospitalisation; and between BC (11.7% increase (95% CI: 4.8, 17.4)), PM(2.5) (6.5% increase (95% CI: 1.1, 11.4)), and CO (5.5% increase (95% CI: 1.1, 9.5)) and the risk of pneumonia hospitalisation. CONCLUSIONS: The pattern of associations seen for myocardial infarction and pneumonia (strongest associations with NO(2), CO, and BC) suggests that traffic exposure is primarily responsible for the association with heart attacks.     

Long-term effects of traffic-related air pollution on mortality in a Dutch cohort (NLCS-AIR study)

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 < or = 2.5 microm (PM(2.5)), 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-microg/m(3) 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 NO(2) and PM(2.5), but no associations were found for SO(2). 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 NO(2) and BS. These results add to the evidence that long-term exposure to ambient air pollution is associated with increased mortality.     

Health impact assessment of particulate pollution in Tallinn using fine spatial resolution and modeling techniques

Background

Higher exposure to outdoor air pollution is associated with increased cardiopulmonary deaths, but there is limited evidence about the association between outdoor air pollution and diagnosed cardiovascular disease. Our study aimed to estimate the size of the association between long term exposure to outdoor air pollution and prevalent cardiovascular disease.

Methods

We carried out a cross-sectional analysis of data on more than 19,000 white adults aged 45 and older who participated in three representative surveys of the English population in 1994, 1998 and 2003, examining the relationship between self-reported doctor-diagnosed cardiovascular disease and exposure to outdoor air pollutants using multilevel regression techniques and meta-analysis.

Results

The combined estimates suggested that an increase of 1 μg m^-3 in concentration of particulate matter less than 10 microns in diameter was associated with an increase of 2.9% (95% CI -0.6% to 6.5%) in prevalence of cardiovascular disease in men, and an increase of 1.6% (95%CI -2.1% to 5.5%) in women. The year-specific analyses showed strongly positive associations in 2003 between odds of cardiovascular disease in both men and women and exposure to particulate matter but not in 1994 or 1998. We found no consistent associations between exposure to gaseous air pollutants and doctor-diagnosed cardiovascular disease.

Conclusion

The associations of prevalent cardiovascular disease with concentration of particulate matter less than 10 microns in diameter, while only weakly positive, were consistent with the effects reported in cohort studies. The results provide evidence of the size of the association between particulate air pollution and the prevalence of cardiovascular disease but no evidence for an association with gaseous pollutants. We found strongly positive associations between particulate matter and cardiovascular disease in 2003 only, which highlights the importance of replicating findings in more than one population.     

Acute effect of sulphur dioxide from a power plant on pulmonary function of children, Thailand

BACKGROUND: Epidemiological studies have shown reversible declines of lung function in response to air pollution, but research on the independent effect of short-term exposure to ambient sulphur dioxide (SO2) on pulmonary function is limited. This study evaluated the association of short-term exposure to increased ambient SO2 and daily pulmonary function changes among children with and without asthma. METHODS: The associations of daily exposure to SO2 and particulate matter 10 microm in diameter (PM10) with pulmonary function were examined in 175 asthmatic and non-asthmatic children aged 6-14 years who resided near a coal-fired power plant in Thailand. Each child performed daily pulmonary function tests during the 61-day study period. General linear mixed models were used to estimate the association of air pollution and pulmonary function controlling for time, temperature, co-pollutants, and autocorrelation. RESULTS: In the asthmatic children, a daily increase in SO2 was associated with negligible declines in pulmonary function, but a small negative association was found between PM10 and pulmonary function. A 10-microg/m(3) increment was associated with changes in the highest forced vital capacity (FVC) (-6.3 ml, 95% CI: -9.8, -2.8), forced expiratory volume at 1 second (FEV(1)) (-6.0 ml, 95% CI: -9.2, 2.7), peak expiratory flow rate (PEFR) (-18.9 ml.sec(-1), 95% CI: -28.5, -9.3) and forced expiratory flow 25 to 75% of the FVC (FEF(25-75%)) (-3.7 ml.sec(-1), 95% CI: -10.9, 3.5). No consistent associations between air pollution and pulmonary function were found for non-asthmatic children. CONCLUSION: Declines in pulmonary function among asthmatic children were associated with increases in particulate air pollution, rather than with increases in SO2.     

Ambient air pollution and apnea and bradycardia in high-risk infants on home monitors

Background: Evidence suggests that increased ambient air pollution concentrations are associated with health effects, although relatively few studies have specifically examined infants.Objective: We examined associations of daily ambient air pollution concentrations with central apnea (prolonged pauses in breathing) and bradycardia (low heart rate) events among infants prescribed home cardiorespiratory monitors.Methods: The home monitors record the electrocardiogram, heart rate, and respiratory effort for detected apnea and bradycardia events in high-risk infants [primarily premature and low birth weight (LBW) infants]. From August 1998 through December 2002, 4,277 infants had 8,960 apnea event-days and 29,450 bradycardia event-days in > 179,000 days of follow-up. We assessed the occurrence of apnea and bradycardia events in relation to speciated particulate matter and gaseous air pollution levels using a 2-day average of air pollution (same day and previous day), adjusting for temporal trends, temperature, and infant age.Results: We observed associations between bradycardia and 8-hr maximum ozone [odds ratio (OR) = 1.049 per 25-ppb increase; 95% confidence interval (CI), 1.021–1.078] and 1-hr maximum nitrogen dioxide (OR =1.025 per 20-ppb increase; 95% CI, 1.000–1.050). The association with ozone was robust to different methods of control for time trend and specified correlation structure. In secondary analyses, associations of apnea and bradycardia with pollution were generally stronger in infants who were full term and of normal birth weight than in infants who were both premature and LBW.Conclusions: These results suggest that higher air pollution concentrations may increase the occurrence of apnea and bradycardia in high-risk infants.     

Ambient Air Pollution and Autism in Los Angeles County,California

Background: The prevalence of autistic disorder (AD), a serious developmental condition, has risen dramatically over the past two decades, but high-quality population-based research addressing etiology is limited.Objectives: We studied the influence of exposures to traffic-related air pollution during pregnancy on the development of autism using data from air monitoring stations and a land use regression (LUR) model to estimate exposures.Methods: Children of mothers who gave birth in Los Angeles, California, who were diagnosed with a primary AD diagnosis at 3–5 years of age during 1998–2009 were identified through the California Department of Developmental Services and linked to 1995–2006 California birth certificates. For 7,603 children with autism and 10 controls per case matched by sex, birth year, and minimum gestational age, birth addresses were mapped and linked to the nearest air monitoring station and a LUR model. We used conditional logistic regression, adjusting for maternal and perinatal characteristics including indicators of SES.Results: Per interquartile range (IQR) increase, we estimated a 12–15% relative increase in odds of autism for ozone [odds ratio (OR) = 1.12, 95% CI: 1.06, 1.19; per 11.54-ppb increase] and particulate matter ≤ 2.5 µm (OR = 1.15; 95% CI: 1.06, 1.24; per 4.68-μg/m³ increase) when mutually adjusting for both pollutants. Furthermore, we estimated 3–9% relative increases in odds per IQR increase for LUR-based nitric oxide and nitrogen dioxide exposure estimates. LUR-based associations were strongest for children of mothers with less than a high school education.Conclusion: Measured and estimated exposures from ambient pollutant monitors and LUR model suggest associations between autism and prenatal air pollution exposure, mostly related to traffic sources.     

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.     

A cohort study of traffic-related air pollution impacts on birth outcomes

BACKGROUND: Evidence suggests that air pollution exposure adversely affects pregnancy outcomes. Few studies have examined individual-level intraurban exposure contrasts. OBJECTIVES: We evaluated the impacts of air pollution on small for gestational age (SGA) birth weight, low full-term birth weight (LBW), and preterm birth using spatiotemporal exposure metrics. METHODS: With linked administrative data, we identified 70,249 singleton births (1999-2002) with complete covariate data (sex, ethnicity, parity, birth month and year, income, education) and maternal residential history in Vancouver, British Columbia, Canada. We estimated residential exposures by month of pregnancy using nearest and inverse-distance weighting (IDW) of study area monitors [carbon monoxide, nitrogen dioxide, nitric oxide, ozone, sulfur dioxide, and particulate matter < 2.5 (PM2.5) or < 10 (PM10) microm in aerodynamic diameter], temporally adjusted land use regression (LUR) models (NO, NO2, PM2.5, black carbon), and proximity to major roads. Using logistic regression, we estimated the risk of mean (entire pregnancy, first and last month of pregnancy, first and last 3 months) air pollution concentrations on SGA (< 10th percentile), term LBW (< 2,500 g), and preterm birth. RESULTS: Residence within 50 m of highways was associated with a 26% increase in SGA [95% confidence interval (CI), 1.07-1.49] and an 11% (95% CI, 1.01-1.23) increase in LBW. Exposure to all air pollutants except O3 was associated with SGA, with similar odds ratios (ORs) for LUR and monitoring estimates (e.g., LUR: OR = 1.02; 95% CI, 1.00-1.04; IDW: OR = 1.05; 95% CI, 1.03-1.08 per 10-microg/m3 increase in NO). For preterm births, associations were observed with PM2.5 for births < 37 weeks gestation (and for other pollutants at < 30 weeks). No consistent patterns suggested exposure windows of greater relevance. CONCLUSION: Associations between traffic-related air pollution and birth outcomes were observed in a population-based cohort with relatively low ambient air pollution exposure.     

Air pollution, asthma attacks, and socioeconomic deprivation: a small-area case-crossover study

With few exceptions, studies of short-term health effects of air pollution use pollutant concentrations that are averaged citywide as exposure indicators. They are thus prone to exposure misclassification and consequently to bias. Measurement of the relations between air pollution and health, generally and in specific populations, could be improved by employing more geographically precise exposure estimates. The authors investigated short-term relations between ambient air pollution estimated in small geographic areas (French census blocks) and asthma attacks in Strasbourg, France, in 2000-2005--in the general population and in populations with contrasting levels of socioeconomic deprivation. Emergency health-care networks provided data on 4,683 telephone calls made for asthma attacks. Deprivation was estimated using a block-level index constructed from census data. Hourly concentrations of particulate matter less than 10 microm in aerodynamic diameter (PM(10)), sulfur dioxide, nitrogen dioxide, and ozone were modeled by block with ADMS-Urban software. Adjusted case-crossover analyses showed that asthma calls were positively but not significantly associated with PM(10) (for a 10-microg x m(-3) increase, odds ratio (OR) = 1.035, 95% confidence interval (CI): 0.997, 1.075), sulfur dioxide (OR = 1.056, 95% CI: 0.979, 1.139), and nitrogen dioxide (OR = 1.025, 95% CI: 0.990, 1.062). No association was observed for ozone (OR = 0.998, 95% CI: 0.965, 1.032). Socioeconomic deprivation had no significant influence on these relations.     

The effect of ozone and PM10 on hospital admissions for pneumonia and chronic obstructive pulmonary disease: a national multicity study

A case-crossover study was conducted in 36 US cities to evaluate the effect of ozone and particulate matter with an aerodynamic diameter of < or =10 microm (PM10) on respiratory hospital admissions and to identify which city characteristics may explain the heterogeneity in risk estimates. Respiratory hospital admissions and air pollution data were obtained for 1986-1999. In a meta-analysis based on the city-specific regression models, several city characteristics were evaluated as effect modifiers. During the warm season, the 2-day cumulative effect of a 5-ppb increase in ozone was a 0.27% (95% confidence interval (CI): 0.08, 0.47) increase in chronic obstructive pulmonary disease admissions and a 0.41% (95% CI: 0.26, 0.57) increase in pneumonia admissions. Similarly, a 10-microg/m(3) increase in PM10 during the warm season resulted in a 1.47% (95% CI: 0.93, 2.01) increase in chronic obstructive pulmonary disease at lag 1 and a 0.84% (95% CI: 0.50, 1.19) increase in pneumonia at lag 0. Percentage of households with central air conditioning reduced the effect of air pollution, and variability of summer apparent temperature reduced the effect of ozone on chronic obstructive pulmonary disease. The study confirmed, in a large sample of cities, that exposure to ozone and PM10 is associated with respiratory hospital admissions and provided evidence that the effect of air pollution is modified by certain city characteristics.     

The lag structure between particulate air pollution and respiratory and cardiovascular deaths in 10 US cities.

To assess differences in the lag structure pattern between particulate matter < 10 microns/100 microns in diameter (PM10) and cause-specific mortality, we performed a time-series analysis in 10 US cities using generalized additive Poisson regressions in each city; nonparametric smooth functions were used to control for long time trend, weather, and day of the week. The PM10 effect was estimated based on its daily mean, 2-day moving average, and the cumulative 7-day effect by means of an unconstrained distributed lag model. A 10-microgram/m3 increase in the 7-day mean of PM10 was associated with increases in deaths due to pneumonia (2.7%, 95% confidence interval [CI]: 1.5, 3.9), chronic obstructive pulmonary disease (1.7%, 95% CI: 0.1, 3.3), and all cardiovascular diseases (1.0%, 95% CI: 0.6, 1.4). A 10-microgram/m3 increase in the 2-day mean of PM10 was associated with a 0.7% (95% CI: 0.3, 1.1) increase in deaths from myocardial infarction. When the distributed lag was assessed, two different patterns could be observed: respiratory deaths were more affected by air pollution levels on the previous days, whereas cardiovascular deaths were more affected by same-day pollution. These results contribute to the overall efforts so far in understanding how exposure to air pollution promotes adverse health effects.     

Air pollution and heart rate variability: effect modification by chronic lead exposure

BACKGROUND: Outdoor air pollution and lead exposure can disturb cardiac autonomic function, but the effects of both these exposures together have not been studied. METHODS: We examined whether higher cumulative lead exposures, as measured by bone lead, modified cross-sectional associations between air pollution and heart rate variability among 384 elderly men from the Normative Aging Study. We used linear regression, controlling for clinical, demographic, and environmental covariates. RESULTS: We found graded, significant reductions in both high-frequency and low-frequency powers of heart rate variability in relation to ozone and sulfate across the quartiles of tibia lead. Interquartile range increases in ozone and sulfate were associated respectively, with 38% decrease (95% confidence interval = -54.6% to -14.9%) and 22% decrease (-40.4% to 1.6%) in high frequency, and 38% decrease (-51.9% to -20.4%) and 12% decrease (-28.6% to 9.3%) in low frequency, in the highest quartile of tibia lead after controlling for potential confounders. We observed similar but weaker effect modification by tibia lead adjusted for education and cumulative traffic (residuals of the regression of tibia lead on education and cumulative traffic). Patella lead modified only the ozone effect on heart rate variability. CONCLUSIONS: People with long-term exposure to higher levels of lead may be more sensitive to cardiac autonomic dysfunction on high air pollution days. Efforts to understand how environmental exposures affect the health of an aging population should consider both current levels of pollution and history of lead exposure as susceptibility factors.