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BackgroundAcute pollutant-related lung function changes among children varies across pollutants and lag periods. We examined whether short-term air pollutant fluctuations were related to daily lung function among a panel of children and whether these effects are modified by airway hyperresponsiveness, location and asthma severity.MethodsStudents from randomly selected grade 4 classrooms at seven primary schools in Durban, participated, together with asthmatic children from grades 3–6 (n=423). The schools were from high pollutant exposed communities (south) and compared with schools from communities with lower levels of pollution (north), with similar socioeconomic profiles. Interviews, spirometry and methacholine challenge testing were conducted. Bihourly lung function measurements were performed over a 3-week period in four phases. During all schooldays, students blew into their personal digital monitors every 1.5–2 hours. Nitrogen dioxide (NO2), nitrogen oxide (NO), sulphur dioxide and particulate matter (<10 μm diameter) (PM10) were measured at each school. Generalised estimating equations assessed lag effects, using single-pollutant (single or distributed lags) models.ResultsFEV1 declines ranged from 13 to 18 mL per unit increase in IQR for NO and 14–23 mL for NO2. Among the 5-day average models, a 20 mL and 30 mL greater drop in FEV1 per IQR for NO2 and NO, respectively, among those with airway hyperresponsiveness compared with those without. Effects were seen among those with normal airways.ConclusionsThis first panel study in sub-Saharan Africa, showed significant declines in lung function, in response to NO and NO2 with effects modified by airway hyperresponsiveness or persistent asthma.

Exposure to traffic-related air pollutants is an important public health issue. Here, we present a systematic review and meta-analysis of research examining the relationship of measures of nitrogen oxides (NOx) and of various measures of traffic-related air pollution exposure with lung cancer. We conducted random-effects meta-analyses of studies examining exposure to nitrogen dioxide (NO2) and NOx and its association with lung cancer. We identified 20 studies that met inclusion criteria and provided information necessary to estimate the change in lung cancer per 10-μg/m3 increase in exposure to measured NO2. Further, we qualitatively assessed the evidence of association between distance to roadways and traffic volume associated with lung cancer. The meta-estimate for the change in lung cancer associated with a 10-μg/m3 increase in exposure to NO2 was 4% (95% CI: 1%, 8%). The meta-estimate for change in lung cancer associated with a 10-μg/m3 increase in NOx was similar and slightly more precise, 3% (95% CI: 1%, 5%). The NO2 meta-estimate was robust to different confounding adjustment sets as well as the exposure assessment techniques used. Trim-and-fill analyses suggest that if publication bias exists, the overall meta-estimate is biased away from the null. Forest plots for measures of traffic volume and distance to roadways largely suggest a modest increase in lung cancer risk. We found consistent evidence of a relationship between NO2, as a proxy for traffic-sourced air pollution exposure, with lung cancer. Studies of lung cancer related to residential proximity to roadways and NOx also suggest increased risk, which may be attributable partly to air pollution exposure. The International Agency for Research on Cancer recently classified outdoor air pollution and particulate matter as carcinogenic (Group 1). These meta-analyses support this conclusion, drawing particular attention to traffic-sourced air pollution. Hamra GB, Laden F, Cohen AJ, Raaschou-Nielsen O, Brauer M, Loomis D. 2015. Lung cancer and exposure to nitrogen dioxide and traffic: a systematic review and meta-analysis. Environ Health Perspect 123:1107-1112; http://dx.doi.org/10.1289/ehp.1408882.

Learning more about how pollutants enter and damage the body would reduce disease and deaths, say Jos Lelieveld and Ulrich Pöschl. Learning more about how pollutants enter and damage the body would reduce disease and deaths, say Jos Lelieveld and Ulrich Pöschl.

Few studies have investigated effects of air pollution on the incidence of cerebrovascular events. We assessed the association between long-term exposure to multiple air pollutants and the incidence of stroke in European cohorts. Data from 11 cohorts were collected, and occurrence of a first stroke was evaluated. Individual air pollution exposures were predicted from land-use regression models developed within the European Study of Cohorts for Air Pollution Effects (ESCAPE). The exposures were: PM2.5 [particulate matter (PM) ≤ 2.5 μm in diameter], coarse PM (PM between 2.5 and 10 μm), PM10 (PM ≤ 10 μm), PM2.5 absorbance, nitrogen oxides, and two traffic indicators. Cohort-specific analyses were conducted using Cox proportional hazards models. Random-effects meta-analysis was used for pooled effect estimation. A total of 99,446 study participants were included, 3,086 of whom developed stroke. A 5-μg/m3 increase in annual PM2.5 exposure was associated with 19% increased risk of incident stroke [hazard ratio (HR) = 1.19, 95% CI: 0.88, 1.62]. Similar findings were obtained for PM10. The results were robust to adjustment for an extensive list of cardiovascular risk factors and noise coexposure. The association with PM2.5 was apparent among those ≥ 60 years of age (HR = 1.40, 95% CI: 1.05, 1.87), among never-smokers (HR = 1.74, 95% CI: 1.06, 2.88), and among participants with PM2.5 exposure < 25 μg/m3 (HR = 1.33, 95% CI: 1.01, 1.77). We found suggestive evidence of an association between fine particles and incidence of cerebrovascular events in Europe, even at lower concentrations than set by the current air quality limit value.

There is evidence for adverse effects of outdoor air pollution on lung function of children. Quantitative summaries of the effects of air pollution on lung function, however, are lacking due to large differences among studies. We aimed to study the association between residential exposure to air pollution and lung function in five European birth cohorts with a standardized exposure assessment following a common protocol. As part of the European Study of Cohorts for Air Pollution Effects (ESCAPE) we analyzed data from birth cohort studies situated in Germany, Sweden, the Netherlands, and the United Kingdom that measured lung function at 6-8 years of age (n = 5,921). Annual average exposure to air pollution [nitrogen oxides (NO2, NOx), mass concentrations of particulate matter with diameters < 2.5, < 10, and 2.5-10 μm (PM2.5, PM10, and PMcoarse), and PM2.5 absorbance] at the birth address and current address was estimated by land-use regression models. Associations of lung function with estimated air pollution levels and traffic indicators were estimated for each cohort using linear regression analysis, and then combined by random effects meta-analysis. Estimated levels of NO2, NOx, PM2.5 absorbance, and PM2.5 at the current address, but not at the birth address, were associated with small decreases in lung function. For example, changes in forced expiratory volume in 1 sec (FEV1) ranged from -0.86% (95% CI: -1.48, -0.24%) for a 20-μg/m3 increase in NOx to -1.77% (95% CI: -3.34, -0.18%) for a 5-μg/m3 increase in PM2.5. Exposure to air pollution may result in reduced lung function in schoolchildren.

Associations between long-term exposure to nitrogen oxides (NO x ) and cause-specific mortality remain insufficiently explored. This study utilizes data from 502,040 participants registered in the UK Biobank. Time-varying Cox regression is used to estimate mortality risks associated with NO x . Cause-specific mortality risks, including non-accidental, accidental and 15 major disease categories across 103 subcategories, are assessed for each 10 μg/m 3 increase in NO x . Positive associations are observed between NO x and mortality from all-cause (HR: 1.036; 95% CI: 1.024, 1.049) and non-accidental diseases (HR: 1.032; 95% CI: 1.019, 1.045). We further identify 20 specific diseases related to NO x , notably respiratory diseases, mental and behavioral disorders, and circulatory diseases, with generally linear exposure-response relationships. Sex and residential areas are potential modifiers of the observed associations. Our findings suggest long-term exposure to NO x may increase mortality risks from a range of diseases, emphasizing the urgent need for clean air policies to alleviate the health burden. There is a critical gap in understanding the full spectrum of health effects associated with NO x exposure. Here, the authors find using UK Biobank data that mortality from all-cause, non-accidental and other 20 specific diseases was significantly associated with NO x .

Background Previous studies have reported adverse effects of either regional or near-roadway air pollution (NRAP) on lung function. However, there has been little study of the joint effects of these exposures. Objectives To assess the joint effects of NRAP and regional pollutants on childhood lung function in the Children's Health Study. Methods Lung function was measured on 1811 children from eight Southern Californian communities. NRAP exposure was assessed based on (1) residential distance to the nearest freeway or major road and (2) estimated near-roadway contributions to residential nitrogen dioxide (NO2), nitric oxide (NO) and total nitrogen oxides (NOx). Exposure to regional ozone (O3), NO2, particulate matter with aerodynamic diameter <10 µm (PM10) and 2.5 µm (PM2.5) was measured continuously at community monitors. Results An increase in near-roadway NOx of 17.9 ppb (2 SD) was associated with deficits of 1.6% in forced vital capacity (FVC) (p=0.005) and 1.1% in forced expiratory volume in 1 s (FEV1) (p=0.048). Effects were observed in all communities and were similar for NO2 and NO. Residential proximity to a freeway was associated with a reduction in FVC. Lung function deficits of 2–3% were associated with regional PM10 and PM2.5 (FVC and FEV1) and with O3 (FEV1), but not NO2 across the range of exposure between communities. Associations with regional pollution and NRAP were independent in models adjusted for each. The effects of NRAP were not modified by regional pollutant concentrations. Conclusions The results indicate that NRAP and regional air pollution have independent adverse effects on childhood lung function.

Long-term exposure to air pollution has been hypothesized to elevate arterial blood pressure (BP). The existing evidence is scarce and country specific. We investigated the cross-sectional association of long-term traffic-related air pollution with BP and prevalent hypertension in European populations. We analyzed 15 population-based cohorts, participating in the European Study of Cohorts for Air Pollution Effects (ESCAPE). We modeled residential exposure to particulate matter and nitrogen oxides with land use regression using a uniform protocol. We assessed traffic exposure with traffic indicator variables. We analyzed systolic and diastolic BP in participants medicated and nonmedicated with BP-lowering medication (BPLM) separately, adjusting for personal and area-level risk factors and environmental noise. Prevalent hypertension was defined as ≥ 140 mmHg systolic BP, or ≥ 90 mmHg diastolic BP, or intake of BPLM. We combined cohort-specific results using random-effects meta-analysis. In the main meta-analysis of 113,926 participants, traffic load on major roads within 100 m of the residence was associated with increased systolic and diastolic BP in nonmedicated participants [0.35 mmHg (95% CI: 0.02, 0.68) and 0.22 mmHg (95% CI: 0.04, 0.40) per 4,000,000 vehicles × m/day, respectively]. The estimated odds ratio (OR) for prevalent hypertension was 1.05 (95% CI: 0.99, 1.11) per 4,000,000 vehicles × m/day. Modeled air pollutants and BP were not clearly associated. In this first comprehensive meta-analysis of European population-based cohorts, we observed a weak positive association of high residential traffic exposure with BP in nonmedicated participants, and an elevated OR for prevalent hypertension. The relationship of modeled air pollutants with BP was inconsistent.

Air pollution has the potential to disrupt ecologically- and economically-beneficial services provided by invertebrates, including pollination and natural pest regulation. To effectively predict and mitigate this disruption requires an understanding of how the impacts of air pollution vary between invertebrate groups. Here we conduct a global meta-analysis of 120 publications comparing the performance of different invertebrate functional groups in unpolluted and polluted atmospheres. We focus on the pollutants ozone, nitrogen oxides, sulfur dioxide and particulate matter. We show that beneficial invertebrate performance is reduced by air pollution, whereas the performance of plant pest invertebrates is not significantly affected. Ozone pollution has the most detrimental impacts, and these occur at concentrations below national and international air quality standards. Changes in invertebrate performance are not dependent on air pollutant concentrations, indicating that even low levels of pollution are damaging. Predicted increases in tropospheric ozone could result in unintended consequences to global invertebrate populations and their valuable ecological services. Air pollution has the potential to harm invertebrates. This meta-analysis compares invertebrate performance in unpolluted and polluted atmospheres, finding negative impacts on beneficial invertebrates and detrimental impacts from low levels of ozone.

Background: Accumulating evidence from laboratory animal and human studies suggests that air pollution exposure during pregnancy affects cognitive and psychomotor development in childhood. Methods: We analyzed data from 6 European population-based birth cohorts—GENERATION R (The Netherlands), DUISBURG (Germany), EDEN (France), GASPII (Italy), RHEA (Greece), and INMA (Spain)—that recruited mother-infant pairs from 1997 to 2008. Air pollution levels—nitrogen oxides (NO2, NOx) in all regions and particulate matter (PM) with diameters of <2.5, <10, and 2.5–10 μm (PM2.5, PM10, and PMcoarse, respectively) and PM2.5 absorbance in a subgroup—at birth addresses were estimated by land-use regression models, based on monitoring campaigns performed primarily between 2008 and 2011. Levels were back-extrapolated to exact pregnancy periods using background monitoring sites. Cognitive and psychomotor development was assessed between 1 and 6 years of age. Adjusted region-specific effect estimates were combined using random-effects meta-analysis. Results: A total of 9482 children were included. Air pollution exposure during pregnancy, particularly NO2, was associated with reduced psychomotor development (global psychomotor development score decreased by 0.68 points [95% confidence interval = −1.25 to −0.11] per increase of 10 μg/m3 in NO2). Similar trends were observed in most regions. No associations were found between any air pollutant and cognitive development. Conclusions: Air pollution exposure during pregnancy, particularly NO2 (for which motorized traffic is a major source), was associated with delayed psychomotor development during childhood. Due to the widespread nature of air pollution exposure, the public health impact of the small changes observed at an individual level could be considerable.