Long-term trend and spatial pattern of PM2.5 induced premature mortality in China

With rapid economic growth, China has witnessed increasingly frequent and severe haze and smog episodes over the past decade, posing serious health impacts to the Chinese population, especially those in densely populated city clusters. Quantification of the spatial and temporal variation of health impacts attributable to ambient fine particulate matter (PM_2.5) has important implications for China's policies on air pollution control. In this study, we evaluated the spatial distribution of premature deaths in China between 2000 and 2010 attributable to ambient PM_2.5 in accord with the Global Burden of Disease based on a high resolution population density map of China, satellite retrieved PM_2.5 concentrations, and provincial health data. Our results suggest that China's anthropogenic ambient PM_2.5 led to 1,255,400 premature deaths in 2010, 42% higher than the level in 2000. Besides increased PM_2.5 concentration, rapid urbanization has attracted large population migration into the more developed eastern coastal urban areas, intensifying the overall health impact. In addition, our analysis implies that health burdens were exacerbated in some developing inner provinces with high population density (e.g. Henan, Anhui, Sichuan) because of the relocation of more polluting and resource-intensive industries into these regions. In order to avoid such national level environmental inequities, China's regulations on PM_2.5 should not be loosened in inner provinces. Furthermore policies should create incentive mechanisms that can promote transfer of advanced production and emissions control technologies from the coastal regions to the interior regions.     

Health effects from Sahara dust episodes in Europe: Literature review and research gaps

The adverse consequences of particulate matter (PM) on human health have been well documented. Recently, special attention has been given to mineral dust particles, which may be a serious health threat. The main global source of atmospheric mineral dust is the Sahara desert, which produces about half of the annual mineral dust. Sahara dust transport can lead to PM levels that substantially exceed the established limit values. A review was undertaken using the ISI web of knowledge database with the objective to identify all studies presenting results on the potential health impact from Sahara dust particles. The review of the literature shows that the association of fine particles, PM_2.5, with total or cause‐specific daily mortality is not significant during Saharan dust intrusions. However, regarding coarser fractions PM₁₀ and PM_2.5–10 an explicit answer cannot be given. Some of the published studies state that they increase mortality during Sahara dust days while other studies find no association between mortality and PM₁₀ or PM_2.5–10. The main conclusion of this review is that health impact of Saharan dust outbreaks needs to be further explored. Considering the diverse outcomes for PM₁₀ and PM_2.5–10, future studies should focus on the chemical characterization and potential toxicity of coarse particles transported from Sahara desert mixed or not with anthropogenic pollutants. The results of this review may be considered to establish the objectives and strategies of a new European directive on ambient air quality. An implication for public policy in Europe is that to protect public health, anthropogenic sources of particulate pollution need to be more rigorously controlled in areas highly impacted by the Sahara dust.     

Projecting future air pollution-related mortality under a changing climate: progress,uncertainties and research needs

BackgroundClimate change may affect mortality associated with air pollutants, especially for fine particulate matter (PM_2.5) and ozone (O₃). Projection studies of such kind involve complicated modelling approaches with uncertainties.ObjectivesWe conducted a systematic review of researches and methods for projecting future PM_2.5-/O₃-related mortality to identify the uncertainties and optimal approaches for handling uncertainty.MethodsA literature search was conducted in October 2013, using the electronic databases: PubMed, Scopus, ScienceDirect, ProQuest, and Web of Science. The search was limited to peer-reviewed journal articles published in English from January 1980 to September 2013.DiscussionFifteen studies fulfilled the inclusion criteria. Most studies reported that an increase of climate change-induced PM_2.5 and O₃ may result in an increase in mortality. However, little research has been conducted in developing countries with high emissions and dense populations. Additionally, health effects induced by PM_2.5 may dominate compared to those caused by O₃, but projection studies of PM_2.5-related mortality are fewer than those of O₃-related mortality.There is a considerable variation in approaches of scenario-based projection researches, which makes it difficult to compare results. Multiple scenarios, models and downscaling methods have been used to reduce uncertainties. However, few studies have discussed what the main source of uncertainties is and which uncertainty could be most effectively reduced.ConclusionsProjecting air pollution-related mortality requires a systematic consideration of assumptions and uncertainties, which will significantly aid policymakers in efforts to manage potential impacts of PM_2.5 and O₃ on mortality in the context of climate change.     

Cause-specific premature death from ambient PM2.5 exposure in India: Estimate adjusted for baseline mortality

In India, more than a billion population is at risk of exposure to ambient fine particulate matter (PM_2.5) concentration exceeding World Health Organization air quality guideline, posing a serious threat to health. Cause-specific premature death from ambient PM_2.5 exposure is poorly known for India. Here we develop a non-linear power law (NLP) function to estimate the relative risk associated with ambient PM_2.5 exposure using satellite-based PM_2.5 concentration (2001 − 2010) that is bias-corrected against coincident direct measurements. We show that estimate of annual premature death in India is lower by 14.7% (19.2%) using NLP (integrated exposure risk function, IER) for assumption of uniform baseline mortality across India (as considered in the global burden of disease study) relative to the estimate obtained by adjusting for state-specific baseline mortality using GDP as a proxy. 486,100 (811,000) annual premature death in India is estimated using NLP (IER) risk functions after baseline mortality adjustment. 54.5% of premature death estimated using NLP risk function is attributed to chronic obstructive pulmonary disease (COPD), 24.0% to ischemic heart disease (IHD), 18.5% to stroke and the remaining 3.0% to lung cancer (LC). 44,900 (5900–173,300) less premature death is expected annually, if India achieves its present annual air quality target of 40 μg m^− 3. Our results identify the worst affected districts in terms of ambient PM_2.5 exposure and resulting annual premature death and call for initiation of long-term measures through a systematic framework of pollution and health data archive.     

WATCH

Abstract

The characteristics of fine particulate pollution (PM₁₀ and PM_2.5) were measured at urban and suburban sites in Jinan during the 2008–2009 heating and non-heating seasons. The results showed that PM₁₀ and PM_2.5 pollution was quite serious, and PM mass concentration was higher during the heating season than the non-heating season. PM was the highest in the chemical factory and lowest in the development zone. The mass concentrations of PM₁₀ and PM_2.5 were linearly related, and the mass concentration ratio of PM_2.5/PM₁₀ was up to 0.59 in urban areas. PM pollution in Jinan was related to local meteorological factors: PM_2.5 mass concentration and humidity were positively correlated, and PM_2.5 mass concentration was negatively correlated with both click on the temperature and wind speed, although wind speed varied more.     

Traffic-related air pollution and hyperactivity/inattention,dyslexia and dyscalculia in adolescents of the German GINIplus and LISAplus birth cohorts

BackgroundFew studies have examined the link between air pollution exposure and behavioural problems and learning disorders during late childhood and adolescence.ObjectivesTo determine whether traffic-related air pollution exposure is associated with hyperactivity/inattention, dyslexia and dyscalculia up to age 15 years using the German GINIplus and LISAplus birth cohorts (recruitment 1995–1999).MethodsHyperactivity/inattention was assessed using the German parent-completed (10 years) and self-completed (15 years) Strengths and Difficulties Questionnaire. Responses were categorized into normal versus borderline/abnormal. Parent-reported dyslexia and dyscalculia (yes/no) at age 10 and 15 years were defined using parent-completed questionnaires. Individual-level annual average estimates of nitrogen dioxide (NO₂), particulate matter (PM)₁₀ mass, PM_2.5 mass and PM_2.5 absorbance concentrations were assigned to each participant's birth, 10 year and 15 year home address. Longitudinal associations between the air pollutants and the neurodevelopmental outcomes were assessed using generalized estimation equations, separately for both study areas, and combined in a random-effects meta-analysis. Odds ratios and 95% confidence intervals are given per interquartile range increase in pollutant concentration.ResultsThe prevalence of abnormal/borderline hyperactivity/inattention scores and parental-reported dyslexia and dyscalculia at 15 years of age was 12.9%, 10.5% and 3.4%, respectively, in the combined population (N = 4745). In the meta- analysis, hyperactivity/inattention was associated with PM_2.5 mass estimated to the 10 and 15 year addresses (1.12 [1.01, 1.23] and 1.11 [1.01, 1.22]) and PM_2.5 absorbance estimated to the 10 and 15 year addresses (1.14 [1.05, 1.25] and 1.13 [1.04, 1.23], respectively).ConclusionsWe report associations suggesting a potential link between air pollution exposure and hyperactivity/inattention scores, although these findings require replication.     

Exposure to long-term air pollution and road traffic noise in relation to cholesterol: A cross-sectional study

BackgroundExposure to traffic noise and air pollution have both been associated with cardiovascular disease, though the mechanisms behind are not yet clear.ObjectivesWe aimed to investigate whether the two exposures were associated with levels of cholesterol in a cross-sectional design.MethodsIn 1993–1997, 39,863 participants aged 50–64 year and living in the Greater Copenhagen area were enrolled in a population-based cohort study. For each participant, non-fasting total cholesterol was determined in whole blood samples on the day of enrolment. Residential addresses 5-years preceding enrolment were identified in a national register and road traffic noise (L_den) were modeled for all addresses. For air pollution, nitrogen dioxide (NO₂) was modeled at all addresses using a dispersion model and PM_2.5 was modeled at all enrolment addresses using a land-use regression model. Analyses were done using linear regression with adjustment for potential confounders as well as mutual adjustment for the three exposures.ResultsBaseline residential exposure to the interquartile range of road traffic noise, NO₂ and PM_2.5 was associated with a 0.58 mg/dl (95% confidence interval: − 0.09; 1.25), a 0.68 mg/dl (0.22; 1.16) and a 0.78 mg/dl (0.22; 1.34) higher level of total cholesterol in single pollutant models, respectively. In two pollutant models with adjustment for noise in air pollution models and vice versa, the association between air pollution and cholesterol remained for both air pollution variables (NO₂: 0.72 (0.11; 1.34); PM_2.5: 0.70 (0.12; 1.28) mg/dl), whereas there was no association for noise (− 0.08 mg/dl). In three-pollutant models (NO₂, PM_2.5 and road traffic noise), estimates for NO₂ and PM_2.5 were slightly diminished (NO₂: 0.58 (− 0.05; 1.22); PM_2.5: 0.57 (− 0.02; 1.17) mg/dl).ConclusionsAir pollution and possibly also road traffic noise may be associated with slightly higher levels of cholesterol, though associations for the two exposures were difficult to separate.     

Annual and diurnal variations of gaseous and particulate pollutants in 31 provincial capital cities based on in situ air quality monitoring data from China National Environmental Monitoring Center

Long-term air quality data with high temporal and spatial resolutions are needed to understand some important processes affecting the air quality and corresponding environmental and health effects. The annual and diurnal variations of each criteria pollutant including PM_2.5 and PM₁₀ (particulate matter with aerodynamic diameter less than 2.5 μm and 10 μm, respectively), CO (carbon monoxide), NO₂ (nitrogen dioxide), SO₂ (sulfur dioxide) and O₃ (ozone) in 31 provincial capital cities between April 2014 and March 2015 were investigated by cluster analysis to evaluate current air pollution situations in China, and the cities were classified as severely, moderately, and slightly polluted cities according to the variations. The concentrations of air pollutants in winter months were significantly higher than those in other months with the exception of O₃, and the cities with the highest CO and SO₂ concentrations were located in northern China. The annual variation of PM_2.5 concentrations in northern cities was bimodal with comparable peaks in October 2014 and January 2015, while that in southern China was unobvious with slightly high PM_2.5 concentrations in winter months. The concentrations of particulate matter and trace gases from primary emissions (SO₂ and CO) and NO₂ were low in the afternoon (~ 16:00), while diurnal variation of O₃ concentrations was opposite to that of other pollutants with the highest values in the afternoon. The most polluted cities were mainly located in North China Plain, while slightly polluted cities mostly focus on southern China and the cities with high altitude such as Lasa. This study provides a basis for the formulation of future urban air pollution control measures in China.     

Seasonal variation in outdoor,indoor, and personal air pollution exposures of women using wood stoves in the Tibetan Plateau: Baseline assessment for an energy intervention study

Cooking and heating with coal and biomass is the main source of household air pollution in China and a leading contributor to disease burden. As part of a baseline assessment for a household energy intervention program, we enrolled 205 adult women cooking with biomass fuels in Sichuan, China and measured their 48-h personal exposure to fine particulate matter (PM_2.5) and carbon monoxide (CO) in winter and summer. We also measured the indoor 48-h PM_2.5 concentrations in their homes and conducted outdoor PM_2.5 measurements during 101 (74) days in summer (winter). Indoor concentrations of CO and nitrogen oxides (NO, NO₂) were measured over 48-h in a subset of ~ 80 homes. Women's geometric mean 48-h exposure to PM_2.5 was 80 μg/m³ (95% CI: 74, 87) in summer and twice as high in winter (169 μg/m³ (95% CI: 150, 190), with similar seasonal trends for indoor PM_2.5 concentrations (winter: 252 μg/m³; 95% CI: 215, 295; summer: 101 μg/m³; 95% CI: 91, 112). We found a moderately strong relationship between indoor PM_2.5 and CO (r = 0.60, 95% CI: 0.46, 0.72), and a weak correlation between personal PM_2.5 and CO (r = 0.41, 95% CI: − 0.02, 0.71). NO₂/NO ratios were higher in summer (range: 0.01 to 0.68) than in winter (range: 0 to 0.11), suggesting outdoor formation of NO₂ via reaction of NO with ozone is a more important source of NO₂ than biomass combustion indoors. The predictors of women's personal exposure to PM_2.5 differed by season. In winter, our results show that primary heating with a low-polluting fuel (i.e., electric stove or wood-charcoal) and more frequent kitchen ventilation could reduce personal PM_2.5 exposures. In summer, primary use of a gaseous fuel or electricity for cooking and reducing exposure to outdoor PM_2.5 would likely have the greatest impacts on personal PM_2.5 exposure.     

DNA hypomethylation and its mediation in the effects of fine particulate air pollution on cardiovascular biomarkers: A randomized crossover trial

BackgroundShort-term exposure to fine particulate matter (PM_2.5) air pollution has been associated with altered DNA methylation in observational studies, but it remains unclear whether this change mediates the effects on cardiovascular biomarkers.ObjectiveTo examine the impact of ambient PM_2.5 on gene-specific DNA methylation and its potential mediation in the acute effects of PM_2.5 on cardiovascular biomarkers.MethodsWe designed a randomized, double-blind crossover trial using true or sham air purifiers for 48 h among 35 healthy college students in Shanghai, China, in 2014. We measured blood global methylation estimated in long interspersed nucleotide element-1 (LINE‑1) and Alu repetitive elements, methylation in ten specific genes, and ten cardiovascular biomarkers. We used linear mixed-effect models to examine the associations between PM_2.5 and methylation. We also performed causal mediation analyses to evaluate the potential mediation of methylation in the associations between PM_2.5 and biomarkers.ResultsAir purification increased DNA methylation in repetitive elements and all candidate genes. An IQR increase (64 μg/m³) in PM_2.5 was significantly associated with reduction of methylation in LINE-1 (1.44%), one pro-inflammatory gene (CD40LG, 9.13%), two pro-coagulant genes (F3, 15.20%; SERPINE1, 3.69%), and two pro-vasoconstriction genes (ACE, 4.64%; EDN1, 9.74%). There was a significant mediated effect (17.82%, P = 0.03) of PM_2.5 on sCD40L protein through CD40LG hypomethylation. Hypomethylation in other candidate genes generally showed positive but non-significant mediation.ConclusionsThis intervention study provided robust human evidence that ambient PM_2.5 could induce rapid decreases in DNA methylation and consequently partly mediate its effects on cardiovascular biomarkers.     

Smoke-haze pollution: a review of the 1997 episode in Southeast Asia

In the second half of 1997, large areas in Southeast Asia were severely affected by a smoke-haze pollution episode caused by the emissions of an estimated 45,600 km² of vegetation that burnt on the Indonesian islands Kalimantan and Sumatra. To document the impacts of these fires on air quality, data for total suspended particulate matter (TSP) and for particulate matter below or equal to 10 microns in diameter (PM₁₀) from selected sites in Indonesia, Malaysia and Singapore are analysed in this paper. These data are supplemented by meteorological data, satellite images and a summary of related research. TSP was above 2,000 μg m^–3 for several days in Indonesian locations close to the most extensive fire activity. In Malaysia and Singapore, ambient particle concentrations increased to several times their average September levels. Characteristically for emissions from vegetation burning, the additional atmospheric particle loading during the smoke-haze episode was predominantly due to an increase of the fraction below or equal to 2.5 microns in diameter (PM_2.5). Due to the dominance of respirable particles (PM_2.5) in the smoke-haze, air quality reporting based on TSP or PM₁₀ may be inadequate to assess the health risk. Upgrading of PM_2.5 monitoring facilities is therefore needed. Reducing the probability of similar smoke-haze events in future would require appropriate fire use and smoke management strategies. Electronic Publication     

Estimation of exposure to atmospheric pollutants during pregnancy integrating space–time activity and indoor air levels: Does it make a difference?

Studies of air pollution effects during pregnancy generally only consider exposure in the outdoor air at the home address. We aimed to compare exposure models differing in their ability to account for the spatial resolution of pollutants, space–time activity and indoor air pollution levels. We recruited 40 pregnant women in the Grenoble urban area, France, who carried a Global Positioning System (GPS) during up to 3 weeks; in a subgroup, indoor measurements of fine particles (PM_2.5) were conducted at home (n = 9) and personal exposure to nitrogen dioxide (NO₂) was assessed using passive air samplers (n = 10). Outdoor concentrations of NO₂, and PM_2.5 were estimated from a dispersion model with a fine spatial resolution. Women spent on average 16 h per day at home. Considering only outdoor levels, for estimates at the home address, the correlation between the estimate using the nearest background air monitoring station and the estimate from the dispersion model was high (r = 0.93) for PM_2.5 and moderate (r = 0.67) for NO₂. The model incorporating clean GPS data was less correlated with the estimate relying on raw GPS data (r = 0.77) than the model ignoring space–time activity (r = 0.93). PM_2.5 outdoor levels were not to moderately correlated with estimates from the model incorporating indoor measurements and space–time activity (r = − 0.10 to 0.47), while NO₂ personal levels were not correlated with outdoor levels (r = − 0.42 to 0.03). In this urban area, accounting for space–time activity little influenced exposure estimates; in a subgroup of subjects (n = 9), incorporating indoor pollution levels seemed to strongly modify them.     

Inequalities in cumulative environmental burdens among three urbanized counties in California

Low-income communities and communities of color often suffer from multiple environmental hazards that pose risks to their health. Here we extended a cumulative environmental hazard inequality index (CEHII) – developed to assess inequalities in air pollution hazards – to compare the inequality among three urban counties in California: Alameda, San Diego, and Los Angeles. We included a metric for heat stress to the analysis because exposure to excessively hot weather is increasingly recognized as a threat to human health and well-being. We determined if inequalities from heat stress differed between the three regions and if this added factor modified the metric for inequality from cumulative exposure to air pollution. This analysis indicated that of the three air pollutants considered, diesel particulate matter had the greatest inequality, followed by nitrogen dioxide (NO₂) and fine particulate matter (PM_2.5). As measured by our index, the inequalities from cumulative exposure to air pollution were greater than those of single pollutants. Inequalities were significantly different among single air pollutant hazards within each region and between regions; however, inequalities from the cumulative burdens did not differ significantly between any two regions. Modeled absolute and relative heat stress inequalities were small except for relative heat stress in San Diego which had the second highest inequality. Our analysis, techniques, and results provide useful insights for policy makers to assess inequalities between regions and address factors that contribute to overall environmental inequality within each region.     

Personal exposure to fine particulate matter and blood pressure: A role of angiotensin converting enzyme and its DNA methylation

BackgroundThe underlying intermediate mechanisms about the association between fine particulate matter (PM_2.5) air pollution and blood pressure (BP) were unclear. Few epidemiological studies have explored the potential mediation effects of angiotensin-converting enzyme (ACE) and its DNA methylation.MethodsWe designed a longitudinal panel study with 4 follow-ups among 36 healthy college students in Shanghai, China from December 17, 2014 to July 11, 2015. We measured personal real-time exposure to PM_2.5, serum ACE level, and blood methylation of ACE gene and the repetitive elements. We applied linear mixed-effects models to examine the effects of PM_2.5 on ACE protein, DNA methylation and BP markers. Furthermore, we conducted mediation analyses to evaluate the potential pathways.ResultsAn interquartile range increase (26.78 μg/m³) in 24-h average exposure to PM_2.5 was significantly associated with 1.12 decreases in ACE average methylation (%5mC), 13.27% increase in ACE protein, and increments of 1.13 mmHg in systolic BP, 0.66 mmHg in diastolic BP and 0.82 mmHg in mean arterial pressure. ACE hypomethylation mediated 11.78% (P = 0.03) of the elevated ACE protein by PM_2.5. Increased ACE protein accounted for 3.90 ~ 13.44% (P = 0.35 ~ 0.68) of the elevated BP by PM_2.5. Repetitive-element methylation was also decreased but did not significantly mediate the association between PM_2.5 and BP.ConclusionsThis investigation provided strong evidence that short-term exposure to PM_2.5 was significantly associated with BP, ACE protein and ACE methylation. Our findings highlighted a possible involvement of ACE and ACE methylation in the effects of PM_2.5 on elevating BP.     

Acute health impacts of airborne particles estimated from satellite remote sensing

Satellite-based remote sensing provides a unique opportunity to monitor air quality from space at global, continental, national and regional scales. Most current research focused on developing empirical models using ground measurements of the ambient particulate. However, the application of satellite-based exposure assessment in environmental health is still limited, especially for acute effects, because the development of satellite PM_2.5 model depends on the availability of ground measurements. We tested the hypothesis that MODIS AOD (aerosol optical depth) exposure estimates, obtained from NASA satellites, are directly associated with daily health outcomes. Three independent healthcare databases were used: unscheduled outpatient visits, hospital admissions, and mortality collected in Beijing metropolitan area, China during 2006. We use generalized linear models to compare the short-term effects of air pollution assessed by ground monitoring (PM₁₀) with adjustment of absolute humidity (AH) and AH-calibrated AOD. Across all databases we found that both AH-calibrated AOD and PM₁₀ (adjusted by AH) were consistently associated with elevated daily events on the current day and/or lag days for cardiovascular diseases, ischemic heart diseases, and COPD. The relative risks estimated by AH-calibrated AOD and PM₁₀ (adjusted by AH) were similar. Additionally, compared to ground PM₁₀, we found that AH-calibrated AOD had narrower confidence intervals for all models and was more robust in estimating the current day and lag day effects. Our preliminary findings suggested that, with proper adjustment of meteorological factors, satellite AOD can be used directly to estimate the acute health impacts of ambient particles without prior calibrating to the sparse ground monitoring networks.     

Associations among plasma metabolite levels and short-term exposure to PM2.5 and ozone in a cardiac catheterization cohort

RationaleExposure to ambient particulate matter (PM) and ozone has been associated with cardiovascular disease (CVD). However, the mechanisms linking PM and ozone exposure to CVD remain poorly understood.ObjectiveThis study explored associations between short-term exposures to PM with a diameter < 2.5 μm (PM_2.5) and ozone with plasma metabolite concentrations.Methods and resultsWe used cross-sectional data from a cardiac catheterization cohort at Duke University, North Carolina (NC), USA, accumulated between 2001 and 2007. Amino acids, acylcarnitines, ketones and total non-esterified fatty acid plasma concentrations were determined in fasting samples. Daily concentrations of PM_2.5 and ozone were obtained from a Bayesian space-time hierarchical model, matched to each patient's residential address. Ten metabolites were selected for the analysis based on quality criteria and cluster analysis. Associations between metabolites and PM_2.5 or ozone were analyzed using linear regression models adjusting for long-term trend and seasonality, calendar effects, meteorological parameters, and participant characteristics.We found delayed associations between PM_2.5 or ozone and changes in metabolite levels of the glycine-ornithine-arginine metabolic axis and incomplete fatty acid oxidation associated with mitochondrial dysfunction. The strongest association was seen for an increase of 8.1 μg/m³ in PM_2.5 with a lag of one day and decreased mean glycine concentrations (− 2.5% [95% confidence interval: − 3.8%; − 1.2%]).ConclusionsShort-term exposures to ambient PM_2.5 and ozone is associated with changes in plasma concentrations of metabolites in a cohort of cardiac catheterization patients. Our findings might help to understand the link between air pollution and cardiovascular disease.     

Association between long-term exposure to air pollution and mortality in France: A 25-year follow-up study

IntroductionLong-term exposure to air pollution (AP) has been shown to have an impact on mortality in numerous countries, but since 2005 no data exists for France.ObjectivesWe analyzed the association between long-term exposure to air pollution and mortality at the individual level in a large French cohort followed from 1989 to 2013.MethodsThe study sample consisted of 20,327 adults working at the French national electricity and gas company EDF-GDF. Annual exposure to PM₁₀, PM_10–2.5, PM_2.5, NO₂, O₃, SO₂, and benzene was assessed for the place of residence of participants using a chemistry-transport model and taking residential history into account. Hazard ratios were estimated using a Cox proportional-hazards regression model, adjusted for selected individual and contextual risk factors. Hazard ratios were computed for an interquartile range (IQR) increase in air pollutant concentrations.ResultsThe cohort recorded 1967 non-accidental deaths. Long-term exposures to baseline PM_2.5, PM_10-25, NO₂ and benzene were associated with an increase in non-accidental mortality (Hazard Ratio, HR = 1.09; 95% CI: 0.99, 1.20 per 5.9 μg/m³, PM_10-25; HR = 1.09;95% CI: 1.04, 1.15 per 2.2 μg/m³, NO₂: HR = 1.14; 95% CI: 0.99, 1.31 per 19.3 μg/m³ and benzene: HR = 1.10; 95% CI: 1.00, 1.22 per 1.7 μg/m³).The strongest association was found for PM₁₀: HR = 1.14; 95% CI: 1.05, 1.25 per 7.8 μg/m³. PM₁₀, PM_10-25 and SO₂ were associated with non-accidental mortality when using time varying exposure. No significant associations were observed between air pollution and cardiovascular and respiratory mortality.ConclusionLong-term exposure to fine particles, nitrogen dioxide, sulfur dioxide and benzene is associated with an increased risk of non-accidental mortality in France. Our results strengthen existing evidence that outdoor air pollution is a significant environmental risk factor for mortality. Due to the limited sample size and the nature of our study (occupational), further investigations are needed in France with a larger representative population sample.     

Recent versus chronic exposure to particulate matter air pollution in association with neurobehavioral performance in a panel study of primary schoolchildren

Children's neuropsychological abilities are in a developmental stage. Recent air pollution exposure and neurobehavioral performance are scarcely studied. In a panel study, we repeatedly administered to each child the following neurobehavioral tests: Stroop Test (selective attention) and Continuous Performance Test (sustained attention), Digit Span Forward and Backward Tests (short-term memory), and Digit-Symbol and Pattern Comparison Tests (visual information processing speed). At school, recent inside classroom particulate matter ≤ 2.5 or 10 μm exposure (PM_2.5, PM₁₀) was monitored on each examination day. At the child's residence, recent (same day up to 2 days before) and chronic (365 days before examination) exposures to PM_2.5, PM₁₀ and black carbon (BC) were modeled. Repeated neurobehavioral test performances (n = 894) of the children (n = 310) reflected slower Stroop Test (p = 0.05) and Digit-Symbol Test (p = 0.01) performances with increasing recent inside classroom PM_2.5 exposure. An interquartile range (IQR) increment in recent residential outdoor PM_2.5 exposure was associated with an increase in average latency of 0.087 s (SE: ± 0.034; p = 0.01) in the Pattern Comparison Test. Regarding chronic exposure at residence, an IQR increment of PM_2.5 exposure was associated with slower performances in the Continuous Performance (9.45 ± 3.47 msec; p = 0.007) and Stroop Tests (59.9 ± 26.5 msec; p = 0.02). Similar results were obtained for PM₁₀ exposure. In essence, we showed differential neurobehavioral changes robustly and adversely associated with recent or chronic ambient exposure to PM air pollution at residence, i.e., with recent exposure for visual information processing speed (Pattern Comparison Test) and with chronic exposure for sustained and selective attention.     

Modelling future impacts of air pollution using the multi-scale UK Integrated Assessment Model (UKIAM)

Integrated assessment modelling has evolved to support policy development in relation to air pollutants and greenhouse gases by providing integrated simulation tools able to produce quick and realistic representations of emission scenarios and their environmental impacts without the need to re-run complex atmospheric dispersion models. The UK Integrated Assessment Model (UKIAM) has been developed to investigate strategies for reducing UK emissions by bringing together information on projected UK emissions of SO₂, NO_x, NH₃, PM₁₀ and PM_2.5, atmospheric dispersion, criteria for protection of ecosystems, urban air quality and human health, and data on potential abatement measures to reduce emissions, which may subsequently be linked to associated analyses of costs and benefits. We describe the multi-scale model structure ranging from continental to roadside, UK emission sources, atmospheric dispersion of emissions, implementation of abatement measures, integration with European-scale modelling, and environmental impacts. The model generates outputs from a national perspective which are used to evaluate alternative strategies in relation to emissions, deposition patterns, air quality metrics and ecosystem critical load exceedance. We present a selection of scenarios in relation to the 2020 Business-As-Usual projections and identify potential further reductions beyond those currently being planned.     

Modeling indoor air pollution of outdoor origin in homes of SAPALDIA subjects in Switzerland

Given the shrinking spatial contrasts in outdoor air pollution in Switzerland and the trends toward tightly insulated buildings, the Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults (SAPALDIA) needs to understand to what extent outdoor air pollution remains a determinant for residential indoor exposure. The objectives of this paper are to identify determining factors for indoor air pollution concentrations of particulate matter (PM), ultrafine particles in the size range from 15 to 300 nm, black smoke measured as light absorbance of PM (PM_absorbance) and nitrogen dioxide (NO₂) and to develop predictive indoor models for SAPALDIA. Multivariable regression models were developed based on indoor and outdoor measurements among homes of selected SAPALDIA participants in three urban (Basel, Geneva, Lugano) and one rural region (Wald ZH) in Switzerland, various home characteristics and reported indoor sources such as cooking. Outdoor levels of air pollutants were important predictors for indoor air pollutants, except for the coarse particle fraction. The fractions of outdoor concentrations infiltrating indoors were between 30% and 66%, the highest one was observed for PM_absorbance. A modifying effect of open windows was found for NO₂ and the ultrafine particle number concentration. Cooking was associated with increased particle and NO₂ levels. This study shows that outdoor air pollution remains an important determinant of residential indoor air pollution in Switzerland.