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.     

The contributions to long-term health-relevant particulate matter at the UK EMEP supersites between 2010 and 2013: Quantifying the mitigation challenge

Human health burdens associated with long-term exposure to particulate matter (PM) are substantial. The metrics currently recommended by the World Health Organization for quantification of long-term health-relevant PM are the annual average PM₁₀ and PM_2.5 mass concentrations, with no low concentration threshold. However, within an annual average, there is substantial variation in the composition of PM associated with different sources. To inform effective mitigation strategies, therefore, it is necessary to quantify the conditions that contribute to annual average PM₁₀ and PM_2.5 (rather than just short-term episodic concentrations). PM₁₀, PM_2.5, and speciated water-soluble inorganic, carbonaceous, heavy metal and polycyclic aromatic hydrocarbon components are concurrently measured at the two UK European Monitoring and Evaluation Programme (EMEP) ‘supersites’ at Harwell (SE England) and Auchencorth Moss (SE Scotland). In this work, statistical analyses of these measurements are integrated with air-mass back trajectory data to characterise the ‘chemical climate’ associated with the long-term health-relevant PM metrics at these sites. Specifically, the contributions from different PM concentrations, months, components and geographic regions are detailed. The analyses at these sites provide policy-relevant conclusions on mitigation of (i) long-term health-relevant PM in the spatial domain for which these sites are representative, and (ii) the contribution of regional background PM to long-term health-relevant PM.At Harwell the mean (± 1 sd) 2010–2013 annual average concentrations were PM₁₀ = 16.4 ± 1.4 μg m^− 3 and PM_2.5 = 11.9 ± 1.1 μg m^− 3 and at Auchencorth PM₁₀ = 7.4 ± 0.4 μg m^− 3 and PM_2.5 = 4.1 ± 0.2 μg m^− 3. The chemical climate state at each site showed that frequent, moderate hourly PM₁₀ and PM_2.5 concentrations (defined as approximately 5–15 μg m^− 3 for PM₁₀ and PM_2.5 at Harwell and 5–10 μg m^− 3 for PM₁₀ at Auchencorth) determined the magnitude of annual average PM₁₀ and PM_2.5 to a greater extent than the relatively infrequent high, episodic PM₁₀ and PM_2.5 concentrations. These moderate PM₁₀ and PM_2.5 concentrations were derived across the range of chemical components, seasons and air-mass pathways, in contrast to the highest PM concentrations which tended to associate with specific conditions. For example, the largest contribution to moderate PM₁₀ and PM_2.5 concentrations – the secondary inorganic aerosol components, specifically NO₃⁻ – were accumulated during the arrival of trajectories traversing the spectrum of marine, UK, and continental Europe areas. Mitigation of the long-term health-relevant PM impact in the regions characterised by these two sites requires multilateral action, across species (and hence source sectors), both nationally and internationally; there is no dominant determinant of the long-term PM metrics to target.     

Long-term effects of elemental composition of particulate matter on inflammatory blood markers in European cohorts

BackgroundEpidemiological studies have associated long-term exposure to ambient particulate matter with increased mortality from cardiovascular and respiratory disorders. Systemic inflammation is a plausible biological mechanism behind this association. However, it is unclear how the chemical composition of PM affects inflammatory responses.ObjectivesTo investigate the association between long-term exposure to elemental components of PM and the inflammatory blood markers high-sensitivity C-reactive protein (hsCRP) and fibrinogen as part of the European ESCAPE and TRANSPHORM multi-center projects.MethodsIn total, 21,558 hsCRP measurements and 17,428 fibrinogen measurements from cross-sections of five and four cohort studies were available, respectively. Residential long-term concentrations of particulate matter < 10 μm (PM₁₀) and < 2.5 μm (PM_2.5) in diameter and selected elemental components (copper, iron, potassium, nickel, sulfur, silicon, vanadium, zinc) were estimated based on land-use regression models. Associations between components and inflammatory markers were estimated using linear regression models for each cohort separately. Cohort-specific results were combined using random effects meta-analysis. As a sensitivity analysis the models were additionally adjusted for PM mass.ResultsA 5 ng/m³ increase in PM_2.5 copper and a 500 ng/m³ increase in PM₁₀ iron were associated with a 6.3% [0.7; 12.3%] and 3.6% [0.3; 7.1%] increase in hsCRP, respectively. These associations between components and fibrinogen were slightly weaker. A 10 ng/m³ increase in PM_2.5 zinc was associated with a 1.2% [0.1; 2.4%] increase in fibrinogen; confidence intervals widened when additionally adjusting for PM_2.5.ConclusionsLong-term exposure to transition metals within ambient particulate matter, originating from traffic and industry, may be related to chronic systemic inflammation providing a link to long-term health effects of particulate matter.     

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.     

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.     

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.     

Exposure to fine particle matter,nitrogen dioxide and benzene during pregnancy and cognitive and psychomotor developments in children at 15 months of age

BackgroundPrenatal exposure to air pollutants has recently been identified as a potential risk factor for neuropsychological impairment.ObjectivesTo assess whether prenatal exposure to fine particulate matter (PM_2.5), nitrogen dioxide (NO₂) and benzene were associated with impaired development in infants during their second year of life.MethodsRegression analyses, based on 438 mother–child pairs, were performed to estimate the association between mother exposure to air pollutants during pregnancy and neurodevelopment of the child. The average exposure to PM_2.5, NO₂ and benzene over the whole pregnancy was calculated for each woman. During the second year of life, infant neuropsychological development was assessed using the Bayley Scales of Infant Development. Regression analyses were performed to estimate the association between exposure and outcomes, accounting for potential confounders.ResultsWe estimated that a 1 μg/m³ increase during pregnancy in the average levels of PM_2.5 was associated with a − 1.14 point decrease in motor score (90% CI: − 1.75; − 0.53) and that a 1 μg/m³ increase of NO₂ exposure was associated with a − 0.29 point decrease in mental score (90% CI: − 0.47; − 0.11). Benzene did not show any significant association with development. Considering women living closer (≤ 100 m) to metal processing activities, we found that motor scores decreased by − 3.20 (90% CI: − 5.18; − 1.21) for PM_2.5 and − 0.51 (− 0.89; − 0.13) for NO₂, while mental score decreased by − 2.71 (90% CI: − 4.69; − 0.74) for PM_2.5, and − 0.41 (9% CI: − 0.76; − 0.06) for NO₂.ConclusionsOur findings suggest that prenatal residential exposure to PM_2.5 and NO₂ adversely affects infant motor and cognitive developments. This negative effect could be higher in the proximity of metal processing plants.     

A method to derive the relationship between the annual and short-term air quality limits—Analysis using the WHO Air Quality Guidelines for health protection

The World Health Organization (WHO) Air Quality Guidelines (AQG) were launched in 2006, but gaps remain in evidence on health impacts and relationships between short-term and annual AQG needed for health protection. We tested whether relationships between WHO short-term and annual AQG for particulates (PM₁₀ and PM_2.5) and nitrogen dioxide (NO₂) are concordant worldwide and derived the annual limits for sulfur dioxide (SO₂) and ozone (O₃) based on the short-term AQG. We obtained air pollutant data over seven years (2004–2010) in seven cities from Asia-Pacific, North America and Europe. Based on probability distribution concept using maximum as the short-term limit and arithmetic mean as the annual limit, we developed a new method to derive limit value one from another in each paired limits for each pollutant with capability to account for allowable exceedances. We averaged the limit derived each year for each city, then used meta-analysis to pool the limit values in all cities. Pooled mean short-term limit for NO₂ (140.5 μg/m³ [130.6–150.4]) was significantly lower than the WHO AQG of 200 μg/m³ while for PM₁₀ (46.4 μg/m³ [95CI:42.1–50.7]) and PM_2.5 (28.6 μg/m³ [24.5–32.6]) were not significantly different from the WHO AQG of 50 and 25 μg/m³ respectively. Pooled mean annual limits for SO₂ and O₃ were 4.6 μg/m³ [3.7–5.5] and 27.0 μg/m³ [21.7–32.2] respectively. Results were robust in various sensitivity analyses. The distribution relationships between the current WHO short-term and annual AQG are supported by empirical data from seven cities for PM₁₀ and PM_2.5, but not for NO₂. The short-term AQG for NO₂ should be lowered for concordance with the selected annual AQG for health protection.     

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.     

Exposure to coarse particulate matter during gestation and birth weight in the U.S.

Few studies have explored the relationship between coarse particles (PM_10-2.5) and adverse birth outcomes. We examined associations between gestational exposure of PM_10-2.5 and birth weight. U.S. birth certificates data (1999–2007) were acquired for 8,017,865 births. Gestational and trimester exposures of PM_10-2.5 were estimated using co-located PM₁₀ and PM_2.5 monitors ≤ 35 km from the population-weighted centroid of mothers' residential counties. A linear regression model was applied, adjusted by potential confounders. As sensitivity analyses, we explored alternative PM_10-2.5 estimations, adjustment for PM_2.5, and stratification by regions. Gestational exposure to PM_10-2.5 was associated with 6.6 g (95% Confidence Interval: 5.9, 7.2) lower birth weight per interquartile range increase (7.8 μg/m³) in PM_10-2.5 exposures. All three trimesters showed associations. Under different exposure methods for PM_10-2.5, associations remained consistent but with different magnitudes. Results were robust after adjusting for PM_2.5, and regional analyses showed associations in all four regions with larger estimates in the South. Our results suggest that PM_10-2.5 is associated with birth weight in addition to PM_2.5. Regional heterogeneity may reflect differences in population, measurement error, region-specific emission pattern, or different chemical composition within PM_10-2.5. Most countries do not set health-based standards for PM_10-2.5, but our findings indicate potentially important health effects of PM_10-2.5.     

Chronic disease prevalence in women and air pollution — A 30-year longitudinal cohort study

BackgroundAir pollution, such as fine particulate matter (PM_2.5), can increase risk of adverse health events among people with heart disease, diabetes, asthma and chronic obstructive pulmonary disease (COPD) by aggravating these conditions. Identifying the influence of PM_2.5 on prevalence of these conditions may help target interventions to reduce disease morbidity among high-risk populations.ObjectivesThe objective of this study is to measure the association of exposure of PM_2.5 with prevalence risk of various chronic diseases among a longitudinal cohort of women.MethodsWomen from Ontario who enrolled in the Canadian National Breast Screening Study (CNBSS) from 1980 to 1985 (n = 29,549) were linked to provincial health administrative data from April 1, 1992 to March 31, 2013 to determine the prevalence of major chronic disease and conditions (heart disease, diabetes, asthma, COPD, acute myocardial infarction, angina, stroke and cancers). Exposure to PM_2.5 was measured using satellite data collected from January 1, 1998 to December 31, 2006 and assigned to resident postal-code at time of entry into study. Poisson regression models were used to describe the relationship between exposure to ambient PM_2.5 and chronic disease prevalence. Prevalence rate ratios (PRs) were estimated while adjusting for potential confounders: baseline age, smoking, BMI, marital status, education and occupation. Separate models were run for each chronic disease and condition.ResultsCongestive heart failure (PR = 1.31, 95% CI: 1.13, 1.51), diabetes (PR = 1.28, 95% CI: 1.16, 1.41), ischemic heart disease (PR = 1.22, 95% CI: 1.14, 1.30), and stroke (PR = 1.21, 95% CI: 1.09, 1.35) showed over a 20% increase in PRs per 10 μg/m³ increase in PM_2.5 after adjusting for risk factors. Risks were elevated in smokers and those with BMI greater than 30.ConclusionsThis study estimated significant elevated prevalent rate ratios per unit increase in PM_2.5 in nine of the ten chronic diseases studied.     

Status and characteristics of ambient PM2.5 pollution in global megacities

Ambient PM_2.5 pollution is a substantial threat to public health in global megacities. This paper reviews the PM_2.5 pollution of 45 global megacities in 2013, based on mass concentration from official monitoring networks and composition data reported in the literature. The results showed that the five most polluted megacities were Delhi, Cairo, Xi'an, Tianjin and Chengdu, all of which had an annual average concentration of PM_2.5 greater than 89 μg/m³. The five cleanest megacities were Miami, Toronto, New York, Madrid and Philadelphia, the annual averages of which were less than 10 μg/m³. Spatial distribution indicated that the highly polluted megacities are concentrated in east-central China and the Indo-Gangetic Plain. Organic matter and SNA (sum of sulfate, nitrate and ammonium) contributed 30% and 36%, respectively, of the average PM_2.5 mass for all megacities. Notable seasonal variation of PM_2.5 polluted days was observed, especially for the polluted megacities of China and India, resulting in frequent heavy pollution episodes occurring during more polluted seasons such as winter. Marked differences in PM_2.5 pollution between developing and developed megacities require more effort on local emissions reduction as well as global cooperation to address the PM_2.5 pollution of those megacities mainly in Asia.     

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.     

Prenatal particulate air pollution and neurodevelopment in urban children: Examining sensitive windows and sex-specific associations

BackgroundBrain growth and structural organization occurs in stages beginning prenatally. Toxicants may impact neurodevelopment differently dependent upon exposure timing and fetal sex.ObjectivesWe implemented innovative methodology to identify sensitive windows for the associations between prenatal particulate matter with diameter ≤ 2.5 μm (PM_2.5) and children's neurodevelopment.MethodsWe assessed 267 full-term urban children's prenatal daily PM_2.5 exposure using a validated satellite-based spatio-temporally resolved prediction model. Outcomes included IQ (WISC-IV), attention (omission errors [OEs], commission errors [CEs], hit reaction time [HRT], and HRT standard error [HRT-SE] on the Conners' CPT-II), and memory (general memory [GM] index and its components — verbal [VEM] and visual [VIM] memory, and attention-concentration [AC] indices on the WRAML-2) assessed at age 6.5 ± 0.98 years. To identify the role of exposure timing, we used distributed lag models to examine associations between weekly prenatal PM_2.5 exposure and neurodevelopment. Sex-specific associations were also examined.ResultsMothers were primarily minorities (60% Hispanic, 25% black); 69% had ≤ 12 years of education. Adjusting for maternal age, education, race, and smoking, we found associations between higher PM_2.5 levels at 31–38 weeks with lower IQ, at 20–26 weeks gestation with increased OEs, at 32–36 weeks with slower HRT, and at 22–40 weeks with increased HRT-SE among boys, while significant associations were found in memory domains in girls (higher PM_2.5 exposure at 18–26 weeks with reduced VIM, at 12–20 weeks with reduced GM).ConclusionsIncreased PM_2.5 exposure in specific prenatal windows may be associated with poorer function across memory and attention domains with variable associations based on sex. Refined determination of time window- and sex-specific associations may enhance insight into underlying mechanisms and identification of vulnerable subgroups.     

Associations between ultrafine and fine particles and mortality in five central European cities — Results from the UFIREG study

BackgroundEvidence on health effects of ultrafine particles (UFP) is still limited as they are usually not monitored routinely. The few epidemiological studies on UFP and (cause-specific) mortality so far have reported inconsistent results.ObjectivesThe main objective of the UFIREG project was to investigate the short-term associations between UFP and fine particulate matter (PM) < 2.5 μm (PM_2.5) and daily (cause-specific) mortality in five European Cities. We also examined the effects of PM < 10 μm (PM₁₀) and coarse particles (PM_2.5–10).MethodsUFP (20–100 nm), PM and meteorological data were measured in Dresden and Augsburg (Germany), Prague (Czech Republic), Ljubljana (Slovenia) and Chernivtsi (Ukraine). Daily counts of natural and cardio-respiratory mortality were collected for all five cities. Depending on data availability, the following study periods were chosen: Augsburg and Dresden 2011–2012, Ljubljana and Prague 2012–2013, Chernivtsi 2013–March 2014. The associations between air pollutants and health outcomes were assessed using confounder-adjusted Poisson regression models examining single (lag 0–lag 5) and cumulative lags (lag 0–1, lag 2–5, and lag 0–5). City-specific estimates were pooled using meta-analyses methods.ResultsResults indicated a delayed and prolonged association between UFP and respiratory mortality (9.9% [95%-confidence interval: − 6.3%; 28.8%] increase in association with a 6-day average increase of 2750 particles/cm³ (average interquartile range across all cities)). Cardiovascular mortality increased by 3.0% [− 2.7%; 9.1%] and 4.1% [0.4%; 8.0%] in association with a 12.4 μg/m³ and 4.7 μg/m³ increase in the PM_2.5- and PM_2.5–10-averages of lag 2–5.ConclusionsWe observed positive but not statistically significant associations between prolonged exposures to UFP and respiratory mortality, which were independent of particle mass exposures. Further multi-centre studies are needed investigating several years to produce more precise estimates on health effects of UFP.     

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.     

High resolution exposure modelling of heat and air pollution and the impact on mortality

BackgroundElevated temperature and air pollution have been associated with increased mortality. Exposure to heat and air pollution, as well as the density of vulnerable groups varies within cities. The objective was to investigate the extent of neighbourhood differences in mortality risk due to heat and air pollution in a city with a temperate maritime climate.MethodsA case-crossover design was used to study associations between heat, air pollution and mortality. Different thermal indicators and air pollutants (PM₁₀, NO₂, O₃) were reconstructed at high spatial resolution to improve exposure classification. Daily exposures were linked to individual mortality cases over a 15 year period.ResultsSignificant interaction between maximum air temperature (Ta_max) and PM₁₀ was observed. During “summer smog” days (Ta_max > 25 °C and PM₁₀ > 50 μg/m³), the mortality risk at lag 2 was 7% higher compared to the reference (Ta_max 15 °C and PM₁₀ 15 μg/m³). Persons above age 85 living alone were at highest risk.ConclusionWe found significant synergistic effects of high temperatures and air pollution on mortality. Single living elderly were the most vulnerable group. Due to spatial differences in temperature and air pollution, mortality risks varied substantially between neighbourhoods, with a difference up to 7%.     

Racial isolation and exposure to airborne particulate matter and ozone in understudied US populations: Environmental justice applications of downscaled numerical model output

BackgroundResearchers and policymakers are increasingly focused on combined exposures to social and environmental stressors, especially given how often these stressors tend to co-locate. Such exposures are equally relevant in urban and rural areas and may accrue disproportionately to particular communities or specific subpopulations.ObjectivesTo estimate relationships between racial isolation (RI), a measure of the extent to which minority racial/ethnic group members are exposed to only one another, and long-term particulate matter with an aerodynamic diameter of < 2.5 μ (PM_2.5) and ozone (O₃) levels in urban and nonurban areas of the eastern two-thirds of the US.MethodsLong-term (5 year average) census tract-level PM_2.5 and O₃ concentrations were calculated using output from a downscaler model (2002–2006). The downscaler uses a linear regression with additive and multiplicative bias coefficients to relate ambient monitoring data with gridded output from the Community Multi-scale Air Quality (CMAQ) model. A local, spatial measure of RI was calculated at the tract level, and tracts were classified by urbanicity, RI, and geographic region. We examined differences in estimated pollutant exposures by RI, urbanicity, and demographic subgroup (e.g., race/ethnicity, education, socioeconomic status, age), and used linear models to estimate associations between RI and air pollution levels in urban, suburban, and rural tracts.ResultsHigh RI tracts (≥ 80th percentile) had higher average PM_2.5 levels in each category of urbanicity compared to low RI tracts (< 20th percentile), with the exception of the rural West. Patterns in O₃ levels by urbanicity and RI differed by region. Linear models indicated that PM_2.5 concentrations were significantly and positively associated with RI. The largest association between PM_2.5 and RI was observed in the rural Midwest, where a one quintile increase in RI was associated with a 0.90 μg/m³ (95% confidence interval: 0.83, 0.99 μg/m³) increase in PM_2.5 concentration. Associations between O₃ and RI in the Northeast, Midwest and West were positive and highest in suburban and rural tracts, even after controlling for potential confounders such as percentage in poverty.ConclusionRI is associated with higher 5 year estimated PM_2.5 concentrations in urban, suburban, and rural census tracts, adding to evidence that segregation is broadly associated with disparate air pollution exposures. Disproportionate burdens to adverse exposures such as air pollution may be a pathway to racial/ethnic disparities in health.     

Respiratory medication sales and urban air pollution in Brussels (2005 to 2011)

BackgroundWe investigated the associations between daily sales of respiratory medication and air pollutants in the Brussels-Capital Region between 2005 and 2011.MethodsWe used over-dispersed Poisson Generalized Linear Models to regress daily individual reimbursement data of prescribed asthma and COPD medication from the social security database against each subject's residential exposure to outdoor particulate matter (PM₁₀) or NO₂ estimated, by interpolation from monitoring stations. We calculated cumulative risk ratios (RR) and their 95% confidence intervals (CI) for interquartile ranges (IQR) of exposure for different windows of past exposure for the entire population and for seven age groups.ResultsMedian daily concentrations of PM₁₀ and NO₂ were 25 μg/m³ (IQR = 17.1) and 38 μg/m³ (IQR = 20.5), respectively. PM₁₀ was associated with daily medication sales among individuals aged 13 to 64 y. For NO₂, significant associations were observed among all age groups except > 84 y. The highest RR were observed for NO₂, among adolescents, including three weeks lags (RR = 1.187 95%CI: 1.097–1.285).ConclusionThe associations found between temporal changes in exposure to air pollutants and daily sales of respiratory medication in Brussels indicate that urban air pollution contributes to asthma and COPD morbidity in the general population.     

Health effects of ambient air pollution: Do different methods for estimating exposure lead to different results?

BackgroundSpatially resolved exposure models are increasingly used in epidemiology. We previously reported that, although exhibiting a moderate correlation, pregnancy nitrogen dioxide (NO₂) levels estimated by the nearest air quality monitoring station (AQMS) model and a geostatistical model, showed similar associations with infant birth weight.ObjectivesWe extended this study by comparing a total of four exposure models, including two highly spatially resolved models: a land-use regression (LUR) model and a dispersion model. Comparisons were made in terms of predicted NO₂ and particle (aerodynamic diameter < 10 μm, PM₁₀) exposure and adjusted association with birth weight.MethodsThe four exposure models were implemented in two French metropolitan areas where 1026 pregnant women were followed as part of the EDEN mother–child cohort.ResultsCorrelations between model predictions were high (≥ 0.70), except for NO₂ between the AQMS and both the LUR (r = 0.54) and dispersion models (r = 0.63). Spatial variations as estimated by the AQMS model were greater for NO₂ (95%) than for PM₁₀ (22%). The direction of effect estimates of NO₂ on birth weight varied according to the exposure model, while PM₁₀ effect estimates were more consistent across exposure models.ConclusionsFor PM₁₀, highly spatially resolved exposure model agreed with the poor spatial resolution AQMS model in terms of estimated pollutant levels and health effects. For more spatially heterogeneous pollutants like NO₂, although predicted levels from spatially resolved models (all but AQMS) agreed with each other, our results suggest that some may disagree with each other as well as with the AQMS regarding the direction of the estimated health effects.