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.     

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.     

Measurement and health risk assessment of PM2.5, flame retardants,carbonyls and black carbon in indoor and outdoor air in kindergartens in Hong Kong

Indoor air pollution is closely related to children's health. Polybrominated diphenyl ethers (PBDEs) and dechlorane plus (DP) transmitted through indoor PM_2.5 and dust, along with carbonyl compounds and black carbon (BC) aerosol were analysed in five Hong Kong kindergartens. The results showed that 60% of the median PM_2.5 levels (1.3 × 10¹ to 2.9 × 10¹ μg/m³ for indoor; 9.5 to 8.8 × 10¹ μg/m³ for outdoor) in the five kindergartens were higher than the guidelines set by the World Health Organization (2.5 × 10¹ μg/m³). Indoor PM_2.5 mass concentrations were correlated with outdoor PM_2.5 in four of the kindergartens. The PBDEs (0.10–0.64 ng/m³ in PM_2.5; 0.30–2.0 × 10² ng/g in dust) and DP (0.05–0.10 ng/m³ in PM_2.5; 1.3–8.7 ng/g in dust) were detected in 100% of the PM_2.5 and dust samples. Fire retardant levels in the air were not correlated with the levels of dust in this study. The median BC concentrations varied by > 7-fold from 8.8 × 10² ng/m^− 3 to 6.7 × 10³ ng/m^− 3 and cooking events might have caused BC concentrations to rise both indoors and outdoors. The total concentrations of 16 carbonyls ranged from 4.7 × 10¹ μg/m³ to 9.3 × 10¹ μg/m³ indoors and from 1.9 × 10¹ μg/m³ to 4.3 × 10¹ μg/m³ outdoors, whilst formaldehyde was the most abundant air carbonyl. Indoor carbonyl concentrations were correlated with outdoor carbonyls in three kindergartens. The health risk assessment showed that hazard indexes (HIs) HIs of non-cancer risks from PBDEs and DPs were all lower than 0.08, whilst non-cancer HIs of carbonyl compounds ranged from 0.77 to 1.85 indoors and from 0.50 to 0.97 outdoors. The human intake of PBDEs and DP through inhalation of PM_2.5 accounted for 78% to 92% of the total intake. The cancer hazard quotients (HQs) of formaldehyde ranged from 4.5E − 05 to 2.1E − 04 indoors and from 1.9E − 05 to 6.2E − 05 outdoors. In general, the indoor air pollution in the five Hong Kong kindergartens might present adverse effects to children, although different schools showed distinct pollution levels, so indoor air quality might be improved through artificial measures. The data will be useful to developing a feasible management protocol for indoor environments.     

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.     

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.     

Effect of the shape of the exposure-response function on estimated hospital costs in a study on non-elective pneumonia hospitalizations related to particulate matter

ObjectiveWe used log-linear and log-log exposure-response (E-R) functions to model the association between PM_2.5 exposure and non-elective hospitalizations for pneumonia, and estimated the attributable hospital costs by using the effect estimates obtained from both functions.MethodsWe used hospital discharge data on 3519 non-elective pneumonia admissions from UZ Brussels between 2007 and 2012 and we combined a case-crossover design with distributed lag models. The annual averted pneumonia hospitalization costs for a reduction in PM_2.5 exposure from the mean (21.4 μg/m³) to the WHO guideline for annual mean PM_2.5 (10 μg/m³) were estimated and extrapolated for Belgium.ResultsNon-elective hospitalizations for pneumonia were significantly associated with PM_2.5 exposure in both models. Using a log-linear E-R function, the estimated risk reduction for pneumonia hospitalization associated with a decrease in mean PM_2.5 exposure to 10 μg/m³ was 4.9%. The corresponding estimate for the log-log model was 10.7%. These estimates translate to an annual pneumonia hospital cost saving in Belgium of €15.5 million and almost €34 million for the log-linear and log-log E-R function, respectively.DiscussionAlthough further research is required to assess the shape of the association between PM_2.5 exposure and pneumonia hospitalizations, we demonstrated that estimates for health effects and associated costs heavily depend on the assumed E-R function. These results are important for policy making, as supra-linear E-R associations imply that significant health benefits may still be obtained from additional pollution control measures in areas where PM levels have already been reduced.     

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.     

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.     

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.     

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.     

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.     

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.     

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%.     

Combustion particles emitted during church services: Implications for human respiratory health

Burning candles and incense generate particulate matter (PM) that produces poor indoor air quality and may cause human pulmonary problems. This study physically characterised combustion particles collected in a church during services. In addition, the emissions from five types of candles and two types of incense were investigated using a combustion chamber. The plasmid scission assay was used to determine the oxidative capacities of these church particles. The corresponding risk factor (CRf) was derived from the emission factor (Ef) and the oxidative DNA damage, and used to evaluate the relative respiratory exposure risks. Real-time PM measurements in the church during candle–incense burning services showed that the levels (91.6 μg/m³ for PM₁₀; 38.9 μg/m³ for PM_2.5) exceeded the European Union (EU) air quality guidelines. The combustion chamber testing, using the same environmental conditions, showed that the incense Ef for both PM₁₀ (490.6–587.9 mg/g) and PM_2.5 (290.1–417.2 mg/g) exceeded that of candles; particularly the PM_2.5 emissions. These CRf results suggested that the exposure to significant amounts of incense PM could result in a higher risk of oxidative DNA adducts (27.4–32.8 times) than tobacco PM. The generation and subsequent inhalation of PM during church activities may therefore pose significant risks in terms of respiratory health effects.     

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.     

Air pollution and diabetes association: Modification by type 2 diabetes genetic risk score

Exposure to ambient air pollution (AP) exposure has been linked to type 2 diabetes (T2D) risk. Evidence on the impact of T2D genetic variants on AP susceptibility is lacking. Compared to single variants, joint genetic variants contribute substantially to disease risk. We investigated the modification of AP and diabetes association by a genetic risk score (GRS) covering 63 T2D genes in 1524 first follow-up participants of the Swiss cohort study on air pollution and lung and heart diseases in adults. Genome-wide data and covariates were available from a nested asthma case-control study design. AP was estimated as 10-year mean residential particulate matter < 10 μm (PM₁₀). We computed count-GRS and weighted-GRS, and applied PM₁₀ interaction terms in mixed logistic regressions, on odds of diabetes. Analyses were stratified by pathways of diabetes pathology and by asthma status. Diabetes prevalence was 4.6% and mean exposure to PM₁₀ was 22 μg/m³. Odds of diabetes increased by 8% (95% confidence interval: 2, 14%) per T2D risk allele and by 35% (− 8, 97%) per 10 μg/m³ exposure to PM₁₀. We observed a positive interaction between PM₁₀ and count-GRS on diabetes [OR_interaction = 1.10 (1.01, 1.20)], associations being strongest among participants at the highest quartile of count-GRS [OR: 1.97 (1.00, 3.87)]. Stronger interactions were observed with variants of the GRS involved in insulin resistance [(OR_interaction = 1.22 (1.00, 1.50)] than with variants related to beta-cell function. Interactions with count-GRS were stronger among asthma cases. We observed similar results with weighted-GRS. Five single variants near GRB14, UBE2E2, PTPRD, VPS26A and KCNQ1 showed nominally significant interactions with PM₁₀ (P < 0.05). Our results suggest that genetic risk for T2D may modify susceptibility to air pollution through alterations in insulin sensitivity. These results need confirmation in diabetes cohort consortia.     

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.     

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.     

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.     

Long-term air pollution exposure and diabetes in a population-based Swiss cohort

Air pollution is an important risk factor for global burden of disease. There has been recent interest in its possible role in the etiology of diabetes mellitus. Experimental evidence is suggestive, but epidemiological evidence is limited and mixed. We therefore explored the association between air pollution and prevalent diabetes, in a population-based Swiss cohort.We did cross-sectional analyses of 6392 participants of the Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults [SAPALDIA], aged between 29 and 73 years. We used estimates of average individual home outdoor PM₁₀ [particulate matter <10 μm in diameter] and NO₂ [nitrogen dioxide] exposure over the 10 years preceding the survey. Their association with diabetes was modeled using mixed logistic regression models, including participants' study area as random effect, with incremental adjustment for confounders.There were 315 cases of diabetes (prevalence: 5.5% [95% confidence interval (CI): 2.8, 7.2%]). Both PM₁₀ and NO₂ were associated with prevalent diabetes with respective odds ratios of 1.40 [95% CI: 1.17, 1.67] and 1.19 [95% CI: 1.03, 1.38] per 10 μg/m³ increase in the average home outdoor level. Associations with PM₁₀ were generally stronger than with NO₂, even in the two-pollutant model. There was some indication that beta blockers mitigated the effect of PM₁₀. The associations remained stable across different sensitivity analyses.Our study adds to the evidence that long term air pollution exposure is associated with diabetes mellitus. PM₁₀ appears to be a useful marker of aspects of air pollution relevant for diabetes. This association can be observed at concentrations below air quality guidelines.