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.     

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.     

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.     

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.     

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.     

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.     

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.     

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.     

Acute respiratory response to traffic-related air pollution during physical activity performance

BackgroundPhysical activity (PA) has beneficial, whereas exposure to traffic related air pollution (TRAP) has adverse, respiratory effects. Few studies, however, have examined if the acute effects of TRAP upon respiratory outcomes are modified depending on the level of PA.ObjectivesThe aim of our study was to disentangle acute effects of TRAP and PA upon respiratory outcomes and assess the impact of participants TRAP pre-exposure.MethodsWe conducted a real-world crossover study with repeated measures of 30 healthy adults. Participants completed four 2-h exposure scenarios that included either rest or intermittent exercise in high- and low-traffic environments. Measures of respiratory function were collected at three time points. Pre-exposure to TRAP was ascertained from land-use-modeled address-attributed values. Mixed-effects models were used to estimate the impact of TRAP and PA on respiratory measures as well as potential effect modifications.ResultsWe found that PA was associated with a statistically significant increases of FEV₁ (48.5 mL, p = 0.02), FEV₁/FVC (0.64%, p = 0.005) and FEF_25–75% (97.8 mL, p = 0.02). An increase in exposure to one unit (1 μg/m³) of PM_coarse was associated with a decrease in FEV₁ (− 1.31 mL, p = 0.02) and FVC (− 1.71 mL, p = 0.01), respectively. On the other hand, for an otherwise equivalent exposure an increase of PA by one unit (1%Heart rate max) was found to reduce the immediate negative effects of particulate matter (PM) upon PEF (PM_2.5, 0.02 L/min, p = 0.047; PM₁₀, 0.02 L/min p = 0.02; PM_coarse, 0.03 L/min, p = 0.02) and the several hours delayed negative effects of PM upon FVC (PM_coarse, 0.11 mL, p = 0.02). The negative impact of exposure to TRAP constituents on FEV₁/FVC and PEF was attenuated in those participants with higher TRAP pre-exposure levels.ConclusionsOur results suggest that associations between various pollutant exposures and respiratory measures are modified by the level of PA during exposure and TRAP pre-exposure of participants.     

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.     

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.     

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.     

Saharan dust,particulate matter and cause-specific mortality: A case–crossover study in Barcelona (Spain)

BackgroundStudies measuring health effects of Saharan dust based on large particulate matter (PM) fraction groups may be masking some effects. Long distant transport reduces the amount of heavier and larger particles in the Saharan air masses increasing the relative contribution of smaller particles that may be more innocuous. This study investigates the association between different PM fractions and daily mortality during Saharan and non-Saharan days in Barcelona, Spain.MethodsWe collected daily PM₁, PM_2.5–1 and PM_10–2.5 fractions, and cause-specific mortality (cardiovascular, respiratory and cerebrovascular) between March 2003 and December 2007. Changes of effects between Saharan and non-Saharan dust days were assessed using a time-stratified case–crossover design.ResultsDuring non-Saharan dust days we found statistically significant (p < 0.05) effects of PM_10–2.5 for cardiovascular (odds ratio for increase of an interquartile range, OR = 1.033, 95% confidence interval: 1.006–1.060) and respiratory mortality (OR = 1.044, 95% CI: 1.001–1.089). During Saharan dust days strongest cardiovascular effects were found for the same fraction (OR = 1.085, 95% CI: 1.017–1.158) with an indication of effect modification (p = 0.111). Effects of PM_2.5–1 during Saharan dust days were about the double than in non-dust days for cardiovascular and respiratory mortality, but these differences were not statistically significant.ConclusionOur results using independent fractions of PMs provide further evidence that the effects of short-term exposure to PM during Saharan dust days are associated with both cardiovascular and respiratory mortality. A better understanding of which of the different PM size fractions brought by Saharan dust is more likely to accelerate adverse effects may help better understand mechanisms of toxicity.     

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.     

Air pollution exposure increases the risk of rheumatoid arthritis: A longitudinal and nationwide study

ObjectiveRheumatoid arthritis (RA) has been associated with inhaled pollutants in several studies, and it is a disease of chronic inflammation. The association between air pollution and the risk of RA remains unclear. Therefore, we conducted this nationwide, retrospective, sex-stratification study to evaluate this association.MethodsWe collected data from the Longitudinal Health Insurance Database (LHID), maintained by the Taiwan Bureau of National Health Insurance, and the Taiwan Air Quality-Monitoring Database (TAQMD), released by the Taiwan Environmental Protection Agency. The TAQMD provides the daily concentrations of particulate matter with the aerodynamic diameter < 2.5 μm (PM_2.5) and nitrogen dioxide (NO₂) from 74 ambient air quality-monitoring stations distributed all over Taiwan during 1998–2010. The LHID and TAQMD were linked according to the residential areas of insurants and the areas where the air quality-monitoring stations were located. A residential area was defined according to the location of the clinic and hospital that treated acute upper respiratory tract infections. The yearly average air pollutant concentrations were categorized into 4 levels based on quartiles. We evaluated the risk of RA in residents exposed to 4 levels of PM_2.5 and NO₂ concentrations.ResultsWe detected an increased risk of RA in participants exposed to PM_2.5 and NO₂. Among four quartiles of NO₂ concentration, namely Q1, Q2, Q3, and Q4, the adjusted hazard ratios (aHRs) in Q2, Q3, and Q4 compared with that in Q1 were 1.07 (95% confidence interval [CI] = 0.76–1.50), 1.63 (95% CI = 1.16–2.31),and 1.49 (95% CI = 1.05–2.12), respectively. Regarding the PM_2.5 concentrations, the aHRs after exposure to the Q2, Q3, and Q4 levels were 1.22 (95% CI = 0.85–1.74), 1.15 (95% CI = 0.82–1.62), and 0.79 (95% CI = 0.53–1.16), respectively.ConclusionThe results of this nationwide study suggest an increased risk of RA in residents exposed to NO₂.     

Air pollution exposure and telomere length in highly exposed subjects in Beijing,China: A repeated-measure study

BackgroundAmbient particulate matter (PM) exposure has been associated with short- and long-term effects on cardiovascular disease (CVD). Telomere length (TL) is a biomarker of CVD risk that is modified by inflammation and oxidative stress, two key pathways for PM effects. Whether PM exposure modifies TL is largely unexplored.ObjectivesTo investigate effects of PM on blood TL in a highly-exposed population.MethodsWe measured blood TL in 120 blood samples from truck drivers and 120 blood samples from office workers in Beijing, China. We measured personal PM_2.5 and Elemental Carbon (EC, a tracer of traffic particles) using light-weight monitors. Ambient PM₁₀ was obtained from local monitoring stations. We used covariate-adjusted regression models to estimate percent changes in TL per an interquartile-range increase in exposure.ResultsCovariate-adjusted TL was higher in drivers (mean = 0.87, 95%CI: 0.74; 1.03) than in office workers (mean = 0.79, 95%CI: 0.67; 0.93; p = 0.001). In all participants combined, TL increased in association with personal PM_2.5 (+ 5.2%, 95%CI: 1.5; 9.1; p = 0.007), personal EC (+ 4.9%, 95%CI: 1.2; 8.8; p = 0.01), and ambient PM₁₀ (+ 7.7%, 95%CI: 3.7; 11.9; p < 0.001) on examination days. In contrast, average ambient PM₁₀ over the 14 days before the examinations was significantly associated with shorter TL (− 9.9%, 95%CI: − 17.6; − 1.5; p = 0.02).ConclusionsShort-term exposure to ambient PM is associated with increased blood TL, consistent with TL roles during acute inflammatory responses. Longer exposures may shorten TL as expected after prolonged pro-oxidant exposures. The observed TL alterations may participate in the biological pathways of short- and long-term PM effects.     

The mortality effect of ship-related fine particulate matter in the Sydney greater metropolitan region of NSW,Australia

This study investigates the mortality effect of primary and secondary PM_2.5 related to ship exhaust in the Sydney greater metropolitan region of Australia. A detailed inventory of ship exhaust emissions was used to model a) the 2010/11 concentration of ship-related PM_2.5 across the region, and b) the reduction in PM_2.5 concentration that would occur if ships used distillate fuel with a 0.1% sulfur content at berth or within 300 km of Sydney. The annual loss of life attributable to 2010/11 levels of ship-related PM_2.5 and the improvement in survival associated with use of low-sulfur fuel were estimated from the modelled concentrations.In 2010/11, approximately 1.9% of the region-wide annual average population weighted-mean concentration of all natural and human-made PM_2.5 was attributable to ship exhaust, and up to 9.4% at suburbs close to ports. An estimated 220 years of life were lost by people who died in 2010/11 as a result of ship exhaust-related exposure (95% CI_β: 140–290, where CI_β is the uncertainty in the concentration-response coefficient only). Use of 0.1% sulfur fuel at berth would reduce the population weighted-mean concentration of PM_2.5 related to ship exhaust by 25% and result in a gain of 390 life-years over a twenty year period (95% CI_β: 260–520). Use of 0.1% sulfur fuel within 300 km of Sydney would reduce the concentration by 56% and result in a gain of 920 life-years over twenty years (95% CI_β: 600–1200).Ship exhaust is an important source of human exposure to PM_2.5 in the Sydney greater metropolitan region. This assessment supports intervention to reduce ship emissions in the GMR. Local strategies to limit the sulfur content of fuel would reduce exposure and will become increasingly beneficial as the shipping industry expands. A requirement for use of 0.1% sulfur fuel by ships within 300 km of Sydney would provide more than twice the mortality benefit of a requirement for ships to use 0.1% sulfur fuel at berth.     

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.