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.     

Fibrin clot structure is affected by levels of particulate air pollution exposure in patients with venous thrombosis

BackgroundParticulate air pollution is a risk factor for cardiovascular diseases and thrombosis. Long-term exposure to particulate matter with a diameter < 10 μm (PM₁₀) has been associated with an increased risk of venous thrombosis.ObjectivesThe aim of this study was to investigate whether or not particulate air pollution alters fibrin clot structure and thus modulates thrombosis risk.MethodsWe investigated fibrin polymerization by turbidity (maximum absorbance mOD), clot structure by confocal microscopy (fibre number per μm) and fibrin pore size by permeability (Ks × 10^− 10 cm²) in 103 patients with deep vein thrombosis and 121 healthy controls, for whom levels of air pollution exposure had been recorded. Exposure groups were defined by mean PM₁₀ concentrations over the 730 days before the event.ResultsWe found a higher average number of fibres per clot area in patients than controls, but no difference in Ks or fibre thickness. When the two groups were divided into high or low exposure to PM₁₀, a significantly denser fibrin clot network structure with thicker fibres (higher maximum absorbance, p < 0.05), decreased permeability (lower Ks value, p < 0.05) and higher average fibre numbers per clot area (p < 0.05) was observed in patients in the high exposure group compared to those with low exposure. There were no significant differences in fibrin clot structure between the two exposure levels in healthy subjects.ConclusionsPM₁₀ levels are associated with altered fibrin clot structure in patients with deep vein thrombosis but not in controls, suggesting that air pollution may trigger differences in fibrin clot structure only in patients predisposed to thrombotic disease.     

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.     

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.     

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.     

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.     

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.     

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.     

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.     

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.     

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.     

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.     

Short-term effects of air pollution on respiratory morbidity at Rio de Janeiro — Part II: Health assessment

The effects of air pollution on health have been studied worldwide. Given that air pollution triggers oxidative stress and inflammation, it is plausible that high levels of air pollutants cause higher number of hospitalisations. This study aimed to assess the impact of air pollution on the emergency hospitalisation for respiratory disease in Rio de Janeiro, Brazil. The study was divided in two parts: Part I specifically addressing the air pollution assessment and Part II addressing the health assessment. Accordingly, this Part II aimed to estimate the association between the concentrations of PM₁₀, SO₂ and CO observed in Rio de Janeiro and the number of emergency hospitalisations at a central hospital due to respiratory diseases. The pollutant concentrations were measured at two different sites in Rio de Janeiro, but the excess relative risks were calculated based on the concentrations observed at one of the sites, where limits were generally exceeded more frequently, between September 2000 and December 2005. A time series analysis was performed using the number of hospitalisations, divided in three categories (children until 1 year old, children aged between 1 and 5 years old and elderly with 65 years old or more) as independent variable, the concentrations of pollutants as dependent variables and temperature, relative humidity, long term trend, and seasonality as confounders. Data were analysed using generalised additive models with smoothing for some of the dependent variables. Results showed an excess risk of hospitalisation for respiratory disease higher than 2% per 10 μg m^− 3 increase in PM₁₀ concentrations for children under 5 years old, of 2% per 10 μg m^− 3 increase in SO₂ for elderly above 65 years old and around 0.1% per 10 μg m^− 3 increase in CO for children under 1 year and elderly. Other studies have found associations that are in agreement with the results achieved in this study.The study suggests that the ambient levels of air pollutants experienced in Rio de Janeiro between 2000 and 2005 were linked to the number of hospitalisations for respiratory diseases among children and elderly.     

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.     

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.     

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.     

Long-term exposure to traffic-related PM10 and decreased heart rate variability: Is the association restricted to subjects taking ACE inhibitors?

BackgroundAlterations in heart rate variability (HRV) are a potential link between exposure to traffic-related air pollution and cardiovascular mortality.ObjectivesWe investigated whether long-term exposure to traffic-related PM₁₀ (TPM₁₀) is associated with HRV in older subjects and/or in participants taking specific cardiovascular treatment or with self-reported heart disease.MethodsWe included 1607 subjects from the general population aged 50 to 72 years. These participants from the SAPALDIA cohort underwent ambulatory 24-hr electrocardiogram monitoring. Associations of average annual exposure to TPM₁₀ over 10 years with HRV parameters from time and frequency domains were estimated using multivariable mixed linear models. Effect estimates are expressed as percent changes in geometric means.ResultsHRV was only associated with TPM₁₀ in participants under ACE inhibitor therapy (N = 94). A 1 μg/m³ increment, approximately equivalent to an interquartile range, in 10 year average TPM₁₀ was associated with decrements of 14.5% (95% confidence interval (CI), − 25.9 to − 1.3) in high frequency (HF) power, of 4.5% (− 8.2 to − 0.5) in the standard deviation of all normal-to-normal RR intervals (SDNN), of 10.6% (− 18.5 to − 1.9) in total power (TP) and an increase of 9.2% (0.8 to 20.2) in the LF/HF power ratio.ConclusionsIn the absence of an overall effect our results suggest that alterations in HRV, a measure of autonomic control of the cardiac rhythm, may not be a central mechanism by which long-term exposure to TPM₁₀ increases cardiovascular mortality. Novel evidence on an effect in persons under ACE inhibitor treatment needs to be confirmed in future studies.     

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.     

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.