Low Levels Of Air Pollution Research Articles

Long-term exposure to fine particle elemental components and mortality in Europe: Results from six European administrative cohorts within the ELAPSE project

Evidence for the association between long-term exposure to ambient particulate matter components and mortality from natural causes is sparse and inconsistent. We evaluated this association in six large administrative cohorts in the framework of the Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE) project.We analyzed data from country-wide administrative cohorts in Norway, Denmark, the Netherlands, Belgium, Switzerland and in Rome (Italy). Annual 2010 mean concentrations of copper (Cu), iron (Fe), potassium (K), nickel (Ni), sulfur (S), silicon (Si), vanadium (V) and zinc (Zn) in fine particulate matter (PM2.5) were estimated using 100 × 100 m Europe-wide hybrid land use regression models assigned to the participants' residential addresses. We applied cohort-specific Cox proportional hazard models controlling for area- and individual-level covariates to evaluate associations with natural mortality. Two pollutant models adjusting for PM2.5 total mass or nitrogen dioxide (NO2) were also applied. We pooled cohort-specific estimates using a random effects meta-analysis.We included almost 27 million participants contributing more than 240 million person-years. All components except Zn were significantly associated with natural mortality [pooled Hazard Ratios (HRs) (95% CI): 1.037 (1.014, 1.060) per 5 ng/m3 Cu; 1.069 (1.031, 1.108) per 100 ng/m3 Fe; 1.039 (1.018, 1.062) per 50 ng/m3 K; 1.024 (1.006, 1.043) per 1 ng/m3 Ni; 1.036 (1.016, 1.057) per 200 ng/m3 S; 1.152 (1.048, 1.266) per 100 ng/m3 Si; 1.020 (1.006, 1.034) per 2 ng/m3 V]. Only K and Si were robust to PM2.5 or NO2 adjustment [pooled HRs (95% CI) per 50 ng/m3 in K: 1.025 (1.008, 1.044), 1.020 (0.999, 1.042) and per 100 ng/m3 in Si: 1.121 (1.039, 1.209), 1.068 (1.022, 1.117) adjusted for PM2.5 and NO2 correspondingly].Our findings indicate an association of natural mortality with most components, which was reduced after adjustment for PM2.5 and especially NO2.

New WHO global air quality guidelines: more pressure on nations to reduce air pollution levels

New WHO global air quality guidelines: more pressure on nations to reduce air pollution levels

Comparative Analysis of COVID-19 Prevalence in Coastal Versus Inland Populations of North Carolina

Statement of Significance This study aimed to assess geographic trends in COVID-19 cases and deaths across North Carolina (NC). Our study found that population-adjusted COVID-19 cases and deaths were lower in the coastal region of NC during the study period, independent of demographic composition and population-density within the region. This represents an interesting finding regarding COVID-19 transmission that deserves further investigation. One possible explanation for this finding is differing environmental conditions between the inland and coastal region. Background: Existing literature has explored the geographic and spatial variations in COVID-19 prevalence. Some studies suggest that the transmission and total prevalence of COVID-19 is diminished in areas with low levels of air pollution, high humidity, and more sunlight. The coastal regions of NC are more likely to have these environmental characteristics than the inland regions. Given these trends, we analyzed and compared population-adjusted COVID-19 case and death counts in the coastal and inland regions of NC. Methods: Time series data displaying the prevalence of population adjusted COVID-19 case and death counts from 15 March 2020 to 15 August 2020 were plotted for a variety of North Carolina regional and population density classifications. A local regression analysis was computed to further assess the observed relationships. Basic demographic characteristics were also compared for the coastal versus inland region. Results: There were fewer population-adjusted COVID-19 cases and deaths in the coastal region (889 cases/100,000; 12.5 deaths/100,000) than in the inland region (1426 cases/100,000; 23.5 deaths/100,000) at the endpoint of this study. This trend is observed even when controlling for population density, and in the absence of significant demographic differences between the two regions. Conclusions: The prevalence of population-adjusted COVID-19 cases and deaths was lower in coastal versus inland NC during this study period. Given that the NC coastal region is associated with lower pollution, higher humidity, and more exposure to sunlight, our findings suggest that more research should be done to explore the correlation between environmental variables and the spread of COVID-19.

Long term exposure to low level air pollution and mortality in eight European cohorts within the ELAPSE project: pooled analysis

ObjectiveTo investigate the associations between air pollution and mortality, focusing on associations below current European Union, United States, and World Health Organization standards and guidelines.DesignPooled analysis of eight cohorts.SettingMulticentre project...

Long-term exposure to low-level ambient air pollution and incidence of stroke and coronary heart disease: a pooled analysis of six European cohorts within the ELAPSE project

Long-term exposure to outdoor air pollution increases the risk of cardiovascular disease, but evidence is unclear on the health effects of exposure to pollutant concentrations lower than current EU and US standards and WHO guideline limits. Within the multicentre study Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE), we investigated the associations of long-term exposures to fine particulate matter (PM2·5), nitrogen dioxide (NO2), black carbon, and warm-season ozone (O3) with the incidence of stroke and acute coronary heart disease. We did a pooled analysis of individual data from six population-based cohort studies within ELAPSE, from Sweden, Denmark, the Netherlands, and Germany (recruited 1992-2004), and harmonised individual and area-level variables between cohorts. Participants (all adults) were followed up until migration from the study area, death, or incident stroke or coronary heart disease, or end of follow-up (2011-15). Mean 2010 air pollution concentrations from centrally developed European-wide land use regression models were assigned to participants' baseline residential addresses. We used Cox proportional hazards models with increasing levels of covariate adjustment to investigate the association of air pollution exposure with incidence of stroke and coronary heart disease. We assessed the shape of the concentration-response function and did subset analyses of participants living at pollutant concentrations lower than predefined values. From the pooled ELAPSE cohorts, data on 137 148 participants were analysed in our fully adjusted model. During a median follow-up of 17·2 years (IQR 13·8-19·5), we observed 6950 incident events of stroke and 10 071 incident events of coronary heart disease. Incidence of stroke was associated with PM2·5 (hazard ratio 1·10 [95% CI 1·01-1·21] per 5 μg/m3 increase), NO2 (1·08 [1·04-1·12] per 10 μg/m3 increase), and black carbon (1·06 [1·02-1·10] per 0·5 10-5/m increase), whereas coronary heart disease incidence was only associated with NO2 (1·04 [1·01-1·07]). Warm-season O3 was not associated with an increase in either outcome. Concentration-response curves indicated no evidence of a threshold below which air pollutant concentrations are not harmful for cardiovascular health. Effect estimates for PM2·5 and NO2 remained elevated even when restricting analyses to participants exposed to pollutant concentrations lower than the EU limit values of 25 μg/m3 for PM2·5 and 40 μg/m3 for NO2. Long-term air pollution exposure was associated with incidence of stroke and coronary heart disease, even at pollutant concentrations lower than current limit values. Health Effects Institute.

Impact of Air Pollution on High-Caliber Athletic Performance

BACKGROUND AND AIM: Athletes who regularly train and compete outdoors experience elevated levels of exposure to air pollutants due to high minute ventilation rates. While many sports committees use the US Environmental Protection Agency’s Air Quality Index (AQI) to monitor the safety of high pollution events, little is known about the effect of repeated exposure to lower levels of air pollution. To quantify the burden, we estimated the association between repeated exposure to particulate matter (PM2.5) and ozone and race performance of collegiate athletes using pollutant concentrations, two-pollutant (PM2.5 and ozone) version of the AQI, and a summed version of the AQI. METHODS: We aggregated data on 334 collegiate male track & field athletes from 46 universities across the United States during the years 2010-2014, comprising a total of 1,104 5-km meter race outcomes. Using distributed lag non-linear models (DLNMs), we analyzed the relationship between race performance and air pollution exposures 21 days prior to the race. We reported cumulative effect estimates for the change in average race time associated with increases in exposure from the 20th to 80th percentile. RESULTS:We observed a 12.8 (95% CI: 1.3, 24.2) second and 11.5 (95% CI: 0.8, 22.1) second increase in 5-km race times from 21 days of exposure to PM2.5 concentration (10.3 μg/m3 versus 4.9μg/m3) and ozone concentration (54.9ppm vs. 36.9ppm), respectively. Exposure measured by the two-pollutant AQI was not significantly associated with race time (95% CI: -5.23, 16.60); however, the association for summed two-pollutant AQI was similar to the associations for the individual pollutants (12.4 seconds, 95% CI: 1.8, 23.0). CONCLUSIONS:Training and competing at consistently higher levels of air pollution were associated with higher race times. This is a first step at identifying the association between pollution and running performance and a foundation for why coaches should consider approaches to reduce air pollution exposure. KEYWORDS: athletic performance, air pollution, particulate matter, ozone

Long-term exposure to low concentrations of air pollution and cause-specific mortality beyond cardiorespiratory disease: A Danish nationwide cohort study

BACKGROUND AND AIM: The association between air pollution and mortality from cardiorespiratory disease is well established, yet evidence for other causes is limited. We examined the associations of long-term exposure to air pollution with mortality from lower respiratory infection (LRI), diabetes, dementia, Alzheimer’s disease (AD), and psychiatric disease (PD) in a Danish nationwide cohort study. METHODS: We linked 3,083,227 subjects aged ≥30 years in 2000 to the Danish Cause of Death Registry until 2017. Annual mean concentrations of fine particulate matter (PM₂.₅), nitrogen dioxide (NO₂), and black carbon (BC) in 2010 at 100x100m resolution were estimated with European-wide hybrid land-use regression models developed within ELAPSE (Effects of Low-Level Air Pollution: A Study in Europe). We applied Cox proportional hazard models with age as time scale, parish as cluster, and adjusting for sex, country of origin, income, education, employment status, marital status, and parish and region-level indicators of income and employment. RESULTS:During the follow-up, 805,838 subject died: 30,578 from LRI, 20,735 from diabetes, 41,178 from dementia, 11,894 from AD, and 12,801 from PD. Mean levels of PM₂.₅, NO₂ and BC were 12.4 µg/m³, 20.3 µg/m³ and 1.0 10⁻⁵/m, respectively. Hazard ratios (95% confidence intervals) for associations of PM₂.₅, NO₂, and BC with LRI mortality were 1.16 (1.10-1.21) per 5 µg/m³, 1.07 (1.04-1.09) per 10 µg/m³, and 1.05 (1.03-1.08) per 0.5 10⁻⁵/m, respectively. Corresponding estimates for diabetes mortality were 1.11 (1.04-1.17), 1.03 (1.00-1.05), and 1.00 (0.98-1.03); for dementia mortality were 1.05 (1.00-1.10), 1.05 (1.03-1.07), and 1.03 (1.01-1.05); for AD mortality were 1.24 (1.14-1.36), 1.18 (1.13-1.22), and 1.15 (1.11-1.19); and for PD mortality were 1.39 (1.28-1.51), 1.24 (1.20-1.28), and 1.22 (1.18-1.27). CONCLUSIONS:Long-term exposures to PM₂.₅, NO₂, and BC were associated with mortality other than cardiorespiratory diseases, even stronger for mortality from Alzheimer’s and psychiatric disease. The indirect adjustment for missing risk factors will be applied. KEYWORDS: Air pollution, Big data, Long-term exposure, Mortality, Neurodegenerative outcomes

Long-term exposure to ambient particulate matter components and mortality: results from six European administrative cohorts within the ELAPSE project

BACKGROUND AND AIM: Evidence of the association between long-term exposure to ambient particulate matter components and mortality is inconsistent. We evaluated this association in six large administrative cohorts in the Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE) project. METHODS: We analysed data from country-wide administrative cohorts in Norway, Denmark, the Netherlands, Belgium, Switzerland and in Rome (Italy). Annual 2010 mean concentrations of copper (Cu), iron (Fe), sulfur (S) and zinc (Zn) in PM2.5 were estimated using 100x100m Europe-wide land use regression models assigned to the participants’ residential addresses. We applied cohort-specific Cox proportional hazard models controlling for area- and individual-level covariates to evaluate associations with natural, cardiovascular, non-malignant respiratory and lung cancer mortality. Two pollutant models adjusting for PM2.5 or NO2 were also applied. We pooled cohort specific estimates using a random effects meta-analysis. RESULTS:We included 27 million participants contributing more than 240 million person-years. Cu, Fe and S were associated with natural mortality [Hazard Ratios (HRs) (95% CI): 1.037 (1.014, 1.060) per 5 ng/m³ Cu; 1.069 (1.031, 1.108) per 100 ng/m³ Fe; 1.036 (1.016, 1.057) per 200 ng/m³ S] even after controlling for PM2.5 [e.g. 1.048 (1.022, 1.074) for Fe]. Adjustment for NO2 decreased HRs to unity [e.g. 0.994 (0.954, 1.036) for Fe]. Associations with cardiovascular mortality were weaker and non-significant. We found positive significant associations of Cu, Fe and S with non-malignant respiratory [HRs: 1.047, 1.099 and 1.043, respectively] and lung cancer mortality [HRs: 1.091, 1.160 and 1.102, respectively] in single pollutant models, though only the effect of Fe persisted after control for PM2.5. CONCLUSIONS:Our results indicate associations of long-term exposure to PM2.5 components with natural and cause-specific mortality outcomes related to non-tailpipe emissions (Cu and Fe) and long-range transport (S). However, associations did not persist after NO2 adjustment. KEYWORDS: Air pollution, Particle components, Long-term exposure, Environmental epidemiology, Survival, Mortality

Long-term air pollution exposure and mortality due to dementia, Parkinson’s Disease and psychiatric disorders: the ELAPSE project

BACKGROUND AND AIM: Ambient air pollution exposure has been linked to neurodegenerative and psychiatric disorders, but evidence remains limited. We examined the association between long-term air pollution exposure and mortality due to dementia, Alzheimer’s Disease (AD), Parkinson’s Disease (PD), psychiatric disorders and suicides in a pooled analysis of eight European cohorts. METHODS: Within the project ‘Effects of Low-Level Air Pollution: A Study in Europe’ (ELAPSE), we pooled data from eight cohorts from six European countries. Annual mean residential concentrations in 2010 for fine particulate matter (PM2.5), nitrogen dioxide (NO2), black carbon (BC) and ozone (O3) were estimated using Europe-wide hybrid land use regression models. We applied stratified Cox proportional hazard models, adjusting for potential confounders, to investigate the associations between air pollution and mortality due to dementia, AD, PD, psychiatric disorders, and suicides. RESULTS:Of 325,367 participants, 1167 died from dementia (528 from AD), 468 from PD, 995 from psychiatric disorders, and 273 from suicides, during a mean follow-up of 19.5 years. We observed positive associations of NO2, PM2.5 and BC with PD (hazard ratio; 95% confidence intervals: 1.14; 0.98-1.33 per 10 µg/m3 in NO2, 1.26; 1.03-1.55 per 5 µg/m3 in PM2.5, and 1.09; 0.93-1.27 per 5 10-5m-1 in BC), psychiatric disorders (1.08; 0.98-1.19; 1.21; 1.02-1.43; 1.12; 1.01-1.24) and suicides (1.16; 0.98-1.37; 1.14; 0.79-1.65; 1-10; 0.93-1.31). We found weak negative associations of NO2, PM2.5 and BC with dementia (0.92; 0.84-1.00; 0.92; 0.79-1.07; 0.91; 0.83-1.00) or AD (0.93; 0.82-1.06; 0.85; 0.69-1.03; 0.89; 0.78-1.03). CONCLUSIONS:Long-term exposures to NO2, PM2.5 and BC may be associated with premature mortality from PD, psychiatric diseases and suicides. KEYWORDS: air pollution, dementia, Alzheimer's Disease, Parkinson's Disease, pyshiatric disorders, suicide

Low-concentration air pollution and mortality in American older adults: A national cohort analysis (2001-2017)

BACKGROUND AND AIM: Mounting epidemiological evidence has documented the associations between air pollution and mortality. There is a pressing need to determine whether risks persist at low concentrations including below current national standards. Better understanding of the health effects of low-level air pollution is essential for the amendment of National Ambient Air Quality Standards. METHODS: A nationwide, population-based, open cohort study was conducted to estimate the association between long-term exposure to low-level PM2.5, NO2, O3 and mortality. The study population included all Medicare enrollees in the contiguous United States from 2001-2017. We further defined three low-exposure sub-cohorts comprised of Medicare enrollees who were always exposed to low-level PM2.5 (annual mean ≤12 µg/m3), NO2 (annual mean ≤53 ppb), and O3 (warm-season mean ≤50 ppb), respectively, over the study period. We applied multiple statistical methods and compared causal modeling methods to standard methods, to provide strong epidemiologic evidence. RESULTS:Of the 68.7-million Medicare enrollees, 33.1%, 93.8%, 65.0% were always exposed to low-level annual PM2.5, annual NO2, and warm-season O3 over the study period, respectively. Among the low-exposure cohorts, a 10-µg/m3 increase in PM2.5, 10-ppb increase in NO2, and 10-ppb increase in warm-season O3, was respectively associated with an increase in mortality rate ranging between 10-13%, 2-4%, and 12-14% in single-pollutant models, and between 6-8%, 1-3%, and 9-11% in tri-pollutant models, using three statistical approaches. There was strong evidence of linearity in concentration-response relationships for PM2.5 and NO2 at levels below the current NAAQS, suggesting that no safe threshold exists for health-harmful pollution levels. For O3, the concentration-response relationship shows an increasingly positive association at levels above 30-ppb. CONCLUSIONS:Long-term exposures to PM2.5, NO2, and O3 were significantly associated with an increased risk of all-cause mortality, particularly at levels below the current NAAQS standards, suggesting that implementing more stringent regulations in air quality may yield substantial health benefits. KEYWORDS: low concentration, air pollution, NAAQS, survival analysis, causal modeling

Long-term exposure to air pollution and liver cancer incidence in six European cohorts.

Particulate matter air pollution and diesel engine exhaust have been classified as carcinogenic for lung cancer, yet few studies have explored associations with liver cancer. We used six European adult cohorts which were recruited between 1985 and 2005, pooled within the "Effects of low-level air pollution: A study in Europe" (ELAPSE) project, and followed for the incidence of liver cancer until 2011 to 2015. The annual average exposure to nitrogen dioxide (NO2 ), particulate matter with diameter <2.5μm (PM2.5 ), black carbon (BC), warm-season ozone (O3 ), and eight elemental components of PM2.5 (copper, iron, zinc, sulfur, nickel, vanadium, silicon, and potassium) were estimated by European-wide hybrid land-use regression models at participants' residential addresses. We analyzed the association between air pollution and liver cancer incidence by Cox proportional hazards models adjusting for potential confounders. Of 330 064 cancer-free adults at baseline, 512 developed liver cancer during a mean follow-up of 18.1 years. We observed positive linear associations between NO2 (hazard ratio, 95% confidence interval: 1.17, 1.02-1.35 per 10μg/m3 ), PM2.5 (1.12, 0.92-1.36 per 5μg/m3 ), and BC (1.15, 1.00-1.33 per 0.5 10-5 /m) and liver cancer incidence. Associations with NO2 and BC persisted in two-pollutant models with PM2.5 . Most components of PM2.5 were associated with the risk of liver cancer, with the strongest associations for sulfur and vanadium, which were robust to adjustment for PM2.5 or NO2 . Our study suggests that ambient air pollution may increase the risk of liver cancer, even at concentrations below current EU standards.

Long-term exposure to low-level air pollution and incidence of asthma: the ELAPSE project.

Long-term exposure to ambient air pollution has been linked to childhood-onset asthma, although evidence is still insufficient. Within the multicentre project Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE), we examined the associations of long-term exposures to particulate matter with a diameter <2.5 µm (PM2.5), nitrogen dioxide (NO2) and black carbon (BC) with asthma incidence in adults. We pooled data from three cohorts in Denmark and Sweden with information on asthma hospital diagnoses. The average concentrations of air pollutants in 2010 were modelled by hybrid land-use regression models at participants' baseline residential addresses. Associations of air pollution exposures with asthma incidence were explored with Cox proportional hazard models, adjusting for potential confounders. Of 98 326 participants, 1965 developed asthma during a mean follow-up of 16.6 years. We observed associations in fully adjusted models with hazard ratios of 1.22 (95% CI 1.04-1.43) per 5 μg·m-3 for PM2.5, 1.17 (95% CI 1.10-1.25) per 10 µg·m-3 for NO2 and 1.15 (95% CI 1.08-1.23) per 0.5×10-5 m-1 for BC. Hazard ratios were larger in cohort subsets with exposure levels below the European Union and US limit values and possibly World Health Organization guidelines for PM2.5 and NO2. NO2 and BC estimates remained unchanged in two-pollutant models with PM2.5, whereas PM2.5 estimates were attenuated to unity. The concentration-response curves showed no evidence of a threshold. Long-term exposure to air pollution, especially from fossil fuel combustion sources such as motorised traffic, was associated with adult-onset asthma, even at levels below the current limit values.

Association of Prenatal Ambient Air Pollution Exposure With Placental Mitochondrial DNA Copy Number, Telomere Length and Preeclampsia.

Background: Studies have shown that ambient air pollution is linked to preeclampsia (PE), possibly via generation of oxidative stress in the placenta. Telomere length and mitochondrial DNA copy number (mtDNAcn) are sensitive to oxidative stress damage.Objective: To study the association between prenatal exposure to ambient nitrogen oxides (NOx, a marker for traffic-related air pollution), and PE, as well as potential mediation effects by placental telomere length and mtDNAcn.Methods: This is a cross-sectional study of 42 preeclamptic and 95 arbitrarily selected normotensive pregnant women with gestational ambient NOx exposure assessment in southern Scania, Sweden. Hourly concentrations of NOx were estimated at the residential addresses by a Gaussian-plume dispersion model with 100 × 100 m spatial resolutions and aggregated into trimester-specific mean concentrations. Placental relative mtDNAcn and telomere length were measured using qPCR. Linear and logistic regression models were used to investigate associations, adjusted for perinatal and seasonal characteristics.Results: Exposure was categorized into low and high exposures by median cut-offs during first [11.9 μg/m3; interquartile range (IQR) 7.9, 17.9], second (11.6 μg/m3; IQR: 7.1, 21.1), third trimesters (11.9 μg/m3; IQR: 7.7, 19.5) and entire pregnancy (12.0 μg/m3; IQR: 7.6, 20.1). Increased risk of PE was found for high prenatal NOx exposure during the first trimester (OR 4.0; 95% CI: 1.4, 11.1; p = 0.008), and entire pregnancy (OR 3.7; 95% CI: 1.3, 10.4; p = 0.012). High exposed group during the first trimester had lower placental relative mtDNAcn compared with low exposed group (−0.20; 95% CI: −0.36, −0.04; p = 0.01). Changes in relative mtDNAcn did not mediate the association between prenatal NOx exposure and PE. No statistically significant association was found between placental relative telomere length, prenatal NOx exposure and PE.Conclusion: In this region with relatively low levels of air pollution, ambient NOx exposure during the first trimester was associated with reduced placental relative mtDNAcn and an increased risk of PE. However, we did not find any evidence that mtDNAcn or TL mediated the association between air pollution and PE. Future research should further investigate the role of mtDNAcn for pregnancy complications in relation to exposure to ambient air pollution during pregnancy.

The impact of the climate crisis on brain health

Long-term exposure to air pollution is harmful to human health, causing damage to respiratory and cardiovascular systems. A new study provides evidence that even short-term, relatively low-level air pollution can be detrimental for cognitive function, and suggests the possibility that a commonly used drug might help reduce the harmful effects.

Long-term exposure to air pollution and mortality in a prospective cohort: The Ontario Health Study

BackgroundAir pollution has been associated with increased mortality. However, updated evidence from cohort studies with detailed information on various risk factors is needed, especially in regions with low air pollution levels. We investigated the associations between long-term exposure to air pollution and mortality in a prospective cohort. MethodsWe studied 88,615 participants aged ≥30 years from an ongoing cohort study in Ontario, Canada from 2009 to 2017. Exposure to ambient fine particulate matter (PM2.5) and nitrogen dioxide (NO2) was estimated at participants’ residence. Cox proportional hazard models were used to investigate the associations between air pollution and non-accidental, cardiovascular, and respiratory mortality, adjusted for a wide array of individual-level and contextual covariates. Potential effect modification by socio-demographic and behavioral factors was also examined in exploratory stratified analyses. ResultsThe fully adjusted hazard ratios (HRs) per 1 µg/m3 increment in PM2.5 were 1.037 [95% confidence interval (CI): 1.018, 1.057]¸ 1.083 (95% CI: 1.040, 1.128) and 1.109 (95% CI: 1.035, 1.187) for non-accidental, cardiovascular, and respiratory mortality, respectively. Positive associations were also found for NO2; the corresponding HRs per 1 ppb increment were 1.027 (95% CI: 1.021, 1.034), 1.032 (95% CI: 1.019, 1.046) and 1.044 (95% CI: 1.020, 1.068). We found suggestive evidence of stronger associations in physically active participants, smokers, and those with lower household income. ConclusionsLong-term exposure to PM2.5 and NO2 was associated with increased risks for non-accidental, cardiovascular, and respiratory mortality, suggesting potential benefits of further improvement in air quality even in low-exposure environments.

Outdoor Air Pollution and Depression in Canada: A Population-Based Cross-Sectional Study from 2011 to 2016.

To assess whether exposure to increased levels of outdoor air pollution is associated with psychological depression, six annual iterations of the Canadian Community Health Survey (n ≈ 127,050) were used to estimate the prevalence of a major depressive episode (2011–2014) or severity of depressive symptoms (2015–2016). Survey data were linked with outdoor air pollution data obtained from the Canadian Urban Environmental Health Research Consortium, with outdoor air pollution represented by fine particulate matter ≤2.5 micrometers (μm) in diameter (PM2.5), ozone (O3), sulfur dioxide (SO2), and nitrogen dioxide (NO2). Log-binomial models were used to estimate the association between outdoor air pollution and depression, and included adjustment for age, sex, marital status, income, education, employment status, urban versus rural households, cigarette smoking, and chronic illness. No evidence of associations for either depression outcomes were found. Given the generally low levels of outdoor air pollution in Canada, these findings should be generalized with caution. It is possible that a meaningful association with major depression may be observed in regions of the world where the levels of outdoor air pollution are greater, or during high pollution events over brief time intervals. Future research is needed to replicate these findings and to further investigate these associations in other regions and populations.

Modeling multi-level survival data in multi-center epidemiological cohort studies: Applications from the ELAPSE project

BackgroundWe evaluated methods for the analysis of multi-level survival data using a pooled dataset of 14 cohorts participating in the ELAPSE project investigating associations between residential exposure to low levels of air pollution (PM2.5 and NO2) and health (natural-cause mortality and cerebrovascular, coronary and lung cancer incidence). MethodsWe applied five approaches in a multivariable Cox model to account for the first level of clustering corresponding to cohort specification: (1) not accounting for the cohort or using (2) indicator variables, (3) strata, (4) a frailty term in frailty Cox models, (5) a random intercept under a mixed Cox, for cohort identification. We accounted for the second level of clustering due to common characteristics in the residential area by (1) a random intercept per small area or (2) applying variance correction. We assessed the stratified, frailty and mixed Cox approach through simulations under different scenarios for heterogeneity in the underlying hazards and the air pollution effects. ResultsEffect estimates were stable under approaches used to adjust for cohort but substantially differed when no adjustment was applied. Further adjustment for the small area grouping increased the effect estimates’ standard errors. Simulations confirmed identical results between the stratified and frailty models. In ELAPSE we selected a stratified multivariable Cox model to account for between-cohort heterogeneity without adjustment for small area level, due to the small number of subjects and events in the latter. ConclusionsOur study supports the need to account for between-cohort heterogeneity in multi-center collaborations using pooled individual level data.

Effects of the spread of COVID-19 on public health of polluted cities: results of the first wave forexplaining the dejà vu in the second wave of COVID-19pandemic and epidemics of future vital agents.

The pandemic of coronavirus disease 2019 (COVID-19), caused by the novel coronavirus SARS-CoV-2, is generating a high number of deaths worldwide. One of the current questions in the field of environmental science is to explain how air pollution can affect the impact of COVID-19 pandemic on public health. The research here focuses on a case study of Italy. Results suggest that the diffusion of COVID-19 in cities with high levels of air pollution is generating higher numbers of COVID-19 related infected individuals and deaths. In particular, results reveal that the number of infected people was higher in cities with more than 100 days per year exceeding limits set for PM10 or ozone, cities located in hinterland zones (i.e. away from the coast), cities having a low average speed of wind and cities with a lower average temperature. In hinterland cities having a high level of air pollution, coupled with low wind speed, the average number of infected people in April 2020—during the first wave of the COVID-19 pandemic—is more than tripled compared to cities with low levels of air pollution. In addition, results show that more than 75% of infected individuals and about 81% of deaths of the first wave of COVID-19 pandemic in Italy are in industrialized regions with high levels of air pollution. Although these vital results of the first wave of the COVID-19 from February to August 2020, policymakers have had a low organizational capacity to plan effective policy responses for crisis management to cope with COVID-19 pandemic that is generating recurring waves with again negative effects, déjà vu, on public health and of course economic systems.

Effects of the Spread of COVID-19 on Public Health of Polluted Cities: Results of the First Wave for Explaining the Dejà Vu in the Second Wave of COVID-19

The pandemic of coronavirus disease 2019 (COVID-19), caused by the novel coronavirus SARS-CoV-2, is generating a high number of deaths worldwide. One of the current questions in the field of environmental science is to explain how air pollution can affect the impact of COVID-19 on public health. The research here focuses on a case study of Italy. Results suggest that the diffusion of COVID-19 in cities with high levels of air pollution is generating higher numbers of COVID-19 related infected individuals and deaths. In particular, results reveal that, among Italian cities, the number of infected people was higher in cities with more than 100 days per year exceeding limits set for PM10 or ozone, cities located in hinterland zones (i.e. away from the coast), cities having a low average speed of wind and cities with a lower average temperature. In hinterland cities (mostly those bordering large urban conurbations) having a high level of air pollution, coupled with low wind speed, the average number of infected people in April 2020during the first wave of the COVID-19 is more than tripled compared to cities that low levels of air pollution. In addition, results show that more than 75% of infected individuals and about 81% of deaths of the first wave of COVID-19 in Italy are in industrialized regions with high levels of air pollution. Although these vital results of the first wave of the COVID-19 from February to August 2020, policymakers have had a low organizational capacity to plan effective policy responses for crisis management to cope with recurring COVID-19 pandemic that is generating a new wave with again negative effects, déjà vu, on public health and of course economic systems.

Park municipalities and air quality

In Italy, 23 percent of the 7,903 municipalities include protected areas, while 6.4 percent (which we define as park municipalities) national parks. We investigate the relationship between park areas and quality of air and find that park municipalities experienced far lower levels of air pollution in the last three years, the gross difference ranging from 25 to 30 percent lower levels of particulate matter (PM10 and PM2.5) and three times lower levels of nitrogen dioxide. In our econometric analysis we find that part (but not all) of this difference depends on the lower population density and manufacturing activity in municipalities with national parks. We as well show that park municipalities have progressively reduced particulate matter over the last three years and that parks have a “green lung” function since, in non-park municipalities, air pollution grows in the distance from national parks. Based on our average of estimated parameters of the impact of the main air pollutants on mortality in the literature we calculate that living in park municipalities reduces mortality rates by around 10 percent.