Long-Term Exposure to Low-Level PM2.5 and Mortality: Investigation of Heterogeneity by Harmonizing Analyses in Large Cohort Studies in Canada, United States, and Europe.

BACKGROUND: Studies across the globe generally reported increased mortality risks associated with particulate matter with aerodynamic diameter ≤2.5µm (PM2.5) exposure with large heterogeneity in the magnitude of reported associations and the shape of concentration-response functions (CRFs). We aimed to evaluate the impact of key study design factors (including confounders, applied exposure model, population age, and outcome definition) on PM2.5 effect estimates by harmonizing analyses on three previously published large studies in Canada [Mortality-Air Pollution Associations in Low Exposure Environments (MAPLE), 1991-2016], the United States (Medicare, 2000-2016), and Europe [Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE), 2000-2016] as much as possible. METHODS: We harmonized the study populations to individuals 65+ years of age, applied the same satellite-derived PM2.5 exposure estimates, and selected the same sets of potential confounders and the same outcome. We evaluated whether differences in previously published effect estimates across cohorts were reduced after harmonization among these factors. Additional analyses were conducted to assess the influence of key design features on estimated risks, including adjusted covariates and exposure assessment method. A combined CRF was assessed with meta-analysis based on the extended shape-constrained health impact function (eSCHIF). RESULTS: More than 81 million participants were included, contributing 692 million person-years of follow-up. Hazard ratios and 95% confidence intervals (CIs) for all-cause mortality associated with a 5-µg/m3 increase in PM2.5 were 1.039 (1.032, 1.046) in MAPLE, 1.025 (1.021, 1.029) in Medicare, and 1.041 (1.014, 1.069) in ELAPSE. Applying a harmonized analytical approach marginally reduced difference in the observed associations across the three studies. Magnitude of the association was affected by the adjusted covariates, exposure assessment methodology, age of the population, and marginally by outcome definition. Shape of the CRFs differed across cohorts but generally showed associations down to the lowest observed PM2.5 levels. A common CRF suggested a monotonically increased risk down to the lowest exposure level. https://doi.org/10.1289/EHP12141.

Air pollution deaths attributable to fossil fuels: observational and modelling study.

OBJECTIVES: To estimate all cause and cause specific deaths that are attributable to fossil fuel related air pollution and to assess potential health benefits from policies that replace fossil fuels with clean, renewable energy sources. DESIGN: Observational and modelling study. METHODS: An updated atmospheric composition model, a newly developed relative risk model, and satellite based data were used to determine exposure to ambient air pollution, estimate all cause and disease specific mortality, and attribute them to emission categories. DATA SOURCES: Data from the global burden of disease 2019 study, observational fine particulate matter and population data from National Aeronautics and Space Administration (NASA) satellites, and atmospheric chemistry, aerosol, and relative risk modelling for 2019. RESULTS: Globally, all cause excess deaths due to fine particulate and ozone air pollution are estimated at 8.34 million (95% confidence interval 5.63 to 11.19) deaths per year. Most (52%) of the mortality burden is related to cardiometabolic conditions, particularly ischaemic heart disease (30%). Stroke and chronic obstructive pulmonary disease both account for 16% of mortality burden. About 20% of all cause mortality is undefined, with arterial hypertension and neurodegenerative diseases possibly implicated. An estimated 5.13 million (3.63 to 6.32) excess deaths per year globally are attributable to ambient air pollution from fossil fuel use and therefore could potentially be avoided by phasing out fossil fuels. This figure corresponds to 82% of the maximum number of air pollution deaths that could be averted by controlling all anthropogenic emissions. Smaller reductions, rather than a complete phase-out, indicate that the responses are not strongly non-linear. Reductions in emission related to fossil fuels at all levels of air pollution can decrease the number of attributable deaths substantially. Estimates of avoidable excess deaths are markedly higher in this study than most previous studies for these reasons: the new relative risk model has implications for high income (largely fossil fuel intensive) countries and for low and middle income countries where the use of fossil fuels is increasing; this study accounts for all cause mortality in addition to disease specific mortality; and the large reduction in air pollution from a fossil fuel phase-out can greatly reduce exposure. CONCLUSION: Phasing out fossil fuels is deemed to be an effective intervention to improve health and save lives as part the United Nations' goal of climate neutrality by 2050. Ambient air pollution would no longer be a leading, environmental health risk factor if the use of fossil fuels were superseded by equitable access to clean sources of renewable energy.

Daily Summer Temperatures and Hospitalization for Acute Cardiovascular Events: Impact of Outdoor PM 2.5 Oxidative Potential on Observed Associations Across Canada.

BACKGROUND: Oxidative stress plays an important role in the health impacts of both outdoor fine particulate air pollution (PM 2.5 ) and thermal stress. However, it is not clear how the oxidative potential of PM 2.5 may influence the acute cardiovascular effects of temperature. METHODS: We conducted a case-crossover study of hospitalization for cardiovascular events in 35 cities across Canada during the summer months (July-September) between 2016 and 2018. We collected three different metrics of PM 2.5 oxidative potential each month in each location. We estimated associations between lag-0 daily temperature (per 5ºC) and hospitalization for all cardiovascular (n = 44,876) and ischemic heart disease (n = 14,034) events across strata of monthly PM 2.5 oxidative potential using conditional logistical models adjusting for potential time-varying confounders. RESULTS: Overall, associations between lag-0 temperature and acute cardiovascular events tended to be stronger when outdoor PM 2.5 oxidative potential was higher. For example, when glutathione-related oxidative potential (OP GSH ) was in the highest tertile, the odds ratio (OR) for all cardiovascular events was 1.040 (95% confidence intervals [CI] = 1.004, 1.074) compared with 0.980 (95% CI = 0.943, 1.018) when OP GSH was in the lowest tertile. We observed a greater difference for ischemic heart disease events, particularly for older subjects (age >70 years). CONCLUSIONS: The acute cardiovascular health impacts of summer temperature variations may be greater when outdoor PM 2.5 oxidative potential is elevated. This may be particularly important for ischemic heart disease events.

Reversal of trends in global fine particulate matter air pollution.

Ambient fine particulate matter (PM2.5) is the world's leading environmental health risk factor. Quantification is needed of regional contributions to changes in global PM2.5 exposure. Here we interpret satellite-derived PM2.5 estimates over 1998-2019 and find a reversal of previous growth in global PM2.5 air pollution, which is quantitatively attributed to contributions from 13 regions. Global population-weighted (PW) PM2.5 exposure, related to both pollution levels and population size, increased from 1998 (28.3 µg/m3) to a peak in 2011 (38.9 µg/m3) and decreased steadily afterwards (34.7 µg/m3 in 2019). Post-2011 change was related to exposure reduction in China and slowed exposure growth in other regions (especially South Asia, the Middle East and Africa). The post-2011 exposure reduction contributes to stagnation of growth in global PM2.5-attributable mortality and increasing health benefits per µg/m3 marginal reduction in exposure, implying increasing urgency and benefits of PM2.5 mitigation with aging population and cleaner air.

Air pollution and the sequelae of COVID-19 patients: A multistate analysis.

IMPORTANCE: Recent evidence links air pollution to the severity COVID-19 symptoms and to death from the disease. To date, however, few studies have assessed whether air pollution affects the sequelae to more severe states or recovery from COVID-19 in a cohort with individual data. OBJECTIVE: To assess how air pollution affects the transition to more severe COVID-19 states or to recovery from COVID-19 infection in a cohort with detailed patient information. DESIGN AND OUTCOMES: We used a cohort design that followed patients admitted to hospital in the Kaiser Permanente Southern California (KPSC) Health System, which has 4.7 million members with characteristics similar to the general population. Enrollment began on 06/01/2020 and ran until 01/30/2021 for all patients admitted to hospital while ill with COVID-19. All possible states of sequelae were considered, including deterioration to intensive care, to death, discharge to recovery, or discharge to death. Transition risks were estimated with a multistate model. We assessed exposure using chemical transport model that predicted ambient concentrations of nitrogen dioxide, ozone, and fine particulate matter (PM2.5) at a 1 km scale. RESULTS: Each increase in PM2.5 concentration equivalent to the interquartile range was associated with increased risk of deterioration to intensive care (HR of 1.16; 95% CI: 1.12-1.20) and deterioration to death (HR of 1.11; 95% CI: 1.04-1.17). Results for ozone were consistent with PM2.5 effects, but ozone also affected the transition from recovery to death: HR of 1.24 (95% CI: 1.01-1.51). NO2 had weaker effects but displayed some elevated risks. CONCLUSIONS: PM2.5 and ozone were significantly associated with transitions to more severe states while in hospital and to death after discharge from hospital. Reducing air pollution could therefore lead to improved prognosis for COVID-19 patients and a sustainable means of reducing the health impacts of coronaviruses now and in the future.

Using Parametric g-Computation to Estimate the Effect of Long-Term Exposure to Air Pollution on Mortality Risk and Simulate the Benefits of Hypothetical Policies: The Canadian Community Health Survey Cohort (2005 to 2015).

BACKGROUND: Numerous epidemiological studies have documented the adverse health impact of long-term exposure to fine particulate matter [particulate matter ≤2.5µm in aerodynamic diameter (PM2.5)] on mortality even at relatively low levels. However, methodological challenges remain to consider potential regulatory intervention's complexity and provide actionable evidence on the predicted benefits of interventions. We propose the parametric g-computation as an alternative analytical approach to such challenges. METHOD: We applied the parametric g-computation to estimate the cumulative risks of nonaccidental death under different hypothetical intervention strategies targeting long-term exposure to PM2.5 in the Canadian Community Health Survey cohort from 2005 to 2015. On both relative and absolute scales, we explored the benefits of hypothetical intervention strategies compared with the natural course that a) set the simulated exposure value at each follow-up year to a threshold value if exposure was above the threshold (8.8 µg/m3, 7.04 µg/m3, 5 µg/m3, and 4 µg/m3), and b) reduced the simulated exposure value by a percentage (5% and 10%) at each follow-up year. We used the 3-y average PM2.5 concentration with 1-y lag at the postal code of respondents' annual mailing addresses as their long-term exposure to PM2.5. We considered baseline and time-varying confounders, including demographics, behavior characteristics, income level, and neighborhood socioeconomic status. We also included the R syntax for reproducibility and replication. RESULTS: All hypothetical intervention strategies explored led to lower 11-y cumulative mortality risks than the estimated value under the natural course without intervention, with the smallest reduction of 0.20 per 1,000 participants (95% CI: 0.06, 0.34) under the threshold of 8.8 µg/m3, and the largest reduction of 3.40 per 1,000 participants (95% CI: -0.23, 7.03) under the relative reduction of 10% per interval. The reductions in cumulative risk, or numbers of deaths that would have been prevented if the intervention was employed instead of maintaining the status quo, increased over time but flattened toward the end of the follow-up period. Estimates among those ≥65 years of age were greater with a similar pattern. Our estimates were robust to different model specifications. DISCUSSION: We found evidence that any intervention further reducing the long-term exposure to PM2.5 would reduce the cumulative mortality risk, with greater benefits in the older population, even in a population already exposed to low levels of ambient PM2.5. The parametric g-computation used in this study provides flexibilities in simulating real-world interventions, accommodates time-varying exposure and confounders, and estimates adjusted survival curves with clearer interpretation and more information than a single hazard ratio, making it a valuable analytical alternative in air pollution epidemiological research. https://doi.org/10.1289/EHP11095.

Air pollution and meteorology as risk factors for COVID-19 death in a cohort from Southern California.

BACKGROUND: Recent evidence links ambient air pollution to COVID-19 incidence, severity, and death, but few studies have analyzed individual-level mortality data with high quality exposure models. METHODS: We sought to assess whether higher air pollution exposures led to greater risk of death during or after hospitalization in confirmed COVID-19 cases among patients who were members of the Kaiser Permanente Southern California (KPSC) healthcare system (N=21,415 between 06-01-2020 and 01-31-2022 of whom 99.85 % were unvaccinated during the study period). We used 1 km resolution chemical transport models to estimate ambient concentrations of several common air pollutants, including ozone, nitrogen dioxide, and fine particle matter (PM2.5). We also derived estimates of pollutant exposures from ultra-fine particulate matter (PM0.1), PM chemical species, and PM sources. We employed Cox proportional hazards models to assess associations between air pollution exposures and death from COVID-19 among hospitalized patients. FINDINGS: We found significant associations between COVID-19 death and several air pollution exposures, including: PM2.5 mass, PM0.1 mass, PM2.5 nitrates, PM2.5 elemental carbon, PM2.5 on-road diesel, and PM2.5 on-road gasoline. Based on the interquartile (IQR) exposure increment, effect sizes ranged from hazard ratios (HR) = 1.12 for PM2.5 mass and PM2.5 nitrate to HR âˆ¼ 1.06-1.07 for other species or source markers. Humidity and temperature in the month of diagnosis were also significant negative predictors of COVID-19 death and negative modifiers of the air pollution effects. INTERPRETATION: Air pollution exposures and meteorology were associated the risk of COVID-19 death in a cohort of patients from Southern California. These findings have implications for prevention of death from COVID-19 and for future pandemics.

Impact of lowering fine particulate matter from major emission sources on mortality in Canada: A nationwide causal analysis.

Emissions of fine particulate matter (PM2.5) from human activities have been linked to substantial disease burdens, but evidence regarding how reducing PM2.5 at its sources would improve public health is sparse. We followed a population-based cohort of 2.7 million adults across Canada from 2007 through 2016. For each participant, we estimated annual mean concentrations of PM2.5 and the fractional contributions to PM2.5 from the five leading anthropogenic sources at their residential address using satellite observations in combination with a global atmospheric chemistry transport model. For each source, we estimated the causal effects of six hypothetical interventions on 10-y nonaccidental mortality risk using the parametric g-formula, a structural causal model. We conducted stratified analyses by age, sex, and income. This cohort would have experienced tangible health gains had contributions to PM2.5 from any of the five sources been reduced. Compared with no intervention, a 10% annual reduction in PM2.5 contributions from transportation and power generation, Canada's largest and fifth-largest anthropogenic sources, would have prevented approximately 175 (95%CI: 123-226) and 90 (95%CI: 63-117) deaths per million by 2016, respectively. A more intensive 50% reduction per year in PM2.5 contributions from the two sources would have averted 360 and 185 deaths per million, respectively, by 2016. The potential health benefits were greater among men, older adults, and low-income earners. In Canada, where PM2.5 levels are among the lowest worldwide, reducing PM2.5 contributions from anthropogenic sources by as little as 10% annually would yield meaningful health gains.

Chronic Exposure to Fine Particulate Matter Increases Mortality Through Pathways of Metabolic and Cardiovascular Disease: Insights From a Large Mediation Analysis.

Background Long-term exposure to outdoor fine particulate matter (PM2.5) is the leading environmental risk factor for premature mortality worldwide. Characterizing important pathways through which PM2.5 increases individuals' mortality risk can clarify the PM2.5-mortality relationship and identify possible points of interventions. Recent evidence has linked PM2.5 to the onset of diabetes and cardiovascular disease, but to what extent these associations contribute to the effect of PM2.5 on mortality remains poorly understood. Methods and Results We conducted a population-based cohort study to investigate how the effect of PM2.5 on nonaccidental mortality is mediated by its impacts on incident diabetes, acute myocardial infarction, and stroke. Our study population comprised ≈200 000 individuals aged 20 to 90 years who participated in population-based health surveys in Ontario, Canada, from 1996 to 2014. Follow-up extended until December 2017. Using causal mediation analyses with Aalen additive hazards models, we decomposed the total effect of PM2.5 on mortality into a direct effect and several path-specific indirect effects mediated by diabetes, each cardiovascular event, or both combined. A series of sensitivity analyses were also conducted. After adjusting for various individual- and neighborhood-level covariates, we estimated that for every 1000 adults, each 10 µg/m3 increase in PM2.5 was associated with ≈2 incident cases of diabetes, ≈1 major cardiovascular event (acute myocardial infarction and stroke combined), and ≈2 deaths annually. Among PM2.5-related deaths, 31.7% (95% CI, 17.2%-53.2%) were attributable to diabetes and major cardiovascular events in relation to PM2.5. Specifically, 4.5% were explained by PM2.5-induced diabetes, 22.8% by PM2.5-induced major cardiovascular events, and 4.5% through their interaction. Conclusions This study suggests that a significant portion of the estimated effect of long-term exposure to PM2.5 on deaths can be attributed to its effect on diabetes and cardiovascular diseases, highlighting the significance of PM2.5 on deteriorating cardiovascular health. Our findings should raise awareness among professionals that improving metabolic and cardiovascular health may reduce mortality burden in areas with higher exposure to air pollution.

How low can you go? Air pollution affects mortality at very low levels.

The World Health Organization (WHO) recently released new guidelines for outdoor fine particulate air pollution (PM2.5) recommending an annual average concentration of 5 µg/m3. Yet, our understanding of the concentration-response relationship between outdoor PM2.5 and mortality in this range of near-background concentrations remains incomplete. To address this uncertainty, we conducted a population-based cohort study of 7.1 million adults in one of the world's lowest exposure environments. Our findings reveal a supralinear concentration-response relationship between outdoor PM2.5 and mortality at very low (<5 µg/m3) concentrations. Our updated global concentration-response function incorporating this new information suggests an additional 1.5 million deaths globally attributable to outdoor PM2.5 annually compared to previous estimates. The global health benefits of meeting the new WHO guideline for outdoor PM2.5 are greater than previously assumed and indicate a need for continued reductions in outdoor air pollution around the world.

Long-term Exposure to Oxidant Gases and Mortality: Effect Modification by PM 2.5 Transition Metals and Oxidative Potential.

BACKGROUND: Populations are simultaneously exposed to outdoor concentrations of oxidant gases (i.e., O 3 and NO 2 ) and fine particulate air pollution (PM 2.5 ). Since oxidative stress is thought to be an important mechanism explaining air pollution health effects, the adverse health impacts of oxidant gases may be greater in locations where PM 2.5 is more capable of causing oxidative stress. METHODS: We conducted a cohort study of 2 million adults in Canada between 2001 and 2016 living within 10 km of ground-level monitoring sites for outdoor PM 2.5 components and oxidative potential. O x exposures (i.e., the redox-weighted average of O 3 and NO 2 ) were estimated using a combination of chemical transport models, land use regression models, and ground-level data. Cox proportional hazards models were used to estimate associations between 3-year moving average O x and mortality outcomes across strata of transition metals and sulfur in PM 2.5 and three measures of PM 2.5 oxidative potential adjusting for possible confounding factors. RESULTS: Associations between O x and mortality were consistently stronger in regions with elevated PM 2.5 transition metal/sulfur content and oxidative potential. For example, each interquartile increase (6.27 ppb) in O x was associated with a 14.9% (95% CI = 13.0, 16.9) increased risk of nonaccidental mortality in locations with glutathione-related oxidative potential (OP GSH ) above the median whereas a 2.50% (95% CI = 0.600, 4.40) increase was observed in regions with OP GSH levels below the median (interaction P value <0.001). CONCLUSION: Spatial variations in PM 2.5 composition and oxidative potential may contribute to heterogeneity in the observed health impacts of long-term exposures to oxidant gases.

Air Pollution and Pediatric Respiratory Hospitalizations: Effect Modification by Particle Constituents and Oxidative Potential.

Rationale: Outdoor particulate and gaseous air pollutants impair respiratory health in children, and these associations may be influenced by particle composition. Objectives: To examine whether associations between short-term variations in fine particulate air pollution, oxidant gases, and respiratory hospitalizations in children are modified by particle constituents (metals and sulfur) or oxidative potential. Methods: We conducted a case-crossover study of 10,500 children (0-17 years of age) across Canada. Daily fine particle mass concentrations and oxidant gases (nitrogen dioxide and ozone) were collected from ground monitors. Monthly estimates of fine particle constituents (metals and sulfur) and oxidative potential were also measured. Conditional logistic regression models were used to estimate associations between air pollutants and respiratory hospitalizations, above and below median values for particle constituents and oxidative potential. Measurements and Main Results: Lag-1 fine particulate matter mass concentrations were not associated with respiratory hospitalizations (odds ratio and 95% confidence interval per 10 µg/m3 increase in fine particulate matter: 1.004 [0.955-1.056]) in analyses ignoring particle constituents and oxidative potential. However, when models were examined above or below median metals, sulfur, and oxidative potential, positive associations were observed above the median. For example, the odds ratio and 95% confidence interval per 10 µg/m3 increase in fine particulate matter were 1.084 (1.007-1.167) when copper was above the median and 0.970 (0.929-1.014) when copper was below the median. Similar trends were observed for oxidant gases. Conclusions: Stronger associations were observed between outdoor fine particles, oxidant gases, and respiratory hospitalizations in children when metals, sulfur, and particle oxidative potential were elevated.

Longest sediment flows yet measured show how major rivers connect efficiently to deep sea.

Here we show how major rivers can efficiently connect to the deep-sea, by analysing the longest runout sediment flows (of any type) yet measured in action on Earth. These seafloor turbidity currents originated from the Congo River-mouth, with one flow travelling >1,130 km whilst accelerating from 5.2 to 8.0 m/s. In one year, these turbidity currents eroded 1,338-2,675 [>535-1,070] Mt of sediment from one submarine canyon, equivalent to 19-37 [>7-15] % of annual suspended sediment flux from present-day rivers. It was known earthquakes trigger canyon-flushing flows. We show river-floods also generate canyon-flushing flows, primed by rapid sediment-accumulation at the river-mouth, and sometimes triggered by spring tides weeks to months post-flood. It is demonstrated that strongly erosional turbidity currents self-accelerate, thereby travelling much further, validating a long-proposed theory. These observations explain highly-efficient organic carbon transfer, and have important implications for hazards to seabed cables, or deep-sea impacts of terrestrial climate change.

Long-term exposure to wildfires and cancer incidence in Canada: a population-based observational cohort study.

BACKGROUND: Wildfires emit many carcinogenic pollutants that contaminate air, water, terrestrial, and indoor environments. However, little is known about the relationship between exposure to wildfires and cancer risk. We aimed to assess the associations between residential exposure to wildfires and the incidence of several cancer outcomes (lung cancer, brain cancer, non-Hodgkin lymphoma, multiple myeloma, and leukaemia) in Canada. METHODS: We did a population-based observational cohort study of participants in the 1996 Canadian Census Health and Environment Cohort. The 1996 Canadian Census Health and Environment Cohort is a nationally representative sample of Canadian adults, followed up for cancer incidence and mortality from 1996 to 2015. For this analysis, we excluded participants who lived in major Canadian cities (with a population size greater than 1·5 million people), recent immigrants, and individuals younger than 25 years or 90 years of age or older at baseline. Exposures to wildfires were assigned on the basis of area burned within a 20 km or 50 km radius of residential locations and updated for annual residential mobility. Multivariable Cox proportional hazards models were used to estimate associations between exposure to wildfires and specific cancers associated with carcinogenic compounds released by wildfires, including lung and brain cancer, non-Hodgkin lymphoma, multiple myeloma, and leukaemia, adjusted for many personal and neighbourhood-level covariates. FINDINGS: Our analyses included more than 2 million people followed up for a median of 20 years, for a total of 34 million person-years. Wildfire exposure was associated with slightly increased incidence of lung cancer and brain tumours. For example, cohort members exposed to a wildfire within 50 km of residential locations in the past 10 years had a 4·9% relatively higher incidence (adjusted hazard ratio [HR] 1·049, 95% CI 1·028-1·071) of lung cancer than unexposed populations, and a 10% relatively higher incidence (adjusted HR 1·100, 1·026-1·179) of brain tumours. Similar associations were observed for the 20 km buffer size. Wildfires were not associated with haematological cancers in this study, and concentration-response trends were not readily apparent when area burned was modelled as a continuous variable. INTERPRETATION: Long-term exposure to wildfires might increase the risk of lung cancer and brain tumours. Further work is needed to develop long-term estimates of wildfire exposures that capture the complex mixture of environmental pollutants released during these events. FUNDING: Canadian Institute for Health Research and Fonds de recherche du Quebec.

Associations of long-term exposure to fine particulate matter and its constituents with cardiovascular mortality: A prospective cohort study in China.

BACKGROUND: Few studies have evaluated long-term cardiovascular effects of fine particulate matter (PM2.5) and its constituents in countries with high air pollution levels. We aimed to investigate the associations of long-term exposure to PM2.5 and constituents with cardiovascular mortality in China. METHODS: We conducted a prospective cohort study of 90,672 adults ≥ 18 years from 2010 to 2017 in 161 districts/counties across China. The residential annual-average exposure to PM2.5 and 6 main components from 2011 to 2017 were estimated by satellite-based and chemical transport models. Associations of PM2.5 and constituents with cardiovascular mortality were analyzed by competing-risk Cox proportional hazards regression. RESULTS: The average PM2.5 exposure throughout the whole period was 46 ± 22 µg/m3. The hazard ratios of mortality (95% confidence intervals) per 10 µg/m3 increase in PM2.5 concentrations were 1.02 (1.00, 1.05) for overall cardiovascular disease, 1.05 (1.01, 1.09) for ischemic heart disease, 1.03 (1.00, 1.06) for overall stroke, 0.99 (0.94, 1.04) for hemorrhagic stroke, and 1.11 (1.04, 1.19) for ischemic stroke. PM2.5 constituents from fossil fuel combustion (i.e., black carbon, organic matter, nitrate, ammonium, and sulfate) showed larger hazard ratios than PM2.5 total mass, while soil dust showed no risks. CONCLUSIONS: This nationwide cohort study demonstrated associations of long-term exposure to PM2.5 and its constituents with increased risks of cardiovascular mortality in the general population of China. Our study highlighted the importance of PM2.5 constituents from fossil fuel combustion in the long-term cardiovascular effects of PM2.5 in China.

Designing health impact functions to assess marginal changes in outdoor fine particulate matter.

Estimating health benefits from improvements in ambient air quality requires the characterization of the magnitude and shape of the association between marginal changes in exposure and marginal changes in risk, and its uncertainty. Several attempts have been made to do this, each requiring different assumptions. These include the Log-Linear(LL), IntegratedExposure-Response(IER), and GlobalExposureMortalityModel(GEMM). In this paper we develop an improved relative risk model suitable for use in health benefits analysis that incorporates features of existing models while addressing limitations in each model. We model the derivative of the relative risk function within a meta-analytic framework; a quantity directly applicable to benefits analysis, incorporating a Fusion of algebraic functions used in previous models. We assume a constant derivative in concentration over low exposures, like the LL model, a declining derivative over moderate exposures observed in cohort studies, and a derivative declining as the inverse of concentration over high global exposures in a similar manner to the GEMM. The model properties are illustrated with examples of fitting it to data for the six specific causes of death previously examined by the GlobalBurdenofDisease program with ambient fine particulate matter (PM2.5). In a test case analysis assuming a 1% (benefits analysis) or 100% (burden analysis), reduction in country-specific fine particulate matter concentrations, corresponding estimated global attributable deaths using the Fusion model were found to lie between those of the IER and LL models, with the GEMM estimates similar to those based on the LL model.

Cardiopulmonary Mortality and Fine Particulate Air Pollution by Species and Source in a National U.S. Cohort.

The purpose of this study was to estimate cardiopulmonary mortality associations for long-term exposure to PM2.5 species and sources (i.e., components) within the U.S. National Health Interview Survey cohort. Exposures were estimated through a chemical transport model for six species (i.e., elemental carbon (EC), primary organic aerosols (POA), secondary organic aerosols (SOA), sulfate (SO4), ammonium (NH4), nitrate (NO3)) and five sources of PM2.5 (i.e., vehicles, electricity-generating units (EGU), non-EGU industrial sources, biogenic sources (bio), "other" sources). In single-pollutant models, we found positive, significant (p < 0.05) mortality associations for all components, except POA. After adjusting for remaining PM2.5 (total PM2.5 minus component), we found significant mortality associations for EC (hazard ratio (HR) = 1.36; 95% CI [1.12, 1.64]), SOA (HR = 1.11; 95% CI [1.05, 1.17]), and vehicle sources (HR = 1.06; 95% CI [1.03, 1.10]). HRs for EC, SOA, and vehicle sources were significantly larger in comparison to those for remaining PM2.5 (per unit µg/m3). Our findings suggest that cardiopulmonary mortality associations vary by species and source, with evidence that EC, SOA, and vehicle sources are important contributors to the PM2.5 mortality relationship. With further validation, these findings could facilitate targeted pollution regulations that more efficiently reduce air pollution mortality.

Ambient air pollution and the risk of acute myocardial infarction and stroke: A national cohort study.

We used a large national cohort in Canada to assess the incidence of acute myocardial infarction (AMI) and stroke hospitalizations in association with long-term exposure to fine particulate matter (PM2.5), nitrogen dioxide (NO2), and ozone (O3). The study population comprised 2.7 million respondents from the 2006 Canadian Census Health and Environment Cohort (CanCHEC), followed for incident hospitalizations of AMI or stroke between 2006 and 2016. We estimated 10-year moving average estimates of PM2.5, NO2, and O3, annually. We used Cox proportional hazards models to examine the associations adjusting for various covariates. For AMI, each interquartile range (IQR) increase in exposure was found to be associated with a hazard ratio of 1.026 (95% CI: 1.007-1.046) for PM2.5, 1.025 (95% CI: 1.001-1.050) for NO2, and 1.062 (95% CI: 1.041-1.084) for O3, respectively. Similarly, for stroke, an IQR increase in exposure was associated with a hazard ratio of 1.078 (95% CI: 1.052-1.105) for PM2.5, 0.995 (95% CI: 0.965-1.030) for NO2, and 1.055 (95% CI: 1.028-1.082) for O3, respectively. We found consistent evidence of positive associations between long-term exposures to PM2.5, and O3, and to a lesser degree NO2, with incident AMI and stroke hospitalizations.

Differential Mortality Risks Associated With PM2.5 Components: A Multi-Country, Multi-City Study.

BACKGROUND: The association between fine particulate matter (PM2.5) and mortality widely differs between as well as within countries. Differences in PM2.5 composition can play a role in modifying the effect estimates, but there is little evidence about which components have higher impacts on mortality. METHODS: We applied a 2-stage analysis on data collected from 210 locations in 16 countries. In the first stage, we estimated location-specific relative risks (RR) for mortality associated with daily total PM2.5 through time series regression analysis. We then pooled these estimates in a meta-regression model that included city-specific logratio-transformed proportions of seven PM2.5 components as well as meta-predictors derived from city-specific socio-economic and environmental indicators. RESULTS: We found associations between RR and several PM2.5 components. Increasing the ammonium (NH4+) proportion from 1% to 22%, while keeping a relative average proportion of other components, increased the RR from 1.0063 (95% confidence interval [95% CI] = 1.0030, 1.0097) to 1.0102 (95% CI = 1.0070, 1.0135). Conversely, an increase in nitrate (NO3-) from 1% to 71% resulted in a reduced RR, from 1.0100 (95% CI = 1.0067, 1.0133) to 1.0037 (95% CI = 0.9998, 1.0077). Differences in composition explained a substantial part of the heterogeneity in PM2.5 risk. CONCLUSIONS: These findings contribute to the identification of more hazardous emission sources. Further work is needed to understand the health impacts of PM2.5 components and sources given the overlapping sources and correlations among many components.

Association of Sulfur, Transition Metals, and the Oxidative Potential of Outdoor PM2.5 with Acute Cardiovascular Events: A Case-Crossover Study of Canadian Adults.

BACKGROUND: We do not currently understand how spatiotemporal variations in the composition of fine particulate air pollution [fine particulate matter with aerodynamic diameter ≤2.5µm (PM2.5)] affects population health risks. However, recent evidence suggests that joint concentrations of transition metals and sulfate may influence the oxidative potential (OP) of PM2.5 and associated health impacts. OBJECTIVES: The purpose of the study was to evaluate how combinations of transition metals/OP and sulfur content in outdoor PM2.5 influence associations with acute cardiovascular events. METHODS: We conducted a national case-crossover study of outdoor PM2.5 and acute cardiovascular events in Canada between 2016 and 2017 (93,344 adult cases). Monthly mean transition metal and sulfur (S) concentrations in PM2.5 were determined prospectively along with estimates of OP using acellular assays for glutathione (OPGSH), ascorbate (OPAA), and dithiothreitol depletion (OPDTT). Conditional logistic regression models were used to estimate odds ratios (OR) [95% confidence intervals (CI)] for PM2.5 across strata of transition metals/OP and sulfur. RESULTS: Among men, the magnitudes of observed associations were strongest when both transition metal and sulfur content were elevated. For example, an OR of 1.078 (95% CI: 1.049, 1.108) (per 10µg/m3) was observed for cardiovascular events in men when both copper and S were above the median, whereas a weaker association was observed when both elements were below median values (OR=1.019, 95% CI: 1.007, 1.031). A similar pattern was observed for OP metrics. PM2.5 was not associated with acute cardiovascular events in women. DISCUSSION: The combined transition metal and sulfur content of outdoor PM2.5 influences the strength of association with acute cardiovascular events in men. Regions with elevated concentrations of both sulfur and transition metals in PM2.5 should be examined as priority areas for regulatory interventions. https://doi.org/10.1289/EHP9449.