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BACKGROUND: Numerous studies have linked fine particulate matter (PM2.5) to increased cardiovascular mortality. Less is known how the PM2.5-cardiovascular mortality association varies by use of cardiovascular medications. This study sought to quantify effect modification by statin use status on the associations between long-term exposure to PM2.5 and mortality from any cardiovascular cause, coronary heart disease (CHD), and stroke. METHODS: In this nested case-control study, we followed 1.2 million community-dwelling adults aged ≥66 years who lived in Ontario, Canada from 2000 through 2018. Cases were patients who died from the three causes. Each case was individually matched to up to 30 randomly selected controls using incidence density sampling. Conditional logistic regression models were used to estimate odds ratios (ORs) for the associations between PM2.5 and mortality. We evaluated the presence of effect modification considering both multiplicative (ratio of ORs) and additive scales (the relative excess risk due to interaction, RERI). RESULTS: Exposure to PM2.5 increased the risks for cardiovascular, CHD, and stroke mortality. For all three causes of death, compared with statin users, stronger PM2.5-mortality associations were observed among non-users [e.g. for cardiovascular mortality corresponding to each interquartile range increase in PM2.5, OR = 1.042 (95% CI, 1.032-1.053) vs OR = 1.009 (95% CI, 0.996-1.022) in users, ratio of ORs = 1.033 (95% CI, 1.019-1.047), RERI = 0.039 (95% CI, 0.025-0.050)]. Among users, partially adherent users exhibited a higher risk of PM2.5-associated mortality than fully adherent users. CONCLUSIONS: The associations of chronic exposure to PM2.5 with cardiovascular and CHD mortality were stronger among statin non-users compared to users.
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Enfermedades Cardiovasculares , Inhibidores de Hidroximetilglutaril-CoA Reductasas , Material Particulado , Humanos , Material Particulado/efectos adversos , Material Particulado/análisis , Masculino , Anciano , Femenino , Inhibidores de Hidroximetilglutaril-CoA Reductasas/efectos adversos , Estudios de Casos y Controles , Ontario/epidemiología , Enfermedades Cardiovasculares/mortalidad , Anciano de 80 o más Años , Enfermedad Coronaria/mortalidad , Enfermedad Coronaria/epidemiología , Accidente Cerebrovascular/mortalidad , Accidente Cerebrovascular/epidemiología , Exposición a Riesgos Ambientales/efectos adversos , Modelos Logísticos , Factores de Riesgo , Vida Independiente , Oportunidad RelativaRESUMEN
RATIONALE: Outdoor fine particulate air pollution (PM2.5) contributes to millions of deaths around the world each year, but much less is known about the long-term health impacts of other particulate air pollutants including ultrafine particles (a.k.a. nanoparticles) which are in the nanometer size range (<100 nm), widespread in urban environments, and not currently regulated. OBJECTIVES: Estimate the associations between long-term exposure to outdoor ultrafine particles and mortality. METHODS: Outdoor air pollution levels were linked to the residential addresses of a large, population-based cohort from 2001 - 2016. Associations between long-term exposure to outdoor ultrafine particles and nonaccidental and cause-specific mortality were estimated using Cox proportional hazards models. MEASUREMENTS: An increase in long-term exposure to outdoor ultrafine particles was associated with an increased risk of nonaccidental mortality (Hazard Ratio = 1. 073, 95% Confidence Interval = 1. 061, 1. 085) and cause-specific mortality, the strongest of which was respiratory mortality (Hazard Ratio = 1.174, 95% Confidence Interval = 1.130, 1.220). MAIN RESULTS: Long-term exposure to outdoor ultrafine particles was associated with increased risk of mortality. We estimated the mortality burden for outdoor ultrafine particles in Montreal and Toronto, Canada to be approximately 1100 additional nonaccidental deaths every year. Furthermore, we observed possible confounding by particle size which suggests that previous studies may have underestimated or missed important health risks associated with ultrafine particles. CONCLUSIONS: As outdoor ultrafine particles are not currently regulated, there is great potential for future regulatory interventions to improve population health by targeting these common outdoor air pollutants.
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In California, wildfire risk and severity have grown substantially in the last several decades. Research has characterized extensive adverse health impacts from exposure to wildfire-attributable fine particulate matter (PM2.5), but few studies have quantified long-term outcomes, and none have used a wildfire-specific chronic dose-response mortality coefficient. Here, we quantified the mortality burden for PM2.5 exposure from California fires from 2008 to 2018 using Community Multiscale Air Quality modeling system wildland fire PM2.5 estimates. We used a concentration-response function for PM2.5, applying ZIP code-level mortality data and an estimated wildfire-specific dose-response coefficient accounting for the likely toxicity of wildfire smoke. We estimate a total of 52,480 to 55,710 premature deaths are attributable to wildland fire PM2.5 over the 11-year period with respect to two exposure scenarios, equating to an economic impact of $432 to $456 billion. These findings extend evidence on climate-related health impacts, suggesting that wildfires account for a greater mortality and economic burden than indicated by earlier studies.
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Material Particulado , Incendios Forestales , California , Material Particulado/efectos adversos , Material Particulado/análisis , Humanos , Exposición a Riesgos Ambientales/efectos adversos , Contaminantes Atmosféricos/efectos adversos , Contaminantes Atmosféricos/análisis , Contaminantes Atmosféricos/toxicidad , Contaminación del Aire/efectos adversos , Contaminación del Aire/análisis , Humo/efectos adversos , Mortalidad/tendenciasRESUMEN
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.
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Contaminantes Atmosféricos , Contaminación del Aire , Humanos , Anciano , Contaminantes Atmosféricos/análisis , Exposición a Riesgos Ambientales/análisis , Programas Nacionales de Salud , Contaminación del Aire/análisis , Material Particulado/análisis , Europa (Continente)/epidemiología , Estudios de Cohortes , Canadá/epidemiologíaRESUMEN
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.
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Contaminantes Atmosféricos , Contaminación del Aire , Ozono , Humanos , Combustibles Fósiles/efectos adversos , Contaminación del Aire/efectos adversos , Contaminación del Aire/análisis , Ozono/efectos adversos , Ozono/análisis , Material Particulado/efectos adversos , Material Particulado/análisis , Renta , Contaminantes Atmosféricos/efectos adversos , Contaminantes Atmosféricos/análisisRESUMEN
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.
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Hospitalización , Isquemia Miocárdica , Humanos , Anciano , Estudios Cruzados , Temperatura , Canadá/epidemiología , Isquemia Miocárdica/epidemiología , Polvo , Estrés OxidativoRESUMEN
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.
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Contaminación del Aire , Contaminación del Aire/efectos adversos , Contaminación Ambiental , África , Material Particulado/efectos adversosRESUMEN
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.
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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.
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Contaminantes Atmosféricos , Contaminación del Aire , Humanos , Contaminantes Atmosféricos/análisis , Salud Pública , Reproducibilidad de los Resultados , Canadá/epidemiología , Material Particulado/análisis , Encuestas Epidemiológicas , Exposición a Riesgos AmbientalesRESUMEN
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 â¼ 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.
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Contaminantes Atmosféricos , Contaminación del Aire , COVID-19 , Humanos , Meteorología , Contaminación del Aire/efectos adversos , Contaminación del Aire/análisis , Contaminantes Atmosféricos/análisis , Material Particulado/efectos adversos , Material Particulado/análisis , Factores de Riesgo , California/epidemiología , Nitratos , Exposición a Riesgos Ambientales/efectos adversosRESUMEN
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.
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Renta , Material Particulado , Masculino , Humanos , Anciano , Causalidad , Canadá/epidemiología , TransportesRESUMEN
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.
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Contaminantes Atmosféricos , Contaminación del Aire , Enfermedades Cardiovasculares , Infarto del Miocardio , Accidente Cerebrovascular , Humanos , Adulto , Material Particulado/efectos adversos , Material Particulado/análisis , Análisis de Mediación , Enfermedades Cardiovasculares/epidemiología , Contaminantes Atmosféricos/efectos adversos , Contaminantes Atmosféricos/análisis , Estudios de Cohortes , Contaminación del Aire/efectos adversos , Infarto del Miocardio/epidemiología , Ontario/epidemiología , Exposición a Riesgos Ambientales/efectos adversosRESUMEN
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.
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Contaminantes Atmosféricos , Contaminación del Aire , Adulto , Contaminantes Atmosféricos/análisis , Contaminación del Aire/efectos adversos , Contaminación del Aire/análisis , Estudios de Cohortes , Exposición a Riesgos Ambientales/efectos adversos , Exposición a Riesgos Ambientales/análisis , Gases , Glutatión , Humanos , Oxidantes , Oxidación-Reducción , Estrés Oxidativo , Material Particulado/análisis , AzufreRESUMEN
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.
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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.
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Contaminantes Atmosféricos , Contaminación del Aire , Niño , Humanos , Contaminantes Atmosféricos/efectos adversos , Contaminantes Atmosféricos/análisis , Contaminación del Aire/efectos adversos , Contaminación del Aire/análisis , Cobre/efectos adversos , Cobre/análisis , Estudios Cruzados , Exposición a Riesgos Ambientales/efectos adversos , Exposición a Riesgos Ambientales/análisis , Hospitalización , Dióxido de Nitrógeno/efectos adversos , Oxidantes/efectos adversos , Estrés Oxidativo , Material Particulado/efectos adversos , Material Particulado/análisis , Azufre/efectos adversos , Azufre/análisis , Recién Nacido , Lactante , Preescolar , AdolescenteRESUMEN
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.
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Sedimentos Geológicos , Ríos , Carbono , Monitoreo del Ambiente , Inundaciones , Estaciones del AñoRESUMEN
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.
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Contaminantes Atmosféricos , Neoplasias Encefálicas , Leucemia , Neoplasias Pulmonares , Linfoma no Hodgkin , Mieloma Múltiple , Incendios Forestales , Adulto , Contaminantes Atmosféricos/análisis , Canadá/epidemiología , Estudios de Cohortes , Exposición a Riesgos Ambientales/efectos adversos , Exposición a Riesgos Ambientales/análisis , Humanos , Incidencia , Neoplasias Pulmonares/epidemiología , Linfoma no Hodgkin/epidemiología , Linfoma no Hodgkin/etiología , Mieloma Múltiple/epidemiología , Material Particulado/análisisRESUMEN
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.
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Contaminantes Atmosféricos , Contaminación del Aire , Enfermedades Cardiovasculares , Adulto , Contaminantes Atmosféricos/efectos adversos , Contaminantes Atmosféricos/análisis , Contaminación del Aire/efectos adversos , Contaminación del Aire/análisis , Enfermedades Cardiovasculares/epidemiología , China/epidemiología , Estudios de Cohortes , Exposición a Riesgos Ambientales/efectos adversos , Exposición a Riesgos Ambientales/análisis , Combustibles Fósiles , Humanos , Material Particulado/efectos adversos , Material Particulado/análisis , Estudios ProspectivosRESUMEN
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.
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Contaminantes Atmosféricos , Contaminación del Aire , Material Particulado , Contaminantes Atmosféricos/análisis , Contaminantes Atmosféricos/toxicidad , Contaminación del Aire/estadística & datos numéricos , Ciudades/epidemiología , Exposición a Riesgos Ambientales/estadística & datos numéricos , Humanos , Mortalidad , Nitratos/efectos adversos , Material Particulado/análisis , Material Particulado/toxicidadRESUMEN
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.