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A spatial joint analysis of metal constituents of ambient particulate matter and mortality in England.

ABSTRACT: Few studies have investigated associations between metal components of particulate matter on mortality due to well-known issues of multicollinearity. Here, we analyze these exposures jointly to evaluate their associations with mortality on small area data. We fit a Bayesian profile regression (BPR) to account for the multicollinearity in the elemental components (iron, copper, and zinc) of PM10 and PM2.5. The models are developed in relation to mortality from cardiovascular and respiratory disease and lung cancer incidence in 2008-2011 at a small area level, for a population of 13.6 million in the London-Oxford area of England. From the BPR, we identified higher risks in the PM10 fraction cluster likely to represent the study area, excluding London, for cardiovascular mortality relative risk (RR) 1.07 (95% credible interval [CI] 1.02, 1.12) and for respiratory mortality RR 1.06 (95%CI 0.99, 1.31), compared with the study mean. For PM2.5 fraction, higher risks were seen for cardiovascular mortality RR 1.55 (CI 95% 1.38, 1.71) and respiratory mortality RR 1.51 (CI 95% 1.33, 1.72), likely to represent the "highways" cluster. We did not find relevant associations for lung cancer incidence. Our analysis showed small but not fully consistent adverse associations between health outcomes and particulate metal exposures. The BPR approach identified subpopulations with unique exposure profiles and provided information about the geographical location of these to help interpret findings.

SUBMITTER: Lavigne A

PROVIDER: S-EPMC7423532 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature

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A spatial joint analysis of metal constituents of ambient particulate matter and mortality in England.

Lavigne Aurore A Freni-Sterrantino Anna A Fecht Daniela D Liverani Silvia S Blangiardo Marta M de Hoogh Kees K Molitor John J Hansell Anna L AL

Environmental epidemiology (Philadelphia, Pa.) 20200716 4

Few studies have investigated associations between metal components of particulate matter on mortality due to well-known issues of multicollinearity. Here, we analyze these exposures jointly to evaluate their associations with mortality on small area data. We fit a Bayesian profile regression (BPR) to account for the multicollinearity in the elemental components (iron, copper, and zinc) of PM<sub>10</sub> and PM<sub>2.5.</sub> The models are developed in relation to mortality from cardiovascular ...[more]

PMID: 32832837

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Project description:BackgroundNumerous studies have linked fine particles [? 2.5 µm in aerodynamic diameter (PM(2.5))] and health. Most studies focused on the total mass of the particles, although the chemical composition of the particles varies substantially. Which chemical components of fine particles that are the most harmful is not well understood, and research on the chemical composition of PM(2.5) and the components that are the most harmful is particularly limited in Asia.ObjectivesWe characterized PM(2.5) chemical composition and estimated the effects of cause-specific mortality of PM(2.5) mass and constituents in Seoul, Korea. We compared the chemical composition of particles to those of the eastern and western United States.MethodsWe examined temporal variability of PM(2.5) mass and its composition using hourly data. We applied an overdispersed Poisson generalized linear model, adjusting for time, day of week, temperature, and relative humidity to investigate the association between risk of mortality and PM(2.5) mass and its constituents in Seoul, Korea, for August 2008 through October 2009.ResultsPM(2.5) and chemical components exhibited temporal patterns by time of day and season. The chemical characteristics of Seoul's PM(2.5) were more similar to PM(2.5) found in the western United States than in the eastern United States. Seoul's PM(2.5) had lower sulfate (SO(4)) contributions and higher nitrate (NO(3)) contributions than that of the eastern United States, although overall PM(2.5) levels in Seoul were higher than in the United States. An interquartile range (IQR) increase in magnesium (Mg) (0.05 ?g/m³) was associated with a 1.4% increase (95% confidence interval: 0.2%, 2.6%) in total mortality on the following day. Several components that were among the largest contributors to PM(2.5) total mass--NO(3), SO(4), and ammonium (NH(4))--were moderately associated with same-day cardiovascular mortality at the p < 0.10 level. Other components with smaller mass contributions [Mg and chlorine (Cl)] exhibited moderate associations with respiratory mortality on the following day (p < 0.10).ConclusionsOur findings link PM(2.5) constituents with mortality and have implications for policy making on sources of PM(2.5) and on the relevance of PM(2.5) health studies from other areas to this region.

Project description:Murine Pulmonary Responses to Ambient Baltimore Particulate Matter: Genomic Analysis and Contribution to Airway Hyperresponsiveness Asthma is a complex disease characterized by airway hyperresponsiveness (AHR) and chronic airway inflammation. Environmental factors such as ambient particulate matter (PM), a major air pollutant, has been demonstrated in epidemiological studies to contribute to asthma exacerbation and increased asthma prevalence. OBJECTIVE: We investigated the genomic and pathophysiological effects of Baltimore PM (median diameter 1.78 µm) in a murine model of asthma to identify potential biomarkers. METHODS: A/J mice with ovalbumin (OVA) –induced AHR were exposed to PM (20 mg/kg, intratracheal), and both AHR and bronchoalveolar lavage (BAL) were assayed on days 1, 4, and 7 post exposure. Lung gene expression profiling (Affymetrix Mouse430_ 2.0) by PM (20 mg/kg, intratracheal) were assayed on OVA- and / or PM--challenged mice. RESULTS: Significant increases of airway responsiveness in OVA-treated mice were observed, indicating an asthmatic phenotype. Ambient PM exposure induced significant changes in AHR in both naive mice and OVA-induced asthmatic mice. In both naive and OVA challenged asthmatic mice, PM induced eosinophil and neutrophil infiltration into airways, elevated BAL protein content, and stimulated secretion of TH1 cytokines (IFN-g, IL-6, and TNF-a) and TH2 cytokines (IL-4, IL-5, and eotaxin) into BAL. Consistent with these results, PM induced expression of genes of innate immune response, chemotaxis and complementary system. CONCLUSION: These studies, consistent with epidemiological data, indicate that PM increases AHR and lung inflammation in naïve mice and exacerbates the asthma phenotype of increased AHR and gene expression pattern changes correlated with acute lung inflammation and airway damage. We used microarrays to detail the global programme of gene expression induced by rhPBEF treatment and VALI. Keywords: gene expression

Project description:BACKGROUND:The link between PM2.5 exposure and adverse health outcomes is well documented from studies across the world. However, the reported effect estimates vary across studies, locations and constituents. We aimed to conduct a meta-analysis on associations between short-term exposure to PM2.5 constituents and mortality using city-specific estimates, and explore factors that may explain some of the observed heterogeneity. METHODS:We systematically reviewed epidemiological studies on particle constituents and mortality using PubMed and Web of Science databases up to July 2015.We included studies that examined the association between short-term exposure to PM2.5 constituents and all-cause, cardiovascular, and respiratory mortality, in the general adult population. Each study was summarized based on pre-specified study key parameters (e.g., location, time period, population, diagnostic classification standard), and we evaluated the risk of bias using the Office of Health Assessment and Translation (OHAT) Method for each included study. We extracted city-specific mortality risk estimates for each constituent and cause of mortality. For multi-city studies, we requested the city-specific risk estimates from the authors unless reported in the article. We performed random effects meta-analyses using city-specific estimates, and examined whether the effects vary across regions and city characteristics (PM2.5 concentration levels, air temperature, elevation, vegetation, size of elderly population, population density, and baseline mortality). RESULTS:We found a 0.89% (95% CI: 0.68, 1.10%) increase in all-cause, a 0.80% (95% CI: 0.41, 1.20%) increase in cardiovascular, and a 1.10% (95% CI: 0.59, 1.62%) increase in respiratory mortality per 10?g/m3 increase in PM2.5. Accounting for the downward bias induced by studies of single days, the all-cause mortality estimate increased to 1.01% (95% CI: 0.81, 1.20%). We found significant associations between mortality and several PM2.5 constituents. The most consistent and stronger associations were observed for elemental carbon (EC) and potassium (K). For most of the constituents, we observed high variability of effect estimates across cities. CONCLUSIONS:Our meta-analysis suggests that (a) combustion elements such as EC and K have a stronger association with mortality, (b) single lag studies underestimate effects, and (c) estimates of PM2.5 and constituents differ across regions. Accounting for PM mass in constituent's health models may lead to more stable and comparable effect estimates across different studies. SYSTEMATIC REVIEW REGISTRATION:PROSPERO: CRD42017055765.

Project description:BackgroundSurvivors of acute myocardial infarction (AMI) are at increased risk of dying within several hours to days following exposure to elevated levels of ambient air pollution. Little is known, however, about the influence of long-term (months to years) air pollution exposure on survival after AMI.ObjectiveWe conducted a population-based cohort study to determine the impact of long-term exposure to fine particulate matter ? 2.5 ?m in diameter (PM2.5) on post-AMI survival.MethodsWe assembled a cohort of 8,873 AMI patients who were admitted to 1 of 86 hospital corporations across Ontario, Canada in 1999-2001. Mortality follow-up for this cohort extended through 2011. Cumulative time-weighted exposures to PM2.5 were derived from satellite observations based on participants' annual residences during follow-up. We used standard and multilevel spatial random-effects Cox proportional hazards models and adjusted for potential confounders.ResultsBetween 1999 and 2011, we identified 4,016 nonaccidental deaths, of which 2,147 were from any cardiovascular disease, 1,650 from ischemic heart disease, and 675 from AMI. For each 10-?g/m3 increase in PM2.5, the adjusted hazard ratio (HR10) of nonaccidental mortality was 1.22 [95% confidence interval (CI): 1.03, 1.45]. The association with PM2.5 was robust to sensitivity analyses and appeared stronger for cardiovascular-related mortality: ischemic heart (HR10 = 1.43; 95% CI: 1.12, 1.83) and AMI (HR10 = 1.64; 95% CI: 1.13, 2.40). We estimated that 12.4% of nonaccidental deaths (or 497 deaths) could have been averted if the lowest measured concentration in an urban area (4 ?g/m3) had been achieved at all locations over the course of the study.ConclusionsLong-term air pollution exposure adversely affects the survival of AMI patients.CitationChen H, Burnett RT, Copes R, Kwong JC, Villeneuve PJ, Goldberg MS, Brook RD, van Donkelaar A, Jerrett M, Martin RV, Brook JR, Kopp A, Tu JV. 2016. Ambient fine particulate matter and mortality among survivors of myocardial infarction: population-based cohort study. Environ Health Perspect 124:1421-1428;?http://dx.doi.org/10.1289/EHP185.

Project description:We present a systematic review of studies assessing the association between ambient particulate matter (PM) and premature mortality and the results of a Bayesian hierarchical meta-analysis while accounting for population differences of the included studies. The review protocol was registered in the PROSPERO systematic review registry. Medline, CINAHL and Global Health databases were systematically searched. Bayesian hierarchical meta-analysis was conducted using a non-informative prior to assess whether the regression coefficients differed across observations due to the heterogeneity among studies. We identified 3248 records for title and abstract review, of which 309 underwent full text screening. Thirty-six studies were included, based on the inclusion criteria. Most of the studies were from China (n = 14), India (n = 6) and the USA (n = 3). PM2.5 was the most frequently reported pollutant. PM was estimated using modelling techniques (22 studies), satellite-based measures (four studies) and direct measurements (ten studies). Mortality data were sourced from country-specific mortality statistics for 17 studies, Global Burden of Disease data for 16 studies, WHO data for two studies and life tables for one study. Sixteen studies were included in the Bayesian hierarchical meta-analysis. The meta-analysis revealed that the annual estimate of premature mortality attributed to PM2.5 was 253 per 1,000,000 population (95% CI: 90, 643) and 587 per 1,000,000 population (95% CI: 1, 39,746) for PM10. 253 premature deaths per million population are associated with exposure to ambient PM2.5. We observed an unstable estimate for PM10, most likely due to heterogeneity among the studies. Future research efforts should focus on the effects of ambient PM10 and premature mortality, as well as include populations outside Asia. Key messages: Ambient PM2.5 is associated with premature mortality. Given that rapid urbanization may increase this burden in the coming decades, our study highlights the urgency of implementing air pollution mitigation strategies to reduce the risk to population and planetary health.

Dataset Information

A spatial joint analysis of metal constituents of ambient particulate matter and mortality in England.

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A spatial joint analysis of metal constituents of ambient particulate matter and mortality in England.

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