Reduction in fine particulate air pollution and mortality: Extended follow-up of the Harvard Six Cities study.
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ABSTRACT: Rationale
A large body of epidemiologic literature has found an association of increased fine particulate air pollution (PM2.5) with acute and chronic mortality. The effect of improvements in particle exposure is less clear.Objectives
Earlier analysis of the Harvard Six Cities adult cohort study showed an association between long-term ambient PM2.5 and mortality between enrollment in the mid-1970s and follow-up until 1990. We extended mortality follow-up for 8 yr in a period of reduced air pollution concentrations.Methods
Annual city-specific PM2.5 concentrations were measured between 1979 and 1988, and estimated for later years from publicly available data. Exposure was defined as (1) city-specific mean PM2.5 during the two follow-up periods, (2) mean PM2.5 in the first period and change between these periods, (3) overall mean PM2.5 across the entire follow-up, and (4) year-specific mean PM2.5. Mortality rate ratios were estimated with Cox proportional hazards regression controlling for individual risk factors.Measurements and main results
We found an increase in overall mortality associated with each 10 microg/m3 increase in PM2.5 modeled either as the overall mean (rate ratio [RR], 1.16; 95% confidence interval [CI], 1.07-1.26) or as exposure in the year of death (RR, 1.14; 95% CI, 1.06-1.22). PM2.5 exposure was associated with lung cancer (RR, 1.27; 95% CI, 0.96-1.69) and cardiovascular deaths (RR, 1.28; 95% CI, 1.13-1.44). Improved overall mortality was associated with decreased mean PM2.5 (10 microg/m3) between periods (RR, 0.73; 95% CI, 0.57-0.95).Conclusion
Total, cardiovascular, and lung cancer mortality were each positively associated with ambient PM2.5 concentrations. Reduced PM2.5 concentrations were associated with reduced mortality risk.
SUBMITTER: Laden F
PROVIDER: S-EPMC2662950 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundEpidemiologic studies have reported associations between fine particles (aerodynamic diameter ? 2.5 µm; PM2.5) and mortality. However, concerns have been raised regarding the sensitivity of the results to model specifications, lower exposures, and averaging time.ObjectiveWe addressed these issues using 11 additional years of follow-up of the Harvard Six Cities study, incorporating recent lower exposures.MethodsWe replicated the previously applied Cox regression, and examined different time lags, the shape of the concentration-response relationship using penalized splines, and changes in the slope of the relation over time. We then conducted Poisson survival analysis with time-varying effects for smoking, sex, and education.ResultsSince 2001, average PM2.5 levels, for all six cities, were < 18 µg/m3. Each increase in PM2.5 (10 µg/m3) was associated with an adjusted increased risk of all-cause mortality (PM2.5 average on previous year) of 14% [95% confidence interval (CI): 7, 22], and with 26% (95% CI: 14, 40) and 37% (95% CI: 7, 75) increases in cardiovascular and lung-cancer mortality (PM2.5 average of three previous years), respectively. The concentration-response relationship was linear down to PM2.5 concentrations of 8 µg/m3. Mortality rate ratios for PM2.5 fluctuated over time, but without clear trends despite a substantial drop in the sulfate fraction. Poisson models produced similar results.ConclusionsThese results suggest that further public policy efforts that reduce fine particulate matter air pollution are likely to have continuing public health benefits.
| S-EPMC3404667 | biostudies-literature
Project description:BackgroundThe systematic evaluation of the results of time-series studies of air pollution is challenged by differences in model specification and publication bias.MethodsWe evaluated the associations of inhalable particulate matter (PM) with an aerodynamic diameter of 10 ?m or less (PM10) and fine PM with an aerodynamic diameter of 2.5 ?m or less (PM2.5) with daily all-cause, cardiovascular, and respiratory mortality across multiple countries or regions. Daily data on mortality and air pollution were collected from 652 cities in 24 countries or regions. We used overdispersed generalized additive models with random-effects meta-analysis to investigate the associations. Two-pollutant models were fitted to test the robustness of the associations. Concentration-response curves from each city were pooled to allow global estimates to be derived.ResultsOn average, an increase of 10 ?g per cubic meter in the 2-day moving average of PM10 concentration, which represents the average over the current and previous day, was associated with increases of 0.44% (95% confidence interval [CI], 0.39 to 0.50) in daily all-cause mortality, 0.36% (95% CI, 0.30 to 0.43) in daily cardiovascular mortality, and 0.47% (95% CI, 0.35 to 0.58) in daily respiratory mortality. The corresponding increases in daily mortality for the same change in PM2.5 concentration were 0.68% (95% CI, 0.59 to 0.77), 0.55% (95% CI, 0.45 to 0.66), and 0.74% (95% CI, 0.53 to 0.95). These associations remained significant after adjustment for gaseous pollutants. Associations were stronger in locations with lower annual mean PM concentrations and higher annual mean temperatures. The pooled concentration-response curves showed a consistent increase in daily mortality with increasing PM concentration, with steeper slopes at lower PM concentrations.ConclusionsOur data show independent associations between short-term exposure to PM10 and PM2.5 and daily all-cause, cardiovascular, and respiratory mortality in more than 600 cities across the globe. These data reinforce the evidence of a link between mortality and PM concentration established in regional and local studies. (Funded by the National Natural Science Foundation of China and others.).
| S-EPMC7891185 | biostudies-literature
Project description:Using daily fine particulate matter (PM2.5) composition data from the 2000-2005 U.S. EPA Chemical Speciation Network (CSN) for over 200 sites, we applied multivariate methods to identify and quantify the major fine particulate matter (PM2.5) source components in the U.S. Novel aspects of this work were: (1) the application of factor analysis (FA) to multi-city daily data, drawing upon both spatial and temporal variations of chemical species; and, (2) the exclusion of secondary components (sulfates, nitrates and organic carbon) from the source identification FA to more clearly discern and apportion the PM2.5 mass to primary emission source categories. For the quantification of source-related mass, we considered two approaches based upon the FA results: 1) using single key tracers for sources identified by FA in a mass regression; and, 2) applying Absolute Principal Component Analysis (APCA). In each case, we followed a two-stage mass regression approach, in which secondary components were first apportioned among the identified sources, and then mass was apportioned to the sources and to other secondary mass not explained by the individual sources. The major U.S. PM2.5 source categories identified via FA (and their key elements) were: Metals Industry (Pb, Zn); Crustal/Soil Particles (Ca, Si); Motor Vehicle Traffic (EC, NO2); Steel Industry (Fe, Mn); Coal Combustion (As, Se); Oil Combustion (V, Ni); Salt Particles (Na, Cl) and Biomass Burning (K). Nationwide spatial plots of the source-related PM2.5 impacts were confirmatory of the factor interpretations: ubiquitous sources, such as Traffic and Soil, were found to be spread across the nation, more unique sources (such as Steel and Metals Processing) being highest in select industrialized cities, Biomass Burning was highest in the U.S. Northwest, while Residual Oil combustion was highest in cities in the Northeastern U.S. and in cities with major seaports. The sum of these source contributions and the secondary PM2.5 components agreed well with the U.S. PM2.5 observed during the study period (mean=14.3 ug/m3; R2= 0.91). Apportionment regression analyses using single-element tracers for each source category gave results consistent with the APCA estimates. Comparisons of nearby sites indicated that the PM2.5 mass and the secondary aerosols were most homogenous spatially, while traffic PM2.5 and its tracer, EC, were among the most spatially representative of the source-related components. Comparison of apportionment results to a previous analysis of the 1979-1982 IP Network revealed similar and correlated major U.S. source category factors, albeit at lower levels than in the earlier period, suggesting a consistency in the U.S. spatial patterns of these source-related exposures over time, as well. These results indicate that applying source apportionment methods to the nationwide CSN can be an informative avenue for identifying and quantifying source components for the subsequent estimation of source-specific health effects, potentially contributing to more efficient regulation of PM2.5.
| S-EPMC3951912 | biostudies-literature
Project description:Short-term changes in levels of fine ambient particulate matter (PM2.5) may increase the risk of acute ischemic stroke; however, results from prior studies have been inconsistent. We examined this hypothesis using data from a multicenter prospective stroke registry.We analyzed data from 9202 patients hospitalized with acute ischemic stroke, having a documented date and time of stroke onset, and residing within 50 km of a PM2.5 monitor in 8 cities in Ontario, Canada. We evaluated the risk of ischemic stroke onset associated with PM2.5 in each city using a time-stratified case-crossover design, matching on day of week and time of day. We then combined these city-specific estimates using random-effects meta-analysis techniques. We examined whether the effects of PM2.5 differed across strata defined by patient characteristics and ischemic stroke etiology.Overall, PM2.5 was associated with a -0.7% change in ischemic stroke risk per 10-?g/m increase in PM2.5 (95% confidence interval = -6.3% to 5.1%). These overall negative results were robust to a number of sensitivity analyses. Among patients with diabetes mellitus, PM2.5 was associated with an 11% increase in ischemic stroke risk (1% to 22%). The association between PM2.5 and ischemic stroke risk varied according to stroke etiology, with the strongest associations observed for strokes due to large-artery atherosclerosis and small-vessel occlusion.These results do not support the hypothesis that short-term increases in PM2.5 levels are associated with ischemic stroke risk overall. However, specific patient subgroups may be at increased risk of particulate-related ischemic strokes.
| S-EPMC3102528 | biostudies-literature
Project description:Objectives To estimate the short term effect of particulate air pollution (particle diameter <10 ?m, or PM10) on mortality and explore the heterogeneity of particulate air pollution effects in major cities in China.Design Generalised linear models with different lag structures using time series data.Setting 38 of the largest cities in 27 provinces of China (combined population >200 million).Participants 350?638 deaths (200?912 in males, 149?726 in females) recorded in 38 city districts by the Disease Surveillance Point System of the Chinese Center for Disease Control and Prevention from 1 January 2010 to 29 June 2013.Main outcome measure Daily numbers of deaths from all causes, cardiorespiratory diseases, and non-cardiorespiratory diseases and among different demographic groups were used to estimate the associations between particulate air pollution and mortality.Results A 10 µg/m3 change in concurrent day PM10 concentrations was associated with a 0.44% (95% confidence interval 0.30% to 0.58%) increase in daily number of deaths. Previous day and two day lagged PM10 levels decreased in magnitude by one third and two thirds but remained statistically significantly associated with increased mortality. The estimate for the effect of PM10 on deaths from cardiorespiratory diseases was 0.62% (0.43% to 0.81%) per 10 µg/m3 compared with 0.26% (0.09% to 0.42%) for other cause mortality. Exposure to PM10 had a greater impact on females than on males. Adults aged 60 and over were more vulnerable to particulate air pollution at high levels than those aged less than 60. The PM10 effect varied across different cities and marginally decreased in cities with higher PM10 concentrations.Conclusion Particulate air pollution has a greater impact on deaths from cardiorespiratory diseases than it does on other cause mortality. People aged 60 or more have a higher risk of death from particulate air pollution than people aged less than 60. The estimates of the effect varied across cities and covered a wide range of domain.
| S-EPMC6287590 | biostudies-literature
Project description:ObjectiveFew studies investigating associations between fine particulate air pollution and hemorrhagic stroke have considered subtypes. Additionally, less is known about the modification of such association by factors measured at the individual level. We aimed to investigate the risk of fatal intracerebral hemorrhage (ICH) incidence in case of PM2.5 (particles ??2.5??m in aerodynamic diameter) exposure.MethodsData on incidence of fatal ICH from 1 June 2012 to 31 May 2014 were extracted from the acute stroke mortality database in Shanghai Municipal Center for Disease Control and Prevention (SCDC). We used the time-stratified case-crossover approach to assess the association between daily concentrations of PM2.5 and fatal ICH incidence in Shanghai, China.ResultsA total of 5286 fatal ICH cases occurred during our study period. The averaged concentration of PM2.5 was 77.45??g/m3. The incidence of fatal ICH was significantly associated with PM2.5 concentration. Substantial differences were observed among subjects with diabetes compared with those without; following the increase of PM2.5 in lag2, the OR (95% CI) for subjects with diabetes was 1.26 (1.09-1.46) versus 1.05 (0.98-1.12) for those without. We did not find evidence of effect modification by hypertension and cigarette smoking.ConclusionsFatal ICH incidence was associated with PM2.5 exposure. Our results also suggested that diabetes may increase the risk for ICH incidence in relation to PM2.5.
| S-EPMC6545210 | biostudies-literature
Project description:BackgroundMaternal exposure to fine particulate air pollution (PM2.5) during pregnancy is associated with lower newborn birthweight, which is a risk factor for chronic disease. Existing studies typically report the average association related with PM2.5 increase, which does not offer information about potentially varying associations at different points of the birthweight distribution.MethodsWe retrieved all birth records in Massachusetts between 2001 and 2013 then restricted our analysis to full-term live singletons (n = 775,768). Using the birthdate, gestational age, and residential address reported at time of birth, we estimated the average maternal PM2.5 exposure during pregnancy of each birth. PM2.5 predictions came from a model that incorporates satellite, land use, and meteorologic data. We applied quantile regression to quantify the association between PM2.5 and birthweight at each decile of birthweight, adjusted for individual and neighborhood covariates. We considered effect modification by indicators of individual and neighborhood socioeconomic status (SES).ResultsPM2.5 was negatively associated with birthweight. An interquartile range increase in PM2.5 was associated with a 16 g [95% confidence interval (CI) = 13, 19] lower birthweight on average, 19 g (95% CI = 15, 23) lower birthweight at the lowest decile of birthweight, and 14 g (95% CI = 9, 19) lower birthweight at the highest decile. In general, the magnitudes of negative associations were larger at lower deciles. We did not find evidence of effect modification by individual or neighborhood SES.ConclusionsIn full-term live births, PM2.5 and birthweight were negatively associated with more severe associations at lower quantiles of birthweight.
| S-EPMC6686872 | biostudies-literature
Project description:We studied globally representative data to quantify how daily fine particulate matter (PM2.5) concentrations influence both daily stock market returns and volatility. Time-series analysis was applied on 47 city-level environmental and economic datasets and meta-analysis of the city-specific estimates was used to generate a global summary effect estimate. We found that, on average, a 10 μg/m3 increase in PM2.5 reduces same day returns by 1.2% (regression coefficient: - 0.012, 95% confidence interval: - 0.021, - 0.003) Based on a meta-regression, these associations are stronger in areas where the average PM2.5 concentrations are lower, the mean returns are higher, and where the local stock market capitalization is low. Our results suggest that a 10 μg/m3 increase in PM2.5 exposure increases stock market volatility by 0.2% (regression coefficient 0.002, 95% CI 0.000, 0.004), but the city-specific estimates were heterogeneous. Meta-regression analysis did not explain much of the between-city heterogeneity. Our results provide global evidence that short-term exposure to air pollution both reduces daily stock market returns and increases volatility.
| S-EPMC8060286 | biostudies-literature
Project description:Epidemiological evidence indicates that exposures to fine particulate matter air pollution (PM2.5) contribute to global burden of disease, primarily as a result of increased risk of cardiovascular morbidity and mortality. However, mechanisms by which PM2.5 exposure induces cardiovascular injury remain unclear. PM2.5-induced endothelial dysfunction and systemic inflammation have been implicated, but direct evidence is lacking.To examine whether acute exposure to PM2.5 is associated with endothelial injury and systemic inflammation.Blood was collected from healthy, nonsmoking, young adults during 3 study periods that included episodes of elevated PM2.5 levels. Microparticles and immune cells in blood were measured by flow cytometry, and plasma cytokine/growth factors were measured using multiplexing laser beads. PM2.5 exposure was associated with the elevated levels of endothelial microparticles (annexin V+/CD41-/CD31+), including subtypes expressing arterial-, venous-, and lung-specific markers, but not microparticles expressing CD62+. These changes were accompanied by suppressed circulating levels of proangiogenic growth factors (EGF [epidermal growth factor], sCD40L [soluble CD40 ligand], PDGF [platelet-derived growth factor], RANTES [regulated on activation, normal T-cell-expressed and secreted], GRO? [growth-regulated protein ?], and VEGF [vascular endothelial growth factor]), and an increase in the levels of antiangiogenic (TNF? [tumor necrosis factor ?], IP-10 [interferon ?-induced protein 10]), and proinflammatory cytokines (MCP-1 [monocyte chemoattractant protein 1], MIP-1?/? [macrophage inflammatory protein 1?/?], IL-6 [interleukin 6], and IL-1? [interleukin 1?]), and markers of endothelial adhesion (sICAM-1 [soluble intercellular adhesion molecule 1] and sVCAM-1 [soluble vascular cellular adhesion molecule 1]). PM2.5 exposure was also associated with an inflammatory response characterized by elevated levels of circulating CD14+, CD16+, CD4+, and CD8+, but not CD19+ cells.Episodic PM2.5 exposures are associated with increased endothelial cell apoptosis, an antiangiogenic plasma profile, and elevated levels of circulating monocytes and T, but not B, lymphocytes. These changes could contribute to the pathogenic sequelae of atherogenesis and acute coronary events.
| S-EPMC5215745 | biostudies-literature
Project description:With 2.8 billion biomass users globally, household air pollution remains a public health threat in many low- and middle-income countries. However, little evidence on pollution levels and health effects exists in low-income settings, especially slums. This study assesses the levels and sources of household air pollution in the urban slums of Nairobi. This cross-sectional study was embedded in a prospective cohort of pregnant women living in two slum areas-Korogocho and Viwandani-in Nairobi. Data on fuel and stove types and ventilation use come from 1058 households, while air quality data based on the particulate matters (PM2.5) level were collected in a sub-sample of 72 households using the DustTrak™ II Model 8532 monitor. We measured PM2.5 levels mainly during daytime and using sources of indoor air pollutions. The majority of the households used kerosene (69.7%) as a cooking fuel. In households where air quality was monitored, the mean PM2.5 levels were high and varied widely, especially during the evenings (124.6 µg/m³ SD: 372.7 in Korogocho and 82.2 µg/m³ SD: 249.9 in Viwandani), and in households using charcoal (126.5 µg/m³ SD: 434.7 in Korogocho and 75.7 µg/m³ SD: 323.0 in Viwandani). Overall, the mean PM2.5 levels measured within homes at both sites (Korogocho = 108.9 µg/m³ SD: 371.2; Viwandani = 59.3 µg/m³ SD: 234.1) were high. Residents of the two slums are exposed to high levels of PM2.5 in their homes. We recommend interventions, especially those focusing on clean cookstoves and lighting fuels to mitigate indoor levels of fine particles.
| S-EPMC5606663 | biostudies-literature