Dataset Information

PM2.5 air pollution and cause-specific cardiovascular disease mortality.

ABSTRACT:

Background

Ambient air pollution is a modifiable risk factor for cardiovascular disease, yet uncertainty remains about the size of risks at lower levels of fine particulate matter (PM2.5) exposure which now occur in the USA and elsewhere.

Methods

We investigated the relationship of ambient PM2.5 exposure with cause-specific cardiovascular disease mortality in 565 477 men and women, aged 50 to 71?years, from the National Institutes of Health-AARP Diet and Health Study. During 7.5 x 106 person-years of follow up, 41 286 cardiovascular disease deaths, including 23 328 ischaemic heart disease (IHD) and 5894 stroke deaths, were ascertained using the National Death Index. PM2.5 was estimated using a hybrid land use regression (LUR) geostatistical model. Multivariate Cox regression models were used to estimate relative risks (RRs) and 95% confidence intervals (CI).

Results

Each increase of 10 ??g/m3 PM2.5 (overall range, 2.9-28.0? ?g/m3) was associated, in fully adjusted models, with a 16% increase in mortality from ischaemic heart disease [hazard ratio (HR) 1.16; 95% CI 1.09-1.22] and a 14% increase in mortality from stroke (HR 1.14; CI 1.02-1.27). Compared with PM2.5 exposure <8? ?g/m3 (referent), risks for CVD were increased in relation to PM2.5 exposures in the range of 8-12? ?g/m3 (CVD: HR 1.04; 95% CI 1.00-1.08), in the range 12-20? ?g/m3 (CVD: HR 1.08; 95% CI 1.03-1.13) and in the range 20+ ?g/m3 (CVD: HR 1.19; 95% CI 1.10-1.28). Results were robust to alternative approaches to PM2.5 exposure assessment and statistical analysis.

Conclusions

Long-term exposure to fine particulate air pollution is associated with ischaemic heart disease and stroke mortality, with excess risks occurring in the range of and below the present US long-term standard for ambient exposure to PM2.5 (12? µg/m3), indicating the need for continued improvements in air pollution abatement for CVD prevention.

SUBMITTER: Hayes RB

PROVIDER: S-EPMC7124502 | biostudies-literature | 2020 Feb

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

PM2.5 air pollution and cause-specific cardiovascular disease mortality.

Hayes Richard B RB Lim Chris C Zhang Yilong Y Cromar Kevin K Shao Yongzhao Y Reynolds Harmony R HR Silverman Debra T DT Jones Rena R RR Park Yikyung Y Jerrett Michael M Ahn Jiyoung J Thurston George D GD

International journal of epidemiology 20200201 1

<h4>Background</h4>Ambient air pollution is a modifiable risk factor for cardiovascular disease, yet uncertainty remains about the size of risks at lower levels of fine particulate matter (PM2.5) exposure which now occur in the USA and elsewhere.<h4>Methods</h4>We investigated the relationship of ambient PM2.5 exposure with cause-specific cardiovascular disease mortality in 565 477 men and women, aged 50 to 71 years, from the National Institutes of Health-AARP Diet and Health Study. During 7.5 x ...[more]

PMID: 31289812

Similar Datasets

Project description:ImportanceAmbient fine particulate matter (PM2.5) air pollution is associated with increased risk of several causes of death. However, epidemiologic evidence suggests that current knowledge does not comprehensively capture all causes of death associated with PM2.5 exposure.ObjectiveTo systematically identify causes of death associated with PM2.5 pollution and estimate the burden of death for each cause in the United States.Design, setting, and participantsIn a cohort study of US veterans followed up between 2006 and 2016, ensemble modeling was used to identify and characterize morphology of the association between PM2.5 and causes of death. Burden of death associated with PM2.5 exposure in the contiguous United States and for each state was then estimated by application of estimated risk functions to county-level PM2.5 estimates from the US Environmental Protection Agency and cause-specific death rate data from the Centers for Disease Control and Prevention.Main outcomes and measuresNonlinear exposure-response functions of the association between PM2.5 and causes of death and burden of death associated with PM2.5.ExposuresAnnual mean PM2.5 levels.ResultsA cohort of 4 522 160 US veterans (4 243 462 [93.8%] male; median [interquartile range] age, 64.1 [55.7-75.5] years; 3 702 942 [82.0%] white, 667 550 [14.8%] black, and 145 593 [3.2%] other race) was followed up for a median (interquartile range) of 10.0 (6.8-10.2) years. In the contiguous United States, PM2.5 exposure was associated with excess burden of death due to cardiovascular disease (56 070.1 deaths [95% uncertainty interval {UI}, 51 940.2-60 318.3 deaths]), cerebrovascular disease (40 466.1 deaths [95% UI, 21 770.1-46 487.9 deaths]), chronic kidney disease (7175.2 deaths [95% UI, 5910.2-8371.9 deaths]), chronic obstructive pulmonary disease (645.7 deaths [95% UI, 300.2-2490.9 deaths]), dementia (19 851.5 deaths [95% UI, 14 420.6-31 621.4 deaths]), type 2 diabetes (501.3 deaths [95% UI, 447.5-561.1 deaths]), hypertension (30 696.9 deaths [95% UI, 27 518.1-33 881.9 deaths]), lung cancer (17 545.3 deaths [95% UI, 15 055.3-20 464.5 deaths]), and pneumonia (8854.9 deaths [95% UI, 7696.2-10 710.6 deaths]). Burden exhibited substantial geographic variation. Estimated burden of death due to nonaccidental causes was 197 905.1 deaths (95% UI, 183 463.3-213 644.9 deaths); mean age-standardized death rates (per 100 000) due to nonaccidental causes were higher among black individuals (55.2 [95% UI, 50.5-60.6]) than nonblack individuals (51.0 [95% UI, 46.4-56.1]) and higher among those living in counties with high (65.3 [95% UI, 56.2-75.4]) vs low (46.1 [95% UI, 42.3-50.4]) socioeconomic deprivation; 99.0% of the burden of death due to nonaccidental causes was associated with PM2.5 levels below standards set by the US Environmental Protection Agency.Conclusions and relevanceIn this study, 9 causes of death were associated with PM2.5 exposure. The burden of death associated with PM2.5 was disproportionally borne by black individuals and socioeconomically disadvantaged communities. Effort toward cleaner air might reduce the burden of PM2.5-associated deaths.

Project description:BACKGROUND:Recent experimental evidence suggests that nutritional supplementation can blunt adverse cardiopulmonary effects induced by acute air pollution exposure. However, whether usual individual dietary patterns can modify the association between long-term air pollution exposure and health outcomes has not been previously investigated. We assessed, in a large cohort with detailed diet information at the individual level, whether a Mediterranean diet modifies the association between long-term exposure to ambient air pollution and cardiovascular disease mortality risk. METHODS:The National Institutes of Health-American Association for Retired Persons Diet and Health Study, a prospective cohort (N=548 845) across 6 states and 2 cities in the United States and with a follow-up period of 17 years (1995-2011), was linked to estimates of annual average exposures to fine particulate matter and nitrogen dioxide at the residential census-tract level. The alternative Mediterranean Diet Index, which uses a 9-point scale to assess conformity with a Mediterranean-style diet, was constructed for each participant from information in cohort baseline dietary questionnaires. We evaluated mortality risks for cardiovascular disease, ischemic heart disease, cerebrovascular disease, or cardiac arrest associated with long-term air pollution exposure. Effect modification of the associations between exposure and the mortality outcomes by alternative Mediterranean Diet Index was examined via interaction terms. RESULTS:For fine particulate matter, we observed elevated and significant associations with cardiovascular disease (hazard ratio [HR] per 10 μg/m3, 1.13; 95% CI, 1.08-1.18), ischemic heart disease (HR, 1.16; 95% CI, 1.10-1.23), and cerebrovascular disease (HR, 1.15; 95% CI, 1.03-1.28). For nitrogen dioxide, we found significant associations with cardiovascular disease (HR per 10 ppb, 1.06; 95% CI, 1.04-1.08) and ischemic heart disease (HR, 1.08; 95% CI, 1.05-1.11). Analyses indicated that Mediterranean diet modified these relationships, as those with a higher alternative Mediterranean Diet Index score had significantly lower rates of cardiovascular disease mortality associated with long-term air pollution exposure ( P-interaction<0.05). CONCLUSIONS:A Mediterranean diet reduced cardiovascular disease mortality risk related to long-term exposure to air pollutants in a large prospective US cohort. Increased consumption of foods rich in antioxidant compounds may aid in reducing the considerable disease burden associated with ambient air pollution.

Project description:ImportanceHispanics are the largest minority group in the United States and face a disproportionate burden of risk factors for cardiovascular disease (CVD) and low socioeconomic position. However, Hispanics paradoxically experience lower all-cause mortality rates compared with their non-Hispanic white (NHW) counterparts. This phenomenon has been largely observed in Mexicans, and whether this holds true for other Hispanic subgroups or whether these favorable trends persist over time remains unknown.ObjectiveTo disaggregate a decade of national CVD mortality data for the 3 largest US Hispanic subgroups.Design, setting, and participantsDeaths from CVD for the 3 largest US Hispanic subgroups-Mexicans, Puerto Ricans, and Cubans-compared with NHWs were extracted from the US National Center for Health Statistics mortality records using the underlying cause of death based on coding from the International Statistical Classification of Diseases and Related Health Problems, Tenth Revision (I00-II69). Mortality data were evaluated from January 1, 2003, to December 31, 2012. Population estimates were calculated using linear interpolation from the 2000 and 2010 US Census reports. Data were analyzed from November 2015 to July 2016.Main outcomes and measuresMortality due to CVD.ResultsParticipants included 688 074 Mexican, 163 335 Puerto Rican, 130 397 Cuban, and 19 357 160 NHW individuals (49.0% men and 51.0% women; mean [SD] age, 75 [15] years). At the time of CVD death, Mexicans (age, 67 [18] years) and Puerto Ricans (age, 68 [17] years) were younger compared with NHWs (age, 76 [15] years). Mortality rates due to CVD decreased from a mean of 414.2 per 100 000 in 2003 to 303.3 per 100 000 in 2012. Estimated decreases in mortality rate for CVD from 2003 to 2012 ranged from 85 per 100 000 for all Hispanic women to 144 per 100 000 for Cuban men, but rate differences between groups vary substantially, with Puerto Ricans exhibiting similar mortality patterns to NHWs, and Mexicans experiencing lower mortality. Puerto Ricans experienced higher mortality rates for ischemic and hypertensive heart disease compared with other subgroups, whereas Mexicans experienced higher rates of cerebrovascular disease deaths.Conclusions and relevanceSignificant differences in CVD mortality rates and changes over time were found among the 3 largest Hispanic subgroups in the United States. Findings suggest that the current aggregate classification of Hispanics masks heterogeneity in CVD mortality reporting, leading to an incomplete understanding of health risks and outcomes in this population.

Project description:BACKGROUND:Coarse particulate matter with aerodynamic diameter between 2.5 and [Formula: see text] ([Formula: see text]) air pollution is a severe environmental problem in developing countries, but its challenges to public health were rarely evaluated. OBJECTIVE:We aimed to investigate the associations between day-to-day changes in [Formula: see text] and cause-specific mortality in China. METHODS:We conducted a nationwide daily time-series analysis in 272 main Chinese cities from 2013 to 2015. The associations between [Formula: see text] concentrations and mortality were analyzed in each city using overdispersed generalized additive models. Two-stage Bayesian hierarchical models were used to estimate national and regional average associations, and random-effect models were used to pool city-specific concentration-response curves. Two-pollutant models were adjusted for fine particles with aerodynamic diameter [Formula: see text] ([Formula: see text]) or gaseous pollutants. RESULTS:Overall, we observed positive and approximately linear concentration-response associations between [Formula: see text] and daily mortality. A [Formula: see text] increase in [Formula: see text] was associated with higher mortality due to nonaccidental causes [0.23%; 95% posterior interval (PI): 0.13, 0.33], cardiovascular diseases (CVDs; 0.25%; 95% PI: 0.13, 0.37), coronary heart disease (CHD; 0.21%; 95% PI: 0.05, 0.36), stroke (0.21%; 95% PI: 0.08, 0.35), respiratory diseases (0.26%; 95% PI: 0.07, 0.46), and chronic obstructive pulmonary disease (COPD; 0.34%; 95% PI: 0.12, 0.57). Associations were stronger for cities in southern vs. northern China, with significant differences for total and cardiovascular mortality. Associations with [Formula: see text] were of similar magnitude to those for [Formula: see text] in both single- and two-pollutant models with mutual adjustment. Associations were robust to adjustment for gaseous pollutants other than nitrogen dioxide and sulfur dioxide. Meta-regression indicated that a larger positive correlation between [Formula: see text] and [Formula: see text] predicted stronger city-specific associations between [Formula: see text] and total mortality. CONCLUSIONS:This analysis showed significant associations between short-term [Formula: see text] exposure and daily nonaccidental and cardiopulmonary mortality based on data from 272 cities located throughout China. Associations appeared to be independent of exposure to [Formula: see text], carbon monoxide, and ozone. https://doi.org/10.1289/EHP2711.

Project description:Psychosocial and environmental stress exposures across the life course have been shown to be relevant in the development of cardiovascular disease (CVD). Assessing more than one stressor from different domains (e.g., individual and neighborhood) and across the life course moves us towards a more integrated picture of how stress affects health and well-being. Furthermore, these individual and neighborhood psychosocial stressors act on biologic pathways, including immune function and inflammatory response, which are also impacted by ubiquitous environmental exposures such as air pollution. The objective of this study is to evaluate the interaction between psychosocial stressors, at both the individual and neighborhood level, and air pollution on CVD. This study used data from the 2009-2011 Behavioral Risk Factor Surveillance System (BRFSS) from Washington State. Adverse childhood experiences (ACEs) measured at the individual level, and neighborhood deprivation index (NDI) measured at the zip code level, were the psychosocial stressors of interest. Exposures to three air pollutants-particulate matter (both PM2.5 and PM10) and nitrogen dioxide (NO?)-were also calculated at the zip code level. Outcome measures included several self-reported CVD-related health conditions. Both multiplicative and additive interaction quantified using the relative excess risk due to interaction (RERI), were evaluated. This study included 32,151 participants in 502 unique zip codes. Multiplicative and positive additive interactions were observed between ACEs and PM10 for diabetes, in models adjusted for NDI. The prevalence of diabetes was 1.58 (95% CI: 1.40, 1.79) times higher among those with both high ACEs and high PM10 compared to those with low ACEs and low PM10 (p-value = 0.04 for interaction on the multiplicative scale). Interaction was also observed between neighborhood-level stressors (NDI) and air pollution (NO?) for the stroke and diabetes outcomes on both multiplicative and additive scales. Modest interaction was observed between NDI and air pollution, supporting prior literature on the importance of neighborhood-level stressors in cardiovascular health and reinforcing the importance of NDI on air pollution health effects. ACEs may exert health effects through selection into disadvantaged neighborhoods and more work is needed to understand the accumulation of risk in multiple domains across the life course.

Dataset Information

PM2.5 air pollution and cause-specific cardiovascular disease mortality.

Background

Methods

Results

Conclusions

Publications

PM2.5 air pollution and cause-specific cardiovascular disease mortality.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets