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      Disparities in Air Pollution Exposure in the United States by Race/Ethnicity and Income, 1990–2010

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          Abstract

          Background:

          Few studies have investigated air pollution exposure disparities by race/ethnicity and income across criteria air pollutants, locations, or time.

          Objective:

          The objective of this study was to quantify exposure disparities by race/ethnicity and income throughout the contiguous United States for six criteria air pollutants, during the period 1990 to 2010.

          Methods:

          We quantified exposure disparities among racial/ethnic groups (non-Hispanic White, non-Hispanic Black, Hispanic (any race), non-Hispanic Asian) and by income for multiple spatial units (contiguous United States, states, urban vs. rural areas) and years (1990, 2000, 2010) for carbon monoxide (CO), nitrogen dioxide ( NO 2 ), ozone ( O 3 ), particulate matter with aerodynamic diameter 2.5 μ m ( PM 2.5 ; excluding year-1990), particulate matter with aerodynamic diameter 10 μ m ( PM 10 ), and sulfur dioxide ( SO 2 ). We used census data for demographic information and a national empirical model for ambient air pollution levels.

          Results:

          For all years and pollutants, the racial/ethnic group with the highest national average exposure was a racial/ethnic minority group. In 2010, the disparity between the racial/ethnic group with the highest vs. lowest national-average exposure was largest for NO 2 [54% ( 4.6  ppb )], smallest for O 3 [3.6% ( 1.6  ppb )], and intermediate for the remaining pollutants (13%–19%). The disparities varied by U.S. state; for example, for PM 2.5 in 2010, exposures were at least 5% higher than average in 63% of states for non-Hispanic Black populations; in 33% and 26% of states for Hispanic and for non-Hispanic Asian populations, respectively; and in no states for non-Hispanic White populations. Absolute exposure disparities were larger among racial/ethnic groups than among income categories (range among pollutants: between 1.1 and 21 times larger). Over the period studied, national absolute racial /ethnic exposure disparities declined by between 35% ( 0.6 6 μ g / m 3 ; PM 2.5 ) and 88% ( 0.35  ppm ; CO); relative disparities declined to between 0.99 × ( PM 2.5 ; i.e., nearly zero change) and 0.71 × (CO; i.e., a 29 % reduction).

          Discussion:

          As air pollution concentrations declined during the period 1990 to 2010, absolute (and to a lesser extent, relative) racial/ethnic exposure disparities also declined. However, in 2010, racial/ethnic exposure disparities remained across income levels, in urban and rural areas, and in all states, for multiple pollutants. https://doi.org/10.1289/EHP8584

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          Most cited references53

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          Global, regional, and national comparative risk assessment of 84 behavioural, environmental and occupational, and metabolic risks or clusters of risks for 195 countries and territories, 1990–2017: a systematic analysis for the Global Burden of Disease Study 2017

          Summary Background The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2017 comparative risk assessment (CRA) is a comprehensive approach to risk factor quantification that offers a useful tool for synthesising evidence on risks and risk–outcome associations. With each annual GBD study, we update the GBD CRA to incorporate improved methods, new risks and risk–outcome pairs, and new data on risk exposure levels and risk–outcome associations. Methods We used the CRA framework developed for previous iterations of GBD to estimate levels and trends in exposure, attributable deaths, and attributable disability-adjusted life-years (DALYs), by age group, sex, year, and location for 84 behavioural, environmental and occupational, and metabolic risks or groups of risks from 1990 to 2017. This study included 476 risk–outcome pairs that met the GBD study criteria for convincing or probable evidence of causation. We extracted relative risk and exposure estimates from 46 749 randomised controlled trials, cohort studies, household surveys, census data, satellite data, and other sources. We used statistical models to pool data, adjust for bias, and incorporate covariates. Using the counterfactual scenario of theoretical minimum risk exposure level (TMREL), we estimated the portion of deaths and DALYs that could be attributed to a given risk. We explored the relationship between development and risk exposure by modelling the relationship between the Socio-demographic Index (SDI) and risk-weighted exposure prevalence and estimated expected levels of exposure and risk-attributable burden by SDI. Finally, we explored temporal changes in risk-attributable DALYs by decomposing those changes into six main component drivers of change as follows: (1) population growth; (2) changes in population age structures; (3) changes in exposure to environmental and occupational risks; (4) changes in exposure to behavioural risks; (5) changes in exposure to metabolic risks; and (6) changes due to all other factors, approximated as the risk-deleted death and DALY rates, where the risk-deleted rate is the rate that would be observed had we reduced the exposure levels to the TMREL for all risk factors included in GBD 2017. Findings In 2017, 34·1 million (95% uncertainty interval [UI] 33·3–35·0) deaths and 1·21 billion (1·14–1·28) DALYs were attributable to GBD risk factors. Globally, 61·0% (59·6–62·4) of deaths and 48·3% (46·3–50·2) of DALYs were attributed to the GBD 2017 risk factors. When ranked by risk-attributable DALYs, high systolic blood pressure (SBP) was the leading risk factor, accounting for 10·4 million (9·39–11·5) deaths and 218 million (198–237) DALYs, followed by smoking (7·10 million [6·83–7·37] deaths and 182 million [173–193] DALYs), high fasting plasma glucose (6·53 million [5·23–8·23] deaths and 171 million [144–201] DALYs), high body-mass index (BMI; 4·72 million [2·99–6·70] deaths and 148 million [98·6–202] DALYs), and short gestation for birthweight (1·43 million [1·36–1·51] deaths and 139 million [131–147] DALYs). In total, risk-attributable DALYs declined by 4·9% (3·3–6·5) between 2007 and 2017. In the absence of demographic changes (ie, population growth and ageing), changes in risk exposure and risk-deleted DALYs would have led to a 23·5% decline in DALYs during that period. Conversely, in the absence of changes in risk exposure and risk-deleted DALYs, demographic changes would have led to an 18·6% increase in DALYs during that period. The ratios of observed risk exposure levels to exposure levels expected based on SDI (O/E ratios) increased globally for unsafe drinking water and household air pollution between 1990 and 2017. This result suggests that development is occurring more rapidly than are changes in the underlying risk structure in a population. Conversely, nearly universal declines in O/E ratios for smoking and alcohol use indicate that, for a given SDI, exposure to these risks is declining. In 2017, the leading Level 4 risk factor for age-standardised DALY rates was high SBP in four super-regions: central Europe, eastern Europe, and central Asia; north Africa and Middle East; south Asia; and southeast Asia, east Asia, and Oceania. The leading risk factor in the high-income super-region was smoking, in Latin America and Caribbean was high BMI, and in sub-Saharan Africa was unsafe sex. O/E ratios for unsafe sex in sub-Saharan Africa were notably high, and those for alcohol use in north Africa and the Middle East were notably low. Interpretation By quantifying levels and trends in exposures to risk factors and the resulting disease burden, this assessment offers insight into where past policy and programme efforts might have been successful and highlights current priorities for public health action. Decreases in behavioural, environmental, and occupational risks have largely offset the effects of population growth and ageing, in relation to trends in absolute burden. Conversely, the combination of increasing metabolic risks and population ageing will probably continue to drive the increasing trends in non-communicable diseases at the global level, which presents both a public health challenge and opportunity. We see considerable spatiotemporal heterogeneity in levels of risk exposure and risk-attributable burden. Although levels of development underlie some of this heterogeneity, O/E ratios show risks for which countries are overperforming or underperforming relative to their level of development. As such, these ratios provide a benchmarking tool to help to focus local decision making. Our findings reinforce the importance of both risk exposure monitoring and epidemiological research to assess causal connections between risks and health outcomes, and they highlight the usefulness of the GBD study in synthesising data to draw comprehensive and robust conclusions that help to inform good policy and strategic health planning. Funding Bill & Melinda Gates Foundation.
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            Estimates and 25-year trends of the global burden of disease attributable to ambient air pollution: an analysis of data from the Global Burden of Diseases Study 2015

            Summary Background Exposure to ambient air pollution increases morbidity and mortality, and is a leading contributor to global disease burden. We explored spatial and temporal trends in mortality and burden of disease attributable to ambient air pollution from 1990 to 2015 at global, regional, and country levels. Methods We estimated global population-weighted mean concentrations of particle mass with aerodynamic diameter less than 2·5 μm (PM2·5) and ozone at an approximate 11 km × 11 km resolution with satellite-based estimates, chemical transport models, and ground-level measurements. Using integrated exposure–response functions for each cause of death, we estimated the relative risk of mortality from ischaemic heart disease, cerebrovascular disease, chronic obstructive pulmonary disease, lung cancer, and lower respiratory infections from epidemiological studies using non-linear exposure–response functions spanning the global range of exposure. Findings Ambient PM2·5 was the fifth-ranking mortality risk factor in 2015. Exposure to PM2·5 caused 4·2 million (95% uncertainty interval [UI] 3·7 million to 4·8 million) deaths and 103·1 million (90·8 million 115·1 million) disability-adjusted life-years (DALYs) in 2015, representing 7·6% of total global deaths and 4·2% of global DALYs, 59% of these in east and south Asia. Deaths attributable to ambient PM2·5 increased from 3·5 million (95% UI 3·0 million to 4·0 million) in 1990 to 4·2 million (3·7 million to 4·8 million) in 2015. Exposure to ozone caused an additional 254 000 (95% UI 97 000–422 000) deaths and a loss of 4·1 million (1·6 million to 6·8 million) DALYs from chronic obstructive pulmonary disease in 2015. Interpretation Ambient air pollution contributed substantially to the global burden of disease in 2015, which increased over the past 25 years, due to population ageing, changes in non-communicable disease rates, and increasing air pollution in low-income and middle-income countries. Modest reductions in burden will occur in the most polluted countries unless PM2·5 values are decreased substantially, but there is potential for substantial health benefits from exposure reduction. Funding Bill & Melinda Gates Foundation and Health Effects Institute.
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              The contribution of outdoor air pollution sources to premature mortality on a global scale.

              Assessment of the global burden of disease is based on epidemiological cohort studies that connect premature mortality to a wide range of causes, including the long-term health impacts of ozone and fine particulate matter with a diameter smaller than 2.5 micrometres (PM2.5). It has proved difficult to quantify premature mortality related to air pollution, notably in regions where air quality is not monitored, and also because the toxicity of particles from various sources may vary. Here we use a global atmospheric chemistry model to investigate the link between premature mortality and seven emission source categories in urban and rural environments. In accord with the global burden of disease for 2010 (ref. 5), we calculate that outdoor air pollution, mostly by PM2.5, leads to 3.3 (95 per cent confidence interval 1.61-4.81) million premature deaths per year worldwide, predominantly in Asia. We primarily assume that all particles are equally toxic, but also include a sensitivity study that accounts for differential toxicity. We find that emissions from residential energy use such as heating and cooking, prevalent in India and China, have the largest impact on premature mortality globally, being even more dominant if carbonaceous particles are assumed to be most toxic. Whereas in much of the USA and in a few other countries emissions from traffic and power generation are important, in eastern USA, Europe, Russia and East Asia agricultural emissions make the largest relative contribution to PM2.5, with the estimate of overall health impact depending on assumptions regarding particle toxicity. Model projections based on a business-as-usual emission scenario indicate that the contribution of outdoor air pollution to premature mortality could double by 2050.
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                Author and article information

                Journal
                Environ Health Perspect
                Environ Health Perspect
                EHP
                Environmental Health Perspectives
                Environmental Health Perspectives
                0091-6765
                1552-9924
                15 December 2021
                December 2021
                : 129
                : 12
                : 127005
                Affiliations
                [ 1 ]Department of Civil & Environmental Engineering, University of Washington , Seattle, Washington, USA
                [ 2 ]Department of Epidemiology, University of Washington , Seattle, Washington, USA
                [ 3 ]Department of Cancer Control and Population Health, Graduate School of Cancer Science and Policy, National Cancer Center , Goyang-si, Gyeonggi-do, Korea
                [ 4 ]Department of Mechanical Engineering & Department of Engineering and Public Policy, Carnegie Mellon University , Pittsburgh, Pennsylvania, USA
                [ 5 ]Department of Biostatistics, University of Washington , Seattle, Washington, USA
                [ 6 ]Department of Environmental and Occupational Health Sciences, University of Washington , Seattle, Washington, USA
                Author notes
                Address correspondence to Julian Marshall, Department of Civil & Environmental Engineering, University of Washington, 201 More Hall, Seattle, WA 98195 USA. Telephone: (206) 685-2591. Email: jdmarsh@ 123456uw.edu
                Author information
                https://orcid.org/0000-0003-3400-992X
                https://orcid.org/0000-0001-8076-5457
                https://orcid.org/0000-0002-7110-3395
                https://orcid.org/0000-0002-1819-083X
                https://orcid.org/0000-0003-1622-508X
                Article
                EHP8584
                10.1289/EHP8584
                8672803
                34908495
                8ee0e195-6d53-4d8c-a243-4fe8761f4e73

                EHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted.

                History
                : 29 October 2020
                : 20 October 2021
                : 09 November 2021
                Categories
                Research

                Public health
                Public health

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