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How low can you go? Air pollution affects mortality at very low levels.

ABSTRACT: The World Health Organization (WHO) recently released new guidelines for outdoor fine particulate air pollution (PM_2.5) recommending an annual average concentration of 5 μg/m³. Yet, our understanding of the concentration-response relationship between outdoor PM_2.5 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 PM_2.5 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 PM_2.5 annually compared to previous estimates. The global health benefits of meeting the new WHO guideline for outdoor PM_2.5 are greater than previously assumed and indicate a need for continued reductions in outdoor air pollution around the world.

SUBMITTER: Weichenthal S

PROVIDER: S-EPMC9519036 | biostudies-literature | 2022 Sep

REPOSITORIES: biostudies-literature

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How low can you go? Air pollution affects mortality at very low levels.

Weichenthal Scott S Pinault Lauren L Christidis Tanya T Burnett Richard T RT Brook Jeffrey R JR Chu Yen Y Crouse Dan L DL Erickson Anders C AC Hystad Perry P Li Chi C Martin Randall V RV Meng Jun J Pappin Amanda J AJ Tjepkema Michael M van Donkelaar Aaron A Weagle Crystal L CL Brauer Michael M

Science advances 20220928 39

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 lo ...[more]

PMID: 36170354

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Project description:Zinc (Zn) is a major elemental component of respirable ambient particulate matter (PM) detected often at alarming levels in urban air. Exposure to PM has been widely associated with increased cardiovascular morbidity and mortality, however, it is not known what components or sources of PM are causative. We recently demonstrated that long-term episodic inhalation of combustion PM, having similar amount of Zn found in urban PM, caused myocardial lesions in rats. We further demonstrated that a single pulmonary exposure to Zn at high concentration is associated with disturbances in cardiac mitochondrial function, ion channel regulation, calcium homeostasis, and cell signaling. Therefore, in this study we investigated the role of PM-associated Zn in cardiac injury using multiple exposure scenarios. Male Wistar-Kyoto (WKY) rats of 12-14 wks age were intratracheally exposed (once per wk x 8 or16 wks) to either (1) saline (control); (2) PM having no soluble Zn; (3) combustion PM suspension containing 14.5 ug/mg water-soluble Zn at high and (4) low dose levels, (5) the aqueous fraction of this suspension devoid of solid insoluble particulate fraction (14.5 ug/mg soluble Zn), or (6) Zn sulfate. Zn concentrations were identical in groups 3, 5 and 6. Pulmonary toxicity was apparent in all exposure groups when compared to saline as determined by recovery of cells in bronchoalveolar lavage fluid. Long-term exposure to PM with or without soluble Zn, or Zn sulfate caused distinct myocardial lesions characterized by subepicardial and randomly distributed myocardial inflammation, degeneration, and fibrosis. The lesion severity was higher in those groups receiving Zn PM. Because cardiac mitochondria are likely the primary target of inhaled metal or other absorbed PM components, we analyzed mitochondrial DNA damage using QPCR and found that all exposure groups except those exposed to PM without Zn caused variable degree of damage. Aconitase activity, sensitive to inhibition by oxidative stress was inhibited slightly but significantly in rats receiving zinc sulfate. Although modest, microarray (Affymetrix) analysis revealed expression changes in the heart reflective of effects on cell signaling, inflammation/oxidative stress, mitochondrial fatty acid metabolisms and cell cycle regulation in rats exposed to zinc sulfate. However, these changes were minimal following exposure to PM devoid of soluble metals. We demonstrate that episodic subchronic pulmonary exposure to zinc sulfate causes cardiac injury and mitochondrial DNA damage. Thus, water-soluble PM-associated zinc may be one of the PM components responsible for cardiovascular morbidity. Experiment Overall Design: Group 1 received Saline to serve as a control. Group 2 received Mount St. Helenâs ash, which does not contain any water-soluble zinc or other metals such that we can delineate any cardiac effect secondary to pulmonary deposition of these particles as these fine mode particles themselves are not likely to translocate to the heart. Group 3 received whole saline suspension of the same fugitive oil combustion particle sample used in the previous study, which contained insoluble components plus water-soluble zinc (Kodavanti et al., 2003; 14.5 ug/mg zinc) and also a small amount of water-soluble nickel (3.0 Âµg/mg). Elemental composition of this PM is comparable to Ottawa urban PM (Kodavanti et al., 2003). Group 4 also received same particle sample but at half the dose than group 3. Group 5 received saline-soluble or leachable fraction of PM-HD devoid of any solid material but contained soluble components including zinc and nickel. And, group 6 received zinc sulfate at concentration that was present in groups 3 or 5. This design allowed us to test if cardiac injury in rats was due to leached of zinc or solid particles. There were 4 replicates per treatment group.

Project description:Zinc (Zn) is a major elemental component of respirable ambient particulate matter (PM) detected often at alarming levels in urban air. Exposure to PM has been widely associated with increased cardiovascular morbidity and mortality, however, it is not known what components or sources of PM are causative. We recently demonstrated that long-term episodic inhalation of combustion PM, having similar amount of Zn found in urban PM, caused myocardial lesions in rats. We further demonstrated that a single pulmonary exposure to Zn at high concentration is associated with disturbances in cardiac mitochondrial function, ion channel regulation, calcium homeostasis, and cell signaling. Therefore, in this study we investigated the role of PM-associated Zn in cardiac injury using multiple exposure scenarios. Male Wistar-Kyoto (WKY) rats of 12-14 wks age were intratracheally exposed (once per wk x 8 or16 wks) to either (1) saline (control); (2) PM having no soluble Zn; (3) combustion PM suspension containing 14.5 ug/mg water-soluble Zn at high and (4) low dose levels, (5) the aqueous fraction of this suspension devoid of solid insoluble particulate fraction (14.5 ug/mg soluble Zn), or (6) Zn sulfate. Zn concentrations were identical in groups 3, 5 and 6. Pulmonary toxicity was apparent in all exposure groups when compared to saline as determined by recovery of cells in bronchoalveolar lavage fluid. Long-term exposure to PM with or without soluble Zn, or Zn sulfate caused distinct myocardial lesions characterized by subepicardial and randomly distributed myocardial inflammation, degeneration, and fibrosis. The lesion severity was higher in those groups receiving Zn PM. Because cardiac mitochondria are likely the primary target of inhaled metal or other absorbed PM components, we analyzed mitochondrial DNA damage using QPCR and found that all exposure groups except those exposed to PM without Zn caused variable degree of damage. Aconitase activity, sensitive to inhibition by oxidative stress was inhibited slightly but significantly in rats receiving zinc sulfate. Although modest, microarray (Affymetrix) analysis revealed expression changes in the heart reflective of effects on cell signaling, inflammation/oxidative stress, mitochondrial fatty acid metabolisms and cell cycle regulation in rats exposed to zinc sulfate. However, these changes were minimal following exposure to PM devoid of soluble metals. We demonstrate that episodic subchronic pulmonary exposure to zinc sulfate causes cardiac injury and mitochondrial DNA damage. Thus, water-soluble PM-associated zinc may be one of the PM components responsible for cardiovascular morbidity. Keywords: Pulmonary exposure, Cardiac gene expression

Project description:BackgroundStudies have shown that long-term exposure to air pollution increases mortality. However, evidence is limited for air-pollution levels below the most recent National Ambient Air Quality Standards. Previous studies involved predominantly urban populations and did not have the statistical power to estimate the health effects in underrepresented groups.MethodsWe constructed an open cohort of all Medicare beneficiaries (60,925,443 persons) in the continental United States from the years 2000 through 2012, with 460,310,521 person-years of follow-up. Annual averages of fine particulate matter (particles with a mass median aerodynamic diameter of less than 2.5 μm [PM2.5]) and ozone were estimated according to the ZIP Code of residence for each enrollee with the use of previously validated prediction models. We estimated the risk of death associated with exposure to increases of 10 μg per cubic meter for PM2.5 and 10 parts per billion (ppb) for ozone using a two-pollutant Cox proportional-hazards model that controlled for demographic characteristics, Medicaid eligibility, and area-level covariates.ResultsIncreases of 10 μg per cubic meter in PM2.5 and of 10 ppb in ozone were associated with increases in all-cause mortality of 7.3% (95% confidence interval [CI], 7.1 to 7.5) and 1.1% (95% CI, 1.0 to 1.2), respectively. When the analysis was restricted to person-years with exposure to PM2.5 of less than 12 μg per cubic meter and ozone of less than 50 ppb, the same increases in PM2.5 and ozone were associated with increases in the risk of death of 13.6% (95% CI, 13.1 to 14.1) and 1.0% (95% CI, 0.9 to 1.1), respectively. For PM2.5, the risk of death among men, blacks, and people with Medicaid eligibility was higher than that in the rest of the population.ConclusionsIn the entire Medicare population, there was significant evidence of adverse effects related to exposure to PM2.5 and ozone at concentrations below current national standards. This effect was most pronounced among self-identified racial minorities and people with low income. (Supported by the Health Effects Institute and others.).

Project description:Mounting epidemiological evidence has documented the associations between long-term exposure to multiple air pollutants and increased mortality. There is a pressing need to determine whether risks persist at low concentrations including below current national standards. Air pollution levels have decreased in the United States, and better understanding of the health effects of low-level air pollution is essential for the amendment of National Ambient Air Quality Standards (NAAQS). A nationwide, population-based, open cohort study was conducted to estimate the association between long-term exposure to low-level PM2.5, NO2, O3, and all-cause mortality. The study population included all Medicare enrollees (ages 65 years or older) in the contiguous U.S. from 2001 to 2017. We further defined three low-exposure subcohorts comprised of Medicare enrollees who were always exposed to low-level PM2.5 (annual mean ≤12-μg/m3), NO2 (annual mean ≤53-ppb), and O3 (warm-season mean ≤50-ppb), respectively, over the study period. Of the 68.7-million Medicare enrollees, 33.1% (22.8-million, mean age 75.9 years), 93.8% (64.5-million, mean age 76.2 years), and 65.0% (44.7-million, mean age 75.6 years) were always exposed to low-level annual PM2.5, annual NO2, and warm-season O3 over the study period, respectively. Among the low-exposure cohorts, a 10-μg/m3 increase in PM2.5, 10-ppb increase in NO2, and 10-ppb increase in warm-season O3, were, respectively, associated with an increase in mortality rate ranging between 10 and 13%, 2 and 4%, and 12 and 14% in single-pollutant models, and between 6 and 8%, 1 and 3%, and 9 and 11% in tripollutant models, using three statistical approaches. There was strong evidence of linearity in concentration-response relationships for PM2.5 and NO2 at levels below the current NAAQS, suggesting that no safe threshold exists for health-harmful pollution levels. For O3, the concentration-response relationship shows an increasingly positive association at levels above 40-ppb. In conclusion, exposure to low levels of PM2.5, NO2, and warm-season O3 was associated with an increased risk of all-cause mortality.

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How low can you go? Air pollution affects mortality at very low levels.

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How low can you go? Air pollution affects mortality at very low levels.

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