Fine particle air pollution and lung cancer risk: Extending the long list of health risks.

Exposures to fine particulate matter (PM2.5) concentrations above the WHO guidelines affect 99% of the world population. In a recent issue of Nature, Hill et al. dissect the tumor promotion paradigm orchestrated by PM2.5 inhalation exposures in lung carcinogenesis, supporting the hypothesis that PM2.5 can increase your risk of lung carcinoma without ever smoking.

Environmental pollutants and the immune response.

Environmental pollution is one of the most serious challenges to health in the modern world. Pollutants alter immune responses and can provoke immunotoxicity. In this Review, we summarize the major environmental pollutants that are attracting wide-ranging concern and the molecular basis underlying their effects on the immune system. Xenobiotic receptors, including the aryl hydrocarbon receptor (AHR), sense and respond to a subset of environmental pollutants by activating the expression of detoxification enzymes to protect the body. However, chronic activation of the AHR leads to immunotoxicity. KEAP1-NRF2 is another important system that protects the body against environmental pollutants. KEAP1 is a sensor protein that detects environmental pollutants, leading to activation of the transcription factor NRF2. NRF2 protects the body from immunotoxicity by inducing the expression of genes involved in detoxification, antioxidant and anti-inflammatory activities. Intervening in these sensor-response systems could protect the body from the devastating immunotoxicity that can be induced by environmental pollutants.

The mechanism for directional hearing in fish.

Locating sound sources such as prey or predators is critical for survival in many vertebrates. Terrestrial vertebrates locate sources by measuring the time delay and intensity difference of sound pressure at each ear1-5. Underwater, however, the physics of sound makes interaural cues very small, suggesting that directional hearing in fish should be nearly impossible6. Yet, directional hearing has been confirmed behaviourally, although the mechanisms have remained unknown for decades. Several hypotheses have been proposed to explain this remarkable ability, including the possibility that fish evolved an extreme sensitivity to minute interaural differences or that fish might compare sound pressure with particle motion signals7,8. However, experimental challenges have long hindered a definitive explanation. Here we empirically test these models in the transparent teleost Danionella cerebrum, one of the smallest vertebrates9,10. By selectively controlling pressure and particle motion, we dissect the sensory algorithm underlying directional acoustic startles. We find that both cues are indispensable for this behaviour and that their relative phase controls its direction. Using micro-computed tomography and optical vibrometry, we further show that D. cerebrum has the sensory structures to implement this mechanism. D. cerebrum shares these structures with more than 15% of living vertebrate species, suggesting a widespread mechanism for inferring sound direction.

Global population exposure to landscape fire air pollution from 2000 to 2019.

Wildfires are thought to be increasing in severity and frequency as a result of climate change1-5. Air pollution from landscape fires can negatively affect human health4-6, but human exposure to landscape fire-sourced (LFS) air pollution has not been well characterized at the global scale7-23. Here, we estimate global daily LFS outdoor fine particulate matter (PM2.5) and surface ozone concentrations at 0.25° × 0.25° resolution during the period 2000-2019 with the help of machine learning and chemical transport models. We found that overall population-weighted average LFS PM2.5 and ozone concentrations were 2.5 µg m-3 (6.1% of all-source PM2.5) and 3.2 µg m-3 (3.6% of all-source ozone), respectively, in 2010-2019, with a slight increase for PM2.5, but not for ozone, compared with 2000-2009. Central Africa, Southeast Asia, South America and Siberia experienced the highest LFS PM2.5 and ozone concentrations. The concentrations of LFS PM2.5 and ozone were about four times higher in low-income countries than in high-income countries. During the period 2010-2019, 2.18 billion people were exposed to at least 1 day of substantial LFS air pollution per year, with each person in the world having, on average, 9.9 days of exposure per year. These two metrics increased by 6.8% and 2.1%, respectively, compared with 2000-2009. Overall, we find that the global population is increasingly exposed to LFS air pollution, with socioeconomic disparities.

The contribution of wildfire to PM2.5 trends in the USA.

Steady improvements in ambient air quality in the USA over the past several decades, in part a result of public policy1,2, have led to public health benefits1-4. However, recent trends in ambient concentrations of particulate matter with diameters less than 2.5 µm (PM2.5), a pollutant regulated under the Clean Air Act1, have stagnated or begun to reverse throughout much of the USA5. Here we use a combination of ground- and satellite-based air pollution data from 2000 to 2022 to quantify the contribution of wildfire smoke to these PM2.5 trends. We find that since at least 2016, wildfire smoke has influenced trends in average annual PM2.5 concentrations in nearly three-quarters of states in the contiguous USA, eroding about 25% of previous multi-decadal progress in reducing PM2.5 concentrations on average in those states, equivalent to 4 years of air quality progress, and more than 50% in many western states. Smoke influence on trends in the number of days with extreme PM2.5 concentrations is detectable by 2011, but the influence can be detected primarily in western and mid-western states. Wildfire-driven increases in ambient PM2.5 concentrations are unregulated under current air pollution law6 and, in the absence of further interventions, we show that the contribution of wildfire to regional and national air quality trends is likely to grow as the climate continues to warm.

Krill body size drives particulate organic carbon export in West Antarctica.

The export of carbon from the ocean surface and storage in the ocean interior is important in the modulation of global climate1-4. The West Antarctic Peninsula experiences some of the largest summer particulate organic carbon (POC) export rates, and one of the fastest warming rates, in the world5,6. To understand how warming may alter carbon storage, it is necessary to first determine the patterns and ecological drivers of POC export7,8. Here we show that Antarctic krill (Euphausia superba) body size and life-history cycle, as opposed to their overall biomass or regional environmental factors, exert the dominant control on the POC flux. We measured POC fluxes over 21 years, the longest record in the Southern Ocean, and found a significant 5-year periodicity in the annual POC flux, which oscillated in synchrony with krill body size, peaking when the krill population was composed predominately of large individuals. Krill body size alters the POC flux through the production and export of size-varying faecal pellets9, which dominate the total flux. Decreases in winter sea ice10, an essential habitat for krill, are causing shifts in the krill population11, which may alter these export patterns of faecal pellets, leading to changes in ocean carbon storage.

Lung adenocarcinoma promotion by air pollutants.

A complete understanding of how exposure to environmental substances promotes cancer formation is lacking. More than 70 years ago, tumorigenesis was proposed to occur in a two-step process: an initiating step that induces mutations in healthy cells, followed by a promoter step that triggers cancer development1. Here we propose that environmental particulate matter measuring ≤2.5 µm (PM2.5), known to be associated with lung cancer risk, promotes lung cancer by acting on cells that harbour pre-existing oncogenic mutations in healthy lung tissue. Focusing on EGFR-driven lung cancer, which is more common in never-smokers or light smokers, we found a significant association between PM2.5 levels and the incidence of lung cancer for 32,957 EGFR-driven lung cancer cases in four within-country cohorts. Functional mouse models revealed that air pollutants cause an influx of macrophages into the lung and release of interleukin-1ß. This process results in a progenitor-like cell state within EGFR mutant lung alveolar type II epithelial cells that fuels tumorigenesis. Ultradeep mutational profiling of histologically normal lung tissue from 295 individuals across 3 clinical cohorts revealed oncogenic EGFR and KRAS driver mutations in 18% and 53% of healthy tissue samples, respectively. These findings collectively support a tumour-promoting role for  PM2.5 air pollutants  and provide impetus for public health policy initiatives to address air pollution to reduce disease burden.

Air pollution exposure disparities across US population and income groups.

Air pollution contributes to the global burden of disease, with ambient exposure to fine particulate matter of diameters smaller than 2.5 µm (PM2.5) being identified as the fifth-ranking risk factor for mortality globally1. Racial/ethnic minorities and lower-income groups in the USA are at a higher risk of death from exposure to PM2.5 than are other population/income groups2-5. Moreover, disparities in exposure to air pollution among population and income groups are known to exist6-17. Here we develop a data platform that links demographic data (from the US Census Bureau and American Community Survey) and PM2.5 data18 across the USA. We analyse the data at the tabulation area level of US zip codes (N is approximately 32,000) between 2000 and 2016. We show that areas with higher-than-average white and Native American populations have been consistently exposed to average PM2.5 levels that are lower than areas with higher-than-average Black, Asian and Hispanic or Latino populations. Moreover, areas with low-income populations have been consistently exposed to higher average PM2.5 levels than areas with high-income groups for the years 2004-2016. Furthermore, disparities in exposure relative to safety standards set by the US Environmental Protection Agency19 and the World Health Organization20 have been increasing over time. Our findings suggest that more-targeted PM2.5 reductions are necessary to provide all people with a similar degree of protection from environmental hazards. Our study is observational and cannot provide insight into the drivers of the identified disparities.

Continuous air purification by aqueous interface filtration and absorption.

The adverse impact of particulate air pollution on human health1,2 has prompted the development of purification systems that filter particulates out of air3-5. To maintain performance, the filter units must inevitably be replaced at some point, which requires maintenance, involves costs and generates solid waste6,7. Here we show that an ion-doped conjugated polymer-coated matrix infiltrated with a selected functional liquid enables efficient, continuous and maintenance-free air purification. As the air to be purified moves through the system in the form of bubbles, the functional fluid provides interfaces for filtration and for removal of particulate matter and pollutant molecules from air. Theoretical modelling and experimental results demonstrate that the system exhibits high efficiency and robustness: its one-time air purification efficiency can reach 99.6%, and its dust-holding capacity can reach 950 g m-2. The system is durable and resistant to fouling and corrosion, and the liquid acting as filter can be reused and adjusted to also enable removal of bacteria or odours. We anticipate that our purification approach will be useful for the development of specialist air purifiers that might prove useful in a settings such as hospitals, factories and mines.

Liquefied Petroleum Gas or Biomass Cooking and Severe Infant Pneumonia.

BACKGROUND: Exposure to household air pollution is a risk factor for severe pneumonia. The effect of replacing biomass cookstoves with liquefied petroleum gas (LPG) cookstoves on the incidence of severe infant pneumonia is uncertain. METHODS: We conducted a randomized, controlled trial involving pregnant women 18 to 34 years of age and between 9 to less than 20 weeks' gestation in India, Guatemala, Peru, and Rwanda from May 2018 through September 2021. The women were assigned to cook with unvented LPG stoves and fuel (intervention group) or to continue cooking with biomass fuel (control group). In each trial group, we monitored adherence to the use of the assigned cookstove and measured 24-hour personal exposure to fine particulate matter (particles with an aerodynamic diameter of ≤2.5 µm [PM2.5]) in the women and their offspring. The trial had four primary outcomes; the primary outcome for which data are presented in the current report was severe pneumonia in the first year of life, as identified through facility surveillance or on verbal autopsy. RESULTS: Among 3200 pregnant women who had undergone randomization, 3195 remained eligible and gave birth to 3061 infants (1536 in the intervention group and 1525 in the control group). High uptake of the intervention led to a reduction in personal exposure to PM2.5 among the children, with a median exposure of 24.2 µg per cubic meter (interquartile range, 17.8 to 36.4) in the intervention group and 66.0 µg per cubic meter (interquartile range, 35.2 to 132.0) in the control group. A total of 175 episodes of severe pneumonia were identified during the first year of life, with an incidence of 5.67 cases per 100 child-years (95% confidence interval [CI], 4.55 to 7.07) in the intervention group and 6.06 cases per 100 child-years (95% CI, 4.81 to 7.62) in the control group (incidence rate ratio, 0.96; 98.75% CI, 0.64 to 1.44; P = 0.81). No severe adverse events were reported to be associated with the intervention, as determined by the trial investigators. CONCLUSIONS: The incidence of severe pneumonia among infants did not differ significantly between those whose mothers were assigned to cook with LPG stoves and fuel and those whose mothers were assigned to continue cooking with biomass stoves. (Funded by the National Institutes of Health and the Bill and Melinda Gates Foundation; HAPIN ClinicalTrials.gov number, NCT02944682.).

Effects of Cooking with Liquefied Petroleum Gas or Biomass on Stunting in Infants.

BACKGROUND: Household air pollution is associated with stunted growth in infants. Whether the replacement of biomass fuel (e.g., wood, dung, or agricultural crop waste) with liquefied petroleum gas (LPG) for cooking can reduce the risk of stunting is unknown. METHODS: We conducted a randomized trial involving 3200 pregnant women 18 to 34 years of age in four low- and middle-income countries. Women at 9 to less than 20 weeks' gestation were randomly assigned to use a free LPG cookstove with continuous free fuel delivery for 18 months (intervention group) or to continue using a biomass cookstove (control group). The length of each infant was measured at 12 months of age, and personal exposures to fine particulate matter (particles with an aerodynamic diameter of ≤2.5 µm) were monitored starting at pregnancy and continuing until the infants were 1 year of age. The primary outcome for which data are presented in the current report - stunting (defined as a length-for-age z score that was more than two standard deviations below the median of a growth standard) at 12 months of age - was one of four primary outcomes of the trial. Intention-to-treat analyses were performed to estimate the relative risk of stunting. RESULTS: Adherence to the intervention was high, and the intervention resulted in lower prenatal and postnatal 24-hour personal exposures to fine particulate matter than the control (mean prenatal exposure, 35.0 µg per cubic meter vs. 103.3 µg per cubic meter; mean postnatal exposure, 37.9 µg per cubic meter vs. 109.2 µg per cubic meter). Among 3061 live births, 1171 (76.2%) of the 1536 infants born to women in the intervention group and 1186 (77.8%) of the 1525 infants born to women in the control group had a valid length measurement at 12 months of age. Stunting occurred in 321 of the 1171 infants included in the analysis (27.4%) of the infants born to women in the intervention group and in 299 of the 1186 infants included in the analysis (25.2%) of those born to women in the control group (relative risk, 1.10; 98.75% confidence interval, 0.94 to 1.29; P = 0.12). CONCLUSIONS: An intervention strategy starting in pregnancy and aimed at mitigating household air pollution by replacing biomass fuel with LPG for cooking did not reduce the risk of stunting in infants. (Funded by the National Institutes of Health and the Bill and Melinda Gates Foundation; HAPIN ClinicalTrials.gov number, NCT02944682.).

Measuring long-term exposure to wildfire PM2.5 in California: Time-varying inequities in environmental burden.

Wildfires have become more frequent and intense due to climate change and outdoor wildfire fine particulate matter (PM2.5) concentrations differ from relatively smoothly varying total PM2.5. Thus, we introduced a conceptual model for computing long-term wildfire PM2.5 and assessed disproportionate exposures among marginalized communities. We used monitoring data and statistical techniques to characterize annual wildfire PM2.5 exposure based on intermittent and extreme daily wildfire PM2.5 concentrations in California census tracts (2006 to 2020). Metrics included: 1) weeks with wildfire PM2.5 < 5 µg/m3; 2) days with non-zero wildfire PM2.5; 3) mean wildfire PM2.5 during peak exposure week; 4) smoke waves (≥2 consecutive days with <15 µg/m3 wildfire PM2.5); and 5) mean annual wildfire PM2.5 concentration. We classified tracts by their racial/ethnic composition and CalEnviroScreen (CES) score, an environmental and social vulnerability composite measure. We examined associations of CES and racial/ethnic composition with the wildfire PM2.5 metrics using mixed-effects models. Averaged 2006 to 2020, we detected little difference in exposure by CES score or racial/ethnic composition, except for non-Hispanic American Indian and Alaska Native populations, where a 1-SD increase was associated with higher exposure for 4/5 metrics. CES or racial/ethnic × year interaction term models revealed exposure disparities in some years. Compared to their California-wide representation, the exposed populations of non-Hispanic American Indian and Alaska Native (1.68×, 95% CI: 1.01 to 2.81), white (1.13×, 95% CI: 0.99 to 1.32), and multiracial (1.06×, 95% CI: 0.97 to 1.23) people were over-represented from 2006 to 2020. In conclusion, during our study period in California, we detected disproportionate long-term wildfire PM2.5 exposure for several racial/ethnic groups.

Reductions in premature deaths from heat and particulate matter air pollution in South Asia, China, and the United States under decarbonization.

Following a sustainable development pathway designed to keep warming below 2 °C will benefit human health. We quantify premature deaths attributable to fine particulate matter (PM2.5) air pollution and heat exposures for China, South Asia, and the United States using projections from multiple climate models under high- and low-emission scenarios. Projected changes in premature deaths are typically dominated by population aging, primarily reflecting increased longevity leading to greater sensitivity to environmental risks. Changes in PM2.5 exposure typically have small impacts on premature deaths under a high-emission scenario but provide substantial benefits under a low-emission scenario. PM2.5-attributable deaths increase in South Asia throughout the century under both scenarios but shift to decreases by late century in China, and US values decrease throughout the century. In contrast, heat exposure increases under both scenarios and combines with population aging to drive projected increases in deaths in all countries. Despite population aging, combined PM2.5- and heat-related deaths decrease under the low-emission scenario by ~2.4 million per year by midcentury and ~2.9 million by century's end, with ~3% and ~21% of these reductions from heat, respectively. Intermodel variations in exposure projections generally lead to uncertainties of <40% except for US and China heat impacts. Health benefits of low emissions are larger from reduced heat exposure than improved air quality by the late 2090s in the United States. In contrast, in South and East Asia, the PM2.5-related benefits are largest throughout the century, and their valuation exceeds the cost of decarbonization, especially in China, over the next 30 y.

Adopting electric school buses in the United States: Health and climate benefits.

Electric school buses have been proposed as an alternative to reduce the health and climate impacts of the current U.S. school bus fleet, of which a substantial share are highly polluting old diesel vehicles. However, the climate and health benefits of electric school buses are not well known. As they are substantially more costly than diesel buses, assessing their benefits is needed to inform policy decisions. We assess the health benefits of electric school buses in the United States from reduced adult mortality and childhood asthma onset risks due to exposure to ambient fine particulate matter (PM2.5). We also evaluate climate benefits from reduced greenhouse-gas emissions. We find that replacing the average diesel bus in the U.S. fleet in 2017 with an electric bus yields $84,200 in total benefits. Climate benefits amount to $40,400/bus, whereas health benefits amount to $43,800/bus due to 4.42*10-3 fewer PM2.5-attributable deaths ($40,000 of total) and 7.42*10-3 fewer PM2.5-attributable new childhood asthma cases ($3,700 of total). However, health benefits of electric buses vary substantially by driving location and model year (MY) of the diesel buses they replace. Replacing old, MY 2005 diesel buses in large cities yields $207,200/bus in health benefits and is likely cost-beneficial, although other policies that accelerate fleet turnover in these areas deserve consideration. Electric school buses driven in rural areas achieve small health benefits from reduced exposure to ambient PM2.5. Further research assessing benefits of reduced exposure to in-cabin air pollution among children riding buses would be valuable to inform policy decisions.

PM2.5 exposure contributes to anxiety and depression-like behaviors via phenyl-containing compounds interfering with dopamine receptor.

As a global problem, fine particulate matter (PM2.5) really needs local fixes. Considering the increasing epidemiological relevance to anxiety and depression but inconsistent toxicological results, the most important question is to clarify whether and how PM2.5 causally contributes to these mental disorders and which components are the most dangerous for crucial mitigation in a particular place. In the present study, we chronically subjected male mice to a real-world PM2.5 exposure system throughout the winter heating period in a coal combustion area and revealed that PM2.5 caused anxiety and depression-like behaviors in adults such as restricted activity, diminished exploratory interest, enhanced repetitive stereotypy, and elevated acquired immobility, through behavioral tests including open field, elevated plus maze, marble-burying, and forced swimming tests. Importantly, we found that dopamine signaling was perturbed using mRNA transcriptional profile and bioinformatics analysis, with Drd1 as a potential target. Subsequently, we developed the Drd1 expression-directed multifraction isolating and nontarget identifying framework and identified a total of 209 compounds in PM2.5 organic extracts capable of reducing Drd1 expression. Furthermore, by applying hierarchical characteristic fragment analysis and molecular docking and dynamics simulation, we clarified that phenyl-containing compounds competitively bound to DRD1 and interfered with dopamine signaling, thereby contributing to mental disorders. Taken together, this work provides experimental evidence for researchers and clinicians to identify hazardous factors in PM2.5 and prevent adverse health outcomes and for local governments and municipalities to control source emissions for diminishing specific disease burdens.

Health and equity implications of individual adaptation to air pollution in a changing climate.

Future climate change can cause more days with poor air quality. This could trigger more alerts telling people to stay inside to protect themselves, with potential consequences for health and health equity. Here, we study the change in US air quality alerts over this century due to fine particulate matter (PM2.5), who they may affect, and how they may respond. We find air quality alerts increase by over 1 mo per year in the eastern United States by 2100 and quadruple on average. They predominantly affect areas with high Black populations and leakier homes, exacerbating existing inequalities and impacting those less able to adapt. Reducing emissions can offer significant annual health benefits ($5,400 per person) by mitigating the effect of climate change on air pollution and its associated risks of early death. Relying on people to adapt, instead, would require them to stay inside, with doors and windows closed, for an extra 142 d per year, at an average cost of $11,000 per person. It appears likelier, however, that people will achieve minimal protection without policy to increase adaptation rates. Boosting adaptation can offer net benefits, even alongside deep emission cuts. New adaptation policies could, for example: reduce adaptation costs; reduce infiltration and improve indoor air quality; increase awareness of alerts and adaptation; and provide measures for those working or living outdoors. Reducing emissions, conversely, lowers everyone's need to adapt, and protects those who cannot adapt. Equitably protecting human health from air pollution under climate change requires both mitigation and adaptation.

Phosphocholine-induced energy source shift alleviates mitochondrial dysfunction in lung cells caused by geospecific PM2.5 components.

Fine particulate matter (PM2.5) is globally recognized for its adverse implications on human health. Yet, remain limited the individual contribution of particular PM2.5 components to its toxicity, especially considering regional disparities. Moreover, prevention solutions for PM2.5-associated health effects are scarce. In the present study, we comprehensively characterized and compared the primary PM2.5 constituents and their altered metabolites from two locations: Taiyuan and Guangzhou. Analysis of year-long PM2.5 samples revealed 84 major components, encompassing organic carbon, elemental carbon, ions, metals, and organic chemicals. PM2.5 from Taiyuan exhibited higher contamination, associated health risks, dithiothreitol activity, and cytotoxicities than Guangzhou's counterpart. Applying metabolomics, BEAS-2B lung cells exposed to PM2.5 from both cities were screened for significant alterations. A correlation analysis revealed the metabolites altered by PM2.5 and the critical toxic PM2.5 components in both regions. Among the PM2.5-down-regulated metabolites, phosphocholine emerged as a promising intervention for PM2.5 cytotoxicities. Its supplementation effectively attenuated PM2.5-induced energy metabolism disorder and cell death via activating fatty acid oxidation and inhibiting Phospho1 expression. The highlighted toxic chemicals displayed combined toxicities, potentially counteracted by phosphocholine. Our study offered a promising functional metabolite to alleviate PM2.5-induced cellular disorder and provided insights into the geo-based variability in toxic PM2.5 components.

Air Pollution-Related Neurotoxicity Across the Life Span.

Air pollution is a complex mixture of gases and particulate matter, with adsorbed organic and inorganic contaminants, to which exposure is lifelong. Epidemiological studies increasingly associate air pollution with multiple neurodevelopmental disorders and neurodegenerative diseases, findings supported by experimental animal models. This breadth of neurotoxicity across these central nervous system diseases and disorders likely reflects shared vulnerability of their inflammatory and oxidative stress-based mechanisms and a corresponding ability to produce brain metal dyshomeo-stasis. Future research to define the responsible contaminants of air pollution underlying this neurotoxicity is critical to understanding mechanisms of these diseases and disorders and protecting public health.

Air Pollution and Mortality at the Intersection of Race and Social Class.

BACKGROUND: Black Americans are exposed to higher annual levels of air pollution containing fine particulate matter (particles with an aerodynamic diameter of ≤2.5 µm [PM2.5]) than White Americans and may be more susceptible to its health effects. Low-income Americans may also be more susceptible to PM2.5 pollution than high-income Americans. Because information is lacking on exposure-response curves for PM2.5 exposure and mortality among marginalized subpopulations categorized according to both race and socioeconomic position, the Environmental Protection Agency lacks important evidence to inform its regulatory rulemaking for PM2.5 standards. METHODS: We analyzed 623 million person-years of Medicare data from 73 million persons 65 years of age or older from 2000 through 2016 to estimate associations between annual PM2.5 exposure and mortality in subpopulations defined simultaneously by racial identity (Black vs. White) and income level (Medicaid eligible vs. ineligible). RESULTS: Lower PM2.5 exposure was associated with lower mortality in the full population, but marginalized subpopulations appeared to benefit more as PM2.5 levels decreased. For example, the hazard ratio associated with decreasing PM2.5 from 12 µg per cubic meter to 8 µg per cubic meter for the White higher-income subpopulation was 0.963 (95% confidence interval [CI], 0.955 to 0.970), whereas equivalent hazard ratios for marginalized subpopulations were lower: 0.931 (95% CI, 0.909 to 0.953) for the Black higher-income subpopulation, 0.940 (95% CI, 0.931 to 0.948) for the White low-income subpopulation, and 0.939 (95% CI, 0.921 to 0.957) for the Black low-income subpopulation. CONCLUSIONS: Higher-income Black persons, low-income White persons, and low-income Black persons may benefit more from lower PM2.5 levels than higher-income White persons. These findings underscore the importance of considering racial identity and income together when assessing health inequities. (Funded by the National Institutes of Health and the Alfred P. Sloan Foundation.).

Personal Strategies to Reduce the Cardiovascular Impacts of Environmental Exposures.

Ubiquitous environmental exposures increase cardiovascular disease risk via diverse mechanisms. This review examines personal strategies to minimize this risk. With regard to fine particulate air pollution exposure, evidence exists to recommend the use of portable air cleaners and avoidance of outdoor activity during periods of poor air quality. Other evidence may support physical activity, dietary modification, omega-3 fatty acid supplementation, and indoor and in-vehicle air conditioning as viable strategies to minimize adverse health effects. There is currently insufficient data to recommend specific personal approaches to reduce the adverse cardiovascular effects of noise pollution. Public health advisories for periods of extreme heat or cold should be observed, with limited evidence supporting a warm ambient home temperature and physical activity as strategies to limit the cardiovascular harms of temperature extremes. Perfluoroalkyl and polyfluoroalkyl substance exposure can be reduced by avoiding contact with perfluoroalkyl and polyfluoroalkyl substance-containing materials; blood or plasma donation and cholestyramine may reduce total body stores of perfluoroalkyl and polyfluoroalkyl substances. However, the cardiovascular impact of these interventions has not been examined. Limited utilization of pesticides and safe handling during use should be encouraged. Finally, vasculotoxic metal exposure can be decreased by using portable air cleaners, home water filtration, and awareness of potential contaminants in ground spices. Chelation therapy reduces physiological stores of vasculotoxic metals and may be effective for the secondary prevention of cardiovascular disease.