Indoor Air Sources of Outdoor Air Pollution: Health Consequences, Policy, and Recommendations: An Official American Thoracic Society Workshop Report.

Indoor sources of air pollution worsen indoor and outdoor air quality. Thus, identifying and reducing indoor pollutant sources would decrease both indoor and outdoor air pollution, benefit public health, and help address the climate crisis. As outdoor sources come under regulatory control, unregulated indoor sources become a rising percentage of the problem. This American Thoracic Society workshop was convened in 2022 to evaluate this increasing proportion of indoor contributions to outdoor air quality. The workshop was conducted by physicians and scientists, including atmospheric and aerosol scientists, environmental engineers, toxicologists, epidemiologists, regulatory policy experts, and pediatric and adult pulmonologists. Presentations and discussion sessions were centered on 1) the generation and migration of pollutants from indoors to outdoors, 2) the sources and circumstances representing the greatest threat, and 3) effective remedies to reduce the health burden of indoor sources of air pollution. The scope of the workshop was residential and commercial sources of indoor air pollution in the United States. Topics included wood burning, natural gas, cooking, evaporative volatile organic compounds, source apportionment, and regulatory policy. The workshop concluded that indoor sources of air pollution are significant contributors to outdoor air quality and that source control and filtration are the most effective measures to reduce indoor contributions to outdoor air. Interventions should prioritize environmental justice: Households of lower socioeconomic status have higher concentrations of indoor air pollutants from both indoor and outdoor sources. We identify research priorities, potential health benefits, and mitigation actions to consider (e.g., switching from natural gas to electric stoves and transitioning to scent-free consumer products). The workshop committee emphasizes the benefits of combustion-free homes and businesses and recommends economic, legislative, and education strategies aimed at achieving this goal.

PM2.5 and cardiovascular diseases: State-of-the-Art review.

Air pollution, especially exposure to particulate matter 2.5 (PM2.5), has been associated with an increase in morbidity and mortality around the world. Specifically, it seems that PM2.5 promotes the development of cardiovascular risk factors such as hypertension and atherosclerosis, while being associated with an increased risk of cardiovascular diseases, including myocardial infarction (MI), stroke, heart failure, and arrhythmias. In this review, we seek to elucidate the pathophysiological mechanisms by which exposure to PM2.5 can result in adverse cardiovascular outcomes, in addition to understanding the link between exposure to PM2.5 and cardiovascular events. It is hypothesized that PM2.5 functions via 3 mechanisms: increased oxidative stress, activation of the inflammatory pathway of the immune system, and stimulation of the autonomic nervous system which ultimately promote endothelial dysfunction, atherosclerosis, and systemic inflammation that can thus lead to cardiovascular events. It is important to note that the various cardiovascular associations of PM2.5 differ regarding the duration of exposure (short vs long) to PM2.5, the source of PM2.5, and regulations regarding air pollution in the area where PM2.5 is prominent. Current strategies to reduce PM2.5 exposure include personal strategies such as avoiding high PM2.5 areas such as highways or wearing masks outdoors, to governmental policies restricting the amount of PM2.5 produced by organizations. This review, by highlighting the significant impact between PM2.5 exposure and cardiovascular health will hopefully bring awareness and produce significant change regarding dealing with PM2.5 levels worldwide.

Gaps and future directions in research on health effects of air pollution.

Despite progress in many countries, air pollution, and especially fine particulate matter air pollution (PM2.5) remains a global health threat: over 6 million premature cardiovascular and respiratory deaths/yr. have been attributed to household and outdoor air pollution. In this viewpoint, we identify present gaps in air pollution monitoring and regulation, and how they could be strengthened in future mitigation policies to more optimally reduce health impacts. We conclude that there is a need to move beyond simply regulating PM2.5 particulate matter mass concentrations at central site stations. A greater emphasis is needed on: new portable and affordable technologies to measure personal exposures to particle mass; the consideration of a submicron (PM1) mass air quality standard; and further evaluations of effects by particle composition and source. We emphasize the need to enable further studies on exposure-health relationships in underserved populations that are disproportionately impacted by air pollution, but not sufficiently represented in current studies.

Life Expectancy and Built Environments in the U.S.: A Multilevel Analysis.

INTRODUCTION: The purpose of this study is to examine the associations between built environments and life expectancy across a gradient of urbanicity in the U.S. METHODS: Census tract‒level estimates of life expectancy between 2010 and 2015, except for Maine and Wisconsin, from the U.S. Small-Area Life Expectancy Estimates Project were analyzed in 2022. Tract-level measures of the built environment included: food, alcohol, and tobacco outlets; walkability; park and green space; housing characteristics; and air pollution. Multilevel linear models for each of the 4 urbanicity types were fitted to evaluate the associations, adjusting for population and social characteristics. RESULTS: Old housing (built before 1979) and air pollution were important built environment predictors of life expectancy disparities across all gradients of urbanicity. Convenience stores were negatively associated with life expectancy in all urbanicity types. Healthy food options were a positive predictor of life expectancy only in high-density urban areas. Park accessibility was associated with increased life expectancy in all areas, except rural areas. Green space in neighborhoods was positively associated with life expectancy in urban areas but showed an opposite association in rural areas. CONCLUSIONS: After adjusting for key social characteristics, several built environment characteristics were salient risk factors for decreased life expectancy in the U.S., with some measures showing differential effects by urbanicity. Planning and policy efforts should be tailored to local contexts.

PM2.5 and Cardiovascular Health Risks.

PM2.5 is a frequently studied particulate matter metric, due to its wide range of identified overall adverse health effects, particularly cardiovascular health risks. However, there are no clear clinical practice guidelines for air pollution in regard to the prevention of cardiovascular health risks, since most of the current medical guidelines for CVD focus on metabolic risk factors such as hyperlipidemia or diabetes. We sought to determine the relationship between PM2.5 and cardiovascular disease, cardiovascular events, and all-cause mortality by performing a systematic review and meta-analysis. We searched Ovid MEDLINE, Ovid Embase, Ovid Cochrane Database of Systematic Reviews, Scopus, and Web of Science from the database inception to December 2022 for studies that reported an association between PM2.5 and cardiovascular disease, cardiovascular events, and all-cause mortality. We used the DerSimonian & Laird random-effects method to pool hazard ratios or risk ratios separately from the included studies. Of the total 18 prospective studies, 7,300,591 individuals were followed for a median follow-up of 9 years. Compared to low long-term exposure to PM 2.5 levels, an increase in exposure to PM 2.5 levels resulted in an increase in all-cause mortality (HR 1.08 95% CI of 1.05-1.11, P < 0.05). Similarly, when compared to a low long-term exposure to PM 2.5 levels, an increase in exposure to PM 2.5 levels resulted in an increase in cardiovascular disease (HR 1.09, 95% CI of 1.00-1.18, P < 0.05) and an increase in cardiovascular disease mortality (HR 1.12, 95% CI of 1.07-1.18, P < 0.05). Increased exposure to PM 2.5 levels is significantly associated with an increased risk of all-cause mortality, cardiovascular disease, and cardiovascular disease mortality. Although federal primary and secondary standards are in place, those standards are not low enough to prevent CVD health effects. Clinicians should emphasize PM2.5 as a modifiable CV risk factors for their patients to potentially reduce the development of CV complications. A clinical action guideline is needed specifically for air pollution effects on CVD, and how to mitigate them.

Long-Term Exposure to Source-Specific Fine Particles and Mortality─A Pooled Analysis of 14 European Cohorts within the ELAPSE Project.

We assessed mortality risks associated with source-specific fine particles (PM2.5) in a pooled European cohort of 323,782 participants. Cox proportional hazard models were applied to estimate mortality hazard ratios (HRs) for source-specific PM2.5 identified through a source apportionment analysis. Exposure to 2010 annual average concentrations of source-specific PM2.5 components was assessed at baseline residential addresses. The source apportionment resulted in the identification of five sources: traffic, residual oil combustion, soil, biomass and agriculture, and industry. In single-source analysis, all identified sources were significantly positively associated with increased natural mortality risks. In multisource analysis, associations with all sources attenuated but remained statistically significant with traffic, oil, and biomass and agriculture. The highest association per interquartile increase was observed for the traffic component (HR: 1.06; 95% CI: 1.04 and 1.08 per 2.86 µg/m3 increase) across five identified sources. On a 1 µg/m3 basis, the residual oil-related PM2.5 had the strongest association (HR: 1.13; 95% CI: 1.05 and 1.22), which was substantially higher than that for generic PM2.5 mass, suggesting that past estimates using the generic PM2.5 exposure response function have underestimated the potential clean air health benefits of reducing fossil-fuel combustion. Source-specific associations with cause-specific mortality were in general consistent with findings of natural mortality.

Particle toxicity's role in air pollution.

[Figure: see text].

Respiratory Emergency Department Visit Associations with Exposures to Fine Particulate Matter Mass, Constituents, and Sources in Dhaka, Bangladesh Air Pollution.

Rationale: To date, there is no published local epidemiological evidence documenting the respiratory health effects of source-specific air pollution in South Asia, where particulate matter ⩽2.5 µm in aerodynamic diameter (PM2.5) composition is different from past studies. Differences include more biomass and residue crop-burning emissions, which may have differing health implications. Objectives: We assessed PM2.5 associations with respiratory emergency department (ED) visits in a biomass-burning-dominated high-pollution region and evaluated their variability by pollution source and composition. Methods: Time-series regression modeling was applied to daily ED visits from January 2014 through December 2017. Air pollutant effect sizes were estimated after addressing long-term trends and seasonality, day of week, holidays, relative humidity, ambient temperature, and the effect modification by season, age, and sex. Results: PM2.5 yielded a significant association with increased respiratory ED visits (0.84%; 95% confidence interval, 0.33-1.35%) per 10-µg/m3 increase. The PM2.5 health effect size varied with season, the highest being during monsoon season, when fossil-fuel combustion sources dominated exposures. Results from a source-specific health effect analysis were also consistent with fossil-fuel PM2.5 having a larger effect size per 10 µg/m3 than PM2.5 from other sources (fossil-fuel PM2.5: 2.79% [0.33-5.31%], biomass-burning PM2.5: 1.27% [0-2.54%], and other PM2.5: 0.95% [0.06-1.85%]). Age-specific associations varied, with children and older adults being disproportionately affected by the air pollution, especially by the combustion-related particles. Conclusions: This study provided novel and important evidence that respiratory health in Dhaka is significantly affected by particle air pollution, with a greater health impact by fossil-fuel combustion-derived PM2.5.

Cardiovascular morbidity and mortality associations with biomass- and fossil-fuel-combustion fine-particulate-matter exposures in Dhaka, Bangladesh.

BACKGROUND: Fine-particulate-matter (i.e. with an aerodynamic diameter of ≤2.5 µm, PM2.5) air pollution is commonly treated as if it had 'equivalent toxicity', irrespective of the source and composition. We investigate the respective roles of fossil-fuel- and biomass-combustion particles in the PM2.5 relationship with cardiovascular morbidity and mortality using tracers of sources in Dhaka, Bangladesh. Results provide insight into the often observed levelling of the PM2.5 exposure-response curve at high-pollution levels. METHODS: A time-series regression model, adjusted for potentially confounding influences, was applied to 340 758 cardiovascular disease (CVD) emergency-department visits (EDVs) during January 2014 to December 2017, 253 407 hospital admissions during September 2013 to December 2017 and 16 858 CVD deaths during January 2014 to October 2017. RESULTS: Significant associations were confirmed between PM2.5-mass exposures and increased risk of cardiovascular EDV [0.27%, (0.07% to 0.47%)] at lag-0, hospitalizations [0.32% (0.08% to 0.55%)] at lag-0 and deaths [0.87%, (0.27% to 1.47%)] at lag-1 per 10-µg/m3 increase in PM2.5. However, the relationship of PM2.5 with morbidity and mortality effect slopes was less steep and non-significant at higher PM2.5 concentrations (during crop-burning-dominated exposures) and varied with PM2.5 source. Fossil-fuel-combustion PM2.5 had roughly a four times greater effect on CVD mortality and double the effect on CVD hospital admissions on a per-µg/m3 basis than did biomass-combustion PM2.5. CONCLUSION: Biomass burning was responsible for most PM2.5 air pollution in Dhaka, but fossil-fuel-combustion PM2.5 dominated the CVD adverse health impacts. Such by-source variations in the health impacts of PM2.5 should be considered in conducting ambient particulate-matter risk assessments, as well as in prioritizing air-pollution-mitigation measures and clinical advice.

Evaluation of a commercial database to estimate residence histories in the los angeles ultrafines study.

BACKGROUND: Commercial databases can be used to identify participant addresses over time, but their quality and impact on environmental exposure assessment is uncertain. OBJECTIVE: To evaluate the performance of a commercial database to find residences and estimate environmental exposures for study participants. METHODS: We searched LexisNexis® for participant addresses in the Los Angeles Ultrafines Study, a prospective cohort of men and women aged 50-71 years. At enrollment (1995-1996) and follow-up (2004-2005), we evaluated attainment (address found for the corresponding time period) and match rates to survey addresses by participant characteristics. We compared geographically-referenced predictors and estimates of ultrafine particulate matter (UFP) exposure from a land use regression model using LexisNexis and survey addresses at enrollment. RESULTS: LexisNexis identified an address for 69% of participants at enrollment (N = 50,320) and 95% of participants at follow-up (N = 24,432). Attainment rate at enrollment modestly differed (≥5%) by age, smoking status, education, and residential mobility between surveys. The match rate at both survey periods was high (82-86%) and similar across characteristics. When using LexisNexis versus survey addresses, correlations were high for continuous values of UFP exposure and its predictors (rho = 0.86-0.92). SIGNIFICANCE: Time period and population characteristics influenced the attainment of addresses from a commercial database, but accuracy and subsequent estimation of specific air pollution exposures were high in our older study population.

Exposure assessment of emissions from mobile food carts on New York City streets.

Food carts are common along streets in cities throughout the world. In North America, food cart vendors generally use propane, charcoal, or both propane and charcoal (P and C) for food preparation. Although cooking emissions are known to be a major source of indoor air pollution, there is limited knowledge on outdoor cooking's impact on the ambient environment and, in particular, the relative contribution of the different cooking fuels. This field study investigated the air pollution the public is exposed to in the micro-environment around 19 food carts classified into 3 groups: propane, charcoal, and P and C carts. Concentrations near the food carts were measured using both real-time and filter-based methods. Mean real-time concentrations of PM2.5, BC2.5, and particle counts were highest near the charcoal food carts: 196 µg/m3, 5.49 µg/m3, and 69,000 particles/cm3, respectively, with peak exposures of 1520 µg/m3, 67.9 µg/m3, and 235,000 particles/cm3, respectively. In order of pollution emission impacts: charcoal > P and C > propane carts. Thus, significant differences in air pollution emissions occurred in the vicinity of mobile food carts, depending on the fuel used in food preparation. Local air pollution polices should consider these emission factors in regulating food cart vendor operations.

Assessing the PM2.5 impact of biomass combustion in megacity Dhaka, Bangladesh.

In Dhaka, Bangladesh, fine particulate matter (PM2.5) air pollution shows strong seasonal trends, with significantly higher mean concentrations during winter than during the monsoon (winter = 178.1 µg/m3 vs. monsoon = 30.2 µg/m3). Large-scale open burning of post-harvest agricultural waste across the Indo-Gangetic Plain is a major source of PM2.5 air pollution in northern India during the non-monsoon period. This study evaluates the extent to which the seasonal differences in PM2.5 pollution concentrations in Dhaka are accounted for by biomass-burning vs. fossil-fuel combustion sources. To assess this, an index was developed based on elemental potassium (K) as a marker for biomass particulate matter, after adjusting for soil-associated K contributions. Alternatively, particulate sulfur was employed as a tracer index for fossil-fuel combustion PM2.5. By simultaneously regressing total PM2.5 on S and adjusted K, the PM2.5 mass for each day was apportioned into: 1) fossil-fuels combustion associated PM2.5; 2) biomass-burning associated PM2.5; and, 3) all other PM2.5. The results indicated that fossil-fuel combustion contributed 21.6% (19.5 µg/m3), while biomass contributed 40.2% (36.3 µg/m3) of overall average PM2.5 from September 2013 to December 2017. However, the mean source contributions varied by season: PM2.5 in Dhaka during the monsoon season was dominated by fossil-fuels sources (44.3%), whereas PM2.5 mass was dominated by biomass-burning (41.4%) during the remainder of the year. The contribution to PM2.5 and each of its source components by transport of pollution into Dhaka during non-monsoon time was also evaluated by: 1) Conditional bivariate (CBPF) and pollution rose plots; 2) Concentration weighted trajectories (CWT), and; 3) NASA satellite photos to identify aerosol loading and fire locations on high pollution days. The collective evidence indicates that, while the air pollution in Dhaka is contributed to by both local and transboundary sources, the highest pollution days were dominated by biomass-related PM2.5, during periods of crop-burning in the Indo-Gangetic Plain.

Outdoor Air Pollution and New-Onset Airway Disease. An Official American Thoracic Society Workshop Report.

Although it is well accepted that air pollution exposure exacerbates preexisting airway disease, it has not been firmly established that long-term pollution exposure increases the risk of new-onset asthma or chronic obstruction pulmonary disease (COPD). This Workshop brought together experts on mechanistic, epidemiological, and clinical aspects of airway disease to review current knowledge regarding whether air pollution is a causal factor in the development of asthma and/or COPD. Speakers presented recent evidence in their respective areas of expertise related to air pollution and new airway disease incidence, followed by interactive discussions. A writing committee summarized their collective findings. The Epidemiology Group found that long-term exposure to air pollution, especially metrics of traffic-related air pollution such as nitrogen dioxide and black carbon, is associated with onset of childhood asthma. However, the evidence for a causal role in adult-onset asthma or COPD remains insufficient. The Mechanistic Group concluded that air pollution exposure can cause airway remodeling, which can lead to asthma or COPD, as well as asthma-like phenotypes that worsen with long-term exposure to air pollution, especially fine particulate matter and ozone. The Clinical Group concluded that air pollution is a plausible contributor to the onset of both asthma and COPD. Available evidence indicates that long-term exposure to air pollution is a cause of childhood asthma, but the evidence for a similar determination for adult asthma or COPD remains insufficient. Further research is needed to elucidate the exact biological mechanism underlying incident childhood asthma, and the specific air pollutant that causes it.

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

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 µg/m3 PM2.5 (overall range, 2.9-28.0 µg/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 µg/m3 (referent), risks for CVD were increased in relation to PM2.5 exposures in the range of 8-12 µg/m3 (CVD: HR 1.04; 95% CI 1.00-1.08), in the range 12-20 µg/m3 (CVD: HR 1.08; 95% CI 1.03-1.13) and in the range 20+ µg/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.

Air Pollution Monitoring for Health Research and Patient Care. An Official American Thoracic Society Workshop Report.

Air quality data from satellites and low-cost sensor systems, together with output from air quality models, have the potential to augment high-quality, regulatory-grade data in countries with in situ monitoring networks and provide much-needed air quality information in countries without them. Each of these technologies has strengths and limitations that need to be considered when integrating them to develop a robust and diverse global air quality monitoring network. To address these issues, the American Thoracic Society, the U.S. Environmental Protection Agency, the National Aeronautics and Space Administration, and the National Institute of Environmental Health Sciences convened a workshop in May 2017 to bring together global experts from across multiple disciplines and agencies to discuss current and near-term capabilities to monitor global air pollution. The participants focused on four topics: 1) current and near-term capabilities in air pollution monitoring, 2) data assimilation from multiple technology platforms, 3) critical issues for air pollution monitoring in regions without a regulatory-quality stationary monitoring network, and 4) risk communication and health messaging. Recommendations for research and improved use were identified during the workshop, including a recognition that the integration of data across monitoring technology groups is critical to maximizing the effectiveness (e.g., data accuracy, as well as spatial and temporal coverage) of these monitoring technologies. Taken together, these recommendations will advance the development of a global air quality monitoring network that takes advantage of emerging technologies to ensure the availability of free, accessible, and reliable air pollution data and forecasts to health professionals, as well as to all global citizens.

Air Pollution, Oxidative Stress, and Diabetes: a Life Course Epidemiologic Perspective.

PURPOSE OF REVIEW: Ambient air pollution is strongly linked to cardiovascular and respiratory diseases. We summarize available published evidence regarding similar associations with diabetes across the life course. RECENT FINDINGS: We performed a life-course survey of the recent literature, including prenatal, gestational, childhood/adolescence, and adult exposures to air pollution. Oxidative stress is identified as a key factor in both metabolic dysfunction and the effects of air pollution exposure, especially from fossil fuel combustion products, providing a plausible mechanism for air pollution-diabetes associations. The global burden of diabetes attributed to air pollution exposure is substantial, with a recent estimate that ambient fine particulate matter (PM2.5) exposure contributes to more than 200,000 deaths from diabetes annually. There is a growing body of literature linking air pollution exposure during childhood and adulthood with diabetes etiology and related cardiometabolic biomarkers. A small number of studies found that exposure to air pollution during pregnancy is associated with elevated gestational diabetes risk among mothers. Studies examining prenatal air pollution exposure and diabetes risk among the offspring, as well as potential transgenerational effects of air pollution exposure, are very limited thus far. This review provides insight into how air pollutants affect diabetes and other metabolic dysfunction-related diseases across the different life stages.