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.

Acute exposure to pollen and airway inflammation in adolescents.

INTRODUCTION: Pollen exposure is known to exacerbate allergic asthma and allergic rhinitis symptoms, yet few studies have investigated if exposure to pollen affects lung function or airway inflammation in healthy children. METHODS: We evaluated the extent to which higher pollen exposure was associated with differences in airway inflammation and lung function among 490 early adolescent participants (mean age of 12.9 years) in Project Viva, a prebirth cohort based in Massachusetts. We obtained regional daily total pollen counts, including tree, grass, and weed pollen, from a Rotorod pollen counter. We evaluated associations of 3- and 7-day moving averages of pollen with fractional exhaled nitric oxide (FeNO) and lung function using linear regression models and evaluated the linearity of associations with penalized splines. We tested if associations of pollen with FeNO and lung function were modified by current asthma diagnosis, history of allergic rhinitis, aeroallergen sensitivity, temperature, precipitation, and air pollution. RESULTS: Three- and 7-day median pollen concentrations were 19.0 grains/m3 (IQR: 73.4) and 20.9 grains/m3 (IQR: 89.7). In main models, higher concentrations of total pollen over the preceding 3 and 7 days were associated with a 4.6% (95% CI: 0.1,9.2) and 7.4% (95% CI: 0.9,14.3) higher FeNO per IQR of pollen, respectively. We did not find associations of pollen with lung function in main models. Asthma, allergic rhinitis, precipitation, and air pollution (nitrogen dioxide and ozone) modified associations of pollen with lung function (Pinteraction < 0.1), while temperature, sex, and aeroallergen sensitization did not. CONCLUSION: Short-term exposure to pollen was associated with higher FeNO in early adolescents, even in the absence of allergic sensitization and asthma.

Protocol for the air purification for eosinophilic COPD study (APECS): a randomised controlled trial of home air filtration by HEPA.

INTRODUCTION: Exposure to particulate matter (PM) pollution has been associated with lower lung function in adults with chronic obstructive pulmonary disease (COPD). Patients with eosinophilic COPD have been found to have higher levels of airway inflammation, greater responsiveness to anti-inflammatory steroid inhalers and a greater lung function response to PM pollution exposure compared with those with lower eosinophil levels. This study will evaluate if reducing home PM exposure by high-efficiency particulate air (HEPA) air filtration improves respiratory health in eosinophilic COPD. METHODS AND ANALYSIS: The Air Purification for Eosinophilic COPD Study (APECS) is a double-blinded randomised placebo-controlled trial that will enrol 160 participants with eosinophilic COPD living in the area of Boston, Massachusetts. Real and sham air purifiers will be placed in the bedroom and living rooms of the participants in the intervention and control group, respectively, for 12 months. The primary trial outcome will be the change in forced expiratory volume in 1 s (FEV1). Lung function will be assessed twice preintervention and three times during the intervention phase (at 7 days, 6 months and 12 months postrandomisation). Secondary trial outcomes include changes in (1) health status by St. George's Respiratory Questionnaire; (2) respiratory symptoms by Breathlessness, Cough and Sputum Scale (BCSS); and (3) 6-Minute Walk Test (6MWT). Inflammatory mediators were measured in the nasal epithelial lining fluid (NELF). Indoor PM will be measured in the home for the week preceding each study visit. The data will be analysed to contrast changes in outcomes in the intervention and control groups using a repeated measures framework. ETHICS AND DISSEMINATION: Ethical approval was obtained from the Institutional Review Board of Beth Israel Deaconess Medical Centre (protocol #2019P0001129). The results of the APECS trial will be presented at scientific conferences and published in peer-reviewed journals. TRIAL REGISTRATION: NCT04252235. Version: October 2023.

Neighborhood Environmental Burden and Cardiovascular Health in the US.

Importance: Cardiovascular disease is the leading cause of death in the US. However, little is known about the association between cumulative environmental burden and cardiovascular health across US neighborhoods. Objective: To evaluate the association of neighborhood-level environmental burden with prevalence of cardiovascular risk factors and diseases, overall and by levels of social vulnerability. Design, Settings, and Participants: This was a national cross-sectional study of 71 659 US Census tracts. Environmental burden (EBI) and social vulnerability indices from the US Centers for Disease Control and Prevention (CDC) and Agency for Toxic Substances and Disease Registry were linked to the 2020 CDC PLACES data set. Data were analyzed from March to October 2023. Exposures: The EBI, a measure of cumulative environmental burden encompassing 5 domains (air pollution, hazardous or toxic sites, built environment, transportation infrastructure, and water pollution). Main Outcomes and Measures: Neighborhood-level prevalence of cardiovascular risk factors (hypertension, diabetes, and obesity) and cardiovascular diseases (coronary heart disease and stroke). Results: Across the US, neighborhoods with the highest environmental burden (top EBI quartile) were more likely than those with the lowest environmental burden (bottom EBI quartile) to be urban (16 626 [92.7%] vs 13 414 [75.4%]), in the Midwest (5191 [28.9%] vs 2782 [15.6%]), have greater median (IQR) social vulnerability scores (0.64 [0.36-0.85] vs 0.42 [0.20-0.65]), and have higher proportions of adults in racial or ethnic minority groups (median [IQR], 34% [12-73] vs 12% [5-30]). After adjustment, neighborhoods with the highest environmental burden had significantly higher rates of cardiovascular risk factors than those with the lowest burden, including hypertension (mean [SD], 32.83% [7.99] vs 32.14% [6.99]; adjusted difference, 0.84%; 95% CI, 0.71-0.98), diabetes (mean [SD], 12.19% [4.33] vs 10.68% [3.27]; adjusted difference, 0.62%; 95% CI, 0.53-0.70), and obesity (mean [SD], 33.57% [7.62] vs 30.86% [6.15]; adjusted difference, 0.77%; 95% CI, 0.60-0.94). Similarly, neighborhoods with the highest environmental burden had significantly higher rates of coronary heart disease (mean [SD], 6.66% [2.15] vs 6.82% [2.41]; adjusted difference, 0.28%; 95% CI, 0.22-0.33) and stroke (mean [SD], 3.65% [1.47] vs 3.31% [1.12]; adjusted difference, 0.19%; 95% CI, 0.15-0.22). Results were consistent after matching highest and lowest environmentally burdened neighborhoods geospatially and based on other covariates. The associations between environmental burden quartiles and cardiovascular risk factors and diseases were most pronounced among socially vulnerable neighborhoods. Conclusions and Relevance: In this cross-sectional study of US neighborhoods, cumulative environmental burden was associated with higher rates of cardiovascular risk factors and diseases, although absolute differences were small. The strongest associations were observed in socially vulnerable neighborhoods. Whether initiatives that address poor environmental conditions will improve cardiovascular health requires additional prospective investigations.

Global Burden of Chronic Obstructive Pulmonary Disease Through 2050.

Importance: Chronic obstructive pulmonary disease (COPD) is a respiratory condition that is associated with significant health and economic burden worldwide. Previous studies assessed the global current-day prevalence of COPD, but to better facilitate resource planning and intervention development, long-term projections are needed. Objective: To assess the global burden of COPD through 2050, considering COPD risk factors. Design, Setting, and Participants: In this modeling study, historical data on COPD prevalence was extracted from a recent meta-analysis on 2019 global COPD prevalence, and 2010 to 2018 historical prevalence was estimated using random-effects meta-analytical models. COPD risk factor data were obtained from the Global Burden of Disease database. Main Outcomes and Measures: To project global COPD prevalence to 2050, generalized additive models were developed, including smoking prevalence, indoor and outdoor air pollution, and development indices as predictors, and stratified by age, sex, and World Bank region. Results: The models estimated that the number of COPD cases globally among those aged 25 years and older will increase by 23% from 2020 to 2050, approaching 600 million patients with COPD globally by 2050. Growth in the burden of COPD was projected to be the largest among women and in low- and middle-income regions. The number of female cases was projected to increase by 47.1% (vs a 9.4% increase for males), and the number of cases in low- and middle-income regions was expected to be more than double that of high-income regions by 2050. Conclusions and Relevance: In this modeling study of future COPD burden, projections indicated that COPD would continue to affect hundreds of millions of people globally, with disproportionate growth among females and in low-middle income regions through 2050. Further research, prevention, and advocacy are needed to address these issues so that adequate preparation and resource allocation can take place.

Personal and community-level exposure to air pollution and daily changes in respiratory symptoms and oxygen saturation among adults with COPD.

Background: Air pollution exposure is associated with hospital admissions for Chronic Obstructive Pulmonary Disease (COPD). Few studies have investigated whether daily personal exposure to air pollutants affects respiratory symptoms and oxygenation among COPD patients. Methodology: We followed 30 former smokers with COPD for up to 4 non-consecutive 30-day periods in different seasons. Participants recorded worsening of respiratory symptoms (sub-categorized as breathing or bronchitis symptoms) by daily questionnaire, and oxygen saturation by pulse oximeter. Personal and community-level exposure to fine particulate matter (PM2.5), nitrogen dioxide (NO2), and ozone (O3) were measured by portable air quality monitors and stationary monitors in the Boston area. We used generalized and multi-level linear mixed-effects models to estimate associations of the 24-hour average of each pollutant in the previous day with changes in respiratory symptoms and oxygen saturation. Results: Higher community-level exposure to air pollutants was associated with worsening respiratory symptoms. An interquartile range (IQR) higher community-level O3 was associated with a 1.35 (95%CI: 1.07-1.70) higher odds of worsening respiratory symptoms. The corresponding ORs for community-level PM2.5 and NO2 were 1.18 (95%CI: 1.02-1.37) and 1.06 (95%CI: 0.90-1.25), respectively. Community-level NO2 was associated with worsening bronchitis symptoms (OR=1.25, 95%CI: 1.00-1.56), but not breathing symptoms. Personal PM2.5 exposure was associated with lower odds of worsening respiratory symptoms (OR=0.91; 95%CI: 0.81-1.01). Personal exposure to NO2 was associated with 0.11% lower oxygen saturation (95%CI: -0.22, 0.00) per IQR. Conclusions: In this COPD population, there was a pattern of worsening respiratory symptoms associated with community-level exposure to O3 and PM2.5, and worsening oxygenation associated with personal exposure to NO2.

Impact of Global Climate Change on Pulmonary Health: Susceptible and Vulnerable Populations.

As fossil fuel combustion continues to power the global economy, the rate of climate change is accelerating, causing severe respiratory health impacts and large disparities in the degree of human suffering. Hotter and drier climates lead to longer and more severe wildland fire seasons, impairing air quality around the globe. Hotter temperatures lead to higher amounts of ozone and particles, causing the exacerbation of chronic respiratory diseases and premature mortality. Longer pollen seasons and higher pollen concentrations provoke allergic airway diseases. In arid regions, accelerated land degradation and desertification are promoting dust pollution and impairing food production and nutritional content that are essential to respiratory health. Extreme weather events and flooding impede healthcare delivery and can lead to poor indoor air quality due to mold overgrowth. Climate and human activities that harm the environment and ecosystem may also affect the emergence and spread of viral infections, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and associated morbidity and mortality exacerbated by air pollution. Children and elderly individuals are more susceptible to the adverse health effects of climate change. Geographical and socioeconomic circumstances, together with a decreased capacity to adapt, collectively increase vulnerability to the adverse effects of climate change. Successful mitigation of anthropogenic climate change is dependent on the commitment of energy-intensive nations to manage greenhouse gas emissions, as well as societal support and response to aggravating factors. In this review, we focus on the respiratory health impacts of global climate change, with an emphasis on susceptible and vulnerable populations and low- and middle-income countries.

Comparison of multiplexed protein analysis platforms for the detection of biomarkers in the nasal epithelial lining fluid of healthy subjects.

BACKGROUND: Multiplexed protein analysis platforms are a novel and efficient way to characterize biomarkers in a variety of biological samples. Few studies have compared protein quantitation and reproducibility of results across platforms. We utilize a novel nasosorption technique to collect nasal epithelial lining fluid (NELF) from healthy subjects, and compare the detection of proteins in NELF across three commonly used platforms. METHODS: NELF was collected from both nares of twenty healthy subjects using an absorbent fibrous matrix and analyzed using three different protein analysis platforms: Luminex, Meso Scale Discovery (MSD), and Olink. Twenty-three protein analytes were shared across two or more platforms, and correlations across platforms were assessed using Spearman correlations. RESULTS: Among the twelve proteins represented on all three platforms, IL1⍺ and IL6 were very highly correlated (Spearman correlation coefficient [r] ≥ 0.9); CCL3, CCL4, and MCP1 were highly correlated (r ≥ 0.7); and IFNÉ£, IL8, and TNF⍺ were moderately correlated (r ≥ 0.5). Four proteins (IL2, IL4, IL10, IL13) were poorly correlated across at least two platform comparisons (r < 0.5); for two of these proteins (IL10 and IL13), the majority of observations were below the limits of detection for Olink and Luminex. DISCUSSION: Multiplexed protein analysis platforms are a promising method for analyzing nasal samples for biomarkers of interest in respiratory health research. For most proteins evaluated, there was good correlation across platforms, although results were less consistent for low abundance proteins. Of the three platforms tested, MSD had the highest sensitivity for analyte detection.

Personal air pollution exposure and metals in the nasal epithelial lining fluid of COPD patients.

Sampling of the nasal epithelial lining fluid is a potential method to assess exposure to air pollution within the respiratory tract among high risk populations. We investigated associations of short- and long-term particulate matter exposure (PM) and pollution-related metals in the nasal fluid of people with chronic obstructive pulmonary disease (COPD). This study included 20 participants with moderate-to-severe COPD from a larger study who measured long-term personal exposure to PM2.5 using portable air monitors and short-term PM2.5 and black carbon (BC) using in-home samplers for the seven days preceding nasal fluid collection. Nasal fluid was sampled from both nares by nasosorption, and inductively coupled plasma mass spectrometry was used to determine the concentration of metals with major airborne sources. Correlations of selected elements (Fe, Ba, Ni, Pb, V, Zn, Cu) were determined within the nasal fluid. Associations between personal long-term PM2.5 and seven day home PM2.5 and BC exposure and nasal fluid metal concentrations were determined by linear regression. Within nasal fluid samples, concentrations of vanadium and nickel (r = 0.8) and lead and zinc (r = 0.7) were correlated. Seven day and long-term PM2.5 exposure were both associated with higher levels of copper, lead, and vanadium in the nasal fluid. BC exposure was associated with higher levels of nickel in the nasal fluid. Levels of certain metals in the nasal fluid may serve as biomarkers of air pollution exposure in the upper respiratory tract.

Physical Activity, Air Pollution Exposure, and Lung Function Interactions Among Adults with COPD.

Rationale: Although physical activity is strongly encouraged for patients with chronic obstructive pulmonary disease (COPD), it is unknown if physical activity affects daily exposure to air pollution, or whether it attenuates or exacerbates the effects of pollution on the airways among adults with COPD. Methods: Thirty former smokers with moderate-to-severe COPD in Boston were followed for 4 non-consecutive months in different seasons. We assessed daily lung function (forced expiratory volume in 1 second [FEV1] and forced vital capacity [FVC]), prior-day personal pollutant exposure measured by portable air quality monitors (fine particulate matter [PM2.5] nitrogen oxide [NO2], and ozone [O3]), and daily step count. We constructed multi-level linear mixed-effects models with random intercepts for person and person-observation month, adjusting for demographic/seasonal covariates to test if step count was associated with daily pollution exposure, and if associations between prior-day pollution and lung function differed based on prior-day step count. Where effect modification was found, we performed stratified analyses by tertile of step count. Results: Higher daily step count was associated with higher same-day personal exposure to PM2.5, and O3 but not NO2. Each interquartile range (IQR) increment in step count was associated with 0.97 µg/m3 (95%CI: 0.30, 1.64) higher exposure to PM2.5 and 0.15 parts per billion (95% CI: -0.05, 0.35) higher exposure to O3 in adjusted models. We observed an interaction between prior-day NO2 and step count on FEV1 and FVC (Pinteraction<0.05) in which the negative associations between NO2 and lung function were reduced or absent at higher levels of daily activity. For example, FEV1 was 28.5mL (95%CI: -41.0, -15.9) lower per IQR of NO2 in the lowest tertile of step count, but there was no association in the highest tertile of step count (-1.6mL, 95% CI: -18.4, 15.2). Conclusions: Higher physical activity was associated with modestly higher daily exposure to PM2.5 and O3 and may attenuate the association between NO2 exposure and lung function.

Precipitation and Adolescent Respiratory Health in the Northeast United States.

Rationale: With more frequent and intense precipitation events across the globe due to a changing climate, there is a need to understand the relationship between precipitation and respiratory health. Precipitation may trigger asthma exacerbations, but little is known about how precipitation affects lung function and airway inflammation in early adolescents. Objectives: To determine if short-term precipitation exposure is associated with lung function and airway inflammation in early adolescents and if ever having a diagnosis of asthma modifies associations of precipitation with lung function and airway inflammation. Methods: In a prospective prebirth cohort, Project Viva, that included 1,019 early adolescents born in the northeastern United States, we evaluated associations of 1-, 2-, 3-, and 7-day moving averages of precipitation in the preceding week and forced expiratory volume in 1 second, forced vital capacity, and fractional exhaled nitric oxide (FeNO) using linear regression. We used log-transformed FeNO with effect estimates presented as percentage change. We adjusted for maternal education and household income at enrollment; any smoking in the home in early adolescence; child sex, race/ethnicity, and ever asthma diagnosis; and age, height, weight, date, and season (as sine and cosine functions of visit date) at the early adolescent visit and moving averages for mean daily temperature (same time window as exposure). Results: In fully adjusted linear models, 3- and 7-day moving averages for precipitation were positively associated with FeNO but not lung function. Every 2-mm increase in the 7-day moving average for precipitation was associated with a 4.0% (95% confidence interval, 1.1, 6.9) higher FeNO. There was evidence of effect modification by asthma status: Precipitation was associated with lower forced vital capacity and higher FeNO among adolescents with asthma. We also found that outdoor aeroallergen sensitization (immunoglobulin E against common ragweed, oak, ryegrass, or silver birch) modified associations of precipitation with FeNO, with higher FeNO in sensitized adolescents compared with nonsensitized adolescents. The associations of precipitation with FeNO were not explained by relative humidity or air pollution exposure. Conclusions: We found that greater short-term precipitation may trigger airway inflammation in adolescents, particularly among those with asthma.

Nasal biomarkers of immune function differ based on smoking and respiratory disease status.

Respiratory biomarkers have the potential to identify airway injury by revealing inflammatory processes within the respiratory tract. Currently, there are no respiratory biomarkers suitable for clinical use to identify patients that warrant further diagnostic work-up, counseling, and treatment for toxic inhalant exposures or chronic airway disease. Using a novel, noninvasive method of sampling the nasal epithelial lining fluid, we aimed to investigate if nasal biomarker patterns could distinguish healthy nonsmoking adults from active smokers and those with chronic upper and lower airway disease in this exploratory study. We compared 28 immune mediators from healthy nonsmoking adults (n = 32), former smokers with COPD (n = 22), chronic rhinosinusitis (CRS) (n = 22), and smoking adults without airway disease (n = 13). Using ANOVA, multinomial logistic regressions, and weighted gene co-expression network analysis (WGCNA), we determined associations between immune mediators and each cohort. Six mediators (IL-7, IL-10, IL-13, IL-12p70, IL-15, and MCP-1) were lower among disease groups compared to healthy controls. Participants with lower levels of IL-10, IL-12p70, IL-13, and MCP-1 in the nasal fluid had a higher odds of being in the COPD or CRS group. The cluster analysis identified groups of mediators that correlated with disease status. Specifically, the cluster of IL-10, IL-12p70, and IL-13, was positively correlated with healthy and negatively correlated with COPD groups, and two clusters were correlated with active smoking. In this exploratory study, we preliminarily identified groups of nasal mucosal mediators that differed by airway disease and smoking status. Future prospective, age-matched studies that control for medication use are needed to validate these patterns and determine if nasosorption has diagnostic utility for upper and lower airway disease or injury.