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This study was conducted in a school center in Finland that had been the focus of intense public concern over 2 years because of suspected mold and health problems. Because several attempts to find solutions to the problem within the community were not satisfactory, outside specialists were needed for support in solving the problem. The study group consisted of experts in civil engineering, indoor mycology, and epidemiology. The studies were conducted in close cooperation with the city administration. Structures at risk were opened, moisture and temperature were measured, and the causes of damage were analyzed. Microbial samples were taken from the air, surfaces, and materials. Health questionnaires were sent to the school children and personnel. Information on the measurements and their results was released regularly to school employees, students and their parents, and to the media. Repairs were designed on the basis of this information. Moisture damage was caused mainly by difficult moisture conditions at the building site, poor ventilation, and water leaks. Fungal genera typical to buildings with mold problems were collected from the indoor air and surfaces of the school buildings. Where moisture-prone structures were identified and visible signs of damage or elevated moisture content were recorded, the numbers of microbes also were high; thus microbial results from material samples supported the conclusions made in the structural studies. Several irritative and recurrent symptoms were common among the upper secondary and high school students. The prevalence of asthma was high (13 percent) among the upper secondary school students. During the last 4 years, the incidence of asthma was three-fold that of the previous 4-year period. (Contains 18 references.) (Author/EV)

BACKGROUND: The prenatal environment influences lifetime health; epigenetic mechanisms likely predominate. In 2016, the first international consortium paper on cigarette smoking during pregnancy and offspring DNA methylation identified extensive, reproducible exposure signals. This finding raised expectations for epigenome-wide association studies (EWAS) of other exposures. OBJECTIVE: We review the current state-of-the-science for DNA methylation associations across prenatal exposures in humans and provide future recommendations. METHODS: We reviewed 134 prenatal environmental EWAS of DNA methylation in newborns, focusing on 51 epidemiological studies with meta-analysis or replication testing. Exposures spanned cigarette smoking, alcohol consumption, air pollution, dietary factors, psychosocial stress, metals, other chemicals, and other exogenous factors. Of the reproducible DNA methylation signatures, we examined implementation as exposure biomarkers. RESULTS: Only 19 (14%) of these prenatal EWAS were conducted in cohorts of 1,000 or more individuals, reflecting the still early stage of the field. To date, the largest perinatal EWAS sample size was 6,685 participants. For comparison, the most recent genome-wide association study for birth weight included more than 300,000 individuals. Replication, at some level, was successful with exposures to cigarette smoking, folate, dietary glycemic index, particulate matter with aerodynamic diameter <10 μm and <2.5 μm, nitrogen dioxide, mercury, cadmium, arsenic, electronic waste, PFAS, and DDT. Reproducible effects of a more limited set of prenatal exposures (smoking, folate) enabled robust methylation biomarker creation. DISCUSSION: Current evidence demonstrates the scientific premise for reproducible DNA methylation exposure signatures. Better powered EWAS could identify signatures across many exposures and enable comprehensive biomarker development. Whether methylation biomarkers of exposures themselves cause health effects remains unclear. We expect that larger EWAS with enhanced coverage of epigenome and exposome, along with improved single-cell technologies and evolving methods for integrative multi-omics analyses and causal inference, will expand mechanistic understanding of causal links between environmental exposures, the epigenome, and health outcomes throughout the life course. [ABSTRACT FROM AUTHOR]

BACKGROUND: Dementia is a devastating neurologic condition that is common in older adults. We previously reviewed the epidemiological evidence examining the hypothesis that long-term exposure to air pollution affects dementia risk. Since then, the evidence base has expanded rapidly. OBJECTIVES: With this update, we collectively review new and previously identified epidemiological studies on air pollution and late-life cognitive health, highlighting new developments and critically discussing the merits of the evidence. METHODS: Using a registered protocol (PROSPERO 2020 CRD42020152943), we updated our literature review to capture studies published through 31 December 2020, extracted data, and conducted a bias assessment. RESULTS: We identified 66 papers (49 new) for inclusion in this review. Cognitive level remained the most commonly considered outcome, and particulate matter (PM) remained the most commonly considered air pollutant. Since our prior review, exposure estimation methods in this research have improved, and more papers have looked at cognitive change, neuroimaging, and incident cognitive impairment/dementia, though methodological concerns remain common. Many studies continue to rely on administrative records to ascertain dementia, have high potential for selection bias, and adjust for putative mediating factors in primary models. A subset of 35 studies met strict quality criteria. Although high-quality studies of fine particulate matter with aerodynamic diameter =2.5 µm (PM2.5) and cognitive decline generally supported an adverse association, other findings related to PM2.5 and findings related to particulate matter with aerodynamic diameter =10 µm (PM10, NO2, and NOx) were inconclusive, and too few papers reported findings with ozone to comment on the likely direction of association. Notably, only a few findings on dementia were included for consideration on the basis of quality criteria. DISCUSSION: Strong conclusions remain elusive, although the weight of the evidence suggests an adverse association between PM2.5 and cognitive decline. However, we note a continued need to confront methodological challenges in this line of research. [ABSTRACT FROM AUTHOR]

Background: Exposure to PM 2.5 arising from solid fuel combustion is estimated to result in ∼ 2.3 million premature deaths and 91 million lost disability-adjusted life years annually. Interventions attempting to mitigate this burden have had limited success in reducing exposures to levels thought to provide substantive health benefits., Objectives: This paper reports exposure reductions achieved by a liquified petroleum gas (LPG) stove and fuel intervention for pregnant mothers in the Household Air Pollution Intervention Network (HAPIN) randomized controlled trial., Methods: The HAPIN trial included 3,195 households primarily using biomass for cooking in Guatemala, India, Peru, and Rwanda. Twenty-four-hour exposures to PM 2.5 , carbon monoxide (CO), and black carbon (BC) were measured for pregnant women once before randomization into control ( n = 1,605 ) and LPG ( n = 1,590 ) arms and twice thereafter (aligned with trimester). Changes in exposure were estimated by directly comparing exposures between intervention and control arms and by using linear mixed-effect models to estimate the impact of the intervention on exposure levels., Results: Median postrandomization exposures of particulate matter (PM) with aerodynamic diameter ≤ 2.5 μ m ( PM 2.5 ) in the intervention arm were lower by 66% at the first (71.5 vs. 24.1   μ g / m 3 ), and second follow-up visits (69.5 vs. 23.7   μ g / m 3 ) compared to controls. BC exposures were lower in the intervention arm by 72% (9.7 vs. 2.7   μ g / m 3 ) and 70% (9.6 vs. 2.8   μ g / m 3 ) at the first and second follow-up visits, respectively, and carbon monoxide exposure was 82% lower at both visits (1.1 vs. 0.2  ppm ) in comparison with controls. Exposure reductions were consistent over time and were similar across research locations., Discussion: Postintervention PM 2.5 exposures in the intervention arm were at the lower end of what has been reported for LPG and other clean fuel interventions, with 69% of PM 2.5 samples falling below the World Health Organization Annual Interim Target 1 of 35   μ g / m 3 . This study indicates that an LPG intervention can reduce PM 2.5 exposures to levels at or below WHO targets. https://doi.org/10.1289/EHP10295.

BACKGROUND: Studies have reported that ambient air pollution is associated with an increased risk of developing or dying from coronavirus-2 (COVID-19). Methodological approaches to investigate the health impacts of air pollution on epidemics should differ from those used for chronic diseases, but the methods used in these studies have not been appraised critically. OBJECTIVES: Our study aimed to identify and critique the methodological approaches of studies of air pollution on infections and mortality due to COVID-19 and to identify and critique the methodological approaches of similar studies concerning severe acute respiratory syndrome (SARS). METHODS: Published and unpublished papers of associations between air pollution and developing or dying from COVID-19 or SARS that were reported as of 10 May 2020 were identified through electronic databases, internet searches, and other sources. RESULTS: All six COVID-19 studies and two of three SARS studies reported positive associations. Two were time series studies that estimated associations between daily changes in air pollution, one was a cohort that assessed associations between air pollution and the secondary spread of SARS, and six were ecological studies that used area-wide exposures and outcomes. Common shortcomings included possible cross-level bias in ecological studies, underreporting of health outcomes, using grouped data, the lack of highly spatially resolved air pollution measures, inadequate control for confounding and evaluation of effect modification, not accounting for regional variations in the timing of outbreaks’ temporal changes in at-risk populations, and not accounting for nonindependence of outcomes. DISCUSSION: Studies of air pollution and novel coronaviruses have relied mainly on ecological measures of exposures and outcomes and are susceptible to important sources of bias. Although longitudinal studies with individual-level data may be imperfect, they are needed to adequately address this topic. The complexities involved in these types of studies underscore the need for careful design and for peer review. [ABSTRACT FROM AUTHOR]

The authors comment on a study which investigated the bias from measurement error (ME) in long-term estimates of particulate matter 2.5 micrometers in aerodynamic diameter in residential areas of participants on the mortality effect estimates. Topics covered include the several exceptional methodological features of the study, the study's strengths and limitations, and some aspects of the paper that are unique and lead to a smaller reported magnitude of bias.

BACKGROUND: High quality personal exposure data is fundamental to understanding the health implications of household energy interventions, interpreting analyses across assigned study arms, and characterizing exposure–response relationships for household air pollution. This paper describes the exposure data collection for the Household Air Pollution Intervention Network (HAPIN), a multicountry randomized controlled trial of liquefied petroleum gas stoves and fuel among 3,200 households in India, Rwanda, Guatemala, and Peru. OBJECTIVES: The primary objectives of the exposure assessment are to estimate the exposure contrast achieved following a clean fuel intervention and to provide data for analyses of exposure–response relationships across a range of personal exposures. METHODS: Exposure measurements are being conducted over the 3-y time frame of the field study. We are measuring fine particulate matter [PM < 2.5 μm in aerodynamic diameter (PM2.5)] with the Enhanced Children’s MicroPEM™ (RTI International), carbon monoxide (CO) with the USB-EL-CO (Lascar Electronics), and black carbon with the OT21 transmissometer (Magee Scientific) in pregnant women, adult women, and children < 1 year of age, primarily via multiple 24-h personal assessments (three, six, and three measurements, respectively) over the course of the 18-month follow-up period using lightweight monitors. For children we are using an indirect measurement approach, combining data from area monitors and locator devices worn by the child. For a subsample (up to 10%) of the study population, we are doubling the frequency of measurements in order to estimate the accuracy of subject-specific typical exposure estimates. In addition, we are conducting ambient air monitoring to help characterize potential contributions of PM2.5 exposure from background concentration. Stove use monitors (Geocene) are being used to assess compliance with the intervention, given that stove stacking (use of traditional stoves in addition to the intervention gas stove) may occur. CONCLUSIONS: The tools and approaches being used for HAPIN to estimate personal exposures build on previous efforts and take advantage of new technologies. In addition to providing key personal exposure data for this study, we hope the application and learnings from our exposure assessment will help inform future efforts to characterize exposure to household air pollution and for other contexts. [ABSTRACT FROM AUTHOR]

Background: Although numerous epidemiologic studies now use models of intra-urban exposure, there has been little systematic evaluation of the performance of different models. Objectives: In this paper we proposed a modeling framework for assessing exposure model performance and the role of spatial autocorrelation in health effects estimation. Methods: Data was obtained from an exposure measurement substudy of subjects from the Southern California Children's Health Study. We examine how the addition of spatial correlations to a previously described unified exposure and health outcome modeling framework affects estimates of exposure-response relationships using the substudy data. The methods proposed build upon the authors' previous work, which developed measurement-error techniques to estimate long-term nitrogen dioxide (NO2) exposure and its effect on lung function in children. This paper further develops these methods by introducing between and within-community spatial autocorrelation error terms to evaluate effects of air pollution on forced vital capacity (FVC). The analytical methods developed are set in a Bayesian framework where multi-stage models are fitted jointly, properly incorporating parameter estimation uncertainty at all levels of the modeling process. Results: Findings suggest that the inclusion of residual spatial error terms improves the prediction of health effects. The results also demonstrate how residual spatial error may be used as a diagnostic for comparing exposure model performance. [ABSTRACT FROM AUTHOR]

The article discusses the results of a study on how to lower the health disparities of the effect of air pollution on racial/ethnic communities in the U.S. Topics mentioned include the use of race-specific concentration-response functions (CRFs) in calculating the link between exposure to fine particulates and mortality for Asian, African American, and Hispanic Americans, the impact of federal policies to improve air quality on communities of color, and the various aspects of systemic racism.

Background: Long-term air pollution exposure has been associated with age-related cognitive impairment, possibly because of enhanced inflammation. Leukocytes with longer telomere length (TL) are more responsive to inflammatory stimuli, yet TL has not been evaluated in relation to air pollution and cognition., Objectives: We assessed whether TL modifies the association of 1-year exposure to black carbon (BC), a marker of traffic-related air pollution, with cognitive function in older men, and we examined whether this modification is independent of age and of C-reactive protein (CRP), a marker of inflammation., Methods: Between 1999 and 2007, we conducted 1-3 cognitive examinations of 428 older men in the Veterans Affairs (VA) Normative Aging Study. We used covariate-adjusted repeated-measure logistic regression to estimate associations of 1-year BC exposure with relative odds of being a low scorer (≤ 25) on the Mini-Mental State Examination (MMSE), which is a proxy of poor cognition. Confounders included age, CRP, and lifestyle and sociodemographic factors., Results: Each doubling in BC level was associated with 1.57 (95% CI: 1.20, 2.05) times higher odds of low MMSE scores. The BC-MMSE association was greater only among individuals with longer blood TL (5th quintile) (OR = 3.23; 95% CI: 1.37, 7.59; p = 0.04 for BC-by-TL-interaction). TL and CRP were associated neither with each other nor with MMSE. However, CRP modified the BC-MMSE relationship, with stronger associations only at higher CRP (5th quintile) and reference TL level (1st quintile) (OR = 2.68; 95% CI: 1.06, 6.79; p = 0.04 for BC-by-CRP-interaction)., Conclusions: TL and CRP levels may help predict the impact of BC exposure on cognitive function in older men. Citation: Colicino E, Wilson A, Frisardi MC, Prada D, Power MC, Hoxha M, Dioni L, Spiro A III, Vokonas PS, Weisskopf MG, Schwartz JD, Baccarelli AA. 2017. Telomere length, long-term black carbon exposure, and cognitive function in a cohort of older men: the VA Normative Aging Study. Environ Health Perspect 125:76-81; http://dx.doi.org/10.1289/EHP241., Competing Interests: The views expressed in this paper are those of the authors and do not necessarily represent the views of the U.S. Department of VA. The authors declare they have no actual or potential competing financial interests.

Background: Among nondiabetic individuals, higher fasting blood glucose (FBG) independently predicts diabetes risk, cardiovascular disease, and dementia. Ambient PM2.5 (particulate matter with aerodynamic diameter ≤ 2.5 μm) is an emerging determinant of glucose dysregulation. PM2.5 effects and mechanisms are understudied among nondiabetic individuals., Objectives: Our goals were to investigate whether PM2.5 is associated with an increase in FBG and to explore potential mediating roles of epigenetic gene regulation., Methods: In 551 nondiabetic participants in the Normative Aging Study, we measured FBG, and DNA methylation of four inflammatory genes (IFN-γ, IL-6, ICAM-1, and TLR-2), up to four times between 2000 and 2011 (median = 2). We estimated short- and medium-term (1-, 7-, and 28-day preceding each clinical visit) ambient PM2.5 at each participant's address using a validated hybrid land-use regression satellite-based model. We fitted covariate-adjusted regression models accounting for repeated measures., Results: Mean FBG was 99.8 mg/dL (SD = 10.7), 18% of the participants had impaired fasting glucose (IFG; i.e., 100-125 mg/dL FBG) at first visit. Interquartile increases in 1-, 7-, and 28-day PM2.5 were associated with 0.57 mg/dL (95% CI: 0.02, 1.11, p = 0.04), 1.02 mg/dL (95% CI: 0.41, 1.63, p = 0.001), and 0.89 mg/dL (95% CI: 0.32, 1.47, p = 0.003) higher FBG, respectively. The same PM2.5 metrics were associated with 13% (95% CI: -3%, 33%, p = 0.12), 27% (95% CI: 6%, 52%, p = 0.01) and 32% (95% CI: 10%, 58%, p = 0.003) higher odds of IFG, respectively. PM2.5 was negatively correlated with ICAM-1 methylation (p = 0.01), but not with other genes. Mediation analysis estimated that ICAM-1 methylation mediated 9% of the association of 28-day PM2.5 with FBG., Conclusions: Among nondiabetics, short- and medium-term PM2.5 were associated with higher FBG. Mediation analysis indicated that part of this association was mediated by ICAM-1 promoter methylation. Citation: Peng C, Bind MA, Colicino E, Kloog I, Byun HM, Cantone L, Trevisi L, Zhong J, Brennan K, Dereix AE, Vokonas PS, Coull BA, Schwartz JD, Baccarelli AA. 2016. Particulate air pollution and fasting blood glucose in nondiabetic individuals: associations and epigenetic mediation in the Normative Aging Study, 2000-2011. Environ Health Perspect 124:1715-1721; http://dx.doi.org/10.1289/EHP183., Competing Interests: The views expressed in this paper are those of the authors and do not necessarily represent the views of the U.S. Department of Veterans Affairs. The authors declare they have no actual or potential competing financial interests.

BACKGROUND: Polyunsaturated fatty acids (PUFAs) have been shown to protect against fine particulate matter <2.5 μm in aerodynamic diameter (PM2.5)-induced hazards. However, limited evidence is available for respiratory health, particularly in pregnant women and their offspring. OBJECTIVES: We aimed to investigate the association of prenatal exposure to PM2.5 and its chemical components with allergic rhinitis (AR) in children and explore effect modification by maternal erythrocyte PUFAs. METHODS: This prospective birth cohort study involved 657 mother–child pairs from Guangzhou, China. Prenatal exposure to residential PM2.5 mass and its components [black carbon (BC), organic matter (OM), sulfate (SO42- ), nitrate (NO3 - ), and ammonium (NH4 +)] were estimated by an established spatiotemporal model. Maternal erythrocyte PUFAs during pregnancy were measured using gas chromatography. The diagnosis of AR and report of AR symptoms in children were assessed up to 2 years of age. We used Cox regression with the quantile-based g-computation approach to assess the individual and joint effects of PM2.5 components and examine the modification effects of maternal PUFA levels. RESULTS: Approximately 5.33% and 8.07% of children had AR and related symptoms, respectively. The average concentration of prenatal PM2.5 was 35.50 ± 5.31 μg/m³. PM2.5 was positively associated with the risk of developing AR [hazard ratio (HR)= 1.85; 95% confidence interval (CI): 1.16, 2.96 per 5 μg/m³] and its symptoms (HR = 1.79; 95% CI: 1.22, 2.62 per 5 μg/m³) after adjustment for confounders. Similar associations were observed between individual PM2.5 components and AR outcomes. Each quintile change in a mixture of components was associated with an adjusted HR of 3.73 (95% CI: 1.80, 7.73) and 2.69 (95% CI: 1.55, 4.67) for AR and AR symptoms, with BC accounting for the largest contribution. Higher levels of n-3 docosapentaenoic acid and lower levels of n-6 linoleic acid showed alleviating effects on AR symptoms risk associated with exposure to PM2.5 and its components. CONCLUSION: Prenatal exposure to PM2.5 and its chemical components, particularly BC, was associated with AR/symptoms in early childhood. We highlight that PUFA biomarkers could modify the adverse effects of PM2.5 on respiratory allergy. [ABSTRACT FROM AUTHOR]

Background: Previous studies have observed associations between air pollution and heart disease. Susceptibility to air pollution effects has been examined mostly with a test of effect modification, but little evidence is available whether air pollution distorts cardiovascular risk factor distribution., Objectives: This paper aims to examine distributional and heterogeneous effects of air pollution on known cardiovascular biomarkers., Methods: A total of 1,112 men from the Normative Aging Study and residents of the greater Boston, Massachusetts, area with mean age of 69 years at baseline were included in this study during the period 1995-2013. We used quantile regression and random slope models to investigate distributional effects and heterogeneity in the traffic-related responses on blood pressure, heart rate variability, repolarization, lipids, and inflammation. We considered 28-day averaged exposure to particle number, PM2.5 black carbon, and PM2.5 mass concentrations (measured at a single monitor near the site of the study visits)., Results: We observed some evidence suggesting distributional effects of traffic-related pollutants on systolic blood pressure, heart rate variability, corrected QT interval, low density lipoprotein (LDL) cholesterol, triglyceride, and intercellular adhesion molecule-1 (ICAM-1). For example, among participants with LDL cholesterol below 80 mg/dL, an interquartile range increase in PM2.5 black carbon exposure was associated with a 7-mg/dL (95% CI: 5, 10) increase in LDL cholesterol, while among subjects with LDL cholesterol levels close to 160 mg/dL, the same exposure was related to a 16-mg/dL (95% CI: 13, 20) increase in LDL cholesterol. We observed similar heterogeneous associations across low versus high percentiles of the LDL distribution for PM2.5 mass and particle number., Conclusions: These results suggest that air pollution distorts the distribution of cardiovascular risk factors, and that, for several outcomes, effects may be greatest among individuals who are already at high risk., Citation: Bind MA, Peters A, Koutrakis P, Coull B, Vokonas P, Schwartz J. 2016. Quantile regression analysis of the distributional effects of air pollution on blood pressure, heart rate variability, blood lipids, and biomarkers of inflammation in elderly American men: the Normative Aging Study. Environ Health Perspect 124:1189-1198; http://dx.doi.org/10.1289/ehp.1510044.

BACKGROUND: Air pollution risk assessments do not generally quantify health impacts using multipollutant risk estimates, but instead use results from single-pollutant or copollutant models. Multipollutant epidemiological models account for pollutant interactions and joint effects but can be computationally complex and data intensive. Risk estimates from multipollutant studies are therefore challenging to implement in the quantification of health impacts. OBJECTIVES: Our objective was to conduct a case study using a developmental multipollutant version of the Environmental Benefits Mapping and Analysis Program—Community Edition (BenMAP-CE) to estimate the health impact associated with changes in multiple air pollutants using both a single and multipollutant approach. METHODS: BenMAP-CE was used to estimate the change in the number of pediatric asthma emergency department (ED) visits attributable to simulated changes in air pollution between 2011 and 2025 in Atlanta, Georgia, applying risk estimates from an epidemiological study that examined shortterm single-pollutant and multipollutant (with and without first-order interactions) exposures. Analyses examined individual pollutants (i.e., ozone, fine particulate matter, carbon monoxide, nitrogen dioxide (NO2), sulfur dioxide, and particulate matter components) and combinations of these pollutants meant to represent shared properties or predefined sources (i.e., oxidant gases, secondary pollutants, traffic, power plant, and criteria pollutants). Comparisons were made between multipollutant health impact functions (HIF) and the sum of single-pollutant HIFs for the individual pollutants that constitute the respective pollutant groups. RESULTS: Photochemical modeling predicted large decreases in most of the examined pollutant concentrations between 2011 and 2025 based on sector specific (i.e., source-based) estimates of growth and anticipated controls. Estimated number of avoided asthma ED visits attributable to any given multipollutant group were generally higher when using results from models that included interaction terms in comparison with those that did not. We estimated the greatest number of avoided pediatric asthma ED visits for pollutant groups that include NO2 (i. e., criteria pollutants, oxidants, and traffic pollutants). In models that accounted for interaction, year-round estimates for pollutant groups that included NO2 ranged from 27.1 [95% confidence interval (CI): 1.6, 52.7; traffic pollutants] to 55.4 (95% CI: 41.8, 69.0; oxidants) avoided pediatric asthma ED visits. Year-round results using multipollutant risk estimates with interaction were comparable to the sum of the single-pollutant results corresponding to most multipollutant groups [e.g., 52.9 (95% CI: 43.6, 62.2) for oxidants] but were notably lower than the sum of the single-pollutant results for some pollutant groups [e.g., 77.5 (95% CI: 66.0, 89.0) for traffic pollutants]. DISCUSSION: Performing a multipollutant health impact assessment is technically feasible but computationally complex. It requires time, resources, and detailed input parameters not commonly reported in air pollution epidemiological studies. Results estimated using the sum of single-pollutant models are comparable to those quantified using a multipollutant model. Although limited to a single study and location, assessing the trade-offs between a multipollutant and single-pollutant approach is warranted. [ABSTRACT FROM AUTHOR]

The article explores the direct health effects of gas stove emissions. Topics discussed include association of childhood asthma cases in the U.S. to gas stove use, association of natural gas connections in residential and commercial construction to carbon emissions and climate change, pollutants produced by gas burners such as volatile organic compounds and liquefied petroleum gas or propane, and concentration of nitrogen dioxide in kitchens with overhead range hood versus sealed off kitchens.

BACKGROUND: Extreme heat and air pollution are important human health concerns; exposure can affect mental and physical well-being, particularly during periods of co-occurrence. Yet, the impacts on people are largely determined by underlying health conditions, coupled with the length and intensity of exposure. Preexisting adverse health conditions and prolonged exposure times are more common for people experiencing homelessness, particularly those with intersectional identity characteristics (e.g., disease, ability, age, etc.). Partially due to methodological limitations, such as data scarcity, there is a lack of research at the intersection of this at-risk population within the climate-health domain. OBJECTIVES: We have three distinct objectives throughout this article: a) to advance critical discussions around the state of concurrent high heat and air pollution exposure research as it relates to people experiencing homelessness; b) to assert the importance of heat and air pollution exposure research among a highly vulnerable, too-often homogenized population—people experiencing homelessness; and c) to underline challenges in this area of study while presenting potential ways to address such shortcomings. DISCUSSION: The health insights from concurrent air pollution and heat exposure studies are consequential when studying unhoused communities who are already overexposed to harmful environmental conditions. Without holistic data sets and more advanced methods to study concurrent exposures, appropriate and targeted prevention and intervention strategies cannot be developed to protect this at-risk population. We highlight that a) concurrent high heat and air pollution exposure research among people experiencing homelessness is significantly underdeveloped considering the pressing human health implications; b) the severity of physiological responses elicited by high heat and air pollution are predicated on exposure intensity and time, and thus people without means of seeking climate-controlled shelter are most at risk; and c) collaboration among transdisciplinary teams is needed to resolve data resolution issues and enable targeted prevention and intervention strategies. [ABSTRACT FROM AUTHOR]

BACKGROUND: Wildfire activity is predicted to increase in many parts of the world due to changes in temperature and precipitation patterns from global climate change. Wildfire smoke contains numerous hazardous air pollutants and many studies have documented population health effects from this exposure. OBJECTIVES: We aimed to assess the evidence of health effects from exposure to wildfire smoke and to identify susceptible populations. METHODS: We reviewed the scientific literature for studies of wildfire smoke exposure on mortality and on respiratory, cardiovascular, mental, and perinatal health. Within those reviewed papers deemed to have minimal risk of bias, we assessed the coherence and consistency of findings. DISCUSSION: Consistent evidence documents associations between wildfire smoke exposure and general respiratory health effects, specifically exacerbations of asthma and chronic obstructive pulmonary disease. Growing evidence suggests associations with increased risk of respiratory infections and all-cause mortality. Evidence for cardiovascular effects is mixed, but a few recent studies have reported associations for specific cardiovascular end points. Insufficient research exists to identify specific population subgroups that are more susceptible to wildfire smoke exposure. CONCLUSIONS: Consistent evidence from a large number of studies indicates that wildfire smoke exposure is associated with respiratory morbidity with growing evidence supporting an association with all-cause mortality. More research is needed to clarify which causes of mortality may be associated with wildfire smoke, whether cardiovascular outcomes are associated with wildfire smoke, and if certain populations are more susceptible. [ABSTRACT FROM AUTHOR]

The article discusses a study published in the journal which used a novel type of clock based on urinary peptides to assess the relationship between ambient air pollutants, biological aging, and cardiovascular mortality. Topics include finding on earlier research about air pollutants, differences observed on pollutants, and an alternative mechanism by which vitamin K may influence cardiovascular health.

Background: This paper presents an application of quantitative ion character-activity relationships (QICAR) to estimate associations of human cardiovascular (CV) diseases (CVDs) with a set of metal ion properties commonly observed in ambient air pollutants. QICAR has previously been used to predict ecotoxicity of inorganic metal ions based on ion properties., Objectives: The objective of this work was to examine potential associations of biological end points with a set of physical and chemical properties describing inorganic metal ions present in exposures using QICAR., Methods: Chemical and physical properties of 17 metal ions were obtained from peer-reviewed publications. Associations of cardiac arrhythmia, myocardial ischemia, myocardial infarction, stroke, and thrombosis with exposures to metal ions (measured as inference scores) were obtained from the Comparative Toxicogenomics Database (CTD). Robust regressions were applied to estimate the associations of CVDs with ion properties., Results: CVD was statistically significantly associated (Bonferroni-adjusted significance level of 0.003) with many ion properties reflecting ion size, solubility, oxidation potential, and abilities to form covalent and ionic bonds. The properties are relevant for reactive oxygen species (ROS) generation, which has been identified as a possible mechanism leading to CVDs., Conclusion: QICAR has the potential to complement existing epidemiologic methods for estimating associations between CVDs and air pollutant exposures by providing clues about the underlying mechanisms that may explain these associations.

Background: Hierarchical Bayesian methods have been used in previous papers to estimate national mean effects of air pollutants on daily deaths in time-series analyses., Objectives: We obtained maximum likelihood estimates of the common national effects of the criteria pollutants on mortality based on time-series data from ≤ 108 metropolitan areas in the United States., Methods: We used a subsampling bootstrap procedure to obtain the maximum likelihood estimates and confidence bounds for common national effects of the criteria pollutants, as measured by the percentage increase in daily mortality associated with a unit increase in daily 24-hr mean pollutant concentration on the previous day, while controlling for weather and temporal trends. We considered five pollutants [PM10, ozone (O3), carbon monoxide (CO), nitrogen dioxide (NO2), and sulfur dioxide (SO2)] in single- and multipollutant analyses. Flexible ambient concentration-response models for the pollutant effects were considered as well. We performed limited sensitivity analyses with different degrees of freedom for time trends., Results: In single-pollutant models, we observed significant associations of daily deaths with all pollutants. The O3 coefficient was highly sensitive to the degree of smoothing of time trends. Among the gases, SO2 and NO2 were most strongly associated with mortality. The flexible ambient concentration-response curve for O3 showed evidence of nonlinearity and a threshold at about 30 ppb., Conclusions: Differences between the results of our analyses and those reported from using the Bayesian approach suggest that estimates of the quantitative impact of pollutants depend on the choice of statistical approach, although results are not directly comparable because they are based on different data. In addition, the estimate of the O3-mortality coefficient depends on the amount of smoothing of time trends.

BACKGROUND: Recently enacted environmental justice policies in the United States at the state and federal level emphasize addressing place-based inequities, including persistent disparities in air pollution exposure and associated health impacts. Advances in air quality measurement, models, and analytic methods have demonstrated the importance of finer-scale data and analysis in accurately quantifying the extent of inequity in intraurban pollution exposure, although the necessary degree of spatial resolution remains a complex and context-dependent question. OBJECTIVE: The objectives of this commentary were to a) discuss ways to maximize and evaluate the effectiveness of efforts to reduce air pollution disparities, and b) argue that environmental regulators must employ improved methods to project, measure, and track the distributional impacts of new policies at finer geographic and temporal scales. DISCUSSION: The historic federal investments from the Inflation Reduction Act, the Infrastructure Investment and Jobs Act, and the Biden Administration's commitment to Justice40 present an unprecedented opportunity to advance climate and energy policies that deliver real reductions in pollution-related health inequities. In our opinion, scientists, advocates, policymakers, and implementing agencies must work together to harness critical advances in air quality measurements, models, and analytic methods to ensure success. [ABSTRACT FROM AUTHOR]

BACKGROUND: The three-ringed polycyclic aromatic hydrocarbon (PAH) phenanthrene (Phe) has been implicated in the cardiotoxicity of petroleum based pollution in aquatic systems, where it disrupts the contractile and electrical function of the fish heart. Phe is also found adsorbed to particulate matter and in the gas phase of air pollution, but to date, no studies have investigated the impact of Phe on mammalian cardiac function. OBJECTIVES: Our objectives were to determine the arrhythmogenic potential of acute Phe exposure on mammalian cardiac function and define the underlying mechanisms to provide insight into the toxicity risk to humans. METHODS: Ex vivo Langendorff-perfused mouse hearts were used to test the arrhythmogenic potential of Phe on myocardial function, and voltage and current-clamp recordings were used to define underlying cellular mechanisms in isolated cardiomyocytes. RESULTS: Mouse hearts exposed to ∼8 μM Phe for 15-min exhibited a significantly slower heart rate (푝=0.0006, 푁 =10 hearts), a prolonged PR interval (푝=0.036, 푁 =8 hearts), and a slower conduction velocity (푝=0.0143, 푁 =7 hearts). Whole-cell recordings from isolated cardiomyocytes revealed action potential (AP) duration prolongation (at 80% repolarization; 푝=0.0408, 푛=9 cells) and inhibition of key murine repolarizing currents- transient outward potassium current (I[sub to]) and ultrarapid potassium current (I[sub Kur])-following Phe exposure. A significant reduction in AP upstroke velocity (푝=0.0445, 푛=9 cells) and inhibition of the fast sodium current (I[sub Na]; 푝=0.001, 푛=8 cells) and calcium current (I[sub Ca]; 푝=0.0001) were also observed, explaining the slowed conduction velocity in intact hearts. Finally, acute exposure to ∼8 μM Phe significantly increased susceptibility to arrhythmias (푝=0.0455, 푁 =9 hearts). DISCUSSION: To the best of our knowledge, this is the first evidence of direct inhibitory effects of Phe on mammalian cardiac electrical activity at both the whole-heart and cell levels. This electrical dysfunction manifested as an increase in arrhythmia susceptibility due to impairment of both conduction and repolarization. Similar effects in humans could have serious health consequences, warranting greater regulatory attention and toxicological investigation into this ubiquitous PAH pollutant generated from fossil-fuel combustion. [ABSTRACT FROM AUTHOR]

Objective: There is growing interest in disentangling the health effects of spatially clustered social and physical environmental exposures and in exploring potential synergies among them, with particular attention directed to the combined effects of psychosocial stress and air pollution. Both exposures may be elevated in lower-income urban communities, and it has been hypothesized that stress, which can influence immune function and susceptibility, may potentiate the effects of air pollution in respiratory disease onset and exacerbation. In this paper, we attempt to synthesize the relevant research from social and environmental epidemiology, toxicology, immunology, and exposure assessment to provide a useful framework for environmental health researchers aiming to investigate the health effects of environmental pollution in combination with social or psychological factors., Data Synthesis: We review the existing epidemiologic and toxicologic evidence on synergistic effects of stress and pollution, and then describe the physiologic effects of stress and key issues related to measuring and evaluating stress as it relates to physical environmental exposures and susceptibility. Finally, we identify some of the major methodologic challenges ahead as we work toward disentangling the health effects of clustered social and physical exposures and accurately describing the interplay among these exposures., Conclusions: There is still tremendous work to be done toward understanding the combined and potentially synergistic health effects of stress and pollution. As this research proceeds, we recommend careful attention to the relative temporalities of stress and pollution exposures, to nonlinearities in their independent and combined effects, to physiologic pathways not elucidated by epidemiologic methods, and to the relative spatial distributions of social and physical exposures at multiple geographic scales.

In this paper, we present national maps of relative rates of mortality associated with short-term exposure to particulate matter < 10 micro m in aerodynamic diameter (PM(10)). We report results for 88 of the largest metropolitan areas in the United States from 1987 to 1994 for all-cause mortality, combined cardiovascular and respiratory deaths, and other causes of mortality. Maximum likelihood estimates of the relative rate of mortality associated with PM(10)and the degree of statistical uncertainty were obtained for each of the 88 cities by fitting a separate log-linear regression of the daily mortality rate on air pollution level and potential confounders. We obtained Bayesian estimates of the relative rates by fitting a hierarchical model that takes into account spatial correlation among the true city-specific relative rates. We found that daily variations of PM(10) are positively associated with daily variations of mortality. In particular, the relative rate estimates of cardiovascular and respiratory mortality associated with PM(10) are larger on average than the relative rate estimates of all-cause and other-cause mortality. The estimated increase in the relative rate of death from cardiovascular and respiratory mortality, all-cause mortality, and other-cause mortality were 0.31% (95% posterior interval, 0.15-0.5), 0.22% (95% posterior interval, 0.1-0.38), and 0.13% (95% posterior interval, -0.05 to 0.29), respectively. Bayesian estimates of the city-specific relative rates ranged from 0.23% to 0.35% for cardiovascular and respiratory mortality, from 0.18% to 0.27% for all causes, and from 0.10% to 0.20% for other causes of mortality. The spatial characterization of effects across cities offers the potential to identify factors that could influence the effect of PM(10) on health, including particle characteristics, offering insights into mechanisms by which PM(10) causes adverse health effects.

The authors' response to a commentary on their article "Impacts of Sugarcane Fires on Air Quality and Public Health in South Florida," which appeared in the issue, is presented. Topics covered include the errors in the description of the study's methods and in the observation that the analysis neglected meteorological conditions or the temporal specifics of actual harvest activities and the reason why the study focused on the years 2009-2018.

The article comments on a study on exposure to ambient air pollution during the prehypertension stage, which references a research paper by S. Zhang et al., published within the issue. Topics discussed include the link between a mixture of air pollutants and dynamic progression of cardiovascular disease, limitations to the methodology available for analyzing multivariate dynamic processes, and key issues related to environmental health that were not addressed in the study.

In this paper we examine scientific evidence and related uncertainties in two steps of benefit-cost analyses of ozone reduction: estimating the health improvements attributable to reductions in ozone and determining the appropriate monetary values of these improvements. Although substantial evidence exists on molecular and physiologic impacts, the evidence needed to establish concentration-response functions is somewhat limited. Furthermore, because exposure to ozone depends on factors such as air conditioning use, past epidemiologic studies may not be directly applicable in unstudied settings. To evaluate the evidence likely to contribute significantly to benefits, we focus on four health outcomes: premature mortality, chronic asthma, respiratory hospital admissions, and minor restricted activity days. We determine concentration-response functions for these health outcomes for a hypothetical case study in Houston, Texas, using probabilistic weighting reflecting our judgment of the strength of the evidence and the possibility of confounding. We make a similar presentation for valuation, where uncertainty is due primarily to the lack of willingness-to-pay data for the population affected by ozone. We estimate that the annual monetary value of health benefits from reducing ozone concentrations in Houston is approximately $10 per person per microgram per cubic meter (24-hr average) reduced (95% confidence interval, $0.70-$40). The central estimate exceeds past estimates by approximately a factor of five, driven by the inclusion of mortality. We discuss the implications of our findings for future analyses and determine areas of research that might help reduce the uncertainties in benefit estimation.

Misclassification of exposure is a well-recognized inherent limitation of epidemiologic studies of disease and the environment. For many agents of interest, exposures take place over time and in multiple locations; accurately estimating the relevant exposures for an individual participant in epidemiologic studies is often daunting, particularly within the limits set by feasibility, participant burden, and cost. Researchers have taken steps to deal with the consequences of measurement error by limiting the degree of error through a study's design, estimating the degree of error using a nested validation study, and by adjusting for measurement error in statistical analyses. In this paper, we address measurement error in observational studies of air pollution and health. Because measurement error may have substantial implications for interpreting epidemiologic studies on air pollution, particularly the time-series analyses, we developed a systematic conceptual formulation of the problem of measurement error in epidemiologic studies of air pollution and then considered the consequences within this formulation. When possible, we used available relevant data to make simple estimates of measurement error effects. This paper provides an overview of measurement errors in linear regression, distinguishing two extremes of a continuum-Berkson from classical type errors, and the univariate from the multivariate predictor case. We then propose one conceptual framework for the evaluation of measurement errors in the log-linear regression used for time-series studies of particulate air pollution and mortality and identify three main components of error. We present new simple analyses of data on exposures of particulate matter < 10 microm in aerodynamic diameter from the Particle Total Exposure Assessment Methodology Study. Finally, we summarize open questions regarding measurement error and suggest the kind of additional data necessary to address them.

BACKGROUND: Previous studies aiming at relating exposure to phenols and phthalates with child social behavior characterized exposure using one or a few spot urine samples, resulting in substantial exposure misclassification. Moreover, early infancy exposure was rarely studied. OBJECTIVES: We aimed to examine the associations of phthalates and phenols with child social behavior in a cohort with improved exposure assessment and to a priori identify the chemicals supported by a higher weight of evidence. METHODS: Among 406 mother-child pairs from the French Assessment of Air Pollution exposure during Pregnancy and Effect on Health (SEPAGES) cohort, 25 phenols/phthalate metabolites were measured in within-subject pools of repeated urine samples collected at the second and third pregnancy trimesters (∼21 samples/trimester) and at 2 months and 1-year of age (∼7 samples/period). Social behavior was parent-reported at 3 years of age of the child using the Social Responsiveness Scale (SRS). A structured literature review of the animal and human evidence was performed to prioritize the measured phthalates/phenols based on their likelihood to affect social behavior. Both adjusted linear regression and Bayesian Weighted Quantile Sum (BWQS) regression models were fitted. False discovery rate (FDR) correction was applied only to nonprioritized chemicals. RESULTS: Prioritized compounds included bisphenol A, bisphenol S, triclosan (TCS), diethyl-hexyl phthalate (RDEHP), mono-ethyl phthalate (MEP), mono-n-butyl phthalate (MnBP), and mono-benzyl phthalate (MBzP). With the exception of bisphenols, which showed a mixed pattern of positive and negative associations in pregnant mothers and neonates, few prenatal associations were observed. Most associations were observed with prioritized chemicals measured in 1-y-old infants: Each doubling in urinary TCS (β=0.78; 95% CI: 0.00, 1.55) and MEP (β=0.92; 95% CI: -0.11, 1.96) concentrations were associated with worse total SRS scores, whereas MnBP and RDEHP were associated with worse Social Awareness (β=0.25; 95% CI: 0.01, 0.50) and Social Communication (β=0.43; 95% CI: -0.02, 0.89) scores, respectively. BWQS also suggested worse total SRS [Beta 1=1.38; 95% credible interval (CrI): -0.18, 2.97], Social Awareness (Beta 1=0.37; 95% CrI: 0.06, 0.70), and Social Communication (Beta 1=0.91; 95% CrI: 0.31, 1.53) scores per quartile increase in the mixture of prioritized compounds assessed in 1-y-old infants. The few associations observed with nonprioritized chemicals did not remain after FDR correction, with the exception of benzophenone-3 exposure in 1-y-old infants, which was suggestively associated with worse Social Communication scores (corrected 푝=0.07). DISCUSSION: The literature search allowed us to adapt our statistical analysis according to the weight of evidence and create a corpus of experimental and epidemiological knowledge to better interpret our findings. Early infancy appears to be a sensitive exposure window that should be further investigated. [ABSTRACT FROM AUTHOR]

BACKGROUND: Concentrated animal feeding operations (CAFOs) emit pollutants that can cause negative impacts on human health. The concentration of hog production in North Carolina raises concerns regarding the disproportionate exposure of vulnerable communities to air pollution from CAFOs. OBJECTIVES: We investigated whether exposure to gaseous ammonia (NH3) and hydrogen sulfide (H2S) (in 2019) differs between subpopulations by examining demographics, including race/ethnicity, age, educational attainment, language proficiency, and socioeconomic status. METHODS: We used an Air Monitoring Station (AMS)/Environmental Protection Agency (EPA) Regulatory Model (AERMOD)–based Human Exposure Model (version 3) to estimate ambient concentrations of NH3 and H2S from hog farms in Duplin County and its surrounding counties in North Carolina and estimate subsequent exposures of communities within 50 km of Duplin County, North Carolina, or the Duplin County Region. We combined estimated exposures with 2016 American Community Summary Census data, at the block group level, using spatial analysis to investigate whether exposures to these pollutants differ by race and ethnicity, age, income, education, and language proficiency. Based on these estimations, we assessed associated exposure risks to the impacted communities and used multivariable regression modeling to evaluate the relationship between average ammonia exposures from Duplin regional hog farms and the presence of vulnerable populations. RESULTS: The average [± standard deviation (SD)] annual estimated concentration of NH3 and H2S in the Duplin County Region is 1.75±2.81 μg/m³ and 0.0087±0.014 μg/m³, respectively. The maximum average annual ambient concentrations are estimated at 54.27±4.12 μg/m³ and 0.54±0.041 μg/m³ for NH3 and H2S, respectively. Our descriptive analysis reveals that people of low income, people of color, people with low educational attainment, and the linguistically isolated in the Duplin Region are disproportionately exposed to higher levels of pollutants than the average exposure for residents. Alternatively, our statistical results suggests that after adjusting for covariates, communities of color are associated with 1.70% (95% CI: -3.79, 0.44) lower NH3 concentrations per 1-SD increase. One-standard deviation increases in the adults with low educational attainment and children <19 years of age is associated with 1.26%(95% CI: -0.77, 3.33) and 1.20%(95% CI: -0.62, 3.05) higher NH3 exposure per 1-SDincrease, respectively. DISCUSSION: Exposures to NH3 and H2S differed by race and ethnicity, educational attainment, language proficiency, and socioeconomic status. The observed associations between exposure to CAFO-generated pollutants and sociodemographic indicators differed among demographics. The disproportionate distribution of hog facilities and resulting pollutant exposures among communities may have adverse environmental and human health impacts, raising environmental justice concerns. [ABSTRACT FROM AUTHOR]

BACKGROUND: Although overall air quality has improved in the United States, air pollution remains unevenly distributed across neighborhoods, producing disproportionate environmental burdens for minoritized and socioeconomically disadvantaged residents for whom greater exposure to other structurally rooted neighborhood stressors is also more frequent. These interrelated dynamics and layered vulnerabilities each have well-documented associations with physical and psychological health outcomes; however, much remains unknown about the joint effects of environmental hazards and neighborhood socioeconomic factors on self-reported health status. OBJECTIVES: We examined the nexus of air pollution exposure, neighborhood socioeconomic disadvantage, and self-rated health (SRH) among adults in the United States. METHODS: This observational study used individual-level data from the Panel Study of Income Dynamics merged with contextual information, including neighborhood socioeconomic and air pollution data at the census tract and census block levels, spanning the period of 1999–2015. We estimated ordinary least squares regression models predicting SRH by 10-y average exposures to fine particulate matter [particles =2.5 μm in aerodynamic diameter (PM2.5)] and neighborhood socioeconomic disadvantage while controlling for individual-level correlates of health. We also investigated the interaction effects of air pollution and neighborhood socioeconomic disadvantage on SRH. RESULTS: On average, respondents in our sample rated their health as 3.41 on a scale of 1 to 5. Respondents in neighborhoods with higher 10-y average PM2.5 concentrations or socioeconomic disadvantage rated their health more negatively after controlling for covariates [β= -0.024 (95% CI: -0.034, -0.014); β= -0.107 (95% CI: -0.163, -0.052), respectively]. We also found that the deleterious associations of PM2.5 exposure with SRH were weaker in the context of greater neighborhood socioeconomic disadvantage (β=0.007; 95% CI: 0.002, 0.011). DISCUSSION: Study results indicate that the effects of air pollution on SRH may be less salient in socioeconomically disadvantaged neighborhoods compared with more advantaged areas, perhaps owing to the presence of other more proximate structurally rooted health risks and vulnerabilities in disinvested areas (e.g., lack of economic resources, health access, healthy food options). This intersection may further underscore the importance of meaningful involvement and political power building among community stakeholders on issues concerning the nexus of environmental and socioeconomic justice, particularly in structurally marginalized communities. [ABSTRACT FROM AUTHOR]

BACKGROUND: Growing evidence shows ultrafine particles (UFPs) are detrimental to cardiovascular, cerebrovascular, and respiratory health. Historically, racialized and low-income communities are exposed to higher concentrations of air pollution. OBJECTIVES: Our aim was to conduct a descriptive analysis of present-day air pollution exposure disparities in the greater Seattle, Washington, area by income, race, ethnicity, and historical redlining grade. We focused on UFPs (particle number count) and compared with black carbon, nitrogen dioxide, and fine particulate matter (PM2.5) levels. METHODS: We obtained race and ethnicity data from the 2010 U.S. Census, median household income data from the 2006-2010 American Community Survey, and Home Owners' Loan Corporation (HOLC) redlining data from the University of Richmond's Mapping Inequality. We predicted pollutant concentrations at block centroids from 2019 mobile monitoring data. The study region encompassed much of urban Seattle, with redlining analyses restricted to a smaller region. To analyze disparities, we calculated population-weighted mean exposures and regression analyses using a generalized estimating equation model to account for spatial correlation. RESULTS: Pollutant concentrations and disparities were largest for blocks with median household income of <$20,000, Black residents, HOLC Grade D, and ungraded industrial areas. UFP concentrations were 4% lower than average for non-Hispanic White residents and higher than average for racialized groups (Asian, 3%; Black, 15%; Hispanic, 6%; Native American, 8%; Pacific Islander, 11%). For blocks with median household incomes of <$20,000, UFP concentrations were 40% higher than average, whereas blocks with incomes of >$110,000 had UFP concentrations 16% lower than average. UFP concentrations were 28% higher for Grade D and 49% higher for ungraded industrial areas compared with Grade A. Disparities were highest for UFPs and lowest for PM2.5 exposure levels. DISCUSSION: Our study is one of the first to highlight large disparities with UFP exposures compared with multiple pollutants. Higher exposures to multiple air pollutants and their cumulative effects disproportionately impact historically marginalized groups. [ABSTRACT FROM AUTHOR]

BACKGROUND: Heart failure (HF) poses a significant global disease burden. The current evidence on the impact of air pollution on HF remains inconsistent. OBJECTIVES: We aimed to conduct a systematic review of the literature and meta-analysis to provide a more comprehensive and multiperspective assessment of the associations between short- and long-term air pollution exposure and HF from epidemiological evidences. METHODS: Three databases were searched up to 31 August 2022 for studies investigating the association between air pollutants (PM2.5, PM10, NO2, SO2, CO, O3) and HF hospitalization, incidence, or mortality. A random effects model was used to derive the risk estimations. Subgroup analysis was conducted by geographical location, age of participants, outcome, study design, covered area, the methods of exposure assessment, and the length of exposure window. Sensitivity analysis and adjustment for publication bias were performed to test the robustness of the results. RESULTS: Of 100 studies covering 20 countries worldwide, 81 were for short-term and 19 were for long-term exposure. Almost all air pollutants were adversely associated with the risk of HF in both short- and long-term exposure studies. For short-term exposures, we found the risk of HF increased by 1.8% [relative risk (RR)=1.018, 95% confidence interval (CI): 1.011, 1.025] and 1.6% (RR=1.016, 95% CI: 1.011, 1.020) per 10-μg/m³ increment of PM2.5 and PM10, respectively. HF was also significantly associated with NO2, SO2, and CO, but not O3. Positive associations were stronger when exposure was considered over the previous 2 d (lag 0–1) rather than on the day of exposure only (lag 0). For long-term exposures, there were significant associations between several air pollutants and HF with RR (95% CI) of 1.748 (1.112, 2.747) per 10-μg/m³ increment in PM2.5, 1.212 (1.010, 1.454) per 10-μg/m³ increment in PM10, and 1.204 (1.069, 1.356) per 10-ppb increment in NO2, respectively. The adverse associations of most pollutants with HF were greater in low- and middle-income countries than in high-income countries. Sensitivity analysis demonstrated the robustness of our results. DISCUSSION: Available evidence highlighted adverse associations between air pollution and HF regardless of short- and long-term exposure. Air pollution is still a prevalent public health issue globally and sustained policies and actions are called for to reduce the burden of HF. [ABSTRACT FROM AUTHOR]

The 1990 amendments to the Clean Air Act required the EPA to institute new pollution control technology requirements for industrial sources of air pollution. In part because agreement could not be reached on the best way for the EPA to determine whether any significant risks to human health will remain after the technology controls are in place, the amendments also created a Commission on Risk Assessment and Risk Management and gave the commission a broad mandate to review and make recommendations concerning risk assessment and risk management in federal regulatory programs. In its March 1997 final report to Congress and the administration, the commission recommended a tiered approach to assessing such residual risks. That approach included the idea that when decisions about managing residual risks are made, emissions should be evaluated in the context of other sources of air pollution. Evaluating risks in their larger contexts is consistent with what the commission called a public health approach to environmental risk management. This paper describes the public health approach and how it applies to evaluating residual risks under the Clean Air Act.

Naturally occurring and man-made (synthetic) fibers of respirable sizes are substances that have been identified by the U.S. Environmental Protection Agency (U.S. EPA) as priority substances for risk reduction and pollution prevention under the Toxic Substances Control Act (TSCA). The health concern for respirable fibers is based on the link of occupational asbestos exposure and environmental erionite fiber exposure to the development of chronic respiratory diseases, including interstitial lung fibrosis, lung cancer, and mesothelioma in humans. There is also considerable laboratory evidence indicating that a variety of fibers of varying physical and chemical characteristics can elicit fibrogenic and carcinogenic effects in animals under certain exposure conditions. This paper discusses key scientific issues and major default assumptions and uncertainties pertaining to the risk assessment of inhaled fibers. This is followed by a description of the types of assessment performed by the U.S. EPA to support risk management actions of new fibers and existing fibers under TSCA. The scope and depth of these risk assessments, however, vary greatly depending on whether the substance under review is an existing or a new fiber, the purpose of the assessment, the availability of data, time, and resources, and the intended nature of regulatory action. In general, these risk assessments are of considerable uncertainty because health hazard and human exposure information is often incomplete for most fibers. Furthermore, how fibers cause diseases and what specific determinants are critical to fiber-induced toxicity and carcinogenicity are still not completely understood. Further research to improve our knowledge base in fiber toxicology and additional toxicity and exposure data gathering are needed to more accurately characterize the health risks of inhaled fibers.

Ambient air is a complex mixture containing a variety of substances, some of which are known to be carcinogenic. To develop a homogeneous approach for regulating the emission of these compounds, their individual carcinogenic potential needs to be placed on a comparable scale. The unit risk may be considered as an appropriate measure that condensates dose-response analyses of epidemiologic data into a single, easily interpretable estimate. Given the information on the carcinogenic potency of single compounds, more information on the occurrence of the components and the relation of emissions to specific emittents needs to be considered. In Germany, an approach has been developed that combines different assumptions on complex mixtures for the regulation of the overall risk. This paper outlines some of the principal aspects of the underlying concepts.

A major field study was conducted in Boise, Idaho, during the heating season of 1986 to 1987 as part of the Integrated Air Cancer Project. Filter samples were systematically collected in residences and in the ambient air across the community to characterize the particle-bound pollutants. The extractable organic matter (EOM) from the filter samples was apportioned to its source of origin, either residential wood combustion (RWC) or mobile sources (MS). Two composite samples, with apportioned contributions from RWC and MS, were prepared from the Boise ambient samples and tested for tumor-initiation potency. A comparative potency lung cancer risk estimate has been made based on the two ambient composite samples from this airshed. In addition, a microenvironmental exposure model was developed from the Boise data and from national survey data to estimate the exposure to EOM from RWC and MS. In this paper, the microenvironmental model is extrapolated to provide an estimate of the average annual exposure and dose in Boise to EOM from RWC and MS. The annual model considers actual pollutant levels in Boise, historical changes in RWC usage and meteorological dilution factors and the likely activities in the various microenvironmental zones and their resultant inhalation rates. Combined with the lifetime risk estimates, the average annual dose suggests a risk of about 4 x 10(-4) based upon the composite ambient samples. Despite the fact that RWC accounts for 73% of the EOM on an annual average basis, it accounts for only about 20% of the estimated lifetime risk.

This study deals with some methods of making human exposure estimates, aimed at describing the human exposure for selected air pollutants in Sweden that are suspected carcinogens. Nitrogen oxides (NOx) have been chosen as an indicator substance for estimating the concentration of the urban plume. Earlier investigations have shown that the traffic in Swedish cities contributes around 85% to the measured NOx concentrations, and that most of the mutagenicity in urban air originates from traffic. The first section of this paper describes measurements in Stockholm of some unregulated light hydrocarbons, such as ethene, ethyne, propane, propene, butane, and isobutane. In addition, measurements of some volatile aromatic hydrocarbons are presented. Simultaneous measurements of carbon monoxide (CO) were made. The ratios between CO and the individual specific compounds were determined by linear regression analysis. By analysis of relationships between CO and NOx, NOx concentrations can be used as a tracer to describe the exposure for these specific compounds. NOx are considered to be a better tracer than CO, because NOx or NO2 values exist for many places over a long time, while CO is measured mostly in streets with high concentrations. At low concentrations, instruments that measure normal CO levels give no detectable signals. Through use of atmospheric dispersion models and models that describe how people live and work in urban areas it has been possible to describe the average exposure to NOx in cities of different sizes. The exposure to NOx for people living in the countryside has also been estimated. In this way, it has been possible to calculate the average exposure dose for NOx for the Swedish population. This figure is 23 micrograms/m3. By use of the relationships between NOx and specific compounds the average dose has been calculated for the following compounds: polyaromatic compounds (PAH); ethene, propene, and butadiene; benzene, toluene, and xylene; formaldehyde and actaldehyde; nickel, chromium (VI), arsenic, and cadmium; asbestos; and silicon.

Indoor exposures to aerosols and gases are associated with both indoor and outdoor air pollution sources. The identification of sources and the assessment of their relative contribution can be a complicated process due to a) the presence of numerous indoor sources, which can vary from building to building; b) the uncertainties associated with the estimation of the impact of outdoor sources on indoor air quality; c) the interactions between pollutants; and d) the importance of reactions between pollutants and indoor surfaces. It is well established that fine particles (diameter less than or equal to 2.5 microns) originating from outdoor sources such as automobiles, oil and coal combustion, incineration, and diverse industrial activities can penetrate into the indoor environment. Indoor/outdoor ratios, usually varying between 0.4 and 0.8, depend on parameters such as particle size and density, air exchange rate, and the surface-to-volume ratio of the indoor environment. Determining fine particle elemental composition makes it possible to identify the contribution of different outdoor sources. This paper focuses on the origin and the concentration of indoor aerosols and acid gases by highlighting the results from two indoor air quality studies.

The Clean Air Act requires that sensitive subgroups of exposed populations be protected from adverse health effects of air pollution exposure. Hence, data suggesting the existence of sensitive subgroups can have an important impact on regulatory decisions. Some investigators have interpreted differences among individuals in observed pulmonary function response to air pollution episodes as evidence that individuals differ in their sensitivity. An alternative explanation is that the differences are due entirely to normal variation in repeated pulmonary function measurements. This paper investigates this question by reanalyzing data from three studies of children exposed to air pollution episodes to determine whether the observed variability in pulmonary function response indicates differences in sensitivity or natural interoccasion variability. One study investigated exposures to total suspended particulates (TSP), the other two investigated exposure to ozone. In all studies, each child's response to air pollution exposures was summarized by regressing that child's set of pulmonary function measurements on the air pollution concentrations on the day or days before measurement. The within-child and between-child variances of these slopes were used to test the hypothesis of variable sensitivity. Regression slopes did not vary significantly among children exposed to episodes of high TSP concentration, but there was evidence of heterogeneity in both studies of ozone exposures. The finding of heterogeneous response to ozone exposure is consistent with the epidemiologic and chamber studies of ozone exposures, but the lack of evidence for heterogeneous response to TSP exposures implies that observed variation in response can be explained by sampling variability rather than the presence of sensitive subgroup.

The article discusses a study that examines how socioeconomic status may impact the urban exposome among pregnant women in six European countries. Topics mentioned include the definition of exposome by researcher Christopher Wild, the Human Early Life Exposome project, and the triple jeopardy hypothesis.

The article investigates the case of terminal lakes or shrinking inland seas that expose salty particulates, metals and other compounds. Topics discussed are potential effect of dust from Salton Sea in California on the respiratory health of children, presence of arsenic in the bed of Great Salt Lake Utah, global water diversion and climate change, and approaches to mitigate dust emissions from dry lakes.

BACKGROUND: Exposures to environmental contaminants can be influenced by social determinants of health. As a result, persons living in socially disadvantaged communities may experience disproportionate health risks from environmental exposures. Mixed methods research can be used to understand community-level and individual-level exposures to chemical and nonchemical stressors contributing to environmental health disparities. Furthermore, community-based participatory research (CBPR) approaches can lead to more effective interventions. OBJECTIVES: We applied mixed methods to identify environmental health perceptions and needs among metal recyclers and residents living in disadvantaged neighborhoods near metal recycling facilities in Houston, Texas, in a CBPR study, Metal Air Pollution Partnership Solutions (MAPPS). Informed by what we learned and our previous findings from cancer and noncancer risk assessments of metal air pollution in these neighborhoods, we developed an action plan to lower metal aerosol emissions from metal recycling facilities and enhance community capacity to address environmental health risks. METHODS: Key informant interviews, focus groups, and community surveys were used to identify environmental health concerns of residents. A diverse group from academia, an environmental justice advocacy group, the community, the metal recycling industry, and the local health department collaborated and translated these findings, along with results from our prior risk assessments, to inform a multifaceted public health action plan. RESULTS: An evidence-based approach was used to develop and implement neighborhood-specific action plans. Plans included a voluntary framework of technical and administrative controls to reduce metal emissions in the metal recycling facilities, direct lines of communication among residents, metal recyclers, and local health department officials, and environmental health leadership training. DISCUSSION: Using a CBPR approach, health risk assessment findings based on outdoor air monitoring campaigns and community survey results informed a multipronged environmental health action plan to mitigate health risks associated with metal air pollution. [ABSTRACT FROM AUTHOR]

BACKGROUND: The role of chronic exposure to ambient air pollutants in increasing COVID-19 fatality is still unclear. OBJECTIVES: The study aimed to investigate the association between long-term exposure to air pollutants and mortality among 4 million COVID-19 cases in Italy. METHODS: We obtained individual records of all COVID-19 cases identified in Italy from February 2020 to June 2021. We assigned 2016-2019 mean concentrations of particulate matter (PM) with aerodynamic diameter =10 μm (PM10), PM with aerodynamic diameter = 2.5 μm (PM2.5), and nitrogen dioxide (NO2) to each municipality (푛 = 7,800) as estimates of chronic exposures. We applied a principal component analysis (PCA) and a generalized propensity score (GPS) approach to an extensive list of area-level covariates to account for major determinants of the spatial distribution of COVID-19 case-fatality rates. Then, we applied generalized negative binomial models matched on GPS, age, sex, province, and month. As additional analyses, we fit separate models by pandemic periods, age, and sex; we quantified the numbers of COVID-19 deaths attributable to exceedances in annual air pollutant concentrations above predefined thresholds; and we explored associations between air pollution and alternative outcomes of COVID-19 severity, namely hospitalizations or accesses to intensive care units. RESULTS: We analyzed 3,995,202 COVID-19 cases, which generated 124,346 deaths. Overall, case-fatality rates increased by 0.7% [95% confidence interval (CI): 0.5%, 0.9%], 0.3% (95% CI: 0.2%, 0.5%), and 0.6% (95% CI: 0.5%, 0.8%) per 1 μg/m³ increment in PM2.5, PM10, and NO2, respectively. Associations were higher among elderly subjects and during the first (February 2020-June 2020) and the third (December 2020-June 2021) pandemic waves. We estimated ~8%COVID-19 deaths were attributable to pollutant levels above the World Health Organization 2021 air quality guidelines. DISCUSSION: We found suggestive evidence of an association between long-term exposure to ambient air pollutants with mortality among 4 million COVID-19 cases in Italy. [ABSTRACT FROM AUTHOR]

BACKGROUND: Understanding the mechanistic basis of air pollution toxicity is dependent on accurately characterizing both exposure and biological responses. Untargeted metabolomics, an analysis of small-molecule metabolic phenotypes, may offer improved estimation of exposures and corresponding health responses to complex environmental mixtures such as air pollution. The field remains nascent, however, with questions concerning the coherence and generalizability of findings across studies, study designs and analytical platforms. OBJECTIVES: We aimed to review the state of air pollution research from studies using untargeted high-resolution metabolomics (HRM), highlight the areas of concordance and dissimilarity in methodological approaches and reported findings, and discuss a path forward for future use of this analytical platform in air pollution research. METHODS: We conducted a state-of-the-science review to a) summarize recent research of air pollution studies using untargeted metabolomics and b) identify gaps in the peer-reviewed literature and opportunities for addressing these gaps in future designs. We screened articles published within Pubmed and Web of Science between 1 January 2005 and 31 March 2022. Two reviewers independently screened 2,065 abstracts, with discrepancies resolved by a third reviewer. RESULTS: We identified 47 articles that applied untargeted metabolomics on serum, plasma, whole blood, urine, saliva, or other biospecimens to investigate the impact of air pollution exposures on the human metabolome. Eight hundred sixteen unique features confirmed with level-1 or -2 evidence were reported to be associated with at least one or more air pollutants. Hypoxanthine, histidine, serine, aspartate, and glutamate were among the 35 metabolites consistently exhibiting associations with multiple air pollutants in at least 5 independent studies. Oxidative stress and inflammation-related pathways—including glycerophospholipid metabolism, pyrimidine metabolism, methionine and cysteine metabolism, tyrosine metabolism, and tryptophan metabolism—were the most commonly perturbed pathways reported in >70% of studies. More than 80% of the reported features were not chemically annotated, limiting the interpretability and generalizability of the findings. CONCLUSIONS: Numerous investigations have demonstrated the feasibility of using untargeted metabolomics as a platform linking exposure to internal dose and biological response. Our review of the 47 existing untargeted HRM–air pollution studies points to an underlying coherence and consistency across a range of sample analytical quantitation methods, extraction algorithms, and statistical modeling approaches. Future directions should focus on validation of these findings via hypothesis-driven protocols and technical advances in metabolic annotation and quantification. [ABSTRACT FROM AUTHOR]

BACKGROUND: Ambient air pollution exposure has been associated with childhood asthma, but previous studies have primarily focused on prevalence of asthma and asthma-related outcomes and urban traffic-related exposures. OBJECTIVE: We examined nationwide associations between pre- and postnatal exposure to ambient air pollution components and asthma incidence in children age 0–19 y. METHODS: Asthma incidence was identified from hospital admission, emergency room, and outpatient contacts among all live-born singletons born in Denmark between 1998 and 2016. We linked registry data with monthly mean concentrations of particulate matter (PM) with aerodynamic diameter ≤2.5 μm (PM2.5) and PM with aerodynamic diameter ≤10 μm (PM10), nitrogen dioxide (NO2), nitrogen oxides, elemental carbon, and organic carbon (OC), sulfur dioxide, ozone, sulfate, nitrate, ammonium, secondary organic aerosols, and sea salt. Associations were estimated with Cox proportional hazard models using fixed prenatal exposure means and time-varying postnatal exposures. RESULTS: Of the 1,060,154 children included, 6.1% had asthma during the mean follow-up period of 8.8 y. The risk of asthma increased with increasing prenatal exposure to all pollutants except for O3 and sea salt. We also observed increased risk after restriction to asthma after age 4 y, after additional adjustment for area-specific socioeconomic status, and for postnatal exposure to most pollutants. The hazard ratio (HR) associated with an interquartile range increase of 2.4 and 8.7 µg/m³ in prenatal exposure was 1.06 [95% confidence interval (CI): 1.04, 1.08] for PM2.5 and 1.04 (95% CI: 1.02, 1.05) for NO2, respectively. This association with PM2.5 was stable after adjustment for NO2, whereas it attenuated for NO2 to 1.01 (95% CI: 0.99, 1.03) after adjustment for PM2.5. For a 0.5-µg/m³ increase in prenatal OC exposure, for which biomass is an important source, the HR was 1.08 (95% CI: 1.06, 1.10), irrespective of adjustment for PM2.5. DISCUSSION: These findings suggest that early-life exposure to ambient air pollution from multiple sources contributes to asthma development. [ABSTRACT FROM AUTHOR]

BACKGROUND: Air pollution is negatively associated with cardiovascular health. Impediments to efficient regulation include lack of knowledge about which sources of air pollution contributes most to health burden and few studies on effects of the potentially more potent ultrafine particles (UFP). OBJECTIVE: The authors aimed to investigate myocardial infarction (MI) morbidity and specific types and sources of air pollution. METHODS: We identified all persons living in Denmark in the period 2005–2017, age >50 y and never diagnosed with MI. We quantified 5-y running time-weighted mean concentrations of air pollution at residencies, both total and apportioned to traffic and nontraffic sources. We evaluated particulate matter (PM) with aerodynamic diameter ≤ 2.5 μm (PM2.5), <0.1 μm (UFP), elemental carbon (EC), and nitrogen dioxide (NO2). We used Cox proportional hazards models, with adjustment for time-varying exposures, and personal and area-level demographic and socioeconomic covariates from high-quality administrative registers. RESULTS: In this nationwide cohort of 1,964,702 persons (with 18 million person-years of follow-up and 71,285 cases of MI), UFP and PM2.5 were associated with increased risk of MI with hazard ratios (HRs) per interquartile range (IQR) of 1.040 [95% confidence interval (CI): 1.025, 1.055] and 1.053 (95% CI: 1.035, 1.071), respectively. HRs per IQR of UFP and PM2.5 from nontraffic sources were similar to the total (1.034 and 1.051), whereas HRs for UFP and PM2.5 from traffic sources were smaller (1.011 and 1.011). The HR for EC from traffic sources was 1.013 (95% CI: 1.003, 1.023). NO2 from nontraffic sources was associated with MI (HR =1.048; 95% CI: 1.034, 1.062) but not from traffic sources. In general, nontraffic sources contributed more to total air pollution levels than national traffic sources. CONCLUSIONS: PM2.5 and UFP from traffic and nontraffic sources were associated with increased risk of MI, with nontraffic sources being the dominant source of exposure and morbidity. [ABSTRACT FROM AUTHOR]