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Air pollution exposure is ranked as a leading environmental risk factor for not only cardiopulmonary diseases but also for systemic health ailments including diabetes, reproductive abnormalities, and neuropsychiatric disorders, likely mediated by central neural stress mechanisms. Current experimental evidence links many air pollution health outcomes with activation of neuroendocrine sympathetic-adrenal-medullary and hypothalamic-pituitary-adrenal (HPA) stress axes associated with resultant increases in adrenal-derived hormone levels acting as circulating mediators of multi-organ stress reactions. Epidemiological and experimental investigations also demonstrated sex-specific responses to air pollutant inhalation, which may be attributed to hormonal interactions within the stress and reproductive axes. Sex hormones (androgens and estrogens) interact with neuroendocrine functions to influence hypothalamic responses, subsequently augmenting stress-mediated metabolic and immune changes. These neurohormonal interactions may contribute to innate sex-specific responses to inhaled irritants, inducing differing individual susceptibility. The aim of this review was to: (1) examine neuroendocrine co-regulation of the HPA axis by gonadal hormones, (2) provide experimental evidence demonstrating sex-specific respiratory and systemic effects attributed to air pollutant inhalation exposure, and (3) postulate proposed mechanisms of stress and sex hormone interactions during air pollution-related stress.

Using a high-resolution, 1.33 km by 1.33 km coupled Weather Research and Forecasting-Community Multi-scale Air Quality Model (WRF-CMAQ), we quantify the impact of emissions of nitrogen oxides (NOx) from high energy demand day (HEDD) electricity generating units (EGU) and onroad vehicles on ambient ozone air quality in the Long Island Sound Tropospheric Ozone Study (LISTOS) region covering New York City (NYC); Long Island, NY; coastal Connecticut; and neighboring areas. We test sensitivity scenarios to quantify HEDD EGU NOx contributions to ozone: (1) zero out HEDD EGU emissions, (2) dispatch HEDD EGUs starting with the lowest NOx emitting units first, (3) reduce onroad emissions by 90%, (4) combine zero out HEDD EGU emissions and reducing onroad emissions by 90%, and (5) dispatch HEDD EGUs starting with the lowest emitting units coupled with a reduction in onroad emissions by 90%. Results determine that HEDD EGUs lead to highly localized impacts on ambient concentrations of ozone while onroad emission reductions lead to large-scale regional concentration impacts. Further, reducing onroad emissions by 90% leads to spatially smaller VOC-limited regions and spatially larger transitional and NO X -limited regions around NYC. Despite the limited scale at which the EGU emission reductions occur, modifying HEDD EGU NO X emissions still provides substantial benefits in reducing ozone concentrations in the region, particularly at elevated ozone concentrations above 70 ppb. Implications: High-resolution coupled meteorology-chemistry modeling was used to quantify the impacts of high energy demand day (HEDD) electricity generating units (EGUs) and onroad transportation emissions changes on ozone air quality in the LISTOS region. Despite being highly localized and variable, HEDD EGUs NO X emissions sensitivity tests led to quantifiable changes in ozone. Further, reducing onroad emissions by 90% produced large decreases in ozone concentrations and led to a more NO X -sensitive ozone photochemical regime. With a transition to greater NO X -sensitivity, urban NO X -titration weakens and ozone is more likely to decline with the removal of additional NO X from sources like HEDD EGUs.

Air pollution is a significant environmental health risk for urban areas and developing countries. Air pollution may contribute to the incidence of cardiopulmonary and metabolic diseases. Evidence also points to the role of air pollution in worsening or developing neurological and neuropsychiatric conditions. Inhaled pollutants include compositionally differing mixtures of respirable gaseous and particulate components of varied sizes, solubilities, and chemistry. Inhalation of combustibles and volatile organic compounds (VOCs) or other irritant particulate matter (PM) may trigger lung sensory afferents which initiate a sympathetic stress response via activation of the hypothalamic-pituitary-adrenal (HPA) and sympathetic-adrenal-medullary (SAM) axes. Activation of SAM and HPA axes are associated with selective inhibition of hypothalamic-pituitary-gonadal (HPG) and hypothalamic-pituitary-thyroid (HPT) axes following exposure. Regarding chronic exposure in susceptible hosts, these changes may become pathological by causing neuroinflammation, neurotransmitter, and neuroendocrine imbalances. Soluble PM, such as metals and nano-size particles may translocate across the olfactory, trigeminal, or vagal nerves through retrograde axonal transport, or through systemic circulation which may disrupt the blood-brain barrier (BBB) and deposit in neural tissue. Neuronal deposition of metallic components can have a negative impact through multiple molecular mechanisms. In addition to systemic translocation, the release of pituitary and stress hormones, altered metabolic hormonal status and resultant circulating metabolic milieu, and sympathetically and HPA-mediated changes in immune markers, may secondarily impact the brain through a variety of regulatory adrenal hormone-dependent mechanisms. Several reviews covering air pollution as a risk factor for neuropsychiatric disorders have been published, but no reviews discuss the in-depth intersection between molecular and stress-related neuroendocrine mechanisms, thereby addressing adaptation and susceptibility variations and link to peripheral tissue effects. The purpose of this review is to discuss evidence regarding neurochemical, neuroendocrine, and molecular mechanisms which may contribute to neuropathology from air pollution exposure. This review also covers bi-directional neural and systemic interactions which may raise the risk for air pollution-related systemic illness.

Personal exposure to air pollution is influenced by an individual's time-activity patterns, but data regarding personal exposure to air pollution among children populations is lacking. The objective of this study was to characterize personal exposure to both PM 2.5 and ultrafine particles (UFPs) using two portable real-time monitors, combined with GPS logging, and describe the relationship between these exposures across time and microenvironments among adolescents with asthma. Participants completed personal exposure monitoring for seven consecutive days and PM2.5 and UFP concentrations experienced in five microenvironments were determined using GPS location and mobility data. Average UFP and PM 2.5 exposure varied across microenvironments with the highest average UFP exposure concentrations observed in transit (10,910 ± 27,297 p/cc), though correlations between UFP and PM 2.5 concentrations in transit were low (0.24) and did not reach statistical significance (p > 0.05). We calculated exposure time ratios for each participant. Across participants, UFP exposures within the transit environment demonstrated the highest ratio (average exposure-time ratio = 1.91) though only 3 % of overall sampling time among all participants was monitored in transit (74/2840 h). We did not observe similar trends among PM 2.5 exposures. The correlations between UFP and PM 2.5 exposures varied throughout the day, with an overall correlation ranging from moderate to high among participants. Identifying microenvironments and activities where high exposure to PM occurs may offer potential targets for interventions to reduce overall exposures among sensitive groups., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Background: Experimental studies suggest ultrafine particles (UFPs), the smallest size fraction of particulate matter, may be more toxic than larger particles, however personal sampling studies in children are lacking., Objective: The objective of this analysis was to examine individual, housing, and neighborhood characteristics associated with personal UFP concentrations as well as the differences in exposures that occur within varying microenvironments., Methods: We measured weekly personal UFP concentrations and GPS coordinates in 117 adolescents ages 13-17 to describe exposures across multiple microenvironments. Individual, home, and neighborhood characteristics were collected by caregiver completed questionnaires., Results: Participants regularly exposed to secondhand tobacco smoke had significantly higher indoor concentrations of UFPs compared to participants who were not. We observed that the 'home' microenvironment dominated the relative contribution of overall UFP concentrations and sampling time, however, relative proportion of integrated UFP exposure were higher in 'other' environments., Impact Statement: In this study, we employed a novel panel study design, involving real-time measurement of UFP exposure within the multiple microenvironments of adolescents. We found a combination of personal sampling and detailed activity patterns should be used in future studies to accurately describe exposure-behavior relationships., (© 2024. The Author(s), under exclusive licence to Springer Nature America, Inc.)

Epidemiological evidence suggests the potential for air pollutants to induce male reproductive toxicity. In experimental studies, exposure to ozone during sensitive windows in the sperm lifecycle has been associated with impaired sperm motility. Subsequently, we sought to investigate the effects of episodic exposure to ozone during sperm maturation in the rat. Long-Evans rats were exposed to either filtered air or ozone (0.4 or 0.8 ppm) for five non-consecutive days over two weeks. Ozone exposure did not impact male reproductive organ weights or sperm motility ∼24 hours following the final exposure. Furthermore, circulating sex hormones remained unchanged despite increased T 3 and T 4 in the 0.8 ppm group. While there was indication of altered adrenergic signaling attributable to ozone exposure in the testis, there were minimal impacts on small non-coding RNAs detected in cauda sperm. Only two piwi-interacting RNAs (piRNAs) were altered in the mature sperm of ozone-exposed rats (piR-rno-346434 and piR-rno-227431). Data across all rats were next analyzed to identify any non-coding RNAs that may be correlated with reduced sperm motility. A total of 7 microRNAs (miRNAs), 8 RNA fragments, and 1682 piRNAs correlated well with sperm motility. Utilizing our exposure paradigm herein, we were unable to substantiate the relationship between ozone exposure during maturation with sperm motility. However, these approaches served to identify a suite of non-coding RNAs that were associated with sperm motility in rats. With additional investigation, these RNAs may prove to have functional roles in the acquisition of motility or be unique biomarkers for male reproductive toxicity., Competing Interests: Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Corresponding author is co-editor for special issue on reproductive toxicology and air pollution and current sits on the editorial board - CM If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Published by Elsevier Inc.)

Background: Personal exposure to fine particulate matter (PM 2.5 ) is impacted by different sources each with different chemical composition. Determining these sources is important for reducing personal exposure and its health risks especially during pregnancy., Objective: Identify main sources and their contributions to the personal PM 2.5 exposure in 213 women in the 3rd trimester of pregnancy in Los Angeles, CA., Methods: We measured 48-hr integrated personal PM 2.5 exposure and analyzed filters for PM 2.5 mass, elemental composition, and optical carbon fractions. We used the EPA Positive Matrix Factorization (PMF) model to resolve and quantify the major sources of personal PM 2.5 exposure. We then investigated bivariate relationships between sources, time-activity patterns, and environmental exposures in activity spaces and residential neighborhoods to further understand sources., Results: Mean personal PM 2.5 mass concentration was 22.3 (SD = 16.6) μg/m 3 . Twenty-five species and PM 2.5 mass were used in PMF with a final R 2 of 0.48. We identified six sources (with major species in profiles and % contribution to PM 2.5 mass) as follows: secondhand smoking (SHS) (brown carbon, environmental tobacco smoke; 65.3%), fuel oil (nickel, vanadium; 11.7%), crustal (aluminum, calcium, silicon; 11.5%), fresh sea salt (sodium, chlorine; 4.7%), aged sea salt (sodium, magnesium, sulfur; 4.3%), and traffic (black carbon, zinc; 2.6%). SHS was significantly greater in apartments compared to houses. Crustal source was correlated with more occupants in the household. Aged sea salt increased with temperature and outdoor ozone, while fresh sea salt was highest on days with westerly winds from the Pacific Ocean. Traffic was positively correlated with ambient NO 2 and traffic-related NO x at residence. Overall, 76.8% of personal PM 2.5 mass came from indoor or personal compared to outdoor sources., Impact: We conducted source apportionment of personal PM 2.5 samples in pregnancy in Los Angeles, CA. Among identified sources, secondhand smoking contributed the most to the personal exposure. In addition, traffic, crustal, fuel oil, fresh and aged sea salt sources were also identified as main sources. Traffic sources contained markers of combustion and non-exhaust wear emissions. Crustal source was correlated with more occupants in the household. Aged sea salt source increased with temperature and outdoor ozone and fresh sea salt source was highest on days with westerly winds from the Pacific Ocean., (© 2024. The Author(s).)

We developed spatially detailed source-impact estimates of population health burden measures of air pollution for the United States and Canada by quantifying sources-receptor relationships using the benefit-per-ton (BPT 1 ) metric. We calculated BPTs as the valuations of premature mortality counts due to fine particulate matter (PM 2.5 ; particulate matter ≤2.5 μm in aerodynamic diameter) exposure resulting from emissions of one ton of a given pollutant. Our BPT estimates, while accounting for a large portion of societal impact, do not include morbidity, acute exposure mortality, or chronic exposure mortality due to exposure to other pollutants such as ozone., The adjoint version of a widely used chemical transport model (CTM) allowed us to calculate location-specific BPTs at a high level of granularity for source-impact characterization. Location-specific BPTs provides a means for exploiting the disparities in source impact of emissions at different locations. For instance, estimated BPTs show that 20% of primary PM 2.5 and ammonia emissions in the United States account for approximately 50% and 60% of the burden of each species, respectively, for an estimated burden of $370B USD. Similarly, 10% of the most harmful emissions of primary PM 2.5 and ammonia emissions in Canada account for approximately 60% and 50% of their burden, respectively. By delineating differences and disparities in source impacts, adjoint-based BPT provides a direct means for prioritizing and targeting emissions that are most damaging., Sensitivity analyses evaluated the impact of our assumptions and study design on the estimated BPTs. The choice of concentration-response function had a substantial impact on the estimated BPTs and is likely to constitute the largest source of uncertainty in those estimates. Our method for constructing annual BPT estimates based on episodic simulations introduces low uncertainty, while uncertainties associated with the spatial resolution of the CTM were evaluated to be of medium importance. Finally, while recognizing that the use of BPTs entails an implied assumption of linearity, we show that BPTs for primary PM 2.5 emissions are stable across different emission levels in North America. While BPTs for precursors of secondary inorganic aerosols showed sensitivity to emission levels in the past, we found that those have stabilized with lower emissions and pollutant concentrations in the North American atmosphere., We used BPTs to provide location-specific and sectoral estimates for the cobenefits of reducing carbon dioxide emissions from a range of combustion sources. Cobenefit estimates rely heavily on the emission characteristics of the sector and therefore exhibit more pronounced sectoral fingerprints than do BPTs. We provide cobenefit estimates for various subsectors of on-road transportation, thermal electricity generation, and off-road engines. Off-road engines and various heavy-duty diesel vehicles had the largest cobenefits, which in most urban locations far exceeded estimates of the social cost of carbon. Based on our cobenefit estimations, we also provide per-vehicle burden estimates for different vintages of vehicle subsectors such as transit buses and short-haul trucks in major US cities., (© 2024 Health Effects Institute. All rights reserved.)

Communities near transportation sources can be impacted by higher concentrations of particulate matter (PM) and other air pollutants. Few studies have reported on air quality in complex urban environments with multiple transportation sources. To better understand these environments, the Kansas City Transportation and Local-Scale Air Quality Study (KC-TRAQS) was conducted in three neighborhoods in Southeast Kansas City, Kansas. This area has several emissions sources including transportation (railyards, vehicles, diesel trucks), light industry, commercial facilities, and residential areas. Stationary samples were collected for 1-year (October 24, 2017, to October 31, 2018) at six sites using traditional sampling methods and lower-cost air sensor packages. This work examines PM less than 2.5 μm in diameter (PM 2.5 ), black carbon (BC), and trace metals data collected during KC-TRAQS. PM 2.5 filter samples showed the highest 24-h mean concentrations (9.34 μg/m 3 ) at the sites located within 20-50 m of the railyard. Mean 24-h PM 2.5 concentrations, ranging from 7.96 to 9.34 μg/m 3 , at all sites were lower than that of the nearby regulatory site (9.83 μg/m 3 ). Daily maximum PM 2.5 concentrations were higher at the KC-TRAQS sites (ranging from 25.31 to 43.76 μg/m 3 ) compared to the regulatory site (20.50 μg/m 3 ), suggesting short-duration impacts of localized emissions sources. Across the KC-TRAQS sites, 24-h averaged PM 2.5 concentrations from the sensor package (P-POD) ranged from 3.24 to 5.69 µg/m 3 showing that, out-of-the-box, the PM sensor underestimated the reference concentrations. KC-TRAQS was supplemented by elemental and organic carbon (EC/OC) and trace metal analysis of filter samples. The EC/OC data suggested the presence of secondary organic aerosol formation, with the highest mean concentrations observed at the site within 20 m of the railyard. Trace metals data showed daily, monthly, and seasonal variations for iron, copper, zinc, chromium, and nickel, with elevated concentrations occurring during the summer at most of the sites. Implications : This work reports on findings from a year-long air quality study in Southeast Kansas City, Kansas to understand micro-scale air quality in neighborhoods impacted by multiple emissions sources such as transportation sources (including a large railyard operation), light industry, commercial facilities, and residential areas. While dozens of studies have reported on air quality near roadways, this work will provide more information on PM 2.5 , black carbon, and trace metals concentrations near other transportation sources in particular railyards. This work can also inform additional field studies near railyards.

Background: Outdoor air pollution is a ubiquitous exposure that includes endocrine-disrupting and carcinogenic compounds that may contribute to the risk of hormone-sensitive outcomes such as uterine cancer. However, there is limited evidence about the relationship between outdoor air pollution and uterine cancer incidence., Methods: We investigated the associations of residential exposure to particulate matter less than 2.5 µm in aerodynamic diameter (PM2.5) and nitrogen dioxide (NO2) with uterine cancer among 33 417 Sister Study participants with an intact uterus at baseline (2003-2009). Annual average air pollutant concentrations were estimated at participants' geocoded primary residential addresses using validated spatiotemporal models. Cox proportional hazards models were used to estimate hazard ratios and 95% confidence intervals for the association between time-varying 12-month PM2.5 (µg/m3) and NO2 (parts per billion; ppb) averages and uterine cancer incidence., Results: Over a median follow-up period of 9.8 years, 319 incident uterine cancer cases were identified. A 5-ppb increase in NO2 was associated with a 23% higher incidence of uterine cancer (hazard ratio = 1.23, 95% confidence interval = 1.04 to 1.46), especially among participants living in urban areas (hazard ratio = 1.53, 95% confidence interval = 1.13 to 2.07), but  PM2.5 was not associated with increased uterine cancer incidence., Conclusion: In this large US cohort, NO2, a marker of vehicular traffic exposure, was associated with a higher incidence of uterine cancer. These findings expand the scope of health effects associated with air pollution, supporting the need for policy and other interventions designed to reduce air pollutant exposure., (Published by Oxford University Press 2024.)

Per- and polyfluoroalkyl substances (PFAS) are a unique class of chemicals synthesized to aid in industrial processes, fire-fighting products, and to benefit consumer products such as clothing, cosmetics, textiles, carpets, and coatings. The widespread use of PFAS and their strong carbon-fluorine bonds has led to their ubiquitous presence throughout the world. Airborne transport of PFAS throughout the atmosphere has also contributed to environmental pollution. Due to the potential environmental and human exposure concerns of some PFAS, research has extensively focused on water, soil, and organismal detection, but the presence of PFAS in the air has become an area of growing concern. Methods to measure polar PFAS in various matrices have been established, while the investigation of polar and nonpolar PFAS in air is still in its early development. This literature review aims to present the last two decades of research characterizing PFAS in outdoor and indoor air, focusing on active and passive air sampling and analytical methods. The PFAS classes targeted and detected in air samples include fluorotelomer alcohols (FTOHs), perfluoroalkane sulfonamides (FASAs), perfluoroalkane sulfonamido ethanols (FASEs), perfluorinated carboxylic acids (PFCAs), and perfluorinated sulfonic acids (PFSAs). Although the manufacturing of perfluorooctanoic acid (PFOA) and perfluorooctane sulfonic acid (PFOS) has been largely phased out, these two PFAS are still often detected in air samples. Additionally, recent estimates indicate that there are thousands of PFAS that are likely present in the air that are not currently monitored in air methods. Advances in air sampling methods are needed to fully characterize the atmospheric transport of PFAS., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Published by Elsevier Ltd.)

Inhalation exposure to plastic incineration emissions (PIEs) is a problem of increasing human relevance, as plastic production and waste creation have drastically increased since mainstream integration during the 20th century. We investigated the effects of PIEs on human nasal epithelial cells (HNECs) to understand if such exposures cause damage and dysfunction to respiratory epithelia. Primary HNECs from male and female donors were cultured at air-liquid interface (ALI), and 16HBE cells were cultured on coverslips. Smoke condensates were generated from incineration of plastic at flaming (640°C) and smoldering (500°C) temperatures, and cells were subsequently exposed to these materials at 5-50 μg/cm2 concentrations. HNECs were assessed for mitochondrial dysfunction and 16HBE cells for glutathione oxidation in real-time analyses. HNEC culture supernatants and total RNA were collected at 4-h postexposure for cytokine and gene expression analysis, and results show that PIEs can acutely induce inflammation, oxidative stress, and mitochondrial dysfunction in HNECs, and that incineration temperature modifies biological responses. Specifically, condensates from flaming and smoldering PIEs significantly increased HNEC secretion of cytokines IL-8, IL-1β, and IL-13, as well as expression of xenobiotic metabolism pathways and genes such as CYP1A1 and CYP1B1 at 5 and 20 μg/cm2 concentrations. Only 50 μg/cm2 flaming PIEs significantly increased glutathione oxidation in 16HBEs, and decreased respiration and ATP production in HNEC mitochondria. Impact Statement: Our data reveal the impact of incineration temperatures on biological outcomes associated with PIE exposures, emphasizing the importance of temperature as a factor when evaluating respiratory disease associated with PIEs exposure., (© The Author(s) 2024. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Background: Chronic kidney disease (CKD) affects more than 38 million people in the United States, predominantly those over 65 years of age. While CKD etiology is complex, recent research suggests associations with environmental exposures., Methods: Our primary objective is to examine creatinine-based estimated glomerular filtration rate (eGFR cr ) and diagnosis of CKD and potential associations with fine particulate matter (PM 2.5 ), ozone (O 3 ), and nitrogen dioxide (NO 2 ) using a random sample of North Carolina electronic healthcare records (EHRs) from 2004 to 2016. We estimated eGFR cr using the serum creatinine-based 2021 CKD-EPI equation. PM 2.5 and NO 2 data come from a hybrid model using 1 km 2 grids and O 3 data from 12 km 2 CMAQ grids. Exposure concentrations were 1-year averages. We used linear mixed models to estimate eGFR cr per IQR increase of pollutants. We used multiple logistic regression to estimate associations between pollutants and first appearance of CKD. We adjusted for patient sex, race, age, comorbidities, temporality, and 2010 census block group variables., Results: We found 44,872 serum creatinine measurements among 7,722 patients. An IQR increase in PM2.5 was associated with a 1.63 mL/min/1.73m 2 (95% CI: -1.96, -1.31) reduction in eGFRcr, with O 3 and NO 2 showing positive associations. There were 1,015 patients identified with CKD through e-phenotyping and ICD codes. None of the environmental exposures were positively associated with a first-time measure of eGFR cr  < 60 mL/min/1.73m 2 . NO 2 was inversely associated with a first-time diagnosis of CKD with aOR of 0.77 (95% CI: 0.66, 0.90)., Conclusions: One-year average PM 2.5 was associated with reduced eGFR cr , while O 3 and NO 2 were inversely associated. Neither PM 2.5 or O 3 were associated with a first-time identification of CKD, NO 2 was inversely associated. We recommend future research examining the relationship between air pollution and impaired renal function., (© 2024. This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply.)

Evidence of the potential causal links between long-term exposure to particulate matters (PM, i.e., PM 1 , PM 2.5 , and PM 1-2.5 ) and T2DM mortality based on large cohorts is limited. In contrast, the existing evidence usually suffers from inherent bias with the traditional association assessment. A prospective cohort of 580,757 participants in the southern region of China were recruited during 2009 and 2015 and followed up through December 2020. PM exposure at each residential address was estimated by linking to the well-established high-resolution simulation dataset. Hazard ratios (HRs) were calculated using time-varying marginal structural Cox models, an established causal inference approach, after adjusting for potential confounders. During follow-up, a total of 717 subjects died from T2DM. For every 1 μg/m 3 increase in PM 2.5 , the adjusted HRs and 95% confidence interval (CI) for T2DM mortality was 1.036 (1.019-1.053). Similarly, for every 1 μg/m 3 increase in PM 1 and PM 1-2.5 , the adjusted HRs and 95% CIs were 1.032 (1.003-1.062) and 1.085 (1.054-1.116), respectively. Additionally, we observed a generally more pronounced impact among individuals with lower levels of education or lower residential greenness which as measured by the Normalized Difference Vegetation Index (NDVI). We identified substantial interactions between NDVI and PM 1 (P-interaction = 0.003), NDVI and PM 2.5 (P-interaction = 0.019), as well as education levels and PM 1 (P-interaction = 0.049). The study emphasizes the need to consider environmental and socio-economic factors in strategies to reduce T2DM mortality. We found that PM 1 , PM 2.5 , and PM 1-2.5 heighten the peril of T2DM mortality, with education and green space exposure roles in modifying it., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Oxidative stress is a prominent pathway for the health effects associated with fine particulate matter (PM 2.5 ) exposure. Oxidative potential (OP) of PM has been associated to several health endpoints, but studies on its impact on biomarkers of oxidative stress remains insufficient. 300 pregnant women from the SEPAGES cohort (France) carried personal PM 2.5 samplers for a week and OP was measured using ascorbic acid (AA) and dithiothreitol (DTT) assays, and normalized by 1) PM 2.5 mass (OP m ) and 2) sampled air volume (OP v ). A pool of three urine spots collected on the 7th day of PM sampling was analyzed for biomarkers, namely 8-hydroxy-2-deoxyguanosine (8-OHdG), malondialdehyde (MDA) and 8-isoprostaglandin-F2α (8-isoPGF2α). Associations were investigated using adjusted multiple linear regressions. OP effects were additionally investigated by stratifying by median PM 2.5 concentration (14 μg m -3 ). In the main models, no association was observed with 8-isoPGF2α, nor MDA. An interquartile range (IQR) increase in OP m AA exposure was associated with increased 8-OHdG (percent change: 6.2 %; 95 % CI: 0.2 % to 12.6 %). In the stratified analysis, exposure to OP m AA was associated with 8-OHdG for participants exposed to low levels of PM 2.5 (percent change: 11.4 %; 95 % CI: 3.3 % to 20.1 %), but not for those exposed to high levels (percent change: -1.0 %; 95 % CI: -10.6 % to 9.6 %). Associations for OP m DTT also followed a similar pattern (p-values for OP m AA -PM and OP m DTT -PM interaction terms were 0.12 and 0.11, respectively). Overall, our findings suggest that OP m AA may be associated with increased DNA oxidative damage. This association was not observed with PM 2.5 mass concentration exposure. The effects of OP m AA in 8-OHdG tended to be stronger at lower (below median) vs. higher concentrations of PM 2.5 . Further epidemiological, toxicological and aerosol research are needed to further investigate the OP m AA effects on 8-OHdG and the potential modifying effect of PM mass concentration on this association., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Background: Ambient air pollution contributes to an estimated 6.67 million deaths annually, and has been linked to cardiovascular disease (CVD), the leading cause of death. Short-term increases in air pollution have been associated with increased risk of CVD event, though relatively few studies have directly compared effects of multiple pollutants using fine-scale spatio-temporal data, thoroughly adjusting for co-pollutants and temperature, in an exhaustive citywide hospitals dataset, towards identifying key pollution sources within the urban environment to most reduce, and reduce disparities in, the leading cause of death worldwide., Objectives: We aimed to examine multiple pollutants against multiple CVD diagnoses, across lag days, in models adjusted for co-pollutants and meteorology, and inherently adjusted by design for non-time-varying individual and aggregate-level covariates, using fine-scale space-time exposure estimates, in an exhaustive dataset of emergency department visits and hospitalizations across an entire city, thereby capturing the full population-at-risk., Methods: We used conditional logistic regression in a case-crossover design - inherently controlling for all confounders not varying within case month - to examine associations between spatio-temporal nitrogen dioxide (NO 2 ), fine particulate matter (PM 2.5 ), sulfur dioxide (SO 2 ), and ozone (O 3 ) in New York City, 2005-2011, on individual risk of acute CVD event (n = 837,523), by sub-diagnosis [ischemic heart disease (IHD), heart failure (HF), stroke, ischemic stroke, acute myocardial infarction]., Results: We found significant same-day associations between NO 2 and risk of overall CVD, IHD, and HF - and between PM 2.5 and overall CVD or HF event risk - robust to all adjustments and multiple comparisons. Results were comparable by sex and race - though median age at CVD was 10 years younger for Black New Yorkers than White New Yorkers. Associations for NO 2 were comparable for adults younger or older than 69 years, though PM 2.5 associations were stronger among older adults., Discussion: Our results indicate immediate, robust effects of combustion-related pollution on CVD risk, by sub-diagnosis. Though acute impacts differed minimally by age, sex, or race, the much younger age-at-event for Black New Yorkers calls attention to cumulative social susceptibility., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Fine particulate matter (PM2.5) has been inconsistently associated with breast cancer incidence, however, few studies have considered historic exposure when levels were higher., Methods: Outdoor residential PM2.5 concentrations were estimated using a nationwide spatiotemporal model for women in the National Institutes of Health-AARP Diet and Health Study, a prospective cohort located in 6 states (California, Florida, Louisiana, New Jersey, North Carolina, and Pennsylvania) and 2 metropolitan areas (Atlanta, GA, and Detroit, MI) and enrolled in 1995-1996 (n = 196 905). Annual average PM2.5 concentrations were estimated for a 5-year historical period 10 years prior to enrollment (1980-1984). We used Cox regression to estimate adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between a 10 µg/m3 increase in PM2.5 and breast cancer incidence overall and by estrogen receptor status and catchment area., Results: With follow-up of participants through 2017, a total of 15 870 breast cancer cases were identified. A 10 ug/m3 increase in PM2.5 was statistically significantly associated with overall breast cancer incidence (HR = 1.08, 95% CI = 1.02 to 1.13). The association was evident for estrogen receptor-positive (HR = 1.10, 95% CI = 1.04 to 1.17) but not estrogen receptor-negative tumors (HR = 0.97, 95% CI = 0.84 to 1.13; Pheterogeneity = .3). Overall breast cancer hazard ratios were more than 1 across the catchment areas, ranging from a hazard ratio of 1.26 (95% CI = 0.96 to 1.64) for North Carolina to a hazard ratio of 1.04 (95% CI = 0.68 to 1.57) for Louisiana (Pheterogeneity = .9)., Conclusions: In this large US cohort with historical air pollutant exposure estimates, PM2.5 was associated with risk of estrogen receptor-positive breast cancer. State-specific estimates were imprecise but suggest that future work should consider region-specific associations and the potential contribution of PM2.5 chemical constituency in modifying the observed association., (Published by Oxford University Press 2023.)

This paper focuses on the impact of solid barriers located upwind of a highway in reducing vehicle related concentrations that occur downwind of the roadway, compared to a highway without barriers. Measurements made in the United States Environmental Protection Agency's meteorological wind tunnel show that the mitigating impact of an upwind barrier is comparable to that of a downwind barrier. Upwind barriers lead to reductions in pollution concentrations by drawing emissions in from the highway toward the barrier. The emissions are then entrained into the flow above the recirculation zone and dispersed vertically as they are advected downwind. This upwind transport of vehicle emissions leads to concentrations at the center of the roadways that are roughly 200-300% higher than those measured on roadways with downwind barriers. This difference between on-road concentrations indicates that although both types of barriers mitigate the impact of vehicle emissions downwind of a roadway, the upwind barrier may create adverse air quality impacts for the people on the road.We have formulated a semiempirical dispersion model that incorporates the physics revealed by the wind tunnel measurements. This model improves upon a model proposed by Ahangar et al. (2017) by adjusting the wind speed to get a more realistic plume dispersion just downwind of the upwind barrier and also by providing vertical profiles of concentrations in addition to ground-level concentrations. The upwind barrier model proposed in this paper and the downwind barrier model described in Francisco et al. (2022) have been incorporated into AERMOD (version 21112) as a nonregulatory option, including the new two-barrier option when modeling both barriers on the same roadway. Implications: Our paper presents an air dispersion model algorithm for modeling the effect of upwind noise barriers on dispersion of traffic-related emissions from roadways, which was incorporated into EPA's AERMOD and then evaluated using observations from a wind tunnel experiment. The results are compared and contrasted with results from both a no-barrier case and downwind barrier cases. This manuscript expands on previously published work analyzing the effect of barrier height and source-to-barrier distance on downwind dispersion (Atmos. Pollut. Res., 13:101385, 2022, https://doi.org/10.1016/j.apr.2022.101385). The current manuscript uses the same wind tunnel setup as reported there, but focuses on a different subset of cases, namely the upwind barrier cases, when developing dispersion model algorithms to simulate the observed effects. We believe the evaluations of the vertical profiles from the wind tunnel study, development, and incorporation of the upwind barrier algorithms into AERMOD, and model evaluation of these new algorithms are significant contributions to understanding the effects of these commonly used roadside barriers.

Background: Air pollutants may contribute to the development of Parkinson's disease (PD), but empirical evidence is limited and inconsistent., Objectives: This study aimed to prospectively investigate the associations of PD with ambient exposures to fine particulate matter with aerodynamic diameter ≤ 2.5 μ m ( PM 2.5 ) and nitrogen dioxide ( NO 2 )., Methods: We analyzed data from 47,108 US women from the Sister Study, enrolled from 2003-2009 (35-80 years of age) and followed through 2018. Exposures of interest included address-level ambient PM 2.5 and NO 2 in 2009 and their cumulative averages from 2009 to PD diagnosis with varying lag-years. The primary outcome was PD diagnosis between 2009 and 2018 ( n = 163 ). We used multivariable Cox proportional hazards and time-varying Cox models to calculate hazard ratios (HRs) and 95% confidence intervals (CIs)., Results: NO 2 exposure in 2009 was associated with PD risk in a dose-response manner. The HR and 95% CI were 1.22 (95% CI: 1.03, 1.46) for one interquartile [4.8 parts per billion (ppb)] increment in NO 2 , adjusting for age, race and ethnicity, education, smoking status, alcohol drinking, caffeine intake, body mass index, physical activity, census region, residential area type, area deprivation index (ADI), and self-reported health status. The association was confirmed in secondary analyses with time-varying averaged cumulative exposures. For example, the multivariable adjusted HR for PD per 4.8   ppb increment in NO 2 was 1.25 (95% CI: 1.05, 1.50) in the 2-year lag analysis using cumulative average exposure. Post hoc subgroup analyses overall confirmed the association. However, statistical interaction analyses found that the positive association of NO 2 with PD risk was limited to women in urban, rural, and small town areas and women with ≥ 50 th percentile ADI but not among women from suburban areas or areas with < 50 th percentile ADI. In contrast, PM 2.5 exposure was not associated with PD risk with the possible exception for women from the Midwest region of the US ( HR interquartile -range = 2.49 , 95% CI: 1.20, 5.14) but not in other census regions., Discussion: In this nationwide cohort of US women, higher level exposure to ambient NO 2 is associated with a greater risk of PD. This finding needs to be independently confirmed and the underlying mechanisms warrant further investigation. https://doi.org/10.1289/EHP13009.

In the United States (U.S.), studies on nitrogen dioxide (NO 2 ) trends and pollution-attributable health effects have historically used measurements from in situ monitors, which have limited geographical coverage and leave 66% of urban areas unmonitored. Novel tools, including remotely sensed NO 2 measurements and estimates of NO 2 estimates from land-use regression and photochemical models, can aid in assessing NO 2 exposure gradients, leveraging their complete spatial coverage. Using these data sets, we find that Black, Hispanic, Asian, and multiracial populations experience NO 2 levels 15-50% higher than the national average in 2019, whereas the non-Hispanic White population is consistently exposed to levels that are 5-15% lower than the national average. By contrast, the in situ monitoring network indicates more moderate ethnoracial NO 2 disparities and different rankings of the least- to most-exposed ethnoracial population subgroup. Validating these spatially complete data sets against in situ observations reveals similar performance, indicating that all these data sets can be used to understand spatial variations in NO 2 . Integrating in situ monitoring, satellite data, statistical models, and photochemical models can provide a semiobservational record, complete geospatial coverage, and increasingly high spatial resolution, enhancing future efforts to characterize, map, and track exposure and inequality for highly spatially heterogeneous pollutants like NO 2 .

Ambient temperature and relative humidity can affect asthma symptoms. Apparent temperature is a measure of temperature perceived by humans that takes into account the effect of humidity. However, the potential link between personal exposures to apparent temperature and asthma symptoms has not been investigated. We conducted a panel study of 37 asthmatic children, aged 5-11 years, during an early spring season (average daily ambient temperature: 14°C, range: 7-18°C). Asthma symptoms were measured 4 times for each participant with a 2-week interval between consecutive measurements using the Childhood Asthma-Control Test (C-ACT). Average, minimum, and maximum personal apparent temperature exposures, apparent temperature exposure variability (TV), and average ambient temperature were calculated for the 12 hours, 24 hours, week, and 2 weeks prior to each visit. We found that a 10°C lower in 1-week and 2-week average & minimum personal apparent temperature exposures, TV, and average ambient temperature exposures were significantly associated with lower total C-ACT scores by up to 2.2, 1.4, 3.3, and 1.4 points, respectively, indicating worsened asthma symptoms. Our results support that personal apparent temperature exposure is potentially a stronger driver than ambient temperature exposures for the variability in asthma symptom scores. Maintaining a proper personal apparent temperature exposure could be an effective strategy for personalized asthma management., Competing Interests: The authors have declared that no competing interests exist., (Copyright: This is an open access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication.)

Background: DNA methylation-based measures of biological aging have been associated with air pollution and may link pollutant exposures to aging-related health outcomes. However, evidence is inconsistent and there is little information for Black women., Objective: We examined associations of ambient particulate matter <2.5 μm and <10 μm in diameter (PM 2.5 and PM 10 ) and nitrogen dioxide (NO 2 ) with DNA methylation, including epigenetic aging and individual CpG sites, and evaluated whether associations differ between Black and non-Hispanic White (NHW) women., Methods: Validated models were used to estimate annual average outdoor residential exposure to PM 2.5 , PM 10 , and NO 2 in a sample of self-identified Black (n=633) and NHW (n=3493) women residing in the contiguous US. We used sampling-weighted generalized linear regression to examine the effects of pollutants on six epigenetic aging measures (primary: DunedinPACE, GrimAgeAccel, and PhenoAgeAccel; secondary: Horvath intrinsic epigenetic age acceleration [EAA], Hannum extrinsic EAA, and skin & blood EAA) and epigenome-wide associations for individual CpG sites. Wald tests of nested models with and without interaction terms were used to examine effect measure modification by race/ethnicity., Results: Black participants had higher median air pollution exposure than NHW participants. GrimAgeAccel was associated with both PM 10 and NO 2 among Black participants, (Q4 versus Q1, PM 10 : β=1.09, 95% CI: 0.16-2.03; NO 2 : β=1.01, 95% CI 0.08-1.94) but not NHW participants (p-for-heterogeneity: PM 10 =0.10, NO 2 =0.20). In Black participants, we also observed a monotonic exposure-response relationship between NO 2 and DunedinPACE (Q4 versus Q1, NO 2 : β=0.029, 95% CI: 0.004-0.055; p-for-trend=0.03), which was not observed in NHW participants (p-for-heterogeneity=0.09). In the EWAS, pollutants were significantly associated with differential methylation at 19 CpG sites in Black women and one in NHW women., Conclusions: In a US-wide cohort study, our findings suggest that air pollution is associated with DNA methylation alterations consistent with higher epigenetic aging among Black, but not NHW, women., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Partitioning of per- and polyfluoroalkyl substances (PFAS) to indoor materials, including clothing, may prolong the residence time of PFAS indoors and contribute to exposure. During the Indoor PFAS Assessment (IPA) Campaign, we measured concentrations of nine neutral PFAS in air and cotton cloth in 11 homes in North Carolina, for up to 9 months. Fluorotelomer alcohols (i.e., 6:2 FTOH, 8:2 FTOH, and 10:2 FTOH) are the dominant target species in indoor air, with concentrations ranging from 1.8 to 49 ng m - 3 , 1.2 to 53 ng m - 3 , and 0.21 to 5.7 ng m - 3 , respectively. In cloth, perfluorooctane sulfonamidoethanols (i.e., MeFOSE and EtFOSE) accumulated most significantly over time, reaching concentrations of up to 0.26 ng cm - 2 and 0.24 ng cm - 2 , respectively. From paired measurements of neutral PFAS in air and suspended cloth, we derived cloth-air partition coefficients ( K ca ) for 6:2, 8:2, and 10:2 FTOH; ethylperfluorooctane sulfonamide (EtFOSA); MeFOSE; and EtFOSE. Mean log( K ca ) values range from 4.7 to 6.6 and are positively correlated with the octanol-air partition coefficient. We investigated the effect of the cloth storage method on PFAS accumulation and the influence of home characteristics on air concentrations. Temperature had the overall greatest effect. This study provides valuable insights into PFAS distribution, fate, and exposure indoors.

Wildfires have increased in frequency and area burned, trends expected to continue with climate change. Among other effects, fires release pollutants into the atmosphere, representing a risk to human health and downwind terrestrial and aquatic ecosystems. While human health risks are well studied, the ecological impacts to downwind ecosystems are not, and this gap may present a constraint on developing an adequate assessment of the ecological risks associated with downwind wildfire exposure. Here, we first screened the scientific literature to assess general knowledge about pathways and end points of a conceptual model linking wildfire generated pollutants and other materials to downwind ecosystems. We found a substantial body of literature on the composition of wildfire derived pollution and materials in the atmosphere and subsequent transport, yet little observational or experimental work on their effects on downwind ecological end points. This dearth of information raises many questions related to adequately assessing the ecological risk of downwind exposure, especially given increasing wildfire trends. To guide future research, we pose eight questions within the well-established US EPA ecological risk assessment paradigm that if answered would greatly improve ecological risk assessment and, ultimately, management strategies needed to reduce potential wildfire impacts.

Reduced complexity tools that provide a representation of both primarily emitted particulate matter with an aerodynamic diameter less than 2.5 μm (PM 2.5 ), secondarily formed PM 2.5 , and ozone (O 3 ) allow for a quick assessment of many iterations of pollution control scenarios. Here, a new reduced complexity tool, Pattern Constructed Air Pollution Surfaces (PCAPS), that estimates annual average PM 2.5 and seasonal average maximum daily average 8 h (MDA8) O 3 for any source location in the United States is described and evaluated. Typically, reduced complexity tools are not evaluated for skill in predicting change in air pollution by comparison with more sophisticated modeling systems. Here, PCAPS was compared against multiple types of emission control scenarios predicted with state-of-the-science photochemical grid models to provide confidence that the model is realistically capturing the change in air pollution due to changing emissions. PCAPS was also applied with all anthropogenic emissions sources for multiple retrospective years to predict PM 2.5 chemical components for comparison against routine surface measurements. PCAPS predicted similar magnitudes and regional variations in spatial gradients of measured chemical components of PM 2.5 . Model performance for capturing ambient measurements was consistent with other reduced complexity tools. PCAPS also did well at capturing the magnitude and spatial features of changes predicted by photochemical transport models for multiple emissions scenarios for both O 3 and PM 2.5 . PCAPS is a flexible tool that provides source-receptor relationships using patterns of air quality gradients from a training data set of generic modeled sources to create interpolated air pollution gradients for new locations not part of the training database. The flexibility provided for both sources and receptors makes this tool ideal for integration into larger frameworks that provide emissions changes and need estimates of air quality to inform downstream analytics, which often includes an estimate of monetized health effects.

Personal exposure to PM 2.5 , and the elemental composition therein, may vary greatly from ambient measurements at fixed monitoring sites. Here, we characterized the differences between personal, indoor, and outdoor concentrations of PM 2.5 -bound elements, and predicted personal exposures to 21 PM 2.5 -bound elements. Personal-indoor-outdoor PM 2.5 filter samples were collected for five consecutive days across two seasons from 66 healthy non-smoking retired adults in Beijing (BJ) and Nanjing (NJ), China. Personal element-specific models were developed using liner mixed effects models and evaluated by R 2 and root mean square error (RMSE). The mean (SD) concentrations of personal exposures varied by element and city, ranging from 2.5 (1.4) ng/m 3 for Ni in BJ to 4271.2 (1614.8) ng/m 3 for S in NJ. Personal exposures to PM 2.5 and most elements were significantly correlated with both indoor and outdoor (except Ni in BJ) measurements, but frequently exceeded indoor levels and fell below outdoor levels. Indoor and outdoor PM 2.5 elemental concentrations were the strongest determinants of most personal elemental exposures, with R M 2 ranging from 0.074 to 0.975 for indoor and from 0.078 to 0.917 for outdoor levels, respectively. Home ventilation conditions (especially window opening behavior), time-activity patterns, meteorological factors, household characteristics, and season were also key factors influencing personal exposure levels. The final models accounted for 24.2 %-94.0 % (RMSE: 0.135-0.718) of the variance in personal PM 2.5 elemental exposures. By incorporating these crucial determinants, the modeling approach used here can improve PM 2.5 -bound elemental exposure estimates and better associate compositionally dependent PM 2.5 exposures and health risks., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

There is substantial evidence that photochemical reactions in the atmosphere cause physico-chemical transformation of combustion smoke, but how this processing modifies potential health effects in exposed populations is not well understood. Here we utilized a new approach to simulate photochemical aging of anthropogenic smoke emissions (a mixture of plastic, plywood, and cardboard smoke) from two different burning conditions (smoldering vs. flaming) and investigated their adverse outcomes associated with mutagenic activity and the relative potencies of different polycyclic aromatic hydrocarbons (PAHs). Aging resulted in increased oxygenated volatile organic compound (VOC) emissions but largely degraded particle-bound PAH components in the smoke. Chemical transformation during aging was more dramatic for flaming versus smoldering smoke. Due to the PAH degradation, mutagenicity of the aged smoke from flaming combustion was much lower (up to 4 times) than that of the fresh smoke on per-particle mass basis. However, on the basis of particle emitted per fuel mass burned, the aged and fresh smoke particles exhibited similar mutagenic activities, which were up to 3 times higher for smoldering versus flaming smoke emissions. Similarly, the PAH toxicity equivalent (PAH-TEQ) of the aged smoldering smoke was 3 times higher than that of the aged flaming smoke particles, suggesting that some PAHs (e.g., indeno[c,d]pyrene and benzo[b]fluoranthene) in the smoldering smoke were more photochemically stable during aging. These findings increase understanding of the evolution of smoke emitted at different burning conditions and the role of photochemical transformations on mutagenicity and PAH-induced toxicity., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Yong Ho Kim reports financial support was provided by National Institutes of Health. Andrew P. Grieshop reports financial support was provided by National Science Foundation., (Copyright © 2023. Published by Elsevier B.V.)

Ambient air pollution, temperature, and social stressor exposures are linked with asthma risk, with potential synergistic effects. We examined associations for acute pollution and temperature exposures, with modification by neighborhood violent crime and socioeconomic deprivation, on asthma morbidity among children aged 5-17 years year-round in New York City. Using conditional logistic regression in a time-stratified, case-crossover design, we quantified percent excess risk of asthma event per 10-unit increase in daily, residence-specific exposures to PM 2.5 , NO 2 , SO 2 , O 3 , and minimum daily temperature (Tmin). Data on 145,834 asthma cases presenting to NYC emergency departments from 2005 to 2011 were obtained from the New York Statewide Planning and Research Cooperative System (SPARCS). Residence- and day-specific spatiotemporal exposures were assigned using the NYC Community Air Survey (NYCCAS) spatial data and daily EPA pollution and NOAA weather data. Point-level NYPD violent crime data for 2009 (study midpoint) was aggregated, and Socioeconomic Deprivation Index (SDI) scores assigned, by census tract. Separate models were fit for each pollutant or temperature exposure for lag days 0-6, controlling for co-exposures and humidity, and mutually-adjusted interactions (modification) by quintile of violent crime and SDI were assessed. We observed stronger main effects for PM 2.5 and SO 2 in the cold season on lag day 1 [4.90% (95% CI: 3.77-6.04) and 8.57% (5.99-11.21), respectively]; Tmin in the cold season on lag day 0 [2.26% (1.25-3.28)]; and NO 2 and O 3 in the warm season on lag days 1 [7.86% (6.66-9.07)] and 2 [4.75% (3.53-5.97)], respectively. Violence and SDI modified the main effects in a non-linear manner; contrary to hypotheses, we found stronger associations in lower-violence and -deprivation quintiles. At very high stressor exposures, although asthma exacerbations were highly prevalent, pollution effects were less apparent-suggesting potential saturation effects in socio-environmental synergism., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)

Volatile chemical products (VCP) are an increasingly important source of hydrocarbon and oxygenated volatile organic compound (OVOC) emissions to the atmosphere, and these emissions are likely to play an important role as anthropogenic precursors for secondary organic aerosol (SOA). While the SOA from VCP hydrocarbons is often accounted for in models, the formation, evolution, and properties of SOA from VCP OVOCs remain uncertain. We use environmental chamber data and a kinetic model to develop SOA parameters for 10 OVOCs representing glycols, glycol ethers, esters, oxygenated aromatics, and amines. Model simulations suggest that the SOA mass yields for these OVOCs are of the same magnitude as widely studied SOA precursors (e.g., long-chain alkanes, monoterpenes, and single-ring aromatics), and these yields exhibit a linear correlation with the carbon number of the precursor. When combined with emissions inventories for two megacities in the United States (US) and a US-wide inventory, we find that VCP VOCs react with OH to form 0.8-2.5× as much SOA, by mass, as mobile sources. Hydrocarbons (terpenes, branched and cyclic alkanes) and OVOCs (terpenoids, glycols, glycol ethers) make up 60-75 and 25-40% of the SOA arising from VCP use, respectively. This work contributes to the growing body of knowledge focused on studying VCP VOC contributions to urban air pollution.

Background: Epigenome-wide association studies of ambient fine particulate matter (PM 2.5 ) have been reported. However, few have examined PM 2.5 components (PMCs) and sources or included repeated measures. The lack of high-resolution exposure measurements is the key limitation. We hypothesized that significant changes in DNA methylation might vary by PMCs and the sources., Methods: We predicted the annual average of 14 PMCs using novel high-resolution exposure models across the contiguous U.S., between 2000-2018. The resolution was 50 m × 50 m in the Greater Boston Area. We also identified PM 2.5 sources using positive matrix factorization. We repeatedly collected blood samples and measured leukocyte DNAm with the Illumina HumanMethylation450K BeadChip in the Normative Aging Study. We then used median regression with subject-specific intercepts to estimate the associations between long-term (one-year) exposure to PMCs / PM 2.5 sources and DNA methylation at individual cytosine-phosphate-guanine CpG sites. Significant probes were identified by the number of independent degrees of freedom approach, using the number of principal components explaining > 95% of the variation of the DNA methylation data. We also performed regional and pathway analyses to identify significant regions and pathways., Results: We included 669 men with 1,178 visits between 2000-2013. The subjects had a mean age of 75 years. The identified probes, regions, and pathways varied by PMCs and their sources. For example, iron was associated with 6 probes and 6 regions, whereas nitrate was associated with 15 probes and 3 regions. The identified pathways from biomass burning, coal burning, and heavy fuel oil combustion sources were associated with cancer, inflammation, and cardiovascular diseases, whereas there were no pathways associated with all traffic., Conclusions: Our findings showed that the effects of PM 2.5 on DNAm varied by its PMCs and sources., (© 2023. BioMed Central Ltd., part of Springer Nature.)

Background: Poor olfaction is common in older adults and may have profound adverse implications on their health. However, little is known about the potential environmental contributors to poor olfaction., Objective: We investigated ambient fine particulate matter [PM ≤ 2.5 μ m in aerodynamic diameter ( PM 2.5 )] and nitrogen dioxide ( NO 2 ) in relation to poor olfaction in middle-aged to older women., Methods: The Sister Study is a nationwide cohort of 50,884 women in the United States with annual average air pollutant exposures estimated based on participants' residences from enrollment (2003-2009) through 2017. This analysis was limited to 3,345 women, 50-79 years of age as of January 2018, who completed the Brief Smell Identification Test (B-SIT) in 2018-2019. Poor olfaction was defined as a B-SIT score of ≤ 9 in the primary analysis. We conducted multivariable logistic regressions, accounting for covariates and study sampling design., Results: Overall, we found little evidence for associations of air pollutants with poor olfaction. The odds ratio (OR) and 95% confidence interval (CI) of poor olfaction for each interquartile range (IQR) increment of air pollutants in 2006 were 1.03 (95% CI: 0.91, 1.17) for PM 2.5 (per 3.3   μ g / m 3 ) and 1.08 (95% CI: 0.96, 1.22) for NO 2 (per 5.7  ppb ). Results were similar in the analyses using the most recent (2017) or the cumulative average (2006-2017) air pollutant exposure data. Secondary analyses suggested potential association in certain subgroups. The OR per IQR was 1.35 (95% CI: 1.11, 1.65) for PM 2.5 among younger participants ( < 54.2 years of age) and 1.87 (95% CI: 1.29, 2.71) for NO 2 among current smokers., Discussion: This study did not find convincing evidence that air pollutants have lasting detrimental effects on the sense of smell of women 50-79 years of age. The subgroup analyses are exploratory, and the findings need independent confirmation. https://doi.org/10.1289/EHP12066.

Tools for assessing multiple exposures across several domains (e.g., physical, chemical, and social) are of growing importance in social and environmental epidemiology because of their value in uncovering disparities and their impact on health outcomes. Here we describe work done within the Environmental influences on Child Health Outcomes (ECHO)-wide Cohort Study to build a combined exposure index. Our index considered both environmental hazards and social stressors simultaneously with national coverage for a 10-year period. Our goal was to build this index and demonstrate its utility for assessing differences in exposure for pregnancies enrolled in the ECHO-wide Cohort Study. Our unitless combined exposure index, which collapses census-tract level data into a single relative measure of exposure ranging from 0-1 (where higher values indicate higher exposure to hazards), includes indicators for major air pollutants and air toxics, features of the built environment, traffic exposures, and social determinants of health (e.g., lower educational attainment) drawn from existing data sources. We observed temporal and geographic variations in index values, with exposures being highest among participants living in the West and Northeast regions. Pregnant people who identified as Black or Hispanic (of any race) were at higher risk of living in a "high" exposure census tract (defined as an index value above 0.5) relative to those who identified as White or non-Hispanic. Index values were also higher for pregnant people with lower educational attainment. Several recommendations follow from our work, including that environmental and social stressor datasets with higher spatial and temporal resolutions are needed to ensure index-based tools fully capture the total environmental context.

Background: Air pollution exposure is associated with cardiovascular morbidity and mortality. Although exposure to air pollution early in life may represent a critical window for development of cardiovascular disease risk factors, few studies have examined associations of long-term air pollution exposure with markers of cardiovascular and metabolic health in young adults., Objectives: By combining health data from the National Longitudinal Study of Adolescent to Adult Health (Add Health) with air pollution data from the Fused Air Quality Surface using Downscaling (FAQSD) archive, we: (1) calculated multi-year estimates of exposure to ozone (O 3 ) and particulate matter with an aerodynamic diameter ≤ 2.5 µm (PM 2.5 ) for Add Health participants; and (2) estimated associations between air pollution exposures and multiple markers of cardiometabolic health., Methods: Add Health is a nationally representative longitudinal cohort study of over 20,000 adolescents aged 12-19 in the United States (US) in 1994-95 (Wave I). Participants have been followed through adolescence and into adulthood with five in-home interviews. Estimated daily concentrations of O 3 and PM 2.5 at census tracts were obtained from the FAQSD archive and used to generate tract-level annual averages of O 3 and PM 2.5 concentrations. We estimated associations between average O 3 and PM 2.5 exposures from 2002 to 2007 and markers of cardiometabolic health measured at Wave IV (2008-09), including hypertension, hyperlipidemia, body mass index (BMI), diabetes, C-reactive protein, and metabolic syndrome., Results: The final sample size was 11,259 individual participants. The average age of participants at Wave IV was 28.4 years (range: 24-34 years). In models adjusting for age, race/ethnicity, and sex, long-term O 3 exposure (2002-07) was associated with elevated odds of hypertension, with an odds ratio (OR) of 1.015 (95% confidence interval [CI]: 1.011, 1.029); obesity (1.022 [1.004, 1.040]); diabetes (1.032 [1.009,1.054]); and metabolic syndrome (1.028 [1.014, 1.041]); PM 2.5 exposure (2002-07) was associated with elevated odds of hypertension (1.022 [1.001, 1.045])., Conclusion: Findings suggest that long-term ambient air pollution exposure, particularly O 3 exposure, is associated with cardiometabolic health in early adulthood., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Wildfire activity is increasing in the continental U.S. and can be linked to climate change effects, including rising temperatures and more frequent drought conditions. Wildfire emissions and large fire frequency have increased in the western U.S., impacting human health and ecosystems. We linked 15 years (2006-2020) of particulate matter (PM 2.5 ) chemical speciation data with smoke plume analysis to identify PM 2.5 -associated nutrients elevated in air samples on smoke-impacted days. Most macro- and micro-nutrients analyzed (phosphorus, calcium, potassium, sodium, silicon, aluminum, iron, manganese, and magnesium) were significantly elevated on smoke days across all years analyzed. The largest percent increase was observed for phosphorus. With the exception of ammonium, all other nutrients (nitrate, copper, and zinc), although not statistically significant, had higher median values across all years on smoke vs. non-smoke days. Not surprisingly, there was high variation between smoke impacted days, with some nutrients episodically elevated >10 000% during select fire events. Beyond nutrients, we also explored instances where algal blooms occurred in multiple lakes downwind from high-nutrient fires. In these cases, remotely sensed cyanobacteria indices in downwind lakes increased two to seven days following the occurrence of wildfire smoke above the lake. This suggests that elevated nutrients in wildfire smoke may contribute to downwind algal blooms. Since cyanobacteria blooms can be associated with the production of cyanotoxins and wildfire activity is increasing due to climate change, this finding has implications for drinking water reservoirs in the western United States, and for lake ecology, particularly alpine lakes with otherwise limited nutrient inputs.

Exposure to tropospheric ozone pollution impairs photosynthesis and growth in plants and this can have consequences for ecosystems. However, exposure-response research in the United States (U.S.) has historically focused on trees and crops, and less attention has been given to non-crop herbaceous species. We combined U.S. Environmental Protection Agency ozone monitoring data from the entirety of 2016 with published exposure-response relationships from controlled exposure experiments for twenty herbaceous plant species occurring in California. The U.S. Department of Agriculture PLANTS database was used to identify county-level occurrence data of these plant species. A kriged ozone exposure surface for 2016 was generated using data from monitoring stations in California and surrounding states, using Accumulated Ozone exposure over a Threshold of 40 ppb (AOT40) as an exposure metric. County-wide ozone exposure estimations were then combined with published exposure response functions for focal plants, and maps were created to estimate ozone-induced growth losses in the counties where the plants occur. Plant species had estimated annual growth losses from <1 % to >20 % based on exposure levels and sensitivity. Of the 20 species, 17 had predicted biomass loss >5 % in at least one county, emphasizing the vulnerability of herbaceous species at recent ozone concentrations. Butte, Nevada, Plumas, San Luis Obispo, and Shasta Counties, an area of about 31,652 km 2 , had the highest number of species (6) with >10 % estimated biomass loss, the loss threshold for European critical levels. White clover (Trifolium repens L.) was one of the most affected species with more than an estimated 10 % annual estimated growth loss over 59 % of the state. Overall, these estimated growth losses demonstrate potential for shifts in plant communities and negative effects on ecosystems. This study addresses critical policy needs for risk assessments on herbaceous species in a single year of ozone exposure., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Published by Elsevier B.V.)

Context: While strong evidence supports adverse effects of pre-natal air pollution on child's lung function, previous studies rarely considered fine particulate matter (PM 2.5 ) or the potential role of offspring sex and no study examined the effects of pre-natal PM 2.5 on the lung function of the newborn., Aim: We examined overall and sex-specific associations of personal pre-natal exposure to PM 2.5 and nitrogen (NO 2 ) with newborn lung function measurements., Methods: This study relied on 391 mother-child pairs from the French SEPAGES cohort. PM 2.5 and NO 2 exposure was estimated by the average concentration of pollutants measured by sensors carried by the pregnant women during repeated periods of one week. Lung function was assessed with tidal breathing analysis (TBFVL) and nitrogen multiple breath washout (N 2 MBW) test, performed at 7 weeks. Associations between pre-natal exposure to air pollutants and lung function indicators were estimated by linear regression models adjusted for potential confounders, and then stratified by sex., Results: Mean exposure to NO 2 and PM 2.5 during pregnancy was 20.2 μg/m 3 and 14.3 μg/m 3 , respectively. A 10 μg/m 3 increase in PM 2.5 maternal personal exposure during pregnancy was associated with an adjusted 2.5 ml (2.3%) decrease in the functional residual capacity of the newborn (p-value = 0.11). In females, functional residual capacity was decreased by 5.2 ml (5.0%) (p = 0.02) and tidal volume by 1.6 ml (p = 0.08) for each 10 μg/m 3 increase in PM 2.5 . No association was found between maternal NO 2 exposure and newborns lung function., Conclusions: Personal pre-natal PM 2.5 exposure was associated with lower lung volumes in female newborns, but not in males. Our results provide evidence that pulmonary effects of air pollution exposure can be initiated in utero. These findings have long term implications for respiratory health and may provide insights into the underlying mechanisms of PM 2.5 effects., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Background: Despite many efforts, preterm birth (PTB) is poorly understood and remains a major public health problem in the United States. Toxicological work suggests gestational parent (GP) diet may modify the effect of ambient pollutants on birth outcomes. We assessed risk of PTB in humans in relation to fine particulate matter (PM 2.5 ), ozone (O 3 ), and nitrogen dioxide (NO 2 ) and variation by diet., Methods: 684 GP-singleton infant pairs in the Newborn Epigenetics Study prospective birth cohort were attributed ambient air pollutant exposures for each trimester based on residence. Total energy intake, percent of energy intake from saturated fat, and percent of energy intake from total fat were dichotomized at the 75th percentile. >We used log binomial regressions to estimate risk ratios (RR (95%CI)) for PTB by pollutant interquartile ranges, adjusting for GP age, pre-pregnancy body mass index, GP race/ethnicity, GP education, season of conception, household income, and each diet factor. We assessed departure from additivity using interaction contrast ratios (ICRs). We addressed missing covariate data with multiple imputation., Results: Point estimates suggest that O 3 may be inversely associated with PTB when exposure occurs in trimester 2 (min RR: 0.77, 95% CI: 0.39, 1.49), but may be harmful when exposure occurs in trimester 3 (max RR: 1.51, 95% CI: 0.62, 3.64). Additionally, PM 2.5 may be inversely associated with PTB when considered with total fat and saturated fat in trimester 2. Imprecise ICRs suggest departure from additivity (evidence of modification) with some pollutant-diet combinations., Conclusions: While confidence intervals are wide, we observed potential modification of pollutant associations by dietary factors. It is imperative that large cohorts collect the required data to examine this topic, as more power is necessary to investigate the nuances suggested by this work., (© 2023. This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply.)

Background: A critical aspect of air pollution exposure assessments is determining the time spent in various microenvironments (ME), which can have substantially different pollutant concentrations. We previously developed and evaluated a ME classification model, called Microenvironment Tracker (MicroTrac), to estimate time of day and duration spent in eight MEs (indoors and outdoors at home, work, school; inside vehicles; other locations) based on input data from global positioning system (GPS) loggers., Objective: In this study, we extended MicroTrac and evaluated the ability of using geolocation data from smartphones to determine the time spent in the MEs., Method: We performed a panel study, and the MicroTrac estimates based on data from smartphones and GPS loggers were compared to 37 days of diary data across five participants., Results: The MEs were correctly classified for 98.1% and 98.3% of the time spent by the participants using smartphones and GPS loggers, respectively., Significance: Our study demonstrates the extended capability of using ubiquitous smartphone data with MicroTrac to help reduce time-location uncertainty in air pollution exposure models for epidemiologic and exposure field studies., (© 2022. This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply.)

Some dioxins are carcinogenic, but few studies have investigated the relationship between ambient polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/F) and risk of breast cancer. We evaluated associations between proximity-based residential exposure to industrial emissions of PCDD/F and breast cancer risk in a large U.S. cohort. Sister Study participants at enrollment (2003-2009) were followed for incident breast cancer through September 2018. After restricting to participants with ≥10 years of residential history prior to enrollment (n = 35,908), we generated 10-year distance- and toxic equivalency quotient (TEQ)-weighted average emissions indices (AEI [g TEQ/km 2 ]) within 3, 5, or 10 km of participants' residences, overall and by facility type. Multivariable Cox regression models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between AEI quartiles (vs. zero AEI) and risk of breast cancer [invasive or ductal carcinoma in situ]. There were 2670 incident breast cancer cases over 11 years (median) of follow-up. Breast cancer risk was increased for those in the highest quartile [Q] of AEI exposure within 3 km (HR Q4 :1.18, 95% CI: 0.99,1.40, P trend  = 0.03). The HR was higher for the 10-year AEI at 3 km from municipal solid waste facilities (HR  ≥ median.vs.0 :1.50, 95% CI: 0.98, 2.29; P trend  = 0.07). Risk was higher among ever smokers (vs. never smokers) in the top quartile of the 3 km AEI (HR Q4 :1.41, 95% CI:1.12,1.77, P trend  = 0.003; P interaction  = 0.03) and higher risk for ER negative tumors was suggested (HR Q4 :1.47, 95% CI: 0.95, 2.28, P trend  = 0.07, P heterogeneity  = 0.17). Our findings suggest that residential exposure to PCDD/F emissions may confer an increased risk of breast cancer., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Published by Elsevier Inc.)

Particulate matter (PM) is a major primary pollutant emitted during wildland fires that has the potential to pose significant health risks to individuals/communities who live and work in areas impacted by smoke events. Limiting exposure is the principle measure available to mitigate health impacts of smoke and therefore the accurate determination of ambient PM concentrations during wildland fire events is critical to protecting public health. However, monitoring air pollutants in smoke impacted environments has proven challenging in that measurement interferences or sampling conditions can result in both positive and negative artifacts. The EPA has performed research on methods for the measurement of PM 2.5 in a series of laboratory-based studies including evaluation in smoke. This manuscript will summarize the results of the laboratory-based evaluation of federal equivalent method (FEM) monitors for PM 2.5 with particular attention being given to the Teledyne-API Model T640 PM Mass monitor, as compared to the filter-based federal reference method (FRM). The T640 is an optical-based PM monitor and has been gaining wide use by state and local agencies in monitoring for PM 2.5 U.S. National Ambient Air Quality Standards (NAAQS) attainment. At present, the T640 (includes both T640 and T640×) comprises ~44% of the PM 2.5 FEM monitors in U.S. regulatory monitoring networks. In addition, the T640 has increasingly been employed for the higher time resolution comparison/evaluation of low-cost PM sensors including during smoke impacted events. Results from controlled non-smoke laboratory studies using generated ammonium sulfate aerosols demonstrated a generally negative T640 measurement artifact that was significantly related to the PM 2.5 concentration and particle size distribution. Results from biomass burning chamber studies demonstrated positive and negative artifacts significantly associated with PM 2.5 concentration and optical wavelength-dependent absorption properties of the smoke aerosol. Implications : The results detailed in this paper will provide state and local air monitoring agencies with the tools and knowledge to address PM 2.5 measurement challenges in areas frequently impacted by wildland fire smoke. The observed large positive and negative artifacts in the T640 PM mass determination have the potential to result in false exceedances of the PM 2.5 NAAQS or in the disqualification of monitoring data through an exceptional event designation. In addition, the observed artifacts in smoke impacted air will have a detrimental effect on providing reliable public information when wildfires occur and also in identifying reference measurements for small sensor evaluation studies. Other PM 2.5 FEMs such as the BAM-1022 perform better in smoke and are comparable to the filter-based FRM. Care must be taken in choosing high time resolution FEM monitors that will be operated at smoke impacted sites. Accurate methods, such as the FRM and BAM-1022 will reduce the burden of developing and reviewing exceptional event request packages, data loss/disqualification, and provide states with tools to adequately evaluate public exposure risks and provide accurate public health messaging during wildfire/smoke events.

Microenvironmental concentrations and time-activity patterns influence personal exposure to fine particulate matter (PM 2.5 ). However, the variations and contributions of PM 2.5 exposures from various microenvironments (MEs) and activities remain unclear. In this study, gravimetrically corrected real-time personal PM 2.5 measurements were collected during routine activities in different MEs from 66 non-smoking retired adults. Exposure data were collected for five consecutive days over two seasons in Nanjing (NJ) and Beijing (BJ), China. Measured PM 2.5 concentrations varied substantially both between and within different MEs and activities. The highest average concentrations were observed in restaurants (NJ: mean 192 μg/m 3 , SD 242 μg/m 3 ; BJ: mean 91 μg/m 3 , SD 79 μg/m 3 ) and were associated with sources such as passive smoking and cooking emissions. Overall, PM 2.5 concentrations in different MEs and activities were moderately to highly correlated with outdoor PM 2.5 concentrations (Spearman's r = 0.51-0.97) except in restaurants and during passive smoking. The at-home ME contributed approximately 85 % of the total PM 2.5 exposure, corresponding to the participants spending about 87 % of their time there. The majority of household exposures occurred during sleeping, cooking, and other home-based activities. Transportation accounted for <5 % of total exposure. Our results indicate that improving indoor air quality, especially residential indoors, is important to reduce personal exposure to PM 2.5 ., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Air pollutants are being increasingly linked to extrapulmonary multi-organ effects. Specifically, recent studies associate air pollutants with brain disorders including psychiatric conditions, neuroinflammation and chronic diseases. Current evidence of the linkages between neuropsychiatric conditions and chronic peripheral immune and metabolic diseases provides insights on the potential role of the neuroendocrine system in mediating neural and systemic effects of inhaled pollutants (reactive particulates and gases). Autonomically-driven stress responses, involving sympathetic-adrenal-medullary and hypothalamus-pituitary-adrenal axes regulate cellular physiological processes through adrenal-derived hormones and diverse receptor systems. Recent experimental evidence demonstrates the contribution of the very stress system responding to non-chemical stressors, in mediating systemic and neural effects of reactive air pollutants. The assessment of how respiratory encounter of air pollutants induce lung and peripheral responses through brain and neuroendocrine system, and how the impairment of these stress pathways could be linked to chronic diseases will improve understanding of the causes of individual variations in susceptibility and the contribution of habituation/learning and resiliency. This review highlights effects of air pollution in the respiratory tract that impact the brain and neuroendocrine system, including the role of autonomic sensory nervous system in triggering neural stress response, the likely contribution of translocated nano particles or metal components, and biological mediators released systemically in causing effects remote to the respiratory tract. The perspective on the use of systems approaches that incorporate multiple chemical and non-chemical stressors, including environmental, physiological and psychosocial, with the assessment of interactive neural mechanisms and peripheral networks are emphasized.

A growing body of evidence indicates that exposure to air pollution affects cognitive performance; however, few studies have assessed this in the context of repeated measures within a large group of individuals or in a population with a large age range. In this study, we evaluated the associations between long-term exposure to fine particulate matter (PM 2.5 ) and ozone (O 3 ) in large cohort of adults aged 18-90 years. The study cohort included 29,091 Lumosity users in the contiguous US who completed 20 repetitions of the Lost in Migration game between 2017 and 2018. Game scores reflect the ability to filter information and avoid distracting information. Long-term air pollution data included ambient PM 2.5 and O 3 averaged for the 365-day period before each gameplay date. Generalized linear models were used to examine the associations between long-term PM 2.5 and O 3 and game score percentile. Co-pollutant models were adjusted for meteorology, time trend, age, gender, device, education, local socioeconomic factors, and urbanicity. Results represent the change in attention game score percentile per 1 μg/m 3 increase in PM 2.5 or 0.01 ppm increase in O 3 . In the entire cohort, a -0.10 (95% CI: -0.16, -0.04) change in score percentile was associated with PM 2.5 , while no significant association was observed with O 3 . Modification of these associations by age was observed for both PM 2.5 and O 3 , with stronger associations observed in younger users. In users aged 18-29, a -0.25 (-0.45, -0.05) change in score percentile was associated with PM 2.5 , while no associations were observed in other age groups. With O 3 , there was a -2.92 (-4.63, -1.19) and -2.81 (-4.29, -1.25) change in score percentile for users aged 18-29 and 30-39, respectively. We observed that elevated long-term PM 2.5 and O 3 were associated with decreased focus scores in young adults, but follow-up research is necessary to further illuminate these associations., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Dr. Cavin Ward-Caviness is a paid advisor for the Clock Foundation. The Clock Foundation had no involvement in any aspect of this work. The remaining authors have nothing to disclose., (Published by Elsevier Ltd.)

Objective: Inhalation of ozone activates central sympathetic-adrenal-medullary and hypothalamic-pituitary-adrenal stress axes. While airway neural networks are known to communicate noxious stimuli to higher brain centers, it is not known to what extent responses generated from pulmonary airways contribute to neuroendocrine activation., Materials and Methods: Unlike inhalational exposures that involve the entire respiratory tract, we employed intratracheal (IT) instillations to expose only pulmonary airways to either soluble metal-rich residual oil fly ash (ROFA) or compressor-generated diesel exhaust particles (C-DEP). Male Wistar-Kyoto rats (12-13 weeks) were IT instilled with either saline, C-DEP or ROFA (5 mg/kg) and necropsied at 4 or 24 hr to assess temporal effects., Results: IT-instillation of particulate matter (PM) induced hyperglycemia as early as 30-min and glucose intolerance when measured at 2 hr post-exposure. We observed PM- and time-specific effects on markers of pulmonary injury/inflammation (ROFA>C-DEP; 24 hr>4hr) as corroborated by increases in lavage fluid injury markers, neutrophils (ROFA>C-DEP), and lymphocytes (ROFA). Increases in lavage fluid pro-inflammatory cytokines differed between C-DEP and ROFA in that C-DEP caused larger increases in TNF-α whereas ROFA caused larger increases in IL-6. No increases in circulating cytokines occurred. At 4 hr, PM impacts on neuroendocrine activation were observed through depletion of circulating leukocytes, increases in adrenaline (ROFA), and decreases in thyroid-stimulating-hormone, T 3 , prolactin, luteinizing-hormone, and testosterone. C-DEP and ROFA both increased lung expression of genes involved in acute stress and inflammatory processes. Moreover, small increases occurred in hypothalamic Fkbp5 , a glucocorticoid-sensitive gene., Conclusion: Respiratory alterations differed between C-DEP and ROFA, with ROFA inducing greater overall lung injury/inflammation; however, both PM induced a similar degree of neuroendocrine activation. These findings demonstrate neuroendocrine activation after pulmonary-only PM exposure, and suggest the involvement of pituitary- and adrenal-derived hormones.

Most studies of the health effects and chemical characterization of the dust resulting from the catastrophic collapse of the World Trade Center (WTC) on September 11, 2001, have focused on the large inorganic fraction of the dust; however, chemical analyses have identified mutagens and carcinogens in the smaller organic fraction. Here, we determined the mutagenicity of the organic fraction of WTC dust in Salmonella. Only 0.74% of the mass of the particulate matter (PM) <53 μm in diameter was extractable organic matter (EOM). Because the EOM was 10 times more mutagenic in TA100 +S9 than in TA98 +S9 and was negative in TA98 -S9, we inferred, respectively, that polycyclic aromatic hydrocarbons (PAHs) played a role in the mutagenicity and not nitroarenes. In TA98 +S9, the mutagenic potency of the EOM (0.1 revertant/μg EOM) was within the range of EOMs from air and combustion emissions. However, the EOM-based mutagenic potency of the particles (0.0007 revertants/μg PM) was 1-2 orders of magnitude lower than values from a review of 50 combustion emissions and various air samples. We calculated that 37 PAHs analyzed previously in WTC EOM were 5.4% of the EOM mass and 0.04% of the PM mass; some air contained 0.3 μg WTC EOM/m 3 (0.02 μg PAHs/m 3 ). Populations exposed to WTC dust have elevated levels of prostate and thyroid cancer but not lung cancer. Our data support earlier estimates that PAH-associated cancer risk among this population, for example, PAH-associated lung cancer, was unlikely to be significantly elevated relative to background PAH exposures., (Published 2022. This article is a U.S. Government work and is in the public domain in the USA. Environmental and Molecular Mutagenesis published by Wiley Periodicals LLC on behalf of Environmental Mutagen Society.)

Background: Fine particulate matter ( PM 2.5 ) has been found to be detrimental to respiratory health of children, but few studies have examined the effects of prenatal PM 2.5 oxidative potential (OP) on lung function in infants and preschool children., Objectives: We estimated the associations of personal exposure to PM 2.5 and OP during pregnancy on offspring objective lung function parameters and compared the strengths of associations between both exposure metrics., Methods: We used data from 356 mother-child pairs from the SEPAGES cohort. PM filters collected twice during a week were analyzed for OP, using the dithiothreitol (DTT) and the ascorbic acid (AA) assays, quantifying the exposure of each pregnant woman. Lung function was assessed with tidal breathing analysis (TBFVL) and nitrogen multiple-breath washout ( N 2 MBW ) test, performed at 6 wk, and airwave oscillometry (AOS) performed at 3 y. Associations of prenatal PM 2.5 mass and OP with lung function parameters were estimated using multiple linear regressions., Results: In neonates, an interquartile (IQR) increase in OP v DTT ( 0.89  nmol / min / m 3 ) was associated with a decrease in functional residual capacity (FRC) measured by N 2 MBW [ β = - 2.26 mL ; 95% confidence interval (CI): - 4.68 , 0.15]. Associations with PM 2.5 showed similar patterns in comparison with OP v DTT but of smaller magnitude. Lung clearance index (LCI) and TBFVL parameters did not show any clear association with the exposures considered. At 3 y, increased frequency-dependent resistance of the lungs ( Rrs 7 - 19 ) from AOS tended to be associated with higher OP v DTT ( β = 0.09  hPa × s / L ; 95% CI: - 0.06 , 0.24) and OP v AA ( IQR = 1.14  nmol / min / m 3 ; β = 0.12  hPa × s / L ; 95% CI: - 0.04 , 0.27) but not with PM 2.5 ( IQR = 6.9   μ g / m 3 ; β = 0.02  hPa × s / L ; 95% CI: - 0.13 , 0.16). Results for FRC and Rrs 7 - 19 remained similar in OP models adjusted on PM 2.5 ., Discussion: Prenatal exposure to OP v DTT was associated with several offspring lung function parameters over time, all related to lung volumes. https://doi.org/10.1289/EHP11155.

Background: The association between long-term particulate matter (PM) exposure and all-cause mortality has been well-documented. However, evidence is still limited from high-exposed cohorts, especially for PM 1 which is smaller while more toxic than other commonly investigated particles. We aimed to examine the potential casual links of long-term PMs exposure with all-cause mortality in high-exposed areas., Methods: A total of 580,757 participants in southern China were enrolled during 2009-2015 and followed up to 2020. The annual average concentration of PM 1 , PM 2.5 , and PM 10 at 1 km 2 spatial resolution was assessed for each residential address through validated spatiotemporal models. We used marginal structural Cox models to estimate the PM-mortality associations which were further stratified by sociodemographic, lifestyle factors and general exposure levels., Results: 37,578 deaths were totally identified during averagely 8.0 years of follow-up. Increased exposure to all 3 PM size fractions were significantly associated with increased risk of all-cause mortality, with hazard ratios (HRs) of 1.042 (95 % confidence interval (CI): 1.037-1.046), 1.031 (95 % CI: 1.028-1.033), and 1.029 (95 % CI: 1.027-1.031) per 1 μg/m 3 increase in PM 1 , PM 2.5 , and PM 10 concentrations, respectively. We observed greater effect estimates among the elderly (age ≥ 65 years), unmarried participants, and those with low education attainment. Additionally, the effect of PM 1 , PM 2.5 , and PM 10 tend to be higher in the low-exposure group than in the general population., Conclusions: We provided comprehensive evidence for the potential causal links betweenlong-term PM exposureand all-cause mortality, and suggested stronger links for PM 1 compared to large particles and among certain vulnerable subgroups., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022. Published by Elsevier Ltd.)