Gestational exposure to ambient air pollution has been linked to adverse birth outcomes. Folic acid (FA) supplementation supports fetal development, but the optimal timing for protective effects remains uncertain. This study aims to determine whether maternal FA supplementation prior to conception modifies the association between gestational air pollution exposure and birthweight-related outcomes in a population where most women also took FA during pregnancy. We analyzed data from 10,579 mother-child pairs from a preconception cohort in Shanghai, China. Ambient concentrations of PM2.5, PM10, NO2, and ozone were estimated at a residential level using spatiotemporal models for the preconception period and each trimester. We assessed whether preconception FA supplementation modified the association between air pollution exposure and birth outcomes, including birthweight, birthweight Z-score, small-for-gestational age (SGA), and low birthweight (LBW). Linear and logistic regression models with interaction terms, as well as stratified analyses by FA supplementation status, were applied. Children's sex-specific associations were also explored. Significant interactions between preconception FA supplementation and air pollution exposures were observed for birthweight and SGA. A 10 mu g/m(3) increase in PM2.5 exposure during pregnancy was associated with a -62.8 g (95% CI: -97.0, -28.6) change in birthweight and a 1.78 (95% CI: 1.16, 2.73) odds ratio for SGA among women without preconception FA supplementation. No such significant associations were found among women receiving preconception FA supplementation, with an estimated change of -1.7 g in birthweight (95% CI: -65.7 to 62.4) and an odds ratio of 0.70 for SGA (95% CI: 0.32-1.44). The protective effect appeared more pronounced for male infants than females. Maternal preconception FA supplementation can attenuate the adverse effects of gestational air pollution exposure on birthweight and SGA risk in women who also received FA supplementation during pregnancy. These findings support the importance of incorporating preconception FA supplementation as a protective measure against gestational exposure to air pollution.

Personal ozone (O3) exposure is often regarded as a more accurate metric of individual-level O3 exposure relevant to health outcomes than outdoor O3 concentration. However, epidemiological studies of personal O3 exposure health effects have been inconsistent, including paradoxical "protective' effects, suggesting the presence of confounding factors yet to be identified. When O3 enters indoors, it reacts with indoor chemicals to form ozone reaction products (ORPs) that may adversely affect cardiorespiratory health. The correlation between personal ORPs and O3 exposure can vary largely across individuals, which leads us to hypothesize ORPs exposure as a confounder for cardiorespiratory effects of personal O3 exposure. We analyzed two complementary datasets from panel studies in 89 healthy adults and in 43 asthmatic children, each measured four times for cardiorespiratory biomarkers and personal exposures to O3, O3 loss (a proxy for ORPs exposure), and PM2.5, respectively. We found personal O3 and O3 loss exposures were highly correlated in the Adults' Study but poorly correlated in the Children's Study. In the Adults' Study, personal O3 exposure was significantly associated with biomarkers of pulmonary oxidative stress, airway inflammation, lung function, systemic oxidative stress, thrombosis, arterial stiffness, and blood pressure. After adjusting for O3 loss, the O3 effects on many of these biomarkers were largely changed in terms of effect sizes and/or statistical significance. However, similar confounding effects were not observed in the Children's Study. These findings may help explain the inconsistencies in the literature regarding the cardiorespiratory effects of personal O3 exposure and highlight the need to account for potential confounding from ORPs in future studies.

Disease burden of ground-level ozone (O3) may be underestimated partly due to unresolved inconsistencies in O3 health effects reported in the literature. Inaccurate exposure assessment, copollutant confounding, and other methodological issues have not fully explained the inconsistencies. To explore an alternative explanation, we hypothesize that acute cardiorespiratory effects of O3 can be modified by longer-term PM2.5 exposure (30 day average), which may predispose people to heightened susceptibility. We tested the hypothesis by using two complementary approaches, including a panel study in healthy adults and a meta-regression analysis of O3 on cardiorespiratory effects reported in the literature. In the panel study, we observed significantly stronger associations between short-term O3 exposure and decreased lung function (FEV1, FEF25-75, and PEF) and increased systolic and diastolic blood pressure under higher PM2.5 exposure levels (>22 μg/m3). These findings were further supported by the meta-regression analysis, which showed that study areas with higher annual PM2.5 concentrations had greater effect sizes of short-term ozone exposure on both FEV1 and blood pressure. Together, our results suggest that higher background PM2.5 concentrations may amplify the acute adverse cardiorespiratory effects of O3, which may partly explain the inconsistent health effect of ozone exposure reported in prior studies.

Malondialdehyde (MDA), a product of lipid peroxidation, is a biomarker of oxidative stress. We investigated the relationship between ozone exposure and MDA in skin wipes in a series of three controlled full-body chamber studies. Twenty-nine volunteers were exposed under different levels of temperature, relative humidity, ozone concentration, clothing coverage, and ventilation rate. One study also examined age-related differences among teenagers, young adults, and seniors. Exposures lasted between 3 and 6 hours. Skin wipes were collected from the volunteers’ forearms before and after exposure and analyzed for MDA and, in some cases, squalene. To characterize baseline variability, skin wipes were collected from 3 unexposed reference persons twice a day for 5 days. Two skin wipes were collected daily from two additional persons; one from each person was subsequently exposed to chamber air, the other was unexposed. This was to distinguish ozone chemistry on collected skin oil from processes occurring directly on skin. Ozone exposure significantly increased MDA on skin. A higher post/pre-exposure MDA ratio was observed with a longer exposure duration. MDA concentrations were an order of magnitude higher on skin-oil-loaded wipes exposed to ozone than on wipes collected from volunteers exposed to ozone. This suggests that ozone reactions with skin lipids can generate MDA even in the absence of an inflammatory process. Inter- and intra-person variability in skin MDA can be attributed to the combined influence of environmental and personal factors, which drive the production and transformation/uptake of MDA on skin. The lack of association between squalene depletion and MDA production suggests an intricate balance between parallel, possibly interconnected, ozone-initiated formation and loss mechanisms responsible for the measured concentrations of the two compounds.

BACKGROUND:Increased placental oxidative stress is frequently documented in pregnant women with adverse maternal outcomes such as preeclampsia. However, environmental determinants of placental oxidative stress remain poorly understood. OBJECTIVES:To determine whether exposure to air pollution and polycyclic aromatic hydrocarbons (PAHs) are associated with placental levels of malondialdehyde (MDA), a biomarker of oxidative stress; to assess whether placental MDA reflects short-term (lag days 0-7) or longer-term (trimester-specific) exposure; and to evaluate whether these associations differ by fetal sex. METHODS:Participants were drawn from the UPSIDE ECHO BABIES cohort (n = 222). Placental MDA concentrations were quantified using an HPLC method. The ambient PM2.5 and NO2 exposures were estimated using high-resolution random forest models. PAH exposure was assessed using trimester-specific maternal blood concentration of PAH-hemoglobin adducts. Associations between exposure and placental MDA were evaluated using multivariable linear regression and distributed lag non-linear models (DLNMs), adjusting for maternal and demographic covariates. RESULTS:A 1-IQR increase in the second trimester, specifically month 5 p.m.2.5, was associated with a 24.8% (95% CI: 3.3-50.7), and 13.7% (95% CI: 0.1-29.16) increase in MDA concentration, respectively. Similarly, the second-trimester hemoglobin adduct of benzo [a]pyrene showed a positive, non-significant association with MDA. Although week-specific DLNM estimates were not statistically significant, the analysis showed that exposure to PM2.5 during gestational weeks 16-20 was positively associated with MDA concentration. When stratified by placenta sex, female placentas had increased MDA in the second trimester associated with PM2.5, and male placentas had increased MDA in the second trimester associated with PAH-hemoglobin adducts. No significant associations were observed for either pollutant when estimated one lag week before birth. No significant associations were observed for NO2 exposure. CONCLUSIONS:Second-trimester PM2.5 exposure was linked to elevated placental MDA concentration at delivery, indicating that placental MDA may reflect longer-term air pollution exposure. These findings emphasize the importance of investigating specific gestational windows through which air pollution induces oxidative injury to the placenta.

Background: Residential radon exposure is a leading risk factor for lung cancer, and climate change may exacerbate this risk by increasing radon entry into homes. In North Carolina (NC), disparities in lung cancer outcomes and low radon awareness disproportionately affect racially and ethnically diverse and low-income populations. However, little is known about how use of conventional address-based sampling (ABS) compares with community-engaged recruitment strategies for enrolling historically underrepresented populations into such research. Community-engaged approaches are used to improve participation in environmental health research, yet few studies compare their effectiveness with traditional approaches in NC. This manuscript compares recruitment outcomes between ABS and community-engaged approaches within the CLOVER study to address this gap. Materials and Methods: The Climate Impact on Lung Cancer via Exposure to Radon (CLOVER) study is a cross-sectional study examining climate-impacted radon exposure and lung cancer risk in NC. Participants were recruited using either ABS through a commercial address database or targeted community-engaged approaches implemented through partnerships with community organizations and culturally responsive, in-person outreach events. After providing informed consent, participants completed a household survey and a 7-day home radon test. Recruitment outcomes—consent, survey completion, and radon test return—were stratified by race and ethnicity and compared across strategies. Results: Of 236 consented participants, community-engaged recruitment enrolled a higher proportion of Non-Hispanic (NH) Black, Hispanic/Latino, and American Indian participants than ABS (57.3% vs. 41.9%). Community-engaged recruitment also had a higher consent rate than ABS (10.2% vs. 1.3%). Of the 145 participants who completed the survey, ABS participants completed surveys at a higher rate than community-engaged participants (73.3% vs. 54.7%), while of the 86 who returned the radon test kits, community-engaged participants did so at twice the rate of ABS participants (44.7% vs. 22.1%). Conclusions: Community-engaged recruitment enrolled a more racially and ethnically diverse sample and achieved higher consent and return rates than ABS, though ABS participants completed surveys at a higher rate. These findings highlight the importance of community partnerships and in-person recruitment strategies to improve participation of historically underrepresented populations in environmental health research and support equitable approaches to radon mitigation and lung cancer prevention.

BACKGROUND:Air pollution (AP) is a known cause of lung cancer (LC); growing evidence links AP with breast cancer (BC) risk. Many epidemiological studies analyze PM2.5, though AP is a complex mixture of many pollutants. New metrics are necessary to fully represent the carcinogenic constituents of AP. Therefore, we aimed to develop cancer-specific metrics to determine where and what types of AP drive incident cancers. METHODS:We combined databases of AP across the continental US in 2005-2020, including the Risk-Screening Environmental Indicators (RSEI) model and CACES land-use regression-estimated concentrations of criteria air pollutants (CAP). We joined AP concentrations at census tracts and employed meta-analytic cancer-specific risk estimates to weight the CAP and produce a set of combined metrics (AP for BC (APBC), AP for LC (APLC)) from numerous sources. RESULTS:APBC and APLC exhibited positive skew, with certain tracts having values approximately an order of magnitude above the mean, and were typically highest in large cities and along transportation corridors. Relative to RSEI, APBC and APLC were larger in certain regions including Los Angeles and New York City. Both varied with respect to race, ethnicity, and housing and exhibited significant spatial clustering. CONCLUSION:We developed novel AP metrics incorporating emissions from industrial facilities, along transportation corridors, and from power plants to characterize cancer-specific risks. IMPACT:Future research will use these metrics that represent multiple simultaneous sources of AP to identify specific constituents of the AP exposome relevant for BC and LC, informing strategies to reduce their incidence and disparities.

When ozone (O3) enters indoor environments, a substantial portion reacts with indoor chemicals, producing ozone reaction products (ORPs) that have shown adverse cardiorespiratory effects. Some ORPs partition to PM2.5 that can carry these species to the deep lung and may even enter the circulatory system. High-efficiency particulate air (HEPA) filtration has been shown to reduce indoor PM2.5 levels and may decrease the amount of ORPs reaching the deep lung. We, hence, hypothesized that HEPA filtration could mitigate ORPs' cardiorespiratory health effects. We analyzed data from an intervention study with 84 participants, 50 receiving indoor HEPA filtration and 34 serving as controls. Each participant underwent two assessments of cardiorespiratory biomarkers. We measured personal exposures to PM2.5, O3, and O3 loss (a proxy for ORPs exposure). Among participants without HEPA filtration, O3 loss was significantly associated with adverse changes in biomarkers of systemic oxidative stress, vasoconstriction, thrombosis, airway inflammation, and pulmonary oxidative stress. In stark contrast, no significant adverse associations between O3 loss and these biomarkers were observed in participants receiving HEPA filtration. These findings suggest that HEPA filtration, in addition to being effective in reducing PM2.5 exposure, may be useful in mitigating the harmful health effects of ORPs exposure.

Environmental epidemiological studies often use both station-monitored and personal air pollutant exposures, which frequently yield different results. We aimed to identify key considerations when choosing between these measures. In a panel study of 37 college students assessed six times across three seasons for cardiorespiratory outcomes, personal PM2.5 and O3 exposures were monitored for 5 days with wearable sensors before each health assessment, alongside concurrent measurements from nearby monitoring stations. The association between station-monitored and personal concentrations was stronger for PM2.5 (regression coefficient: 0.51 ± 0.16) than for O3 (regression coefficient: 0.19 ± 0.15). Both station-monitored and personal PM2.5 were associated with decreased forced expiratory volume in the first second (FEV1), forced vital capacity (FVC), and increased fractional exhaled nitric oxide (FeNO). In contrast, only station-monitored O3 was associated with decreased FEV1, FVC, increased FeNO, and worsening augmentation index (AI) and blood pressure. Personal O3 showed mostly null associations or even “seemingly beneficial” associations with AI, FEV1, and FVC. These findings suggest station-monitored PM2.5 can serve as a reasonable proxy for personal exposure in studies with minimal indoor PM2.5 sources. However, this may be unsuitable for O3, given its high spatial variability and potential differences in exposure to ozone-derived reaction products.

The wildland-urban interface (WUI) fires have adverse effects on both physical and mental health. However, early biosignals changes related to fires are not well understood. Digital wearables can capture real-time changes in physiological stress and activity patterns, providing insight into the mechanisms of health effects of WUI fires and identifying vulnerable populations during and after WUI fires. This study aimed to assess the immediate and sustained changes in physical activity patterns and physiological stress markers during and after the 2025 Los Angeles wildfires. We conducted a longitudinal study of 15 older adults (mean age 73.2 years) during the 2025 Eaton Fire in Los Angeles, using the digital Oura Ring (Gen 3) continuously. Data were collected at baseline (Dec 9th, 2024 to Jan 6th, 2025), during the fire (Jan 7th, 2025 to Jan 12th, 2025), and after the fire (Jan 13th, 2025 to Jan 27th, 2025). Daily activity patterns (physical activity and sleep duration) and physiological stress (sleep heart rate, heart rate variability, sleep fragmentation, and breath rate) were collected, and linear mixed-effects models were used to investigate how these biosignals changed and how evacuation alerts impacted these changes. During the fire, six out of fifteen participants received evacuation alerts. We observed a 41-minute increase in sedentary time ( P = .007), a 34 min reduction in sleep duration ( P = .002), and a 0.4 BPM increase in sleep breath rate ( P = .009). Although activity patterns returned to baseline post-fire, markers of physiological stress, including sleep heart rate and breath rate, remained elevated. Among participants who received evacuation alerts, the immediate and prolonged impacts are larger. The changes in activity patterns and increases in physiological stress during and after the 2025 Los Angeles wildfire in this cohort can indicate potential health effects. Digital bio-signals may serve as early indicators of adverse health outcomes following a wildfire.

OBJECTIVE:We previously documented that exposure to a spectrum of elements is associated with autism spectrum disorder (ASD). However, there is a lack of mechanistic understanding as to how elemental mixtures contribute to the ASD development. MATERIALS AND METHODS:Serum and urinary concentrations of 26 elements and six biomarkers of ASD-relevant pathophysiologic pathways including serum HIPK 2, serum p53 protein, urine malondialdehyde (MDA), urine 8-OHdG, serum melatonin, and urine carnitine, were measured in 21 ASD cases and 21 age-matched healthy controls of children aged 6-12 years. The Mann-Whitney U test was used to compare the differences in serum elemental levels between ASD and control groups. A principal component analysis (PCA) was used to reduce the dimensionality of multiple elements into uncorrelated predictors that may capture shared patterns. Associations of PC scores with ASD risk or pathway-specific biomarkers were examined using logistic or linear regressions, respectively. Robust linear regressions were conducted to explore the association between serum and urinary elements. RESULTS:We observed significantly higher serum levels of chromium, titanium, lithium, vanadium, calcium, cobalt, magnesium, and arsenic, but lower levels of cadmium and palladium in ASD children. We identified four PCs. PC1 reflects a mixture of 14 elements that were significantly elevated in ASD. PC2 reflects a mixture of elements that were significantly affected by urinary excretion. PC3 reflects a mixture of 5 elements within the 14 elements in PC1. PC4 reflects barium and palladium, both lower in ASD children. PC1 and PC2 were differentially associated with pathway-specific biomarkers. Each interquartile range (IQR) increase in PC1 was associated with increases in HIPK2 (12.96 %, 95 % CI: 3.98 %, 21.94 %) and p53 (8.34 %, 95 % CI: 0.30 %, 16.38 %), and a decrease in urinary carnitine (-24.85 %, 95 % CI: -46.36 %, -3.34 %). An IQR increase in PC2 was associated with increased urinary carnitine by 19.27 % (95 % CI: 3.08 %, 35.47 %). PC4 was not associated with any biomarkers. No PCs were associated with oxidative stress biomarkers of 8-OHdG or MDA. Additionally, increased excretion of essential elements (e.g. phosphorus, calcium, zinc) and the accumulation of metals with higher molecular weight (lead, tin, molybdenum, palladium, and bismuth) were observed in ASD group. CONCLUSIONS:Increased levels of element mixtures of chromium, calcium, magnesium, arsenic, and antimony were associated with pro-apoptotic increases in HIPK2 and p53, whereas increased levels of cobalt, lead, and cadmium were associated with carnitine excretion. Increased urinary excretion of essential elements may contribute to ASD risk through modulating blood elemental levels. The role of oxidative stress was not observed.

Air quality has improved while the lifestyle of children has changed substantially over the past 2 decades in four Chinese cities. It is unknown how these changes affected the lung function of children. We analyzed data collected in 1995-1996 and 2017-2018. In each period, >2000 children 6-13 years were measured for lung function and surveyed for behavioral, residential, and health conditions. Monitored and modeled data for ambient air pollution were obtained. Age- and covariate-adjusted FVC and FEV1 values were lower, and the proportions of children with low FVC and FEV1 were greater in the later period than in the earlier period, while PM2.5, PM10, SO2, NO x , and O3 levels changed by -42.8 μg/m3 (95% CI, -67.3, -18.6 mg/m3), -65.1 μg/m3 (-113.5, -16.7 mg/m3), -34.6 ppb (-69.2, 0.0 ppb), -27.5 ppb (-60.7, 5.7 ppb), and 1.5 ppb (-4.2, 7.1 ppb), respectively. A 4 ppb O3 increase was associated with lower FVC by 105 mL (95% CI: 30, 180 mL) in boys and 76 mL (17, 135 mL) in girls. A generational decline in the lung function of children in the 4 Chinese cities has significant public health ramifications. Our findings imply that the reduction of ambient air pollutant concentrations from the 1995-1996 levels to the 2017-2018 levels were not sufficient to make lung function improvements. Risk factors that were absent or not as prominent in the earlier period may be responsible for lowered lung function during the later period.

Gestational air pollution exposure was associated with childhood obesity. However, little is known about the effect of air pollution exposure during the preconception period, a critical window when environmental exposures may affect body growth trajectory and increase obesity risk. We conducted a population-based prospective cohort study of preconception women and their newborn children followed until 2 years old from metropolitan Shanghai, China to investigate the impact of preconception air pollution on childhood weight and body mass index (BMI) growth trajectories. Exposures to PM2.5, PM10, and NO2 during 3 months before conception and each trimester of pregnancy were estimated using high-resolution spatiotemporal models matched at residential addresses. Children's weight and BMI were assessed postnatally every three months. Multivariate and longitudinal models with piecewise linear mixed effects were used to examine the relationship between preconception air pollution and child growth trajectories of weight, BMI, and standardized BMI (BMIZ). The study population comprised 26,714 women in the baseline enrolled in preconception clinics and 5,834 children reached 2 years included in the analysis with 34,398 longitudinal weight and height measurements. One interquartile range (IQR) increase in preconception PM2.5 (16.2 mu g/m3) was associated with a 0.078 (95% confidence interval (CI): 0.002-0.154, p = 0.04) increase in attained BMIZ and 1 IQR increase of PM10 (21.1 mu g/m3) were associated with an 0.093 (95% CI: 0.002-0.184, p = 0.04) kg/m2 increase in attained BMI, respectively, at the age of two years, after controlling for individual covariates and gestational air pollution exposure. Higher weight, BMI, and BMIZ growth rates during 6-24 months of life were also associated with higher preconception NO2 and PM exposure. Males and children born to mothers less than 35 years old or with overweight/obesity status were more affected by preconception air pollution exposure on weight growth. The 3-month preconception period was a critical time window for air pollution exposure.

Previous studies documented increased nitrative stress and susceptibility to air pollution among individuals with chronic inflammatory conditions. This study examines the role of anti-inflammatory and cardioprotective nitrated fatty acids (i.e., NO2-cLA) in chronic obstructive pulmonary disease (COPD)'s and ischemic heart disease (IHD)'s susceptibility to air pollution. In a randomized crossover study, 40 healthy, 40 COPD, and 39 IHD adults underwent a 2 h walk in a more polluted street or a less polluted park. We measured urinary NO2-cLA before and 24 h after the walk, as well as respiratory inflammatory biomarkers, lung function, airway resistance, and arterial stiffness. Baseline NO2-cLA levels were 2.56 (95% CI: 1.20-5.43)-fold higher among COPD participants than healthy participants, which can be explained by higher fractional exhaled nitric oxide and sputum myeloperoxidase levels. Among COPD but not healthy or IHD participants, the street walk, compared to park, led to a 57.7% (95% CI: 7.6-80.6%) decrease in NO2-cLA levels and sputum biomarker changes indicative of decreased neutrophil inflammation and proresolving responses. Decreased NO2-cLA levels were associated with exposure to black carbon and ultrafine particles and worsened lung function and arterial stiffness. Taken together, nitrated fatty acids partially mediate COPD patients' cardiorespiratory responses to air pollution, explaining their susceptibility.

Urinary hydroxylated-polycyclic aromatic hydrocarbons (PAHs), with half-life less than 2 days, are established biomarkers of short-term exposure to PAHs, a ubiquitous constituent of air pollution mixture. In this study, we explore the use of PAHs-hemoglobin adducts as biomarkers of longer-term exposure to air pollution by leveraging an extant resource of blood samples collected from 235 pregnant women residing in Rochester, NY. We measured red blood cells for benzo[a]pyrene-tetrols (BaPT) and phenanthrene-tetrols (PHET), both of which are hydrolysis products of PAH-hemoglobin adduct. We utilized previously estimated PM2.5 and NO2 concentrations within the 1 km2 grid surrounding each participant's residence, calculated for up to 20 weeks before the blood collection date. Associations between PAHs tetrols and cumulative exposures to ambient PM2.5 or NO2 over different time periods were examined using a linear mixed-effects model with participant-specific random intercepts adjusting for season, gestation age, maternal age, maternal income level, and pre-pregnancy BMI. We observed positive associations between PHET concentration and cumulative PM2.5 exposure over gestational weeks 12-17, and between BaPT concentration and cumulative PM2.5 exposure over gestational weeks 3-16 prior to sample collection. Each interquartile range (IQR) increase in 14 week PM2.5 exposure (1.26 μg m-3) was associated with a 9.02% (95% CI: 0.30%, 17.7%) increase in PHET and a 12.8% (95% CI: 1.09%, 23.5%) increase in BaPT levels. In contrast, no associations were observed between either biomarker and cumulative NO2 exposures. These findings underscore the potential of PAH-hemoglobin adducts as longer-term (weeks to 4 months) exposure biomarkers of ambient PM2.5.

BACKGROUND:Energy burden, defined as the inability to afford residential energy consumption, is a pressing public health issue globally and in the U.S. However, its impact on asthma remains largely unknown. OBJECTIVES:This study aims to examine the association between energy burden and asthma prevalence in U.S. areas and to evaluate whether the association differs by climate zone. METHODS:We merged the energy burden variables at census tract from Low-Income Energy Affordability Data (LEAD) and asthma prevalence from CDC PLACES data. Using the data from five nationally representative datasets including LEAD and CDC, we employed multilevel random intercept model to estimate the association between energy burden and asthma prevalence, controlling for the socioeconomic status and housing characteristics of census tracts across the largest 500 US cities. Further, we conducted a stratification analysis to examine whether this association varies by climate region in the U.S. MAIN RESULTS:Energy burden at the census tract level is significantly and independently associated with asthma prevalence across U.S. census tracts. Census tracts with high energy burdens exhibited a 0.803 % higher asthma prevalence [95 % Confidence Interval (CI): 0.763, 0.834] compared to those with low energy burdens. The significant and positive association between high energy burden and asthma prevalence remains in all climate regions, respectively, after adjusting for socioeconomic and housing characteristics. CONCLUSION:The findings suggest that high energy burden is an emerging environmental determinant of respiratory health in the U.S.

Ozone (O3) is a toxic air pollutant that causes pulmonary inflammation, neutrophil recruitment, and lung injury. Part of the inflammatory response to O3 includes altered expression of formyl peptide receptor 2 (ALX/FPR2), a G protein-coupled receptor expressed primarily in immune cells. ALX/FPR2 is considered either anti-inflammatory/proresolving or proinflammatory depending on its ligands, which include lipoxin A4 or serum amyloid A (SAA). While the anti-inflammatory/proresolving lipoxin A4 ligand has been well studied, there remains a significant knowledge gap in the interaction between proinflammatory SAA and ALX/FPR2. To date, SAA has been shown to increase neutrophil recruitment through ALX/FPR2 and is increased systemically after O3 exposure. However, it is unclear if pulmonary SAA signals through ALX/FPR2 during the O3-induced inflammatory response. We hypothesized that ALX/FPR2-SAA signaling is required to initiate neutrophil recruitment to the lungs following O3 exposure. To test this hypothesis, ALX/FPR2 wild type (FPR2+/+) or knockout (FPR2-/-) mice were exposed to filtered air (FA) or 1 ppm O3 for 3 h. Pulmonary inflammation was assessed 6, 24, and 48 h following O3 exposure. FPR2-/- mice exhibited impaired neutrophil recruitment at 6 and 24 h after O3 exposure. In addition, FPR2-/- mouse pulmonary SAA expression was significantly increased after O3 exposure compared to FPR2+/+ mice. FPR2+/+ mice dosed with SAA via oropharyngeal aspiration had increased pulmonary neutrophils, while neutrophils were not increased in FPR2-/- mice. Taken together, these data indicate that ALX/FPR2 may contribute to SAA-induced pulmonary neutrophilia following O3 exposure.

BACKGROUND:Traffic pollution exposure has been associated with adverse cardiovascular outcomes, but determinants of individual susceptibility remain unclear. To explore whether disease status modifies traffic-related cardiac responses and to examine the cardioprotective role of nitro linoleic acids. METHODS:In a crossover study, 39 chronic obstructive pulmonary disease (COPD) patients, 38 ischemic heart disease (IHD) patients, and 39 healthy participants walked for two hours on traffic-congested Oxford Street and in traffic-free Hyde Park, in random order, on separate days. Cardiac electrical activity, including heart rate, heart rate variability (HRV), QT interval, and ST-segment changes, was continuously monitored for 24 h. At 24 h following the walk, a urine void was collected and analyzed for nitro linoleic acid NO2-cLA (a cardioprotective marker). Mixed-effect models assessed pollution-related cardiac changes. RESULTS:In reference to walking in the park, participants following the street walk exhibited adverse cardiac changes, including increased heart rate, decreased HRV, shortened QT interval, and elevated ST-segment, with larger changes in some parameters observed in COPD participants, though between-group differences were not statistically significant. Among COPD participants, the cardiac effects were more pronounced in those who did not use inhaler medications than in those who used them. NO2-cLA concentrations were significantly lower in COPD participants after the street walk compared to after the park walk (0.0189 vs 0.0323 μg/g creatinine, p = 0.03). Increasing NO2-cLA concentrations were associated with increased pNN50 and QTc and decreased ST elevation. Among measured pollutants, ultrafine particles and black carbon were most elevated in the street and showed the strongest cardiac effects. CONCLUSIONS:Although between-group comparisons were not statistically significant, COPD patients showed numerically larger electrophysiological changes and reductions in NO2-cLA levels following short-term exposure to traffic pollution. Use of inhaler medications lessened these effects, suggesting a potential role of medication use in modifying pollution responses.