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Importance: Socioeconomically disadvantaged subpopulations are more vulnerable to fine particulate matter (PM2.5) exposure. However, as prior studies focused on individual-level socioeconomic characteristics, how contextual deprivation modifies the association of PM2.5 exposure with cardiovascular health remains unclear., Objective: To assess disparities in PM2.5 exposure association with cardiovascular disease among subpopulations defined by different socioeconomic characteristics., Design, Setting, and Participants: This cohort study used longitudinal data on participants with electronic health records (EHRs) from the All of Us Research Program between calendar years 2016 and 2022. Statistical analysis was performed from September 25, 2023, through February 23, 2024., Exposure: Satellite-derived 5-year mean PM2.5 exposure at the 3-digit zip code level according to participants' residential address., Main Outcome and Measures: Incident myocardial infarction (MI) and stroke were obtained from the EHRs. Stratified Cox proportional hazards regression models were used to estimate the hazard ratio (HR) between PM2.5 exposure and incident MI or stroke. We evaluated subpopulations defined by 3 socioeconomic characteristics: contextual deprivation (less deprived, more deprived), annual household income (≥$50 000, <$50 000), and race and ethnicity (non-Hispanic Black, non-Hispanic White). We calculated the ratio of HRs (RHR) to quantify disparities between these subpopulations., Results: A total of 210 554 participants were analyzed (40% age >60 years; 59.4% female; 16.7% Hispanic, 19.4% Non-Hispanic Black, 56.1% Non-Hispanic White, 7.9% other [American Indian, Asian, more than 1 race and ethnicity]), among whom 954 MI and 1407 stroke cases were identified. Higher PM2.5 levels were associated with higher MI and stroke risks. However, disadvantaged groups (more deprived, income <$50 000 per year, Black race) were more vulnerable to high PM2.5 levels. The disparities were most pronounced between groups defined by contextual deprivation. For instance, increasing PM2.5 from 6 to 10 μg/m3, the HR for stroke was 1.13 (95% CI, 0.85-1.51) in the less-deprived vs 2.57 (95% CI, 2.06-3.21) in the more-deprived cohort; 1.46 (95% CI, 1.07-2.01) in the $50 000 or more per year vs 2.27 (95% CI, 1.73-2.97) in the under $50 000 per year cohort; and 1.70 (95% CI, 1.35-2.16) in White individuals vs 2.76 (95% CI, 1.89-4.02) in Black individuals. The RHR was highest for contextual deprivation (2.27; 95% CI, 1.59-3.24), compared with income (1.55; 95% CI, 1.05-2.29) and race and ethnicity (1.62; 95% CI, 1.02-2.58)., Conclusions and Relevance: In this cohort study, while individual race and ethnicity and income remained crucial in the adverse association of PM2.5 with cardiovascular risks, contextual deprivation was a more robust socioeconomic characteristic modifying the association of PM2.5 exposure.

Background: An estimated 3 billion people, largely in low- and middle-income countries, rely on unclean fuels for cooking, heating, and lighting to meet household energy needs. The resulting exposure to household air pollution (HAP) is a leading cause of pneumonia, chronic lung disease, and other adverse health effects. In the last decade, randomized controlled trials of clean cooking interventions to reduce HAP have been conducted. We aim to provide guidance on how to interpret the findings of these trials and how they should inform policy makers and practitioners. Methods: We assembled a multidisciplinary working group of international researchers, public health practitioners, and policymakers with expertise in household air pollution from within academia, the American Thoracic Society, funders, nongovernmental organizations, and global organizations, including the World Bank and the World Health Organization. We performed a literature search, convened four sessions via web conference, and developed consensus conclusions and recommendations via the Delphi method. Results: The committee reached consensus on 14 conclusions and recommendations. Although some trials using cleaner-burning biomass stoves or cleaner-cooking fuels have reduced HAP exposure, the committee was divided (with 55% saying no and 45% saying yes) on whether the studied interventions improved measured health outcomes. Conclusions: HAP is associated with adverse health effects in observational studies. However, it remains unclear which household energy interventions reduce exposure, improve health, can be scaled, and are sustainable. Researchers should engage with policy makers and practitioners working to scale cleaner energy solutions to understand and address their information needs.

Background: Exposure to air pollutants and other environmental factors increases the risk of adverse pregnancy outcomes. There is growing evidence that adverse outcomes related to air pollution disproportionately affect racial and ethnic minorities. The objective of this paper is to explore the importance of race as a risk factor for air pollution-related poor pregnancy outcomes., Methods: Studies investigating the effects of exposure to air pollution on pregnancy outcomes by race were reviewed. A manual search was conducted to identify missing studies. Studies that did not compare pregnancy outcomes among two or more racial groups were excluded. Pregnancy outcomes included preterm births, small for gestational age, low birth weight, and stillbirths., Results: A total of 124 articles explored race and air pollution as risk factors for poor pregnancy outcome. Thirteen percent of these (n=16) specifically compared pregnancy outcomes among two or more racial groups. Findings across all reviewed articles showed more adverse pregnancy outcomes (preterm birth, small for gestational age, low birth weight, and stillbirths) related to exposure to air pollution among Blacks and Hispanics than among non-Hispanic Whites., Conclusion: Evidence support our general understanding of the impact of air pollution on birth outcomes and, specifically, of disparities in exposure to air pollution and birth outcomes for infants born to Black and Hispanic mothers. The factors driving these disparities are multifactorial, mostly social, and economic factors. Reducing or eliminating these disparities require interventions at individual, community, state, and national level., (© 2023. The Author(s).)

Background: Ambient fine particulate matter (PM 2.5 ) exposure has been related to cardiometabolic diseases, but the underlying biological pathways remain unclear at the population level., Objective: To investigate the effect of PM 2.5 exposure on changes in multiple cardiometabolic biomarkers across different exposure durations., Method: Data from a prospective cohort study were analyzed. Ten cardiometabolic biomarkers were measured, including ghrelin, resistin, leptin, C-peptide, creatine kinase myocardial band (CK-MB), monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor alpha (TNF-alpha), N-terminal pro B-type natriuretic peptide (NT-proBNP), troponin, and interleukin-6 (IL-6). PM 2.5 levels across exposure durations from 1 to 36 months were assessed. Mixed effect model was used to estimate changes in biomarker levels against 1 μg/m 3 increase in PM 2.5 level across different exposure durations., Results: Totally, 641 participants were included. The average PM 2.5 exposure level was 9 μg/m 3 . PM 2.5 exposure was inversely associated with ghrelin, and positively associated with all other biomarkers. The magnitudes of these associations were duration-sensitive and exhibited a U-shaped or inverted-U-shaped trend. For example, the association of resistin were β = 0.05 (95% CI: 0.00, 0.09) for 1-month duration, strengthened to β = 0.27 (95% CI: 0.14, 0.41) for 13-month duration, and weakened to β = 0.12 (95% CI: -0.03, 0.26) for 24-month duration. Similar patterns were observed for other biomarkers except for CK-MB, of which the association direction switched from negative to positive as the duration increased. Resistin, leptin, MCP-1, TNF-alpha, and troponin had a sensitive exposure duration of nearly 12 months. Ghrelin and C-peptide were more sensitive to longer-term exposure (>18 months), while NT-proBNP and IL-6 were more sensitive to shorter-term exposure (<6 months)., Conclusion: PM 2.5 exposure was associated with elevated levels in cardiometabolic biomarkers related to insulin resistance, inflammation, and heart injury. The magnitudes of these associations depended on the exposure duration. The most sensitive exposure durations of different biomarkers varied., 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.)

Competing Interests: We declare no competing interests.

Rationale: Studies identify prenatal household air pollution (HAP) exposure and maternal psychological distress (PMPD) as independent factors contributing to gestational ill-health and adverse birth outcomes., Objective: We investigated the impact of PMPD on fetal biometric parameters (FBP) in HAP-exposed pregnant Nigerian women., Methods: The randomized controlled trial (RCT; ClinicalTrials.gov NCT02394574) investigated effects of HAP exposure in pregnant Nigerian women (n = 324), who customarily cooked with polluting fuels (firewood or kerosene). Half of the women (intervention group) were given CleanCook ethanol stoves to use for 156 days during the study. Once a month, all women were administered an abridged version of the SF-12v2TM health-related quality of life questionnaire to assess psychological distress. Using mixed effects linear regression models, adjusted for relevant covariates, we analyzed associations between the women's exposure to PM2·5 (particulate matter with an aerodynamic diameter<2·5 microns) from HAP, their PMPD scores, and FBP (ultrasound estimated fetal weight [UEFW], head circumference [HC], abdominal circumference [AC], femur length [FL], biparietal diameter [BPD], estimated gestational age [GA] and intrauterine growth restriction [IUGR]), and birth anthropometric measures (birth weight [BW] and birth length [BL])., Results: PMPD negatively impacted UEFW, HC, FL, BPD and BL (p<0·05). Controls (kerosene/firewood users) experienced significantly higher PMPD compared with ethanol-stove users (p<0·05). The mediation analysis revealed that the proportion of the outcome (fetal biometrics, birth anthropometrics, IUGR and GA), which can be explained via PMPD by groups (intervention vs. control) after adjusting for confounding variables was 6·2% (0·062). No significant correlation was observed between levels of PM2.5 exposure and PMPD scores., Conclusions: PMPD was an independent mediator of adverse fetal biometric parameters in pregnant women, who were exposed to HAP from burning of firewood/kerosene. Formulating preventative measures to alleviate maternal distress during pregnancy and reducing exposure to HAP is important from public health perspectives., Competing Interests: The authors have declared that no competing interests exist.

Rationale: Lung function is adversely affected by exposure to household air pollution (HAP). Studies investigating the impact of prenatal and postnatal HAP exposure on early childhood lung development are limited, especially from Sub-Saharan Africa., Objective: We used oscillometry to investigate the impact on lung function of prenatal and postnatal HAP exposure of children born to Nigerian women who participated in a randomized controlled cookstove intervention trial., Methods: We performed oscillometric measurements (R: airway resistance; X: airway reactance; Fres: resonant frequency; AX: reactance area) in 223 children starting at age of 2 years (ethanol stove, n = 113; firewood/kerosene, n = 110). Personal exposure monitoring assessed mothers' prenatal exposure to particulate matter less than 2.5 μm in aerodynamic diameter (PM 2.5 ). Postnatal HAP exposure was measured by determining household PM 2.5 levels. We employed linear regression analysis to examine the association of prenatal and postnatal HAP exposures with children's lung function. Models were adjusted for age, gender, weight, height, group (intervention or control), birthweight and gestational age., Results: Mean age of the children was 2.9 years (standard deviation = 0.3); 120 were boys (53.8%) and 103 were girls (46.2%). Higher postnatal PM 2.5 exposures were significantly associated with higher airway reactance at 5 Hz (X5 Hz; p = 0.04) in adjusted models. There were no significant associations between prenatal or postnatal PM 2.5 exposure levels and other oscillometry parameters in adjusted regression analysis., Conclusions: This is the first study to use oscillometry to explore the relationship between HAP exposure and lung function in children as young as 2 years. The findings provide some evidence that increased postnatal HAP exposure may result in poorer lung function in children, although larger studies are needed to confirm observed results. This study indicates that oscillometry is a low-cost and effective method to determine lung function in early childhood., 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 © 2020 The Authors. Published by Elsevier B.V. All rights reserved.)

Background: Maternal exposure to ambient air pollution affects placental growth markers., Objectives: Investigate impact of household air pollution (HAP) on placental growth markers., Methods: Two groups of pregnant women were identified: firewood/kerosene stove-users (A, n=33) and bioethanol stove-users (B, n=44) that participated in a randomized control trial in Ibadan, Nigeria. A third group of non-smoking and presumed liquefied petroleum gas-using Chicago women (C, n=19) were included in this exploratory pilot to assess for possible differences between similar racial groups. Levels of placental growth factor (PlGF) and soluble fms-like tyrosine kinase 1 (sFlt-1) were measured in maternal and cord plasma using ELISA., Results: Maternal and cord blood sFlt-1 and PlGF did not differ significantly between women of groups A and B. Nevertheless, both groups differed significantly from the Chicago group in that group A women had lower maternal sFlt-1 (1372.50 vs. 3194.19) but higher PlGF (1607.87 vs. 442.80), and higher cord blood sFlt-1 (2925.02 vs. 107.53) and PlGF (223.68 vs. 6.92), all p≤0.001. Group B showed similar trends (all p≤0.002). Maternal PlGF levels were positively correlated to minutes of HAP exposure when PM 2.5 concentration was above 100μg/m 3 in Nigerian women., Conclusions: Maternal levels of PlGF and cord blood levels of sFlt-1 and PlGF in Nigerian women with varying HAP exposures were significantly higher than Chicago-based women who had no presumed HAP exposure. It suggests that in-utero exposure to HAP influenced levels of angiogenic factors involved in normal placentation and growth and could represent compensation for pollutants exposure to preserve fetal viability., (Copyright © 2017 The Authors. Published by Elsevier B.V. All rights reserved.)

Background: Low birthweight, intrauterine growth restriction (IUGR) and perinatal mortality have been associated with air pollution. However, intervention studies that use ultrasound measurements to assess the effects of household air pollution (HAP) on fetal biometric parameters (FBP) are rare. We investigated the effect of a cookstove intervention on FBP and IUGR in a randomized controlled trial (RCT) cohort of HAP-exposed pregnant Nigerian women.Methods: We recruited 324 women early in the second trimester of pregnancy. Between 16 and 18 weeks, we randomized them to either continue cooking with firewood/kerosene (control group) or receive a CleanCook stove and ethanol fuel (intervention group). We measured fetal biparietal diameter (BPD), head circumference (HC), femur length (FL), abdominal circumference (AC) and ultrasound-estimated fetal weight (U-EFW) in the second and third trimesters. The women were clinically followed up at six regular time points during their pregnancies. Once during the women's second trimester and once during the third, we made 72-h continuous measurements of their personal exposures to particulate matter having aerodynamic diameter < 2.5 μm (PM2.5). We adopted a modified intent-to-treat approach for the analysis. Differences between the intervention and control groups on impact of HAP on fetal growth trajectories were analyzed using mixed effects regression models.Results: There were no significant differences in fetal growth trajectories between the intervention and control groups.Conclusions: Larger studies in a setting of low ambient air pollution are required to further investigate the effect of transitioning to a cleaner fuel such as ethanol on intrauterine growth.Trial Registration: ClinicalTrials.gov NCT02394574 ; September 2012. [ABSTRACT FROM AUTHOR]

Background Household air pollution (HAP) is associated with adverse pregnancy outcomes. Objectives Investigate impact of in-utero HAP exposure on placental development and chronic hypoxia. Methods Markers of chronic placental hypoxia [Hofbauer cells (HBC), syncytial knots (SK), chorionic vascular density (cVD) and hypoxia-inducible factor (HIF)] were stained by hematoxylin-eosin and/or immunohistochemically in placenta samples collected from firewood −/kerosene-users (A, n = 16), and ethanol-users (B, n = 20) that participated in a randomized controlled intervention trial in Ibadan, Nigeria. A third group of non-smoking and presumed natural gas-using Chicago women (C, n = 12) were included in this exploratory pilot to assess for possible differences in placenta histology between similar racial groups. All patients had uncomplicated pregnancies and delivered at term. Results HBC, SK and cVD were significantly increased among firewood-/kerosene-users compared to ethanol-users and natural gas-using Chicago women (HBC medians 5.5, 3.5, and 2.0, respectively; SK means 55.6, 41.8 and 30.1; cVD means 8.8, 6.2, and 5.2; all p < 0.01). HIF expression was significantly higher in Group A compared to B and C (all p < 0.001). Conclusions In-utero exposure to HAP is associated with pathologic changes and HIF expression consistent with chronic hypoxia in placenta of firewood/kerosene-users compared to ethanol-users with less HAP exposure and Chicago women with no presumed HAP exposure. Presence of chronic hypoxic signature in placenta of women exposed to HAP has implications for adverse pregnancy complications and future growth and development of the young children. Future larger studies need to focus on HAP exposure and placental disorders like preeclampsia and long-term health impact of in-utero exposure to HAP. [ABSTRACT FROM AUTHOR]

Background Household air pollution (HAP) exposure has been linked to adverse pregnancy outcomes. Objectives A randomized controlled trial was undertaken in Ibadan, Nigeria to determine the impact of cooking with ethanol on pregnancy outcomes. Methods Three-hundred-twenty-four pregnant women were randomized to either the control (continued cooking using kerosene/firewood stove, n = 162) or intervention group (received ethanol stove, n = 162). Primary outcome variables were birthweight, preterm delivery, intrauterine growth restriction (IUGR), and occurrence of miscarriage/stillbirth. Results Mean birthweights for ethanol and controls were 3076 and 2988 g, respectively; the difference, 88 g, (95% confidence interval: − 18 g to 194 g), was not statistically significant (p = 0.10). After adjusting for covariates, the difference reached significance (p = 0.020). Rates of preterm delivery were 6.7% (ethanol) and 11.0% (control), (p = 0.22). Number of miscarriages was 1(ethanol) vs. 4 (control) and stillbirths was 3 (ethanol) vs. 7 (control) (both non-significant). Average gestational age at delivery was significantly (p = 0.015) higher in ethanol-users (39.2 weeks) compared to controls (38.2 weeks). Perinatal mortality (stillbirths and neonatal deaths) was twice as high in controls compared to ethanol-users (7.9% vs. 3.9%; p = 0.045, after adjustment for covariates). We did not detect significant differences in exposure levels between the two treatment arms, perhaps due to large seasonal effects and high ambient air pollution levels. Conclusions Transition from traditional biomass/kerosene fuel to ethanol reduced adverse pregnancy outcomes. However, the difference in birthweight was statistically significant only after covariate adjustment and the other significant differences were in tertiary endpoints. Our results are suggestive of a beneficial effect of ethanol use. Larger trials are required to validate these findings. [ABSTRACT FROM AUTHOR]