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BACKGROUND: The frequency and destructiveness of hurricanes and related extreme weather events (e.g., cyclones, severe storms) have been increasing due to climate change. A growing body of evidence suggests that victims of hurricanes have increased incidence of cardiovascular disease (CVD), likely due to increased stressors around time of the hurricane and in their aftermath. OBJECTIVES: The objective was to systematically examine the evidence of the association between hurricanes (and related extreme weather events) and adverse CVD outcomes with the goal of understanding the gaps in the literature. METHODS: A comprehensive literature search of population-level and cohort studies focused on CVD outcomes (i.e., myocardial infarction, stroke, and heart failure) related to hurricanes, cyclones, and severe storms was performed in the following databases from inception to December 2021: Ovid MEDLINE, Ovid EMBASE, Web of Science, and The Cochrane Library. Studies retrieved were then screened for eligibility against predefined inclusion/exclusion criteria. Studies were then qualitatively synthesized based on the time frame of the CVD outcomes studied and special populations that were studied. Gaps in the literature were identified based on this synthesis. RESULTS: Of the 1,103 citations identified, 48 met our overall inclusion criteria. We identified articles describing the relationship between CVD and extreme weather, primarily hurricanes, based on data from the United States (42), Taiwan (3), Japan (2), and France (1). Outcomes included CVD and myocardial infarction–related hospitalizations (30 studies) and CVVD-related mortality (7 studies). Most studies used a retrospective study design, including one case–control study, 39 cohort studies, and 4 time-series studies. DISCUSSION: Although we identified a number of papers that reported evaluations of extreme weather events and short-term adverse CVD outcomes, there were important gaps in the literature. These gaps included a) a lack of rigorous long-term evaluation of hurricane exposure, b) lack of investigation of hurricane exposure on vulnerable populations regarding issues related to environmental justice, c) absence of research on the exposure of multiple hurricanes on populations, and d) absence of an exploration of mechanisms leading to worsened CVD outcomes. Future research should attempt to fill these gaps, thus providing an important evidence base for future disaster-related policy. [ABSTRACT FROM AUTHOR]

BACKGROUND: In spring 2013, groundwater of a vast area of the Veneto Region (northeastern Italy) was found to be contaminated by perfluoroalkyl substances (PFAS) from a PFAS manufacturing plant active since the late 1960s. Residents were exposed to high concentrations of PFAS, particularly perfluorooctanoic acid (PFOA), through drinking water until autumn 2013. A publicly funded health surveillance program is under way to aid in the prevention, early diagnosis, and treatment of chronic disorders possibly associated with PFAS exposure. OBJECTIVES: The objectives of this paper are: a) to describe the organization of the health surveillance program, b) to report serum PFAS concentrations in adolescents and young adults, and c) to identify predictors of serum PFAS concentrations in the studied population. METHODS: The health surveillance program offered to residents of municipalities supplied by contaminated waterworks includes a structured interview, routine blood and urine tests, and measurement of 12 PFAS in serum by high-performance liquid chromatography–tandem mass spectrometry. We studied 18,345 participants born between 1978 and 2002, 14–39 years of age at recruitment. Multivariable linear regression was used to identify sociodemographic, lifestyle, dietary, and reproductive predictors of serum PFAS concentrations. RESULTS: The PFAS with the highest serum concentrations were PFOA [median 44.4 ng/mL, interquartile range (IQR) 19.3–84.9], perfluorohexanesulfonic acid (PFHxS) (median 3.9 ng/mL, IQR 1.9–7.4), and perfluorooctanesulfonic acid (PFOS) (median 3.9 ng/mL, IQR 2.6–5.8). The major predictors of serum levels were gender, municipality, duration of residence in the affected area, and number of deliveries. Overall, the regression models explained 37%, 23%, and 43% of the variance of PFOA, PFOS, and PFHxS, respectively. CONCLUSIONS: Serum PFOA concentrations were high relative to concentrations in populations with background residential exposures only. Interindividual variation of serum PFAS levels was partially explained by the considered predictors. [ABSTRACT FROM AUTHOR]

BACKGROUND: Weather variability is associated with enteric infections in people through a complex interaction of human, animal, and environmental factors. Although Campylobacter infections have been previously associated with precipitation and temperature, the association between precipitation and drought on campylobacteriosis has not been studied. OBJECTIVE: Using data from Arizona, Colorado, New Mexico, and counties in Utah, this ecological study aimed to assess the association between precipitation and the incidence of campylobacteriosis by county from 2009 to 2021 and to determine how this association is modified by prior drought level and animal operations. METHODS: We merged 38,782 cases of campylobacteriosis reported in 127 counties with total precipitation (in inches), temperature (in average degrees Fahrenheit), Palmer Drought Severity Index (PDSI, category), and animal census data (presence, density per square mile) by week from 2009 to 2021. Negative binomial generalized estimating equations adjusted for temperature with a 3-wk lag were used to explore the association between precipitation on campylobacteriosis with resulting incidence rate ratios (IRRs). Stratified analyses explored the association with precipitation following antecedent drought, presence of farm operations, and animal density. RESULTS: A 1-in (25.4 mm) increase in precipitation was associated with a 3% increase in campylobacteriosis reported 3 wks later (IRR=1.03; 95% CI: 1.02, 1.04) after adjusting for average temperature and PDSI. Compared with normal conditions, there were significantly more cases when precipitation followed antecedent extremely wet (IRR=1.15; 95% CI: 1.04, 1.26), very wet (IRR=1.09; 95% CI: 1.01, 1.18), moderately wet (IRR=1.06; 95% CI: 1.01, 1.12), moderate drought (IRR=1.11; 95% CI: 1.07, 1.16), and severe drought (IRR=1.06; 95% CI: 1.02, 1.11) conditions, whereas there were significantly fewer cases (IRR=0.89; 95% CI: 0.85, 0.94) for antecedent extreme drought. Compared to counties with no animal operations, counties with animal operations had significantly more cases following precipitation for every PDSI category except extreme drought. Counties with a higher density of beef cattle, goats for meat, chicken broilers, and chicken layers had significantly higher rates of campylobacteriosis following precipitation than those with no such operations, whereas those with dairy cattle and goats for milk, did not. DISCUSSION: In this majority arid and semiarid environment, precipitation following prior wet conditions and moderate and severe drought were significantly associated with increased rates of campylobacteriosis, and only in prior extreme drought did rates decrease. Where the precipitation fell made a difference; after precipitation, counties with farm operations had significantly more cases compared to counties without farm operations. Further work should assess individual-level risk factors within environmental exposure pathways for Campylobacter. [ABSTRACT FROM AUTHOR]

BACKGROUND: A major industrial fire accident occurred in a tire manufacturing factory in Daejeon, Korea, on 12 March 2023 and lasted for 3 d, generating air pollutant emissions. Although evidence regarding the health effects of urban fires is limited, residents near tire factory may have experienced health hazards due to smoke exposure from fire plumes. OBJECTIVES: Capitalizing on the timing of this fire incident as a natural experiment, we estimated the attributable excess air pollution exposure and associated disease development among residents living near the tire factory. METHODS: We used the generalized synthetic control method to estimate air pollution exposure and health burden attributable to the accident among residents living in smoke-exposed districts. Based on satellite images and air pollution monitoring results, three administrative districts (within 1.2 km from the factory) were defined as smoke-exposed, and the other 79 districts of Daejeon were defined as controls. Among the 11 monitoring stations in Daejeon, the station located 500 m from the factory was used to estimate excess air pollution exposure (PM10, PM2.5, NO2, O3, SO2, and CO) for residents in the exposed districts. The number of daily district-level disease-specific incidence cases were acquired from the National Health Insurance Database and used to estimate excess health burden resulting from the fire. RESULTS: During the first week following the factory fire, residents of exposed districts had an estimated excess exposure to 125.2 [95% confidence interval (CI): 44.9, 156.7] μg/m³ of PM10, 50.4 (95% CI: 12.7, 99.8) ppb of NO2, and 32.0 (95% CI: 21.0, 35.9) ppb of SO2. We also found an average increase in the incidence cases of other diseases of upper respiratory tract [20.6 persons (95% CI: 6.2, 37.4)], lung disease due to external agents [2.5 persons (95% CI: 2.1, 3.3)], urticaria and erythema [5.9 persons (95% CI: -0:6, 11.2)], and episodic and paroxysmal disorders [8.5 persons (95% CI: 3.7, 13.4)] in exposed districts. DISCUSSION: Excessive air pollution exposure and disease incidence were identified among residents living close to the tire factory. Preventive measures, such as a warning system, to avoid health impacts to people breathing fire-related pollution may be beneficial for communities impacted by such events. [ABSTRACT FROM AUTHOR]

BACKGROUND: Accumulating evidence suggests that domestic water hardness is linked to health outcomes, but its association to all-cause and causespecific cancers warrants investigation. OBJECTIVE: The aim of this study was to investigate the association of domestic hard water with all-cause and cause-specific cancers METHODS: In the prospective cohort study, a total of 447,996 participants from UK Biobank who were free of cancer at baseline were included and followed up for 16 y. All-cause and 22 common cause-specific cancer diagnoses were ascertained using hospital inpatient records and self-reported data until 30 November 2022. Domestic water hardness, measured by CaCO3 concentrations, was obtained from the local water supply companies across England, Scotland, and Wales in 2005. Data were analyzed using Cox proportional hazard models, with adjustments for known measured confounders, including demographic, socioeconomic, clinical, biochemical, lifestyle, and environmental factors RESULTS: Over a median follow-up of 13.6 y (range: 12.7–14.4 y), 58,028 all-cause cancer events were documented. A U-shaped relationship between domestic water hardness and all-cause cancers was observed (푝 for nonlinearity <0.001). In comparison with individuals exposed to soft water (0–60 mg/L), the hazard ratios (HRs) and 95% confidence intervals (CIs) of all-cause cancer were 1.00 (95% CI: 0.98, 1.02) for those exposed to moderate hard water (>60–120 mg/L), 0.88 (95% CI: 0.84, 0.91) for those exposed to hard water (>120–180 mg/L) and 1.06 (95% CI: 1.04, 1.08) for those exposed to very hard water (>180 mg/L). Additionally, domestic water hardness was associated with 11 of 22 cause-specific cancers, including cancers of the esophagus, stomach, colorectal tract, lung, breast, prostate, and bladder, as well as non-Hodgkin lymphoma, multiple myeloma, malignant melanoma, and hematological malignancies. Moreover, we observed a positive linear relationship between water hardness and bladder cancer DISCUSSION: Our findings suggest that domestic water hardness was associated with all-cause and multiple cause-specific cancers. Findings from the UK Biobank support a potentially beneficial association between hard water and the incidence of all-cause cancer. However, very hard water may increase the risk of all-cause cancer. [ABSTRACT FROM AUTHOR]

BACKGROUND: Sanitary sewer overflows (SSOs) occur when untreated sewage is discharged into water sources before reaching the treatment facility, potentially contaminating the water source with gastrointestinal pathogens. OBJECTIVES: The objective of this paper is to assess associations between SSO events and rates of gastrointestinal (GI) illness in Massachusetts. METHODS: A case-crossover study design was used to investigate association between SSO events and emergency room (ER) visits with a primary diagnosis of gastrointestinal (GI) illness in Massachusetts for 2006-2007. ER visits for GI were considered exposed if an SSO event occurred in the county of residence within three hazard periods, 0-4 d, 5-9 d, or 10-14 d, before the visit. A time-stratified bidirectional design was used to select control days for each ER visit on the same day of the week during the same month. Fixed effect logistic regression models were used to estimate the risk of ER visits following the SSO event. RESULTS: During the study period, there were 270 SSO events for northeastern Massachusetts and 66,460 ER admissions with GI illness listed as the primary diagnostic code. The overall odds ratio (OR) for ER visits for GI illness was 1.09 [95% confidence interval (CI): 1.03, 1.16] in the 10-14 d period following an SSO event, with positive ORs for all age groups and for three of the four counties. The 0-4 d and 5-9 d periods following an SSO event were not associated with ER visits for GI illness overall, and associations by county or age were inconsistent. CONCLUSIONS: We demonstrated an association between SSO events and ER visits for GI illness using a case-crossover study design. In light of the aging water infrastructure in the United States and the expected increase in heavy rainfall events, our findings suggest a potential health impact associated with sewage overflows. [ABSTRACT FROM AUTHOR]

BACKGROUND: Endocrine-disrupting chemicals may play a role in adiposity development during childhood. Until now literature in this scope suffers from methodologic limitations in exposure assessment using one or few urine samples and missing assessment during the infancy period. OBJECTIVES: We investigated the associations between early-life exposure to quickly metabolized chemicals and post-natal growth, relying on repeated within-subject urine collections over pregnancy and infancy. METHODS: We studied the associations of four phenols, four parabens, seven phthalates, and one nonphthalate plasticizer from weekly pooled urine samples collected from the mother during second and third trimesters (median 18 and 34 gestational weeks, respectively) and infant at 2 and 12 months of age, and child growth until 36 months. We relied on repeated measures of height, weight and head circumference from study visits and the child health booklet to predict growth outcomes at 3 and 36 months using the Jenss-Bayley nonlinear mixed model. We assessed associations with individual chemicals using adjusted linear regression and mixtures of chemicals using a Bayesian kernel machine regression model. RESULTS: The unipollutant analysis revealed few associations. Bisphenol S (BPS) at second trimester was positively associated with all infant growth parameters at 3 and 36 months, with similar patterns between exposure at third trimester and all infant growth parameters at 3 months. Mono-푛-butyl phthalate (MnBP) at 12 months was positively associated with body mass index (BMI), weight, and head circumference at 36 months. Mixture analysis revealed positive associations between exposure at 12 months and BMI and weight at 36 months, with MnBP showing the highest effect size within the mixture. CONCLUSIONS: This study suggests that exposure in early infancy may be associated with increased weight and BMI in early childhood, which are risk factors of obesity in later life. Furthermore, this study highlighted the impact of BPS, a compound replacing bisphenol A, which has never been studied in this context. [ABSTRACT FROM AUTHOR]

BACKGROUND: Per- and polyfluoroalkyl substances (PFAS) are widely detected in pregnant women and associated with adverse outcomes related to impaired placental function. Human chorionic gonadotropin (hCG) is a dimeric glycoprotein hormone that can indicate placental toxicity. OBJECTIVES: Our aim was to quantify the association of serum PFAS with placental hCG, measured as an intact molecule (hCG), as free alpha- (hCGα) and beta-subunits (hCGβ), and as a hyperglycosylated form (h-hCG), and evaluate effect measure modification by social determinants and by fetal sex. METHODS: Data were collected from 326 pregnant women enrolled from 2015 to 2019 in the UPSIDE study in Rochester, New York. hCG forms were normalized for gestational age at the time of blood draw in the first trimester [multiple of the median (MoM)]. Seven PFAS were measured in second-trimester maternal serum. Multivariate imputation by chained equations and inverse probability weighting were used to evaluate robustness of linear associations. PFAS mixture effects were estimated by Bayesian kernel machine regression. RESULTS: Perfluorohexane sulfonic acid (PFHxS) [hCGβ: 0.29 log MoM units per log PFHxS; 95% confidence interval (CI): 0.08, 0.51] and perfluorodecanoic acid (PFDA) (hCG: -0.09; 95% CI: -0.16, -0.02) were associated with hCG in the single chemical and mixture analyses. The PFAS mixture was negatively associated with hCGα and positively with hCGβ. Subgroup analyses revealed that PFAS associations with hCG differed by maternal race/ethnicity and education. Perfluoropentanoic acid (PFPeA) was associated with hCGβ only in Black participants (-0.23; 95% CI: -0.37, -0.09) and in participants with high school education or less (-0.14; 95% CI: -0.26, -0.02); conversely, perfluorononanoic acid (PFNA) was negatively associated with hCGα only in White participants (-0.15; 95% CI: -0.27, -0.03) and with hCGβ only in participants with a college education or greater (-0.19; 95% CI: -0.36, -0.01). These findings were robust to testing for selection bias, confounding bias, and left truncation bias where PFAS detection frequency was <100%. Two associations were negative in male (and null in female) pregnancies: Perfluoroundecanoic acid (PFUnDA) with hCGα, and PFNA with h-hCG. CONCLUSIONS: Evidence was strongest for the association between PFHxS and PFDA with hCG in all participants and for PFPeA and PFNA within subgroups defined by social determinants and fetal sex. PFAS mixture associations with hCGα and hCGβ differed, suggesting subunit-specific types of toxicity and/or regulation. Future studies will evaluate the biological, clinical and public health significance of these findings. [ABSTRACT FROM AUTHOR]

BACKGROUND: Hypertension is a major cause of death worldwide. Although arsenic exposure has been associated with the risk of hypertension, this association appears nonuniform due to inconsistent results from studies conducted in different populations. Moreover, hypertension is a complex condition with multiple underlying mechanisms and factors. One factor is impaired production and bioavailability of vascular nitric oxide (NO). However, the implications of the effects of arsenic exposure on circulating NO and its association with hypertension in humans are largely unknown. OBJECTIVE: We investigated the dose–response relationship between arsenic exposure and hypertension with vascular NO levels as a potential mediator of arsenic-related hypertension in individuals exposed to a broad range of arsenic. METHODS: A total of 828 participants were recruited from low- and high-arsenic exposure areas in Bangladesh. Participants’ drinking water, hair, and nail arsenic concentrations were measured by inductively coupled plasma mass spectroscopy. Hypertension was defined as a systolic blood pressure (SBP) value of = 140 and a diastolic (DBP) value of = 90 mmHg. Serum NO levels reflected by total serum nitrite concentrations were measured by immunoassay. A formal causal mediation analysis was used to assess NO as a mediator of the association between arsenic level and hypertension. RESULTS: Increasing concentrations of arsenic measured in drinking water, hair, and nails were associated with the increasing levels of SBP and DBP. The odds of hypertension were dose-dependently increased by arsenic even in participants exposed to relatively low to moderate levels (10–50 µg/L) of water arsenic [odds ratios (ORs) and 95% confidence intervals (CIs): 2.87 (95% CI: 1.28, 6.44), 2.67 (95% CI: 1.27, 5.60), and 5.04 (95% CI: 2.71, 9.35) for the 10–50 µg/L, 50.01–150 µg/L, and >150 µg/L groups, respectively]. Causal mediation analysis showed a significant mediating effect of NO on arsenic-related SBP, DBP, and hypertension. CONCLUSION: Increasing exposure to arsenic was associated with increasing odds of hypertension. The association was mediated through the reduction of vascular NO bioavailability, suggesting that impaired NO bioavailability was a plausible underlying mechanism of arsenic-induced hypertension in this Bangladeshi population. [ABSTRACT FROM AUTHOR]

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

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

BACKGROUND: Federal housing assistance is an important policy tool to ensure housing security for low-income households. Less is known about its impact on residential environmental exposures, particularly lead. OBJECTIVES: We conducted a quasi-experimental study to investigate the association between federal housing assistance and blood lead levels (BLLs) in a nationally representative US sample age 6 y and older eligible for housing assistance. METHODS: We used the 1999-2018 National Health and Nutrition Examination Survey (NHANES) linked with US Department of Housing and Urban Development (HUD) administrative records to assess BLLs of NHANES participants with concurrent HUD housing assistance (i.e., current recipients, 푛=3,071) and those receiving assistance within 2 y after the survey (i.e., pseudo-waitlist recipients, 푛=1,235). We estimated BLL least squares geometric means (LSGMs), odds ratio (OR) for BLL ≥3.5 μg/dL, and percent differences in LSGMs by HUD housing assistance status adjusting for age, sex, family income-to-poverty ratio, education, country of birth, race/ethnicity, region, and survey year. We also examined effect modification using interaction terms and stratified analyses by program type [i.e., public housing, multifamily, housing choice vouchers (HCV)], and race/ethnicity. RESULTS: Current HUD recipients had a significantly lower LSGM [1.07 μg/dL; 95% confidence interval (CI): 1.02, 1.12] than pseudo-waitlist recipients (1.21 μg/dL; 95% CI: 1.14, 1.28), with an adjusted OR of 0.60 (95% CI: 0.42, 0.87) for BLL ≥3.5 μg/dL. Some effect modification were observed: The protective association of HUD assistance on BLL was strongest among public housing (-19.5% LSGM; 95% CI: -27.5%, -10.7%), multifamily (-12.5% LSGM; 95% CI: -20.7%, -3.5%), and non-Hispanic White (-20:6% LSGM; 95% CI: -29.8%, -10.3%) recipients. It was weaker to null among HCV (-5.7% LSGM; 95% CI: -12.7, 1.7%), non-Hispanic Black (-1.6% LSGM; 95% CI: -8.1%, 5.4%), and Mexican American (-12.5% LSGM; 95% CI: -31.9%, 12.5%) recipients. DISCUSSION: Our research underscores the importance of social-structural determinants like federal housing assistance in providing affordable, stable, and healthy housing to very low-income households. More attention is needed to ensure housing quality and racial equity across HUD's three major housing assistance programs. [ABSTRACT FROM AUTHOR]

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

BACKGROUND: Exposure to environmental metals has been consistently associated with attention and behavioral deficits in children, and these associations may be modified by coexposure to other metals or iron (Fe) status. However, few studies have investigated Fe status as a modifier of a metal mixture, particularly with respect to attention-related behaviors. METHODS: We used cross-sectional data from the Public Health Impact of Metals Exposure study, which included 707 adolescents (10–14 years of age) from Brescia, Italy. Manganese, chromium, and copper were quantified in hair samples, and lead was quantified in whole blood, using inductively coupled plasma mass spectrometry. Concentrations of Fe status markers (ferritin, hemoglobin, transferrin) were measured using immunoassays or luminescence assays. Attention-related behaviors were assessed using the Conners Rating Scales Self-Report Scale–Long Form, Parent Rating Scales Revised–Short Form, and Teacher Rating Scales Revised–Short Form. We employed Bayesian kernel machine regression to examine associations of the metal mixture with these outcomes and evaluate Fe status as a modifier. RESULTS: Higher concentrations of the metals and ferritin were jointly associated with worse self-reported attention-related behaviors: metals and ferritin set to their 90th percentiles were associated with 3.0% [&#946= 0.03; 95% credible interval (CrI): -0.01, 0.06], 4.1% (&#946= 0.04; 95% CrI: 0.00, 0.08), and 4.1% (β= 0.04; 95% CrI: 0.00, 0.08) higher T-scores for self-reported attention deficit/hyperactivity disorder (ADHD) index, inattention, and hyperactivity, respectively, compared with when metals and ferritin were set to their 50th percentiles. These associations were driven by hair manganese, which exhibited nonlinear associations with all self-reported scales. There was no evidence that Fe status modified the neurotoxicity of the metal mixture. The metal mixture was not materially associated with any parent-reported or teacher-reported scale. CONCLUSIONS: The overall metal mixture, driven by manganese, was adversely associated with self-reported attention-related behavior. These findings suggest that exposure to multiple environmental metals impacts adolescent neurodevelopment, which has significant public health implications. [ABSTRACT FROM AUTHOR]

BACKGROUND: There is suggestive epidemiological evidence that maternal dietary polycyclic aromatic hydrocarbons (PAH) may increase the risk of adverse birth outcomes. We sought to summarize the available evidence on the effect of dietary PAH exposure on birth outcomes. METHODS: PubMed and Scopus databases were systematically searched from inception up to November 2022. Studies were included if they were original articles, were conducted in a human population, assessed dietary PAH consumption, and investigated the relationship between dietary PAH consumption and any adverse birth outcomes. Risk of bias in the included studies was assessed qualitatively and quantitatively. A random effects model was used to compute summary effect estimates in the meta-analysis. RESULTS: Six observational studies (five prospective cohort studies, and one prevalence case–control study) were included. The included studies assessed dietary PAH exposure using dietary questionnaires. Information on the outcomes of interest was obtained from medical records. Three of the included studies were rated as good quality with the remaining three studies rated as fair quality. One study was considered as having low risk of bias for selection, information and confounding bias. Dietary PAH consumption was associated with 5.65 g [95% confidence interval (CI): -16.36, 5.06] and 0.04 cm (95% CI: -0.08, 0.01) reductions in birth weight and birth length, respectively, and an increase in head circumference [effect size (ES) = 0.001; 95% CI: -0.003, 0.005]. The CI of all the summary effect estimates, however, included the null value. In the sensitivity analysis that included only studies that assessed dietary PAH exposure as the primary exposure of interest, dietary PAH consumption was associated with much higher reductions in birth weight (ES = -14.61; 95% CI: -21.07, -8.15) and birth length (ES = -0.06; 95% CI: -0.1, -0.03). High statistical heterogeneity was observed in the birth weight and birth length analysis and in the head circumference sensitivity analysis. DISCUSSION: The body of epidemiological evidence suggests that maternal dietary PAH exposure is associated with reduced fetal growth, measured as birth weight and length. There was considerable heterogeneity in the measurement of PAH exposure among the included studies. Also, nonstandardized and validated dietary questionnaires were employed by a majority of the included studies with potential exposure misclassification. These issues are likely to impact the summary effect estimates computed and underscores the need for high-quality epidemiological studies with improved exposure assessment and adequate confounding control to strengthen the evidence base. [ABSTRACT FROM AUTHOR]

BACKGROUND: Previous epidemiological studies found associations between exposure to per- and polyfluoroalkyl substances (PFAS) and some cancer types. Many studies considered highly exposed populations, so relevance to less-exposed populations can be uncertain. Additionally, many studies considered only cancer site, not histology. OBJECTIVES: We conducted a case–cohort study within the American Cancer Society’s prospective Cancer Prevention Study II (CPS-II) LifeLink cohort to examine associations between PFAS exposure and risk of selected cancers, considering histologic subtypes. METHODS: Serum specimens were collected from cohort participants during the period 1998–2001. This study included a subcohort (500 men, 499 women) randomly selected from participants without prior cancer diagnoses at serum collection, and all participants with incident (after serum collection) first cancers of the breast (females only, 푛=786), bladder (푛=401), kidney (푛=158), pancreas (푛=172), prostate (males only, 푛=1,610) or hematologic system (푛=635). PFAS concentrations [perfluorooctanoic acid (PFOA), perfluorooctane sulfonate (PFOS), perfluorohexane sulfonic acid (PFHxS), and perfluorononanoic acid (PFNA)] were measured in stored serum. We assessed associations between PFAS concentrations and incident cancers, by site and histologic subtype, using multivariable Cox proportional hazards models stratified by sex and controlling for age and year at blood draw, education, race/ethnicity, smoking, and alcohol use. RESULTS: Serum PFOA concentrations were positively associated with renal cell carcinoma of the kidney among women [hazard ratio (HR) and 95% confidence interval (CI) per PFOA doubling: 1.54 (95% CI: 1.05, 2.26)] but not men. Among men, we observed a positive association between PFHxS concentrations and chronic lymphocytic leukemia/small lymphocytic lymphoma [CLL/SLL, HR and 95% CI per PFHxS doubling: 1.34 (95% CI: 1.02, 1.75)]. We observed some heterogeneity of associations by histologic subtype within sites. DISCUSSION: This study supports the previously observed association between PFOA and renal cell carcinoma among women and suggests an association between PFHxS and CLL/SLL among men. Consideration of histologic subtypes might be important in future studies of PFAS-cancer associations. [ABSTRACT FROM AUTHOR]

BACKGROUND: Studies across the globe generally reported increased mortality risks associated with particulate matter with aerodynamic diameter ≤2.5 μm (PM2.5) exposure with large heterogeneity in the magnitude of reported associations and the shape of concentration-response functions (CRFs). We aimed to evaluate the impact of key study design factors (including confounders, applied exposure model, population age, and outcome definition) on PM2.5 effect estimates by harmonizing analyses on three previously published large studies in Canada [Mortality-Air Pollution Associations in Low Exposure Environments (MAPLE), 1991-2016], the United States (Medicare, 2000-2016), and Europe [Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE), 2000-2016] as much as possible. METHODS: We harmonized the study populations to individuals 65+ years of age, applied the same satellite-derived PM2.5 exposure estimates, and selected the same sets of potential confounders and the same outcome. We evaluated whether differences in previously published effect estimates across cohorts were reduced after harmonization among these factors. Additional analyses were conducted to assess the influence of key design features on estimated risks, including adjusted covariates and exposure assessment method. A combined CRF was assessed with meta-analysis based on the extended shape-constrained health impact function (eSCHIF). RESULTS: More than 81 million participants were included, contributing 692 million person-years of follow-up. Hazard ratios and 95% confidence intervals (CIs) for all-cause mortality associated with a 5-μg/m³ increase in PM2.5 were 1.039 (1.032, 1.046) in MAPLE, 1.025 (1.021, 1.029) in Medicare, and 1.041 (1.014, 1.069) in ELAPSE. Applying a harmonized analytical approach marginally reduced difference in the observed associations across the three studies. Magnitude of the association was affected by the adjusted covariates, exposure assessment methodology, age of the population, and marginally by outcome definition. Shape of the CRFs differed across cohorts but generally showed associations down to the lowest observed PM2.5 levels. A common CRF suggested a monotonically increased risk down to the lowest exposure level. [ABSTRACT FROM AUTHOR]

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

Background: Although high doses of ionizing radiation have long been linked to circulatory disease, evidence for an association at lower exposures remains controversial. However, recent analyses suggest excess relative risks at occupational exposure levels. Objectives: We performed a systematic review and meta-analysis to summarize information on circulatory disease risks associated with moderate- and low-level whole-body ionizing radiation exposures. Methods: We conducted PubMed/ISI Thomson searches of peer-reviewed papers published since 1990 using the terms "radiation" AND "heart" AND "disease," OR "radiation" AND "stroke," OR "radiation" AND "circulatory" AND "disease." Radiation exposures had to be whole-body, with a cumulative mean dose of < 0.5 Sv, or at a low dose rate (< 10 mSv/day). We estimated population risks of circulatory disease from low-level radiation exposure using excess relative risk estimates from this meta-analysis and current mortality rates for nine major developed countries. Results: Estimated excess population risks for all circulatory diseases combined ranged from 2.5%/Sv [95% confidence interval (CI): 0.8, 4.2] for France to 8.5%/Sv (95% CI: 4.0, 13.0) for Russia. Conclusions: Our review supports an association between circulatory disease mortality and low and moderate doses of ionizing radiation. Our analysis was limited by heterogeneity among studies (particularly for noncardiac end points), the possibility of uncontrolled confounding in some occupational groups by lifestyle factors, and higher dose groups (> 0.5 Sv) generally driving the observed trends. If confirmed, our findings suggest that overall radiation-related mortality is about twice that currently estimated based on estimates for cancer end points alone (which range from 4.2% to 5.6%/Sv for these populations). [ABSTRACT FROM AUTHOR]

BACKGROUND: Per- and polyfluoroalkyl substances (PFAS) are chemical substances spread throughout the environment worldwide. Exposure during pregnancy represents a specific window of vulnerability for child health. OBJECTIVE: Our objective was to assess the impact of prenatal exposure to multiple PFAS on emotional and behavioral functions in 12-y-old children. METHOD: In the PELAGIE mother–child cohort (France), prenatal exposure to nine PFAS was measured from concentrations in cord serum samples. Behavior was assessed at age 12 y using the parent-reported Strengths and Difficulties Questionnaire (SDQ) and the self-reported Dominic Interactive for Adolescents (DIA) for 444 children. Associations were estimated using negative binomial models for each PFAS. Bayesian kernel machine regression (BKMR) models were performed to assess the exposure mixture effect on children’s behavior. RESULTS: In our study population, 73% of mothers had spent more than 12 y in education. Higher scores on SDQ externalizing subscale were observed with increasing cord-serum concentration of perfluorooctanoic acid (PFOA) and perfluorononanoic acid (PFNA) [adjusted mean ratio (aMR)=1.18, 95% confidence interval (CI): 1.03, 1.34, and aMR=1.14 (95% CI: 1.00, 1.29) for every doubling of concentration, respectively]. Results for the hyperactivity score were similar [aMR=1.20 (95% CI: 1.04, 1.40) and aMR=1.18 (95% CI: 1.02, 1.36), respectively]. With regard to major depressive disorder and internalizing subscales, perfluorodecanoic acid (PFDA) was associated with higher self-reported DIA scores [aMR=1.14 (95% CI: 1.01, 1.27) and aMR=1.11 (95% CI: 1.02, 1.21), respectively]. In terms of the anxiety subscale, PFDA and PFNA were associated with higher scores [aMR=1.11 (95% CI: 1.02, 1.21) and aMR=1.10 (95% CI: 1.01, 1.19), respectively]. Concurrent increases in the PFAS concentrations included in the BKMR models showed no change in the SDQ externalizing and DIA internalizing subscales scores. CONCLUSION: Prenatal exposure to PFNA and PFOA were associated with increasing scores for measures of externalizing behaviors, specifically hyperactivity. We also identified associations between PFNA and PFDA prenatal exposure levels and increasing scores related to internalizing behaviors (general anxiety and major depressive disorder), which adds to the as yet sparse literature examining the links between prenatal exposure to PFAS and internalizing disorders. [ABSTRACT FROM AUTHOR]

BACKGROUND: Evidence of the negative impacts of contemporary use insecticides on sperm concentration has increased over the last few decades; however, meta-analyses on this topic are rare. OBJECTIVES: This investigation assessed the qualitative and quantitative strength of epidemiological evidence regarding adult exposure to two classes of contemporary use insecticides—organophosphates (OPs) and 푁-methyl carbamates (NMCs)—and sperm concentration using robust and reproducible systematic review and meta-analysis methods. METHODS: Three scientific databases (PubMed, Scopus, and Web of Science), two U.S. government databases (NIOSHTIC-2 and Science.gov), and five nongovernmental organization websites were searched for relevant primary epidemiological studies published in any language through 11 August 2022. Risk of bias and strength of evidence were evaluated according to Navigation Guide systematic review methodology. Bias-adjusted standardized mean difference effect sizes were calculated and pooled using a three-level, multivariate random-effect meta-analysis model with cluster-robust variance estimation. RESULTS: Across 20 studies, 21 study populations, 42 effect sizes, and 1,774 adult men, the pooled bias-adjusted standardized mean difference in sperm concentration between adult men more- and less-exposed to OP and NMC insecticides was -0.30 (95% CI: -0.49, -0.10; 푃Satt < 0.01). Sensitivity and subgroup analyses explored statistical heterogeneity and validated the model robustness. Although the pooled effect estimate was modified by risk of bias, insecticide class, exposure setting, and recruitment setting, it remained negative in direction across all meta-analyses. The body of evidence was rated to be of moderate quality, with sufficient evidence of an association between higher adult OP and NMC insecticide exposure and lower sperm concentration. DISCUSSION: This comprehensive investigation found sufficient evidence of an association between higher OP and NMC insecticide exposure and lower sperm concentration in adults. Although additional cohort studies can be beneficial to fill data gaps, the strength of evidence warrants reducing exposure to OP and NMC insecticides now to prevent continued male reproductive harm. [ABSTRACT FROM AUTHOR]

BACKGROUND: Widespread insecticide exposure might be a risk factor for neurodevelopment of our children, but few studies examined the mixture effect of maternal coexposure to organophosphate insecticides (OPPs), pyrethroids (PYRs), and neonicotinoid insecticides (NNIs) during pregnancy on child neurodevelopment, and critical windows of exposure are unknown. OBJECTIVES: We aimed to evaluate the association of prenatal exposure to multiple insecticides with children’s neurodevelopment and to identify critical windows of the exposure. METHODS: Pregnant women were recruited into a prospective birth cohort study in Wuhan, China, from 2014–2017. Eight metabolites of OPPs (mOPPs), three metabolites of PYRs (mPYRs), and nine metabolites of NNIs (mNNIs) were measured in 3,123 urine samples collected at their first, second, and third trimesters. Children’s neurodevelopment [mental development index (MDI) and psychomotor development index (PDI)] was assessed using the Bayley Scales of Infant Development at 2 years of age (푁 = 1,041). Multivariate linear regression models, generalized estimating equation models, and weighted quantile sum (WQS) regression were used to estimate the association between the insecticide metabolites and Bayley scores. Potential sex-specific associations were also examined. RESULTS: Single chemical analysis suggested higher urinary concentrations of some insecticide metabolites at the first trimester were significantly associated with lower MDI and PDI scores, and the associations were more prominent among boys. Each 1-unit increase in ln-transformed urinary concentrations of two mOPPs, 3,5,6-trichloro-2-pyridinol and 4-nitrophenol, was associated with a decrease of 3.16 points [95% confidence interval (CI): -5:59, -0:74] and 3.06 points (95% CI: -5.45, -0.68) respectively in boys’ MDI scores. Each 1-unit increase in that of trans-3-(2,2-dichloroethenyl)-2,2-dimethylcyclopropanecarboxylic acid (trans-DCCA; an mPYR) was significantly associated with a decrease of 2.24 points (95% CI: -3.89, -0.58) in boys’ MDI scores and 1.90 points (95% CI: -3.16, -0.64) in boys’ PDI scores, respectively. Significantly positive associations of maternal urinary biomarker concentrations [e.g., dimethyl phosphate (a nonspecific mOPP) and desmethyl-clothianidin (a relatively specific mNNI)] with child neurodevelopment were also observed. Using repeated holdout validation, a 1-quartile increase in the WQS index of the insecticide mixture (in the negative direction) at the first trimester was significantly associated with a decrease of 3.02 points (95% CI: -5.47, -0.57) in MDI scores among the boys, and trans-DCCA contributed the most to the association (18%). CONCLUSIONS: Prenatal exposure to higher levels of certain insecticides and their mixture were associated with lower Bayley scores in children, particularly in boys. Early pregnancy may be a sensitive window for such an effect. Future studies are needed to confirm our findings. [ABSTRACT FROM AUTHOR]

BACKGROUND: Improving mental health is recognized as an important factor for achieving global development goals. Despite strong evidence that neighborhood greenery promotes better mental health, there are environmental justice concerns over the distribution of neighborhood greenery. Underlying these concerns are present-day consequences of historical discriminatory financial investment practices, such as redlining which was established by the U.S. Federal Home Owners’ Loan Corporation (HOLC) in the 1930s. The impacts of redlining on environmental and health disparities have been researched extensively. However, the influences of redlining on the associations between neighborhood environment and health outcomes have not been fully assessed. OBJECTIVES: The aim of this study was to examine whether associations between residential tree cover and depressive symptoms vary across areas subject to HOLC practices. METHODS: Depressive symptoms were defined by the 10-item Center for Epidemiologic Studies Depression Scale collected during the period 2008– 2012 for 3,555 women in the Sister Study cohort residing in cities subject to HOLC practices across the United States. HOLC rating maps were obtained from the Mapping Inequality Project, University of Richmond, with neighborhoods graded as A (best for financial investment, green), B (still desirable, blue), C (declining, yellow), and D (hazardous, red—known as redlined). Tree cover within 500 m and 2,000 m from residences was estimated using 2011 U.S. Forest Service Percent Tree Canopy Cover. Mixed model using climate zone as the random effect was applied to evaluate the associations with adjustments for potential covariates. Analyses were stratified by HOLC grade. RESULTS: Tree cover was significantly higher in neighborhoods with better HOLC grades. A 10% increase in tree cover was associated with reduced odds of depressive symptoms for the full study population, with adjusted odds ratios (AORs) of 0.93 [95% confidence interval (CI): 0.88, 0.99], and 0.91 (0.85, 0.97) for 500-m and 2,000-m buffer, respectively. Across HOLC grades, the strongest associations were observed in redlined neighborhoods, with respective AORs of 0.72 (95% CI: 0.52, 0.99) and 0.63 (95% CI: 0.45, 0.90) for 500-m and 2,000-m buffer. DISCUSSION: Findings support a remediation strategy focused on neighborhood greenery that would address multiple public health priorities, including mental health and environmental justice. [ABSTRACT FROM AUTHOR]

BACKGROUND: The protective effect of urban greenery from adverse heat impacts remains inconclusive. Existing inconsistent findings could be attributed to the different estimation techniques used. OBJECTIVES: We investigated how effect modifications of urban greenery on heat–mortality associations vary when using different greenery measurements reflecting overhead-view and eye-level urban greenery. METHODS: We collected meteorological and daily mortality data for 286 territory planning units between 2005 and 2018 in Hong Kong. Three greenery measurements were extracted for each unit: a) the normalized difference vegetation index (NDVI) from Landsat remote sensing images, b) the percentage of greenspace based on land use data, and c) eye-level street greenery from street view images via a deep learning technique. Time-series analyses were performed using the case time series design with a linear interaction between the temperature term and each of the three greenery measurements. Effect modifications were also estimated for different age groups, sex categories, and cause-specific diseases. RESULTS: Higher mortality risks were associated with both moderate and extreme heat, with relative risks (RRs) of 1.022 (95% CI: 1.000, 1.044) and 1.045 (95% CI: 1.013, 1.079) at the 90th and 99th percentiles of temperatures relative to the minimum mortality temperature (MMT). Lower RRs were observed in greener areas whichever of the three greenery measurements was used, but the disparity of RRs between areas with low and high levels of urban greenery was more apparent when using eye-level street greenery as the index at high temperatures (99th percentile relative to MMT), with RRs for low and high levels of greenery, respectively, of 1.096 (95% CI: 1.035, 1.161) and 0.985 (95% CI: 0.920, 1.055) for NDVI (푝=0.0193), 1.068 (95% CI: 1.021, 1.117) and 0.990 (95% CI: 0.906, 1.081) for the percentage of greenspace (푝=0.1338), and 1.103 (95% CI: 1.034, 1.177) and 0.943 (95% CI: 0.841, 1.057) for eye-level street greenery (푝 =0.0186). Health discrepancies remained for nonaccidental mortality and cardiorespiratory diseases and were more apparent for older adults (≥ 65 years of age) and females. DISCUSSION: This study provides new evidence that eye-level street greenery shows stronger associations with reduced heat–mortality risks compared with overhead-view greenery based on NDVI and percentage of greenspace. The effect modification of urban greenery tends to be amplified as temperatures rise and are more apparent in older adults and females. Heat mitigation strategies and health interventions, in particular with regard to accessible and visible greenery, are needed for helping heat-sensitive subpopulation groups in coping with extreme heat. [ABSTRACT FROM AUTHOR]

BACKGROUND: Per- and polyfluoroalkyl substances (PFAS), endocrine disrupting chemicals with worldwide exposure, cause changes in mammary gland development in rodents. A few human studies report delay in pubertal events with increasing perfluorooctanoic acid (PFOA) exposure, but to our knowledge none have examined reproductive hormone levels at thelarche. METHODS: In a cohort of Greater Cincinnati (GC) and San Francisco Bay Area (SFBA) girls recruited at 6–8 years of age, clinical examinations were conducted annually or semiannually with sequential Tanner staging. PFAS concentrations were measured in the first serum sample of 704 girls. In 304 GC girls, estradiol (E2), estrone (E1), testosterone (T), and dihydroepiandrosterone sulfate (DHEAS) were measured in serum at four time points around puberty. Relationships between PFAS and age at thelarche, pubarche, and menarche were analyzed using survival and structural equation models. The association between PFAS and reproductive hormones was assessed using linear regression models. RESULTS: Median PFOA serum concentrations in GC (푁 = 353, 7.3 ng/mL) and the SFBA (푁 =351, 5.8 ng/mL) were higher than in the U.S. population. In multivariable Cox proportional hazard models [adjusted for race, body mass index (BMI)], increasing serum log-transformed PFOA was associated with a delay in pubarche [hazard ratio (HR)=0.83; 95% CI: 0.70, 0.99] and menarche (HR=0.04; 95% CI: 0.01, 0.25). Structural equation models indicated a triangular relationship between PFOA, BMI percentile, and the age at the pubertal milestone. Increased PFOA had a statistically significant direct effect of delay on all three milestones, as did BMI. Perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDeA), and 2-(N-methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) also were associated with later thelarche, and Me-PFOSA-AcOH also with later pubarche. PFOA was inversely associated with DHEAS (푝<0.01), E1 (푝=0.04), and T (푝=0.03) concentrations at 6 months prior to puberty. CONCLUSIONS: PFAS may delay pubertal onset through the intervening effects on BMI and reproductive hormones. The decreases in DHEAS and E1 associated with PFOA represent biological biomarkers of effect consistent with the delay in onset of puberty. [ABSTRACT FROM AUTHOR]

BACKGROUND: Children are routinely exposed to chemicals known or suspected of harming brain development. Targeting Environmental Neuro- Development Risks (Project TENDR), an alliance of >50 leading scientists, health professionals, and advocates, is working to protect children from these toxic chemicals and pollutants, especially the disproportionate exposures experienced by children from families with low incomes and families of color. OBJECTIVE: This scoping review was initiated to map existing literature on disparities in neurodevelopmental outcomes for U.S. children from population groups who have been historically economically/socially marginalized and exposed to seven exemplar neurotoxicants: combustion-related air pollution (AP), lead (Pb), mercury (Hg), organophosphate pesticides (OPs), phthalates (Phth), polybrominated diphenyl ethers (PBDEs), and polychlorinated biphenyls (PCBs). METHODS: Systematic literature searches for the seven exemplar chemicals, informed by the Population, Exposure, Comparator, Outcome (PECO) framework, were conducted through 18 November 2022, using PubMed, CINAHL Plus (EBSCO), GreenFILE (EBSCO), and Web of Science sources. We examined these studies regarding authors’ conceptualization and operationalization of race, ethnicity, and other indicators of sociodemographic and socioeconomic disadvantage; whether studies presented data on exposure and outcome disparities and the patterns of those disparities; and the evidence of effect modification by or interaction with race and ethnicity. RESULTS: Two hundred twelve individual studies met the search criteria and were reviewed, resulting in 218 studies or investigations being included in this review. AP and Pb were the most commonly studied exposures. The most frequently identified neurodevelopmental outcomes were cognitive and behavioral/psychological. Approximately a third (74 studies) reported investigations of interactions or effect modification with 69% (51 of 74 studies) reporting the presence of interactions or effect modification. However, less than half of the studies presented data on disparities in the outcome or the exposure, and fewer conducted formal tests of heterogeneity. Ninety-two percent of the 165 articles that examined race and ethnicity did not provide an explanation of their constructs for these variables, creating an incomplete picture. DISCUSSION: As a whole, the studies we reviewed indicated a complex story about how racial and ethnic minority and low-income children may be disproportionately harmed by exposures to neurotoxicants, and this has implications for targeting interventions, policy change, and other necessary investments to eliminate these health disparities. We provide recommendations on improving environmental epidemiological studies on environmental health disparities. To achieve environmental justice and health equity, we recommend concomitant strategies to eradicate both neurotoxic chemical exposures and systems that perpetuate social inequities. [ABSTRACT FROM AUTHOR]

BACKGROUND: Personal care products are a notable source of exposure to endocrine-disrupting chemicals (EDCs). Racial/ethnic differences in the use of hair products containing EDCs are reported, with women and children of color more commonly using hair products that are hormonally active and contain EDCs than other racial/ethnic groups. There is limited research examining the neighborhood-level social and economic factors that may contribute to these reported disparities. OBJECTIVES: We aimed to examine the safety of hair products across sociodemographically diverse neighborhoods in Boston, Massachusetts. METHODS: Eight neighborhoods were identified based on indicators of race/ethnicity and socioeconomic status (SES). We randomly selected 50 stores and collected data on the hair products for sale and their corresponding Environmental Working Group (EWG) Skin Deep hazard score. The association between neighborhood and EWG hazard category (low, moderate, high) was examined using a multinomial logistic regression. RESULTS: A total of 14,019 hair products were identified in the eight neighborhoods. When considering products with EWG hazard scores, Roxbury, a lower income community of color, and Mission Hill, a lower income community, were reported to have a higher percentage of high-hazard hair products in comparison with Beacon Hill [12.2% (163/1,332), 11.4% (65/571) vs. 7.9% (30/382), respectively]. Differences between the safety of hair products were observed, with Roxbury and Mission Hill reporting more than a 2-fold higher risk ratio (RR) of finding hair products with high vs. low EWG scores in comparison with that of Beacon Hill [RR for Roxbury: 2.3, 95% confidence interval (CI): 1.1, 4.6; RR for Mission Hill: 2.3, 95% CI: 1.0, 5.4]. Other neighborhoods were also observed to have an increased RR in comparison with Beacon Hill, however, with 95% CIs that extended beyond the null. DISCUSSION: Retail stores in neighborhoods with a higher percentage of residents of color and lower SES were found to be more likely to sell products with high hazard scores than stores in a higher SES and predominately non-Hispanic White neighborhood. [ABSTRACT FROM AUTHOR]

This paper reviews approximate confidence intervals for some effect parameters common in cancer epidemiology. These methods have computational feasibility and give nearly nominal coverage rates. In the analysis of crude data, the simplest type of epidemiologic analysis, parameters of interest are the odds ratio in case-control studies and the rate ratio and difference in cohort studies. These parameters can estimate the instantaneous-incidence-rate ratio and difference that are the most meaningful effect measures in cancer epidemiology. Approximate confidence intervals for these parameters including the classical Cornfield's method are mainly based on efficient scores. When some confounding factors exist, stratified analysis and summary measures for effect parameters are needed. Since the Mantel-Haenszel estimators have been widely used by epidemiologists as summary measures, confidence intervals based on the Mantel-Haenszel estimators are described. The paper also discusses recent developments in these methods.

BACKGROUND: Greenness, referring to a measurement of the density of vegetated land (e.g., gardens, parks, grasslands), has been linked with many human health outcomes. However, the evidence on greenness exposure and human microbiota remains limited, inconclusive, drawn from specific regions, and based on only modest sample size. OBJECTIVES: We aimed to study the association between greenness exposure and human microbial diversity and composition in a large sample across 34 countries and regions. METHODS: We explored associations between residential greenness and human microbial alpha-diversity, composition, and genus abundance using data from 34 countries. Greenness exposure was assessed using the normalized difference vegetation index and the enhanced vegetation index mean values in the month before sampling. We used linear regression models to estimate the association between greenness and microbial alpha-diversity and tested the effect modification of age, sex, climate zone, and pet ownership of participants. Differences in microbial composition were tested by permutational multivariate analysis of variance based on Bray–Curtis distance and differential taxa were detected using the DESeq2 R package between two greenness exposure groups split by median values of greenness. RESULTS: We found that higher greenness was significantly associated with greater richness levels in the palm and gut microbiota but decreased evenness in the gut microbiota. Pet ownership and climate zone modified some associations between greenness and alpha-diversity. Palm and gut microbial composition at the genus level also varied by greenness. Higher abundances of the genera Lactobacillus and Bifidobacterium, and lower abundances of the genera Anaerotruncus and Streptococcus, were observed in people with higher greenness levels. DISCUSSION: These findings suggest that residential greenness was associated with microbial richness and composition in the human skin and gut samples, collected across different geographic contexts. Future studies may validate the observed associations and determine whether they correspond to improvements in human health. [ABSTRACT FROM AUTHOR]

BACKGROUND: More intense cyclones are expected in the future as a result of climate change. A comprehensive review is urgently needed to summarize and update the evidence on the health effects of cyclones. OBJECTIVES: We aimed to provide a systematic review with meta-analysis of current evidence on the risks of all reported health outcomes related to cyclones and to identify research gaps and make recommendations for further research. METHODS: We systematically searched five electronic databases (MEDLINE, Embase, PubMed, Scopus, and Web of Science) for relevant studies in English published before 21 December 2022. Following the Preferred Reporting Items for Systematic reviews and Meta-Analysis (PRISMA) guidelines, we developed inclusion criteria, screened the literature, and included epidemiological studies with a quantitative risk assessment of any mortality or morbidity-related outcomes associated with cyclone exposures. We extracted key data and assessed study quality for these studies and applied meta-analyses to quantify the overall effect estimate and the heterogeneity of comparable studies. RESULTS: In total, 71 studies from eight countries (the United States, China, India, Japan, the Philippines, South Korea, Australia, Brazil), mostly the United States, were included in the review. These studies investigated the all-cause and cause-specific mortality, as well as morbidity related to injury, cardiovascular diseases (CVDs), respiratory diseases, infectious diseases, mental disorders, adverse birth outcomes, cancer, diabetes, and other outcomes (e.g., suicide rates, gender-based violence). Studies mostly included only one high-amplitude cyclone (cyclones with a Saffir–Simpson category of 4 or 5, i.e., Hurricanes Katrina or Sandy) and focused on mental disorders morbidity and all-cause mortality and hospitalizations. Consistently elevated risks of overall mental health morbidity, post-traumatic stress disorder (PTSD), as well as all-cause mortality or hospitalizations, were found to be associated with cyclones. However, the results for other outcomes were generally mixed or limited. A statistically significant overall relative risk of 1.09 [95% confidence interval (CI): 1.04, 1.13], 1.18 (95% CI: 1.12, 1.25), 1.15 (95% CI: 1.13, 1.18), 1.26 (95% CI: 1.05, 1.50) was observed for all-cause mortality, all-cause hospitalizations, respiratory disease, and chronic obstructive pulmonary disease hospitalizations, respectively, after cyclone exposures, whereas no statistically significant risks were identified for diabetes mortality, heart disease mortality, and preterm birth. High between-study heterogeneity was observed. CONCLUSIONS: There is generally consistent evidence supporting the notion that high-amplitude cyclones could significantly increase risks of mental disorders, especially for PTSD, as well as mortality and hospitalizations, but the evidence for other health outcomes, such as chronic diseases (e.g., CVDs, cancer, diabetes), and adverse birth outcomes remains limited or inconsistent. More studies with rigorous exposure assessment, of larger spatial and temporal scales, and using advanced modeling strategy are warranted in the future, especially for those small cyclone-prone countries or regions with low and middle incomes. [ABSTRACT FROM AUTHOR]

BACKGROUND: Neural tube defects (NTDs) affect >300,000 pregnancies worldwide annually. Few nongenetic factors, other than folate deficiency, have been identified that may provide intervenable solutions to reduce the burden of NTDs. Prenatal exposure to toxic metals [arsenic (As), cadmium (Cd), mercury (Hg), manganese (Mn) and lead (Pb)] may increase the risk of NTDs. Although a growing epidemiologic literature has examined associations, to our knowledge no systematic review has been conducted to date. OBJECTIVE: Through adaptation of the Navigation Guide systematic review methodology, we aimed to answer the question “does exposure to As, Cd, Hg, Mn, or Pb during gestation increase the risk of NTDs?” and to assess challenges to evaluating this question given the current evidence. METHODS: We selected available evidence on prenatal As, Cd, Hg, Mn, or Pb exposure and risk of specific NTDs (e.g., spina bifida, anencephaly) or all NTDs via a comprehensive search across MEDLINE, Embase, Web of Science, and TOXLINE databases and applied inclusion/exclusion criteria. We rated the quality and strength of the evidence for each metal. We applied a customized risk of bias protocol and evaluated the sufficiency of evidence of an effect of each metal on NTDs. RESULTS: We identified 30 studies that met our criteria. Risk of bias for confounding and selection was high in most studies, but low for missing data. We determined that, although the evidence was limited, the literature supported an association between prenatal exposure to Hg or Mn and increased risk of NTDs. For the remaining metals, the evidence was inadequate to establish or rule out an effect. CONCLUSION: The role of gestational As, Cd, or Pb exposure in the etiology of NTDs remains unclear and warrants further investigation in high-quality studies, with a particular focus on controlling confounding, mitigating selection bias, and improving exposure assessment. [ABSTRACT FROM AUTHOR]

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

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

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

BACKGROUND: Seasonal temperature variability remains understudied and may be modified by climate change. Most temperature–mortality studies examine short-term exposures using time-series data. These studies are limited by regional adaptation, short-term mortality displacement, and an inability to observe longer-term relationships in temperature and mortality. Seasonal temperature and cohort analyses allow the long-term effects of regional climatic change on mortality to be analyzed. OBJECTIVES: We aimed to carry out one of the first investigations of seasonal temperature variability and mortality across the contiguous United States. We also investigated factors that modify this association. Using adapted quasi-experimental methods, we hoped to account for unobserved confounding and to investigate regional adaptation and acclimatization at the ZIP code level. METHODS: We examined the mean and standard deviation (SD) of daily temperature in the warm (April–September) and cold (October–March) season in the Medicare cohort from 2000 to 2016. This cohort comprised 622,427,230 y of person-time in all adults over the age of 65 y from 2000 to 2016. We used daily mean temperature obtained from gridMET to develop yearly seasonal temperature variables for each ZIP code. We used an adapted difference-in-difference approach model with a three-tiered clustering approach and meta-analysis to observe the relationship between temperature variability and mortality within ZIP codes. Effect modification was assessed with stratified analyses by race and population density. RESULTS: For every 1°C increase in the SD of warm and cold season temperature, the mortality rate increased by 1.54% [95% confidence interval (CI): 0.73%, 2.15%] and 0.69% (95% CI: 0.22%, 1.15%) respectively. We did not see significant effects for seasonal mean temperatures. Participants who were classified by Medicare into an “other” race group had smaller effects than those classified as White for Cold and Cold SD and areas with lower population density had larger effects for Warm SD. DISCUSSION: Warm and cold season temperature variability were significantly associated with increased mortality rates in U.S. individuals over the age of 65 y, even after controlling for seasonal temperature averages. Warm and cold season mean temperatures showed null effects on mortality. Cold SD had a larger effect size for those who were in the racial subgroup other, whereas Warm SD was more harmful for those living in lower population density areas. This study adds to the growing calls for urgent climate mitigation and environmental health adaptation and resiliency. [ABSTRACT FROM AUTHOR]

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

BACKGROUND: We previously reported associations of prenatal exposure to organophosphate (OP) pesticides with poorer neurodevelopment in early childhood and at school age, including poorer cognitive function and more behavioral problems, in the Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS), a birth cohort study in an agriculture community. OBJECTIVE: We investigated the extent to which early-life exposure to OP pesticides is associated with behavioral problems, including mental health, in youth during adolescence and early adulthood. METHODS: We measured urinary dialkylphosphates (DAPs), nonspecific OP metabolites, in urine samples collected from mothers twice during pregnancy (13 and 26 wk) and at five different times in their children (ages 6 months to 5 y). We assessed maternal report and youth report of externalizing and internalizing behavior problems using the Behavior Assessment System for Children, 2nd edition (BASC-2), when the youth were ages 14, 16, and 18 y. Because there was evidence of nonlinearity, we estimated associations across quartiles of DAPs and modeled repeated outcome measures using generalized estimating equations. RESULTS: There were 335 youths with prenatal maternal DAP measures and 14-. 16-, or 18-y BASC-2 scores. Prenatal maternal DAP concentrations (specific gravity–adjusted median, Q1–Q3=159.4, 78:7–350.4 nmol=L) were associated with higher T-scores (more behavior problems) from maternal report, including more hyperactivity [fourth vs. first quartile of exposure β=2.32; 95% confidence interval (CI): 0.18, 4.45], aggression (β=1.90; 95% CI: 0.15, 3.66), attention problems (β=2.78; 95% CI: 0.26, 5.30), and depression (β=2.66; 95% CI: 0.08, 5.24). Associations with youth report of externalizing problems were null, and associations with depression were suggestive (fourth vs. first quartile of exposure β=2.15; 95% CI: -0.36, 4.67). Childhood DAP metabolites were not associated with behavioral problems. DISCUSSION: We found associations of prenatal, but not childhood, urinary DAP concentrations with adolescent/young adult externalizing and internalizing behavior problems. These findings are consistent with prior associations we have reported with neurodevelopmental outcomes measured earlier in childhood in CHAMACOS participants and suggests that prenatal exposure to OP pesticides may have lasting effects on the behavioral health of youth as they mature into adulthood, including their mental health. [ABSTRACT FROM AUTHOR]

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

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

BACKGROUND: Per- and polyfluoroalkyl substances (PFAS) have been previously linked to polycystic ovarian syndrome (PCOS), but only a few legacy PFAS were examined. OBJECTIVES: This study aimed to explore this association with a variety of PFAS, including legacy, branched-chain isomers, and emerging alternatives, as well as a PFAS mixture. METHODS: From 2014 to 2016, we conducted a multicenter, hospital-based case–control study on environmental endocrine disruptors and infertility in China. Three hundred sixty-six women with PCOS-related infertility and 577 control participants without PCOS were included in the current analysis. Twenty-three PFAS, including 3 emerging PFAS alternatives, 6 linear and branched PFAS isomers, 6 short-chain PFAS, and 8 legacy PFAS, were quantified in the plasma. Logistic regression and two multipollutant models [quantile-based g-computation (QGC) and Bayesian kernel machine regression (BKMR) methods] were used to assess the association of individual PFAS and PFAS mixture with PCOS, as well as the potential interactions among the congeners. RESULTS: After adjusting for potential confounders, Each 1-standard deviation higher difference in ln-transformed 6:2 chlorinated perfluoroalkyl ether sulfonic acid (6:2 Cl-PFESA) and hexafluoropropylene oxide dimer acid (HFPO-DA) level was significantly associated with a 29% (95% CI: 1.11, 1.52) and 39% (95% CI:1.16, 1.68) higher odds of PCOS, respectively. Meanwhile, branched isomers of perfluorooctane sulfonate (PFOS) and perfluorohexane sulfonate (PFHxS) (i.e., br-PFHxS, n-PFOS, 1m-PFOS, Σ3,4,5m-PFOS), short-chain PFAS (i.e., PFPeS and PFHxA) and other legacy PFAS [i.e., total concentrations of PFOS (T-PFOS), and perfluorododecanoic acid (PFDoA)] were significantly associated with increased odds of PCOS. The PFAS mixture was positively related to PCOS in the BKMR model. A similar trend was observed in QGC model, a ln-unit increase in the PFAS mixture was associated with a 20% increased risk of PCOS [adjusted odds ratio (aOR)=1.20 (95% CI: 1.06, 1.37)]. After controlling for other PFAS homologs, 6:2 Cl-PFESA, HFPO-DA, Σ3,4,5m-PFOS, and PFDoA were the major contributors based on the QGC and BKMR models. The associations were more pronounced in overweight/obese women. CONCLUSIONS: In this group of women, environmental exposure to a PFAS mixture was associated with an elevated odds of PCOS, with 6:2 Cl- PFESA, HFPO-DA, Σ3,4,5m-PFOS, and PFDoA being the major contributors, especially in overweight/obese women. [ABSTRACT FROM AUTHOR]

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

BACKGROUND: Recent studies have reported the association between air pollution exposure and reduced kidney function. However, it is unclear whether air pollution is associated with an increased risk of acute kidney injury (AKI). OBJECTIVES: To address this gap in knowledge, we investigated the effect estimates of long-term exposures to fine particulate matter [PM ≤ 2.5 μm in aerodynamic diameter (PM2.5)], nitrogen dioxide (NO2), and ozone (O3) on the risk of first hospital admission for AKI using nationwide Medicare data. METHODS: This nationwide population-based longitudinal cohort study included 61,300,754 beneficiaries enrolled in Medicare Part A fee-for-service (FFS) who were ≥65 years of age and resided in the continental United States from the years 2000 through 2016. We applied Cox-equivalent Poisson models to estimate the association between air pollution and first hospital admission for AKI. RESULTS: Exposure to PM2.5, NO2, and O3 was associated with increased risk for first hospital admission for AKI, with hazard ratios (HRs) of 1.17 (95% CI: 1.16, 1.19) for a 5-μg/m³ increase in PM2.5, 1.12 (95% CI: 1.11, 1.13) for a 10-ppb increase in NO2, and 1.03 (95% CI: 1.02, 1.04) for a 10-ppb increase in summer-period O3 (June to September). The associations persisted at annual exposures lower than the current National Ambient Air Quality Standard. DISCUSSION: This study found an association between exposures to air pollution and the risk of the first hospital admission with AKI, and this association persisted even at low concentrations of air pollution. Our findings provide beneficial implications for public health policies and air pollution guidelines to alleviate health care expenditures and the disease burden attributable to AKI. [ABSTRACT FROM AUTHOR]

BACKGROUND: Toxic metals, such as lead (Pb), cadmium (Cd), arsenic (As), and mercury (Hg), may be associated with a higher risk of gestational hypertension and preeclampsia, whereas manganese (Mn) is an essential metal that may be protective. OBJECTIVES: We estimated the individual, independent, and joint associations of Pb, Cd, As, Hg, and Mn on the risk of developing gestational hypertension and preeclampsia in a cohort of Canadian women. METHODS: Metal concentrations were analyzed in first and third trimester maternal blood (푛=1,560). We measured blood pressure after 20 wk gestation to diagnose gestational hypertension, whereas proteinuria and other complications defined preeclampsia. We estimated individual and independent (adjusted for coexposure) relative risks (RRs) for each doubling of metal concentrations and examined interactions between toxic metals and Mn. We used quantile g-computation to estimate the joint effect of trimester-specific exposures. RESULTS: Each doubling of third trimester Pb (RR = 1.54; 95% CI: 1.06, 2.22) and first trimester blood As (RR = 1.25; 95% CI: 1.01, 1.58) was independently associated with a higher risk of developing preeclampsia. First trimester blood As (RR = 3.40; 95% CI: 1.40, 8.28) and Mn (RR = 0.63; 95% CI: 0.42, 0.94) concentrations were associated with a higher and lower risk, respectively, of developing gestational hypertension. Mn modified the association with As such that the deleterious association with As was stronger at lower concentrations of Mn. First trimester urinary dimethylarsinic acid concentrations were not associated with gestational hypertension (RR = 1.31; 95% CI: 0.60, 2.85) or preeclampsia (RR = 0.92; 95% CI: 0.68, 1.24). We did not observe overall joint effects for blood metals. DISCUSSION: Our results confirm that even low blood Pb concentrations are a risk factor for preeclampsia. Women with higher blood As concentrations combined with lower Mn in early pregnancy were more likely to develop gestational hypertension. These pregnancy complications impact maternal and neonatal health. Understanding the contribution of toxic metals and Mn is of public health importance. [ABSTRACT FROM AUTHOR]

BACKGROUND: Household air pollution (HAP) from inefficient combustion of solid fuels is a major health concern worldwide. However, prospective evidence on the health impacts of solid cooking fuels and risks of chronic digestive diseases remains scarce. OBJECTIVES: We explored the effects of self-reported primary cooking fuels on the incidence of chronic digestive diseases. METHODS: The China Kadoorie Biobank recruited 512,726 participants 30–79 years of age from 10 regions across China. Information on primary cooking fuels at the current and previous two residences was collected via self-reporting at baseline. Incidence of chronic digestive diseases was identified through electronic linkage and active follow-up. Cox proportional hazards regression models were used to estimate adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for the associations of self-reported long-term cooking fuel patterns and weighted duration of self-reported solid cooking fuel use with chronic digestive diseases incidence. Linear trend was tested by assigning the medians of weighted duration in each group and then taking those as continuous variables in the models. Subgroup analyses were undertaken across the baseline characteristics of participants. RESULTS: During 9.1±1.6 y of follow-up, 16,810 new cases of chronic digestive diseases were documented, among which 6,460 were diagnosed as cancers. Compared with long-term cleaner fuel use, self-reported long-term use of solid cooking fuels (i.e., coal, wood) was associated with elevated risks of chronic digestive diseases (HR=1.08; 95% CI: 1.02, 1.13), including nonalcoholic fatty liver disease (NAFLD) (HR=1.43; 95% CI: 1.10, 1.87), hepatic fibrosis/cirrhosis (HR=1.35; 95% CI: 1.05, 1.73), cholecystitis (HR=1.19; 95% CI: 1.07, 1.32), and peptic ulcers (HR=1.15; 95% CI: 1.00, 1.33). The longer the weighted duration of self-reported solid cooking fuel use, the higher the risks of chronic digestive diseases, hepatic fibrosis/cirrhosis, peptic ulcers, and esophageal cancer (푝Trend <0.05). The aforementioned associations were modified by sex and body mass index (BMI). Positive associations of always solid cooking fuel use with chronic digestive disease, hepatic fibrosis/cirrhosis, NAFLD, and cholecystitis were observed among women but not men. The longer the weighted duration of self-reported solid cooking fuel use, the higher the risk of NAFLDamong those with a BMI≥28 kg/m². DISCUSSION: Long-term self-reported solid cooking fuels use was associated with higher risks of chronic digestive diseases. The positive association of HAP from solid cooking fuels with chronic digestive diseases indicates for an imminent promotion of cleaner fuels as public health interventions. [ABSTRACT FROM AUTHOR]

BACKGROUND: Regulatory toxicity values used to assess and manage chemical risks rely on the determination of the point of departure (POD) for a critical effect, which results from a comprehensive and systematic assessment of available toxicity studies. However, regulatory assessments are only available for a small fraction of chemicals. OBJECTIVES: Using in vivo experimental animal data from the U.S. Environmental Protection Agency’s Toxicity Value Database, we developed a semiautomated approach to determine surrogate oral route PODs, and corresponding toxicity values where regulatory assessments are unavailable. METHODS: We developed a curated data set restricted to effect levels, exposure routes, study designs, and species relevant for deriving toxicity values. Effect levels were adjusted to chronic human equivalent benchmark doses (BMDh). We hypothesized that a quantile of the BMDh distribution could serve as a surrogate POD and determined the appropriate quantile by calibration to regulatory PODs. Finally, we characterized uncertainties around the surrogate PODs from intra- and interstudy variability and derived probabilistic toxicity values using a standardized workflow. RESULTS: The BMD[sub h] distribution for each chemical was adequately fit by a lognormal distribution, and the 25th percentile best predicted the available regulatory PODs [푅² =0.78, residual standard error (RSE)=0.53 log10 units]. We derived surrogate PODs for 10,145 chemicals from the curated data set, differentiating between general noncancer and reproductive/developmental effects, with typical uncertainties (at 95% confidence) of a factor of 10 and 12, respectively. From these PODs, probabilistic reference doses (1% incidence at 95% confidence), as well as human population effect doses (10% incidence), were derived. DISCUSSION: In providing surrogate PODs calibrated to regulatory values and deriving corresponding toxicity values, we have substantially expanded the coverage of chemicals from 744 to 8,023 for general noncancer effects, and from 41 to 6,697 for reproductive/developmental effects. These results can be used across various risk assessment and risk management contexts, from hazardous site and life cycle impact assessments to chemical prioritization and substitution. [ABSTRACT FROM AUTHOR]

BACKGROUND: Numerous epidemiological studies have documented the adverse health impact of long-term exposure to fine particulate matter [particulate matter ≤2.5 μm in aerodynamic diameter (PM2.5)] on mortality even at relatively low levels. However, methodological challenges remain to consider potential regulatory intervention's complexity and provide actionable evidence on the predicted benefits of interventions. We propose the parametric g-computation as an alternative analytical approach to such challenges. METHOD: We applied the parametric g-computation to estimate the cumulative risks of nonaccidental death under different hypothetical intervention strategies targeting long-term exposure to PM2.5 in the Canadian Community Health Survey cohort from 2005 to 2015. On both relative and absolute scales, we explored the benefits of hypothetical intervention strategies compared with the natural course that a) set the simulated exposure value at each follow-up year to a threshold value if exposure was above the threshold (8.8 μg/m³, 7.04 μg/m³, 5 μg/m³, and 4 μg/m³), and b) reduced the simulated exposure value by a percentage (5% and 10%) at each follow-up year. We used the 3-y average PM2.5 concentration with 1-y lag at the postal code of respondents’ annual mailing addresses as their long-term exposure to PM2.5. We considered baseline and time-varying confounders, including demographics, behavior characteristics, income level, and neighborhood socioeconomic status. We also included the R syntax for reproducibility and replication. RESULTS: All hypothetical intervention strategies explored led to lower 11-y cumulative mortality risks than the estimated value under the natural course without intervention, with the smallest reduction of 0.20 per 1,000 participants (95% CI: 0.06, 0.34) under the threshold of 8:8 μg/m³, and the largest reduction of 3.40 per 1,000 participants (95% CI: -0.23, 7.03) under the relative reduction of 10% per interval. The reductions in cumulative risk, or numbers of deaths that would have been prevented if the intervention was employed instead of maintaining the status quo, increased over time but flattened toward the end of the follow-up period. Estimates among those ≥65 years of age were greater with a similar pattern. Our estimates were robust to different model specifications. DISCUSSION: We found evidence that any intervention further reducing the long-term exposure to PM2.5 would reduce the cumulative mortality risk, with greater benefits in the older population, even in a population already exposed to low levels of ambient PM2.5. The parametric g-computation used in this study provides flexibilities in simulating real-world interventions, accommodates time-varying exposure and confounders, and estimates adjusted survival curves with clearer interpretation and more information than a single hazard ratio, making it a valuable analytical alternative in air pollution epidemiological research. [ABSTRACT FROM AUTHOR]

BACKGROUND: Large electricity-generating wind turbines emit both audible sound and inaudible infrasound at very low frequencies that are outside of the normal human range of hearing. Sufferers of wind turbine syndrome (WTS) have attributed their ill-health and particularly their sleep disturbance to the signature pattern of infrasound. Critics have argued that these symptoms are psychological in origin and are attributable to nocebo effects. OBJECTIVES: We aimed to test the effects of 72 h of infrasound (1.6–20 Hz at a sound level of ~90 dB pk re 20 μPa, simulating a wind turbine infrasound signature) exposure on human physiology, particularly sleep. METHODS: We conducted a randomized double-blind triple-arm crossover laboratory-based study of 72 h exposure with a >10-d washout conducted in a noise-insulated sleep laboratory in the style of a studio apartment. The exposures were infrasound (~90 dB pk), sham infrasound (same speakers not generating infrasound), and traffic noise exposure [active control; at a sound pressure level of 40–50 dB LAeq,night and 70 dB LAFmax transient maxima, night (2200 to 0700 hours)]. The following physiological and psychological measures and systems were tested for their sensitivity to infrasound: wake after sleep onset (WASO; primary outcome) and other measures of sleep physiology, wake electroencephalography, WTS symptoms, cardiovascular physiology, and neurobehavioral performance. RESULTS: We randomized 37 noise-sensitive but otherwise healthy adults (18–72 years of age; 51% female) into the study before a COVID19-related public health order forced the study to close. WASO was not affected by infrasound compared with sham infrasound (-1.36 min; 95% CI: -6.60, 3.88, 푝 = 0.60) but was worsened by the active control traffic exposure compared with sham by 6.07 min (95% CI: 0.75, 11.39, 푝 = 0.02). Infrasound did not worsen any subjective or objective measures used. DISCUSSION: Our findings did not support the idea that infrasound causes WTS. High level, but inaudible, infrasound did not appear to perturb any physiological or psychological measure tested in these study participants. [ABSTRACT FROM AUTHOR]

BACKGROUND: Evidence for a potential link between air pollution and rheumatoid arthritis (RA) is inconsistent, and the modified effect of genetic susceptibility on the relationship between air pollution and RA has not been well studied. OBJECTIVE: Using a general population cohort from the UK Biobank, this study aimed to investigate the associations between various air pollutants and the risk of incident RA and to further estimate the impact of combined exposure to ambient air pollutants on the risk of developing RA under the modification effect of genetic predisposition. METHODS: A total of 342,973 participants with completed genotyping data and who were free of RA at baseline were included in the study. An air pollution score was constructed by summing the concentrations of each pollutant weighted by the regression coefficients with RA from single-pollutant models to assess the combined effect of air pollutants, including particulate matter (PM) with diameters ≤ 2.5 µm (PM2.5), between 2.5 and 10 µm (PM2.5–10), and ≤ 10 µm (PM10), as well as nitrogen dioxide (NO2) and nitrogen oxides (NOx). In addition, the polygenic risk score (PRS) of RA was calculated to characterize individual genetic risk. The Cox proportional hazard model was used to estimate hazard ratios (HRs) and 95% confidence intervals (95% CIs) of associations of single air pollutant, air pollution score, or PRS with incident RA. RESULTS: During a median follow-up time of 8.1 y, 2,034 incident events of RA were recorded. The HRs (95% CIs) of incident RA per interquartile range increment in PM2.5, PM2.5-10, PM10, NO2, and NOx were 1.07 (1.01, 1.13), 1.00 (0.96, 1.04), 1.01 (0.96, 1.07), 1.03 (0.98, 1.09), and 1.07 (1.02, 1.12), respectively. We also found a positive exposure-response relationship between air pollution score and RA risk (푝Trend = 0.000053). The HR(95% CI) of incident RA was 1.14 (1.00, 1.29) in the highest quartile group compared with the lowest quartile group of the air pollution score. Furthermore, the results of the combined effect of air pollution score and PRS on the RA risk showed that the risk of RA incidence in the highest genetic risk and air pollution score group was almost twice that of the lowest genetic risk and air pollution score group [incidence rate (IR) per 100,000 person-years: 98.46 vs. 51.19, and HR= 1.73 (95% CI: 1.39, 2.17) vs. 1 (reference)], although no statistically significant interaction between the air pollution and genetic risk for incident RA was found (푝Interaction >0.05). DISCUSSION: The results revealed that long-term combined exposure to ambient air pollutants might increase the risk of RA, particularly in those with high genetic risk. [ABSTRACT FROM AUTHOR]

BACKGROUND: Exposure to air pollution has been associated with a higher risk of type 2 diabetes (T2D), but studies investigating whether deprived groups are more susceptible to the harmful effects of air pollution are inconsistent. OBJECTIVES: We aimed to investigate whether the association between air pollution and T2D differed according to sociodemographic characteristics, comorbidity, and coexposures. METHODS: We estimated residential exposure to PM2.5, ultrafine particles (UFP), elemental carbon, and NO2 for all persons living in Denmark in the period 2005–2017. In total, 1.8 million persons 50–80 y of age were included for main analyses of whom 113,985 developed T2D during follow-up. We conducted additional analyses on 1.3 million persons age 35–50 y. Using Cox proportional hazards model (relative risk) and Aalens additive hazard model (absolute risk), we calculated associations between 5-y time-weighted running means of air pollution and T2D in strata of sociodemographic variables, comorbidity, population density, road traffic noise, and green space proximity. RESULTS: Air pollution was associated with T2D, especially among people age 50-80 y, with hazard ratios of 1.17 [95% confidence interval (CI): 1.13, 1.21] per 5 μg/m³ PM2.5 and 1.16 (95% CI: 1.13, 1.19) per 10,000 UFP/cm³. In the age 50-80 y population, we found higher associations between air pollution and T2D among men in comparison with women, people with lower education vs. individuals with high education, people with medium income vs. those with low or high income, people cohabiting vs. those living alone, and people with comorbidities vs. those without comorbidities. We observed no marked changes according to occupation, population density, road noise, or surrounding greenness. In the age 35-50 y population, similar tendencies were observed, except in relation to sex and occupation, where we observed associations with air pollution only among women and blue-collar workers. DISCUSSION: We found stronger associations between air pollution and T2D among people with existing comorbidities and weaker associations among people with high socioeconomic status in comparison with those with lower socioeconomic status. [ABSTRACT FROM AUTHOR]

BACKGROUND: Fine particulate matter (PM2.5) has been found to be detrimental to respiratory health of children, but few studies have examined the effects of prenatal PM2.5 oxidative potential (OP) on lung function in infants and preschool children. OBJECTIVES: We estimated the associations of personal exposure to PM2.5  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 (N2MBW) test, performed at 6 wk, and airwave oscillometry (AOS) performed at 3 y. Associations of prenatal PM2.5  mass and OP with lung function parameters were estimated using multiple linear regressions. RESULTS: In neonates, an interquartile (IQR) increase in OPDTTv (0.89nmol/min/m³) was associated with a decrease in functional residual capacity (FRC) measured by N2MBW  [β = -2.26 mL ; 95% confidence interval (CI): -4.68, 0.15]. Associations with PM2.5  showed similar patterns in comparison with OPDTTv  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 (Rrs7-19) from AOS tended to be associated with higher OPDTTv  (β = 0.09hPa×s/L ; 95% CI: -0.06, 0.24) and OPAAv  (IQR = 1.14nmol/min/m³ ; β = 0.12hPa×s/L ; 95% CI: -0.04, 0.27) but not with PM2.5  (IQR = 6.9µg/m³ ; β = 0.02hPa×s/L ; 95% CI: -0.13, 0.16). Results for FRC and Rrs7-19 remained similar in OP models adjusted on PM2.5. DISCUSSION: Prenatal exposure to OPDTTv was associated with several offspring lung function parameters over time, all related to lung volumes. [ABSTRACT FROM AUTHOR]