The Joint Effects of Thunderstorms and Power Outages on Respiratory-Related Emergency Visits and Modifying and Mediating Factors of This Relationship.

BACKGROUND: While limited studies have evaluated the health impacts of thunderstorms and power outages (POs) separately, few have assessed their joint effects. We aimed to investigate the individual and joint effects of both thunderstorms and POs on respiratory diseases, to identify disparities by demographics, and to examine the modifications and mediations by meteorological factors and air pollution. METHODS: Distributed lag nonlinear models were used to examine exposures during three periods (i.e., days with both thunderstorms and POs, thunderstorms only, and POs only) in relation to emergency department visits for respiratory diseases (2005-2018) compared to controls (no thunderstorm/no PO) in New York State (NYS) while controlling for confounders. Interactions between thunderstorms and weather factors or air pollutants on health were assessed. The disparities by demographics and seasons and the mediative effects by particulate matter with aerodynamic diameter ≤2.5µm (PM2.5) and relative humidity (RH) were also evaluated. RESULTS: Thunderstorms and POs were independently associated with total and six subtypes of respiratory diseases in NYS [highest risk ratio (RR) = 1.12; 95% confidence interval (CI): 1.08, 1.17], but the impact was stronger when they co-occurred (highest RR = 1.44; 95% CI: 1.22, 1.70), especially during grass weed, ragweed, and tree pollen seasons. The stronger thunderstorm/PO joint effects were observed on chronic obstructive pulmonary diseases, bronchitis, and asthma (lasted 0-10 d) and were higher among residents who lived in rural areas, were uninsured, were of Hispanic ethnicity, were 6-17 or over 65 years old, and during spring and summer. The number of comorbidities was significantly higher by 0.299-0.782/case. Extreme cold/heat, high RH, PM2.5, and ozone concentrations significantly modified the thunderstorm-health effect on both multiplicative and additive scales. Over 35% of the thunderstorm effects were mediated by PM2.5 and RH. CONCLUSION: Thunderstorms accompanied by POs showed the strongest respiratory effects. There were large disparities in thunderstorm-health associations by demographics. Meteorological factors and air pollution levels modified and mediated the thunderstorm-health effects. https://doi.org/10.1289/EHP13237.

Bridging Differences in Cohort Analyses of the Relationship between Secondhand Smoke Exposure during Pregnancy and Birth Weight: The Transportability Framework in the ECHO Program.

BACKGROUND: Estimates for the effects of environmental exposures on health outcomes, including secondhand smoke (SHS) exposure, often present considerable variability across studies. Knowledge of the reasons behind these differences can aid our understanding of effects in specific populations as well as inform practices of combining data from multiple studies. OBJECTIVES: This study aimed to assess the presence of effect modification by measured sociodemographic characteristics on the effect of SHS exposure during pregnancy on birth weights that may drive differences observed across cohorts. We also aimed to quantify the extent to which differences in the cohort mean effects observed across cohorts in the Environmental influences on Child Health Outcomes (ECHO) consortium are due to differing distributions of these characteristics. METHODS: We assessed the presence of effect modification and transportability of effect estimates across five ECHO cohorts in a total of 6,771 mother-offspring dyads. We assessed the presence of effect modification via gradient boosting of regression trees based on the H-statistic. We estimated individual cohort effects using linear models and targeted maximum likelihood estimation (TMLE). We then estimated transported effects from one cohort to each of the remaining cohorts using a robust nonparametric estimation approach relying on TMLE estimators and compared them to the original effect estimates for these cohorts. RESULTS: Observed effect estimates varied across the five cohorts, ranging from significantly lower birth weight associated with exposure [-167.3g; 95% confidence interval (CI): -270.4, -64.1] to higher birth weight with wide CIs, including the null (42.4g; 95% CI: -15.0, 99.8). Transported effect estimates only minimally explained differences in the point estimates for two out of the four cohort pairs. DISCUSSION: Our findings of weak to moderate evidence of effect modification and transportability indicate that unmeasured individual-level and contextual factors and sources of bias may be responsible for differences in the effect estimates observed across ECHO cohorts. https://doi.org/10.1289/EHP13961.

Association between PM2.5 constituents and cardiometabolic risk factors: Exploring individual and combined effects, and mediating inflammation.

BACKGROUND: The individual and combined effects of PM2.5 constituents on cardiometabolic risk factors are sparsely investigated. Besides, the key cardiometabolic risk factor that PM2.5 constituents targeted and the biological mechanisms remain unclear. METHOD: A multistage, stratified cluster sampling survey was conducted in two typically air-polluted Chinese cities. The PM2.5 and its constituents including sulfate, nitrate, ammonium, organic matter, and black carbon were predicted using a machine learning model. Twenty biomarkers in three category were simultaneously adopted as cardiometabolic risk factors. We explored the individual and mixture association of long-term PM2.5 constituents with these markers using generalized additive model and quantile-based g-computation, respectively. To minimize potential confounding effects, we accounted for covariates including demographic, lifestyle, meteorological, temporal trends, and disease-related information. We further used ROC curve and mediation analysis to identify the key subclinical indicators and explore whether inflammatory mediators mediate such association, respectively. RESULT: PM2.5 constituents was positively correlated with HOMA-B, TC, TG, LDL-C and LCI, and negatively correlated with PP and RC. Further, PM2.5 constituent mixture was positive associated with DBP, MAP, HbA1c, HOMA-B, AC, CRI-1 and CRI-2, and negative associated with PP and HDL-C. The ROC analysis further reveals that multiple cardiometabolic risk factors can collectively discriminate exposure to PM2.5 constituents (AUC>0.9), among which PP and CRI-2 as individual indicators exhibit better identifiable performance for nitrate and ammonium (AUC>0.75). We also found that multiple blood lipid indicators may be affected by PM2.5 and its constituents, possibly mediated through complement C3 or hsCRP. CONCLUSION: Our study suggested associations of individual and combined PM2.5 constituents exposure with cardiometabolic risk factors. PP and CRI-2 were the targeted markers of long-term exposure to nitrate and ammonium. Inflammation may serve as a mediating factor between PM2.5 constituents and dyslipidemia, which enhance current understanding of potential pathways for PM2.5-induced preclinical cardiovascular responses.

Effects of chemical composition of ambient PM2.5 measured in Seoul on potential health risks and generation of reactive oxygen species.

This study assesses the health effects associated with the chemical species of ambient particulate matter (PM) with an aerodynamic diameter ≤2.5 µm (PM2.5) in Seoul, focusing on identifying key chemical constituents and their sources. We employed two approaches to estimate health risks: (1) evaluating carcinogenic and noncarcinogenic risks using IRIS (Integrated Risk Information System) data from the US EPA (Environmental Protection Agency), and (2) quantifying the generation of hydroxyl radicals (·OH) following exposure to PM2.5 in surrogate lung fluid (SLF). Our results show a significant impact on human health from certain elements (Cr, Ni, As, and Cd) and polycyclic aromatic hydrocarbons (PAHs) (DaeP, DahA, and BaP for carcinogenic risks; BaP and BeP for noncarcinogenic risks). Notably, Cr and BaP, which are influential in both risk assessment and ·OH generation, highlight their significant roles in human health impacts. However, other components (e.g., CPP, BaP, BghiP, BaA, CHR, PYR, FLT, Ca, Mg, and Cu), though contributors to ·OH generation, were not included in the EPA's health risk assessment, suggesting a need for a broader PM2.5 compositional analysis to more accurately determine exposure concentrations and assess inhalation risks. These components predominantly originate from anthropogenic sources, such as combustion, vehicles, and industrial activities, underscoring the significant health implications of the pollutants emitted from these sources. The study concluded that focusing solely on the mass reduction of PM2.5 may not suffice; a dual approach that reduces both mass concentration and chemical-specific health risks is imperative for effective public health protection.

Diurnal rail noise measurement, analysis, and evaluation of associated health impacts on residents living in the proximity of rail track area.

In India, railway is the major transportation mode for carrying goods and people. The tracks for the movement of the rail were initially constructed in the city for the pre-eminence and expediency of the vantage of the people. Rapid modernization and increasing population in the city crammed the area around the railway tracks. Moving rail on the tracks passing through the city is not compatible, which is creating problems for the nearby residents. In the urban and suburban regions, the railway noise has become a major problem. This study was conducted to examine the perception of the physiological and psychological effects of railway noise in the nearby areas of railway stations in Delhi, India. For this purpose, 10 sites near the railway station were selected for the study. To assess the impact of railway noise pollution on the health of humans, a questionnaire survey was conducted. The data of 344 individuals were collected through the questionnaire survey and analyzed to get the perception towards railway noise. Noise level was monitored by a Sound Level Meter (SLM) and the equivalent noise level (Leq) in dB(A) was used to compute the noise pollution in three shifts, i.e., morning, noon, and evening time. Results showed that 57.65% of female and 86.11% of male respondents in the survey reported the disturbance due to railway noise. The level of noise pollution was found higher in the evening time as compared to the noon and morning period, which exceeds the limit set by the Central Pollution Control Board (CPCB) at all the monitored locations. Findings of the study show that the primary cause of the health problems is railroad noise, which is negatively impacting the health of the residents, who are living in the proximity of the rail track region. The perception survey reported that headache, sleep disturbance, irritation, and stress are common health issues among the locals residing around the railway track proximity in Delhi.

Trends in childhood leukemia incidence in urban countries and their relation to environmental factors, including space weather.

Leukemia is the most common cancer in children. Its incidence has been increasing worldwide since 1910th, suggesting the presence of common sources of the disease, most likely related to people's lifestyle and environment. Understanding the relationship between childhood leukemia and environmental conditions is critical to preventing the disease. This discussion article examines established potentially-carcinogenic environmental factors, such as vehicle emissions and fires, alongside space weather-related parameters like cosmic rays and the geomagnetic field. To discern the primary contributor, we analyze trends and annual variations in leukemia incidence among 0-14-year-olds in the United States, Canada, Australia, and Russia from 1990 to 2018. Comparisons are drawn with the number of vehicles (representing gasoline emissions) and fire-affected land areas (indicative of fire-related pollutants), with novel data for Russia introduced for the first time. While childhood leukemia incidence is rising in all countries under study, the rate of increase in Russia is twice that of other nations, possibly due to a delayed surge in the country's vehicle fleet compared to others. This trend in Russia may offer insights into past leukemia levels in the USA, Canada, and Australia. Our findings highlight vehicular emissions as the most substantial environmental hazard for children among the factors examined. We also advocate for the consideration of potential modulation of carcinogenic effects arising from variations in cosmic ray intensity, as well as the protective role of the geomagnetic field. To support the idea, we provide examples of potential space weather effects at both local and global scales. The additional analysis includes statistical data from 49 countries and underscores the significance of the magnetic field dip in the South Atlantic Anomaly in contributing to a peak in childhood leukemia incidence in Peru, Ecuador and Chile. We emphasize the importance of collectively assessing all potentially carcinogenic factors for the successful future predictions of childhood leukemia risk in each country.

Sources and human health risks associated with potentially toxic elements (PTEs) in urban dust: A global perspective.

Long-term exposure to urban dust containing potentially toxic elements (PTEs) poses detrimental impacts on human health. However, studies estimating human health risks in urban dusts from a global perspective are scarce. We evaluated data for twelve PTEs in urban dusts across 59 countries from 463 published articles, including their concentrations, input sources, and probabilistic risks to human health. We found that 34.1 and 60.3% of those investigated urban dusts have been heavily contaminated with As and Cd, respectively. The input of PTEs was significantly correlated with economic structure due to emissions of industrial activities and traffic emissions being the major sources. Based on the Monte Carlo simulation, we found that the mean hazard index below the safe threshold (1.0) could still cause non-negligible risks to human health. Arsenic and Cr were the major PTEs threatening human health, and relatively high risk levels were observed in cities in China, Korea, Chile, Malaysia, and Australia. Importantly, our analysis suggested that PTEs threaten the health of approximately 92 million adults and 280 million children worldwide. Overall, our study provides important foundational understanding and guidance for policy decision-making to reduce the potential risks associated with PTE exposure and to promote sustainable development of urban economies.

Early life ambient air pollution, household fuel use, and under-5 mortality in Ghana.

INTRODUCTION: Environmental exposures, such as ambient air pollution and household fuel use affect health and under-5 mortality (U5M) but there is a paucity of data in the Global South. This study examined early-life exposure to ambient particulate matter with a diameter of 2.5 µm or less (PM2.5), alongside household characteristics (including self-reported household fuel use), and their relationship with U5M in the Navrongo Health and Demographic Surveillance Site (HDSS) in northern Ghana. METHODS: We employed Satellite-based spatiotemporal models to estimate the annual average PM2.5 concentrations with the Navrongo HDSS area (1998 to 2016). Early-life exposure levels were determined by pollution estimates at birth year. Socio-demographic and household data, including cooking fuel, were gathered during routine surveillance. Cox proportional hazards models were applied to assess the link between early-life PM2.5 exposure and U5M, accounting for child, maternal, and household factors. FINDINGS: We retrospectively studied 48,352 children born between 2007 and 2017, with 1872 recorded deaths, primarily due to malaria, sepsis, and acute respiratory infection. Mean early-life PM2.5 was 39.3 µg/m3, and no significant association with U5M was observed. However, Children from households using "unclean" cooking fuels (wood, charcoal, dung, and agricultural waste) faced a 73 % higher risk of death compared to those using clean fuels (adjusted HR = 1.73; 95 % CI: 1.29, 2.33). Being born female or to mothers aged 20-34 years were linked to increased survival probabilities. INTERPRETATION: The use of "unclean" cooking fuel in the Navrongo HDSS was associated with under-5 mortality, highlighting the need to improve indoor air quality by introducing cleaner fuels.

Mechanistic insights into cardiovascular effects of ultrafine particle exposure: A longitudinal panel study.

BACKGROUND: Ultrafine particle (UFP) has been linked with higher risks of cardiovascular diseases; however, the biological mechanisms remain to be fully elucidated. OBJECTIVES: This study aims to investigate the cardiovascular responses to short-term UFP exposure and the biological pathways involved. METHODS: A longitudinal panel study was conducted among 32 healthy, non-smoking young adults in Shanghai, China, who were engaged in five rounds of follow-ups between December 2020 and November 2021. Individual exposures were calculated based on the indoor and outdoor real-time measurements. Blood pressure, arterial stiffness, targeted biomarkers, and untargeted proteomics and metabolomics were examined during each follow-up. Linear mixed-effect models were applied to analyze the exposure and health data. The differential proteins and metabolites were used for pathway enrichment analyses. RESULTS: Short-term UFP exposure was associated with significant increases in blood pressure and arterial stiffness. For example, systolic blood pressure increased by 2.10 % (95 % confidence interval: 0.63 %, 3.59 %) corresponding to each interquartile increase in UFP concentrations at lag 0-3 h, while pulse wave velocity increased by 2.26 % (95 % confidence interval: 0.52 %, 4.04 %) at lag 7-12 h. In addition, dozens of molecular biomarkers altered significantly. These effects were generally present within 24 h after UFP exposure, and were robust to the adjustment of co-pollutants. Molecular changes detected in proteomics and metabolomics analyses were mainly involved in systemic inflammation, oxidative stress, endothelial dysfunction, coagulation, and disturbance in lipid transport and metabolism. DISCUSSION: This study provides novel and compelling evidence on the detrimental subclinical cardiovascular effects in response to short-term UFP exposure. The multi-omics profiling further offers holistic insights into the underlying biological pathways.

Unveiling the intricate connection between per- and polyfluoroalkyl substances and prostate hyperplasia.

The presence of perfluoroalkyl and polyfluoroalkyl substances (PFAS) in various everyday products has raised concerns about their potential impact on prostate health. This study aimed to investigate the effects of different types of PFAS on prostate health, including PFDeA, PFOA, PFOS, PFHxS, and PFNA. To assess the relationship between PFAS exposure and prostate injury, machine learning algorithms were employed to analyze prostate-specific antigen (PSA) metrics. The analysis revealed a linear and positive dose-dependent association between PFOS and the ratio of free PSA to total PSA (f/tPSA). Non-linear dose-response relationships were observed between the other four types of PFAS and the f/tPSA ratio. Additionally, the analysis showed a positive association between the mixture of PFAS and prostate hyperplasia, with PFNA having the highest impact followed by PFOS. These findings suggest that elevated serum levels of PFDeA, PFOA, PFOS, and PFNA are linked to prostate hyperplasia. Therefore, this study utilized advanced machine learning techniques to uncover potential hazardous effects of PFAS exposure on prostate health, specifically the positive association between PFAS and prostate hyperplasia.

Informal E-waste dismantling activities accelerated the releasing of liquid crystal monomers (LCMs) in Pakistan: Occurrence, distribution, and exposure assessment.

Liquid crystal monomers (LCMs) are emerging contaminants characterized by their persistence, bioaccumulation potential, and toxicity. They have been observed in several environmental matrices associated with electronic waste (e-waste) dismantling activities, particularly in China. However, there is currently no information on the pollution caused by LCMs in other developing countries, such as Pakistan. In this study, we collected soil samples (n = 59) from e-waste dismantling areas with different functions in Pakistan for quantification analysis of 52 target LCMs. Thirty out of 52 LCMs were detected in the soil samples, with the concentrations ranging from 2.14 to 191 ng/g (median: 16.3 ng/g), suggesting widespread contamination by these emerging contaminants. Fluorinated LCMs (median: 10.4 ng/g, range: 1.27-116 ng/g) were frequently detected and their levels were significantly (P < 0.05) higher than those of non-fluorinated LCMs (median: 6.11 ng/g, range: not detected (ND)-76.7 ng/g). The concentrations and profiles of the observed LCMs in the soil samples from the four functional areas varied. The informal dismantling of e-waste poses a potential exposure risk to adults and infants, with median estimated daily intake (EDI, ng/kg bw/day) values of 0.0420 and 0.1013, respectively. Calculation of the hazard quotient (HQ) suggested that some LCMs (e.g., ETFMBC (1.374) and EDFPB (1.257)) may pose potential health risks to occupational workers and their families. Considering the widespread contamination and risks associated with LCMs, we strongly recommend enhancing e-waste management and regulation in Pakistan.

Air pollutants, genetic susceptibility, and incident schizophrenia in later life: A prospective study in the UK Biobank.

OBJECTIVE: Air pollution has been linked to multiple psychiatric disorders, but little is known on its long-term association with schizophrenia. The interaction between air pollution and genetic susceptibility on incident schizophrenia has never been reported. We aimed to explore the associations between long-term air pollution exposure and late-onset schizophrenia and evaluate whether genetic susceptibility could modify the association. METHODS: This population-based prospective cohort study included 437,802 middle-aged and elderly individuals free of schizophrenia at baseline in the UK Biobank. Land use regression models were applied in the estimation of the annual average concentrations of nitrogen dioxide (NO2), nitrogen oxides (NOx), fine particulate matter (PM2.5), and inhalable particulate matter (PM10) at residence. The associations between air pollutants and schizophrenia were evaluated by using Cox proportional hazard models. A polygenic risk score of schizophrenia was constructed for exploring potential interaction of air pollutants with genetic susceptibility. RESULTS: An interquartile range increase in PM2.5, PM10, NO2, and NOx was associated with the hazard ratios (HR) for incident schizophrenia at 1.19, 1.16, 1.22, and 1.09, respectively. The exposure-response curves for the association of air pollution with incident schizophrenia were approximately linear. There are additive interactions of air pollution score (APS), PM10, NO2, and NOx with genetic risk. Specifically, compared with participants with low genetic susceptibility and low APS, the HR was 3.23 for individuals with high genetic risk and high APS, among which 0.49 excess risk could be attributed to the additive interaction, accounting for 15 % of the schizophrenia risk. CONCLUSION: This large-scale, prospective cohort study conveys the first-hand evidence that long-term air pollution exposure could elevate schizophrenia incidence in later life, especially for individuals with higher genetic risks. The findings highlight the importance of improving air quality for preventing the late-onset schizophrenia in an aging era, especially among those with high genetic risks.

The association between exposure to volatile organic chemicals and serum α-Klotho in USA middle to old aged population: A cross-sectional study from NHANES 2011-2016.

BACKGROUND: Volatile Organic Compounds (VOCs) constitute an omnipresent category of environmental contaminants. Numerous studies have identified associations between various VOCs and human diseases. The anti-aging protein α-Klotho has been shown to exert protective influences across a variety of disease origins and progressions. This study aims to explore the relationship between serum α-Klotho levels and exposure to VOCs in humans. METHODS: This analysis utilized data from 1672 participants aged from 40 to 79 years in 2011-2016 NHANES. Exposure to VOCs was assessed through measurements of urinary VOC metabolites (mVOCs), with 16 mVOCs selected for analysis. Multivariate generalized linear models (GLM), restricted cubic splines (RCS), weighted quantile sum (WQS) regression models, and Bayesian kernel machine regression (BKMR) models were employed to examine the connection between serum α-Klotho and individual mVOCs and mVOCs mixtures, as well as to identify the primary monomeric mVOCs responsible for these associations. RESULTS: Our research revealed that 8 mVOCs exhibited inverse associations with serum α-Klotho levels in GLM and RCS models. Particularly noteworthy, N-Acetyl-S-(2-cyanoethyl)-L-cysteine (CYMA), a metabolite of acrylonitrile, emerged as the most influential mVOC in both WQS and BKMR models. Furthermore, the mVOCs mixture was found to be negatively correlated with serum α-Klotho. The detrimental effects of mVOCs on serum α-Klotho were observed to significantly diminish in individuals with elevated serum vitamin D levels. CONCLUSION: Our study highlights a significant inverse relationship between serum α-Klotho and the mixture of mVOCs, indicating that exposure to VOCs may impact the molecular pathways of aging and related diseases by influencing α-Klotho concentrations. Remarkably, the attenuation of this association by high serum vitamin D levels implies potential therapeutic strategies. Our study underscores the importance of minimizing VOCs exposure to mitigate the adverse effects on α-Klotho. Further research is warranted to elucidate the underlying mechanisms of these relationships.

Pesticide exposure and increased breast cancer risk in women population studies.

Pesticide exposure is emerging as a risk factor for various human diseases. Breast cancer (BC) is a multifactorial disease with known genetic and non-genetic risk factors. Most BC cases are attibutable to non-genetic risk factors, with a history of adverse environmental exposures playing a significant role. Pesticide exposure can occur at higher levels in female populations participating in rural activities such as spraying of pesticides in the field, unprotected handling of pesticides at home, and washing of contaminated clothes. Exposure can also be significant in the drinking water of certain populations. Here, we reviewed the literature on women's exposure to pesticides and the risk of BC. We summarize the main links between pesticide exposure and BC and discuss the role of dose and exposure context, as well as potential mechanisms of toxicity. Overall, reports reviewed here have documented stronger associations between higher levels of exposure and BC risk, including documenting direct and acute pesticide exposure in certain female populations. However, discrepancies among studies regarding dose and mode of exposure may result in misunderstandings about the risks posed by pesticide exposure. Plausible mechanisms linking pesticides to breast cancer risk include their impacts as endocrine disruptors, as well as their roles as genotoxic agents, and modulators of the epigenome. Besides establishing links between pesticide exposure and breast cancer, the literature also highlights the critical need to understand the routes and doses of women's exposure to pesticides and the specific associations and mechanisms that are determinants of disease etiology and prognosis.

Heat Exposure and Cause-Specific Hospital Admissions in Spain: A Nationwide Cross-Sectional Study.

BACKGROUND: More frequent and intense exposure to extreme heat conditions poses a serious threat to public health. However, evidence on the association between heat and specific diagnoses of morbidity is still limited. We aimed to comprehensively assess the short-term association between cause-specific hospital admissions and high temperature, including the added effect of temperature variability and heat waves and the effect modification by humidity and air pollution. METHODS: We used data on cause-specific hospital admissions, weather (i.e., temperature and relative humidity), and air pollution [i.e., fine particulate matter with aerodynamic diameter ≤2.5µm (PM2.5), fine particulate matter with aerodynamic diameter ≤10µm (PM10), NO2, and ozone (O3)] for 48 provinces in mainland Spain and the Balearic Islands between 1 January 2006 and 31 December 2019. The statistical analysis was performed for the summer season (June-September) and consisted of two steps. We first applied quasi-Poisson generalized linear regression models in combination with distributed lag nonlinear models (DLNM) to estimate province-specific temperature-morbidity associations, which were then pooled through multilevel univariate/multivariate random-effect meta-analysis. RESULTS: High temperature had a generalized impact on cause-specific hospitalizations, while the added effect of temperature variability [i.e., diurnal temperature range (DTR)] and heat waves was limited to a reduced number of diagnoses. The strongest impact of heat was observed for metabolic disorders and obesity [relative risk (RR) = 1.978; 95% empirical confidence interval (eCI): 1.772, 2.208], followed by renal failure (1.777; 95% eCI: 1.629, 1.939), urinary tract infection (1.746; 95% eCI: 1.578, 1.933), sepsis (1.543; 95% eCI: 1.387, 1.718), urolithiasis (1.490; 95% eCI: 1.338, 1.658), and poisoning by drugs and nonmedicinal substances (1.470; 95% eCI: 1.298, 1.665). We also found differences by sex (depending on the diagnosis of hospitalization) and age (very young children and the elderly were more at risk). Humidity played a role in the association of heat with hospitalizations from acute bronchitis and bronchiolitis and diseases of the muscular system and connective tissue, which were higher in dry days. Moreover, heat-related effects were exacerbated on high pollution days for metabolic disorders and obesity (PM2.5) and diabetes (PM10, O3). DISCUSSION: Short-term exposure to heat was found to be associated with new diagnoses (e.g., metabolic diseases and obesity, blood diseases, acute bronchitis and bronchiolitis, muscular and connective tissue diseases, poisoning by drugs and nonmedicinal substances, complications of surgical and medical care, and symptoms, signs, and ill-defined conditions) and previously identified diagnoses of hospital admissions. The characterization of the vulnerability to heat can help improve clinical and public health practices to reduce the health risks posed by a warming planet. https://doi.org/10.1289/EHP13254.

Associations between organophosphate esters and bone mineral density in adults in the United States: 2011-2018 NHANES.

BACKGROUND: Organophosphate esters (OPEs) are used extensively as flame retardants and plasticizers. Laboratory studies have shown that OPEs exhibit osteotoxicity by inhibiting osteoblast differentiation; however, little is known about how OPEs exposure is associated with bone health in humans. OBJECTIVES: We conducted a cross-sectional study to investigate the association between OPEs exposure and bone mineral density (BMD) in adults in the United States using data from the 2011-2018 National Health and Nutrition Examination Survey (NHANES). METHODS: Multivariate linear regression models were used to assess the association between concentrations of individual OPE metabolites and BMDs. We also used the Bayesian kernel machine regression (BKMR) and quantile g-computation (qgcomp) models to estimate joint associations between OPE mixture exposure and BMDs. All the analyses were stratified according to gender. RESULTS: A total of 3546 participants (median age, 40 years [IQR, 30-50 years]; 50.11% male) were included in this study. Five urinary OPE metabolites with a detection rate of > 50% were analyzed. After adjusting for the potential confounders, OPE metabolite concentrations were associated with decreased total-body BMD and lumbar spine BMD in males, although some associations only reached significance for bis(1-chloro-2-propyl) phosphate (BCPP), dibutyl phosphate (DBUP), and bis(2-chloroethyl) phosphate (BCEP) (ß = -0.013, 95% CI: -0.026, -0.001 for BCPP and total-body BMD; ß = -0.022, 95% CI: -0.043, -0.0001 for DBUP and lumbar spine BMD; ß=-0.018, 95% CI: -0.034, -0.002 for BCEP and lumbar spine BMD). OPE mixture exposure was also inversely associated with BMD in males, as demonstrated in the BMKR and qgcomp models. CONCLUSIONS: This study provides preliminary evidence that urinary OPE metabolite concentrations are inversely associated with BMD. The results also suggested that males were more vulnerable than females. However, further studies are required to confirm these findings.

Human molybdenum exposure risk in industrial regions of China: New critical effect indicators and reference dose.

Evidence increasingly suggests molybdenum exposure at environmental levels is still associated with adverse human health, emphasizing the necessity to establish a more protective reference dose (RfD). Herein, we conducted a study measuring 15 urinary metals and 30 clinical health indicators in 2267 participants residing near chemical enterprises across 11 Chinese provinces to investigate their relationships. The kidney and cystatin-C emerged as the most sensitive organ and critical effect indicator of molybdenum exposure, respectively. Odds of cystatin-C-defined chronic kidney disease (CKD) in the highest quantile of molybdenum exposure significantly increased by 133.5% (odds ratio [OR]: 2.34, 95% CI: 1.78, 3.11) and 75.8% (OR: 1.76, 95% CI: 1.24, 2.49) before and after adjusting for urinary 14 metals, respectively. Intriguingly, cystatin-C significantly mediated 15.9-89.5% of molybdenum's impacts on liver and lung function, suggesting nephrotoxicity from molybdenum exposure may trigger hepatotoxicity and pulmonary toxicity. We derived a new RfD for molybdenum exposure (0.87 µg/kg-day) based on cystatin-C-defined estimated glomerular filtration rate by employing Bayesian Benchmark Dose modeling analysis. This RfD is significantly lower than current exposure guidance values (5-30 µg/kg-day). Remarkably, >90% of participants exceeded the new RfD, underscoring the significant health impacts of environmental molybdenum exposure on populations in industrial regions of China.

Phthalate exposure and subfecundity in preconception couples: A nested case-control study.

BACKGROUND: Phthalates (PAEs) are endocrine-disrupting chemicals ubiquitously found in the environment. This study aimed to examine the association between exposure of PAEs and subfecundity in preconception couples. METHODS: This is a nested case-control study based on preconception cohort. Preconception couples with intention to conceive were enrolled and followed up until a clinically confirmed pregnancy or 12 menstrual cycles of preparation for conception. A total of 107 couples with subfecundity- time to pregnancy (TTP) more than 12 menstrual cycles, and 144 couples ≤12 cycles were included in the analysis. The levels of PAE metabolites in one spot urine samples were detected and compared between the groups. The weighted quantile sum (WQS) regression model and Bayesian kernel machine regression (BKMR) model were used to examine the joint effects of couples' exposure to PAEs on subfecundity. RESULTS: Using the multivariate binary logistic regression model, compared to the lowest quartile of urinary ∑PAEs concentration group, both preconception females (aOR=2.42, 95% CI: 1.10-5.30, p=0.027) and males (aOR=2.99, 95% CI: 1.36-6.58, p=0.006) in the highest quartile group had an increased risk of subfecundity, and a dose-response relationship was observed between PAEs and the risk of subfecundity. The WQS analyses found that co-exposure to PAE mixture was a risk factor for subfecundity in preconception female (aOR=1.76, 95% CI: 1.38-2.26, p<0.001), male (aOR=1.58, 95% CI: 1.20-2.08, p=0.001), and couple (aOR=2.39, 95% CI: 1.61-3.52, p<0.001). The BKMR model found a positive combined effect of mixed exposure to PAEs on the risk of subfecundity. CONCLUSIONS: PAEs increase the risk of subfecundity in preconception couples. Our research reinforced the need of monitoring PAE exposure for the purpose of improving human reproductive health.

Associations of phthalates with accelerated aging and the mitigating role of physical activity.

Phthalates are positioned as potential risk factors for health-related diseases. However, the effects of exposure to phthalates on accelerated aging and the potential modifications of physical activity remain unclear. A total of 2317 participants containing complete study-related information from the National Health and Nutrition Examination Survey 2007-2010 were included in the current study. We used two indicators, the Klemera-Doubal method biological age acceleration (BioAgeAccel) and phenotypic age acceleration (PhenoAgeAccel), to assess the accelerated aging status of the subjects. Multiple linear regression (single pollutant models), weighted quantile sum (WQS) regression, Quantile g-computation, and Bayesian kernel machine regression (BKMR) models were utilized to explore the associations between urinary phthalate metabolites and accelerated aging. Three groups of physical activity with different intensities were used to evaluate the modifying effects on the above associations. Results indicated that most phthalate metabolites were significantly associated with BioAgeAccel and PhenoAgeAccel, with effect values (ß) ranging from 0.16 to 0.21 and 0.16-0.37, respectively. The WQS indices were positively associated with BioAgeAccel (0.33, 95% CI: 0.11, 0.54) and PhenoAgeAccel (0.50, 95% CI: 0.19, 0.82). Quantile g-computation indicated that phthalate mixtures were associated with accelerated aging, with effect values of 0.15 (95% CI: 0.02, 0.28) for BioAgeAccel and 0.39 (95% CI: 0.12, 0.67) for PhenoAgeAccel respectively. The BKMR models indicated a significant positive association between the concentrations of urinary phthalate mixtures with the two indicators. In addition, we found that most phthalate metabolites showed the strongest effects on accelerated aging in the no physical activity group and that the effects decreased gradually with increasing levels of physical activity (P < 0.05 for trend). Similar results were also observed in the mixed exposure models (WQS and Quantile g-computation). This study indicates that phthalates exposure is associated with accelerated aging, while physical activity may be a crucial barrier against phthalates exposure-related aging.

Environmental triggers of autoimmunity: The association between bisphenol analogues and systemic lupus erythematosus.

The aim of this research was to examine the correlation between the exposure to bisphenol analogues (BPs), such as bisphenol A (BPA), bisphenol F (BPF), and bisphenol S (BPS), and the risk of developing systemic lupus erythematosus (SLE). Ultra performance liquid chromatography/tandem mass spectrometry (UPLC-MS/MS) was utilized to measure the levels of BPA, BPF, and BPS in the urine of 168 female participants diagnosed with SLE and 175 female participants who were deemed healthy controls. Logistic regression models were utilized to assess the connections between levels of bisphenol and the risk of SLE. The findings indicated that levels of BPA and BPF in the urine of individuals with SLE were markedly elevated compared to those in the control group. Higher exposure to BPA and BPF exhibited positive dose-response relationships with increased SLE risk. No significant associations were identified between BPS and the risk of SLE. These findings suggest exposure to BPA and BPF may be implicated as novel environmental triggers in the development of autoimmunity such as SLE. The significantly increased levels of these bisphenol analogues detected in SLE patients versus healthy controls, along with the associations between higher exposures and elevated SLE risk, which offers crucial hints for comprehending how endocrine-disrupting substances contribute to the genesis of autoimmune illnesses. Further research using robust longitudinal assessments of bisphenol analogue exposures is warranted to corroborate these epidemiological findings. Overall, this study highlights potential environmental risk factors for SLE while calling for additional investigation into the impact of bisphenol exposures on autoimmunity development.