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This study delves into the relationship between environmental metal exposure and QT interval corrected for heart rate (QTc) prolongation, a critical marker for cardiovascular risk in the elderly. Although the interplay between metal exposure and QTc prolongation is important for predicting sudden cardiac death, it remains underexplored. Our analysis of 6478 participants from the Shenzhen aging-related disorder cohort involved measuring urinary concentrations of 22 trace metals and using mitochondrial DNA copy number (mtDNA-CN) as an indicator of mitochondrial dysfunction. Utilizing Bayesian kernel machine regression, and structural equation modeling, we assessed the effects of mixed trace metals on QTc prolongation. Our findings indicated a direct association between certain metals (Sb, Cu, Zn) and a 7 % increase in QTc prolongation risk, while Li, V, and Rb were associated with a 5 % reduction in risk. Elevated levels of V, Ti, and Cr corresponded to higher mtDNA-CN. Notably, restricted cubic splines revealed a U-shaped, nonlinear relationship between mtDNA-CN and QTc prolongation. After adjusting for metal exposure, an inverse correlation was observed between mtDNA-CN and QTc prolongation, suggesting mitochondrial dysfunction as a partial mediator., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier B.V.)

Recent decades of epidemiological and clinical research have suggested that heat exposure could be a potential risk factor for ischemic stroke. Despite climate factors having a minor impact on individuals compared with established risk factors such as smoking, their widespread and persistent effects significantly affect public health. The mechanisms by which heat exposure triggers ischemic stroke are currently unclear. However, several potential mechanisms, such as the impact of temperature variability on stroke risk factors, inflammation, oxidative stress, and coagulation system changes, have been proposed. This article details the potential mechanisms by which heat exposure may induce ischemic stroke, aiming to guide the prevention and treatment of high-risk groups in hot climates and support public health policy development., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Background: Impaired cognitive function following exposure to heavy metals has emerged as a significant global health concern. Nevertheless, the impact of combined exposure to multiple heavy metals on cognitive impairment remains unclear., Objective: This study aimed to explore the association between multiple heavy metals exposure and cognitive function to provide theoretical evidence to guide prevention strategies., Methods: The blood levels of lead (Pb), cadmium (Cd), mercury (Hg), selenium (Se), copper (Cu) and zinc (Zn) and the results of the cognitive function tests were extracted from 811 elderly Americans who completed the NHANES between 2011 and 2014. Quantile regression (QR), restricted cubic splines (RCS), and Bayesian kernel machine regression (BKMR) were used to explore the individual and joint association between heavy metals exposure and performance in 4 standardized cognitive tests; Item Response Theory (IRT), Delayed Recall Test (DRT), Animal Fluency Test (AFT) and Digit Symbol Substitution Test (DSST)., Results: A negative association was noted between Cd levels and IRT (p = 0.048, 95%CI: -2.7, -0.1). Se concentrations ranging between 2.197 µg/L (95%CI: 0.004, 0.15) to 2.29 µg/L (95%CI: 2.56, 7.64) (log 10 Se) was postively associated with DSST (p = 0.001 ). Cu was negatively associated with DSST (p = 0.049, 95%CI: -37.75, -0.09), while Zn was positively associated with IRT (p = 0.022, 95%CI: 0.55, 11.73). Exposure to the 6 heavy metals combined showed a positive linear association with IRT, DRT, and a negative linear association with DSST. An interaction between Cd and the other heavy metals (excepted for Pb)., Conclusion: Exposure to Pb, Cd, Hg, Se, Cu, and Zn was associated with cognitive function. Joint exposure to the 6 heavy metals showed a positive linear association with IRT, DRT, contrarily, a negative linear association with DSST., Competing Interests: Declarations Ethics approval and consent to participate The NHANES database is publicly available and has been approved by the Institutional Review Board of the National Center for Health Statistics (NCHS). All participants provided written informed consent during their participation in the national survey conducted in the United States. Ethical review and approval were waived for this study as it involved secondary analysis and did not necessitate additional institutional review board approval. Consent for publication Not applicable. Competing interests The authors declare no competing interests. Highlight Pb, Cd, Hg, Se, Cu, and Zn were significantly associated with cognitive function.An interaction between Cd and the other heavy metals (excepted for Pb).Exposure to the 6 heavy metals combined showed a positive linear association with IRT, DRT and a negative linear association with DSST., (© 2024. The Author(s).)

Background: Whether genetic susceptibility to cardiovascular diseases (CVDs) enhances the vulnerability to adverse cardiovascular outcomes by air pollution is unknown. We assessed the combined effect of air pollution and genetic predispositions on CVD risk., Methods and Results: From the UK Biobank cohort, we selected genetically unrelated White British participants without CVD. Levels of ambient particulate matter with a diameter of <2.5 μm (PM 2.5 ) and <10 μm were estimated using land use regression models. An individual's genetic predisposition to CVDs was determined by polygenic risk scores for coronary artery disease, myocardial infarction, stroke, ischemic stroke, heart failure, and atrial fibrillation. We stratified mortality and CVD risk by PM 2.5 exposure across high and low genetic risk groups. A total of 249 082 participants (aged 56.9±8.0 years, 46.8% men) were followed for a median of 10.8 years. The combined effect of PM 2.5 exposure and the genetic predisposition of CVD demonstrated the highest risk of cardiovascular death in the high genetic risk group with the greatest PM 2.5 exposure (adjusted hazard ratios ranging from 1.73 to 2.12 across the polygenic risk score of each CVD). The combination of higher exposure to ambient PM 2.5 and high genetic risk was associated with higher incidence of all CVDs, although no significant interactions were observed between genetic risk and PM 2.5 exposure on cardiovascular death or CVD events., Conclusions: A combination of greater PM 2.5 exposure and higher genetic predisposition to particular CVDs was modestly associated with elevated risks of cardiovascular death and CVDs. Not only alleviating PM 2.5 exposure in the general population but also implementing individualized preventive approach for those at high genetic risk might be beneficial.

Background: Pediatric hypertension is linked to environmental factors like neighborhood noise disrupting sleep, which is crucial for health. The specific interaction between noise and sleep health in causing hypertension still needs to be explored., Methods and Results: We analyzed data from 3320 participants of the ABCD (Adolescent Brain Cognitive Development) study, recruited across 21 US cities and monitored from 2018 to 2020 through 2020 to 2022. Participants with complete data on Fitbit-tracked sleep, blood pressure, height, neighborhood noise, and covariates (biological sex, race and ethnicity, pubertal stage, waist circumference) were included. Hypertension was defined as average blood pressure ≥95th percentile for age, sex, and height. Sleep health was categorized on the basis of daily duration: healthy (9-12 hours), moderately healthy (±1 hour from optimal), and low (≥1 hour deviation). Noise exposure was measured as median nighttime anthropogenic noise levels by zip code. The incidence of hypertension increased from 1.7% (95% CI, 1.4-2.1) in 2018 to 2020 to 2.9% (95% CI, 2.4-3.6) in 2020 to 2022. Adolescents with healthier sleep had a lower risk of developing hypertension (relative risk, 0.63 [95% CI, 0.25-0.82]), while no significant effects were found for neighborhood noise alone or in combination with sleep health., Conclusions: Adequate sleep significantly reduces the risk of hypertension in adolescents, independent of environmental noise exposure. These findings underscore the importance of promoting good sleep hygiene among youth to mitigate hypertension risk.

Background: Assessment of breast cancer (BC) risk generally relies on mammography, family history, reproductive history, and genotyping of major mutations. However, assessing the impact of environmental factors, such as lifestyle, health-related behavior, or external exposures, is still challenging. DNA methylation (DNAm), capturing both genetic and environmental effects, presents a promising opportunity. Previous studies have identified associations and predicted the risk of BC using DNAm in blood; however, these studies did not distinguish between genetic and environmental contributions to these DNAm sites. In this study, associations between DNAm and BC are assessed using paired twin models, which control for shared genetic and environmental effects, allowing testing for associations between DNAm and non-shared environmental exposures and behavior., Results: Pre-diagnosis blood samples of 32 monozygotic (MZ) and 76 dizygotic (DZ) female twin pairs discordant for BC were collected at the mean age of 56.0 years, with the mean age at diagnosis 66.8 years and censoring 75.2 years. We identified 212 CpGs (p < 6.4*10 -8 ) and 15 DMRs associated with BC risk across all pairs using paired Cox proportional hazard models. All but one of the BC risks associated with CpGs were hypomethylated, and 198/212 CpGs had their DNAm associated with BC risk independent of genetic effects. According to previous literature, at least five of the top CpGs were related to estrogen signaling. Following a comprehensive two-sample Mendelian randomization analysis, we found evidence supporting a dual causal impact of DNAm at cg20145695 (gene body of NXN, rs480351) with increased risk for estrogen receptor positive BC and decreased risk for estrogen receptor negative BC., Conclusion: While causal effects of DNAm on BC risk are rare, most of the identified CpGs associated with the risk of BC appear to be independent of genetic effects. This suggests that DNAm could serve as a valuable biomarker for environmental risk factors for BC, and may offer potential benefits as a complementary tool to current risk assessment procedures., Competing Interests: Declarations Ethics approval and consent to participate Informed consent was obtained before the beginning of the FTC studies in 1975, and upon every contact with the study subjects. When clinical investigations were undertaken with sampling of biological material, written informed consent was obtained. Ethics approval of these procedures was provided in multiple studies, the last one on the transfer of biological samples to the THL Biobank by the Hospital District of Helsinki and Uusimaa ethics board in 2018 (#1799/2017). Permission for register linkage to the Finnish Cancer Registry was given by the Finnish Social and Health Data Permit Authority Findata (latest THL/6353/14.06.00/2023). Informed consent The two Danish twin studies (LSADT and MADT) were approved by the Regional Committees on Health Research Ethics for Southern Denmark (S-VF-19980072), and written informed consents were obtained from all participants. Competing interests The authors declare no competing interests., (© 2024. The Author(s).)

Background: A growing body of epidemiologic and toxicologic literature indicates that fine airborne particulate matter (PM 2.5 ) pollution is neurotoxic and threatens children's neurobehavioral development, resulting in reduced cognitive function. Understanding the magnitude of this effect is critical for establishing public health policies that will protect children's health, preserve human capital, and support societal progress., Objective: To quantify the association between ambient PM 2.5 air pollution and loss of cognitive function in children, as measured by Intelligence Quotient (IQ) scores, through a systematic literature review and meta-analysis., Methods: Following PRISMA guidelines, we conducted a systematic literature search across seven databases: Agricultural and Environmental Science, BIOSIS Citation Index, Embase, GreenFILE, PubMed, Scopus, and Web of Science to identify original scientific studies that investigated the impact of PM 2.5 exposure during pre-and postnatal periods on IQ loss during childhood. Using data from studies included for final review, we conducted a meta-analysis, using a random effects model to compute a beta coefficient that quantifies the overall effect of PM 2.5 exposure on Full-Scale IQ (FSIQ), Performance IQ (PIQ), and Verbal IQ (VIQ)., Findings: Of the 1,107 unique publications identified, six studies met the inclusion criteria for final review, representing 4,860 children across three continents (North America, Europe, and Asia). The mean PM 2.5 concentration across all studies was 30.4 ± 24.4 µg/m 3 . Exposure timing ranged from the prenatal period to mid-childhood. Children were an average of 8.9 years old at the time of cognitive testing. We found that each 1 µg/m 3 increase in PM 2.5 concentration is associated with a -0.27 point change in FSIQ (p < 0.001), 0.39 point change in PIQ (p = 0.003), and -0.24 point change in VIQ (p = 0.021)., Conclusion: Through a systematic review and meta-analysis, we identified a statistically significant relationship between increased exposure to PM 2.5 air pollution and reduced cognitive function in children, with the most pronounced impact on PIQ. This analysis will enable estimation of the burden of adverse neurobehavioral development attributable to PM 2.5 in pediatric populations and will inform local and global strategies for exposure prevention., Competing Interests: Declarations Competing interests The authors declare no competing interests., (© 2024. The Author(s).)

Background: Per- and polyfluoroalkyl substances (PFAS) are commonly utilized in consumer products. While earlier studies have suggested potential impacts of certain PFAS on serum concentrations of vitamin D, these investigations were constrained to a limited set of conventional PFAS. Moreover, they did not specifically focus on populations with longer duration of PFAS exposure and potentially higher blood PFAS levels, such as older adults, and lacked adequate evidence to examine sex-related disparities., Methods: This observational investigation utilized cross-sectional data obtained from the U.S. NHANES spanning the years 2003 to 2018. Survey-weighted multiple regression models were employed to evaluate the relationship between PFAS exposure and vitamin D concentrations. Multi-pollutant models were employed to evaluate the association between PFAS mixtures and vitamin D concentrations. Subsequently, environmental risk scores (ERS) were constructed to gauge associations with vitamin D concentrations. ERS was computed through a weighted linear combination of PFAS, utilizing calculations from ridge regression and adaptive elasticity network (adENET) methodologies. All analyses were stratified by sex., Results: The study encompassed 3,853 older adults. Our analysis revealed a negative association between PFOA, PFOS, PFNA, and MeFOSAA and serum vitamin D concentrations. In analyses examining mixed exposures, various models consistently indicated an inverse association between PFAS mixed exposure and vitamin D concentrations. Moreover, an increase in ERS of PFAS across the interquartile range was associated with a decrease in vitamin D concentrations (Q4 vs. Q1, adENET: β: -0.083, 95% CI: -0.117, -0.048; ridge regression: β: -0.077, 95% CI: -0.111, -0.042). Notably, these associations were exclusively observed within the female population., Conclusions: Our study indicates that heightened exposure to PFAS correlates with diminished serum vitamin D concentrations in females aged 60 years and older, evident in both single and mixed exposures. These findings find support in in vitro mechanistic studies, suggesting that PFAS may impact the metabolism of 25(OH)D, consequently affecting vitamin D concentrations., Competing Interests: Declarations Ethics approval and consent to participate Not applicable. Consent for publication Not applicable. Competing interests The authors declare no competing interests., (© 2024. The Author(s).)

Context: Higher mean and rapid increases in body mass index (BMI) during infancy are associated with subsequent obesity and may be influenced by exposure to endocrine-disrupting chemicals such as phenols., Objective: In a prospective US-based cohort conducted 2010-2014, we investigated associations between environmental phenol exposures and BMI in 199 infants., Methods: We measured 7 urinary phenols at ages 6-8 and 12 weeks and assessed BMI z-score at up to 12 study visits between birth and 36 weeks. We examined individual and joint associations of averaged early infancy phenols with level of BMI z-score using mean differences (β [95% CI]) and with BMI z-score trajectories using relative risk ratios (RR [95% CI])., Results: Benzophenone-3, methyl and propyl paraben, and all phenols jointly were positively associated with higher mean BMI z-score (0.07 [-0.05, 0.18], 0.10 [-0.08, 0.27], 0.08 [-0.09, 0.25], 0.17 [-0.08, 0.43], respectively). Relative to a stable trajectory, benzophenone-3, 2,4-dichlorophenol, 2,5-dichlorophenol, and all phenols jointly were positively associated with risk of a rapid increase trajectory (1.46 [0.89, 2.39], 1.33 [0.88, 2.01], 1.66 [1.03, 2.68], 1.41 [0.71, 2.84], respectively)., Conclusion: Early phenol exposure was associated with a higher mean and rapid increase in BMI z-score across infancy, signaling potential long-term cardiometabolic consequences of exposure., (Published by Oxford University Press on behalf of the Endocrine Society 2024.)

Background: Exposure to pesticides in the living environment can be associated with the prevalence of health symptoms. This study investigates associations between health symptoms among residents in areas with fruit crop fields where pesticides are applied, and psychological perceptions and attitudes about environmental aspects and exposures., Methods: A cross-sectional survey combined with routine primary care electronic health records (EHR) data was conducted in 2017 in rural areas of the Netherlands with high concentration of fruit crops (n = 3,321, aged ≥ 16 years). Individual exposure to pesticides was estimated using geocoded data on fruit crops around the home. Validated instruments were used to assess symptom report and psychological perceptions and attitudes. Annual prevalence of various health symptoms was derived from EHRs. Multilevel regression models were used to analyze associations between health symptoms (outcome), fruit crops, and multiple psychological perceptions and attitudes (confounders)., Results: Living in the vicinity of fruit crop fields was generally not associated with self-reported symptom duration and general practitioner (GP) registered symptoms. For self-reported symptoms, symptom prevalence decreased when crop density within 250 m and 500 m from the home increased. No associations were found at other distances. Furthermore, higher levels of environmental worries, perceived exposure, and perceived sensitivity to pesticides and attribution of symptoms to environmental exposures were generally associated with a higher number of self-reported symptoms, and longer symptom duration. Symptoms reported to GPs were not associated with psychological perceptions and attitudes, except for perceived sensitivity to pesticides., Conclusion: Psychological perceptions and attitudes appear to be related to self-reported symptoms, but not to GP-registered symptoms, independent of the actual levels of exposure as measured by the size of the area of crop fields. Perceptions about environmental factors should be taken into account in environmental health risk assessment research when studying health symptoms., Competing Interests: Declarations Ethics approval and consent to participate The use of Electronic Health Records data from the Nivel Primary Care Database, as used for this study, is permitted by the Dutch law – under certain conditions – without having to ask permission from each individual patient, or without review by a medical ethics committee. Nivel Primary Care Database meets the Dutch regulations on data protection and laws on use of health data for epidemiological research purposes (Dutch Civil Law, Article 7:458). According to this legislation, neither obtaining informed consent from patients nor approval by a medical ethics committee is obligatory for observational studies containing no directly identifiable data.For matching the EHR data and the questionnaire data, a Trusted Third Party ensured anonymity of data at all times. For this purpose, a privacy regulation was established, which included the requirement for general practitioners to inform their patients through posters and brochures in the waiting room about participation in the study. The proposal for the study was submitted to the Privacy Committee of Nivel, which provided positive recommendations. For the linkage between datasets (EHR data - distance to fruit cultivation/buffers), a Trusted Third Party (TTP) was used (IVZ, Houten, https://www.sivz.nl/en/datamanagement). Consent for publication Not applicable. Competing interests The authors declare no competing interests., (© 2024. The Author(s).)

Microplastic particles (MPs) have been detected in a variety of environmental samples, including soil, water, food, and air. Cellular studies and animal exposures reported that exposure to MPs composed of different polymers might result in adverse effects at the portal of entry (local) or throughout the body (systemic). The most relevant routes of particle uptake into the body are oral and respiratory exposure. This review describes the various processes that may contribute to the adverse effects of MPs. Only MPs up to 5 µm were found to cross epithelial barriers to a significant extent. However, MPs may also exert a detrimental impact on human health by acting at the epithelial barrier and within the lumen of the orogastrointestinal and respiratory tract. The potential for adverse effects on human health resulting from the leaching, sorption, and desorption of chemicals, as well as the impact of MPs on nutritional status and dysbiosis, are reviewed. In vitro models are suggested as a means of (1) assessing permeation, (2) determining adverse effects on cells of the epithelial barrier, (3) examining influence of digestive fluids on leaching, desorption, and particle properties, and (4) role of microbiota-epithelial cell interactions. The contribution of these mechanisms to human health depends upon exposure levels, which unfortunately have been estimated very differently.

Background: N, N-Diethyl-meta-toluamide (DEET) is the predominant active ingredient found in insect repellents utilized by consumers. Exposure to DEET has been associated with notable risks to human health. Nonetheless, there is a scarcity of extensive cohort studies investigating the precise correlation between DEET exposure and mortality rates among cancer survivors. The objective of this study is to thoroughly evaluate the connection between DEET exposure and mortality rates in cancer survivors., Methods: This study employed individual samples obtained from the National Health and Nutrition Examination Survey (NHANES). Utilizing data from NHANES spanning 2007 to 2016, this study incorporated a cohort of 5,859 cancer survivors for subsequent analysis, following the exclusion of incomplete datasets. Through subgroup analysis, the research examined the impact of quartile levels of 3-diethyl-carbamoyl benzoic acid (DCBA), the primary metabolite of DEET, on cancer survivors across various subgroups within the broader population. Furthermore, the research utilized a multivariable Cox proportional hazards regression model and Kaplan-Meier (KM) curves to investigate the relationship between 3-diethyl-carbamoyl benzoic acid (DCBA), a principal metabolite of DEET, and mortality rates in individuals who have survived cancer., Results: The study identified an association between specific quartiles of DCBA concentration and a decreased risk of all-cause mortality among cancer survivors, specifically in the second (Q2: 0.665-1.95) and third quartiles (Q3: 1.95-6.845). Furthermore, a significant correlation was observed between the third quartile and cancer-specific mortality (Q3: 1.95-6.845), as well as between the second quartile and non-cancer mortality (Q2: 0.665-1.95). The quartiles of DCBA concentration exhibit a statistically significant correlation with total deaths (P < 0.001), cancer-specific deaths (P = 0.009), and non-cancer deaths (P < 0.001) among cancer survivors. The correlation between DCBA and reduced mortality risk in cancer survivors is particularly notable among females and individuals of non-Hispanic Black descent., Conclusion: The detection of DCBA in the urine of adult cancer survivors is strongly associated with increased mortality risks, particularly among females and non-Hispanic Black individuals, warranting further investigation and targeted interventions., Competing Interests: Declarations Ethics approval and consent to participate Not applicable. Consent for publication Not applicable. Competing interests The authors declare no competing interests., (© 2024. The Author(s).)

Background: Growing epidemiological evidence suggests an association between exposure to air pollutants and breast cancer. Yet, the underlying mechanisms remain poorly understood. This study explored the mediating role of thirteen metabolic health biomarkers in the relationship between exposure to three air pollutants, i.e. nitrogen dioxide (NO 2 ), polychlorinated biphenyls 153 (PCB153), and benzo[a]pyrene (BaP), and breast cancer risk., Methods: We used data from a nested case-control study within the French national prospective E3N-Generations cohort, involving 523 breast cancer cases and 523 matched controls. The four-way decomposition mediation of total effects for thirteen biomarkers was applied to estimate interaction and mediation effects (controlled direct, reference interaction, mediated interaction, and pure indirect effects)., Results: The analyses indicated a significant increase in breast cancer risk associated with BaP exposure (odds ratio (OR) Q4 vs Q1  = 2.32, 95% confidence intervals (CI): 1.00-5.37). PCB153 exposure showed a positive association only in the third quartile (OR Q3 vs Q1  = 2.25, CI 1.13-4.57), but it appeared to be non-significant in the highest quartile (OR Q4 vs Q1  = 2.07, CI 0.93-4.61). No association was observed between NO 2 exposure and breast cancer risk. Estradiol was associated with an increased risk of breast cancer (OR per one standard deviation (SD) increment = 1.22, CI 1.05-1.42), while thyroid-stimulating hormone was inversely related to breast cancer risk (OR per 1SD increase = 0.87, CI 0.75-1.00). We observed a suggestive mediated effect of the association between the three pollutants and breast cancer risk, through albumin, high-density lipoproteins cholesterol, low-density lipoprotein cholesterol, parathormone, and estradiol., Conclusion: Although limited by a lack of statistical power, this study provides relevant insights into the potential mediating role of certain biomarkers in the association between air pollutant exposure and breast cancer risk, highlighting the need for further in-depth studies in large populations., Competing Interests: Declarations Ethics approval and consent to participate Our research utilized data from the existing French prospective cohort E3N. All participants provided informed consent and the study received approval from the French National Commission for Data Protection and Privacy (CNIL). Due to ethical considerations and the specific consent signed by the participants, the datasets generated and/or analysed during the current study are not publicly available, however, data can be obtained from the E3N-Generations team through the corresponding author upon reasonable request. Consent for publication Not applicable. Competing interests The authors declare that they have no competing interests., (© 2024. The Author(s).)

In Brief: Clinical drug trials often do not include pregnant people due to health risks; therefore, many medications have an unknown effect on the developing fetus. Machine learning QSAR models have been used successfully to predict the fetal risk of pharmaceutical use during pregnancy., Abstract: Those undergoing pregnancy are often excluded from clinical drug trials due to the risk that participation would pose to their health and the health of the developing fetus. However, they often require pharmaceuticals to manage health conditions that, if left untreated, could harm themselves or the fetus. This can mean that such individuals take one or more pharmaceuticals during pregnancy, many of which have unknown reproductive effects. Machine learning models have been used to successfully predict a number of reproductive toxicological outcomes for pharmaceuticals, including transplacental transfer, US Food and Drug Administration safety rating, and drug interactions. Models use quantitative chemical and structural features of active compounds as inputs to make predictions concerning the outcome of interest using computational algorithms. Models are validated and evaluated rigorously with metrics such as accuracy, area under the receiver operator curve, sensitivity, and precision. Results from these models can be a potential source of valuable information for pregnant people and their medical providers when making decisions regarding therapeutic drug use. This review summarizes current machine learning applications to make predictions about the risk and toxicity of medication use during pregnancy. Our review of the recent literature revealed that machine learning quantitative structure-activity relationship models can be used successfully to predict the transplacental transfer and the US Food and Drug Administration pregnancy safety category of pharmaceuticals; such models have also been employed to predict drug interactions, though not specifically during pregnancy. This latter topic is a potential area for future research. In this review, no single algorithm or descriptor-calculation software emerged as the most widely used, and their performances depend on a variety of factors, including the outcome of interest and combination of such algorithms and software.

Background: Asthma is a prevalent chronic respiratory disease among children, influenced by various climate and environmental factors. Despite its prevalence, the specific effects of these factors on asthma remain unclear. This study aims to systematically assess the epidemiological evidence using spatial and temporal methods on the impact of climate and environmental factors on childhood asthma., Methods: A systematic review was conducted to analyse the impact of climate and environmental factors on childhood asthma and wheezing, focusing on spatial and temporal trends. Searches were carried out in PubMed, Embase, and CINAHL databases for studies published from January 2000 to April 2024, using key search terms 'asthma/wheezing', 'extreme weather, 'green space', 'air pollution' and 'spatial or temporal analyses"., Results: The systematic review analysed 28 studies, with six employing spatial and 22 using temporal analysis methods; however, none incorporated spatio-temporal analysis in their models. The findings reveal that extreme weather events, including heatwaves and heavy rainfall, elevate childhood asthma risks across various climates, with significant effects observed during summer and winter months. Dust storms in arid and subtropical regions are linked to immediate spikes in hospital admissions due to asthma exacerbations. The effects of green spaces on childhood asthma are mixed, with some studies indicating protective effects while others suggest increased risks, influenced by local environmental factors. Air pollutants such as PM 2.5 , NO 2 , and ozone can exacerbate asthma symptoms and along with other environmental factors, contribute to seasonal effects. High temperatures generally correlate with increased asthma risks, though the effects vary by age, sex, and climate., Conclusion: Future research should integrate spatial and temporal methods to better understand the effects of environmental and climate changes on childhood asthma., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)

Air pollutants have been investigated to be associated with many health issues. Recently, increasing epidemiological studies have suggested the association between air pollution exposure and risk of frailty with inconsistent findings. This systematic review and meta-analysis was to summarize and evaluate effects of exposure to various air pollutants on risk of frailty. PubMed, Embase, Scopus and Web of Science were systematically searched for relevant studies published before May 11, 2024. Studies that explored the potential relationship between exposure to air pollutants (PM 2.5 , PM 10 , O 3 , NO x , solid fuel, secondhand tobacco, and air quality) and risk of frailty were included. The quality of cross-sectional and cohort studies was evaluated using an eight-item assessment instrument for epidemiological studies and Newcastle-Ottawa Scale, respectively. A total of 9,929 papers were retrieved, of which 20 met the inclusion criteria. Meta-analysis indicated that PM 2.5 exposure was significantly associated with frailty assessed by the frailty index [OR (95% CI): 1.24 (1,11-1.38) per 10 μg/m 3 increment]. Moreover, solid fuel exposures were significantly associated with an increased risk of frailty assessed by the frailty phenotype [OR (95% CI): 1.91 (1.09-3.34)] or the frailty index [OR (95% CI): 1.25 (1.11-1.41)]. Exposure to PM 2.5 and solid fuel increases the risk of frailty. Environmental protection policies and public health measures should be developed to reduce PM 2.5 concentrations. Effective measures, such as improving stoves and using clean fuels, should be taken to reduce indoor air pollution levels., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Background: Environmental phenols were recognized as endocrine disrupting chemicals (EDCs). However, their impact on childhood anthropometric measures and blood pressure (BP) is still inconclusive. Limited studies have simultaneously considered prenatal and childhood exposures in analyzing mixtures of phenols., Objective: We investigated the relationships between combined prenatal and childhood exposures (two periodic exposures) to phenol mixtures and anthropometric measure and BP, to further identify the vulnerable periods of phenol exposure and to explore the important individual contribution of each phenol., Methods: We analyzed 434 mother-child dyads from the Sheyang Mini Birth Cohort Study (SMBCS). The urinary concentrations of 11 phenolic compounds were measured using gas chromatography tandem mass spectrometry. Generalized linear regression models (GLMs) and hierarchical Bayesian Kernel Machine Regression (hBKMR) were used to examine the effects of individual phenolic compounds at each period and of two periodic exposures., Results: In the single-chemical analysis, prenatal or childhood exposure to specific phenols, especially Benzopheone-3 (BP3), 4-tert-Octylphenol (4-tOP), and Benzyl paraben (BePB) were associated with BMI z-scores (BAZ), Waist-to-height ratio (WHtR), and BP. In the hBKMR models, two periodic exposures to phenol mixtures had a U-shaped association with WHtR, primarily driven by childhood BePB exposure. Moreover, among the phenol mixtures analysis, childhood 4-tOP exposure was identified as the primary contributor to the positive association with diastolic BP. Concurrent exposure to phenol mixtures resulted in greater susceptibility., Conclusions: We found that prenatal and childhood exposure to phenol mixtures might influence childhood obesity and elevate blood pressure levels. Concurrent exposure to 4-tOP may be the primary driver of the positive associations with BP., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests:Zhijun Zhou reports financial support was provided by National Natural Science Foundation of China. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Exposure to ambient ozone (O 3 ) is linked to increased mortality risks from various diseases, but epidemiological investigations delving into its potential implications for cancer mortality are limited. We aimed to examine the association between short-term O 3 exposure and site-specific cancer mortality and investigate vulnerable subgroups in Brazil. In total 3,459,826 cancer death records from 5570 Brazilian municipalities between 2000 and 2019, were included. Municipal average daily O 3 concentration was calculated from a global estimation at 0.25°×0.25° spatial resolution. The time-stratified case-crossover design was applied to assess the O 3 -cancer mortality association. Subgroup analyses by age, sex, season, time-period, region, urban hierarchy, climate classification, quantiles of GDP per capita and illiteracy rates were performed. A linear and non-threshold exposure-response relationship was observed for short-term exposure to O 3 with cancer mortality, with a 1.00% (95% CI: 0.79%-1.20%) increase in all-cancer mortality risks for each 10-μg/m 3 increment of three-day average O 3 . Kidney cancer was most strongly with O 3 exposure, followed by cancers of the prostate, stomach, breast, lymphoma, brain and lung. The associated cancer risks were relatively higher in the warm season and in southern Brazil, with a decreasing trend over time. When restricting O 3 concentration to the national minimum value during 2000-2019, a total of 147,074 (116,690-177,451) cancer deaths could be avoided in Brazil, which included 17,836 (7014-28,653) lung cancer deaths. Notably, these associations persisted despite observed adaptation within the Brazilian population, highlighting the need for a focus on incorporating specific measures to mitigate O 3 exposure into cancer care recommendations., (© 2024 The Author(s). International Journal of Cancer published by John Wiley & Sons Ltd on behalf of UICC.)

People are paying more and more attention to the effects of environmental factors such as heavy metals on depression, and heavy metals may destroy the homeostasis of vitamin D in the body by affecting human metabolism, and the lack of vitamin D will increase the risk of depression. There are few studies on vitamin D deficiency in depression caused by heavy metals, and it is not deep enough. Therefore, this study used logistic regression, restricted cubic spline curve, weighted quantile and Quantile g-computation model to analyze the effects of heavy metal exposure alone and in combination on vitamin D and depression, as well as the potential role of vitamin D deficiency in the process of heavy metal-induced depression. The results showed that cadmium exposure alone or in combination increased the risk of depression (P < 0.05). When Cd increased by 1 unit, the risk of depressive symptoms increased by 1.178 units. Arsenic and its compounds and lead affected vitamin D levels in the body and contributed the second highest or highest weight in the mixture (P < 0.05). It is worth noting that after grouping according to vitamin D deficiency, compared with the normal group, the mixed exposure of heavy metals in the vitamin D deficiency group had more types of metals related to depression and contributed more weight (P < 0.05). This study found that single metal or multi-metal mixed exposure is associated with depression. Vitamin D deficiency may increase the risk of depression. Vitamin D may be a potential factor in the treatment of depression caused by metal, and the specific mechanism of action needs further study., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Background: Particulate matter consisting of fine particles measuring 2.5 microns or less in diameter (PM 2.5 ), a component of air pollution, has been linked to adverse health outcomes. The objective of this study was to assess the association between ambient PM 2.5 exposure and survival in children with cancer in the United States., Methods: Individuals aged birth to 19 years who were diagnosed with cancer between January 1, 2004, and December 31, 2019, were selected from the National Cancer Database. The association between the annual PM 2.5 level at the patient's zip code of residence at the time of diagnosis and overall survival was evaluated using time-varying Cox proportional hazards models (crude and adjusted for diagnosis year and age). To address concerns that exposure to air pollution is correlated with other social determinants of health, the authors tested the association between PM 2.5 levels and survival among sociodemographic subgroups., Results: Of the 172,550 patients included, 27,456 (15.9%) resided in areas with annual PM 2.5 concentrations above the US Environmental Protection Agency (EPA) annual PM 2.5 standard of 12 μg/m 3 . Residing in these high-pollution areas was associated with worse overall survival (adjusted hazard ratio [aHR], 1.06; 95% confidence interval [CI], 1.012-1.10). Similarly, when PM 2.5 was evaluated as a linear measure, each unit increase in PM 2.5 exposure was associated with worse survival (aHR, 1.011; CI, 1.005-1.017). Exposure to PM 2.5 at levels above the EPA standards was also significantly associated with worse overall survival among sociodemographic subgroups., Conclusions: Exposure to PM 2.5 was significantly associated with worse overall survival among children with cancer, even at levels below EPA air quality standards. These results underscore the importance of setting appropriate air quality standards to protect the health of this sensitive population., Plain Language Summary: The authors investigated how living in areas with high air pollution (defined as particulate matter consisting of fine particles measuring 2.5 microns or less in diameter; PM 2.5 ) affects the overall survival of children with cancer in the United States. The results indicated that children living in areas with higher PM 2.5 levels, and even at levels below prior and current US Environmental Protection Agency standards, had lower survival rates than children living in areas with lower levels of PM 2.5 . This finding emphasizes the need for stricter air quality standards to better protect children, particularly those with serious health conditions like childhood cancer., (© 2024 American Cancer Society.)

Background: Previous studies reported that short-term exposure to ground-level ozone is associated with mortality risk. However, due to the limited monitored areas, existing studies were limited in assessing the nationwide risk and suggesting specific vulnerable populations to the ozone-mortality risk., Methods: We performed a nationwide time-stratified case-crossover study to evaluate the association between short-term ozone and cause-specific mortality in South Korea (2015-2019). A machine learning-ensemble prediction model (a test R 2  > 0.96) was used to assess the short-term ozone exposure. Stratification analysis was conducted to examine the high-risk populations, and the excess mortality due to non-compliance with the WHO guideline was also assessed., Results: For all-cause mortality (1,343,077 cases), the risk associated with ozone (lag0- 1) was weakly identified (odd ratio: 1.005 with 95% CI: 0.997-1.014), and the risk was prominent in mortality with circulatory system diseases. In addition, based on the point estimates, the ozone-mortality risk was higher in people aged less than 65y, and this pattern was also observed in circulatory system disease deaths and urban areas., Conclusions: This study provides national estimates of mortality risks associated with short-term ozone. Results showed that the benefits of stricter air quality standards could be greater in vulnerable populations., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Cadmium (Cd) is a toxic contaminant widely spread in natural and industrial environments. Adolescent exposure to Cd increases risk for obesity-related morbidity in young adults including type 2 diabetes and metabolic dysfunction-associated steatotic liver disease (MASLD). Despite this recognition, the direct impact of adolescent Cd exposure on the progression of MASLD later in life, and the mechanisms underlying these effects, remain unclear. Here, adolescent rats received control diet or diets containing 2 mg Cd 2+ /kg feed for 4 weeks, and then HFD containing 15% lard or control diet in young adult rats was selected for 6 weeks to clarify this issue. Data firstly showed that HFD-fed rats in young adulthood due to adolescent Cd exposure exhibited more severe MASLD, evidenced by increased liver damage, disordered serum and hepatic lipid levels, and activated NLRP3 inflammasome. Hepatic transcriptome analysis revealed the potential effects of mitochondrial dysfunction in aggravated MASLD due to Cd exposure. Verification data further confirmed that mitochondrial structure and function were targeted and disrupted during this process, shown by broken mitochondrial ridges, decreased mitochondrial membrane potential, imbalanced mitochondrial dynamic, insufficient ATP concentration, and enhanced mitochondrial ROS generation. However, mitophagy is inactively involved in clearance of damaged mitochondria induced by early Cd in HFD condition due to inhibited mitophagy receptor FUNDC1. In contrast, FUNDC1-dependent mitophagy activation prevents lipotoxicity aggravated by early Cd via suppressing mitochondrial ROS generation. Collectively, our data show that insufficient FUNDC1-dependent mitophagy can drive the transition from HFD-induced MASLD to MASH, and accordingly, these findings will provide a better understanding of potential mechanism of diet-induced metabolic diseases in the context of early environmental Cd exposure., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

The ingestion of soil and dust by children and adults is a potential source of exposure to environmental contaminants. To advance beyond the simple averaging of estimates used in the U.S. EPA's Exposure Factors Handbook (EFH), we describe a novel meta-analysis of all available studies that provided soil or dust ingestion estimates for children or adults conducted in the United States and Canada. Using meta-analytic techniques, we estimate the mean total soil plus dust ingestion rates and confidence intervals (CIs) for eleven age groups (0 - <1 month (m), 1 - <3 m, 3 - <6 m, 6 - <12 m, 1 - <2 years (y), 2 - <3 y, 3 - <6 y, 6 - <11 y, 11 - <16 y, 16 - <21 y, and 21+ y). These age groups were selected for consistency with the EFH update to Chapter 5 and the U.S. EPA's Age Grouping Guidance. For each age group, we calculated best estimates for the three main types of ingestion studies: tracer studies based on the aluminum tracer, biokinetic studies, and activity pattern (modeling) studies, as well as overall estimates for all three study types combined. Our meta-analysis combined study estimates using the alternative statistical approaches of the fixed effect method (inverse variance method, "I-V") and two random effects methods, DerSimonian and Laird's method of moments ("DSL") and the restricted maximum likelihood method ("MIXED"). For each approach, the mean total soil plus dust ingestion rate estimates for each study type generally aligned well with the EFH, ranging from 36 to 68 mg/day for infants, 56-72 mg/day for young children, and 12-32 mg/day for adolescents and adults. When all three study types were combined, the upper bounds of the 95% CI were generally the lowest for the I-V method and the highest for the MIXED method. The estimates produced here can be used for stochastic risk assessments and provide a better estimate of soil and dust ingestion rates across age groups., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Published by Elsevier Inc.)

Introduction: Air pollution and transportation noise pollution has been linked to gastrointestinal (GI) diseases, but their relationship remains unclear., Methods: We extracted the significantly modulated genes and CpG sites related to air pollution (PM2.5, PM10, and NOx) and transportation noise pollution (aircraft, railway, and traffic road noise) from previous published studies. Genome-wide methylation analysis and colocalization analysis with these CpG sites and GWAS data of GI diseases were performed to disentangle the relationship between pollution-related blood DNA methylation (DNAm) alterations and GI diseases risk. Summary-based Mendelian randomization (SMR) analysis assessed the impact of pollution-related genes on GI diseases risk across methylation, gene expression, and protein levels. Enrichment analysis investigated the implicated biological pathways and immune cell types., Results: DNAm at cg00227781 [CD300A] (modulated by NOx exposure) and cg19215199 [ZMIZ1] (modulated by PM2.5 exposure) was significantly linked to increased noninfective enteritis and colitis risk, while cg08500171 [BAT2] (modulated by NOx exposure) is significantly associated with an increased gastroesophageal reflux disease (GERD) risk. Colocalization analysis provides strong evidence supporting a shared causal variant between these associations. Multi-omics levels SMR analysis revealed that pollution-modulated lower DNAm at 5 specific CpG sites were associated with increased expression of 4 genes (IL21R, EVPL, SYNGR1, and WDR46), subsequently increasing the risk of GERD, ulcerative colitis, and gastric ulcer. 7 circulating proteins coded by pollution-modulated genes were observed to be associated with 6 GI diseases risk. Enrichment analysis implicates immune and inflammatory responses, MAPK signaling, and telomere maintenance in these pollution-induced effects., Conclusion: We identified potential links between air and transportation noise pollution-related gene methylation, expression, and protein abundance with GI diseases risk, possibly revealing new therapeutic targets., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Ying-Xuan Chen reports article publishing charges was provided by National Natural Science Foundation of China. Ying-Xuan Chen reports article publishing charges was provided by Shanghai Municipal Education Commission-Gaofeng Clinical Medicine Grant Support. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Background: Cardiovascular consequences of phthalates exposure have been given increasing attention, but the association of phthalates with subclinical cardiovascular disease (CVD) was unknown. Accordingly, this study aimed to investigate the association between phthalates exposure and high-sensitivity cardiac troponin I (hs-cTnI), a marker of myocardial injury, which was detectable in the subclinical stage of CVD., Methods: Participants aged 6 years or older with available urinary phthalates metabolites and serum hs-cTnI concentrations were included in the National Health and Nutrition Examination Survey 2003-2004 cycle. Multivariable linear regression and weighted quantiles sum (WQS) regression were used to assess the association of hs-cTnI with individual phthalates and their co-exposure. Di-2-ethylhexylphthalate (ΣDEHP), high-molecular-weight phthalate (ΣHMWP), and low-molecular-weight phthalate (ΣLMWP) were defined as the molecular sum of phthalates metabolites in urine., Results: 2241 participants were finally included. The percent change of serum hs-cTnI concentrations related to per 1-standard deviation increase of logarithmic urinary phthalates concentrations was 3.4% (0.1-6.7, P = 0.04) for ΣDEHP, 3.6% (0.3-6.9, P = 0.03) for ΣHMWP, and 3.5% (0.2-6.8, P = 0.04) for ΣLMWP. Co-exposure to phthalates metabolites expressed as the WQS index also demonstrated a positive association with hs-cTnI. A similar association pattern was found in the population with no prior CVD., Conclusions: This study indicated the potential of phthalates to myocardial injury which may occur even before clinically apparent CVD was identified, emphasizing the significance of reducing phthalates in the prevention of CVD., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier Inc.)

Background: Substantial inequalities in the overall prevalence and patterns of multimorbidity have been widely reported, but the causal mechanisms are complex and not well understood. This study aimed to identify common patterns of multimorbidity in Serbia and assess their relationship with air pollutant concentrations and water quality indicators., Methods: This ecological study was conducted on a nationally representative sample of the Serbian population. Data were obtained from the European Health Interview (EHIS) Survey, a periodic study designed to assess population health using widely recognized standardized instruments. The study included 13,069 participants aged 15 and older, randomly selected through a multistage stratified sampling design. Multimorbidity was defined as having two or more self-reported diagnoses of chronic non-communicable diseases. Latent class analysis (LCA) was performed to identify clusters of multimorbidity. Concentrations of particulate matter (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), and ozone (O3), as well as water quality indicators, were obtained from the Serbian Environmental Protection Agency., Results: The overall prevalence of multimorbidity was 33.4% [32.6%-34.2%]. Six latent classes of multimorbidity were identified: Healthy, Multicondition, Cardiovascular, Metabolic syndrome, Respiratory, and Musculoskeletal. Annual increases in PM10 and SO2 concentrations, as well as daily increases in O3 concentrations, significantly raised the odds of having multimorbidity (OR = 1.02, 95% CI 1.02-1.03; OR = 1.01, 95% CI 1.00-1.02 and OR = 1.03, 95% CI 1.02-1.03, respectively). A pattern of increased risk was observed with rising levels of water contamination. Exposure to physico-chemical, microbiological and combined contamination was associated with a 3.92%, 5.17% and 5.54% higher probability, respectively, of having multiple chronic conditions. There was strong evidence that air pollutants, as well as chemical and microbial water contamination, were significantly associated with higher odds of the most common clusters of multimorbidity identified by LCA., Conclusion: There is compelling evidence of an association between multimorbidity and environmental pollution, suggesting that exposure to air pollutants and water contaminants may contribute to disease accumulation and help explain geographically and socioeconomically patterned inequalities. These findings underscore the need for extensive studies that simultaneously measure both multimorbidity and pollution to explore their complex interrelationships., Competing Interests: Declarations Ethics approval and consent to participate This study was performed in line with the principles of the Declaration of Helsinki. Approval was granted by the Ethics Committee of the Institute of Public Health of Serbia (date: 10.06.2021; n˚ 3607/1). Informed consent was obtained from all individual participants included in the study. Consent for publication Not applicable. Competing interests The authors declare no competing interests., (© 2024. The Author(s).)

Epidemiologic research and quantitative risk assessment play a crucial role in transferring fundamental scientific knowledge to policymakers so they can take action to reduce the burden of ambient air pollution. This commentary addresses several challenges in quantitative risk assessment of air pollution that require close attention. The background to this discussion provides a summary of and conclusions from the epidemiological evidence on ambient air pollution and health outcomes accumulated since the 1990s. We focus on identifying relevant exposure-health outcome pairs, the associated concentration-response functions to be applied in a risk assessment, and several caveats in their application. We propose a structured and comprehensive framework for assessing the evidence levels associated with each exposure-health outcome pair within a health impact assessment context. Specific issues regarding the use of global or regional concentration-response functions, their shape, and the range of applicability are discussed., Competing Interests: Declarations Ethics approval and consent to participate There was no need to consent as there are no individual data. Consent for publication There was no need of consent. Competing interests The authors declare no competing interests., (© 2024. The Author(s).)

Introduction: While associations between ambient air pollution and respiratory health in chronic obstructive pulmonary disease (COPD) patients are well studied, little is known about individuals' personal exposure to pollution and associated health effects by source., Aim: To separate measured total personal exposure into indoor-generated and outdoor-generated pollution and use these improved metrics in health models for establishing more reliable associations with exacerbations and respiratory symptoms., Methods: We enrolled a panel of 76 patients with COPD and continuously measured their personal exposure to particles and gaseous pollutants and location with portable monitors for 134 days on average. We collected daily health information related to respiratory symptoms through diary cards and peak expiratory flow (PEF). Mixed-effects models were applied to quantify the relationship between total, indoor-generated and outdoor-generated personal exposures to pollutants with exacerbation and symptoms occurrence and PEF., Results: Exposure to nitrogen dioxide from both indoor and outdoor sources was associated with exacerbations and respiratory symptoms. We observed an increase of 33% (22%-45%), 19% (12%-18%) and 12% (5%-20%) in the odds of exacerbation for an IQR increase in total, indoor-generated and outdoor-generated exposures. For carbon monoxide, health effects were mainly attributed to indoor-generated pollution. While no associations were observed for particulate matter 2.5 with COPD exacerbations, indoor-generated particles were associated with a significant decrease in PEF., Conclusions: Indoor-generated and outdoor-generated pollution can deteriorate COPD patients' health. Policy-makers, physicians and patients with COPD should note the importance of decreasing exposure equally to both source types to decrease risk of exacerbation., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY. Published by BMJ.)

The purpose of the study was to determine whether environmental enrichments (EE) can mitigate the adverse effects of chronic low-dose-rate radiation exposure in mice. Female B6C3F1 mice were continuously exposed to 20 mGy d-1 gamma-rays under specific-pathogen-free conditions since 8 weeks of age for 400 d. After completion of the radiation exposure, OV3121 cells, derived from an ovarian granulosa cell tumor, were inoculated subcutaneously alongside age-matched non-irradiated control mice. Irradiated mice were shown to have a significantly reduced ability to eliminate inoculated tumors. The results indicate that EE may be able to mitigate the adverse effects of low-dose-rate radiation exposure, but the effects vary greatly and are complex depending on the type of EE., (© The Author(s) 2024. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)

Purpose of Review: Allergic rhinitis and asthma morbidity has been linked to indoor allergen exposure. Common indoor allergens include dust mites, cats, dogs, rodents, and cockroaches. These allergens are ubiquitous and often difficult to remove from the home, making long-lasting reduction strategies difficult to achieve. Identifying strategies for reducing the presence of indoor allergens in homes could be utilized to decrease allergic disease burden, improve symptomology, reduce healthcare costs, and improve patients' quality of life., Recent Findings: Studies have yielded mixed results with regard to specific environmental control measures in reducing indoor allergen levels and in improving clinical outcomes of allergic disease. In this review, we assess the available evidence of the effectiveness of environmental control measures in reducing indoor allergens and the potential clinical impact of these measures., Competing Interests: Declarations Human and Animal Rights and Informed Consent This article does not contain any studies with human or animal subjects performed by any of the authors. Conflict of Interest TLG receives research support from NIAID. RAW receives research support from NIAID, Aimmune, ALK, DBV, FARE, Genentech, Novartis, and Siolta. Competing Interests The authors declare no competing interests., (© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Background: The prevalence of eczema has increased with industrialization. Industrial practices generate ambient air pollution, including fine particulate matter of diameter ≤ 2.5μm (PM2.5). Studies investigating the relationship between PM2.5 and eczema in the US are scarce. The objective of this study was to determine the risk of eczema with PM2.5 exposure in a diverse national cohort of American adults., Methods: In this cross-sectional study, eczema cases in the All of Us Research Program were linked via three-digit zip code to average annual PM2.5 concentrations from the Center for Air, Climate, and Energy Solutions. Eczema cases and controls were compared using Pearson's χ2 test for categorical variables and one-way analysis of variance for continuous variables. The relationship between PM2.5 and eczema was assessed via logistic regression adjusting for demographic factors, smoking, and atopic comorbidities., Results: Individuals with eczema (n = 12,695) lived in areas with significantly higher PM2.5 concentrations than did individuals without eczema (n = 274,127) (0.83 x 10 μg/m3 v. 0.81 x 10 μg/m3, P < .001). PM2.5 concentration was significantly associated with eczema in univariable analysis (odds ratio 1.97, 95% confidence interval 1.77-2.19, P < .001), and in multivariable analyses, both controlling for demographics and smoking status (odds ratio 2.21, 95% confidence interval 1.98-2.47, P < .001) and with the addition of atopic comorbidities (odds ratio 2.38, 95% confidence interval 2.12-2.67, P < .001)., Conclusions: The odds of eczema increased with greater PM2.5 concentration in this large, diverse, adult American cohort. Ambient air pollution is an environmental hazard that influences inflammatory skin disease, suggesting possible targeted interventions., Competing Interests: The authors have declared that no competing interests exist., (Copyright: © 2024 Chen et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

Background: Lung cancer ranks as the leading cause of cancer-related deaths worldwide. There is evidence that second-hand smoke (SHS) exposure is a risk factor for the development of lung cancer in never-smokers. This systematic review and meta-analysis aims to provide the most accurate quantification of the association between SHS exposure and lung cancer risk in never-smokers., Materials and Methods: Through the use of an innovative method to identify original publications, we conducted a systematic review of the literature, with corresponding meta-analysis, of all epidemiological studies evaluating the association between SHS exposure and lung cancer risk among never-smokers, published up to May 2023. Pooled relative risks were obtained using random-effects models. Dose-response relationships were derived using log-linear functions or cubic splines., Results: Out of 126 identified eligible studies, 97 original articles were included in the meta-analysis. The pooled relative risk for lung cancer for overall exposure to SHS was 1.24 (95% CI 1.16-1.32, number of articles, n=82). Setting-specific relative risks were 1.20 (95% CI 1.12-1.28, n=67) for SHS exposure at home, 1.38 (95% CI 1.28-1.62, n=30) at a workplace, 1.37 (95% CI 1.22-1.53, n=28) at home or a workplace and 1.27 (95% CI 1.11-1.44, n=24) in nonspecified settings. The risk of lung cancer significantly increased with the duration, intensity and pack-years of SHS exposure., Conclusions: This meta-analysis shows that exposure to SHS increases by more than 20% the risk of lung cancer among never-smokers, providing definitive evidence of the association between SHS exposure and lung cancer risk., Competing Interests: Conflict of interest: All authors declare that they have no competing financial interests or personal relationships that could have influenced the work reported in this paper., (Copyright ©The authors 2024.)

To investigate air pollution's effect in the form of PM 2.5 (particulate matter measuring less than 2.5 microns) on head and neck aerodigestive cancer incidence, an epidemiological cohort analysis was performed using data from the Surveillance Epidemiology and End Results national cancer database from the years 2002-2012. The relationship between US county mean PM 2.5 levels and head and neck cancer (HNC) incidence rates were examined using a linear mixed model. Lagged effect of the pollutant's effect on HNC incidence was analyzed. Our results showed a significant association between the incidence of HNC and certain subtypes with PM 2.5 exposure after controlling for demographic characteristics, smoking and alcohol use. We observed the highest association at a 5-year lag period (β = 0.24, p value < 0.001). We observed significant associations at no lag (β = 0.16, p value = 0.02) and up to a 20-year lag period (β = 0.15, p value < 0.001). PM 2.5 exposure is associated with an increased incidence of HNC, with the strongest association at a 5-year lag period. To better understand the relationships between exposure and cancer pathogenesis, further subgroup analysis is needed., Competing Interests: Competing interests The authors declare no competing interests., (© 2024. The Author(s).)

Purpose The relationship between exposure doses of 2.5-micrometer Particulate Matter (PM 2.5 ), Inhalable particles (PM 10 ), Sulfur Dioxide (SO 2 ), Nitrogen Dioxide (NO 2 ) and Ozone (O 3 ) in the first trimester and spontaneous abortion of pregnant women was evaluated by global average method and nearest monitoring station method, respectively. Method Retrospective analysis of the clinical data of pregnant women with spontaneous abortion and full-term pregnant women in the Department of Obstetrics and Gynecology of two third-class hospitals in a valley city in Northwest China. According to the age factor, the eligible pregnant women were matched at a ratio of 1 : 4. The global average method and the nearest monitoring station method were used to evaluate the exposure of pollutants. The rank-sum test and conditional logistic regression were used to analyze the correlation between air pollutants and spontaneous abortion. Results Although the global average method and the nearest monitoring station method are slightly different in the assessment of exposure dose, they do not affect the correlation evaluation with spontaneous abortion. The exposure of pregnant women to PM 2.5 (OR 1  = 1.156, OR 2  = 1.036), SO 2 (OR 1  = 1.432, OR 2  = 1.429) and NO 2 (OR 1  = 1.121, OR 2  = 1.159) in the first trimester is related to the occurrence of spontaneous abortion.(OR 1 : the global average method, OR 2 : the nearest monitoring station method) Conclusion The exposure of PM 2.5 , SO 2 and NO 2 in the first trimester in valley cities is associated with the occurrence of spontaneous abortion in pregnant women., Competing Interests: Declarations Competing interests The authors declare no competing interests., (© 2024. The Author(s).)

Objectives: To evaluate the association between drinking water pollutants and non-syndromic birth defects., Design: Systematic review and meta-analysis synthesis., Data Sources: A search of MEDLINE, EMBASE and Google Scholar was performed to review relevant citations reporting on birth defects in pregnancies exposed to water pollutants between January 1962 and April 2023., Eligibility Criteria: Prospective or retrospective cohort, population studies and case-control studies that provided data on exposure to drinking water pollutants around conception or during pregnancy and non-syndromic birth defects. We included studies published in the English language after the Minamata Bay disaster to reflect on contemporary concerns about the effect of environmental pollution and obstetric outcomes., Data Extraction and Synthesis: Two reviewers independently read the retrieved articles for content, data extraction and analysis. The methodological quality of studies was assessed using the Newcastle-Ottawa Scale. Included studies were assessed for comparability when considered for meta-analysis., Results: 32 studies met inclusion criteria including 17 cohorts (6 389 097 participants) and 15 case-control studies (47 914 cases and 685 712 controls). The most common pollutants investigated were trihalomethanes (11 studies), arsenic (5 studies) and nitrates (4 studies). The studies varied in design with different estimates of exposure, different stages of gestation age and different durations of exposure to pollutants. 21 articles reported data on any birth defects in their population or study groups and the others on specific birth defects including congenital heart defects, neural tube defects, orofacial defects and hypospadias. An increased risk or higher incidence of overall birth defects was reported by 9 studies and for specific birth defects by 14 studies. Eight studies compared the risk or incidence of birth defects with exposure to different concentrations of the pollutants. The analysis showed an association between higher levels of trihalomethanes (TTMs) and arsenic increase in major birth defects (lower vs higher exposure (OR 0.76, 95% CI 0.65 to 0.89; p<0.001 and OR 0.56, 95% CI 0.39 to 0.82; p<0.005, respectively)., Conclusion: The evidence of an association between exposure to average levels of common drinking water chemical pollutants during pregnancy and an increased risk or incidence of birth defects is uncertain. Available evidence indicates that some common chemical pollutants currently found in drinking water may have a direct teratogenic effect at high maternal exposure, however, wide variation in methodology limits the interpretation of the results. Future prospective studies using standardised protocols comparing maternal levels during all three trimesters of pregnancy and cord blood levels at birth are needed to better understand the placental transfer of water pollutants and accurately evaluate individual fetal exposure to drinking water pollutants., Prospero Registration Number: CRD42018112524., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY. Published by BMJ.)

In Brief: This review describes how heat stress causes systemic endocrine and metabolic alterations that contribute to intracellular ovarian perturbations, resulting in female infertility., Abstract: Heat stress (HS) in mammals results from an imbalance in heat accumulation and dissipation. Fertility impairments consequential to HS have been recognized for decades in production animals, and more recently, observations have been extended to other species, including women. There are several systemic impacts of HS that can independently affect reproduction, including metabolic endotoxemia, reduced plane of nutrition, and endocrine disruption. At the level of the ovary, molecular pathways are altered by HS, such as inflammation, JAK-STAT, PI3K, oxidative stress, cell death, and heat shock response. Taken together, impaired ovarian function contributes to seasonal infertility that results from HS. This review paper describes the physiological and endocrine systemic impacts of HS that may independently and collaboratively impair fertility in the porcine model. The review then details ovarian intracellular events that are altered during HS and finally determines future needs in this area of research.

Background: Epidemiological evidence regarding the association between air pollutants and cardiopulmonary disease, mortality in individuals with preserved ratio impaired spirometry (PRISm), and their combined effects remains unclear., Methods: We followed 36,149 participants with PRISm in the UK Biobank study. Annual concentrations of PM 2.5 , PM 10 , NO 2 , NO x , and SO 2 at residential addresses were determined using a bilinear interpolation method, accounting for address changes. A multistate model assessed the dynamic associations between air pollutants and cardiopulmonary diseases and mortality in PRISm. Quantile g-computation was used to investigate the joint effects of air pollutants., Results: Long-term exposure to PM 2.5 , PM 10 , NO 2 , NO x , and SO 2 was significantly associated with the risk of cardiopulmonary disease in PRISm. The corresponding hazard ratios (HRs) [95 % confidence intervals (95 % CIs)] per interquartile range (IQR) were 1.49 (1.43, 1.54), 1.52 (1.46, 1.57), 1.34 (1.30, 1.39), 1.30 (1.26, 1.34), and 1.44 (1.41, 1.48), respectively. For mortality, the corresponding HRs (95 % CIs) per IQR were 1.36 (1.25, 1.47), 1.35 (1.24, 1.46), 1.27 (1.18, 1.36), 1.23 (1.15, 1.31), and 1.29 (1.20, 1.39), respectively. In PRISm, quantile g-computation analysis demonstrated that a quartile increase in exposure to a mixture of all air pollutants was positively associated with the risk of cardiopulmonary disease and mortality, with HRs (95 % CIs) of 1.84 (1.76, 3.84) and 1.45 (1.32, 1.57), respectively., Conclusion: Long-term individual and joint exposure to air pollutants (PM 2.5 , PM 10 , NO 2 , NO x , and SO 2 ) might be an important risk factor for cardiopulmonary disease and mortality in high-risk populations with PRISm., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Introduction: The Nepal Family Cohort study uses a life course epidemiological approach to collect comprehensive data on children's and their parents' environmental, behavioural and metabolic risk factors. These factors can affect the overall development of children to adulthood and the onset of specific diseases. Among the many risk factors, exposure to air pollution and lifestyle factors during childhood may impact lung development and function, leading to the early onset of respiratory diseases. The global incidence and prevalence of respiratory diseases are rapidly increasing, with the rate of increase in Nepal being the highest. Although the cohort will primarily focus on respiratory health, other health outcomes such as cardiovascular, metabolic and mental health will be assessed to provide a comprehensive overall health assessment. All other health outcomes are self-reported following doctor diagnosis. Some of these health outcomes will be quality controlled during the follow-up by measuring disease specific markers. Our cohort study will likely provide evidence of risk factors and policy recommendations., Methods and Analysis: Using a life-course epidemiology approach, we established a longitudinal study to address the determinants of lung health and other health outcomes from childhood to adulthood. The baseline data collection (personal data anonymised) was completed in April 2024, and 16 826 participants (9225 children and 7601 parents) from 5829 families were recruited in different geographical and climate areas (hills and plains) of Nepal. We plan to follow up all the participants every 2-3 years.Descriptive analysis will be used to report demographic characteristics and compare rural and semi-urban regions. A linear regression model will assess the association between air pollution, particularly household air pollution (HAP) exposure, and other lifestyle factors, with lung function adjusted for potential confounders. A two-stage linear regression model will help to evaluate lung development based on exposure to HAP., Ethics: Ethical approval was obtained from the Nepal Health Research Council, Kathmandu, Nepal, and McMaster University, Hamilton, Canada. Permissions were obtained from two municipalities where the study sites are located. Parents provided signed informed consent and children their assent., Dissemination: Findings will be disseminated through traditional academic pathways, including peer-reviewed publications and conference presentations. We will also engage the study population and local media (ie, research blogs and dissemination events) and prepare research and policy briefings for stakeholders and leaders at the local, provincial and national levels., Competing Interests: Competing interests: None declared except PG, who is supported by the NIHR Applied Research Collaboration West Midlands and an NIHR Senior Investigator, and CEB, who is supported by the NIHR Nottingham Biomedical Research Centre., (© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: Air pollution exposure poses significant health risks for the general population, but particularly for women with acute and chronic respiratory conditions. Given the increasing global burden of air pollution-related illnesses, understanding these biomarkers is crucial for developing targeted interventions and improving respiratory health outcomes in vulnerable populations. In this systematic review, we aimed to determine potential dysregulated respiratory inflammatory blood biomarker candidates in adult female patients who experience varying levels and sources of inhaled pollutant exposure., Methods: We searched the Cochrane Library, PubMed, and Web of Science with nuanced search terms to retrieve articles published in English between 1 January 2000 and 12 June 2023, to ensure relevancy. We filtered our findings to generate a focussed narrative analysis and used the Risk of Bias In Non-randomized Studies-of Exposures (ROBINS-E) and Risk-of-bias VISualization (robVIS) tools to ensure the validity of the data and the quality of the conclusions being made., Results: We identified 916 articles from the databases used in our search, 16 of which met the criteria of our focussed narrative analysis. Among blood biomarkers, platelet-activating factor and eosinophilia could be used to assess the severity of asthma conditions, as a lack or reduction thereof indicates specific conditions. Pro-inflammatory cytokines require further validation, as some studies with a high risk of bias have reported conflicting results compared to more recent research on whether these markers are up-regulated or down-regulated. We found one study to be at a very high risk of bias, two had a high risk of bias, one had some concerns of confounding factors which may not have affected their results, and 12 studies had a low risk of bias., Conclusions: There were narrowed-down blood biomarker candidates that could be used in future research and avenues of research like generating specific microRNA sequences to test for prognostic/diagnostic tests., Registration: PROSPERO: 42023435721., Competing Interests: Disclosure of interest: The authors completed the ICMJE Disclosure of Interest Form (available upon request from the corresponding author) and disclose no relevant interests., (Copyright © 2024 by the Journal of Global Health. All rights reserved.)

Background: Although numerous studies have discussed about the impact of air pollution on cognitive function, a consensus has yet to be reached, necessitating further exploration of their relationship. The aim of this study is to reveal the effects of major air pollutants on cognitive function in Chinese middle-aged and older adults, while considering the lagged effects of pollution., Methods: Panel data were constructed by integrating the air pollutants concentration (particulate matter diameter ≤1 µm (μm) (PM 1 ), PM 2.5 , PM 10 , nitrogen dioxide (NO 2 ), and ozone (O 3 )) among 28 provinces in China and the personal characteristics from China Health and Retirement Longitudinal Study participants during the period of 2011-2015. To explore the effects of single pollutants and their interactions on cognitive function, panel linear regression using ordinary least squares method was employed, and first-order lag effects (two-year interval) of air pollution were introduced into the models., Results: Our study revealed that, after adjusting for confounding factors, higher levels of particulate matter (PM 1 , coefficient (Coef.) = -0.093, P = 0.001; PM 2.5 , Coef. = -0.051, P = 0.001; PM 10 , Coef. = -0.030, P = 0.001) and NO 2 (Coef. = -0.094, P = 0.006) were associated with lower cognitive function scores among the participants. Moreover, the interaction between the five major pollutants exhibited a negative effect on cognitive function(Coef. = -2.89, P = 0.004)., Conclusions: PM 1 , PM 2.5 , PM 10 have detrimental effects on the cognitive function of middle-aged and elderly adults in China, where increasing particle diameter correlates with a less negative impacts, providing theoretical underpinnings for the formulation of environmental protection policies., Competing Interests: Disclosure of interest: The authors completed the ICMJE Disclosure of Interest Form (available upon request from the corresponding author) and disclose no relevant interests, (Copyright © 2024 by the Journal of Global Health. All rights reserved.)

Background: Whether including additional environmental risk factors improves cardiovascular disease (CVD) prediction is unclear. We attempted to improve CVD mortality prediction performance beyond traditional CVD risk factors by additionally using metals measured in the urine and blood and with statistical machine learning methods., Methods: Our sample included 7,085 U.S. adults aged 40 years or older from the National Health and Nutrition Examination Survey 2003-2004 through 2015-2016, linked with the National Death Index through December 31, 2019. Data were randomly split into a 50/50 training dataset used to construct CVD mortality prediction models (n = 3542) and testing dataset used as validation to assess prediction performance (n = 3543). Relative to the traditional risk factors (age, sex, race/ethnicity, smoking status, systolic blood pressure, total and high-density lipoprotein cholesterol, hypertension, and diabetes), we compared models with an additional 17 blood and urinary metal concentrations. To build the prediction models, we used Cox proportional hazards, elastic-net (ENET) penalized Cox, and random survival forest methods., Results: 420 participants died from CVD with 8.8 mean years of follow-up. Blood lead, cadmium, and mercury were associated (p < 0.005) with CVD mortality. Including these blood metals in a Cox model, initially containing only traditional risk factors, raised the C-index from 0.845 to 0.847. Additionally, the Net Reclassification Index showed that 23% of participants received a more accurate risk prediction. Further inclusion of urinary metals improved risk reclassification but not risk discrimination., Conclusions: Incorporating blood metals slightly improved CVD mortality risk discrimination, while blood and urinary metals enhanced risk reclassification, highlighting their potential utility in improving cardiovascular risk assessments., (© 2024. The Author(s).)

Background: There is limited evidence regarding the modifying effects of parents' age at childbirth on the relationship between air pollution and obesity in plateau areas. This study aimed to explore the association between particulate matter (PM) and child obesity, specifically investigating whether parents' age at childbirth could modify this relationship in the Tibetan plateau, China., Methods: Satellite-based random forest models were used to estimate the concentrations of PM 2.5 (particulate matter with aerodynamic diameters ≤ 2.5 μm), PM c (particulate matter with aerodynamic diameters between 2.5 μm and 10 μm), and PM 10 (particulate matter with aerodynamic diameters ≤ 10 μm). Linear and logistic regression models were employed to assess associations between PM exposure and obesity indicators, and effect estimates of PM across different particle sizes were compared., Results: The study comprised 2,015 children under five years old. Postnatal exposure to PM was positively associated with overweight and obesity (OWO), waist-to-hip ratio (WHR) and body mass index (BMI). Among these pollutants, PM 10 exhibited the strongest association with BMI and OWO, whereas PM c showed the strongest association with WHR. An interquartile range (IQR) increase in PM 2.5 (5.67 µg/m 3 ), PM c (5.25 µg/m 3 ), and PM 10 (11.06 µg/m 3 ) was positively associated with OWO (odd ratio [OR] for PM 2.5 = 1.52, 95% confidence interval [CI] for PM 2.5 = 1.24 to 1.85; OR for PM c = 1.50, 95% CI for PM c = 1.19 to 1.88; OR for PM 10  = 1.56, 95% CI for PM 10  = 1.25 to 1.96), respectively. Stratified analysis by parents' age at childbirth indicated that the effects of PM on obesity indicators were more pronounced in the advanced age group., Conclusions: Long-term exposure to PM was positively associated with OWO, WHR, and BMI. Our findings also underscore the importance of examining the effects of ambient PM exposure on OWO, particularly in parents of advanced age at childbirth., (© 2024. The Author(s).)

There is a growing interest in the health impacts of PM 2.5 originating from landscape fires. We conducted a time-series study to investigate the association between daily exposure to landscape fire PM 2.5 and hospital admissions for cardiovascular events in 184 major Chinese cities. We developed a machine learning model combining outputs from chemical transport models, meteorological information and observed air pollution data to determine daily concentrations of landscape fire PM 2.5 . Furthermore, we fitted quasi-Poisson regression to evaluate the link between landscape fire PM 2.5 concentrations and cardiovascular hospitalizations in each city, and conducted random-effects meta-analysis to pool the city-specific estimates. Here we show that, on a national scale, a rise of 1-μg/m 3 in landscape fire PM 2.5 concentrations is positively related to a same-day 0.16% (95% confidence interval: 0.01%-0.32%) increase in hospital admissions for cardiovascular disease, 0.28% (0.12%-0.44%) for ischemic heart disease, and 0.25% (0.02%-0.47%) for ischemic stroke. The associations remain significant even after adjusting for other sources of PM 2.5 . Our findings indicate that transient elevation in landscape fire PM 2.5 levels may increase risk of cardiovascular diseases., (© 2024. The Author(s).)

We estimated the association between combined exposure to air pollutants and the development of cardiometabolic multimorbidity (CM) and all-cause mortality. An air pollution score was calculated to determine the combined exposure to five air pollutants. CM was defined as the instance of at least two types of diseases. A genetic risk score (GRS) was calculated for each individual. A multistate regression model was used to investigate the effect of the combined associations of air pollutants on each stage of CM progression. After multivariable adjustment, the air pollution score was related with greater susceptibility of CM and all-cause mortality, and those with a high GRS for cardiovascular disease (CVD) or coronary heart disease (CHD) and a high air pollution score had a greater susceptibility of incident CM and all-cause mortality. The multistate model revealed that the greater air pollution score was connected with the susceptibility of progressing from disease-free baseline to having one cardiometabolic disease, and next to CM, and eventually to death. Combined exposure to five air pollutants were related with greater susceptibility of CM and all-cause mortality in a dose-dependent style and is related with the progression of CM and with all-cause mortality., (© 2024. The Author(s).)

Background: During the COVID-19 pandemic, non-therapeutic interventions (NPIs), such as traffic restrictions, work stoppages, and school suspensions, have led to a sharp decline in the concentration of air pollutants in the epidemic sites. However, few studies focused on the impact of air pollutant changes on the risk of nonaccidental death., Method: We selected Yancheng City, China, as the study site and applied a Generalized Additive Model (GAM) based on the quasi-Poisson distribution to evaluate the impact of atmospheric pollutants exposure on the nonaccidental death of local residents. The time span of this study was set from January 1, 2013, to December 21, 2022, that is, before and after the outbreak of COVID-19., Results: The concentration of some air pollutants has greatly varied after the outbreak of COVID-19, with a significant decline for PM 2.5 (- 43.4%), PM 10 (- 38.5%), SO 2 (- 62.9%), and NO 2 (- 22.6%), but an increase for O 3 (+ 4.3%). Comparative analysis showed that PM 2.5 contributed to an increased risk of nonaccidental death after the outbreak of COVID-19. With an increase in PM 2.5 by 10 µg/m³, the excess relative risks (ER) of nonaccidental death of residents increased by 1.01% (95%CI: 0.19%,1.84%). The stratified analysis revealed that air pollutants impacted nonaccidental deaths in both men and women before the outbreak of COVID-19. After the outbreak of COVID-19, PM 10 had a significant effect on male nonaccidental deaths. The concentrations of PM 2.5 , PM 10 , and SO 2 increased by 10 µg/m³, the ER of PM 2.5 , PM 10 , and SO 2 on female nonaccidental death increased by 1.52% (0.38%,2.67%), 0.58% (0.02%,1.13%), and 15.09% (5.73%,25.28%), respectively. Before the outbreak of COVID-19, five air pollutants had an impact on the death of residents from cardiovascular disease (CVD). After the outbreak of COVID-19, only PM 10 significantly affected the death risk of CVD. In addition, we discovered that PM 2.5 , PM 10 , and SO 2 significantly impacted the risk of death due to respiratory diseases before and after the outbreak of COVID-19., Conclusions: Air pollutants have different effects on nonaccidental deaths before and after the COVID-19 outbreak. A decrease in air pollutant concentration due to the NPIs for COVID-19 had a significant effect on the reduction of the risk of nonaccidental death., (© 2024. The Author(s).)

The cumulative exposures of an individual during their lifetime, known as the exposome, encompass environmental exposures and lifestyle factors that significantly impact cardiovascular health. The exposome concept aims to provide a comprehensive framework for understanding how various exposures combine to influence disease risk and health outcomes over a lifetime. Diet is a well-studied aspect of the exposome, recognized as a critical contributor to cardiovascular health and influencing various other health metrics and behaviors. Furthermore, understanding agricultural food systems and their interrelationships with dietary choice and impacts on environmental and human health requires a systems approach. Through a review of the literature, this publication will (1) elucidate the interconnections between the exposome and cardiovascular diseases through the lens of agricultural systems and environmental health; (2) examine the effect of diet on cardiovascular health; (3) examine the influence of socioeconomic and cultural factors on the agricultural food system and dietary choices; and (4) highlight the importance of adopting a systems approach that integrates dietary interventions with sustainable agricultural practices, emphasizing the need for holistic strategies to address the root causes of cardiovascular health issues through balanced human and environmental health interventions., Competing Interests: The author has no competing interests to declare., (Copyright: © 2024 The Author(s).)

Air pollution, mostly from fossil fuel sources, is the leading environmental cause of global morbidity and mortality and is intricately linked to climate change. There is emerging evidence indicating that air pollution imposes most of its risk through proximate cardiovascular kidney and metabolic (CKM) etiologies. Indeed, there is compelling evidence linking air pollution to the genesis of insulin resistance, type 2 diabetes, hypertension, and other risk factors. Air pollution frequently coexists with factors such as noise, with levels and risks influenced substantially by additional factors such as social determinants and natural and built environment features. Persistent disparities regarding the impact and new sources of air pollution, such as wildfires attributable to climate change, have renewed the urgency to better understand root sources, characterize their health effects, and disseminate this information for personal protection and policy impacts. In this review, we summarize evidence associating air pollution with cardiovascular health, the impact of air pollution on CKM health, and how interactions with other exposures and personal characteristics may modify these associations. Finally, we discuss new integrated approaches to capture risk from air pollution in the context of an exposomic framework., Competing Interests: The authors have no competing interests to declare., (Copyright: © 2024 The Author(s).)

The exposome encompasses the full range of environmental exposures throughout a person's lifetime and plays an important role in cardiovascular health. Interactions with the social, natural, and built components of the exposome significantly impact cardiovascular disease prevalence and mortality. Robust data analytics, including machine learning and geospatial analysis, have advanced our understanding of how these factors converge to influence cardiovascular disease risk. The integration of multiomics platforms and advanced computational approaches enhances our ability to characterize the exposome, leading to targeted public health interventions and innovative risk reduction strategies aimed at improving cardiovascular health globally. These multiomics platforms that integrate factors such as genomics, epigenomics, clinical data, social factors, environmental factors, and wearable technology will characterize the exposome in greater detail concerning cardiovascular health. In this review, we aimed to elucidate the components of the exposome and discuss recent literature regarding their relationship to cardiovascular health., Competing Interests: The authors have no competing interests to declare., (Copyright: © 2024 The Author(s).)

Purpose: Cataract remains the primary cause of blindness in middle-income and low-income countries, with a known association with environmental factors including smoking. However, the relationship between early-life tobacco smoke exposures, including in utero tobacco smoke exposure and early initiation of smoking, and the risk of cataract incidence remains unclear. We aimed to examine the associations of early-life exposure to tobacco smoke with the risk of elderly-onset cataract., Methods: In this prospective study, we included 330,528 participants aged 40 years or older who were recruited between 2006 and 2010. Early-life tobacco smoke exposures, including in utero, childhood, and adolescence exposure to tobacco smoke, as well as the type of tobacco smoke, were ascertained based on questionnaires at baseline. Elderly-onset cataract was ascertained using hospital inpatient records and cataract surgery records. Multivariable-adjusted Cox proportional hazards models were used to examine the association between early-life tobacco smoke exposures and incident cataract. Additionally, the association between different types of tobacco smoke and cataract risk was also explored., Results: During a median follow-up of 12.04 years, 14,754 cases of incident cataract were documented. After adjusting confounders, the incidence of cataract significantly increased among participants with tobacco smoke exposures (hazard ratio [HR] = 1.13, 95% confidence interval [CI] = 1.09-1.18). Furthermore, individuals who were exposed to tobacco smoke in childhood (HR = 1.10, 95% CI = 1.03-1.21), adolescence (HR = 1.15, 95% CI = 1.10-1.21), and adulthood (HR = 1.12, 95% CI = 1.05-1.19) had an increased risk of cataract. Additionally, individuals who smoked cigars or pipes (HR = 1.26, 95% CI = 1.11-1.44), hand-rolled cigarettes (HR = 1.20, 95% CI = 1.05-1.36), and manufactured cigarettes (HR = 1.12, 95% CI = 1.08-1.17) were associated with an increased risk of cataract., Conclusions: Individuals with early-life tobacco smoke exposures in childhood and adolescence significantly elevate the risks of cataract incidence in older age., Translational Relevance: This study identified cataract-associated risks and suggested interventions like banning youth smoking to reduce future cataract incidence.

Cardiovascular disease is a leading cause of death worldwide. There is limited evidence that exposure to current-use pesticides may contribute to cardiovascular disease risk. We examined the association between residential proximity to the application of agricultural pesticides and cardiovascular risk factors among 484 adult women in the Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS) Study, a cohort based in an agricultural region of California. Outcome assessment was completed between 2010 and 2013. Using participant residential addresses and California's Pesticide Use Reporting database, we estimated agricultural pesticide use within 1 km of residences during the 2-year period preceding outcome assessment. We used Bayesian hierarchical modeling to evaluate associations between exposure to 14 agricultural pesticides and continuous measures of waist circumference, body mass index, and blood pressure. Each 10-fold increase in paraquat application around homes was associated with increased diastolic blood pressure (β = 2.60 mm Hg; 95% credible interval [CrI], 0.27-4.89) and each 10-fold increase in glyphosate application was associated with increased pulse pressure (β = 2.26 mm Hg; 95% CrI, 0.09-4.41). No meaningful associations were observed for the other pesticides examined. Our results suggest that paraquat and glyphosate pesticides may affect cardiovascular disease development in women with chronic environmental exposure. This article is part of a Special Collection on Environmental Epidemiology., (© The Author(s) 2024. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)