Impacts of socioeconomic and environmental factors on neoplasms incidence rates using machine learning and GIS: a cross-sectional study in Iran.

Neoplasm is an umbrella term used to describe either benign or malignant conditions. The correlations between socioeconomic and environmental factors and the occurrence of new-onset of neoplasms have already been demonstrated in a body of research. Nevertheless, few studies have specifically dealt with the nature of relationship, significance of risk factors, and geographic variation of them, particularly in low- and middle-income communities. This study, thus, set out to (1) analyze spatiotemporal variations of the age-adjusted incidence rate (AAIR) of neoplasms in Iran throughout five time periods, (2) investigate relationships between a collection of environmental and socioeconomic indicators and the AAIR of neoplasms all over the country, and (3) evaluate geographical alterations in their relative importance. Our cross-sectional study design was based on county-level data from 2010 to 2020. AAIR of neoplasms data was acquired from the Institute for Health Metrics and Evaluation (IHME). HotSpot analyses and Anselin Local Moran's I indices were deployed to precisely identify AAIR of neoplasms high- and low-risk clusters. Multi-scale geographically weight regression (MGWR) analysis was worked out to evaluate the association between each explanatory variable and the AAIR of neoplasms. Utilizing random forests (RF), we also examined the relationships between environmental (e.g., UV index and PM2.5 concentration) and socioeconomic (e.g., Gini coefficient and literacy rate) factors and AAIR of neoplasms. AAIR of neoplasms displayed a significant increasing trend over the study period. According to the MGWR, the only factor that significantly varied spatially and was associated with the AAIR of neoplasms in Iran was the UV index. A good accuracy RF model was confirmed for both training and testing data with correlation coefficients R2 greater than 0.91 and 0.92, respectively. UV index and Gini coefficient ranked the highest variables in the prediction of AAIR of neoplasms, based on the relative influence of each variable. More research using machine learning approaches taking the advantages of considering all possible determinants is required to assess health strategies outcomes and properly formulate policy planning.

Long-term exposure to PM2.5 and mortality in a national cohort in South Korea: effect modification by community deprivation, medical infrastructure, and greenness.

BACKGROUND: Long-term exposure to PM2.5 has been linked to increased mortality risk. However, limited studies have examined the potential modifying effect of community-level characteristics on this association, particularly in Asian contexts. This study aimed to estimate the effects of long-term exposure to PM2.5 on mortality in South Korea and to examine whether community-level deprivation, medical infrastructure, and greenness modify these associations. METHODS: We conducted a nationwide cohort study using the National Health Insurance Service-National Sample Cohort. A total of 394,701 participants aged 30 years or older in 2006 were followed until 2019. Based on modelled PM2.5 concentrations, 1 to 3-year and 5-year moving averages of PM2.5 concentrations were assigned to each participant at the district level. Time-varying Cox proportional-hazards models were used to estimate the association between PM2.5 and non-accidental, circulatory, and respiratory mortality. We further conducted stratified analysis by community-level deprivation index, medical index, and normalized difference vegetation index to represent greenness. RESULTS: PM2.5 exposure, based on 5-year moving averages, was positively associated with non-accidental (Hazard ratio, HR: 1.10, 95% Confidence Interval, CI: 1.01, 1.20, per 10 µg/m3 increase) and circulatory mortality (HR: 1.22, 95% CI: 1.01, 1.47). The 1-year moving average of PM2.5 was associated with respiratory mortality (HR: 1.33, 95% CI: 1.05, 1.67). We observed higher associations between PM2.5 and mortality in communities with higher deprivation and limited medical infrastructure. Communities with higher greenness showed lower risk for circulatory mortality but higher risk for respiratory mortality in association with PM2.5. CONCLUSIONS: Our study found mortality effects of long-term PM2.5 exposure and underlined the role of community-level factors in modifying these association. These findings highlight the importance of considering socio-environmental contexts in the design of air quality policies to reduce health disparities and enhance overall public health outcomes.

Ambient fine particulate matter and daily mortality: a comparative analysis of observed and estimated exposure in 347 cities.

BACKGROUND: Model-estimated air pollution exposure products have been widely used in epidemiological studies to assess the health risks of particulate matter with diameters of ≤2.5 µm (PM2.5). However, few studies have assessed the disparities in health effects between model-estimated and station-observed PM2.5 exposures. METHODS: We collected daily all-cause, respiratory and cardiovascular mortality data in 347 cities across 15 countries and regions worldwide based on the Multi-City Multi-Country collaborative research network. The station-observed PM2.5 data were obtained from official monitoring stations. The model-estimated global PM2.5 product was developed using a machine-learning approach. The associations between daily exposure to PM2.5 and mortality were evaluated using a two-stage analytical approach. RESULTS: We included 15.8 million all-cause, 1.5 million respiratory and 4.5 million cardiovascular deaths from 2000 to 2018. Short-term exposure to PM2.5 was associated with a relative risk increase (RRI) of mortality from both station-observed and model-estimated exposures. Every 10-µg/m3 increase in the 2-day moving average PM2.5 was associated with overall RRIs of 0.67% (95% CI: 0.49 to 0.85), 0.68% (95% CI: -0.03 to 1.39) and 0.45% (95% CI: 0.08 to 0.82) for all-cause, respiratory, and cardiovascular mortality based on station-observed PM2.5 and RRIs of 0.87% (95% CI: 0.68 to 1.06), 0.81% (95% CI: 0.08 to 1.55) and 0.71% (95% CI: 0.32 to 1.09) based on model-estimated exposure, respectively. CONCLUSIONS: Mortality risks associated with daily PM2.5 exposure were consistent for both station-observed and model-estimated exposures, suggesting the reliability and potential applicability of the global PM2.5 product in epidemiological studies.

Ambient air pollution as a time-varying covariate in the survival probability of childhood cancer patients in the upper Northern Thailand.

The objective of this study is to determine the possible association between exposure to air pollution and the risk of death from cancer during childhood in upper northern Thailand. Data were collected on children aged 0-15 years old diagnosed with cancer between January 2003 and December 2018 from the Chiang Mai Cancer Registry. Survival rates were determined by using Kaplan-Meier curves. Cox proportional hazard models were used to investigate associations of potential risk factors with the time-varying air pollution level on the risk of death. Of the 540 children with hematologic cancer, 199 died from any cause (overall mortality rate = 5.3 per 100 Person-Years of Follow-Up (PYFU); 95%CI = 4.6-6.0). Those aged less than one year old (adjusted hazard ratio [aHR] = 2.07; 95%CI = 1.25-3.45) or ten years old or more (aHR = 1.41; 95%CI = 1.04-1.91) at the time of diagnosis had a higher risk of death than those aged one to ten years old. Those diagnosed between 2003 and 2013 had an increased risk of death (aHR = 1.65; 95%CI = 1.13-2.42). Of the 499 children with solid tumors, 214 died from any cause (5.9 per 100 PYFU; 95%CI = 5.1-6.7). Only the cancer stage remained in the final model, with the metastatic cancer stage (HR = 2.26; 95%CI = 1.60-3.21) and the regional cancer stage (HR = 1.53; 95%CI = 1.07-2.19) both associated with an increased risk of death. No association was found between air pollution exposure and all-cause mortality for either type of cancer. A larger-scale analytical study might uncover such relationships.

The Impact of Thallium Exposure in Public Health and Molecular Toxicology: A Comprehensive Review.

This review offers a synthesis of the current understanding of the impact of low-dose thallium (Tl) on public health, specifically emphasizing its diverse effects on various populations and organs. The article integrates insights into the cytotoxic effects, genotoxic potential, and molecular mechanisms of thallium in mammalian cells. Thallium, a non-essential heavy metal present in up to 89 different minerals, has garnered attention due to its adverse effects on human health. As technology and metallurgical industries advance, various forms of thallium, including dust, vapor, and wastewater, can contaminate the environment, extending to the surrounding air, water sources, and soil. Moreover, the metal has been identified in beverages, tobacco, and vegetables, highlighting its pervasive presence in a wide array of food sources. Epidemiological findings underscore associations between thallium exposure and critical health aspects such as kidney function, pregnancy outcomes, smoking-related implications, and potential links to autism spectrum disorder. Thallium primarily exerts cellular toxicity on various tissues through mitochondria-mediated oxidative stress and endoplasmic reticulum stress. This synthesis aims to shed light on the intricate web of thallium exposure and its potential implications for public health, emphasizing the need for vigilant consideration of its risks.

Projecting non-communicable diseases attributable to air pollution in the climate change era: a systematic review.

OBJECTIVES: Climate change is a major global issue with significant consequences, including effects on air quality and human well-being. This review investigated the projection of non-communicable diseases (NCDs) attributable to air pollution under different climate change scenarios. DESIGN: This systematic review was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020 flow checklist. A population-exposure-outcome framework was established. Population referred to the general global population of all ages, the exposure of interest was air pollution and its projection, and the outcome was the occurrence of NCDs attributable to air pollution and burden of disease (BoD) based on the health indices of mortality, morbidity, disability-adjusted life years, years of life lost and years lived with disability. DATA SOURCES: The Web of Science, Ovid MEDLINE and EBSCOhost databases were searched for articles published from 2005 to 2023. ELIGIBILITY CRITERIA FOR SELECTING STUDIES: The eligible articles were evaluated using the modified scale of a checklist for assessing the quality of ecological studies. DATA EXTRACTION AND SYNTHESIS: Two reviewers searched, screened and selected the included studies independently using standardised methods. The risk of bias was assessed using the modified scale of a checklist for ecological studies. The results were summarised based on the projection of the BoD of NCDs attributable to air pollution. RESULTS: This review included 11 studies from various countries. Most studies specifically investigated various air pollutants, specifically particulate matter <2.5 µm (PM2.5), nitrogen oxides and ozone. The studies used coupled-air quality and climate modelling approaches, and mainly projected health effects using the concentration-response function model. The NCDs attributable to air pollution included cardiovascular disease (CVD), respiratory disease, stroke, ischaemic heart disease, coronary heart disease and lower respiratory infections. Notably, the BoD of NCDs attributable to air pollution was projected to decrease in a scenario that promotes reduced air pollution, carbon emissions and land use and sustainable socioeconomics. Contrastingly, the BoD of NCDs was projected to increase in a scenario involving increasing population numbers, social deprivation and an ageing population. CONCLUSION: The included studies widely reported increased premature mortality, CVD and respiratory disease attributable to PM2.5. Future NCD projection studies should consider emission and population changes in projecting the BoD of NCDs attributable to air pollution in the climate change era. PROSPERO REGISTRATION NUMBER: CRD42023435288.

Association between indoor air pollution and depression: a systematic review and meta-analysis of cohort studies.

OBJECTIVES: Incomplete combustion of solid fuel and exposure to secondhand smoke (SHS) are the primary causes of indoor air pollution (IAP), potentially leading to detrimental effects on individual mental health. However, current evidence regarding the association between IAP and depression remains inconclusive. This study aims to systematically investigate the evidence regarding the association between IAP and the risk of depression. DESIGN: Systematic review and meta-analysis of cohort studies. DATA SOURCES: Two independent reviewers searched PubMed, the Cochrane Library, Web of Science and EMBASE for available studies published up to 13 January 2024. ELIGIBILITY CRITERIA: We included all cohort studies published in English that aimed to explore the relationship between IAP from solid fuel use and SHS exposure and the risk of depression. DATA EXTRACTION AND SYNTHESIS: Two independent reviewers extracted data and assessed the risk of bias. The association between IAP and depression was calculated using pooled relative risk (RR) with 95% CIs. Heterogeneity was assessed using the I2 value, and the effect estimates were pooled using fixed-effects or random-effects models depending on the results of homogeneity analysis. RESULTS: We included 12 articles with data from 61 217 participants. The overall findings demonstrated a significant association between IAP exposure and depression (RR=1.22, 95% CI: 1.13 to 1.31), although with substantial heterogeneity (I2=75%). Subgroup analyses based on pollutant type revealed that IAP from solid fuel use was associated with a higher risk of depression (RR=1.20, 95% CI: 1.13 to 1.26; I2=62%; 5 studies, 36 768 participants) than that from SHS exposure (RR=1.11, 95% CI: 0.87 to 1.41; I2=80%; 7 studies, 24 449 participants). In terms of fuel use, the use of solid fuel for cooking (RR: 1.23, 95% CI: 1.16 to 1.31; I2=58%; 4 studies, 34 044 participants) and heating (RR 1.15, 95% CI: 1.04 to 1.27; I2=65%; 3 studies, 24 874 participants) was associated with increased depression risk. CONCLUSIONS: The findings from this systematic review and meta-analysis of cohort studies indicated an association between exposure to IAP and depression. PROSPERO REGISTRATION NUMBER: CRD42022383285.

Atopic Dermatitis: Pathophysiology.

The pathophysiology of atopic dermatitis is complex and multifactorial, involving elements of barrier dysfunction, alterations in cell-mediated immune responses, IgE-mediated hypersensitivity, and environmental factors. Loss-of-function mutations in filaggrin have been implicated in severe atopic dermatitis due to a potential increase in trans-epidermal water loss, pH alterations, and dehydration. Other genetic changes have also been identified, which may alter the skin's barrier function, resulting in an atopic dermatitis phenotype. The imbalance of Th2 to Th1 cytokines observed in atopic dermatitis can create alterations in the cell-mediated immune responses and can promote IgE-mediated hypersensitivity, both of which appear to play a role in the development of atopic dermatitis. One must additionally take into consideration the role of the environment on the causation of atopic dermatitis and the impact of chemicals such as airborne formaldehyde, harsh detergents, fragrances, and preservatives. Use of harsh alkaline detergents in skin care products may also unfavorably alter the skin's pH causing downstream changes in enzyme activity and triggering inflammation. Environmental pollutants can trigger responses from both the innate and adaptive immune pathways. This chapter will discuss the multifaceted etiology of atopic dermatitis, which will help us to elucidate potential therapeutic targets. We will also review existing treatment options and their interaction with the complex inflammatory and molecular triggers of atopic dermatitis.

Cohort profile: the Environmental Reproductive and Glucose Outcomes (ERGO) Study (Boston, Massachusetts, USA) - a prospective pregnancy cohort study of the impacts of environmental exposures on parental cardiometabolic health.

PURPOSE: Pregnancy and the postpartum period are increasingly recognised as sensitive windows for cardiometabolic disease risk. Growing evidence suggests environmental exposures, including endocrine-disrupting chemicals (EDCs), are associated with an increased risk of pregnancy complications that are associated with long-term cardiometabolic risk. However, the impact of perinatal EDC exposure on subsequent cardiometabolic risk post-pregnancy is less understood. The Environmental Reproductive and Glucose Outcomes (ERGO) Study was established to investigate the associations of environmental exposures during the perinatal period with post-pregnancy parental cardiometabolic health. PARTICIPANTS: Pregnant individuals aged ≥18 years without pre-existing diabetes were recruited at <15 weeks of gestation from Boston, Massachusetts area hospitals. Participants completed ≤4 prenatal study visits (median: 12, 19, 26, 36 weeks of gestation) and 1 postpartum visit (median: 9 weeks), during which we collected biospecimens, health histories, demographic and behavioural data, and vitals and anthropometric measurements. Participants completed a postpartum fasting 2-hour 75 g oral glucose tolerance test. Clinical data were abstracted from electronic medical records. Ongoing (as of 2024) extended post-pregnancy follow-up visits occur annually following similar data collection protocols. FINDINGS TO DATE: We enrolled 653 unique pregnancies and retained 633 through delivery. Participants had a mean age of 33 years, 10% (n=61) developed gestational diabetes and 8% (n=50) developed pre-eclampsia. Participant pregnancy and postpartum urinary phthalate metabolite concentrations and postpartum glycaemic biomarkers were quantified. To date, studies within ERGO found higher exposure to phthalates and phthalate mixtures, and separately, higher exposure to radioactive ambient particulate matter, were associated with adverse gestational glycaemic outcomes. Additionally, certain personal care products used in pregnancy, notably hair oils, were associated with higher urinary phthalate metabolite concentrations, earlier gestational age at delivery and lower birth weight. FUTURE PLANS: Future work will leverage the longitudinal data collected on pregnancy and cardiometabolic outcomes, environmental exposures, questionnaires, banked biospecimens and paediatric data within the ERGO Study.

Implications of environmental nanoparticles on neurodegeneration.

The ubiquity of nanoparticles, sourced from both natural environments and human activities, presents critical challenges for public health. While offering significant potential for innovative biomedical applications-especially in enhancing drug transport across the blood-brain barrier-these particles also introduce possible hazards due to inadvertent exposure. This concise review explores the paradoxical nature of nanoparticles, emphasizing their promising applications in healthcare juxtaposed with their potential neurotoxic consequences. Through a detailed examination, we delineate the pathways through which nanoparticles can reach the brain and the subsequent health implications. There is growing evidence of a disturbing association between nanoparticle exposure and the onset of neurodegenerative conditions, highlighting the imperative for comprehensive research and strategic interventions. Gaining a deep understanding of these mechanisms and enacting protective policies are crucial steps toward reducing the health threats of nanoparticles, thereby maximizing their therapeutic advantages.

Environment and systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with a wide range of clinical manifestations and a relapsing-remitting course. SLE pathogenesis is the result of complex interactions between ethnic, genetic, epigenetic, immunoregulatory, hormonal and environmental factors, and several aspects of these multifactorial connections are still unclear. Overall, for the disease development, an environmental trigger may induce immunological dysfunction in genetically predisposed individuals. This review aims to summarise the most relevant data on the impact of environmental factors on the incidence of SLE and on disease activity and damage in patients with an established diagnosis of SLE.

The perils of poly- and perfluorinated chemicals on the reproductive health of humans, livestock, and wildlife.

Poly- and perfluoroalkyl substances (PFAS) are a prominent class of persistent synthetic compound. The widespread use of these substances in various industrial applications has resulted in their pervasive contamination on a global scale. It is therefore concerning that PFAS have a propensity to accumulate in bodily tissues whereupon they have been linked with a range of adverse health outcomes. Despite this, the true extent of the risk posed by PFAS to humans, domestic animals, and wildlife remains unclear. Addressing these questions requires a multidisciplinary approach, combining the fields of chemistry, biology, and policy to enable meaningful investigation and develop innovative remediation strategies. This article combines the perspectives of chemists, soil scientists, reproductive biologists, and health policy researchers, to contextualise the issue of PFAS contamination and its specific impact on reproductive health. The purpose of this article is to describe the challenges associated with remediating PFAS-contaminated soils and waters and explore the consequences of PFAS contamination on health and reproduction. Furthermore, current actions to promote planetary health and protect ecosystems are presented to instigate positive social change among the scientific community.

Regression discontinuity design for the study of health effects of exposures acting early in life.

Regression discontinuity design (RDD) is a quasi-experimental approach to study the causal effect of an exposure on later outcomes by exploiting the discontinuity in the exposure probability at an assignment variable cut-off. With the intent of facilitating the use of RDD in the Developmental Origins of Health and Disease (DOHaD) research, we describe the main aspects of the study design and review the studies, assignment variables and exposures that have been investigated to identify short- and long-term health effects of early life exposures. We also provide a brief overview of some of the methodological considerations for the RDD identification using an example of a DOHaD study. An increasing number of studies investigating the effects of early life environmental stressors on health outcomes use RDD, mostly in the context of education, social and welfare policies, healthcare organization and insurance, and clinical management. Age and calendar time are the mostly used assignment variables to study the effects of various early life policies and programs, shock events and guidelines. Maternal and newborn characteristics, such as age, birth weight and gestational age are frequently used assignment variables to study the effects of the type of neonatal care, health insurance, and newborn benefits, while socioeconomic measures have been used to study the effects of social and welfare programs. RDD has advantages, including intuitive interpretation, and transparent and simple graphical representation. It provides valid causal estimates if the assumptions, relatively weak compared to other non-experimental study designs, are met. Its use to study health effects of exposures acting early in life has been limited to studies based on registries and administrative databases, while birth cohort data has not been exploited so far using this design. Local causal effect around the cut-off, difficulty in reaching high statistical power compared to other study designs, and the rarity of settings outside of policy and program evaluations hamper the widespread use of RDD in the DOHaD research. Still, the assignment variables' cut-offs for exposures applied in previous studies can be used, if appropriate, in other settings and with additional outcomes to address different research questions.

Per- and polyfluoroalkyl substances alter innate immune function: evidence and data gaps.

Per- and polyfluoroalkyl substances (PFASs) are a large class of compounds used in a variety of processes and consumer products. Their unique chemical properties make them ubiquitous and persistent environmental contaminants while also making them economically viable and socially convenient. To date, several reviews have been published to synthesize information regarding the immunotoxic effects of PFASs on the adaptive immune system. However, these reviews often do not include data on the impact of these compounds on innate immunity. Here, current literature is reviewed to identify and incorporate data regarding the effects of PFASs on innate immunity in humans, experimental models, and wildlife. Known mechanisms by which PFASs modulate innate immune function are also reviewed, including disruption of cell signaling, metabolism, and tissue-level effects. For PFASs where innate immune data are available, results are equivocal, raising additional questions about common mechanisms or pathways of toxicity, but highlighting that the innate immune system within several species can be perturbed by exposure to PFASs. Recommendations are provided for future research to inform hazard identification, risk assessment, and risk management practices for PFASs to protect the immune systems of exposed organisms as well as environmental health.

Long-term exposure to ambient air pollution and measures of central hemodynamics and arterial stiffness among multiethnic Chicago residents.

OBJECTIVES: To examine whether long-term air pollution exposure is associated with central hemodynamic and brachial artery stiffness parameters. METHODS: We assessed central hemodynamic parameters including central blood pressure, cardiac parameters, systemic vascular compliance and resistance, and brachial artery stiffness measures [including brachial artery distensibility (BAD), compliance (BAC), and resistance (BAR)] using waveform analysis of the arterial pressure signals obtained from a standard cuff sphygmomanometer (DynaPulse2000A, San Diego, CA). The long-term exposures to particles with an aerodynamic diameter < 2.5 µm (PM2.5) and nitrogen dioxide (NO2) for the 3-year periods prior to enrollment were estimated at residential addresses using fine-scale intra-urban spatiotemporal models. Linear mixed models adjusted for potential confounders were used to examine associations between air pollution exposures and health outcomes. RESULTS: The cross-sectional study included 2,387 Chicago residents (76% African Americans) enrolled in the ChicagO Multiethnic Prevention And Surveillance Study (COMPASS) during 2013-2018 with validated address information, PM2.5 or NO2, key covariates, and hemodynamics measurements. We observed long-term concentrations of PM2.5 and NO2 to be positively associated with central systolic, pulse pressure and BAR, and negatively associated with BAD, and BAC after adjusting for relevant covariates. A 1-µg/m3 increment in preceding 3-year exposures to PM2.5 was associated with 1.8 mmHg higher central systolic (95% CI: 0.98, 4.16), 1.0 mmHg higher central pulse pressure (95% CI: 0.42, 2.87), a 0.56%mmHg lower BAD (95% CI: -0.81, -0.30), and a 0.009 mL/mmHg lower BAC (95% CI: -0.01, -0.01). CONCLUSION: This population-based study provides evidence that long-term exposures to PM2.5 and NO2 is related to central BP and arterial stiffness parameters, especially among African Americans.

Association between exposure to ambient air pollution, meteorological factors and atopic dermatitis consultations in Singapore-a stratified nationwide time-series analysis.

Atopic dermatitis (AD) is a chronic inflammatory skin disease affecting approximately 20% of children globally. While studies have been conducted elsewhere, air pollution and weather variability is not well studied in the tropics. This time-series study examines the association between air pollution and meteorological factors with the incidence of outpatient visits for AD obtained from the National Skin Centre (NSC) in Singapore. The total number of 1,440,844 consultation visits from the NSC from 2009 to 2019 was analysed. Using the distributed lag non-linear model and assuming a negative binomial distribution, the short-term temporal association between outpatient visits for AD and air quality and meteorological variability on a weekly time-scale were examined, while adjusting for long-term trends, seasonality and autocorrelation. The analysis was also stratified by gender and age to assess potential effect modification. The risk of AD consultation visits was 14% lower (RR10th percentile: 0.86, 95% CI 0.78-0.96) at the 10th percentile (11.9 µg/m3) of PM2.5 and 10% higher (RR90th percentile: 1.10, 95% CI 1.01-1.19) at the 90th percentile (24.4 µg/m3) compared to the median value (16.1 µg/m3). Similar results were observed for PM10 with lower risk at the 10th percentile and higher risk at the 90th percentile (RR10th percentile: 0.86, 95% CI 0.78-0.95, RR90th percentile: 1.10, 95% CI 1.01-1.19). For rainfall for values above the median, the risk of consultation visits was higher up to 7.4 mm in the PM2.5 model (RR74th percentile: 1.07, 95% CI 1.00-1.14) and up to 9 mm in the PM10 model (RR80th percentile: 1.12, 95% CI 1.00-1.25). This study found a close association between outpatient visits for AD with ambient particulate matter concentrations and rainfall. Seasonal variations in particulate matter and rainfall may be used to alert healthcare providers on the anticipated rise in AD cases and to time preventive measures to reduce the associated health burden.

Association between plasma metal exposure and health span in very elderly adults: a prospective cohort study with mixture statistical approach.

BACKGROUND: Metals have been linked to a diverse spectrum of age-related diseases; however, the effects of metal exposure on health span remains largely unknown. This cohort study aims to determine the association between plasma metal and health span in elder adults aged ≥ 90 years. METHODS: The plasma concentrations of seven metals were measured at baseline in 300 elder adults. The end of the health span (EHS) was identified as the occurrence of one of eight major morbidities or mortality events. We used Cox regression to assess hazard ratios (HR). The combined effects of multiple metal mixtures were estimated using grouped-weighted quantile sum (GWQS), quantile g-computation (Q-gcomp), and Bayesian kernel machine regression (BKMR) methods. RESULTS: The estimated HR for EHS with an inter-quartile range (IQR) increment for selenium (Se) was 0.826 (95% confidence interval [CI]: 0.737-0.926); magnesium (Mg), 0.806 (95% CI: 0.691-0.941); iron (Fe), 0.756 (95% CI: 0.623-0.917), and copper (Cu), 0.856 (95% CI: 0.750-0.976). The P for trend of Se, Mg, and Fe were all < 0.05. In the mixture analyses, Q-gcomp showed a negative correlation with EHS (P = 0.904), with the sum of the negative coefficients being -0.211. CONCLUSION: Higher plasma Se, Mg, and Fe reduced the risk of premature end of health span, suggesting that essential metal elements played a role in health maintenance in elder adults.

[Association between long-term exposure to ambient ozone and sperm quality in Shandong Province].

Objective: To evaluate the association between long-term exposure to ambient ozone (O3) and sperm quality. Methods: From January 1, 2014, to December 31, 2019, healthy sperm donors were recruited through the Human Sperm Bank of Shandong University Affiliated Reproductive Hospital. A total of 37 977 sperm donation data from 2 971 healthy volunteers were analyzed. The average annual O3 concentration (0.01°× 0.01°) was matched according to household address. A multivariate mixed-effect model was used to analyze the exposure-response relationship between the average O3 exposure concentration and sperm quality in the previous year, with each donor as a random intercept. All results were presented as % changes with 95% confidence intervals (CIs) for all sperm parameters associated with 10 µg/m3 increases in O3. The effects of individual characteristics on the association between O3 and sperm quality were evaluated by stratified analysis. Results: The average O3 concentration in the year before semen collection was (107.09±7.50) µg/m3. Each 10 µg/m3 increase in O3 was associated with declined sperm concentration (-3.12%, 95%CI:-4.55%, -1.67%), total sperm count (-5.21%, 95%CI:-7.28%, -3.09%), total sperm motility (-1.49%, 95%CI:-2.37%, -0.61%), progressive motility (-2.53%, 95%CI:-3.78%, -1.26%), total motile sperm count (-5.82%, 95%CI:-8.17%, -3.41%), and progressively motile sperm count (-6.22%, 95%CI:-8.73%, -3.64%). Men aged 30 and above, obese, and with lower education levels might be more susceptible to the influence of O3 on sperm quality, but the difference was not statistically significant (P>0.05). Conclusion: Long-term exposure to O3 in Shandong Province is associated with a decrease in sperm quality.

[Association between ambient air pollution and biological aging among the middle-aged and older adults: a systematic review].

Objective: To summarize and elucidate the impact of ambient air pollution on biological aging among middle-aged and older adults. Methods: "Air pollution""Biological age""Epigenetic age""Biological aging"and"Epigenetic aging", as well as specific names of air pollutants and biological age were used as search keywords. This study searched the databases of PubMed and Web of Science for eligible English articles and CNKI, CQVIP, Wanfang, CBM, CSTP and other Chinese databases for eligible Chinese articles from inception until June 30, 2023. The language was limited to Chinese and English. Results: Among the 14 included articles, five studies investigated the impact of air pollution on DNA methylation age using different algorithms, while six studies explored the relationship between air pollutants and telomere length. Six studies focused on frailty as an outcome, and an additional study revealed the relationship between fine particulate matter (PM2.5) and its components with composite indicator age (KDM age). The results indicated that, although different forms of biological ages were susceptible to different ambient air pollutants at different degrees, previous studies had consistently found that the increased levels of PM2.5 and one of its major components, black carbon (BC), could significantly accelerate the biological aging of middle-aged and older adults. Similar trends were observed with nitrogen oxides (NOx) and ozone (O3) but with relatively limited evidence. Conclusion: Major air pollutants could accelerate the biological aging of middle-aged and older adults.