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Long-term particulate matter with aerodynamic diameters ≤2.5 μm (PM 2.5 ) exposure has been associated with the occurrence of acute coronary syndrome (ACS). However, the impact of PM 2.5 exposure and its components on the severity of angina pectoris and disease-related health status in patients hospitalized for ACS is understudied. To assess the association between long-term exposure to PM 2.5 components and the angina pectoris severity in ACS patients, as well as the modification effects of genetic factors and disease history in north China. During 2017-2019, 6729 ACS patients were collected in Shandong Province and Beijing, with their angina pectoris severity evaluated using Seattle Angina Questionnaire (SAQ). The 0-3 years' average concentrations of PM 2.5 and its five major components were assigned to each patient's residential address. Linear mixed-effects model, weighted quantile regression, and quantile g-computation were used to estimate the effects of both single and joint associations between PM 2.5 components and SAQ scores. The interactive effect was estimated by polygenic risk scores and disease history. For each interquartile range increase in PM 2.5 , the overall SAQ score changed by -3.71% (95%CI: -4.54% to -2.88%), with score of angina stability more affected than angina frequency and other dimensions of angina pectoris severity. Sulfate and ammonium were major contributors to the effect of PM 2.5 exposure. Significant modification effect was only observed for disease history, especially for the dimension of physical limitation. Among a series of pre-existing diseases, patients with a family history of coronary artery disease, previous percutaneous coronary intervention or coronary artery bypass grafting, and stroke were more susceptible to PM 2.5 exposure than others. Greater exposure to PM 2.5 is associated with more serious angina pectoris and worse disease-related health status in ACS patients. Public health and clinical priority should be given to cutting down key effective components and protecting highly vulnerable individuals., 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.)

Background: Fine particulate matter (PM 2.5 ) has been implicated in various health concerns. However, a comprehensive understanding of the specific PM 2.5 components affecting depression remains limited., Methods: This study conducted a Cox proportional-hazards model to assess the effect of PM 2.5 components on the incidence of depression based on the China Health and Retirement Longitudinal Study (CHARLS). Participants with 10-item Center for Epidemiologic Studies Depression Scale (CESD-10) score of 10 or higher were classified as exhibiting depression., Results: Our findings demonstrated a significant positive correlation between long-term exposure to black carbon (BC), sulfate (SO 4 2- ), and organic matter (OM) components of PM 2.5 and the prevalence of depression. Per 1 Interquartile Range (IQR) increment in 3-year average concentrations of BC, OM, and SO 4 2- were associated with the hazard ratio (HR) of 1.54 (95 % confidence intervals (CI): 1.44, 1.64), 1.24 (95%CI: 1.16, 1.34) and 1.25 (95%CI: 1.16, 1.35). Notably, females, younger individuals, those with lower educational levels, urban residents, individuals who were single, widowed, or divorced, and those living in multi-story houses exhibited heightened vulnerability to the adverse effects of PM 2.5 components on depression., Limitations: Firstly, pollutant data is confined to subjects' fixed addresses, overlooking travel and international residence history. Secondly, the analysis only incorporates five fine particulate components, leaving room for further investigation into the remaining fine particulate components in future studies., Conclusions: This study provides robust evidence supporting the detrimental impact of PM 2.5 components on depression. The identification of specific vulnerable populations contributes to a deeper understanding of the underlying mechanisms involved in the relationship between PM 2.5 components and depression., Competing Interests: Declaration of competing interest The authors declare no competing interests., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Background: The short-term adverse effects of ambient fine particulate matter (PM 2.5 ) and ozone (O 3 ) on anxiety disorders (ADs) remained inconclusive., Methods: We applied an individual-level time-stratified case-crossover study, which including 126,112 outpatient visits for ADs during 2019-2021 in Guangdong province, China, to investigate the association of short-term exposure to PM 2.5 and O 3 with outpatient visits for ADs, and estimate excess outpatient visits in South China. Daily residential air pollutant exposure assessments were performed by extracting grid data (spatial resolution: 1 km × 1 km) from validated datasets. We employed the conditional logistic regression model to quantify the associations and excess outpatient visits., Results: The results of the single-pollutant models showed that each 10 μg/m 3 increase of PM 2.5 and O 3 exposures was significantly associated with a 3.14 % (95 % confidence interval: 2.47 %, 3.81 %) and 0.88 % (0.49 %, 1.26 %) increase in odds of outpatient visits for ADs, respectively. These associations remained robust in 2-pollutant models. The proportion of outpatient visits attributable to PM 2.5 and O 3 exposures was up to 7.20 % and 8.93 %, respectively. Older adults appeared to be more susceptible to PM 2.5 exposure, especially in cool season, and subjects with recurrent outpatient visits were more susceptible to O 3 exposure., Limitation: As our study subjects were from one single hospital in China, it should be cautious when generalizing our findings to other regions., Conclusion: Short-term exposure to ambient PM 2.5 and O 3 was significantly associated with a higher odds of outpatient visits for ADs, which can contribute to considerable excess outpatient visits., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests of personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Introduction: This study investigates the association between maternal exposure to particulate matter (PM 10 ) and nitric dioxide (NO 2 ) during the first, second and third trimester and placental weight and birth weight/placental weight (BW/PW) ratio in twins at birth., Methods: Cross-sectional data of 3340 twins from the East Flanders Prospective Twin Survey was used. Air pollutant exposure was estimated via spatial temporal interpolation. Univariable and multivariable mixed model analyses with a random intercept to account for the relatedness of newborns were conducted for twins with separate placentas. Twin pairs with one placental mass were studied with linear and logistic regression., Results: In the third trimester, for each 10 μm/m 3 increase in PM 10 or NO 2 placental weight decreased -19.7 g (95%-C.I. -35.1; -4.3) and -17.7 g (95%-C.I. -30.4; -0.5) respectively, in moderate to late preterm twins with separate placentas. Consequently, BW/PW ratio increased with higher air pollution exposure. PM 10 exposure in the last week of pregnancy was associated with a higher odds ratio (OR) of 1.20 (95%-C.I. 1.00; 1.44) for a "small for gestational age placenta" (placental weight <10th percentile). Conversely, first trimester air pollutant exposure was associated with lower ORs of 0.55 (95%-C.I. 0.35; 0.88) and 0.60 (95%-C.I. 0.42; 0.84)., Discussion: The association of PM 10 and NO 2 on placental weight is trimester-specific, differs for twins with one versus two placentas and is most pronounced in moderate to late preterm twins. Longitudinal studies are needed to better understand the relationship between air pollutant exposure and placental weight evolution across different trimesters., 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 Ltd.. All rights reserved.)

Introduction: Exposure to ambient air pollution may play a role in the onset of common mental disorders like depressive and anxiety disorders. The association of long-term exposure to particles smaller than 10 μm (PM10) with these diseases remains unclear. This study aimed to estimate the association of long-term exposure to PM10 with mental well-being and the frequency of probable diagnosis of common mental disorders., Methods: A nationally representative cross-sectional study was done in mainland Portugal. Long-term exposure was estimated through one-year average concentrations of PM10, calculated with data from the Portuguese Environment Agency, attributed individually considering individuals' postal codes of residence. The mental well-being and the probable diagnosis of common mental disorders were ascertained through the five-item Mental Health Inventory scale. Linear and Robust Poisson regression models were computed to estimate change percentages, prevalence ratios (PR), and their 95% confidence intervals (95% CI)., Results: The median (interquartile range) concentration of PM10 was 18.6 (15.3 - 19.3) μg/m3. The mental well-being score was 72 (56 - 84) points, on a scale from 0 to 100. A probable diagnosis of common mental disorders was found in 22.7% (95% CI: 20.0 to 25.6). Long-term exposure to PM10 was associated with a non-statistically significant decrease in the mental well-being score [for each 10 μg/m³ increment in one-year average PM10 concentrations, there was a 2% (95% CI: -8 to 4) decrease], and with a non-statistically significant increase in the common mental health frequency (PR = 1.012, 95% CI: 0.979 to 1.045)., Conclusion: We did not find statistically significant associations between long-term exposure to PM10 and mental well-being or the frequency of probable diagnosis of common mental disorders. These results may be explained by the reduced variability in the exposure values, given the geographical distribution and functioning of the network of air quality monitoring stations. This study contributes with evidence for low levels of air pollutants, being one of the first to adjust for individual and aggregate-level variables. Moreover, to the best of our knowledge, this was the first nationally representative, population-based study conducted on the Portuguese population using real-life data. Maintaining a robust and nationwide air quality monitoring network is essential for obtaining quality exposure data.

Background: Enhanced cardiovascular health (CVH) is linked to reduced mortality risks, whereas long-term exposure to fine particulate matter (PM 2.5 ), elevates these risks. Whether long-term exposure to PM 2.5 counteracts the health benefits of high CVH is unknown. The study aims to evaluate whether the association of CVH assessed by Life's Essential 8 (LE8) with death was consistent between participants with different PM 2.5 exposures., Methods: We included 134,727 participants in the field survey of China Chronic Disease and Risk Factor Surveillance which was conducted from August 2013 to June 2014. The deaths of participants were obtained by linking to the National Mortality Surveillance System (2013-2018). The environmental data is obtained by satellite inversion. The participants' CVH scores were calculated using the LE8 method. Hazard ratio (HR) and 95% confidence intervals (95%CI) for mortality were calculated using Cox regression models., Results: A total of 2,936 all-cause deaths and 1,158 cardiovascular disease (CVD) deaths were recorded. Compared to those with low CVH, adults with high CVH demonstrated a reduced risk of all-cause mortality, irrespective of their PM 2.5 exposure levels (P < 0.05, all P for interaction >0.05). Furthermore, in comparison to those with low CVH and highest PM 2.5 exposure, adults with high CVH and lowest PM 2.5 exposure exhibited HR of 0.18 (95%CI, 0.12-0.25) for all-cause mortality and 0.13 (95%CI, 0.08-0.22) for CVD mortality., Conclusions: High CVH is associated with reduced all-cause mortality risk, regardless of PM 2.5 exposure levels. For Chinese adults, sustaining high CVH is advisable, irrespective of their residential location., 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.)

Outdoor air pollution is ubiquitous, and no safe level of exposure has been identified for the most common air pollutants such as ozone and particle pollution. Children are uniquely more susceptible to the harms of outdoor air pollution, which can cause and exacerbate respiratory disease. Although challenging to identify the effects of outdoor air pollution on individual patients, understanding the basics of outdoor air pollution is essential for pediatric respiratory health care providers. This review covers basic information regarding outdoor air pollution, unique considerations for children, mechanisms for increased susceptibility, and association with incident and exacerbation of respiratory disease in children., Competing Interests: Disclosure Dr Rosser's time contribution was supported by NIHK08 HL159333., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Objectives: Our goal was to explore how greenness, air pollution, and residential food environment were linked to excessive gestational weight gain (EGWG), and to estimate their combined effects on this condition., Method: This cross-sectional analysis included 51,507 pregnant women from the Wuhan Maternal and Child Health Management Information System between 2016 and 2019. Generalized linear mixed regression models were employed to explore the relationships between greenness, air pollution, residential food environmental exposure, and EGWG; and the combined effects were further estimated by cluster analysis and principal components analysis., Result: We only found a significant association between convenience store density within the 250 m buffer zone (OR = 1.03 and 95% CI: 1.01,1.05) and EGWG. In terms of air pollution, sulfur dioxide(SO 2 ), particulate matter with a diameter of 10 μm or less(PM 10 ), and particulate matter with a diameter of 2.5 μm or less(PM 2.5 ) were substantially correlated with a higher prevalence of EGWG and higher GWG, with (OR = 1.16 and 95% CI: 1.12,1.21; OR = 1.12 and 95% CI: 1.08,1.16; OR = 1.17 and 95% CI: 1.14,1.21, respectively) per interquartile range(IQR) increase. Cluster analysis revealed the presence of three clusters representing urban exposures. In contrast to urban environment clusters characterized by favourable conditions, those exhibiting elevated air pollution levels, high-density residential food environment and low levels of greenness were found to have increased odds of EGWG (OR = 1.10, 95% CI: 1.03, 1.19)., Conclusion: This study emphasizes that exposure to elevated air pollution, high-density residential neighbourhood food environments, and low levels of greenness is a neighbourhood obesogenic environment for pregnant women., 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.)

Constituents of air pollution, the ultrafine particles (UFP) with a diameter of ≤0.1 μm, are considerably related to traffic emissions. Several studies link air pollution to Alzheimer's disease (AD), yet the exact relationship between the two remains poorly understood. Mitochondria are known targets of environmental toxicants, and their dysfunction is associated with neurodegenerative diseases. The olfactory mucosa (OM), located at the rooftop of the nasal cavity, is directly exposed to the environment and in contact with the brain. Mounting evidence suggests that the UFPs can impact the brain directly through the olfactory tract. By using primary human OM cultures established from nasal biopsies of cognitively healthy controls and individuals diagnosed with AD, we aimed to decipher the effects of traffic-related UFPs on mitochondria. The UFP samples were collected from the exhausts of a modern heavy-duty diesel engine (HDE) without aftertreatment systems, run with renewable diesel (A0) and petroleum diesel (A20), and from an engine of a 2019 model diesel passenger car (DI-E6d) equipped with state-of-the-art aftertreatment devices and run with renewable diesel (Euro6). OM cells were exposed to three different UFPs for 24-h and 72-h, after which cellular processes were assessed on the functional and transcriptomic levels. Our results show that UFPs impair mitochondrial functions in primary human OM cells by hampering oxidative phosphorylation (OXPHOS) and redox balance, and the responses of AD cells differ from cognitively healthy controls. RNA-Seq and IPA® revealed inhibition of OXPHOS and mitochondrial dysfunction in response to UFPs A0 and A20. Functional validation confirmed that A0 and A20 impair cellular respiration, decrease ATP levels, and disturb redox balance by altering NAD and glutathione metabolism, leading to increased ROS and oxidative stress. RNA-Seq and functional assessment revealed the presence of AD-related alterations in human OM cells and that different fuels and engine technologies elicit differential effects., 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.)

Poor sleep quality is a widespread concern. While the influence of particle exposure on sleep disturbances has received considerable attention, research exploring other dimensions of sleep quality and the chemical components of the particles remains limited. We employed a marginal structural model to explore the association of long-term exposure to PM 2.5 and its chemical components with poor sleep quality. The odds ratio (95 % CI) for poor sleep quality was 1.335 (1.292-1.378), 1.097 (1.080-1.113), 1.137 (1.100-1.174), 1.197 (1.156-1.240), and 1.124 (1.107-1.140) per IQR increase in the concentration of PM 2.5 , SO 4 2- , NO 3 - , NH 4 + , and BC, respectively. The score (and 95 % CI) of sleep latency, use of sleep medication, habitual sleep efficiency, subjective sleep quality, and daytime dysfunction were affected by PM 2.5 , with an increase of 0.059 (0.050-0.069), 0.054 (0.049-0.059), 0.011 (0.008-0.014), 0.011 (0.005-0.018), and 0.026 (0.018-0.034) per IQR increase in PM 2.5 concentrations, respectively. This study supports the association of long-term exposure to PM 2.5 and its chemical components with poor sleep quality., 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.)

Objective: To evaluate associations of wildfire fine particulate matter ≤2.5 mm in diameter (PM2.5) with diabetes across multiple countries and territories., Research Design and Methods: We collected data on 3,612,135 diabetes hospitalizations from 1,008 locations in Australia, Brazil, Canada, Chile, New Zealand, Thailand, and Taiwan during 2000-2019. Daily wildfire-specific PM2.5 levels were estimated through chemical transport models and machine-learning calibration. Quasi-Poisson regression with distributed lag nonlinear models and random-effects meta-analysis were applied to estimate associations between wildfire-specific PM2.5 and diabetes hospitalization. Subgroup analyses were by age, sex, location income level, and country or territory. Diabetes hospitalizations attributable to wildfire-specific PM2.5 and nonwildfire PM2.5 were compared., Results: Each 10 µg/m3 increase in wildfire-specific PM2.5 levels over the current day and previous 3 days was associated with relative risks (95% CI) of 1.017 (1.011-1.022), 1.023 (1.011-1.035), 1.023 (1.015-1.032), 0.962 (0.823-1.032), 1.033 (1.001-1.066), and 1.013 (1.004-1.022) for all-cause, type 1, type 2, malnutrition-related, other specified, and unspecified diabetes hospitalization, respectively. Stronger associations were observed for all-cause, type 1, and type 2 diabetes in Thailand, Australia, and Brazil; unspecified diabetes in New Zealand; and type 2 diabetes in high-income locations. An estimate of 0.67% (0.16-1.18%) and 1.02% (0.20-1.81%) for all-cause and type 2 diabetes hospitalizations were attributable to wildfire-specific PM2.5. Compared with nonwildfire PM2.5, wildfire-specific PM2.5 posed greater risks of all-cause, type 1, and type 2 diabetes and were responsible for 38.7% of PM2.5-related diabetes hospitalizations., Conclusions: We show the relatively underappreciated links between diabetes and wildfire air pollution, which can lead to a nonnegligible proportion of PM2.5-related diabetes hospitalizations. Precision prevention and mitigation should be developed for those in advantaged communities and in Thailand, Australia, and Brazil., (© 2024 by the American Diabetes Association.)

Air pollution exposure is linked to an increased risk of stroke. Elevated levels of pollution (carbon monoxide, carbon dioxide, nitrous oxide, sulfur dioxide, coarse particulate matter [PM 10 ], and especially fine particulate matter [PM 2.5 ]) cause systemic inflammation after the particles are inhaled and lodge into lung tissue, causing an increased incidence of stroke, hospitalizations for stroke, and stroke mortality. Until air pollution levels are remediated, assessing Air Quality Index (AQI) and following the guidelines to decrease illness from exposure is imperative. AQI levels are reported hourly, identifying ambient PM 2.5 and ozone levels. When AQI levels are low, the risk of exposure to PM 2.5 is low. As the AQI increases, there is more risk. It is important to take steps to decrease exposure to PM 2.5 , especially for those with cardiovascular comorbidities such as diabetes and those with previous stroke events. This is important information for nurses to understand and share with their patients as a risk reduction strategy., Competing Interests: None.

Background: Recent evidence has linked air pollution with frailty, yet little is known about the role of NO2 in this association. Our aim was to assess the association between frailty and NO2 air concentrations in Mexican older adults., Methods: We used georeferenced data from the population-based Nutrition and Health Survey in Mexico (NHNS) 2021, representative of national and subnational regions, to measure a frailty index based on 31 health deficits in adults aged 50 and older. Air pollution due to NO2 concentrations was estimated from satellite images validated with data from surface-level stations. Maps were produced using Jensen's Natural break method. The association of frailty and NO2 concentrations was measured using the frailty index (multivariate fractional response logit regression) and a frailty binary variable (frailty index [FI] ≥0.36, multivariate logit regression)., Results: There was a positive and significant association of the frailty index with the NO2 concentrations, adjusting for age, sex, urban and rural area, years of education, socioeconomic status, living arrangement, particulate matter smaller than 2.5 microns, and indoor pollution. For each standard deviation increase in NO2 concentrations measured 10 years before the survey, the odds of being frail were 15% higher, and the frailty index was 14.5% higher. The fraction of frailty attributable to NO2 exposure ranged from 1.8% to 23.5% according to different scenarios., Conclusions: Frailty was positively associated with exposure to NO2 concentrations. Mapping frailty and its associated factors like NO2 air concentrations can contribute to the design of targeted pro-healthy aging policies., (© The Author(s) 2024. Published by Oxford University Press on behalf of The Gerontological Society of America.)

Rationale: It is unknown whether air pollution is associated with radiographic features of interstitial lung disease in individuals with chronic obstructive pulmonary disease (COPD). Objectives: To determine whether air pollution increases the prevalence of interstitial lung abnormalities (ILA) or percent high-attenuation areas (HAA) on computed tomography (CT) in individuals with a heavy smoking history and COPD. Methods: We performed a cross-sectional study of SPIROMICS (Subpopulations and Intermediate Outcome Measures in COPD Study), focused on current or former smokers with COPD. Ten-year exposure to particulate matter ⩽2.5 μm in aerodynamic diameter (PM 2.5 ), nitrogen oxides (NO x ), nitrogen dioxide (NO 2 ), and ozone before enrollment CT (completed between 2010 and 2015) were estimated with validated spatiotemporal models at residential addresses. We applied adjusted multivariable modified Poisson regression and linear regression to investigate associations between pollution exposure and relative risk (RR) of ILA or increased percent HAA (between -600 and -250 Hounsfield units), respectively. We assessed for effect modification by MUC5B -promoter polymorphism (variant allele carriers GT or TT vs. GG at rs3705950), smoking status, sex, and percent emphysema. Results: Among 1,272 participants with COPD assessed for HAA, 424 were current smokers, and 249 were carriers of the variant MUC5B allele. A total of 519 participants were assessed for ILA. We found no association between pollution exposure and ILA or HAA. Associations between pollutant exposures and risk of ILA were modified by the presence of MUC5B polymorphism ( P value interaction term for NO x  = 0.04 and PM 2.5  = 0.05) and smoking status ( P value interaction term for NO x  = 0.05; NO 2  = 0.01; and ozone = 0.05). With higher exposure to NO x and PM 2.5 , MUC5B variant carriers had an increased risk of ILA (RR per 26 ppb NO x , 2.41; 95% confidence interval [CI], 0.97-6.0; and RR per 4 μg ⋅ m -3 PM 2.5 , 1.43; 95% CI, 0.93-2.2, respectively). With higher exposure to NO 2 , former smokers had an increased risk of ILA (RR per 10 ppb, 1.64; 95% CI, 1.0-2.7). Conclusions: Exposure to ambient air pollution was not associated with interstitial features on CT in this population of heavy smokers with COPD. MUC5B modified the association between pollution and ILA, suggesting that gene-environment interactions may influence prevalence of interstitial lung features in COPD.

There are growing concerns about the impact of pollution on maternal and infant health. Despite an extensive correlational literature, observational studies which adopt methods that seek to address potential biases due to unmeasured confounders draw mixed conclusions. Using a population database of births in Northern Ireland (NI) linked to localized geographic information on pollution in mothers' postcodes (zipcodes) of residence during pregnancy, we examine whether prenatal exposure to PM 2.5 is associated with a comprehensive range of birth outcomes, including placental health. Overall, we find little evidence that particulate matter is related to infant outcomes at the pollution levels experienced in NI, once we implement a mother fixed effects approach that accounts for time-invariant factors. This contrasts with strong associations in models that adjust for observed confounders but without fixed effects. While reducing ambient air pollution remains an urgent public health priority globally, our results imply that further improvements in short-run levels of prenatal PM 2.5 exposure in a relatively low-pollution, higher-income country context, are unlikely to impact on birth outcomes at the population level., (© 2024 The Author(s). Health Economics published by John Wiley & Sons Ltd.)

Objective: PM2.5 is closed linked to asthma exacerbation. The Notch1 pathway acts as an important pathway, ultimately inducing T-helper cells that express GATA3 and its corresponding Th2 cytokines. The regulatory effects of miR-139-5p on the Notch1 pathway have been indicated in cancer. However, studies on miR-139-5p have not applied asthma-related models. The role of miR-139-5p and its regulatory effects on the Notch1-GATA3 pathway in asthma exacerbation induced by acute PM2.5 exposure has not been elucidated. We hypothesize that acute PM2.5 exposure induces asthma exacerbation by regulating the expression of miR-139-5p and activating the Notch1-GATA3 pathway., Methods: We first employed Diseased Human Bronchial Epithelial Cells-Asthma cells to establish an in vitro model of acute exposure to PM2.5, and explored the relationship between the different concentrations and durations of acute PM2.5 exposure and the activation of Notch1-GATA3 pathway. We investigated the protein and mRNA expression changes of Notch1, upstream Jagged1, downstream GATA3, as well as the regulatory effect of miR-139-5p involved in it., Results: The miR-139-5p expression increased within 24 h of PM2.5 exposure. However, if PM2.5 exposure was sustained, miR-139-5p expression turned to decrease, accompanied by upregulations of the mRNA and protein expression of Notch1-GATA3 pathway. Overexpression of miR-139-5p blocked Notch1-GATA3 pathway activation induced by acute PM2.5 exposure., Conclusion: Acute PM2.5 exposure can activate Notch1-GATA3 pathway in asthma bronchial epithelial cells model, which might be involved in PM2.5-induced asthma exacerbation. miR-139-5p has a potential protective role of inhibiting PM2.5-induced asthma airway inflammation by targeting Notch1.

Background: The association between the concentration of atmospheric particulate matter on the day of surgery and the occurrence of intra-operative hypoxaemia in children receiving general anaesthesia is unclear., Objective: To investigate the association between the exposure to particulate matter on the day of surgery and the occurrence of intra-operative hypoxaemia, defined as a pulse oximetry oxygen saturation of less than 90% for more than 1 min, in children., Design: Retrospective study., Setting: Single-centre., Participants: Children aged 18 years or younger who received general anaesthesia between January 2019 and October 2020., Intervention: Information on daily levels of particulate matter with a diameter 10 μm or less and 2.5 μm or less measured within a neighbourhood corresponding to the area defined by the hospital's zip code was obtained from publicly available air-quality data., Main Outcome Measures: The primary outcome was intra-operative hypoxaemia, defined as a pulse oximetry oxygen saturation of less than 90% lasting for more than 1 min, manually verified by anaesthesiologists using vital sign registry data extracted at 2 s intervals., Results: Of the patients finally analysed, 3.85% (489/13 175) experienced intra-operative hypoxaemia. Higher levels of particulate matter 10 μm or less in diameter (≥81 μg m -3 , 17/275, 6.2%) were associated with an increased occurrence of intra-operative hypoxaemia compared with lower particulate matter concentrations [<81 μg m -3 , 472/12 900, 3.7%; adjusted odds ratio, 1.71; 95% confidence interval (CI), 1.04 to 2.83; P  = 0.035]., Conclusion: The level of particulate matter on the day of surgery pose a risk of intra-operative hypoxaemia in children receiving general anaesthesia. If the concentrations of particulate matter 10 μm or less in diameter on the day of surgery are high, children receiving general anaesthesia should be managed with increased caution., (Copyright © 2024 European Society of Anaesthesiology and Intensive Care. Unauthorized reproduction of this article is prohibited.)

Accumulating evidence has substantiated the potential of ambient particulate matter (PM) to elicit detrimental health consequences in the respiratory system, notably airway inflammation. Macrophages, a pivotal component of the innate immune system, assume a crucial function in responding to exogenous agents. However, the roles and detailed mechanisms in regulating PM-induced airway inflammation remain unclear. The current study revealed that PM had the ability to stimulate the formation of macrophage extracellular traps (METs) both in vitro and in vivo. This effect was dependent on peptidylarginine deiminase type 4 (PAD4)-mediated histone citrullination. Additionally, reactive oxygen species were involved in the formation of PM-induced METs, in parallel with PAD4. Genetic deletion of PAD4 in macrophages resulted in an up-regulation of inflammatory cytokine expression. Moreover, mice with PAD4-specific knockout in myeloid cells exhibited exacerbated PM-induced airway inflammation. Mechanistically, inhibition of METs suppressed the phagocytic ability in macrophages, leading to airway epithelial injuries and an aggravated PM-induced airway inflammation. The present study demonstrates that METs play a crucial role in promoting the phagocytosis and clearance of PM by macrophages, thereby suppressing airway inflammation. Furthermore, it suggests that activation of METs may represent a novel therapeutic strategy for PM-related airway disorders., Competing Interests: Disclosure Statement None declared., (Copyright © 2024 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.)

Environmental health research has suggested that fine particulate matter (PM 2.5 ) exposure can lead to high blood pressures, but it is unclear whether the impacts remain the same for systolic and diastolic blood pressures (SBP and DBP). This study aimed to examine whether the effects of PM 2.5 exposure on SBP and DBP differ using data from a predominantly non-Hispanic Black cohort collected between 2013 and 2019 in the US. PM 2.5 exposure was assessed based on a satellite-derived model across exposure durations from 1 to 36 months. The average PM 2.5 exposure level was between 9.5 and 9.8 μg/m 3 from 1 through 36 months. Mixed effects models were used to estimate the association of PM 2.5 with SBP, DBP, and related hypertension types, adjusted for potential confounders. A total of 6381 participants were included. PM 2.5 exposure was positively associated with both SBP and DBP. The association magnitudes depended on exposure durations. The association with SBP was null at the 1-month duration (β = 0.05, 95% CI: - 0.23, 0.33), strengthened as duration increased, and plateaued at the 24-month duration (β = 1.14, 95% CI: 0.54, 1.73). The association with DBP started with β = 0.29 (95% CI: 0.11, 0.47) at the 1-month duration, and plateaued at the 12-month duration (β = 1.61, 95% CI: 1.23, 1.99). PM 2.5 was associated with isolated diastolic hypertension (12-month duration: odds ratio = 1.20, 95% CI: 1.07, 1.34) and systolic-diastolic hypertension (12-month duration: odds ratio = 1.18, 95% CI: 1.10, 1.26), but not with isolated systolic hypertension. The findings suggest DBP is more sensitive to PM 2.5 exposure and support differing effects of PM 2.5 exposure on SBP and DBP. As elevation of SBP and DBP differentially predict CVD outcomes, this finding is relevant for prevention and treatment., (© 2024. The Author(s).)

Objective: To evaluate the influence of environmental factors and prematurity relating to juvenile dermatomyositis (JDM), its course and refractoriness to treatment., Methods: A case-control study with 35 patients followed up at a tertiary hospital and 124 healthy controls, all residents of São Paulo. Patients were classified according to monocyclic, polycyclic or chronic disease courses and refractoriness to treatment. The daily concentrations of pollutants (inhalable particulate matter-PM 10 , sulfur dioxide-SO 2 , nitrogen dioxide-NO 2 , ozone-O 3 and carbon monoxide-CO) were provided by the Environmental Company of São Paulo. Data from the population were obtained through a questionnaire., Results: Fifteen patients had monocyclic courses, and 19 polycyclic/chronic courses. Eighteen patients were refractory to treatment. Maternal occupational exposure to inhalable agents (OR = 17.88; IC 95% 2.15-148.16, p = 0.01) and exposure to O 3 in the fifth year of life (third tertile > 86.28µg/m 3 ; OR = 6.53, IC95% 1.60-26.77, p = 0.01) were risk factors for JDM in the multivariate logistic regression model. The presence of a factory/quarry at a distance farther than 200 meters from daycare/school (OR = 0.22; IC 95% 0.06-0.77; p = 0.02) was a protective factor in the same analysis. Prematurity, exposure to air pollutants/cigarette smoke/sources of inhalable pollutants in the mother's places of residence and work during the gestational period were not associated with JDM. Prematurity, maternal exposure to occupational pollutants during pregnancy as well as patient's exposure to ground-level pollutants up to the fifth year of life were not associated with disease course and treatment refractoriness., Conclusion: Risk factors for JDM were maternal occupational exposure and exposure to O 3 in the fifth year of life., (© 2024. The Author(s).)

Introduction: Air pollution is a major health risk factor. Ports might be an understudied source of air pollution., Methods: We conducted a spatial health impact assessment (HIA) of port-sourced air pollution for Barcelona for 2017 at the neighbourhood level. Total NO2 and PM10 and port-sourced NO2, PM10 and PM2.5 concentrations were available through the ADMS-Urban model. Population data, mortality and morbidity data, and risk estimates were obtained. We followed standard HIA methodologies and calculated relative risks and impact fractions for 1.35 million adults living in 73 neighbourhoods., Results: The city-wide mean total NO2 and PM10 concentrations were 37.88 μg/m3 (range: 19.61-52.17 μg/m3) and 21.68 μg/m3 (range: 17.33-26.69 μg/m3), respectively, of which 7% (range: 2-36%) and 1% (range: 0-7%) were port-sourced, respectively. The mean port-sourced PM2.5 concentration was 0.19 μg/m3 (range: 0.06-1.38 μg/m3). We estimated that 1,123 (PI: 0-3,060) and 1,230 (95% CI: 0-2,566) premature deaths were attributable to total NO2 and PM10, respectively, of which 8.1% (91; PI: 0-264) and 1.1% (13; 95% CI 0-29) were attributable to port-sourced NO2 and PM10, respectively. 20 (95% CI: 15-26) premature deaths were attributable to port-sourced PM2.5. Additionally, a considerable morbidity burden and losses in life expectancy were attributable to port-sourced air pollution. Neighbourhoods closest to the port in the south-east were most adversely affected, gradually decreasing towards the north-west., Conclusions: The port is an understudied air pollution source in Barcelona with strong health impacts. Cities need local insight into health risk factors, their sources, attributable burdens and distributions for defining targeted policies., Competing Interests: The authors have declared that no competing interests exist., (Copyright: © 2024 Mueller 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.)

Innate lymphoid cells (ILCs) are a heterogeneous population that play diverse roles in airway inflammation after exposure to allergens and infections. However, how ILCs respond after exposure to environmental toxins is not well understood. Here we show a novel method for studying the heterogeneity of rare lung ILC populations by magnetic enrichment for lung ILCs followed by particle-templated instant partition sequencing (PIP-seq). Using this method, we were able to identify novel group 1 and group 2 ILC subsets that exist after exposure to both fungal allergen and burn pit-related constituents (BPC) that include dioxin, aromatic hydrocarbon, and particulate matter. Toxin exposure in combination with fungal allergen induced activation of specific ILC1/NK and ILC2 populations as well as promoted neutrophilic lung inflammation. Oxidative stress pathways and downregulation of specific ribosomal protein genes (Rpl41 and Rps19) implicated in anti-inflammatory responses were present after BPC exposure. Increased IFNγ expression and other pro-neutrophilic mediator transcripts were increased in BPC-stimulated lung innate lymphoid cells. Further, the addition of BPC induced Hspa8 (encodes HSC70) and aryl hydrocarbon transcription factor activity across multiple lung ILC subsets. Overall, using an airway disease model that develops after occupational and environmental exposures, we demonstrate an effective method to better understand heterogenous ILC subset activation., (© 2024. The Author(s).)

Aim: The objective of this study was to visually analyse global research trends and hotspots regarding the role of PM2.5 in ischemic stroke., Methods: The Web of Science core collection database was used to search the literature on PM2.5 and ischemic stroke from 2006 to 2024. Visualization analysis was conducted using CiteSpace, VOSviewer, and an online bibliometric platform., Results: The analysis comprises 190 articles published between 2006 and 2024 by 1229 authors from 435 institutions in 39 countries, across 78 journals. Wellenius GA has the highest number of published and cited papers. China has the highest number of papers, while Canada has the highest citation frequency. Capital Medical University published the highest number of papers, and Harvard University had the highest citation frequency for a single paper. The study investigated the impact of PM2.5 on ischemic stroke in three phases. The first phase analysed hospitalisation rates for correlations. The second phase utilised large-scale multi-cohort data from around the world. The third phase involved studying global exposure risk through machine learning and model construction. Currently, there is limited research on the mechanisms involved, and further in-depth investigation is required., Conclusion: This paper presents a bibliometric analysis of the research framework and hotspots concerning the effect of PM2.5 on ischemic stroke. The analysis aims to provide a comprehensive understanding of this field for researchers. It is expected that research on the effect of PM2.5 on ischemic stroke will remain an important research topic in the future., (© 2024. The Author(s).)

Understanding public awareness of environmental problems is vital for effectively formulating sustainable policies. This paper aims to investigate the impacts of two perspectives-external air pollution and individual health status-on public awareness by leveraging panel data from two waves of the China Family Panel Studies (CFPS) conducted between 2018 and 2020. The model integrates provincial-level PM2.5 concentration indicators and SO 2 , PM s , and NO x emissions. The results reveal a significantly positive correlation between air pollution and public awareness of environmental problems in China. Additionally, this study examines the impact of self-assessed health shock by categorizing it into worse and better health. The influence of better health is insignificant. Conversely, when individuals experience worse health, they may perceive it as a psychological loss, leading to a significant increase in public awareness of environmental problems. This study provides valuable insights for mitigating air pollution and reinforcing public health in developing countries., (© 2024. The Author(s).)

Impaired cognitive health is the leading cause of various disabilities and disorders. Air pollution has been dramatically increasing over the last few decades and has been identified as a potential risk factor for impaired cognitive health. This study investigates the effect of air pollutants, particulate matter (PM 2.5 , PM 10 ), sulfur dioxide (SO 2 ), and ground-level ozone, on global cognitive health. The data on environmental pollutants and cognitive health were recorded from PubMed, Web of Science, Scopus, and Google Scholar. Initially, 790 articles were identified after screening for duplicates and applying the inclusion and exclusion criteria, 21 studies were included, and data was synthesized to get a pooled result. The overall results revealed that increased exposure to PM 2.5 was positively and significantly associated with cognitive decline (OR 1.49; 95% CI 1.11, 1.99; p = 0.01). The risk of cognitive impairment due to PM 10 (OR 1.30; 95% CI 1.00-1.70, p = 0.05), and SO 2  (OR 1.39; 95% CI 1.27-1.51; p < 0.01) exposure were also significantly heightened. The study findings show that overall exposure to particulate matter PM 2.5, PM 10, and SO 2 was associated with an increased risk of a decrease in global cognitive functions. The findings suggest that reducing levels of air pollutants could be a strategic approach to mitigate cognitive health risks in populations worldwide., (© 2024. The Author(s).)

Air pollution stands as an environmental risk to child mental health, with proven relationships hitherto observed only in urban areas. Understanding the impact of pollution in rural settings is equally crucial. The novelty of this article lies in the study of the relationship between air pollution and behavioural and developmental disorders, attention deficit hyperactivity disorder (ADHD), anxiety, and eating disorders in children below 15 living in a rural area. The methodology combines spatio-temporal models, Bayesian inference and Compositional Data (CoDa), that make it possible to study areas with few pollution monitoring stations. Exposure to nitrogen dioxide (NO 2 ), ozone (O 3 ), and sulphur dioxide (SO 2 ) is related to behavioural and development disorders, anxiety is related to particulate matter (PM 10 ), O 3 and SO 2 , and overall pollution is associated to ADHD and eating disorders. To sum up, like their urban counterparts, rural children are also subject to mental health risks related to air pollution, and the combination of spatio-temporal models, Bayesian inference and CoDa make it possible to relate mental health problems to pollutant concentrations in rural settings with few monitoring stations. Certain limitations persist related to misclassification of exposure to air pollutants and to the covariables available in the data sources used., (© 2024. The Author(s).)

Background: Air pollution poses a significant threat to global public health. While broad mitigation policies exist, an understanding of the economic consequences, both in terms of health benefits and mitigation costs, remains lacking. This study systematically reviewed the existing economic implications of air pollution control strategies worldwide., Methods: A predefined search strategy, without limitations on region or study design, was employed to search the PubMed, Scopus, Cochrane Library, Embase, Web of Science, and CEA registry databases for studies from their inception to November 2023 using keywords such as "cost-benefit analyses", "air pollution", and "particulate matter". Focus was placed on studies that specifically considered the health benefits of air pollution control strategies. The evidence was summarized by pollution control strategy and reported using principle economic evaluation measurements such as net benefits and benefit-cost ratios., Results: The search yielded 104 studies that met the inclusion criteria. A total of 75, 21, and 8 studies assessed the costs and benefits of outdoor, indoor, and mixed control strategies, respectively, of which 54, 15, and 3 reported that the benefits of the control strategy exceeded the mitigation costs. Source reduction (n = 42) and end-of-pipe treatments (n = 15) were the most commonly employed pollution control methodologies. The association between particulate matter (PM) and mortality was the most widely assessed exposure-effect relationship and had the largest health gains (n = 42). A total of 32 studies employed a broader benefits framework, examining the impacts of air pollution control strategies on the environment, ecology, and society. Of these, 31 studies reported partially or entirely positive economic evidence. However, despite overwhelming evidence in support of these strategies, the studies also highlighted some policy flaws concerning equity, optimization, and uncertainty characterization., Conclusions: Nearly 70% of the reviewed studies reported that the economic benefits of implementing air pollution control strategies outweighed the relative costs. This was primarily due to the improved mortality and morbidity rates associated with lowering PM levels. In addition to health benefits, air pollution control strategies were also associated with other environmental and social benefits, strengthening the economic case for implementation. However, future air pollution control strategy designs will need to address some of the existing policy limitations., (© 2024. The Author(s).)

Objective: Air pollution is a leading public health issue. This study investigated the effect of air quality and pollutants on pulmonary function and inflammation in patients with asthma in Shanghai., Methods: The study monitored 27 asthma outpatients for a year, collecting data on weather, patient self-management [daily asthma diary, peak expiratory flow (PEF) monitoring, medication usage], spirometry and serum markers. To explore the potential mechanisms of any effects, asthmatic mice induced by ovalbumin (OVA) were exposed to PM 2.5 ., Results: Statistical and correlational analyses revealed that air pollutants have both acute and chronic effects on asthma. Acute exposure showed a correlation between PEF and levels of ozone (O 3 ) and nitrogen dioxide (NO 2 ). Chronic exposure indicated that interleukin-5 (IL-5) and interleukin-13 (IL-13) levels correlated with PM 2.5 and PM 10 concentrations. In asthmatic mouse models, exposure to PM 2.5 increased cytokine levels and worsened lung function. Additionally, PM 2.5 exposure inhibited cell proliferation by blocking the NF-κB and ERK phosphorylation pathways., Conclusion: Ambient air pollutants exacerbate asthma by worsening lung function and enhancing Th2-mediated inflammation. Specifically, PM 2.5 significantly contributes to these adverse effects. Further research is needed to elucidate the mechanisms by which PM 2.5 impacts asthma., (Copyright © 2024 The Editorial Board of Biomedical and Environmental Sciences. Published by China CDC. All rights reserved.)

Objective: In recent decades, China has implemented a series of policies to address air pollution. We aimed to assess the health effects of these policies on stroke burden attributable to ambient fine particulate matter (PM 2.5 )., Methods: Joinpoint regression was applied to explore the temporal tendency of stroke burden based on data from the Global Burden of Disease 2019 study., Results: The age-standardized rates of disability-adjusted life year (DALY) for stroke attributable to ambient PM 2.5 in China, increased dramatically during 1990-2012, subsequently decreased at an annual percentage change (APC) of -1.98 [95% confidence interval ( CI ): -2.26, -1.71] during 2012-2019. For ischemic stroke (IS), the age-standardized DALY rates doubled from 1990 to 2014, and decreased at an APC of -0.83 (95% CI : -1.33, -0.33) during 2014-2019. Intracerebral hemorrhage (ICH) showed a substantial increase in age-standardized DALY rates from 1990 to 2003, followed by declining trends, with APCs of -1.46 (95% CI : -2.74, -0.16) during 2003-2007 and -3.33 (95% CI : -3.61, -3.06) during 2011-2019, respectively. Conversely, the age-standardized DALY rates for subarachnoid hemorrhage (SAH) generally declined during 1990-2019., Conclusion: Our results clarified the dynamic changes of the ambient PM 2.5- attributable stroke burden in China during 1990-2019, highlighting the health effects of air quality improvement policies., (Copyright © 2024 The Editorial Board of Biomedical and Environmental Sciences. Published by China CDC. All rights reserved.)

Fine particulate matter (PM 2.5 ), a significant component of air pollution particulate matter, is inevitable and closely associated with increasing male reproductive disorder. However, the testicular targets of PM 2.5 and its toxicity related molecular mechanisms are still not fully understood. In this study, the conditional knockout (cKO) mice and primary Leydig cells were used to explore the testicular targets of PM 2.5 and the related underlying mechanisms. First, apparent the structure impairment of seminiferous tubules, Leydig cells vacuolization, decline of serum testosterone and sperm quality reduction were found in male wild-type (WT) and Sirt1 knockout mice after exposure to PM 2.5 . Enrichment analyses revealed that differentially expressed genes (DEGs) were enriched in steroid hormone biosynthesis, ferroptosis, and HIF-1 signaling pathway in the mice testes after exposure to PM 2.5 , which were subsequently verified by the molecular biological analyses. Notably, similar enrichment analyses results were also observed in primary Leydig cells after treatment with PM 2.5 . In addition, Knockdown of Sirt1 significantly increased PM 2.5 -induced expression and activation of HIF-1α, which was in parallel to the changes of cellular iron levels, oxidative stress indicators and the ferroptosis markers. In conclusion, this highlights that PM 2.5 triggers ferroptosis via SIRT1/HIF-1α signaling pathway to inhibit testosterone synthesis in males. These findings provide a novel research support for the study that PM 2.5 causes male reproductive injury., 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.)

Background: There is increasing evidence that exposure to PM 2.5 and its constituents is associated with an increased risk of gestational diabetes mellitus (GDM), but studies on the relationship between exposure to PM 2.5 constituents and the risk of GDM are still limited., Methods: A total of 17,855 pregnant women in Guangzhou were recruited for this retrospective cohort study, and the time-varying average concentration method was used to estimate individual exposure to PM 2.5 and its constituents during pregnancy. Logistic regression was used to assess the relationship between exposure to PM 2.5 and its constituents and the risk of GDM, and the expected inflection point between exposure to PM 2.5 and its constituents and the risk of GDM was estimated using logistic regression combined with restricted cubic spline curves. Stratified analyses and interaction tests were performed., Results: After adjustment for confounders, exposure to PM 2.5 and its constituents (NO 3 - , NH 4 + , and OM) was positively associated with the risk of GDM during pregnancy, especially when exposure to NO 3 - and NH 4 + occurred in the first to second trimester, with each interquartile range increase the risk of GDM by 20.2% (95% CI: 1.118-1.293) and 18.2% (95% CI. 1.107-1.263), respectively. The lowest inflection points between PM 2.5 , SO 4 2- , NO 3 - , NH 4 + , OM, and BC concentrations and GDM risk throughout the gestation period were 18.96, 5.80, 3.22, 2.67, 4.77 and 0.97 µg/m 3 , respectively. In the first trimester, an age interaction effect between exposure to SO 4 2- , OM, and BC and the risk of GDM was observed., Conclusions: This study demonstrates a positive association between exposure to PM 2.5 and its constituents and the risk of GDM. Specifically, exposure to NO 3 - , NH 4 + , and OM was particularly associated with an increased risk of GDM. The present study contributes to a better understanding of the effects of exposure to PM 2.5 and its constituents on the risk of GDM., (© 2024. The Author(s).)

Background and Aim: Traffic-related ultrafine particle pollution near highways is associated with adverse health. Reducing exposure by use of portable air purifiers in homes is one approach to reducing this risk. However, the reaction of residents to having air purifiers in homes is not well studied., Methods: Within the framework of our randomized crossover trial of air purifiers in homes near a major highway, we collected data about participants' use and reactions to air purifiers using questionnaires at their 30-day and 90-day home visits, recorded electricity consumption using HOBO monitors, and conducted structured interviews with participants., Results: Nearly all 150 participants reported running the air purifiers virtually 24 h every day in both their living room and their bedroom in the prior month. The units' HOBO electricity use, from a subset of 45 participants, supported the participants' responses from the questionnaire. Approximately 80% of participants reported setting their air purifier on the medium setting. Tolerance to air purifier noise increased significantly between the 30-day and 90-day home visits, with approximately two thirds reporting not being bothered at all by the noise. The qualitative interviews in a subset of 26 participants yielded consistent responses to those from the questionnaires. Size of unit, airflow, and energy consumption were additional concerns that emerged during the interviews., Conclusions: Results from the questionnaires, HOBO data, and structured interviews all suggest participants had positive reactions towards the presence of in-home APs, and therefore may be receptive to using air purifiers in their homes on a regular basis., Trial Registration: ClinicalTrials.gov, NCT04279249 . Registered 09 October 2019., (© 2024. The Author(s).)

Introduction: Air pollution is a significant contributor to morbidity and mortality globally and has been linked to an increased risk of dementia. Previous studies within the Betula cohort in Northern Sweden have demonstrated associations between air pollution and dementia, as well as distinctive metabolomic profiles in dementia patients compared to controls. This study aimed to investigate whether air pollution is associated with quantitative changes in metabolite levels within this cohort, and whether future dementia status would modify this association., Methods: Both short-term and long-term exposure to air pollution were evaluated using high spatial resolution models and measured data. Air pollution from vehicle exhaust and woodsmoke were analyzed separately. Metabolomic profiling was conducted on 321 participants, including 58 serum samples from dementia patients and a control group matched for age, sex, and education level, using nuclear magnetic resonance spectroscopy., Results: No statistically significant associations were found between any metabolites and any measures of short-term or long-term exposure to air pollution. However, there were trends potentially suggesting associations between both long-term and short-term exposure to air pollution with lactate and glucose metabolites. Notably, these associations were observed despite the lack of correlation between long-term and short-term air pollution exposure in this cohort. There were also tendencies for associations between air pollution from woodsmoke to be more pronounced in participants that would later develop dementia, suggesting a potential effect depending on urban/rural factors., Discussion: While no significant associations were found, the trends observed in the data suggest potential links between air pollution exposure and changes in lactate and glucose metabolites. These findings provide some new insights into the link between air pollution and metabolic markers in a low-exposure setting. However, addressing existing limitations is crucial to improve the robustness and applicability of future research in this area. The pronounced associations in participants who later developed dementia may indicate an influence of urban/rural factors, warranting further investigation., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The author(s) declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision., (Copyright © 2024 Raza, Öhman, Kanninen, Jalava, Zeng, de Crom, Ikram and Oudin.)

Background: The evidence on the association of fine particulate matter with an aerodynamic diameter of 2.5 μm or less (PM2.5) with pulmonary tuberculosis (PTB) retreatment is limited. There are no data on whether greenness exposure protects air pollution-related PTB retreatment in patients with prior PTB., Objective: In a population-based retrospective study, we aimed to investigate the influence of PM2.5 and residential greenness on the risk of PTB retreatment., Methods: A total of 26,482 patients with incident PTB, registered in a mandatory web-based reporting system between 2012 and 2019 in Zhengzhou, China, were included in the analysis. The exposure to PM2.5 was assessed based on the China High Air Pollutants dataset, and the level of greenness was estimated using the Normalized Difference Vegetation Index (NDVI) values. The associations of PTB retreatment with exposure to PM2.5 and greenness were evaluated, respectively, considering the local socioeconomic level indicated by the nighttime light index., Results: Among the 26,482 patients (mean age 46.86, SD 19.52 years) with a median follow-up time of 1523 days per patient, 1542 (5.82%) PTB retreatments were observed between 2012 and 2019. Exposure to PM2.5 was observed to be significantly associated with the increased risk of PTB retreatment in fully adjusted models with a hazard ratio of 1.97 (95% CI 1.34-2.83) per 10 μg/m3 increase in PM2.5. Patients living in the regions with relatively high quartiles of NDVI values had a 45% lower risk of PTB retreatment than those living in the regions with the lowest quartile for the 500 m buffers (hazard ratio 0.55, 95% CI 0.40-0.77). Such a protective effect of residential greenness was more pronounced among patients living in lower nighttime light areas. The strength of the association between PM2.5 exposure and the risk of PTB retreatment was attenuated by greenness. No significant association was observed between NDVI and the incidence of drug resistance., Conclusions: Long-term exposure to PM2.5 might be a risk factor for PTB retreatment, while an increased level of residential greenness was found to be associated with reduced risks of PTB retreatment. Our results suggest strengthening the control of ambient air pollution and improving residential greenness may contribute to the reduction of PTB retreatment., (© Tonglei Guo, Fei Shen, Henan Xin, Jiang Du, Xuefang Cao, Boxuan Feng, Yijun He, Lingyu Shen, Yuanzhi Di, Yanxiao Chen, Zihan Li, Qi Jin, Hongzhi Li, Chunming Zhang, Lei Gao. Originally published in JMIR Public Health and Surveillance (https://publichealth.jmir.org).)

Background: Despite accumulating evidence of an association between air pollution and renal disease, studies on the association between long-term exposure to air pollution and renal function are still contradictory. This study aimed to investigate this association in a large population with relatively low exposure and with improved estimation of renal function as well as renal injury biomarkers., Methods: We performed a cross-sectional analysis in the middle-aged general population participating in the Swedish CardioPulmonary bioImaging Study (SCAPIS; n = 30 154). Individual 10-year exposure to total and locally emitted fine particulate matter (PM 2.5 ), inhalable particulate matter (PM 10 ), and nitrogen oxides (NO x ) were modelled using high-resolution dispersion models. Linear regression models were used to estimate associations between exposures and estimated glomerular filtration rate (eGFR, combined creatinine and cystatin C) and serum levels of renal injury biomarkers (KIM-1, MCP-1, IL-6, IL-18, MMP-2, MMP-7, MMP-9, FGF-23, and uric acid), with consideration of potential confounders., Results: Median long-term PM 2.5 exposure was 6.2 µg/m 3 . Almost all participants had a normal renal function and median eGFR was 99.2 mL/min/1.73 m 2 . PM 2.5 exposure was associated with 1.3% (95% CI 0.6, 2.0) higher eGFR per 2.03 µg/m 3 (interquartile range, IQR). PM 2.5 exposure was also associated with elevated serum matrix metalloproteinase 2 (MMP-2) concentration, with 7.2% (95% CI 1.9, 12.8) higher MMP-2 per 2.03 µg/m 3 . There was a tendency towards an association between PM 10 and higher levels of uric acid, but no associations were found with the other biomarkers. Associations with other air pollutants were null or inconsistent., Conclusion: In this large general population sample at low exposure levels, we found a surprising association between PM 2.5 exposure and a higher renal filtration. It seems unlikely that particle function would improve renal function. However, increased filtration is an early sign of renal injury and may be related to the relatively healthy population at comparatively low exposure levels. Furthermore, PM 2.5 exposure was associated with higher serum concentrations of MMP-2, an early indicator of renal and cardiovascular pathology., (© 2024. The Author(s).)

Background: Particulate matter exposure (PM) is a cause of aerodigestive disease globally. The destruction of the World Trade Center (WTC) exposed first responders and inhabitants of New York City to WTC-PM and caused obstructive airways disease (OAD), gastroesophageal reflux disease (GERD) and Barrett's Esophagus (BE). GERD not only diminishes health-related quality of life but also gives rise to complications that extend beyond the scope of BE. GERD can incite or exacerbate allergies, sinusitis, bronchitis, and asthma. Disease features of the aerodigestive axis can overlap, often necessitating more invasive diagnostic testing and treatment modalities. This presents a need to develop novel non-invasive biomarkers of GERD, BE, airway hyperreactivity (AHR), treatment efficacy, and severity of symptoms., Methods: Our observational case-cohort study will leverage the longitudinally phenotyped Fire Department of New York (FDNY)-WTC exposed cohort to identify Biomarkers of Airway Disease, Barrett's and Underdiagnosed Reflux Noninvasively (BAD-BURN). Our study population consists of n = 4,192 individuals from which we have randomly selected a sub-cohort control group (n = 837). We will then recruit subgroups of i. AHR only ii. GERD only iii. BE iv. GERD/BE and AHR overlap or v. No GERD or AHR, from the sub-cohort control group. We will then phenotype and examine non-invasive biomarkers of these subgroups to identify under-diagnosis and/or treatment efficacy. The findings may further contribute to the development of future biologically plausible therapies, ultimately enhance patient care and quality of life., Discussion: Although many studies have suggested interdependence between airway and digestive diseases, the causative factors and specific mechanisms remain unclear. The detection of the disease is further complicated by the invasiveness of conventional GERD diagnosis procedures and the limited availability of disease-specific biomarkers. The management of reflux is important, as it directly increases risk of cancer and negatively impacts quality of life. Therefore, it is vital to develop novel noninvasive disease markers that can effectively phenotype, facilitate early diagnosis of premalignant disease and identify potential therapeutic targets to improve patient care., Trial Registration: Name of Primary Registry: "Biomarkers of Airway Disease, Barrett's and Underdiagnosed Reflux Noninvasively (BADBURN)". Trial Identifying Number: NCT05216133 . Date of Registration: January 31, 2022., (© 2024. The Author(s).)

Fine particulate matter (PM 2.5 ) is a major air pollutant affecting human survival, development and health. By predicting the spatial distribution concentration of PM 2.5 , pollutant sources can be better traced, allowing measures to protect human health to be implemented. Thus, the purpose of this study is to predict and analyze the PM 2.5 concentration of stations based on the integrated deep learning of a convolutional neural network long short-term memory (CNN-LSTM) model. To solve the complexity and nonlinear characteristics of PM 2.5 time series data problems, we adopted the CNN-LSTM deep learning model. We collected the PM 2.5 data of Qingdao in 2020 as well as meteorological factors such as temperature, wind speed and air pressure for pre-processing and characteristic analysis. Then, the CNN-LSTM deep learning model was integrated to capture the temporal and spatial features and trends in the data. The CNN layer was used to extract spatial features, while the LSTM layer was used to learn time dependencies. Through comparative experiments and model evaluation, we found that the CNN-LSTM model can achieve excellent PM 2.5 prediction performance. The results show that the coefficient of determination (R 2 ) is 0.91, and the root mean square error (RMSE) is 8.216 µg/m 3 . The CNN-LSTM model achieves better prediction accuracy and generalizability compared with those of the CNN and LSTM models (R 2 values of 0.85 and 0.83, respectively, and RMSE values of 11.356 and 14.367, respectively). Finally, we analyzed and explained the predicted results. We also found that some meteorological factors (such as air temperature, pressure, and wind speed) have significant effects on the PM 2.5 concentration at ground stations in Qingdao. In summary, by using deep learning methods, we obtained better prediction performance and revealed the association between PM 2.5 concentration and meteorological factors. These findings are of great significance for improving the quality of the atmospheric environment and protecting public health., Competing Interests: The authors declare there are no competing interests., (©2024 Bai et al.)

Background: Air pollution affects residents' health to varying extents according to differences in socioeconomic status. However, there has been a lack of research on whether air pollution contributes to unfair health costs., Methods: In this research, data from the China Labour Force Dynamics Survey are matched with data on PM2.5 average concentration and precipitation, and the influence of air pollution on the health expenditures of residents is analysed with econometric methods involving a two-part model, instrument variables and moderating effects., Results: The findings reveal that air pollution significantly impacts Chinese residents' health costs and leads to low-income people face health inequality. Specifcally, the empirical evidence shows that air pollution has no significant influence on the probability of residents' health costs (β = 0.021, p = 0.770) but that it increases the amount of residents' total outpatient costs (β = 0.379, p < 0.006), reimbursed outpatient cost (β = 0.453, p < 0.044) and out-of-pocket outpatient cost (β = 0.362, p < 0.048). The heterogeneity analysis of income indicates that low-income people face inequality due to health cost inflation caused by air pollution, their total and out-of-pocket outpatient cost significantly increase with PM2.5 (β = 0.417, p = 0.013; β = 0.491, p = 0.020). Further analysis reveals that social basic medical insurance does not have a remarkable positive moderating effect on the influence of air pollution on individual health inflation (β = 0.021, p = 0.292), but supplementary medical insurance for employees could reduce the effect of air pollution on low-income residents' reimbursed and out-of-pocket outpatient cost (β=-1.331, p = 0.096; β=-2.211, p = 0.014)., Conclusion: The study concludes that air pollution increases the amount of Chinese residents' outpatient cost and has no significant effect on the incidence of outpatient cost. However, air pollution has more significant impact on the low-income residents than the high-income residents, which indicates that air pollution leads to the inequity of medical cost. Additionally, the supplementary medical insurance reduces the inequity of medical cost caused by air pollution for the low-income employees., (© 2024. The Author(s).)

Background: Exposure to fine particulate matter (<2.5 um, particulate matter with an aerodynamic diameter <2.5 microns [PM 2.5 ]) has been implicated in atherogenesis. Limited data in animal studies suggest that PM 2.5 exposure leads to myocardial fibrosis and increased incidence of heart failure (HF). Whether PM 2.5 is associated with adverse outcomes in patients with preexisting HF has not been widely studied., Methods and Results: In this retrospective cohort study, Medicare patients hospitalized with first HF between 2013 and 2020 were identified from the Medicare Provider Analysis and Review Part A 100% files. Patients were linked with integrated estimates of ambient PM 2.5 obtained at 1×1 km using the zip code of participants' residence. The study outcomes were all-cause death, HF, and all-cause readmissions burden. A total of 2 599 525 patients were included in this study, with 6 321 731 person-years of follow-up. Mean PM 2.5 was 7.3±1.7 μg/m 3 . Each interquartile range of PM 2.5 was associated with 0.9% increased hazard of all-cause death, 4.5% increased hazard of first HF readmission, 3.1% increased risk of HF hospitalization burden, and 5.2% increase in all-cause readmission burden, after adjusting for 11 sociodemographic and medical factors. Subgroup analyses showed that the effects were more pronounced at levels <7 μg/m 3 and in patients aged <75 years, Asians, and those residing in rural areas., Conclusions: Ambient air pollution is associated with higher risk of adverse events in Medicare beneficiaries with established HF. These associations persist below the National Air Quality Standards (12 μg/m 3 ), supporting that no threshold effect exists for health effects of air pollution exposure.

Background: Recent studies have reported the burden of attention deficit hyperactivity disorder [ADHD], autism spectrum disorder [ASD], and depressive disorder. Also, there is mounting evidence on the effects of environmental factors, such as ambient air pollution, on these disorders among children and adolescents. However, few studies have evaluated the burden of mental disorders attributable to air pollution exposure in children and adolescents., Methods: We estimated the risk ratios of major mental disorders (ADHD, ASD, and depressive disorder) associated with air pollutants among children and adolescents using time-series data (2011-2019) obtained from a nationwide air pollution monitoring network and healthcare utilization claims data in the Republic of Korea. Based on the estimated risk ratios, we determined the population attributable fraction (PAF) and calculated the medical costs of major mental disorders attributable to air pollution., Results: A total of 33,598 patients were diagnosed with major mental disorders during 9 years. The PAFs for all the major mental disorders were estimated at 6.9% (particulate matter < 10 μm [PM 10 ]), 3.7% (PM 2.5 ), and 2.2% (sulfur dioxide [SO 2 ]). The PAF of PM 10 was highest for depressive disorder (9.2%), followed by ASD (8.4%) and ADHD (5.2%). The direct medical costs of all major mental disorders attributable to PM 10 and SO 2 decreased during the study period., Conclusion: This study assessed the burden of major mental disorders attributable to air pollution exposure in children and adolescents. We found that PM 10, PM 2.5 , and SO 2 attributed 7%, 4%, and 2% respectively, to the risk of major mental disorders among children and adolescents., Competing Interests: The authors have no potential conflicts of interest to disclose., (© 2024 The Korean Academy of Medical Sciences.)

Background: Prior research has linked exposure to particulate matter with an aerodynamic diameter of ≤2.5 μm (PM2.5) with preterm birth (PTB). However, the modulating effect of preconception thyroid stimulating hormone (TSH) levels on the relationship between PM2.5 exposure and PTB has not been investigated., Objective: This study aimed to assess whether preconception TSH levels modulate the impact of PM2.5 exposure on PTB., Methods: This cohort study was conducted in Guangdong, China, as a part of the National Free Pre-Pregnancy Checkups Project. PM2.5 exposure was estimated by using the inverse distance weighting method. To investigate the moderating effects of TSH levels on trimester-specific PM2.5 exposure and PTB, we used the Cox proportional hazards model. Additionally, to identify the susceptible exposure windows for weekly specific PM2.5 exposure and PTB, we built distributed lag models incorporating Cox proportional hazards models., Results: A total of 633,516 women who delivered between January 1, 2014, to December 31, 2019, were included. In total, 34,081 (5.4%) of them had abnormal preconception TSH levels. During the entire pregnancy, each 10-μg/m3 increase in PM2.5 was linked to elevated risks of PTB (hazard ratio [HR] 1.559, 95% CI 1.390-1.748), early PTB (HR 1.559, 95% CI 1.227-1.980), and late PTB (HR 1.571, 95% CI 1.379-1.791) among women with abnormal TSH levels. For women with normal preconception TSH levels, PM2.5 exposure during the entire pregnancy was positively associated with the risk of PTB (HR 1.345, 95% CI 1.307-1.385), early PTB (HR 1.203, 95% CI 1.126-1.285), and late PTB (HR 1.386, 95% CI 1.342-1432). The critical susceptible exposure windows were the 3rd-13th and 28th-35th gestational weeks for women with abnormal preconception TSH levels, compared to the 1st-13th and 21st-35th gestational weeks for those with normal preconception TSH levels., Conclusions: PM2.5 exposure was linked with a higher PTB risk, particularly in women with abnormal preconception TSH levels. PM2.5 exposure appears to have a greater effect on pregnant women who are in the early or late stages of pregnancy., (© Ting Xu, Haobo Ni, Xiaoyan Cai, Tingting Dai, Lingxi Wang, Lina Xiao, Qinghui Zeng, Xiaolin Yu, Lu Han, Pi Guo. Originally published in JMIR Public Health and Surveillance (https://publichealth.jmir.org).)

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

Background: Traditional observational studies exploring the association between air pollution and infections have been limited by small sample sizes and potential confounding factors. To address these limitations, we applied Mendelian randomization (MR) to investigate the potential causal relationships between particulate matter (PM2.5, PM2.5-10, and PM10), nitrogen dioxide, and nitrogen oxide and the risks of infections., Methods: Single nucleotide polymorphisms (SNPs) related to air pollution were selected from the genome-wide association study (GWAS) of the UK Biobank. Publicly available summary data for infections were obtained from the FinnGen Biobank and the COVID-19 Host Genetics Initiative. The inverse variance weighted (IVW) meta-analysis was used as the primary method for obtaining the Mendelian randomization (MR) estimates. Complementary analyses were performed using the weighted median method, MR-Egger method, and MR Pleiotropy Residual Sum and Outlier (MR-PRESSO) test., Results: The fixed-effect IVW estimate showed that PM2.5, PM2.5-10 and Nitrogen oxides were suggestively associated with COVID-19 [for PM2.5: IVW (fe): OR 3.573(1.218,5.288), P IVW(fe) = 0.021; for PM2.5-10: IVW (fe): OR 2.940(1.385,6.239), P IVW(fe) = 0.005; for Nitrogen oxides, IVW (fe): OR 1.898(1.318,2.472), P IVW(fe) = 0.010]. PM2.5, PM2.5-10, PM10, and Nitrogen oxides were suggestively associated with bacterial pneumonia [for PM2.5: IVW(fe): OR 1.720 (1.007, 2.937), P IVW(fe) = 0.047; for PM2.5-10: IVW(fe): OR 1.752 (1.111, 2.767), P IVW(fe) = 0.016; for PM10: IVW(fe): OR 2.097 (1.045, 4.208), P IVW(fe) = 0.037; for Nitrogen oxides, IVW(fe): OR 3.907 (1.209, 5.987), P IVW(fe) = 0.023]. Furthermore, Nitrogen dioxide was suggestively associated with the risk of acute upper respiratory infections, while all air pollution were not associated with intestinal infections., Conclusions: Our results support a role of related air pollution in the Corona Virus Disease 2019, bacterial pneumonia and acute upper respiratory infections. More work is need for policy formulation to reduce the air pollution and the emission of toxic and of harmful gas., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Yang, Tong, Wang, Li, Wang and Ni.)

Background: PM 2.5 can induce and aggravate the occurrence and development of cardiovascular diseases (CVDs). The objective of our study is to estimate the causal effect of PM 2.5 on mortality rates associated with CVDs using the instrumental variables (IVs) method., Methods: We extracted daily meteorological, PM 2.5 and CVDs death data from 2016 to 2020 in Binzhou. Subsequently, we employed the general additive model (GAM), two-stage predictor substitution (2SPS), and control function (CFN) to analyze the association between PM 2.5 and daily CVDs mortality., Results: The 2SPS estimated the association between PM 2.5 and daily CVDs mortality as 1.14% (95% CI: 1.04%, 1.14%) for every 10 µg/m 3 increase in PM 2.5 . Meanwhile, the CFN estimated this association to be 1.05% (95% CI: 1.02%, 1.10%). The GAM estimated it as 0.85% (95% CI: 0.77%, 1.05%). PM 2.5 also exhibited a statistically significant effect on the mortality rate of patients with ischaemic heart disease, myocardial infarction, or cerebrovascular accidents (P < 0.05). However, no significant association was observed between PM 2.5 and hypertension., Conclusion: PM 2.5 was significantly associated with daily CVDs deaths (excluding hypertension). The estimates from the IVs method were slightly higher than those from the GAM. Previous studies based on GAM may have underestimated the impact of PM 2.5 on CVDs., (© 2024. The Author(s).)

Although previous studies have suggested that meteorological factors and air pollutants can cause dry eye disease (DED), few clinical cohort studies have determined the individual and combined effects of these factors on DED. We investigated the effects of meteorological factors (humidity and temperature) and air pollutants [particles with a diameter ≤ 2.5 μ m (PM 2.5 ), ozone (O 3 ), nitrogen dioxide (NO 2 ), and carbon monoxide (CO)] on DED. A retrospective cohort study was conducted on 53 DED patients. DED was evaluated by Symptom Assessment in Dry Eye (SANDE), tear secretion, tear film break-up time (TBUT), ocular staining score (OSS), and tear osmolarity. To explore the individual, non-linear, and joint associations between meteorological factors, air pollutants, and DED parameters, we used generalized linear mixed model (GLMM) and Bayesian kernel machine regression (BKMR). After adjusting for all covariates, lower relative humidity or temperature was associated with a higher SANDE (p < 0.05). Higher PM 2.5 , O 3 , and NO 2 levels were associated with higher SANDE and tear osmolarity (p < 0.05). Higher O 3 levels were associated with lower tear secretion and TBUT, whereas higher NO 2 levels were associated with higher OSS (p < 0.05). BKMR analyses indicated that a mixture of meteorological factors and air pollutants was significantly associated with increased SANDE, OSS, tear osmolarity, and decreased tear secretion., (© 2024. The Author(s).)

Asbestos, a group of class I (WHO) carcinogenic fibers, is the main cause of mesothelioma. Asbestos inhalation also increases the risk to develop other solid tumours with lung cancer as the most prominent example [91]. The incidence of asbestos-related lung cancer (ARLC) is estimated to be to six times larger than the mesothelioma incidence thereby becoming an important health issue [86]. Although the pivotal role of asbestos in inducing lung cancer is well established, the precise causal relationships between exposures to asbestos, tobacco smoke, radon and 'particulate' (PM2.5) air pollution remain obscure and new knowledge is needed to establish appropriate preventive measures and to tailor existing screening practices[22,61,65]. We hypothesize that a part of the increasing numbers of lung cancer diagnoses in never-smokers can be explained by (historic and current) exposures to asbestos as well as combinations of different forms of air pollution (PM2.5, asbestos and silica)., 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 Author(s). Published by Elsevier B.V. All rights reserved.)

Chronic kidney disease (CKD) has emerged as a significant global public health concern. Recent epidemiological studies have highlighted the link between exposure to fine particulate matter (PM 2.5 ) and a decline in renal function. PM 2.5 exerts harmful effects on various organs through oxidative stress and inflammation. Acute kidney injury (AKI) resulting from ischaemia-reperfusion injury (IRI) involves biological processes similar to those involved in PM 2.5 toxicity and is a known risk factor for CKD. The objective of this study was to investigate the impact of PM 2.5 exposure on IRI-induced AKI. Through a unique environmentally controlled setup, mice were exposed to urban PM 2.5 or filtered air for 12 weeks before IRI followed by euthanasia 48 h after surgery. Animals exposed to PM 2.5 and IRI exhibited reduced glomerular filtration, impaired urine concentration ability, and significant tubular damage. Further, PM 2.5 aggravated local innate immune responses and mitochondrial dysfunction, as well as enhancing cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway activation. This increased renal senescence and suppressed the anti-ageing protein klotho, leading to early fibrotic changes. In vitro studies using proximal tubular epithelial cells exposed to PM 2.5 and hypoxia/reoxygenation revealed heightened activation of the STING pathway triggered by cytoplasmic mitochondrial DNA, resulting in increased tubular damage and a pro-inflammatory phenotype. In summary, our findings imply a role for PM 2.5 in sensitising proximal tubular epithelial cells to IRI-induced damage, suggesting a plausible association between PM 2.5 exposure and heightened susceptibility to CKD in individuals experiencing AKI. Strategies aimed at reducing PM 2.5 concentrations and implementing preventive measures may improve outcomes for AKI patients and mitigate the progression from AKI to CKD. © 2024 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland., (© 2024 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.)

Background: The literature on the association between fine particulate matter (PM2.5) exposure and gestational diabetes mellitus (GDM) risk has focused mainly on exposure during the first and second trimesters, and the research results are inconsistent. Therefore, this study aimed to investigate the associations between PM2.5 exposure during preconception, the first trimester and second trimester and GDM risk in pregnant women in Guangzhou., Methods: A retrospective cohort study of 26 354 pregnant women was conducted, estimating PM2.5, particulate matter with a diameter >10 µm (PM10), sulphur dioxide (SO2), carbon monoxide (CO) and ozone (O3) exposure during preconception and the first and second trimesters. Analyses were performed using Cox proportional hazards models and nonlinear distributed lag models., Results: The study found that exposure to PM2.5 or a combination of two pollutants (PM2.5+PM10, PM2.5+SO2, PM2.5+CO and PM2.5+O3) was found to be significantly associated with GDM risk (P < 0.05). In the second trimester, with significant interactions found for occupation and anaemia between PM2.5 and GDM. When the PM2.5 concentrations were ≥19.56, ≥25.69 and ≥23.87 μg/m3 during preconception and the first and second trimesters, respectively, the hazard ratio for GDM started to increase. The critical window for PM2.5 exposure was identified to be from 9 to 11 weeks before conception., Conclusions: Our study results suggest that PM2.5 exposure during preconception and the first and second trimesters increases the risk of GDM, with the preconception period appearing to be the critical window for PM2.5 exposure., (© The Author(s) 2024. Published by Oxford University Press on behalf of the European Public Health Association.)

Background: Exposure to environmental stressors like particulate matter (PM) and ultraviolet radiation (UV) induces cutaneous oxidative stress and inflammation and leads to skin barrier dysfunction and premature aging. Metals like iron or copper are abundant in PM and are known to contribute to reactive oxygen species (ROS) production., Aims: Although it has been suggested that topical antioxidants may be able to help in preventing and/or reducing outdoor skin damage, limited clinical evidence under real-life exposure conditions have been reported. The aim of the present study was to evaluate the ability of a topical serum containing 15% ascorbic acid, 0.5% ferulic acid, and 1% tocopherol (CF Mix) to prevent oxinflammatory skin damage and premature aging induced by PM + UV in a human clinical trial., Methods: A 4-day single-blinded, clinical study was conducted on the back of 15 females (18-40 years old). During the 4 consecutive days, the back test zones were treated daily with or without the CF Mix, followed by with/without 2 h of PM and 5 min of UV daily exposure., Results: Application of the CF Mix prevented PM + UV-induced skin barrier perturbation (Involucrin and Loricrin), lipid peroxidation (4HNE), inflammatory markers (COX2, NLRP1, and AhR), and MMP9 activation. In addition, CF Mix was able to prevent Type I Collagen loss., Conclusion: This is the first human study confirming multipollutant cutaneous damage and suggesting the utility of a daily antioxidant topical application to prevent pollution induced skin damage., (© 2024 The Authors. Journal of Cosmetic Dermatology published by Wiley Periodicals LLC.)