Particulate Matter Exposure Research Articles

Impact of particulate matter exposure on melanoma risk: A multicentre case-control study.

The relationship between particulate matter (PM) exposure and melanoma risk remains largely unexplored. This study aims to investigate the association between PM10 and PM2.5 long-term exposure and melanoma risk. Case-control study involving 2575 participants, comprising 1473 melanoma patients and 1102 healthy controls attending Departments of Dermatology of University Hospital in North and Central Italy. Demographic data, smoking status, history of sunburns and skin type were collected. PM10 and PM2.5 exposure levels were estimated for each participant's residential address using a Bayesian hierarchical model, providing daily concentrations at a 1 km2 spatial resolution from 2013 to 2021. Logistic regression analyses were performed to evaluate the association between PM exposure and melanoma risk, adjusting for potential confounders. Melanoma patients and controls were 52% males and had a mean age of 63.89 and 61.66 years, respectively. The majority of melanoma patients had Fitzpatrick phototypes 2 (59%) and 3 (36%). There were no significant differences in the geographical distribution of cases and controls based on ZIP codes (p = 0.894). The average melanoma Breslow thickness was 1.01 mm, with 68.15% of cases diagnosed at stage 0 and IA. The multivariate logistic regression revealed a protective effect for higher PM10 (OR = 0.89, 95%CI: 0.86-0.92, p < 0.001) and PM2.5 levels (OR = 0.72, 95%CI: 0.68-0.76, p < 0.001). Darker skin phototypes (Fitzpatrick 4) and cigarette smoking were also associated with a reduced risk of melanoma. Higher levels of PM10 and PM2.5 may have a protective effect against melanoma, potentially due to the reduction in ultraviolet radiation exposure. Further research to understand the complex interactions between environmental factors and melanoma risk are needed.

The role of mTOR activation in steroid-resistant asthma: insights from particulate matter-induced mouse model and patient studies.

Particulate matter (PM) exposure has been proposed as one of the causes of steroid resistance. However, studies investigating this using patient samples or animals are still lacking. Therefore, in this study, we aimed to investigate the changes in cytokines and mTOR (mammalian target of rapamycin) activation in patients with steroid resistant asthma and the role of mTOR in a mouse model of steroid resistant asthma induced by PM. In mouse experiment, on administering PM10 and allergen (Dp) through the intranasal route for 3 weeks, airway hyperresponsiveness (AHR), eosinophils, and airway inflammation were increased. However, administering rapamycin (mTOR inhibitor) together with PM and Dp led to significant decrease in all of the abovementioned features; additionally, the population of IL-13 + or IL-17 + cells in CD62lowCD44high subset of CD4 + T cells, which serves as an effector/memory cell marker, showed a significant decrease when compared to the group that received PM and Dp. When Dp was administered once after a rest period, the mice exposed to PM and Dp exhibited resurgence in asthma features and elevated effector/memory IL-13 + or IL-17 + cell populations. Rapamycin administration inhibited this effect. In human PBMC, in the steroid Non-Responder (NR) group, cytokines with p-mTOR double-positive population of effector/memory CD4 T cells (CCR7-CD45RA-CD4 + in CD62-CD27-CD45RO+) was significantly higher than that of the Normal or steroid Responder (R) groups. These data demonstrates that rapamycin can inhibit asthmatic features in mouse model of PM induced steroid-resistant asthma. And we suggest that rapamycin could act on effector/memory CD4 + T cells through in vitro and patient sample experiments.

Rural Roads to cognitive Resilience (RRR): A prospective cohort study protocol.

Ambient air pollution, detrimental built and social environments, social isolation (SI), low socioeconomic status (SES), and rural (versus urban) residence have been associated with cognitive decline and risk of Alzheimer's disease and related dementias (ADRD). Research is needed to investigate the influence of ambient air pollution and built and social environments on SI and cognitive decline among rural, disadvantaged, ethnic minority communities. To address this gap, this cohort study will recruit an ethnoracially diverse, rural Florida sample in geographic proximity to seasonal agricultural burning. We will (1) examine contributions of smoke-related fine particulate matter (PM2.5) exposures to SI and cognitive function; (2) determine effects of built and social environments on SI and cognitive function; and (3) contextualize SI and cognitive function among residents from different ethnoracial groups during burn and non-burn seasons. We will recruit 1,087 community-dwelling, dementia-free, ≥45-year-olds from five communities in Florida's Lake Okeechobee region. Over 36 months, participants will complete baseline visits to collect demographics, health history, and health measurements (e.g., blood pressure, body mass index) and 6-month follow-ups assessing cognitive function and social isolation at each visit. A subsample of 120 participants representative of each community will wear smartwatches to collect sensor data (e.g., heart rate) and daily routine and predefined activities (e.g., GPS-captured travel, frequent destinations) over two months. Ecological momentary assessments (EMA) (e.g., whether smoke has bothered participant in last 30 minutes) will occur over two months during agricultural burning and non-burning months. PurpleAir monitors (36 total) will be installed in each community to continuously monitor outdoor PM2.5 levels. We expect to identify individual- and community-level factors that increase the risk for SI and cognitive decline in a vulnerable rural population.

Classroom air quality in a randomized crossover trial with portable HEPA air cleaners.

Children living in communities with lower socioeconomic status and higher minority populations are often disproportionately exposed to particulate matter (PM) compared to children living in other communities. We assessed whether adding HEPA filter air cleaners to classrooms with existing HVAC systems reduces indoor air pollution exposure. From July 2022 to June 2023, using a block randomized crossover trial of 17 Los Angeles Unified School District elementary schools, classroom PM concentrations were monitored and compared for 99 classrooms with HEPA filter air cleaners and 87 classrooms with non-HEPA filter air cleaners. In HEPA classrooms, average school-year PM2.5 was 39.9% lower (0.581 µg/m³; p < 0.001) and infiltration of outdoor PM2.5 into classrooms was 13.8-82.4% lower than non-HEPA classrooms, depending on the school. Few studies have examined HEPA filtration in a classroom environment, and this is one of the first studies since the COVID-19 pandemic to assess PM exposure in the classroom. Using a well powered block randomized crossover trial, we showed that adding portable HEPA air cleaners to classrooms that already had HVAC systems with MERV 13 air filters resulted in lower measurable PM concentrations and less infiltration of outdoor PM2.5 compared to control classrooms with non-HEPA filters. This demonstrates that further improvements in classroom air quality, especially in environmentally burdened communities, can be achieved with additional filtration.

Moderate PM10 exposure increases prostate cancer: a longitudinal nationwide cohort study (2010–2020)

Moderate PM10 exposure increases prostate cancer: a longitudinal nationwide cohort study (2010–2020)

Prenatal exposure to particulates and anthropometry through 9 years of age in a birth cohort.

Previous research observed links between prenatal air pollution and risk of childhood obesity but the timing of the exposure is understudied. We examined prenatal particulate matter (PM10, PM2.5) exposure and child anthropometry. Children's body mass index z-scores (zBMI) at 0-3 (N = 4370) and 7-9 (n = 1191) years were derived from reported anthropometry at paediatric visits. We ran linear mixed models for six windows, adjusting for maternal, child, and neighbourhood factors. PM10 exposure across pregnancy and at multiple windows was associated with higher zBMI in both early and middle childhood. For instance, one interquartile range increase in PM10 exposure during the first 2 weeks of pregnancy was associated with higher zBMI at 0-3 (0.05, 95% CI: 0.01, 0.10) and 7-9 (0.14, 95% CI: 0.02, 0.23). PM2.5 exposure during the final 2 weeks of gestation was associated with higher zBMI at 7-9 years (B: 0.12, 95% CI: 0.04, 0.22). Even at low levels of air pollution, prenatal PM10 exposure was associated with higher zBMI in childhood.

Reliea® combination of Codonopsis lanceolata and Chaenomeles sinensis extract alleviates airway inflammation on particulate matter 10 plus diesel exhaust particles (PM10D) ‑induced respiratory disease mouse model.

Particulate matter (PM, diameter < 10 μm) and Diesel exhaust particles (DEP) exposure can cause severe respiratory disorders. This investigation explored the protective effects of Reliea® (RelA), combination of Codonopsis lanceolata and Chaenomeles sinensis extract, against airway inflammation related to PM10D exposure. RelA treatment suppressed reactive oxygen species, nitric oxide release, cytokine expression (IL-6, IL-1β, iNOS, CXCL-2, MCP-1, and TNF-α), and the related inflammatory mechanisms in PM10-induced alveolar macrophage cells. BALB/c mice were injected with PM10D via intranasal trachea three times over a period of 12 days and RelA were orally dispensed for 12 days. RelA inhibited infiltrating neutrophils, total number of immunocytes in lung and bronchoalveolar lavage fluid (BALF). RelA decreased the expression of interleukin (IL)-17, chemokine (C-X-C motif) ligand (CXCL)-1, thymus and activation-regulated chemokine, macrophage inflammatory protein-2, IL-1α, TNF-α, mucin 5AC, cyclooxygenase-2, and transient receptor potential cation channel subfamily A or V member 1 in BALF and lung, and inhibited IL-1α and macrophage marker F4/80 localization in lung of PM10D-induced mice. RelA treatment decreased serum symmetric dimethyl arginine levels. RelA restored histopathological damage via inhibition of NF-κB and MAPK pathways in the trachea and lung. Lancemaside A and protocatechuic acid as major active compounds of RelA was identified. In addition, RelA showed better expectoration through increased phenol red secretion. These results indicate that Reliea® combination of C. lanceolata and C. sinensis extract might be effective in prevention and treatment of airway inflammation and respiratory diseases.

Novel perspective on particulate matter and Alzheimer's disease: Insights from adverse outcome pathway framework.

Alzheimer's disease (AD) is a neurodegenerative disease, that accounts for 50-75% of all dementia cases. Evidence demonstrates the link between particulate matter (PM) exposure and AD. However, there are still considerable research gaps. This review aims to clarify the mechanism between PM and AD from different levels (subcellular/cellular/system/population) by using an adverse outcome pathway (AOP) framework. We applied a chemical-phenotype interaction network-based workflow to integrate diverse genes and phenotypes. The interactions among PM, genes, phenotypes, and AD were retrieved from the Comparative Toxicogenomics Database (CTD), DisGeNET, MalaCards, Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG), which are publicly available databases. The filtered genes and phenotypes were assembled as molecular initiating events (MIEs) and key events (KEs) according to the upstream and downstream relationships, generating a predictive PM-Gene-Phenotype-AD AOP network. According to the Organization for Economic Co-operation and Development handbook (OECD), a verified AOP network was assessed and applied to determine the effects of PM on AD. PM could increase APP and GSK3B, increase apoptosis, impair cognition and memory, and ultimately lead to AD. Overall, chemical-phenotype interactions are expressed in a formal structured notation using controlled terms for chemicals, phenotypes, taxons, and anatomical descriptors. To our knowledge, this is the first AOP framework focusing on the underlying mechanism of exposure to PM on AD. Our network-based approach not only fills mechanism gaps in PM and AD but sheds light on constructing AOP frameworks for new chemicals.

Lysoglycerophospholipid metabolism alterations associated with ambient fine particulate matter exposure: Insights into the pro-atherosclerotic effects.

The biological pathways connecting ambient fine particulate matter (PM2.5)-induced initial adverse effects to the development of atherosclerotic cardiovascular diseases are not fully understood. We hypothesize that lysoglycerophospholipids (LysoGPLs) are pivotal mediators of atherosclerosis induced by exposure to PM2.5. This study investigated the changes of LysoGPLs in response to PM2.5 exposure and the mediation role of LysoGPLs in the pro-atherosclerotic effects of PM2.5 exposure. In this longitudinal panel study, 110 adults aged 50-65 years from Beijing, China, were followed between 2013 and 2015. Targeted metabolomics analyses were utilized to quantify 18 LysoGPLs from five subclasses in 579 plasma samples. Daily PM2.5 mass concentration was monitored at a station. We used linear mixed-effect models to estimate the responses of LysoGPLs to PM2.5 exposure. Subsequently, mediation analyses were conducted to investigate the mediating role of LysoGPLs in PM2.5-associated changes in non-high density lipoprotein-cholesterol (Non-HDL-C), a biomarker for pro-atherosclerotic apolipoprotein B-containing lipoproteins, and various inflammatory biomarkers, including interleukin (IL)-8, monocyte chemoattractant protein-1 (MCP-1), soluble CD40 ligand, and interferon (IFN)-γ. Short-to medium-term (1-30 days) PM2.5 exposure was associated with significant increases in six lysophosphatidic acids (LPAs), three lysoalkylphosphatidylcholines [LPC(O)s], and three lysophosphatidylglycerols (LPGs), as well as decreases in two LPAs and one lysophosphatidylserine (LysoPS), with maximus changes of 0.5-2.1%, 0.8-2.1%, 1.9-3.0%, -1.4-3.7%, and -8.0%, respectively. Furthermore, the elevated levels of LPA 18:1/18:2, LPC(O) 18:0/18:1, and LPG 16:0/16:1/18:0 significantly mediated the PM2.5-associated increase in Non-HDL-C (18-49%), IL-8 (9-24%), MCP-1 (12-26%), and IFN-γ (4-12%) over 30 days. In conclusion, short-to medium-term PM2.5 exposure was associated with altered metabolism of LysoGPLs, which mediated the PM2.5-associated pro-atherosclerotic response.

Human Monocyte-Derived Macrophages Demonstrate Distinct Responses to Ambient Particulate Matter in a Polarization State- and Particle Seasonality-Specific Manner.

Macrophages are professional phagocytic immune cells that, following activation, polarize on a spectrum between the proinflammatory M1 and the proresolution M2 states. Macrophages have further been demonstrated to retain plasticity, allowing for the reprogramming of their polarization states following exposure to new stimuli. Particulate matter (PM) has been repeatedly shown to modify macrophage function and polarization while also inducing worsening respiratory infection morbidity and mortality. However, limited work has considered the impact of the initial macrophage polarization state on subsequent responses to PM exposure. PM composition can demonstrate seasonality-specific compositional changes based on differences in seasonal weather patterns and energy needs, introducing the need to consider the seasonality-specific effects of airborne PM when investigating its impact on human health. This study sought to determine the impact of airborne PM collected during different seasons of the year in Xinxiang, China, on macrophage function in a polarization state-dependent manner. Macrophages were differentiated using the macrophage colony-stimulating factor (M-CSF) on CD14+CD16- monocytes isolated from the blood of healthy human volunteers. The resulting macrophages were polarized into indicated states using well-characterized polarization methods and assessed for phagocytic function, bioenergetic properties, and secretory profile following exposure to PM collected during a single day during each season of the year. Macrophages demonstrated clear polarization state-dependent phagocytic, bioenergetic, and secretory properties at the baseline and following PM exposure. Specific PM seasonality had a minimal impact on phagocytic function and a minor effect on bioenergetic properties but had clear impacts on the secretory profile as demonstrated by the enriched secretion of well-characterized mediator clusters by particle season. Together, these data suggest that both particle seasonality and macrophage polarization state must be considered when investigating the impact of PM on macrophage function. These factors may contribute to the negative outcomes linked to PM exposure during respiratory infections.

Partial-linear single-index Cox regression models with multiple time-dependent covariates

BackgroundIn cohort studies with time-to-event outcomes, covariates of interest often have values that change over time. The classical Cox regression model can handle time-dependent covariates but assumes linear effects on the log hazard function, which can be limiting in practice. Furthermore, when multiple correlated covariates are studied, it is of great interest to model their joint effects by allowing a flexible functional form and to delineate their relative contributions to survival risk.MethodsMotivated by the World Trade Center (WTC)-exposed Fire Department of New York cohort study, we proposed a partial-linear single-index Cox (PLSI-Cox) model to investigate the effects of repeatedly measured metabolic syndrome indicators on the risk of developing WTC lung injury associated with particulate matter exposure. The PLSI-Cox model reduces the dimensionality of covariates while providing interpretable estimates of their effects. The model’s flexible link function accommodates nonlinear effects on the log hazard function. We developed an iterative estimation algorithm using spline techniques to model the nonparametric single-index component for potential nonlinear effects, followed by maximum partial likelihood estimation of the parameters.ResultsExtensive simulations showed that the proposed PLSI-Cox model outperformed the classical time-dependent Cox regression model when the true relationship was nonlinear. When the relationship was linear, both the PLSI-Cox model and classical time-dependent Cox regression model performed similarly. In the data application, we found a possible nonlinear joint effect of metabolic syndrome indicators on survival risk. Among the different indicators, BMI had the largest positive effect on the risk of developing lung injury, followed by triglycerides.ConclusionThe PLSI-Cox models allow for the evaluation of nonlinear effects of covariates and offer insights into their relative importance and direction. These methods provide a powerful set of tools for analyzing data with multiple time-dependent covariates and survival outcomes, potentially offering valuable insights for both current and future studies.

A Combined Extract from Dioscorea bulbifera and Zingiber officinale Mitigates PM2.5-Induced Respiratory Damage by NF-κB/TGF-β1 Pathway.

This research evaluated the protective role of a combined extract of Dioscorea bulbifera and Zingiber officinale (DBZO) against respiratory dysfunction caused by particulate matter (PM2.5) exposure in BALB/c mice. The bioactive compounds identified in the DBZO are catechin, astragalin, 6-gingerol, 8-gingerol, and 6-shogaol. DBZO ameliorated cell viability and reactive oxygen species (ROS) production in PM2.5-stimulated A549 and RPMI 2650 cells. In addition, it significantly alleviated respiratory dysfunction in BALB/c mice exposed to PM2.5. DBZO improved the antioxidant systems in lung tissues by modulating malondialdehyde (MDA) content, as well as levels of reduced glutathione (GSH) and superoxide dismutase (SOD). Likewise, DBZO restored mitochondrial dysfunction by improving ROS levels, mitochondrial membrane potential, and ATP production. Moreover, DBZO modulated the levels of neutrophils, eosinophils, monocytes, and lymphocytes (specifically CD4+, CD8+, and CD4+IL-4+ T cells) in blood and IgE levels in serum. DBZO was shown to regulate the c-Jun N-terminal kinase (JNK) pathway, nuclear factor kappa B (NF-κB) pathway, and transforming growth factor β (TGF-β)/suppressor of mothers against decapentaplegic (Smad) pathway. Histopathological observation indicated that DBZO mitigates the increase in alveolar septal thickness. These findings indicate that DBZO is a promising natural agent for improving respiratory health.

Association Between Exposure to Particulate Matter Air Pollution with Risk of Obesity Among Children and Adolescents in Northern and Central Taiwan.

The present study investigated the relationship between air pollution, specifically PM2.5 and PM10, and childhood and adolescent obesity in northern and central Taiwan. Previous research has shown a positive correlation between air pollution and pediatric obesity, but no study has been conducted in Taiwan. We used data from the K-12 Education Administration, Ministry of Education, and the Taiwan Air Quality Monitoring Network to analyze the association between PM2.5 and PM10 exposures and obesity rates among elementary and junior high school students. Data on students' height and weight were combined with air pollution data obtained from monitoring stations to assess exposure. A multivariable model estimated the relative risk and 95% confidence intervals of obesity linked to PM2.5 and PM10 exposures. Cities were categorized into quartiles (Q1-Q4) based on pollutant accumulation to compare the obesity rates. Students living in areas with higher PM2.5 and PM10 exposures (Q4) had a significantly higher risk of obesity than those living in areas with lower exposures (Q1). The effect was more pronounced in girls and older students, with PM2.5 exhibiting a stronger relationship than PM10. PM2.5 and PM10 exposures are significantly associated with an increased obesity risk in children and adolescents, particularly in girls and older students. Further research is needed to explore the underlying mechanisms and to control for socioeconomic and demographic factors.

Downregulation of tRNA methyltransferase FTSJ1 by PM2.5 promotes glycolysis and malignancy of NSCLC via facilitating PGK1 expression and translation

Fine particulate matter (PM2.5) exposure has been associated with increased incidence and mortality of lung cancer. However, the molecular mechanisms underlying PM2.5 carcinogenicity remain incompletely understood. Here, we identified that PM2.5 suppressed the expression of tRNA methyltransferase FTSJ1 and Am modification level of tRNA in vitro and in vivo. FTSJ1 downregulation enhanced glycolytic metabolism of non-small cell lung cancer (NSCLC) cells, as indicated by increased levels of lactate, pyruvate, and extracellular acidification rate (ECAR). Whereas treatment with glycolytic inhibitor 2-DG reversed this effect. In contrast, upregulation of FTSJ1 significantly suppressed glycolysis of NSCLC cells. Mechanistically, the silencing of FTSJ1 increased NSCLC cell proliferation and glycolysis through enhancing the expression and translation of PGK1. In human NSCLC tumor samples, FTSJ1 expression was negatively correlated with PGK1 expression level and the SUVmax value of PET/CT scan. In summary, our work reveals a previously unrecognized function of PM2.5-downregulated FTSJ1 on PGK1-mediated glycolysis in NSCLC, suggesting that targeted upregulation of FTSJ1 may represent a potential therapeutic strategy for NSCLC.

Impact of particulate matter and air pollution on ocular surface disease: A systematic review of preclinical and clinical evidence.

Exposure to particulate matter (PM) and air pollution has been implicated in the etiology of ocular surface diseases (OSD). The purpose of this systematic review is to evaluate and synthesize peer-reviewed literature on the impact of PM exposure on the ocular surface, integrating results from preclinical in vitro and in vivo studies with clinical findings to provide a comprehensive understanding of molecular mechanisms, physiological effects, clinical implications, and potential therapies to target acute and chronic PM-induced ocular toxicity. A systematic literature search was performed using PubMed and EMBASE over the period from 2009 to 2024 following the recommendations for the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) reporting guidelines. 102 studies were identified that met the inclusion/exclusion criteria. All studies were assessed for the risk of bias and qualitative data were analyzed. Preclinical studies using models of corneal and conjunctival cells found that exposure to PM and similar air pollutants resulted in apoptosis, primarily via inflammatory and oxidative stress pathways as well as allergic and immune responses. Animal models resulted in phenotypes reminiscent of that of dry eye disease, presenting with reduced tear volumes and ocular surface damage. These results were corroborated by clinical studies, which reported that patients commonly presented with symptoms of itching, burning, and irritation, and ocular surface signs correlated with a diagnosis of dry eye disease, conjunctivitis, and allergic eye disease. This systematic review provides a comprehensive summary of our current understanding of PM exposure on the ocular surface, highlighting the correlation between exposure to PM and ocular surface dysfunction.

Update in association between Lung Cancer and air pollution.

A significant portion of newly diagnosed lung cancer cases occur in populations exposed to air pollution. The World Health Organization has identified air pollution as a human carcinogen, prompting many countries to implement monitoring systems for ambient particulate matter (PM). PM consists of a complex mix of organic and inorganic particles, both solid and liquid, present in the air. Given the carcinogenic properties of PM and the prevalence of lung cancer in exposed populations, it is crucial to explore their connection and clinical implications to effectively prevent lung cancer in this group. This review examines the link between ambient PM and lung cancer. Epidemiological studies have shown a dose-response relationship between PM exposure and lung cancer risk. PM exposure leads to oxidative stress, disrupting the body's redox balance and causing DNA damage, a key factor in cancer development. Recent findings on the strong correlation between ambient PM and adenocarcinoma suggest that understanding the specific molecular and pathological background of pollution-related lung cancer is important. In addition to efforts to control emission sources at the international level, a more individualized approach is necessary to prevent PM-related lung cancer development.

Association of sarcopenia, ambient air pollution and cognitive function in a community-dwelling middle-aged and elderly Korean population: a community-based cohort study

ObjectivesTo investigate the association of sarcopenia, exposure to medium-term to long-term ambient particulate matter 2.5 µm and 10 µm (PM2.5 and PM10) pollution and cognitive function in a community-dwelling cohort...

Maternal exposure to fine particulate matter in the air and risk for fetal congenital heart defects: A case-control study

Prior research into the association between fine particulate matter (PM2.5) exposure and the risk for fetal congenital heart defect (CHD) has yielded inconclusive and conflicting results. More epidemiologic evidence from different regions is necessary. A case-control study was conducted with 360 CHD cases and 3600 healthy newborns. Both the cases and the controls were registered by the mothers in the Prenatal Health Care System during the first trimester and gave birth at hospitals in the Tongzhou District of Beijing between 2013 and 2018. Information on PM2.5 was obtained from satellite remote sensing monitoring data. We estimated average monthly PM2.5 exposure for participants from 3 months before the last menstrual period through 6 months of gestational period. A logistic regression model was used to estimate odd ratio (OR) (95 % confidence interval, CI) for PM2.5 exposure level and fetal risk for CHD. In our study, PM2.5 concentrations before pregnancy and in the first trimester were not associated with CHD risk. In the second trimester, 2nd high quartile PM2.5 group during the second month were associated with a lower CHD risk (adjusted OR(aOR)= 1.42, 95 % CI: 1.04–1.94) and highest quartile level group of PM2.5 exposure in the third month were associated with a reduced risk for fetal CHD (aOR=0.70, 95 % CI: 0.51–0.97). After Bonferroni’s α correction, no comparisons were statistically significant. In conclusion, no associations were found between PM2.5 exposure level and fetal risk for CHD in our study.

Respiratory Benefits of Multisetting Air Purification in Children

Particulate matter exposure has been linked to impaired respiratory health in children, but the respiratory benefits of air purification have not been fully elucidated. To assess the respiratory health outcomes among children exposed to multisetting air purification vs sham purification. This cluster randomized, double-blind, crossover trial was conducted among healthy school-aged children (10-12 years) in China from April to December 2021. Data were analyzed from December 2021 to July 2024. A multisetting (both in classrooms and bedrooms) air purification intervention compared with sham purification in a 2-stage intervention with more than 2 months (76 days) for each period and a washout period (88 days) to estimate the respiratory benefits of air purification. The primary outcomes were pulmonary function, airway inflammation markers, and metabolites in exhaled breath condensate (EBC) before and after the air purification intervention. Linear mixed-effects models were used to estimate the respiratory benefits of children related to air purification. Differential metabolites in EBC were identified using metabolomics analysis to explore their possible mediation roles. A total of 79 children (38 male [48%]; mean [SD] age, 10.3 [0.5] years) were included in the statistical analyses. During the study period, the mean (SD) concentration of outdoor fine particulate matter (PM2.5) at the school site was 32.53 (24.06) μg/m3. The time-weighted personal PM2.5 concentration decreased by 45.14% during the true air purification period (mean [SD], 21.49 [8.72] μg/m3) compared with the sham air purification period (mean [SD], 39.17 [14.25] μg/m3). Air purification improved forced expiratory volume in 1 second by 8.04% (95% CI, 2.15%-13.93%), peak expiratory flow by 16.52% (95% CI, 2.76%-30.28%), forced vital capacity (FVC) by 5.73% (95% CI, 0.48%-10.98%), forced expiratory flow at 25% to 75% of FVC by 17.22% (95% CI, 3.78%-30.67%), maximal expiratory flow at 75% of FVC by 14.60% (95% CI, 0.35%-28.85%), maximal expiratory flow at 50% of FVC by 17.86% (95% CI, 3.65%-32.06%), and maximal expiratory flow at 25% of FVC by 18.22% (95% CI, 1.73%-34.70%). Fractional exhaled nitric oxide in the true air purification group decreased by 22.38% (95% CI, 2.27%-42.48%). Several metabolites in EBC (eg, L-tyrosine and β-alanine) were identified to mediate the effect of air purification on respiratory health. This randomized clinical trial provides robust and holistic evidence that indoor air purification notably improved pulmonary health in children, highlighting the importance of intensified indoor air purification in regions with high air pollution levels. ClinicalTrials.gov Identifier: NCT04835337.

Global Trends and Hotspots in the Research of the Effects of PM2.5 on Asthma: A Bibliometric and Visualized Analysis

BackgroundFine particulate matter (PM2.5) has been identified as a significant environmental and public health challenge, particularly due to its association with respiratory diseases like asthma. With the global rise in urbanization and industrialization, PM2.5-related asthma research has grown substantially over the past two decades. This study aims to provide a comprehensive bibliometric analysis to map global research trends, highlight key contributors, and identify emerging hotspots in the relationship between PM2.5 and asthma.MethodsWe performed a bibliometric analysis using the Web of Science Core Collection database, covering research from January 2004 to September 2024. The selected studies were analyzed using CiteSpace and VOSviewer to assess publication trends, global collaborations, and research hotspots through visualized networks and co-occurrence analyses.ResultsA total of 2035 publications were identified, demonstrating a steady increase in research output over the past two decades. The United States and China emerged as dominant contributors, frequently collaborating with countries like Canada, Australia, and South Korea. Key research areas focused on air quality, particulate matter exposure, and asthma exacerbation, with an increasing emphasis on indoor air pollution and long-term exposure risks. Institutional collaborations were led by prominent universities such as the University of California System and Harvard University. Additionally, research on vulnerable populations, particularly children, and the impact of early-life exposure to PM2.5 has gained attention in recent years.ConclusionsThe global research landscape on PM2.5 and asthma has expanded significantly, with growing attention to interdisciplinary approaches that combine environmental science and public health. Future studies should focus on the global burden of air pollution, particularly in low- and middle-income countries, and address the long-term health impacts of PM2.5 exposure, especially in vulnerable populations.