[Modification of allergic dermatitis on the associations between early-life exposure to size-specific particulate matter and childhood allergic rhinitis].

To evaluate the modification of allergic dermatitis on the association between PM exposure and allergic rhinitis in preschool children. This cross-sectional study was based on a questionnaire conducted between June 2019 and June 2020 to caregivers of children aged 3 to 6 years in the kindergartens of 7 Chinese cities to collect information on allergic rhinitis and allergic dermatitis. A mature machine learning-based space-time extremely randomized trees model was applied to estimate early-life, prenatal, and first-year exposure of PM1, PM2.5 and PM10 at 1 km×1 km resolution. A combination of multilevel logistic regression and restricted cubic spline functions was used to quantitatively assess whether allergic dermatitis modifies the associations between size-specific PM exposure and the risk of childhood allergic rhinitis. The results showed that out of 28 408 children, 14 803 (52.1%) were boys and 13 605 (47.9%) were girls; the age of children ranged from 3.1 to 6.8 years, with a mean age of (4.9±0.9) years, of which 3 586 (12.6%) were diagnosed with allergic rhinitis. Among all children, 17 832 (62.8%) were breastfed for more than 6 months and 769 (2.7%) had parental history of atopy. A total of 21 548 children (75.9%) had a mother with an educational level of university or above and 7 338 (29.6%) had passive household cigarette smoke exposure. The adjusted ORs for childhood allergic rhinitis among the children with allergic dermatitis as per interquartile range (IQR) increase in early-life PM1(9.8 µg/m3), PM2.5 (14.9 µg/m3) and PM10 (37.7 µg/m3) were significantly higher than the corresponding ORs among the children without allergic dermatitis [OR: 1.45, 95%CI (1.26, 1.66) vs. 1.33, 95%CI (1.20, 1.47), for PM1; OR: 1.38, 95%CI (1.23, 1.56) vs. 1.32, 95%CI (1.21, 1.45), for PM2.5; OR: 1.56, 95%CI (1.31, 1.86) vs. 1.46, 95%CI (1.28, 1.67), for PM10]. The interactions between allergic dermatitis and size-specific PM exposure on childhood allergic rhinitis were statistically significant (Z value=19.4, all P for interaction<0.001). The similar patterns were observed for both prenatal and first-year size-specific PM exposure and the results of the dose-response relationship were consistent with those of the logistic regression. In conclusion, allergic dermatitis, as an important part of the allergic disease progression, may modify the association between ambient PM exposure and the risk of childhood allergic rhinitis. Children with allergic dermatitis should pay more attention to minimize outdoor air pollutants exposure to prevent the further progression of allergic diseases.

Bioavailable fractions of heavy metals in the road dust during infrastructure construction at urban Coimbatore and its potential health implications, India.

Over the past two decades the Global South is witnessing unprecedented economic transformation and Asian Cities in particular have a remarkable upsurge. Coimbatore, an industrial city in Southern India with an estimated population of 2 million (in 2022) is witnessing a rapid transition in terms of infrastructure development. In this context, the present study attempts to assess the particulate matter (PM10 and PM2.5) emissions at road network construction sites and the heavy metal fractionation in the road dust/sediment samples with a core focus to quantify the bioavailable fraction of metals (Fe, Cu, Cr, Cd, Pb and Ni) and its source apportionment in the road side dust/sediment samples. About 60 composite road dust/sediment samples were collected for heavy metal fractionation analysis in the six arterial roads that undergo core developments like construction of road over bridges, additional road incorporation and street expansions. PM monitoring revealed that 24 h average PM2.5 (47 µg/m3) and PM10 (69 µg/m3) concentrations at many construction sites exceeded 24 h average recommended by WHO guidelines [PM2.5 (15 µg/m3) and PM10 (45 µg/m3), respectively]. The bioavailable fractions of Fe, Cu, Cr and Cd are notably higher in the roadside sediment samples at road construction sites. Health Risk assessment, such as carcinogenic risks (Children-4.41 × 10-2, Adult-3.598 × 10-6) and non-carcinogenic risks, inferred substantial risks at high intensity construction sites with statistical analyses, including PCA and cluster analysis, indicating considerable anthropogenic influences in the heavy metal fractions.

Health impacts of lifestyle and ambient air pollution patterns on all-cause mortality: a UK Biobank cohort study.

BACKGROUND: Extensive evidence indicates that both lifestyle factors and air pollution are strongly associated with all-cause mortality. However, little studies in this field have integrated these two factors in order to examine their relationship with mortality and explore potential interactions. METHODS: A cohort of 271,075 participants from the UK Biobank underwent analysis. Lifestyles in terms of five modifiable factors, namely smoking, alcohol consumption, physical activity, diet, and sleep quality, were classified as unhealthy (0-1 score), general (2-3 score), and healthy (4-5 score). Air pollution, including particle matter with a diameter ≤ 2.5 µm (PM2.5), particulate matter with a diameter ≤ 10 µm (PM10), particulate matter with a diameter 2.5-10 µm (PM2.5-10), nitrogen dioxide (NO2), and nitrogen oxides (NOx), was divided into three levels (high, moderate, and low) using Latent Profile Analysis (LPA). Cox proportional hazard regression analysis was performed to examine the links between lifestyle, air pollution, and all-cause mortality before and after adjustment for potential confounders. Restricted cubic spline curves featuring three knots were incorporated to determine nonlinear relationships. The robustness of the findings was assessed via subgroup and sensitivity analyses. RESULTS: With unhealthy lifestyles have a significantly enhanced risk of death compared to people with general lifestyles (HR = 1.315, 95% CI, 1.277-1.355), while people with healthy lifestyles have a significantly lower risk of death (HR = 0.821, 95% CI, 0.785-0.858). Notably, the difference in risk between moderate air pollution and mortality risk remained insignificant (HR = 0.993, 95% CI, 0.945-1.044). High air pollution, on the other hand, was independently linked to increased mortality risk as compared to low air pollution (HR = 1.162, 95% CI, 1.124-1.201). The relationship between NOx, PM10, and PM2.5-10 and all-cause mortality was found to be nonlinear (p for nonlinearity < 0.05). Furthermore, no significant interaction was identified between lifestyle and air pollution with respect to all-cause mortality. CONCLUSIONS: Exposure to ambient air pollution elevated the likelihood of mortality from any cause, which was impacted by individual lifestyles. To alleviate this hazard, it is crucial for authorities to escalate environmental interventions, while individuals should proactively embrace and sustain healthy lifestyles.

Vertical transport velocity of fine particles of aluminum smelter emissions.

In this study, the average values of vertical velocity of particles emitted from an aluminum smelter in the surface layer of the atmosphere were estimated using a semi-empirical method. The method is based on regression analysis of the horizontal profile of pollutants measured along the selected direction using moss bioindicators. The selection of epiphytic mosses Sanionia uncinata was carried out in 2013 in the zone of influence of a metallurgical industry enterprise in the city of Kandalaksha, Murmansk region. The concentrations of As, Si, Ni, Zn, Ti, Cd, Na, Pb, Co, K, Ba, Ca, Mg, Mn, Sr, Fe, Al, V, Cr, Cu were determined using atomic emission spectrometry. The conducted assessments showed that the average particle velocity toward the Earth's surface, when considering large spatial and temporal scales, is tens of times higher than gravitational settling velocities.

Socioeconomic and sociodemographic correlations to COVID-19 variability in the United States in 2020.

The COVID-19 pandemic provided an additional spotlight on the longstanding socioeconomic/health impacts of redlining and has added to the myriad of environmental justice issues, which has caused significant loss of life, health, and productive work. The Centers for Disease Control and Prevention (CDC) reports that a person with any selected underlying health conditions is more likely to experience severe COVID-19 symptoms, with more than 81% of COVID-19-related deaths among people aged 65 years and older. The effects of COVID-19 are not homogeneous across populations, varying by socioeconomic status, PM2.5 exposure, and geographic location. This variability is supported by analysis of existing data as a function of the number of cases and deaths per capita/1,00,000 persons. We investigate the degree of correlation between these parameters, excluding health conditions and age. We found that socioeconomic variables alone contribute to ~40% of COVID-19 variability, while socioeconomic parameters, combined with political affiliation, geographic location, and PM2.5 exposure levels, can explain ~60% of COVID-19 variability per capita when using an OLS regression model; socioeconomic factors contribute ~28% to COVID-19-related deaths. Using spatial coordinates in a Random Forest (RF) regressor model significantly improves prediction accuracy by ~120%. Data visualization products reinforce the fact that the number of COVID-19 deaths represents 1% of COVID-19 cases in the US and globally. A larger number of democratic voters, larger per-capita income, and age >65 years is negatively correlated (associated with a decrease) with the number of COVID cases per capita. Several distinct regions of negative and positive correlations are apparent, which are dominated by two major regions of anticorrelation: (1) the West Coast, which exhibits high PM2.5 concentrations and fewer COVID-19 cases; and (2) the middle portion of the US, showing mostly high number of COVID-19 cases and low PM2.5 concentrations. This paper underscores the importance of exercising caution and prudence when making definitive causal statements about the contribution of air quality constituents (such as PM2.5) and socioeconomic factors to COVID-19 mortality rates. It also highlights the importance of implementing better health/lifestyle practices and examines the impact of COVID-19 on vulnerable populations, particularly regarding preexisting health conditions and age. Although PM2.5 contributes comparable deaths (~7M) per year, globally as smoking cigarettes (~8.5M), quantifying any causal contribution toward COVID-19 is non-trivial, given the primary causes of COVID-19 death and confounding factors. This becomes more complicated as air pollution was reduced significantly during the lockdowns, especially during 2020. This statistical analysis provides a modular framework, that can be further expanded with the context of multilevel analysis (MLA). This study highlights the need to address socioeconomic and environmental disparities to better prepare for future pandemics. By understanding how factors such as socioeconomic status, political affiliation, geographic location, and PM2.5 exposure contribute to the variability in COVID-19 outcomes, policymakers and public health officials can develop targeted strategies to protect vulnerable populations. Implementing improved health and lifestyle practices and mitigating environmental hazards will be essential in reducing the impact of future public health crises on marginalized communities. These insights can guide the development of more resilient and equitable health systems capable of responding effectively to similar future scenarios.

Effects and mechanisms of using "clean" smoke particles in the smoking process on the formation of ß-carboline heterocyclic amines (ß-CHAs) in smoked meat patties.

ß-Carboline heterocyclic amines (ß-CHAs), known for their synergistic neurotoxic and carcinogenic effects, are predominantly produced by humans through cigarette smoke and food and are found particularly in meats cooked at high temperatures. Few studies have explored the differences in the mechanisms of accumulation of ß-CHAs in smoked meat and meat processed at high temperatures. In this research, the concentration of ß-CHAs in smoked meats prepared using a variety of wood materials was measured using LCMS/MS. Additionally, key volatile organic compound markers associated with ß-CHAs accumulation in smoke were identified through GCMS and multivariate statistical analysis and subsequently confirmed in a chemical simulation system. Three types of strainers, each with a distinct aperture size, were used to assess the efficacy of particle filtration in reducing ß-CHAs levels in smoked meat. The findings indicated that smoke exposure indeed increases the ß-CHAs content of meat. However, only the strainer capable of filtering PM2.5-sized particles reduced the amount of ß-CHAs present compared to the control group. In contrast, strainers with larger pore sizes facilitated excessive accumulation of ß-CHAs. The presence of aldehydes such as 1 H-pyrrole-2-carboxaldehyde, 5-methylfurfural, benzaldehyde, furfural, and nonanal exhibited a positive correlation with the accumulation of ß-CHAs. Conversely, phenolic compounds, including 2-methoxy-4-vinylphenol, 2-methoxy-5-methylphenol, p-cresol, phenol, 2-methoxy-4-(1-propenyl)-, (Z)-, phenol, 3-ethyl-, and phenol, 4-ethyl-2-methoxy-, showed a negative correlation. Thus, filters made from chelated carbonyl trap materials both chemically and physically disrupt the buildup of ß-CHAs in smoked meats. The use of this approach will not only improve the quality of these products but will also contribute to decreasing the amount of inhalation pollutants released into the environment.

Airborne Aluminum as an Underestimated Source of Human Exposure: Quantification of Aluminum in 24 Human Tissue Types Reveals High Aluminum Concentrations in Lung and Hilar Lymph Node Tissues.

Aluminum (Al) is the most abundant metal in the earth's crust, and humans are exposed to Al through sources like food, cosmetics, and medication. So far, no comprehensive data on the Al distribution between and within human tissues were reported. We measured Al concentrations in 24 different tissue types of 8 autopsied patients using ICP-MS/MS (inductively coupled plasma-tandem mass spectrometry) under cleanroom conditions and found surprisingly high concentrations in both the upper and inferior lobes of the lung and hilar lymph nodes. Al/Si ratios in lung and hilar lymph node samples of 12 additional patients were similar to the ratios reported in urban fine dust. Histological analyses using lumogallion staining showed Al in lung erythrocytes and macrophages, indicating the uptake of airborne Al in the bloodstream. Furthermore, Al was continuously found in PM2.5 and PM10 fine dust particles over 7 years in Upper Austria, Austria. According to our findings, air pollution needs to be reconsidered as a major Al source for humans and the environment.

Air pollution aggravates renal ischaemia-reperfusion-induced acute kidney injury.

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 (PM2.5) and a decline in renal function. PM2.5 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 PM2.5 toxicity and is a known risk factor for CKD. The objective of this study was to investigate the impact of PM2.5 exposure on IRI-induced AKI. Through a unique environmentally controlled setup, mice were exposed to urban PM2.5 or filtered air for 12 weeks before IRI followed by euthanasia 48 h after surgery. Animals exposed to PM2.5 and IRI exhibited reduced glomerular filtration, impaired urine concentration ability, and significant tubular damage. Further, PM2.5 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 PM2.5 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 PM2.5 in sensitising proximal tubular epithelial cells to IRI-induced damage, suggesting a plausible association between PM2.5 exposure and heightened susceptibility to CKD in individuals experiencing AKI. Strategies aimed at reducing PM2.5 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.

Quantitative evaluation of anthropogenic sources and health risks of rare earth elements in airborne particulate matter.

Rare earth elements (REEs) have emerged as contaminants in airborne particulate matter (PM); however, their anthropogenic sources remain poorly quantified, and associated health risks are unknown. This study investigates the REE distribution across eight sizes of airborne PM during July and December in Qingdao, a major Chinese port city. Our results reveal a single coarse-mode distribution with REE concentrations. In contrast, fine PM (size: 0.43-2.1 µm) exhibits notable enrichment of La and Ce compared to Al and other REEs. This study traces La and Ce enrichment to fluid catalytic cracking catalysts (FCCC)-related sources, including refinery and ship emissions, by comparing the REE fractionation in samples with potential sources. We quantify the contributions from FCCC-related sources to La (July: 33.6 % ± 3.2 %, Dec.: 46.4 % ± 5.2 %) and Ce (July: 16.5 % ± 14.3 %, Dec.: 30.3 % ± 12.2 %) by comparing measured concentrations with predictions derived from neighboring REEs, a method previously used exclusively in aquatic systems. For the first time, supply ratios of refinery and ship to FCCC-related La are calculated using a two-component mixing model based on the [La]FCCC/[V]anth, revealing the dominance of refinery emissions (July: 97.3 % ± 0.6 %, Dec.: 99.6 % ± 0.1 %). Furthermore, a global review of La and Ce anomalies that integrates published REE data with our findings reveals a widespread distribution of positive anomalies. The significantly positive correlation between La and Ce anomalies underscores FCCC-related emissions as a global source in fine PM, contributing 0-92 % (mean: 35 % ± 33 %) for La and 0-72 % (mean: 21 % ± 24 %) for Ce. Although the non-carcinogenic health risks of Ce are generally low globally, concerns should be raised in areas near source emissions, where Ce health risks sharply increased along with its concentrations. There is urgently need to establish a threshold value for La, owing to its global enrichment. This study provides novel insights into the sources and health implications of REEs in airborne PM.

Causal association between particulate matter 2.5 and Alzheimer's disease: a Mendelian randomization study.

Background: Although epidemiological evidence implies a link between exposure to particulate matter (PM) and Alzheimer's disease (AD), establishing causality remains a complex endeavor. In the present study, we used Mendelian randomization (MR) as a robust analytical approach to explore the potential causal relationship between PM exposure and AD risk. We also explored the potential associations between PM exposure and other neurodegenerative diseases. Methods: Drawing on extensive genome-wide association studies related to PM exposure, we identified the instrumental variables linked to individual susceptibility to PM. Using summary statistics from five distinct neurodegenerative diseases, we conducted two-sample MR analyses to gauge the causal impact of PM on the risk of developing these diseases. Sensitivity analyses were undertaken to evaluate the robustness of our findings. Additionally, we executed multivariable MR (MVMR) to validate the significant causal associations identified in the two-sample MR analyses, by adjusting for potential confounding risk factors. Results: Our MR analysis identified a notable association between genetically predicted PM2.5 (PM with a diameter of 2.5 µm or less) exposure and an elevated risk of AD (odds ratio, 2.160; 95% confidence interval, 1.481 to 3.149; p < 0.001). A sensitivity analysis supported the robustness of the observed association, thus alleviating concerns related to pleiotropy. No discernible causal relationship was identified between PM and any other neurodegenerative diseases. MVMR analyses-adjusting for smoking, alcohol use, education, stroke, hearing loss, depression, and hypertension-confirmed a persistent causal relationship between PM2.5 and AD. Sensitivity analyses, including MR-Egger and weighted median analyses, also supported this causal association. Conclusion: The present MR study provides evidence to support a plausible causal connection between PM2.5 exposure and AD. The results emphasize the importance of contemplating air quality interventions as a public health strategy for reducing AD risk.

Long-term exposure to particulate matter and all-cause and cause-specific mortality in an analysis of multiple Asian cohorts.

BACKGROUND: Exposure to ambient air pollution is associated with a significant number of deaths. Much of the evidence associating air pollution with adverse effects is from North American and Europe, partially due to incomplete data in other regions limiting location specific examinations. The aim of the current paper is to leverage satellite derived air quality data to examine the relationship between ambient particulate matter and all-cause and cause-specific mortality in Asia. METHODS: Six cohorts from the Asia Cohort Consortium provided residential information for participants, recruited between 1991 and 2008, across six countries (Bangladesh, India, Iran, Japan, South Korea, and Taiwan). Ambient particulate material (PM2·5) levels for the year of enrolment (or 1998 if enrolled earlier) were assigned utilizing satellite and sensor-based maps. Cox proportional models were used to examine the association between ambient air pollution and all-cause and cause-specific mortality (all cancer, lung cancer, cardiovascular and lung disease). Models were additionally adjusted for urbanicity (representing urban and built characteristics) and stratified by smoking status in secondary analyses. Country-specific findings were pooled via random-effects meta-analysis. FINDINGS: More than 300,000 participants across six cohorts were included, representing more than 4-million-person years. A positive relationship was observed between a 5 µg/m (Dockery et al., 1993) increase in PM2·5 and cardiovascular mortality (HR: 1·06, 95 % CI: 0.99, 1·13). The additional adjustment for urbanicity resulted in increased associations between PM2.5 and mortality outcomes, including all-cause mortality (1·04, 95 % CI: 0·97, 1·11). Results were generally similar regardless of whether one was a current, never, or ex-smoker. INTERPRETATION: Using satellite and remote sensing technology we showed that associations between PM2.5 and all-cause and cause-specific Hazard Ratios estimated are similar to those reported for U.S. and European cohorts. FUNDING: This project was supported by the Health Effects Institute. Grant number #4963-RFA/18-5. Specific funding support for individual cohorts is described in the Acknowledgements.

Influence of the atmospheric environment on spatial variation of lung cancer incidence in China.

Conducting this research contributes to a deeper understanding of the correlation between atmospheric environmental quality and lung cancer incidence, and provides the scientific basis for formulating effective environmental protection and lung cancer prevention and control strategies. Lung cancer incidence in China has strong spatial variation. However, few studies have systematically revealed the characteristics of the spatial variation in lung cancer incidence, and have explained the causes of this spatial variation in lung cancer incidence from the perspectives of multiple components of the atmospheric environment to explain this spatial variation in lung cancer incidence. To address research limitations, we first analyze the spatial variation and spatial correlation characteristics of lung cancer incidence in China. Then, we build a spatial regression model using GeoDa software with lung cancer incidence as the dependent variable, five atmospheric environment factors-particulate matter 2.5 (PM2.5) concentration, temperature, atmospheric pressure, and elevation as explanatory variables, and four socio-economic characteristics as control variables to systematically analyze the influence and intensity of these factors on lung cancer incidence. The results show that lung cancer incidence in China has apparent changes in geographical and spatial unevenness, and spatial autocorrelation characteristics. In China, the lung cancer incidence is relatively high in Northeast China, while some areas of high lung cancer incidence still exist in Central China, Southwest China and South China, although the overall lung cancer incidence is relatively low. The atmospheric environment significantly affects lung cancer incidence. Different elements of the atmospheric environment vary in the direction and extent of their influence on the development of lung cancer. A 1% increase in PM2.5 concentration is associated with a level of 0.002975 increase in lung cancer incidence. Atmospheric pressure positively affects lung cancer incidence, and an increase in atmospheric pressure by 1% increases lung cancer incidence by a level of 0.026061. Conversely, a 1% increase in temperature is linked to a level of 0.006443 decreases in lung cancer incidence, and a negative correlation exists between elevation and lung cancer incidence, where an increase in elevation by 1% correlates with a decrease in lung cancer incidence by a level of 0.000934. The core influencing factors of lung cancer incidence in the seven geographical divisions of China exhibit variations. This study facilitates our understanding of the spatial variation characteristics of lung cancer incidence in China on a finer scale, while also offering a more diverse perspective on the impact of the atmospheric environment on lung cancer incidence.

Quantifying air quality co-benefits to industrial decarbonization: the local Air Emissions Tracking Atlas.

Introduction: Many decarbonization technologies have the added co-benefit of reducing short-lived climate pollutants, such as particulate matter (PM), nitrogen oxides (NOx), and sulfur dioxide (SO2), creating a unique opportunity for identifying strategies that promote both climate change solutions and opportunities for air quality improvement. However, stakeholders and decision-makers may struggle to quantify how these co-benefits will impact public health for the communities most affected by industrial air pollution. Methods: To address this problem, the LOCal Air Emissions Tracking Atlas (LOCAETA) fills a data availability and analysis gap by providing estimated air quality benefits from industrial decarbonization options, such as carbon capture and storage (CCS). These co-benefits are calculated using an algorithm that connects disparate datasets that separately report greenhouse gas emissions and other pollutants at U.S. industrial facilities. Results: Version 1.0 of LOCAETA displays the estimated primary PM2.5 emission reduction co-benefits from additional pretreatment equipment for CCS on industrial and power facilities across the state of Louisiana, as well as the potential for VOC and NH3 generation. The emission reductions are presented in the tool alongside facility pollutant emissions information and relevant air quality, environmental, demographic, and public health datasets, such as air toxics cancer risk, satellite and in situ pollutant measurements, and population vulnerability metrics. Discussion: LOCAETA enables regulators, policymakers, environmental justice communities, and industrial and commercial users to compare and contrast quantifiable public health benefits due to air quality impacts from various climate change mitigation strategies using a free and publicly-available tool. Additional pollutant reductions can be calculated using the same methodology and will be available in future versions of the tool.

Particulate matter facilitates amphiregulin-dependent lung cancer proliferation through glutamine metabolism.

Although many cohort studies have reported that long-term exposure to particulate matter (PM) causes lung cancer, the molecular mechanisms underlying the PM-induced increases in lung cancer progression remain unclear. We applied the lung cancer cell line A549 (Parental; A549.Par) to PM for an extended period to establish a mimic PM-exposed lung cancer cell line, A549.PM. Our results indicate that A549.PM exhibits higher cell growth and proliferation abilities compared to A549.Par cells in vitro and in vivo. The RNA sequencing analysis found amphiregulin (AREG) plays a critical role in PM-induced cell proliferation. We observed that PM increases AREG-dependent lung cancer proliferation through glutamine metabolism. In addition, the EGFR/PI3K/AKT/mTOR signaling pathway is involved in PM-induced solute carrier family A1 member 5 (SLC1A5) expression and glutamine metabolism. Our findings offer important insights into how lung cancer proliferation develops upon exposure to PM.

Characterization of airborne endotoxin in personal exposure to fine particulate matter (PM2.5) and bioreactivity for elderly residents in Hong Kong.

The heavy metals and bioreactivity properties of endotoxin in personal exposure to fine particulate matter (PM2.5) were characterized in the analysis. The average personal exposure concentrations to PM2.5 were ranged from 6.8 to 96.6 µg/m3. The mean personal PM2.5 concentrations in spring, summer, autumn, and winter were 32.1±15.8, 22.4±11.8, 35.3±11.9, and 50.2±19.9 µg/m3, respectively. There were 85 % of study targets exceeded the World Health Organization (WHO) PM2.5 threshold (24 hours). The mean endotoxin concentrations ranged from 1.086 ± 0.384-1.912 ± 0.419 EU/m3, with a geometric mean (GM) varied from 1.034 to 1.869. The concentration of iron (Fe) (0.008-1.16 µg/m3) was one of the most abundant transition metals in the samples that could affect endotoxin toxicity under Toll-Like Receptor 4 (TLR4) stimulation. In summer, the interleukin 6 (IL-6) levels showed statistically significant differences compared to other seasons. Spearman correlation analysis showed endotoxin concentrations were positively correlated with chromium (Cr) and nickel (Ni), implying possible roles as nutrients and further transport via adhering to the surface of fine inorganic particles. Mixed-effects model analysis demonstrated that Tumor necrosis factor-α (TNF-α) production was positively associated with endotoxin concentration and Cr as a combined exposure factor. The Cr contained the highest combined effect (0.205-0.262), suggesting that Cr can potentially exacerbate the effect of endotoxin on inflammation and oxidative stress. The findings will be useful for practical policies for mitigating air pollution to protect the public health of the citizens.

How long-term PM exposure may affect all-site cancer mortality: Evidence from a large cohort in southern China.

BACKGROUND: Evidence of a potential causal link between long-term exposure to particulate matter (PM) and all-site cancer mortality from large population cohorts remained limited and suffered from residual confounding issues with traditional statistical methods. AIMS: We aimed to examine the potential causal relationship between long-term PM exposure and all-site cancer mortality in South China using causal inference methods. METHODS: We used a cohort in southern China that recruited 580,757 participants from 2009 through 2015 and tracked until 2020. Annual averages of PM1, PM2.5, and PM10 concentrations were generated with validated spatiotemporal models. We employed a causal inference approach, the Marginal Structural Cox model, based on observational data to evaluate the association between long-term exposure to PM and all-site cancer mortality. RESULTS: With an increase of 1 µg/m³ in PM1, PM2.5, and PM10, the hazard ratios (HRs) and 95% confidence interval (CI) for all-site cancer were 1.033 (95% CI: 1.025-1.041), 1.032 (95% CI: 1.027-1.038), and 1.020 (95% CI: 1.016-1.025), respectively. The HRs (95% CI) for digestive system and respiratory system cancer mortality associated with each 1 µg/m³ increase in PM1 were 1.022 (1.009-1.035) and 1.053 (1.038-1.068), respectively. In addition, inactive participants, who never smoked, or who lived in areas of low surrounding greenness were more susceptible to the effects of PM exposure, the HRs (95% CI) for all-site cancer mortality were 1.042 (1.031-1.053), 1.041 (1.032-1.050), and 1.0473 (1.025-1.070) for every 1 µg/m³ increase in PM1, respectively. The effect of PM1 tended to be more pronounced in the low-exposure group than in the general population, and multiple sensitivity analyses confirmed the robustness of the results. CONCLUSION: This study provided evidence that long-term exposure to PM may elevate the risk of all-site cancer mortality, emphasizing the potential health benefits of improving air quality for cancer prevention.

Ambient air pollution and urological cancer risk: A systematic review and meta-analysis of epidemiological evidence.

Exposure to ambient air pollution has significant adverse health effects; however, whether air pollution is associated with urological cancer is largely unknown. We conduct a systematic review and meta-analysis with epidemiological studies, showing that a 5 µg/m3 increase in PM2.5 exposure is associated with a 6%, 7%, and 9%, increased risk of overall urological, bladder, and kidney cancer, respectively; and a 10 µg/m3 increase in NO2 is linked to a 3%, 4%, and 4% higher risk of overall urological, bladder, and prostate cancer, respectively. Were these associations to reflect causal relationships, lowering PM2.5 levels to 5.8 µg/m3 could reduce the age-standardized rate of urological cancer by 1.5 ~ 27/100,000 across the 15 countries with the highest PM2.5 level from the top 30 countries with the highest urological cancer burden. Implementing global health policies that can improve air quality could potentially reduce the risk of urologic cancer and alleviate its burden.

Occurrence of organic ultraviolet absorbers in the particle and gas samples from plastic greenhouses: Human inhalation intake risk assessment.

The environmental pollution of organic ultraviolet absorbers (UVAs) has attracted global attention. However, the distribution, sources and risk assessment of UVAs in air from plastic greenhouses are rarely reported. This study was the first to investigate the concentrations of ten UVAs in the air samples from plastic greenhouses. The total concentrations of ten UVAs (∑10UVAs) in the air samples ranged from 5.7 × 103 ng/m3 to 6.3 × 103 ng/m3 (median 5.7 × 103 ng/m3) in greenhouses covered with biodegradable mulch film, 288.2 ng/m3 to 376.4 ng/m3 (median 333.9 ng/m3) in greenhouses covered with PE mulch film, and 97.9 ng/m3 to 142.6 ng/m3 (median 114.9 ng/m3) in greenhouses covered without mulch film. The concentrations of ten UVAs in 65 commercial agricultural films were simultaneously analyzed. Additionally, the potential health risks for greenhouse workers exposed to UVAs were estimated. And the migration simulations showed that the health risk in greenhouses may be higher even if only one UVA is added to the biodegradable mulch film. Therefore, the exposure risk of UVAs in plastic greenhouses needs to be highly prioritized.

Residues of atrazine and diuron in rice straw, soils, and air post herbicide-contaminated straw biomass burning.

This study investigates the environmental impact of burning herbicide-contaminated biomass, focusing on atrazine (ATZ) and diuron (DIU) sprayed on rice straw prior to burning. Samples of soil, biomass residues, total suspended particulate (TSP), particulate matter with an aerodynamic diameter ≤ 10 µm (PM10), and aerosols were collected and analyzed. Soil analysis before and after burning contaminated biomass showed significant changes, with 2,4-dichlorophenoxyacetic acid (2,4-D) initially constituting 79.2% and decreasing by 3.3 times post-burning. Atrazine-desethyl, sebuthylazine, and terbuthylazine were detected post-burning. In raw rice straw biomass, terbuthylazine dominated at 80.0%, but burning ATZ-contaminated biomass led to the detection of atrazine-desethyl and notable increases in sebuthylazine and terbuthylazine. Conversely, burning DIU-contaminated biomass resulted in a shift to 2,4-D dominance. Analysis of atmospheric components showed changes in TSP, PM10, and aerosol samples. Linuron in ambient TSP decreased by 1.6 times after burning ATZ-contaminated biomass, while atrazine increased by 2.9 times. Carcinogenic polycyclic aromatic hydrocarbons (PAHs), including benzo[a]anthracene (BaA), benzo[a]pyrene (BaP), and benzo[b]fluoranthene (BbF), increased by approximately 9.9 to 13.9 times after burning ATZ-contaminated biomass. In PM10, BaA and BaP concentrations increased by approximately 11.4 and 19.0 times, respectively, after burning ATZ-contaminated biomass. This study sheds light on the environmental risks posed by burning herbicide-contaminated biomass, emphasizing the need for sustainable agricultural practices and effective waste management. The findings underscore the importance of regulatory measures to mitigate environmental contamination and protect human health.

Air pollution and survival in patients with malignant mesothelioma and asbestos-related lung cancer: a follow-up study of 1591 patients in South Korea.

BACKGROUND: Despite significant advancements in treatments such as surgery, radiotherapy, and chemotherapy, the survival rate for patients with asbestos-related cancers remains low. Numerous studies have provided evidence suggesting that air pollution induces oxidative stress and inflammation, affecting acute respiratory diseases, lung cancer, and overall mortality. However, because of the high case fatality rate, there is limited knowledge regarding the effects of air pollution exposures on survival following a diagnosis of asbestos-related cancers. This study aimed to determine the effect of air pollution on the survival of patients with malignant mesothelioma and asbestos-related lung cancer. METHODS: We followed up with 593 patients with malignant mesothelioma and 998 patients with lung cancer identified as asbestos victims between 2009 and 2022. Data on five air pollutants-sulfur dioxide, carbon monoxide, nitrogen dioxide, fine particulate matter with a diameter < 10 µm, and fine particulate matter with a diameter < 2.5 µm-were obtained from nationwide atmospheric monitoring stations. Cox proportional hazard models were used to estimate the association of cumulative air pollutant exposure with patient mortality, while adjusting for potential confounders. Quantile-based g-computation was used to assess the combined effect of the air pollutant mixture on mortality. RESULTS: The 1-, 3-, and 5-year survival rates for both cancer types decreased with increasing exposure to all air pollutants. The estimated hazard ratios rose significantly with a 1-standard deviation increase in each pollutant exposure level. A quartile increase in the pollutant mixture was associated with a 1.99-fold increase in the risk of malignant mesothelioma-related mortality (95% confidence interval: 1.62, 2.44). For lung cancer, a quartile increase in the pollutant mixture triggered a 1.87-fold increase in the mortality risk (95% confidence interval: 1.53, 2.30). CONCLUSION: These findings support the hypothesis that air pollution exposure after an asbestos-related cancer diagnosis can negatively affect patient survival.