Association between air pollution and skin cutaneous melanoma: A Mendelian randomization study.

There has been a consistent and notable increase in the global prevalence of skin cutaneous melanoma (SKCM). Although genetic factors are closely associated with the occurrence and development of melanoma, the potential influence of environmental factors cannot be overlooked. The existing literature lacks a definitive consensus on the correlation between air pollution and the incidence rate of SKCM. This study seeks to investigate the causal relationship between air pollution, specifically focusing on particulate matter (PM) 2.5, PM2.5-10, PM10, and nitrogen oxides, and the risk of SKCM. A 2-sample Mendelian randomization (MR) method was applied, utilizing extensive publicly accessible genome-wide association studies summary datasets within European populations. The primary analytical method employed was the inverse variance weighted method. Supplementary methods, including the weighted median model, MR-Egger, simple model, and weighted model, were chosen to ensure robust analysis. Heterogeneity assessment was conducted using Cochran's Q test. To identify potential pleiotropy, both MR-Egger regression and the MR-PRESSO global test were employed. Additionally, a sensitivity analysis was performed using the leave-one-out method. The analysis revealed no statistically significant association between air pollution and SKCM risk, with specific findings as follows: PM2.5 (P = .485), PM2.5-10 (P = .535), PM10 (P = .136), and nitrogen oxides (P = .745). While some results exhibited heterogeneity, all findings demonstrated an absence of pleiotropy. This study did not find substantive evidence supporting a causal relationship between air pollution and the risk of SKCM within European populations. The comprehensive MR analysis, encompassing various pollutants, suggests that environmental factors such as air pollution may not be significant contributors to the development of SKCM.

The longitudinal associations between ambient air pollution exposure and dementia in the UK: results from the cognitive function and ageing study II and Wales.

BACKGROUND: Air pollution has been recognised as a potential risk factor for dementia. Yet recent epidemiological research shows mixed evidence. The aim of this study is to investigate the longitudinal associations between ambient air pollution exposure and dementia in older people across five urban and rural areas in the UK. METHODS: This study was based on two population-based cohort studies of 11329 people aged ≥ 65 in the Cognitive Function and Ageing Study II (2008-2011) and Wales (2011-2013). An algorithmic diagnosis method was used to identify dementia cases. Annual concentrations of four air pollutants (NO2, O3, PM10, PM2.5) were modelled for the year 2012 and linked via the participants' postcodes. Multistate modelling was used to examine the effects of exposure to air pollutants on incident dementia incorporating death and adjusting for sociodemographic factors and area deprivation. A random-effect meta-analysis was carried out to summarise results from the current and nine existing cohort studies. RESULTS: Higher exposure levels of NO2 (HR: 1.04; 95% CI: 0.94, 1.14), O3 (HR: 0.90; 95% CI: 0.70, 1.15), PM10 (HR: 1.17; 95% CI: 0.86, 1.58), PM2.5 (HR: 1.41; 95% CI: 0.71, 2.79) were not strongly associated with dementia in the two UK-based cohorts. Inconsistent directions and strengths of the associations were observed across the two cohorts, five areas, and nine existing studies. CONCLUSIONS: In contrast to the literature, this study did not find clear associations between air pollution and dementia. Future research needs to investigate how methodological and contextual factors can affect evidence in this field and clarity the influence of air pollution exposure on cognitive health over the lifecourse.

Air Pollution: Challenges to Human Health in Pakistan.

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

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

Atmosphere particulate matter and respiratory diseases during COVID-19 in Korea.

We aimed to examine the impact of COVID-19 non-pharmaceutical interventions (NPIs) on the relationship between air pollutants and hospital admissions for respiratory and non-respiratory diseases in six metropolitan cities in South Korea. This study compared the associations between particulate matter (PM10 and PM2.5) and hospital admission for respiratory and non-respiratory diseases before (2016-2019) and during (2020) the implementation of COVID-19 NPIs by using distributed lag non-linear models. In the Pre-COVID-19 period, the association between PM10 and admission risk for asthma and COPD showed an inverted U-shaped pattern. For PM2.5, S-shaped and inverted U-shaped changes were observed in asthma and COPD, respectively. Extremely high and low levels of PM10 and extremely low levels of PM2.5 significantly decreased the risk of admission for asthma and COPD. In the Post-COVID-19 outbreak period, the overall cumulative relationship between PM10 and PM2.5 and respiratory diseases and the effects of extreme levels of PM10 and PM2.5 on respiratory diseases were completely changed. For non-respiratory diseases, PM10 and PM2.5 were statistically insignificant for admission risk during both periods. Our study may provide evidence that implementing NPIs and reducing PM10 and PM2.5 exposure during the COVID-19 pandemic has contributed to reducing hospital admissions for environment-based respiratory diseases.

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

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

The effects of meteorological factors and air pollutants on the incidence of tuberculosis in people living with HIV/AIDS in subtropical Guangxi, China.

BACKGROUND: Previous studies have shown the association between tuberculosis (TB) and meteorological factors/air pollutants. However, little information is available for people living with HIV/AIDS (PLWHA), who are highly susceptible to TB. METHOD: Data regarding TB cases in PLWHA from 2014 to2020 were collected from the HIV antiviral therapy cohort in Guangxi, China. Meteorological and air pollutants data for the same period were obtained from the China Meteorological Science Data Sharing Service Network and Department of Ecology and Environment of Guangxi. A distribution lag non-linear model (DLNM) was used to evaluate the effects of meteorological factors and air pollutant exposure on the risk of TB in PLWHA. RESULTS: A total of 2087 new or re-active TB cases were collected, which had a significant seasonal and periodic distribution. Compared with the median values, the maximum cumulative relative risk (RR) for TB in PLWHA was 0.663 (95% confidence interval [CI]: 0.507-0.866, lag 4 weeks) for a 5-unit increase in temperature, and 1.478 (95% CI: 1.116-1.957, lag 4 weeks) for a 2-unit increase in precipitation. However, neither wind speed nor PM10 had a significant cumulative lag effect. Extreme analysis demonstrated that the hot effect (RR = 0.638, 95%CI: 0.425-0.958, lag 4 weeks), the rainy effect (RR = 0.285, 95%CI: 0.135-0.599, lag 4 weeks), and the rainless effect (RR = 0.552, 95%CI: 0.322-0.947, lag 4 weeks) reduced the risk of TB. Furthermore, in the CD4(+) T cells < 200 cells/µL subgroup, temperature, precipitation, and PM10 had a significant hysteretic effect on TB incidence, while temperature and precipitation had a significant cumulative lag effect. However, these effects were not observed in the CD4(+) T cells ≥ 200 cells/µL subgroup. CONCLUSION: For PLWHA in subtropical Guangxi, temperature and precipitation had a significant cumulative effect on TB incidence among PLWHA, while air pollutants had little effect. Moreover, the influence of meteorological factors on the incidence of TB also depends on the immune status of PLWHA.

Continuous Markov Models for Analyzing the Effect of Environmental Personal Exposure on Multiple Sclerosis Progression.

Multiple sclerosis (MS) is an inflammatory autoimmune demyelinating disorder of the central nervous system, leading to progressive functional impairments. Predicting disease progression with a probabilistic and time-dependent approach might help suggest interventions for a better management of the disease. Recently, there has been increasing focus on the impact of air pollutants as environmental factors influencing disease progression. This study employs a Continuous-Time Markov Model (CMM) to explore the impact of air pollution measurements on MS progression using longitudinal data from MS patients in Italy between 2013 and 2022. Preliminary findings indicate a relationship between air pollution and MS progression, with pollutants like Particulate Matter with a diameter of 10 micrometers (PM10) or 2.5 micrometers (PM2.5), Nitrogen Dioxide (NO2), and Carbon Monoxide (CO) showing potential effects on disease activity.

Air pollution and skin diseases: A comprehensive evaluation of the associated mechanism.

Air pollutants deteriorate the survival environment and endanger human health around the world. A large number of studies have confirmed that air pollution jeopardizes multiple organs, such as the cardiovascular, respiratory, and central nervous systems. Skin is the largest organ and the first barrier that protects us from the outside world. Air pollutants such as particulate matter (PM), polycyclic aromatic hydrocarbons (PAHs), volatile organic compounds (VOCs) will affect the structure and function of the skin and bring about the development of inflammatory skin diseases (atopic dermatitis (AD), psoriasis), skin accessory diseases (acne, alopecia), auto-immune skin diseases (cutaneous lupus erythematosus(CLE) scleroderma), and even skin tumors (melanoma, basal cell carcinoma (BCC), squamous-cell carcinoma (SCC)). Oxidative stress, skin barrier damage, microbiome dysbiosis, and skin inflammation are the pathogenesis of air pollution stimulation. In this review, we summarize the current evidence on the effects of air pollution on skin diseases and possible mechanisms to provide strategies for future research.

Model misspecification, measurement error, and apparent supralinearity in the concentration-response relationship between PM2.5 and mortality.

A growing number of studies have produced results that suggest the shape of the concentration-response (C-R) relationship between PM2.5 exposure and mortality is "supralinear" such that incremental risk is higher at the lowest exposure levels than at the highest exposure levels. If the C-R function is in fact supralinear, then there may be significant health benefits associated with reductions in PM2.5 below the current US National Ambient Air Quality Standards (NAAQS), as each incremental tightening of the PM2.5 NAAQS would be expected to produce ever-greater reductions in mortality risk. In this paper we undertake a series of tests with simulated cohort data to examine whether there are alternative explanations for apparent supralinearity in PM2.5 C-R functions. Our results show that a linear C-R function for PM2.5 can falsely appear to be supralinear in a statistical estimation process for a variety of reasons, such as spatial variation in the composition of total PM2.5 mass, the presence of confounders that are correlated with PM2.5 exposure, and some types of measurement error in estimates of PM2.5 exposure. To the best of our knowledge, this is the first simulation-based study to examine alternative explanations for apparent supralinearity in C-R functions.

Changes of PM2.5 and O3 and their impact on human health in the Guangdong-Hong Kong-Macao Greater Bay Area.

In recent years, the combined pollution of PM2.5 and O3 in China, particularly in economically developed regions such as the Guangdong-Hong Kong-Macao Greater Bay Area (GBA), has garnered significant attention due to its potential implications. This study systematically investigated the changes of PM2.5 and O3 and their associated human health effects in the GBA, utilizing observational data spanning from 2015 to 2019. The findings revealed a spatial trend indicating a gradual decrease in PM2.5 levels from the northwest to the southeast, while the spatial distribution of MDA8 O3 demonstrated an opposing pattern to that of PM2.5. The monthly fluctuations of PM2.5 and MDA8 O3 exhibited V-shaped and M-shaped patterns, respectively. Higher MDA8 O3 concentrations were observed in autumn, followed by summer and spring. Over the five-year period, PM2.5 concentrations exhibited a general decline, with an annual reduction rate of 1.7 µg m-3/year, while MDA8 O3 concentrations displayed an annual increase of 3.2 µg m-3. Among the GBA regions, Macao, Foshan, Guangzhou, and Jiangmen demonstrated notable decreases in PM2.5, whereas Jiangmen, Zhongshan, and Guangzhou experienced substantial increases in MDA8 O3 levels. Long-term exposure to PM2.5 in 2019 was associated with 21,113 (95% CI 4968-31,048) all-cause deaths (AD), 1333 (95% CI 762-1714) cardiovascular deaths (CD), and 1424 (95% CI 0-2848) respiratory deaths (RD), respectively, reflecting declines of 27.6%, 28.0%, and 28.4%, respectively, compared to 2015. Conversely, in 2019, estimated AD, CD, and RD attributable to O3 were 16,286 (95% CI 8143-32,572), 7321 (95% CI 2440-14,155), and 6314 (95% CI 0-13,576), respectively, representing increases of 45.9%, 46.2%, and 44.2% over 2015, respectively. Taken together, these findings underscored a shifting focus in air pollution control in the GBA, emphasizing the imperative for coordinated control strategies targeting both PM2.5 and O3.

Research on the spatial and temporal patterns of ozone concentration and population health effects in the Central Plains Urban Agglomeration from 2017 to 2020.

Fine particulate matter (PM2.5) and near-surface ozone (O3) are the main atmospheric pollutants in China. Long-term exposure to high ozone concentrations adversely affects human health. It is of great significance to systematically analyze the spatiotemporal evolution mechanism and health effects of ozone pollution. Based on the ozone data of 91 monitoring stations in the Central Plains Urban Agglomeration from 2017 to 2020, the research used Kriging method and spatial autocorrelation analysis to investigate the spatiotemporal variations of ozone concentration. Additionally, the study assessed the health effects of ozone on the population using the population exposure risk model and exposure-response relationship model. The results indicated that: (1) The number of premature deaths caused by ozone pollution in the warm season were 37,053 at 95% confidence interval (95% CI: 28,190-45,930) in 2017, 37,685 (95% CI: 28,669-46,713) in 2018, and 37,655 (95% CI: 28,647-46,676) in 2019. (2) The ozone concentration of the Central Plains urban agglomeration showed a decreasing trend throughout the year and during the warm season from 2017 to 2020, there are two peaks monthly, one is June, and the other is September. (3) In the warm season, the high-risk areas of population exposure to ozone in the Central Plains Urban Agglomeration were mainly concentrated in urban areas. In general, the population exposure risk of the south is lower than that of the north. The number of premature deaths attributed to ozone concentration during the warm season has decreased, but some southern cities such as Xinyang and Zhumadian have also seen an increase in premature deaths. China has achieved significant results in air pollution control, but in areas with high ozone concentrations and high population density, the health burden caused by air pollution remains heavy, and stricter air pollution control policies need to be implemented.

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

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

Placental DNA methylation signatures of prenatal air pollution exposure and potential effects on birth outcomes: an analysis of three prospective cohorts.

BACKGROUND: Pregnancy air pollution exposure (PAPE) has been linked to a wide range of adverse birth and childhood outcomes, but there is a paucity of data on its influence on the placental epigenome, which can regulate the programming of physiological functions and affect child development. This study aimed to investigate the association between prenatal air pollutant exposure concentrations and changes in placental DNA methylation patterns, and to explore the potential windows of susceptibility and sex-specific alterations. METHODS: This multi-site study used three prospective population-based mother-child cohorts: EDEN, PELAGIE, and SEPAGES, originating from four French geographical regions (Nancy, Poitiers, Brittany, and Grenoble). Pregnant women were included between 2003 and 2006 for EDEN and PELAGIE, and between 2014 and 2017 for SEPAGES. The main eligibility criteria were: being older than 18 years, having a singleton pregnancy, and living and planning to deliver in one of the maternity clinics in one of the study areas. A total of 1539 mother-child pairs were analysed, measuring placental DNA methylation using Illumina BeadChips. We used validated spatiotemporally resolved models to estimate PM2·5, PM10, and NO2 exposure over each trimester of pregnancy at the maternal residential address. We conducted a pooled adjusted epigenome-wide association study to identify differentially methylated 5'-C-phosphate-G-3' (CpG) sites and regions (assessed using the Infinium HumanMethylationEPIC BeadChip array, n=871), including sex-specific and sex-linked alterations, and independently validated our results (assessed using the Infinium HumanMethylation450 BeadChip array, n=668). FINDINGS: We identified four CpGs and 28 regions associated with PAPE in the total population, 469 CpGs and 87 regions in male infants, and 150 CpGs and 66 regions in female infants. We validated 35% of the CpGs available. More than 30% of the identified CpGs were related to one (or more) birth outcome and most significant alterations were enriched for neural development, immunity, and metabolism related genes. The 28 regions identified for both sexes overlapped with imprinted genes (four genes), and were associated with neurodevelopment (nine genes), immune system (seven genes), and metabolism (five genes). Most associations were observed for the third trimester for female infants (134 of 150 CpGs), and throughout pregnancy (281 of 469 CpGs) and the first trimester (237 of 469 CpGs) for male infants. INTERPRETATION: These findings highlight the molecular pathways through which PAPE might affect child health in a widespread and sex-specific manner, identifying the genes involved in the major physiological functions of a developing child. Further studies are needed to elucidate whether these epigenetic changes persist and affect health later in life. FUNDING: French Agency for National Research, Fondation pour la Recherche Médicale, Fondation de France, and the Plan Cancer.

[Research progress on the role of imbalanced high and low molecular weight hyaluronic acid in respiratory system inflammation caused by atmospheric particulate matter].

Atmospheric particulate matter has an association with respiratory system inflammation, and low molecular weight hyaluronic acid (LMW-HA) is a key biomarker of inflammatory cascade reaction. This review summarized the possible pathways and biomarkers of atmospheric particulate matter causing respiratory system inflammation through high molecular weight hyaluronic acid (HMW-HA)/LMW-HA imbalance, including the synthesis and decomposition of HA, the reduction of particulate matter and HMW-HA, the increase of LMW-HA, and the relationship between LMW-HA and respiratory system inflammation. Furthermore, inhibitors and therapeutic drugs targeting certain biomarkers were further listed. This review could shed light on the mechanism of respiratory system inflammation caused by atmospheric particulate matter and the weak points that need attention in subsequent research.

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

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

The Impact of Air Pollution on Asthma Severity among Residents Living near the Main Industrial Complex in Oman: A Cross-Sectional Study.

BACKGROUND: Asthma is a widespread chronic respiratory disease that poses a significant public health challenge. The current study investigated the associations between air pollution and asthma severity among individuals residing near the Sohar industrial port (SIP) in Oman. Despite the presence of multiple major industrial complexes in Oman, limited knowledge regarding their impact on respiratory health is accredited. Hence, the primary objective of this study is to offer valuable insights into the respiratory health consequences of industrial air pollution in Al Batinah North. METHODS: The state health clinics' records for patient visits related to asthma were collected for the timeframe spanning 2014 to 2022. Exposure was defined as the distance from the SIP, Majan Industerial Area (MIA), and Sohar Industerial Zone (SIZ) to determine high-, intermediate-, and low-exposure zones (<6 km, 6-12 km and >12 km, respectively). Exposure effect modifications by age, gender, and smoking status were also examined. RESULTS: The conducted cross-sectional study of 410 patients (46.1% males and 53.9% females) living in over 17 areas around SIP revealed that 73.2% of asthmatics were under 50 years old, with severity significantly associated with closeness to the port. Risk ratios were estimated to be (RR:2.42; CI95%: 1.01-5.78), (RR:1.91; CI95%: 1.01-3.6), and (RR:1.68; CI95%: 0.92-3.09) for SIP, MIP, and SIZ areas, respectively, compared to the control area. Falaj Al Qabail (6.4 km) and Majees (6 km) had the highest number of asthma patients (N 69 and N 72) and highest percentages of severe asthma cases among these patients (28% and 24%) with significant risk ratios (RR:2.97; CI95%: 1.19-7.45 and RR:2.55; CI95%: 1.00-6.48), correspondingly. Moreover, severe asthma prevalence peaked in the 25-50 age group (RR:2.05; CI95%: 1.26-3.33), and this linkage between asthma and age was much more pronounced in males than females. Smoking and exposure to certain contaminants (dust and smoke) also increased the risk of severe asthma symptoms, but their effects were less important in the high-risk zone, suggesting much more important risk factors. A neural network model accurately predicted asthma risk (94.8% accuracy), with proximity to SIP as the most influential predictor. CONCLUSIONS: This study highlights the high asthma burden near SIP, linked to port proximity, smoking, and wind direction as major risk factors. These findings inform vital public health policies to reduce air pollution and improve respiratory health in the region, prompting national policy review.

How air pollution affects corporate total factor productivity?

To explore the relationship between air pollution and total factor productivity and new pathways, This paper examines the impact of air pollution on total factor productivity of A-share listed companies in Shanghai and Shenzhen between 2015 and 2019. It investigates this relationship by considering two pathways: investor sentiment and government attention. The findings indicate that air pollution suppresses total factor productivity of firms. However, air pollution stimulates investor sentiment, which in turn increases R&D investment and total factor productivity, reducing to some extent the dampening effect of air pollution on total factor productivity. There exists a notable positive correlation between air quality and government attention, acting as a mediating variable. This implies that air pollution has the potential to capture the attention of governmental entities, leading to the implementation of appropriate measures aimed at managing and mitigating the occurrence of air pollution caused by industrial enterprises.And the relevant governments should formulate a series of policies to meet the different needs of different enterprises. These two approaches have varying impacts depending on the type of enterprises, thus governments should develop laws to cater to the various demands of different types of enterprises.

Within-city spatial variations in PM2.5 magnetite nanoparticles and brain cancer incidence in Toronto and Montreal, Canada.

Magnetite nanoparticles are small, strongly magnetic iron oxide particles which are produced during high-temperature combustion and friction processes and form part of the outdoor air pollution mixture. These particles can translocate to the brain and have been found in human brain tissue. In this study, we estimated associations between within-city spatial variations in concentrations of magnetite nanoparticles in outdoor fine particulate matter (PM2.5) and brain cancer incidence. We performed a cohort study of 1.29 million participants in four cycles of the Canadian Census Health and Environment Cohort in Montreal and Toronto, Canada who were followed for malignant brain tumour (glioma) incidence. As a proxy for magnetite nanoparticle content, we measured the susceptibility of anhysteretic remanent magnetization (χARM) in PM2.5 samples (N = 124 in Montreal, N = 110 in Toronto), and values were assigned to residential locations. Stratified Cox proportional hazards models were used to estimate hazard ratios (per IQR change in volume-normalized χARM). ARM was not associated with brain tumour incidence (HR = 0.998, 95% CI 0.988, 1.009) after adjusting for relevant potential confounders. Although we found no evidence of an important relationship between within-city spatial variations in airborne magnetite nanoparticles and brain tumour incidence, further research is needed to evaluate this understudied exposure, and other measures of exposure to magnetite nanoparticles should be considered.

Children's food allergy: Effects of environmental influences and antibiotic use across critical developmental windows.

BACKGROUND: Increasing studies linked outdoor air pollution (OAP), indoor environmental factors (IEFs), and antibiotics use (AU) with the first wave of allergies (i.e., asthma, allergic rhinitis, and eczema), yet the role of their exposures on children's second wave of allergy (i.e., food allergy) are unknown. OBJECTIVES: To investigate the association between exposure to OAP and IEFs and childhood doctor-diagnosed food allergy (DFA) during the pre-pregnancy, prenatal, early postnatal, and current periods, and to further explore the effect of OAP and IEFs on DFA in children co-exposed to antibiotics. METHODS: A retrospective cohort study involving 8689 preschoolers was carried out in Changsha, China. Data on the health outcomes, antibiotic use, and home environment of each child were collected through a questionnaire. Temperature and air pollutants data were obtained from 8 and 10 monitoring stations in Changsha, respectively. Exposure levels to temperature and air pollutants at individual home addresses were calculated by the inverse distance weighted (IDW) method. Multiple logistic regression models were employed to assess the associations of childhood DFA with exposure to OAP, IEF, and AU. RESULTS: Childhood ever doctor-diagnosed food allergy (DFA) was linked to postnatal PM10 exposure with OR (95% CI) of 1.18 (1.03-1.36), especially for CO and O3 exposure during the first year with ORs (95% CI) = 1.08 (1.00-1.16) and 1.07 (1.00-1.14), as well as SO2 exposure during the previous year with OR (95% CI) of 1.13 (1.02-1.25). The role of postnatal air pollution is more important for the risk of egg, milk and other food allergies. Renovation-related IAP (new furniture) and dampness-related indoor allergens exposures throughout all time windows significantly increased the risk of childhood DFA, with ORs ranging from 1.23 (1.03-1.46) to 1.54 (1.29-1.83). Furthermore, smoke-related IAP (environmental tobacco smoke [ETS], parental and grandparental smoking) exposure during pregnancy, first year, and previous year was related to DFA. Additionally, exposure to pet-related indoor allergens (cats) during first year and total plant-related allergens (particularly nonflowering plants) during previous year were associated with DFA. Moreover, exposure to plant-related allergy during first and previous year was specifically associated with milk allergy, while keeping cats during first year increased the risk of fruits/vegetables allergy. Life-time and early-life AU was associated with the increased risk of childhood DFA with ORs (95% CI) = 1.57 (1.32-1.87) and 1.46 (1.27-1.67), including different types food allergies except fruit/vegetable allergy. CONCLUSIONS: Postnatal OAP, life-time and early-life IEFs and AU exposure played a vital role in the development of DFA, supporting the "fetal origin of childhood FA" hypothesis.