Aug 2026· Experimental and Clinical Gastroenterology· pp. 99-109· 0 citations· 67 references
TL;DR
No hypothesis clearly characterizes the role of PM in the pathogenesis of the discussed liver diseases, in particular, at the molecular genetic level, and creating a formalized description of the processes mediating the effect of PM on the human body helps to better understand their role.
Abstract
The review highlights current understanding of the role of air pollution with particulate matter (PM) in the pathogenesis of chronic non-infectious liver diseases (CLD). For this purpose, the materials of articles indexed in the PubMed and Russian Science Citation Index (RSCI) databases were used. PM with an aerodynamic diameter of ≤2.5 μm are recognized as the most dangerous. It was found that long-term exposure to fine particulate matter (PM2.5), especially those containing metals, significantly increases the risk and mortality from liver cancer, cirrhosis, and non-alcoholic fatty liver disease. Exposure to PM2.5 can contribute to the development of CLD by causing oxidative stress, systemic inflammation, and dysregulation of lipid metabolism. Damage to the intestinal epithelium and disruption of microbiotic homeostasis causes stress to the endoplasmic reticulum of cells, inducing abnormal expression of specific microRNAs or inflammatory factors. The review discusses modern terminology and hypotheses of the pathogenesis of the most common chronic non-infectious liver diseases. Unfortunately, no hypothesis clearly characterizes the role of PM in the pathogenesis of the discussed liver diseases, in particular, at the molecular genetic level. Creating a formalized description of the processes mediating the effect of PM on the human body helps to better understand their role in the pathogenesis of various diseases, in particular CLD, which can contribute to the improvement of early diagnostic methods, treatment, and preventive measures.
Introduction and Objective. Air pollution is a major environmental health problem associated with increased respiratory morbidity and mortality. Pollutants such as particulate matter (PM2,5, PM10), nitrogen dioxide, sulpher dioxide, ozone, and carbon monoxide may damage the respiratory tract through oxidative stress, epithelial dysfunction, and immune dysregulation. Because the upper airways are the first site of contact with inhaled pollutants, otolaryngological diseases are particularly susceptible to environmental exposure. The aim of this review is to summarize current evidence regarding the impact of air pollution on ENT diseases and their underlying mechanisms. Brief description of the state of knowledge. Current studies demonstrate significant associations between air pollution and disorders such as rhinitis, chronic rhinosinusitis, otitis media, and laryngeal diseases. Both short-and long-term exposure to pollutants increase disease incidence, symptom severity, and healthcare utilisation. Oxidative stress, chronic inflammation, epithelial barrier dysfunction, and impaired mucociliary clearance appear to play central roles in disease pathogenesis. Children and the elderly are especially vulnerable to pollution-related upper airway diseases. Summary. Air pollution is an important environmental determinant of otolaryngological diseases. Its effects involve inflammatory, oxidative, and structural mechanisms contributing to both acute and chronic upper airway pathology. Recognition of environmental exposure, implementation of preventive strategies, and further research on disease mechanisms may improve prevention and clinical management of ENT disorders.
Zuzanna Parfienowicz, A. Drużdżel, M. Krzyżanowska et al.· Environmental Medicine· 0 citations
The deterioration of ambient air quality worldwide has intensified the need to examine the environmental factors associated with the growing burden of respiratory disease. This study aimed to identify broad patterns in the adverse effects of environmental exposures on the respiratory system, while accounting for regional variation and population-specific vulnerability. A systematic literature review was conducted between April and December 2024 using four international databases: PubMed, Web of Science, Scopus, and Google Scholar. Seventy-one relevant publications were included in the final analysis. The findings indicate that, in India, concentrations of particulate matter with aerodynamic diameters of up to 10 μm (PM₁₀) and 2.5 μm (PM₂.₅) exceed recommended limits by a factor of 2.56. In Northern Thailand, reductions of 5.3%–34.3% in particulate matter concentrations were associated with significant declines in hospitalization rates. In China and South Africa, pollutant levels substantially exceed the World Health Organization guideline of 5 μg/m³, while national standards in some settings permit concentrations of up to 40 μg/m³, thereby increasing the risk of chronic inflammatory respiratory conditions. In Bogotá, Colombia, heavy traffic contributes to increased morbidity and mortality from respiratory complications. In Kyrgyzstan, seasonal variation and changes in vegetation patterns have been linked to a rise in allergic reactions, whereas in Slovakia, prolonged pollen seasons are associated with a higher prevalence of bronchial asthma. Children, particularly those under 5 years of age, older adults, and industrial workers were identified as the most vulnerable groups. Climate change further aggravates these risks by intensifying exposure to fine particulate matter and gaseous pollutants. The findings underscore the need for integrated policies focused on emission reduction, environmental monitoring, public awareness, and the harmonization of air-quality standards. The study provides evidence that may support cross-sectoral planning and the development of preventive strategies aimed at reducing the burden of acute and chronic respiratory disease.
Zhanibek Muratov, Aida Zotaj, A. Kalandarova et al.· Luna Azul· 0 citations
The complex relationship between air pollution, the human microbiome, and lung cancer within a One Health framework is explored, highlighting the mechanistic links between air pollution-induced microbial dysbiosis and lung carcinogenesis.
Jawad Hussain, Muhammad Noman· Electronic Journal of Medica...· 0 citations
This study examines the long-term associations between ambient air pollutants and the burden of major respiratory and infectious diseases in this geographically sensitive region. A retrospective analysis was conducted using ICD-10-coded hospital records of patients diagnosed with asthma, chronic obstructive pulmonary disease (COPD), bronchitis, and tuberculosis from January 2020 to June 2026. These data were integrated with in situ air quality measurements, including PM10, PM2.5, and SO2, as well as satellite-derived Aerosol Optical Depth (AOD) from MODIS. Disease incidence was stratified by year, sex, and age groups (0–85+ years) to assess demographic susceptibility patterns. Respiratory diseases constituted a substantial public health burden over the study period. Asthma showed a marked female predominance (≈29,700 females vs. ≈16,000 males) and a bimodal age distribution with peaks in early childhood (0–5 years) and mid-adulthood (35–50 years). COPD was predominantly observed in males (≈8300 males vs. ≈5500 females), with a higher median age range (≈67–70 years). Bronchitis exhibited a similar bimodal pattern, disproportionately affecting both pediatric and elderly populations, while overall case numbers declined over time. Tuberculosis incidence was approximately threefold higher in males than females, with notable age-related divergence, affecting younger females (≈30–32 years) and middle-aged males (≈42–45 years). The findings suggest a spatial–temporal correspondence between elevated pollutant concentrations and respiratory disease prevalence in the Iğdır Basin. The observed sex- and age-specific disparities underscore the potential value of region-specific environmental health strategies, strengthened air quality management, and continuous epidemiological surveillance in enclosed basin environments.
Melahat Batu Ağırkaya, Fatma Şencan, Mehmet Ali Çelik· Pollutants· 0 citations
Airborne particulate matter (PM) is a major component of air pollution and represents a significant global public health concern. Fine and ultrafine particles derived from traffic emissions, industrial processes, biomass burning, and natural sources can penetrate deep into the respiratory tract and, in some cases, enter the systemic circulation. Increasing evidence links exposure to particulate matter, particularly PM2.5 and ultrafine particles, with systemic inflammation, a key underlying mechanism in the development of cardiovascular disease, metabolic disorders, respiratory conditions, and neurodegenerative diseases. This review examines the sources and characteristics of airborne particulate matter, the biological mechanisms that connect inhaled particles to systemic inflammatory responses, and the clinical and epidemiological evidence supporting these associations. Key pathways include oxidative stress, activation of innate immune responses, endothelial dysfunction, and dysregulation of autonomic balance. The role of vulnerable populations and long-term health consequences is discussed, along with emerging biomarkers of exposure and inflammation. Finally, the review highlights policy and public health interventions aimed at reducing exposure and mitigating inflammatory health effects. Understanding the relationship between airborne particulate matter and systemic inflammation is critical for developing effective preventive strategies and reducing the global burden of pollution-related diseases.
Keywords: Particulate matter, Systemic inflammation, Oxidative stress, Cardiovascular disease, Air pollution.
Kungu Erisa· Idosr Journal of Science and...· 0 citations
We use cookies to run the site and, with your consent, for analytics and to show ads.
See our Cookie Policy.
