Environmental exposure to semi-volatile organic compounds and COPD progression: Evidence mapping, exposure assessment and metabolomic insights.

Ambient aromatic hydrocarbons and prostate cancer: mechanistic evidence linking benzene and PAH exposure to tumor progression

Current evidence supports a biologically plausible framework in which AH exposure may contribute to PCa initiation and progression and may intersect with pathways implicated in therapy resistance, although causal inference remains constrained by exposure misclassification, mixture complexity, and limited longitudinal biomarker data.

Short-term effects and attributable burden of ambient volatile organic compound mixtures on pediatric atopic dermatitis and asthma in Seoul.

A Cross-Sectional Study on Immune-Inflammatory Responses: Exposure to Polycyclic Aromatic Hydrocarbons Alters Pteridine Metabolism and Activates the Kynurenine Pathway

Polycyclic aromatic hydrocarbons (PAHs) are common environmental pollutants generated from the incomplete combustion of organic materials and represent an important source of occupational and environmental exposure. Aside from their carcinogenic properties, PAHs are known to exert immunomodulatory and proinflammatory effects. Immune activation is closely associated with alterations in pteridine metabolism and activation of the kynurenine pathway; however, evidence linking PAH exposure to these immune-inflammatory pathways in humans remains limited. This study aimed to investigate the systemic biological effects of occupational exposure to PAHs from asphalt fumes in road construction workers, with a particular focus on alterations in pteridine metabolism and activation of the kynurenine pathway, using a combined panel of exposure and mechanistic biomarkers. Routine clinical parameters remained within normal ranges while urinary 1-hydroxypyrene, a well-established biomarker of internal PAH exposure, was significantly elevated, confirming substantial PAH exposure. Key findings revealed profound alterations in two critical metabolic pathways: (i) Pteridine metabolism was shifted, with increased neopterin and decreased biopterin levels, indicating activation of cell-mediated immunity and reduced cofactor availability; (ii) the kynurenine pathway was concurrently activated, as reflected by elevated kynurenine, reduced tryptophan, and increased estimated indoleamine 2,3-dioxygenase activity. These findings indicate that low-level but chronic PAH exposure induces sustained Th1-type immune activation and metabolic disturbances in the absence of overt clinical pathology, representing a state of subclinical biological adaptation.

PM2.5 chemical constituents and chronic obstructive pulmonary disease mortality risk: The Pearl River Cohort study.

Chronic obstructive pulmonary disease (COPD) imposes a major burden on global health, yet evidence on the prolonged health effects of individual PM2.5 constituents remains limited. Previous research has primarily employed traditional models, which may struggle to capture the complex correlations among the PM2.5 components and be less effective in confounding adjustment. We conducted a prospective cohort study involving 182,009 participants from the Pearl River Cohort (2013-2015) followed through 2020, applying inverse probability-weighted marginal structural Cox models and quantile g-computation (QGC) to assess the associations of individual PM2.5 components and their mixtures with COPD mortality, followed by stratified analyses for effect modification. Over 1.18 million person-years of follow-up, 422 COPD deaths were documented. Long-term exposure to ammonium (NH4+), black carbon (BC), nitrate (NO3-), organic matter (OM) and chloride (Cl-) was associated with higher COPD mortality, with HRs (95% CI) of 2.75 (1.86-4.05), 2.41 (1.64-3.55), 1.86 (1.45-2.39), 1.85 (1.33-2.57) and 1.45 (1.15-1.82), respectively. Mixture analysis showed that each one-quartile increase in the PM2.5 component mixture was associated with a 39% (29%-50%) higher risk of COPD mortality, primarily driven by OM, Cl-, and NO3- (weights = 0.34, 0.34, 0.32). Stratified analyses indicated greater associations among older adults, suggesting increased susceptibility in this group. Our findings underscore the potential contribution of individual PM2.5 constituents and their mixtures in COPD mortality, while suggesting actionable source-control priorities and coordinated precursor-reduction strategies, as well as population-specific prevention approaches.

Association between serum perfluoroalkyl substances and COPD risk: population evidence and in vitro validation.

Mixture exposure showed a significant positive association with chronic obstructive pulmonary disease risk, and these substances disrupt pulmonary homeostasis through concurrent molecular activation and lipid-metabolic disturbance, evidenced by triglyceride-glucose index mediation.

Air Pollution, Microbial Exposure, and Lung Cancer Risk: Integrating One Health Concepts

Lung cancer remains one of the leading causes of cancer-related mortality worldwide, with increasing evidence highlighting the role of environmental and biological interactions in its development. This review explores the complex relationship between air pollution, the human microbiome, and lung cancer within a One Health framework. While smoking remains a major risk factor, air pollution has emerged as a significant modifiable environmental contributor, particularly in urbanized and industrial regions. Pollutants such as particulate matter (PM2.5 and PM10), nitrogen dioxide, and volatile organic compounds are associated with increased lung cancer incidence through mechanisms involving oxidative stress, chronic inflammation, and genetic damage. Recent research has also identified the lung microbiome as an important factor in respiratory health. Once considered sterile, the lungs are now known to host diverse microbial communities that play a role in immune regulation and inflammatory balance. Environmental exposure, particularly polluted air, can disrupt this microbial balance, leading to dysbiosis. Such microbial alterations may contribute to impaired immune responses and enhanced susceptibility to disease. This review further highlights the mechanistic links between air pollution-induced microbial dysbiosis and lung carcinogenesis. Key pathways include chronic inflammation, immune dysregulation, oxidative stress, epigenetic changes, and alterations in the tumor microenvironment. The interaction between the lung and gut microbiome (lung–gut axis) further emphasizes the systemic impact of environmental exposures. The One Health approach provides an integrated framework to understand these interconnected systems, emphasizing the relationship between environmental health, microbial ecosystems, and human disease. However, current research remains fragmented, with gaps in longitudinal data and integrated multi-omics studies.