Aug 2026· Environment & Health· 0 citations· 39 references
TL;DR
Findings suggest urine is a sensitive matrix for detecting acute exposure effects, while serum provides complementary systemic information in firefighters, and integrating both biofluids into NFPA 1582-guided surveillance may enhance occupational health monitoring and support early cancer detection and prevention in firefighters.
Abstract
Firefighters are routinely exposed to complex mixtures of toxicants during fire suppression, and growing evidence links these exposures to elevated cancer risk. Proteomic profiling provides a sensitive means to detect early molecular alterations associated with such occupational hazards. In this study, we performed a comparative label-free proteomic analysis of paired serum (n = 42) and urine (n = 50) samples collected from firefighters at baseline and within 24 h postfire suppression. We identified and quantified 330 protein groups in serum and 1085 in urine. PLS-DA of total protein abundance showed clear separation between pre- and postexposure samples in both biofluids, indicating exposure-related proteomic changes. Volcano plot analysis further revealed multiple significantly altered proteins in both biofluids, wherein the urine-proteome showed a broader range of differential expressions. Proteins altered in at least 70% of samples were subjected to pathway enrichment analysis, identifying associations with several diseases, including small-cell lung cancer. Protein–protein interaction analysis revealed highly interconnected cancer-related networks involving LAMA4, LAMC1, VWF, and B2M. These findings suggest urine is a sensitive matrix for detecting acute exposure effects, while serum provides complementary systemic information. Integrating both biofluids into NFPA 1582-guided surveillance may enhance occupational health monitoring and support early cancer detection and prevention in firefighters.
Firefighters assigned to structure defense had significantly higher increases in PAH metabolites compared to those assigned to wildland firefighting tasks and maximum post-fire concentrations in firefighters also exceeded the BEI for 1-hydroxyprene and trans,trans-muconic acid.
Miriam M Calkins, Alexander C. Mayer, Derek J Urwin et al.· International Journal of Hyg...· 0 citations
It is suggested that air pollution may promote lung cancer partly through metabolic pathways related to inflammatory and oxidative processes, providing key insights into potential mechanisms and targets for prevention.
Sabrina S. Chow, Ying Wang, J. Sarnat et al.· Nature Communications· 0 citations
Hypoxia-driven vascular, immune, and metabolic remodeling is a key biological process involved in cardiovascular diseases, cancer, and other complex systemic disorders. Acute mountain sickness (AMS) is an acute manifestation of hypobaric hypoxia, but its systemic molecular features remain incompletely defined.
We performed integrated plasma proteomic and metabolomic profiling in 81 healthy Han Chinese male participants after rapid high-altitude exposure. Differential analysis, weighted gene co-expression network analysis (WGCNA), tissue-specific protein mapping, regulatory network reconstruction, machine learning, and druggability assessment were applied to characterize AMS-associated molecular alterations and identify candidate biomarkers and targets.
Multi-omics profiling identified 3,137 proteins and 4,104 metabolites and showed clear separation between AMS and non-AMS participants. AMS was characterized by coordinated thrombo-inflammatory activation, coagulation-related disturbance, and metabolic reprogramming, including suppression of oxidative phosphorylation-related signatures. WGCNA identified symptom associated proteomic and metabolomic modules linked to headache severity, oxygen saturation, and hemodynamic traits. Tissue-specific protein mapping revealed a liver-centered but multi-organ circulating proteomic architecture, suggesting hepatic secretory remodeling with additional neural and immune-system contributions. Regulatory network analysis highlighted NOTCH1 as a candidate upstream regulatory hub, whereas druggability analysis prioritized NOTCH1 and the antioxidant-related protein GSTA1 as translational candidates. An mRMR plus logistic regression classifier integrating 15 proteomic features and SpO2 achieved good discriminatory performance, with an AUC of 0.968 in the training cohort and 0.913 in the test cohort.
This study defines a multi-layer molecular framework of human acute hypoxic stress, linking vascular regulation, inflammation, coagulation, metabolic remodeling, tissue origin, and biomarker prioritization. These findings provide mechanistic insight into AMS and support multi-omics-based biomarker discovery and target prioritization in hypoxia-associated systemic diseases.
Wenjing Ding, Yi-Fan Yang, Huaying Wei et al.· Frontiers in Genetics· 0 citations
BACKGROUND
Air pollution has been increasingly associated with epilepsy risk, but the underlying biological mechanisms remain unclear.
METHODS
We conducted a large-scale proteome-wide analysis in a population-based cohort including 51,428 participants and 2254 plasma proteins. Concentrations of particulate matter (PM2.5, PM2.5-10) and gaseous pollutants (NO2 and NO) were estimated using land-use regression models. Principal component analysis was performed to derive an air pollution index (API). Logistic regression and Cox proportional hazards models were applied to examine interactions between plasma proteins and air pollution exposures in relation to epilepsy prevalence and incidence, respectively. Functional enrichment, protein-protein interaction (PPI) network, neuroimaging association, and tissue- and cell-type transcriptomic enrichment analyses were conducted to explore the biological relevance of proteins exhibiting interaction effects.
RESULTS
We identified protein signatures exhibiting consistent interactions with multiple air pollution exposures in relation to epilepsy risk, including CIT-PM₂.₅, PTPRR-NO₂, and BCL2L15-API. Functional enrichment analyses indicated that these proteins were enriched in pathways related to immune regulation, inflammation, and cell death-related processes, which was consistent with PPI network analysis showing a highly interconnected module centered on immune-related proteins. Neuroimaging analyses suggested that these protein-air pollution interactions were associated with structural brain measures, including hippocampal volume and white matter hyperintensities. Additionally, tissue and single-nucleus RNA sequencing analyses showed that the corresponding genes were enriched in immune-related tissues and specific brain cell types, particularly neurons and endothelial cells.
CONCLUSIONS
This study identifies protein signatures that may modify the association between air pollution exposure and epilepsy risk, providing new insights into potential biological links and highlighting candidate molecular signatures for future mechanistic and translational investigations.
Zihua He, Jianqiong Yin, Quan Yang et al.· Ecotoxicology and Environmen...· 0 citations
Radon is a radioactive gas and a lung carcinogen, yet lacks established blood biomarkers for long-term exposure. We aimed to identify circulating metabolomic and exposomics signatures correlated with reconstructed radon-222 exposure. Metabolites and chemical exposomes were profiled using liquid and gas chromatography-high-resolution mass spectrometry from plasma (n=80). Batch effects were corrected using ComBat, and network and pathway analyses were performed using xMWAS and MetaboAnalyst, respectively. A total of 124 metabolites were correlated with radon, including 41 positive correlations. The strongest positive and negative associations involved unidentified features. Network analysis identified six communities, five of which were directly related to radon. Fatty acyls were the most represented class, followed by benzene derivatives and hydroxy acids and derivatives. Pathway analysis showed enrichment in linoleate, fatty acid, and amino acid metabolism. Our findings demonstrate that integrating metabolomic and chemical exposomes may help identify sensitive biomarkers for radon exposure. We recommend further studies to investigate these pathways in greater mechanistic detail to understand the health effects of radon.
Vrinda Kalia, A. Rajendrakumar, Rodrigo Cruz-Nieto et al.· Environmental Research· 0 citations
BACKGROUND
Occupational noise exposure is a recognized risk factor for stroke, yet biomarkers specific to noise-associated stroke (NAS) remain unclear. Oxidative stress (OS) plays a key mechanistic role in noise-induced cerebrovascular damage. We aim to identify OS biomarkers of NAS and conduct risk assessment.
METHODS
Candidate OS biomarkers were screened using Gene Expression Omnibus transcriptomic datasets integrated with eight machine-learning approaches, then verified in UK Biobank longitudinal data and in stroke model mice after 4-week noise exposure. In addition, the relationship between oxidative balance score (OBS) and stroke was evaluated among noise-exposed adults in the National Health and Nutrition Examination Survey (NHANES) 2005-2018 using logistic regression, and quartiles were applied to determine optimal cut-points.
RESULTS
Eight OS-related genes were identified, of which seven were validated in stroke mice. C-C Motif Chemokine Ligand 3 (CCL3) emerged as the key biomarker. In UK Biobank, occupational noise increased CCL3 expression (effect = 0.052, P = 0.038), and higher CCL3 levels predicted greater stroke risk (hazard ratio = 1.15, P < 0.001). Functionally, CCL3 drove neuroinflammation via chemokine signaling. In noise-exposed stroke mice, circulating CCL3 increased ( P = 0.014) and infarct volume enlarged by 12.9% ( P = 0.011). Among 3306 noise-exposed NHANES participants, higher OBS was protective (odd ratio [OR] = 0.97, P = 0.01), whereas OBS <10 markedly elevated stroke risk (OR = 2.40, P = 0.033) compared with the OBS >24 group.
CONCLUSION
CCL3 is a validated OS biomarker linking occupational noise exposure to stroke. Maintaining OBS >18 through dietary and lifestyle strategies may mitigate NAS risk and offer a targeted neuroprotective approach for noise-exposed populations.
Cong-Cong Wu, Xiao Yu, Tian Lv et al.· Noise and Health· 0 citations
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