ReviewFrontiers in immunology2026
Welding fume exposure and respiratory innate immune activation: metal-rich particles, inflammatory biomarkers, and immune-informed occupational prevention.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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3 authors.
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Abstract
Welding fumes are widely recognized occupational aerosols, yet their effects on respiratory immune pathways remain incompletely integrated into exposure-oriented assessment. Generated by welding materials, process parameters, surface conditions, and ventilation, welding fumes contain fine and ultrafine particles that can deposit in the respiratory tract and interact with epithelial cells, alveolar macrophages, neutrophils, monocytes, and circulating immune cells. This Mini Review examines welding fume exposure as a metal-particle stimulus to the respiratory immune system, focusing on how metal-rich particles initiate oxidative and epithelial-innate immune responses, what inflammatory and host-defense markers reveal about early biological effects, and how such evidence can be interpreted alongside exposure assessment. Evidence from human exposure studies, controlled inhalation studies, cell models, and workplace investigations suggests that welding fumes can induce acute-phase proteins, cytokines, chemokines, and neutrophilic responses, while some studies also indicate altered T helper cell activity and weakened responsiveness to bacterial stimuli. Evidence from related metal and particulate models further suggests that TRPA1/TRPV1-mediated sensory signaling may provide a rapid route to cough and acute airway reflex responses, although direct welding-fume-specific human evidence remains limited. However, interpretation remains constrained by differences in fume composition, particle size, soluble metal fraction, exposure pattern, smoking, infection, co-exposures, and limited longitudinal evidence. These findings support an immune-informed view of welding fume exposure in which inflammatory and host-defense markers help identify biologically active residual exposure. Such markers should not replace exposure limits or engineering controls, but they may strengthen the interpretation of airway immune perturbation in occupational metal-particle exposure.
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