Alumina nanoparticles (Al2O3 NPs) can be released in occupational environments in different contexts such as industry, defense, and aerospace. Workers can be exposed by inhalation to these NPs, for instance, through welding fumes or aerosolized propellant combustion residues. Several clinical and epidemiological studies have reported that inhalation of Al2O3 NPs could trigger aluminosis, inflammation in the lung parenchyma, respiratory symptoms such as cough or shortness of breath, and probably long-term pulmonary fibrosis. The present review is a critical update of the current knowledge on underlying toxicological, molecular, and cellular mechanisms induced by exposure to Al2O3 NPs in the lungs. A major part of animal studies also points out inflammatory cells and secreted biomarkers in broncho-alveolar lavage fluid (BALF) and blood serum, while in vitro studies on lung cells indicate contradictory results regarding the toxicity of these NPs.
Solid composite propellants combustion, in aerospace and defense fields, can lead to complex aerosols emission containing high concentrations of alumina nanoparticles (Al2O3 NPs) and hydrogen chlor...
Introduction: Combined exposures to airborne nanoparticles and acidic gases are plausible during industrial accidents and in military settings involving propellants. Aluminum oxide nanoparticles (Al 2 O 3 NPs), widely used in industry and present in propellant formulations, together with hydrogen chloride (HCl), a corrosive combustion by-product, are relevant co-pollutants whose joint impact on lung remodeling remains poorly defined. This study aimed to investigate early airway responses to repeated apical exposures to Al 2 O 3 NPs, HCl, or their mixture in a human air–liquid interface co-culture model of alveolar epithelial (hAELVi) and fibroblast (MRC-5) cells. Methods: Cells were exposed daily for four days, and epithelial viability, barrier integrity, and mediator release were assessed. Conditioned media from exposed cultures were applied to naïve fibroblasts to evaluate proliferation and migration responses. Results: Repeated exposures did not induce cytotoxicity, barrier disruption, or increases in canonical pro-fibrotic or pro-inflammatory mediators such as TGF-β1, CTGF, or IL-8. However, conditioned media from exposed epithelial cells consistently triggered fibroblast activation through non-canonical epithelial–mesenchymal signaling pathways. These effects occurred at sub-toxic exposure levels. Discussion: These findings indicate that early sub-lethal co-exposure to Al 2 O 3 NPs and HCl can trigger fibroblast activation independently of classical cytokine induction. This unconventional paracrine response suggests a mechanistic link between early epithelial stress and fibroblast-driven remodeling, underscoring the importance of investigating non-canonical pathways in lung responses to mixed environmental pollutants.
Background: Submarines represent extremely confined environments where breathing air is continuously recirculated for extended periods with minimal renewal, generating complex multipollutant atmospheres. Objectives: This critical narrative review aims to (i) summarize sources and composition of submarine indoor air, (ii) evaluate respiratory and cardiovascular risks for crews, and (iii) assess current purification technologies. Methods: A narrative review was conducted following PRISMA recommendations applicable to non-systematic reviews. The PubMed search covered all years from inception to September 2025, complemented by backward citation tracking and technical reports. Results: Eligible studies consistently report elevated levels of CO2, VOCs, NOX, CO, PM2.5, and bioaerosols aboard submarines. Evidence from submariner cohorts and toxicological studies indicates risks of airway irritation, impaired mucociliary defenses, endothelial dysfunction, cardiovascular stress, and neurobehavioral alterations. Conclusions: Submarine indoor air quality is a credible determinant of crew health. Existing filtration systems mitigate some risks but do not address multipollutant mixtures adequately. Improved real-time monitoring, advanced filtration, CFD-guided airflow optimization, and longitudinal medical surveillance are necessary.