Chronic Exposure to Secondary Organic Aerosols Causes Lung Tissue Damage

• Published in: Environmental science & technology 2023-04, Vol.57 (15), p.6085-6094
• Main Authors: Déméautis, Tanguy, Bouyssi, Alexandra, Chapalain, Annelise, Guillemot, Johann, Doublet, Patricia, Geloen, Alain, George, Christian, Menotti, Jean, Glehen, Olivier, Devouassoux, Gilles, Bentaher, Abderrazzak
• Format: Article
• Language: English
• Subjects: Aerosols; Air Pollutants - analysis; Air Pollutants - toxicity; Animals; Catalysis; Cell culture; Chemical Sciences; Chronic exposure; Ecotoxicology and Public Health; Environment and Society; Environmental Sciences; Exposure; Gene expression; In vivo methods and tests; Inflammation; Interleukin 6; Lung; Lungs; Macrophages; Matrix metalloproteinase; Matrix metalloproteinases; Metalloproteinase; Mice; Particulate matter; Particulate Matter - analysis; Particulate Matter - toxicity; Pneumonia; Proteolysis; Respiratory Aerosols and Droplets; Tissue analysis; Tissues; Tumor necrosis factor-α
• ISSN: 0013-936X; 1520-5851; 1520-5851
• DOI: 10.1021/acs.est.2c08753

Recently, secondary organic aerosols (SOAs) emerged as a predominant component of fine particulate matter. However, the pathogenic mechanism(s) of SOAs are still poorly understood. Herein, we show that chronic exposure of mice to SOAs resulted in lung inflammation and tissue destruction. Histological analyses found lung airspace enlargement associated with massive inflammatory cell recruitment predominated by macrophages. Concomitant with such cell influx, our results found changes in the levels of a series of inflammatory mediators in response to SOA. Interestingly, we observed that the expression of the genes encoding for TNF-α and IL-6 increased significantly after one month of exposure to SOAs; mediators that have been largely documented to play a role in chronic pulmonary inflammatory pathologies. Cell culture studies confirmed these in vivo findings. Of importance as well, our study indicates increased matrix metalloproteinase proteolytic activity suggesting its contribution to lung tissue inflammation and degradation. Our work represents the first in vivo study, which reports that chronic exposure to SOAs leads to lung inflammation and tissue injury. Thus, we hope that these data will foster new studies to enhance our understanding of the underlying pathogenic mechanisms of SOAs and perhaps help in the design of therapeutic strategies against SOA-mediated lung injury.