Single Exposure to near Roadway Particulate Matter Leads to Confined Inflammatory and Defense Responses: Possible Role of Metals

Inhalation of traffic-associated atmospheric particulate matter (PM2.5) is recognized as a significant health risk. In this study, we focused on a single (“subclinical response”) exposure to water-soluble extracts from PM collected at a roadside site in a major European city to elucidate potential components that drive pulmonary inflammatory, oxidative, and defense mechanisms and their systemic impacts. Intratracheal instillation (IT) of the aqueous extracts induced a 24 h inflammatory response characterized by increased broncho-alveolar lavage fluid (BALF) cells and cytokines (IL-6 and TNF-α), increased reactive oxygen species production, but insignificant lipids and proteins oxidation adducts in mouse lungs. This local response was largely self-resolved by 48 h, suggesting that it could represent a subclinical response to everyday-level exposure. Removal of soluble metals by chelation markedly diminished the pulmonary PM-mediated response. An artificial metal solution (MS) recapitulated the PM extract response. The self-resolving nature of the response is associated with activating defense mechanisms (increased levels of catalase and glutathione peroxidase expression), observed with both PM extract and MS. In conclusion, metals present in PM collected near roadways are largely responsible for the observed transient local pulmonary inflammation and oxidative stress. Simultaneous activation of the antioxidant defense response may protect against oxidative damage

Low Cytotoxicity of Inorganic Nanotubes and Fullerene-Like Nanostructures in Human Bronchial Epithelial Cells: Relation to Inflammatory Gene Induction and Antioxidant Response

The cytotoxicity of tungsten disulfide nano tubes (INT-WS₂) and inorganic fullerene-like molybdenum disulfide (IF-MoS₂) nanoparticles (NPs) used in industrial and medical applications was evaluated in comparison to standard environmental particulate matter. The IF-MoS₂ and INT-WS₂ reside in vesicles/inclusion bodies, suggestive of endocytic vesicles. In cells representing the respiratory, immune and metabolic systems, both IF-MoS₂ and INT-WS₂ NPs remained nontoxic compared to equivalent concentrations (up to 100 μg/mL in the medium) of silica dioxide (SiO₂), diesel engine-derived and carbon black NPs, which induced cell death. Associating with this biocompatibility of IF-MoS₂\INT-WS₂, we demonstrate in nontransformed human bronchial cells (NL-20) relative low induction of the pro-inflammatory cytokines IL-1β, IL-6, IL-8, and TNF-α. Moreover, IF-MoS₂ and INT-WS₂ activated antioxidant response as measured by the antioxidant response element (ARE) using a luciferase reporter, and induced Nrf2-mediated Phase II detoxification genes. Collectively, our findings suggest that the lower cytotoxicity of IF-MoS₂ and INT-WS₂ NPs does not reflect general biological inertness. Rather, compared to other NP’s, it likely results from decreased pro-inflammatory activation, but a comparable significant capacity to induce protective antioxidant/detoxification defense mechanisms

Exposure of Lung Epithelial Cells to Photochemically Aged Secondary Organic Aerosol Shows Increased Toxic Effects

Adverse health effects due to exposure to particulate matter (PM) are among the most important global environmental health risks. However, the effects of exposure to secondary organic aerosols (SOA), a major component of the global aerosol, are largely unknown. Here we exposed lung epithelial cells (A549) to fresh and aged SOA particles and investigated the effect of SOA atmospheric aging on cell viability and gene expression. Naphthalene- and α-pinene-derived SOA were formed in an oxidation flow reactor that simulates atmospheric SOA formation and aging dominated by OH radical oxidation under NO_<i>x</i>-free conditions. The SOA mass and chemical composition were characterized on-line using a scanning mobility particle sizer and aerosol mass spectrometer. Fresh and aged SOA were directed to an air–liquid interface cell exposure system. Aged naphthalene- and α-pinene-derived SOA were somewhat more toxic than fresh SOA. Aged naphthalene SOA contained peroxide levels that were higher than those of fresh SOA. The level of induction of Nrf2 signaling increased following exposure to aged naphthalene SOA. Given the global prevalence of SOA and its observed toxicity, this study calls for more studies aimed at understanding the underlying mechanics

Variation of PM_2.5 Redox Potential and Toxicity During Monsoon in Delhi, India

This study investigates daily variations in redox potential of water- and organic-soluble PM2.5 during Delhi’s monsoon season, offering insights into its chemical composition, cytotoxicity, and oxidative threat to various lung conditions. PM2.5 samples, categorized by pollution levels, showed an average intrinsic oxidative potential (OPmDTT) of 27.5 pmol min–1 μg–1, OH• generation of 51.1 pmol μg–1, and antioxidant capacity (AOC) in both gallic acid and trolox equivalency of 62.5 and 35.3 pmol μg–1, respectively. Water-soluble redox-active compounds (RACs) contributed to approximately 67% of the PM2.5 redox potential. The polar-phase distribution of RACs in PM2.5 can be modified by atmospheric photochemistry and precipitation. Biomass burning emerged as a pivotal pollution source, with polluted PM2.5 samples exhibiting higher cytotoxicity and oxidative stress in A549 cells. All PM2.5 compounds impaired cellular respiration, reducing the oxygen consumption rates in A549 cells. Intrinsic OPmDTT and OH• generation of PM2.5 were influenced by lung fluid variants, such as exogenous nicotine and endogenous inflammatory protein. This study provides a comprehensive perspective on PM2.5 pollution and its toxicity in Delhi, India during distinct pollution periods and also points out the importance of considering population disparities and individual health status in assessing PM2.5 health impacts