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 x -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 αpinene-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.

It has been hypothesized that the cytotoxicity of secondary organic aerosols (SOA) is mediated through the formation of reactive oxygen species (ROS) in the exposed cells. Here, lung epithelial cells (A549) residing at the air–liquid interface were exposed to proxies of anthropogenic and biogenic SOA that were photochemically aged under varying nitrogen oxide (NOx) concentrations in an oxidation flow reactor. The total organic peroxides and ROS radical content in the SOA were quantified by the iodometric spectrophotometric method and by continuous-wave electron paramagnetic resonance. The effect of the exposure was evaluated by measuring cell viability and cellular ROS production following the exposure. The results demonstrate that SOA that aged in the absence of NOx contained more ROS than fresh SOA and were more toxic toward the cells, while varying NOx conditions had no significant influence on levels of the ROS content in fresh SOA and their toxicity. Analysis of ROS in the exposed cells using flow cytometry showed a similar trend with the total ROS content in the SOA. This study provides a first and direct observation of such association.

Consumer-level 3D printers emit ultrafine and fine particles, though little is known about their chemical composition or potential toxicity. We report chemical characteristics of the particles in comparison to raw filaments and assessments of particle toxicity. Particles emitted from polylactic acid (PLA) appeared to be largely composed of the bulk filament material with mass spectra similar to the PLA monomer spectra. Acrylonitrile butadiene styrene (ABS), extruded at a higher temperature than PLA, emitted vastly more particles and their composition differed from that of the bulk filament, suggesting that trace additives may control particle formation. In vitro cellular assays and in vivo mice exposure all showed toxic responses when exposed to PLA and ABS-emitted particles, where PLA-emitted particles elicited higher response levels than ABS-emitted particles at comparable mass doses. A chemical assay widely used in ambient air-quality studies showed that particles from various filament materials had comparable particle oxidative potentials, slightly lower than those of ambient particulate matter (PM 2.5 ). However, particle emissions from ABS filaments are likely more detrimental when considering overall exposure due to much higher emissions. Our results suggest that 3D printer particle emissions are not benign and exposures should be minimized.

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.

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.