Prooxidant and Proinflammatory Potency of Air Pollution Particulate Matter (PM_2.5–0.3) Produced in Rural, Urban, or Industrial Surroundings in Human Bronchial Epithelial Cells (BEAS-2B)

Abstract

Compelling evidence indicates that exposure to air pollution particulate matter (PM) affects human health. However, how PM composition interacts with PM-size to cause adverse health effects needs elucidation. In this study, we were also interested in the physicochemical characteristics and toxicological end points of PM₂.₅₋₀.₃ samples produced in rural, urban, or industrial surroundings, thereby expecting to differentiate their respective in vitro adverse health effects in human bronchial epithelial cells (BEAS-2B). Physicochemical characteristics of the three PM₂.₅₋₀.₃ samples, notably their inorganic and organic components, were closely related to their respective emission sources. Referring also to the dose/response relationships of the three PM₂.₅₋₀.₃ samples, the most toxicologically relevant exposure times (i.e., 24, 48, and 72 h) and doses (i.e., 3.75 μg PM/cm² and 15 μg PM/cm²) to use to study the underlying mechanisms of action involved in PM-induced lung toxicity were chosen. Organic chemicals adsorbed on the three PM₂.₅₋₀.₃ samples (i.e., polycyclic aromatic hydrocarbons) were able to induce the gene expression of xenobiotic-metabolizing enzymes (i.e., Cytochrome P4501A1 and 1B1, and, to a lesser extent, NADPH-quinone oxidoreductase-1). Moreover, intracellular reactive oxygen species within BEAS-2B cells exposed to the three PM₂.₅₋₀.₃ samples induced oxidative damage (i.e., 8-hydroxy-2'-deoxyguanosine formation, malondialdehyde production and/or glutathione status alteration). There were also statistically significant increases of the gene expression and/or protein secretion of inflammatory mediators (i.e., notably IL-6 and IL-8) in BEAS-2B cells after their exposure to the three PM₂.₅₋₀.₃ samples. Taken together, the present findings indicated that oxidative damage and inflammatory response preceeded cytotoxicity in air pollution PM₂.₅₋₀.₃-exposed BEAS-2B cells and supported the idea that PM-size, composition, and origin could interact in a complex manner to determine the in vitro responsiveness to PM.

African Dust Storms Reaching Puerto Rican Coast Stimulate the Secretion of IL-6 and IL-8 and Cause Cytotoxicity to Human Bronchial Epithelial Cells (BEAS-2B)

“…Epidemiological studies by the U.S. CDC and others have reported a high prevalence of asthma, particularly in children [49,69,70]. Similar results have also been reported by other investigations performed in the Caribbean region [46,50,51,54,59,71- 74]. …”

The occurrence of polycyclic aromatic hydrocarbons and their derivatives and the proinflammatory potential of fractionated extracts of diesel exhaust and wood smoke particles

“…[1,2] To further characterize mutagenic and inflammatory effects of complex and variable PM-mixtures, it is of interest to identify specific components which may be responsible for such effects. [3] This knowledge may contribute to the development of more targeted strategies to improve air quality.…”

Toxicity Research of PM2.5 Compositions In Vitro

“…Moreover, intracellular reactive oxygen species within BEAS-2B cells exposed to the three PM (2.5−0.3) samples induced oxidative damage (i.e., 8-hydroxy-2′-deoxyguanosine formation, malondialdehyde production, and/or glutathione status alteration). There were also statistically significant increases of the gene expression and/or protein secretion of inflammatory mediators (i.e., notably IL-6 and IL-8) [33]. …”