The chemical composition of secondary organic aerosols regulates transcriptomic and metabolomic signaling in an epithelial-endothelial in vitro coculture.

Background: The formation of secondary organic aerosols (SOA) by atmospheric oxidation reactions substantially contributes to the burden of fine particulate matter (PM), which has been associated with adverse health effects (e.g., cardiovascular diseases).

Generation, characterization, and toxicological assessment of reference ultrafine soot particles with different organic content for inhalation toxicological studies.

Ultrafine particles (UFP) are the smallest atmospheric particulate matter linked to air pollution-related diseases. The extent to which UFP's physical and chemical properties contribute to its toxicity remains unclear. It is hypothesized that UFP act as carriers for chemicals that drive biological responses.

Biological impact of sequential exposures to allergens and ultrafine particle-rich combustion aerosol on human bronchial epithelial BEAS-2B cells at the air liquid interface.

The prevalence of allergic diseases is constantly increasing since few decades. Anthropogenic ultrafine particles (UFPs) and allergenic aerosols is highly involved in this increase; however, the underlying cellular mechanisms are not yet understood. Studies observing these effects focused mainly on singular in vivo or in vitro exposures of single particle sources, while there is only limited evidence on their subsequent or combined effects.

Processing of carbon-reinforced construction materials releases PM inducing inflammation and (secondary) genotoxicity in human lung epithelial cells and fibroblasts.

Building demolition following domestic fires or abrasive processing after thermal recycling can release particles harmful for the environment and human health. To mimic such situations, particles release during dry-cutting of construction materials was investigated. A reinforcement material consisting of carbon rods (CR), carbon concrete composite (C³) and thermally treated C³ (ttC³) were physicochemically and toxicologically analyzed in monocultured lung epithelial cells, and co-cultured lung epithelial cells and fibroblasts at the air-liquid interface.