On the dose-response association of fine and ultrafine particles in an urban atmosphere: toxicological outcomes on bronchial cells at realistic doses of exposure at the Air Liquid Interface.

Air pollution and particulate matter (PM) are the leading environmental cause of death worldwide. Exposure limits have lowered to increase the protection of human health; accordingly, it becomes increasingly important to understand the toxicological mechanisms on cellular models at low airborne PM concentrations which are relevant for actual human exposure. The use of air liquid interface (ALI) models, which mimic the interaction between airborne pollutants and lung epithelia, is also gaining importance in inhalation toxicological studies.

Associations between fine particulate matter, gene expression, and promoter methylation in human bronchial epithelial cells exposed within a classroom under air-liquid interface.

Associations between indoor air pollution from fine particulate matter (PM with aerodynamic diameter d < 2.5 μm) and human health are poorly understood. Here, we analyse the concentration-response curves for fine and ultrafine PM, the gene expression, and the methylation patterns in human bronchial epithelial cells (BEAS-2B) exposed at the air-liquid interface (ALI) within a classroom in downtown Rome.

Exposure to urban nanoparticles at low PM[Formula: see text] concentrations as a source of oxidative stress and inflammation.

Exposures to fine particulate matter (PM[Formula: see text]) have been associated with health impacts, but the understanding of the PM[Formula: see text] concentration-response (PM[Formula: see text]-CR) relationships, especially at low PM[Formula: see text], remains incomplete. Here, we present novel data using a methodology to mimic lung exposure to ambient air (2[Formula: see text] 60 [Formula: see text]g m[Formula: see text]), with minimized sampling artifacts for nanoparticles. A reference model (Air Liquid Interface cultures of human bronchial epithelial cells, BEAS-2B) was used for aerosol exposure.