Table 2.

In vitro and in vivo models of the respiratory epithelial barrier disruption triggered by air pollution-related substances.

Substance	Evidence	Reference(s)
Particulate matter	PM2.5 exposure in a BEAS-2B cell line increased apoptosis, decreased viability, and decreased ZO-1 and e-cadherin mRNA expression.125	125
	PM2.5 exposure cause ROS activation and apoptosis.138,140	138,140
	PM2.5 and urban PM disrupt TJ molecules of the human nasal epithelium and exacerbate AR.141–143	141–143
	PM10 induces epithelial barrier damage in a primary rat alveolar epithelial cell culture.147	147
Micro- and nano-plastics	Polystyrene micro and nanoparticle exposure induce cytotoxicity, apoptosis, and autophagy in human bronchial and alveolar cell culture models.131,200	131,200
	Polystyrene micro and nanoparticle exposure damage the bronchial epithelial barrier by reducing ZO-1 mRNA expression.	131,200
DEP	DEP induce epithelial barrier damage in human bronchial epithelial cell line.154,155	154,155
	DEP increase IL-33, IL-25, and TSLP cytokine production with Th-2 activation in allergic severe asthma patients.	151–153
Ozone	Ozone exposure causes respiratory barrier injury in mouse models.126,159	126,159

IL: Interleukin; PM: Particulate matter; Th: T helper; TJ: Tight junction; TSLP: Thymic stromal lymphopoietin; ZO: Zonula occludens