Assessment of biological responses of EpiAirway 3-D cell constructs versus A549 cells for determining toxicity of ambient air pollution.

CONTEXT: EpiAirway™ 3-D constructs are human-derived cell cultures of differentiated airway epithelial cells that may represent a more biologically relevant model of the human lung. However, limited information is available on their utility for exposures to air pollutants at the air-liquid interface (ALI). OBJECTIVE: To assess the biological responses of EpiAirway™ cells in comparison to the responses of A549 human alveolar epithelial cells after exposure to air pollutants at ALI. METHODS: Cells were exposed to filtered air, 400 ppb of ozone (O3) or a photochemically aged Synthetic Urban Mixture (SynUrb54) consisting of hydrocarbons, nitrogen oxides, O3 and other secondary oxidation products for 4 h. Basolateral supernatants and apical washes were collected at 9 and 24 h post-exposure. We assessed cytotoxicity by measuring lactate dehydrogenase (LDH) release into the culture medium and apical surface. Interleukin 6 (IL-6) and interleukin 8 (IL-8) proteins were measured in the culture medium and in the apical washes to determine the inflammatory response after exposure. RESULTS: Both O3 and SynUrb54 significantly increased basolateral levels of LDH and IL-8 in A549 cells. No significant changes in LDH and IL-8 levels were observed in the EpiAirway™ cells, however, IL-6 in the apical surface was significantly elevated at 24 h after O3 exposure. CONCLUSION: LDH and IL-8 are robust endpoints for assessing toxicity in A549 cells. The EpiAirway™ cells show minimal adverse effects after exposure suggesting that they are more toxicologically resistant compared to A549 cells. Higher concentrations or longer exposure times are needed to induce effects on EpiAirway™ cells.

Hazard assessment of United Arab Emirates (UAE) incense smoke.

Incense burning inside the home, a common practice in Arabian Gulf countries, has been recognized as a potentially modifiable source of indoor air pollution. To better understand potential adverse effects of incense burning in exposed individuals, we conducted a hazard assessment of incense smoke exposure. The goals of this study were first to characterize the particles and gases emitted from Arabian incense over time when burned, and secondly to examine in vitro human lung cells responses to incense smoke. Two types of incense (from the United Arab Emirates) were burned in a specially designed indoor environmental chamber (22 m(3)) to simulate the smoke concentration in a typical living room and the chamber air was analyzed. Both particulate (PM) concentrations and sizes were measured, as were gases carbon monoxide (CO), sulfur dioxide (SO2), oxides of nitrogen (NOx), formaldehyde (HCHO), and carbonyls. During the burn, peak concentrations were recorded for PM (1.42 mg/m(3)), CO (122 pm), NOx (0.3 ppm), and HCHO (85 ppb) along with pentanal (71.9 µg/m(3)), glyoxal (84.8 µg/m(3)), and several other carbonyls. Particle sizes ranged from 20 to 300 nm with count median diameters ranging from 65 to 92 nm depending on time post burn-out. PM, CO, and NOx time-weighted averages exceeded current government regulation values and emissions seen previously from environmental tobacco smoke. Charcoal emissions were the main contributor to both the high CO and NOx concentrations. A significant cell inflammatory response was observed in response to smoke components formed from incense burning. Our hazard evaluation suggests that incense burning contributes to indoor air pollution and could be harmful to human health.