An air-liquid interface system for toxicity studies of combined exposure to cigarette smoke and radon.
[PURPOSE] While cigarette smoke (CS) is known to modify the risk of radon-induced lung cancer, the mechanisms remain poorly understood.
APA
Boroumand N, Juárez-Facio AT, et al. (2026). An air-liquid interface system for toxicity studies of combined exposure to cigarette smoke and radon.. International journal of radiation biology, 102(5), 536-551. https://doi.org/10.1080/09553002.2026.2629537
MLA
Boroumand N, et al.. "An air-liquid interface system for toxicity studies of combined exposure to cigarette smoke and radon.." International journal of radiation biology, vol. 102, no. 5, 2026, pp. 536-551.
PMID
41770122
Abstract
[PURPOSE] While cigarette smoke (CS) is known to modify the risk of radon-induced lung cancer, the mechanisms remain poorly understood. Experimental studies on their combined effects are limited by the lack of suitable in vitro exposure platforms. This study provides proof-of-concept validation of a novel ALI exposure system for controlled, simultaneous exposure to radon and CS.
[MATERIALS AND METHODS] The system comprises a Ra source, radon monitor, smoking machine, particle counter, siphon mixing unit, and an ALI system. The CS unit maintained the target concentration at 5 mg/m and induced dose-response toxicity in BEAS-2B cells following 0.5, 1 and 2 h exposures. For a 2-h radon exposure, the estimated average dose to the cells was 1 mGy (range 0.3-7.5 mGy), with a localized dose of 171 mGy per hit nucleus.
[RESULTS] Separate exposure to radon (2 h, 228 ± 54 kBq/m) and CS (1 h, 5 mg/m) resulted in 75 ± 9% and 83 ± 16% cell viability, respectively, while combined exposure led to a significantly lower cell viability (55 ± 8%). A trend toward an increase in pro-inflammatory IL-8 secretion was noted for all exposures; however, it did not reach statistical significance.
[CONCLUSION] The developed ALI-based exposure system enables precise dosimetry and biological assessment, establishing a validated proof-of-concept platform for future research on environmental co-exposures.
[MATERIALS AND METHODS] The system comprises a Ra source, radon monitor, smoking machine, particle counter, siphon mixing unit, and an ALI system. The CS unit maintained the target concentration at 5 mg/m and induced dose-response toxicity in BEAS-2B cells following 0.5, 1 and 2 h exposures. For a 2-h radon exposure, the estimated average dose to the cells was 1 mGy (range 0.3-7.5 mGy), with a localized dose of 171 mGy per hit nucleus.
[RESULTS] Separate exposure to radon (2 h, 228 ± 54 kBq/m) and CS (1 h, 5 mg/m) resulted in 75 ± 9% and 83 ± 16% cell viability, respectively, while combined exposure led to a significantly lower cell viability (55 ± 8%). A trend toward an increase in pro-inflammatory IL-8 secretion was noted for all exposures; however, it did not reach statistical significance.
[CONCLUSION] The developed ALI-based exposure system enables precise dosimetry and biological assessment, establishing a validated proof-of-concept platform for future research on environmental co-exposures.
MeSH Terms
Radon; Humans; Smoke; Cell Line; Dose-Response Relationship, Radiation; Toxicity Tests