Cellular burdens and biological effects on tissue level caused by inhaled radon progenies

TL;DR

This study investigates how uneven radon progeny deposition in bronchial airways causes localized cellular damage and potential tumor development, highlighting the importance of spatial distribution in radiation risk assessment.

Contribution

It introduces a computational approach combining fluid dynamics, cellular modeling, and carcinogenesis assessment to analyze radon exposure effects at tissue level.

Findings

Cellular doses can reach up to 1.5 Gy, much higher than tissue doses.

Uneven radon progeny deposition may cause localized tumor formation.

Cancer risk exhibits a non-linear relationship with radiation burden.

Abstract

In the case of radon exposure, the spatial distribution of deposited radioactive particles is highly inhomogeneous in the central airways. The objective of this research is to investigate the consequences of this heterogeneity regarding cellular burdens in the bronchial epithelium and to study the possible biological effects on tissue level. Applying a computational fluid dynamics program, the deposition distribution of inhaled radon daughters has been determined in a bronchial airway model for 23 minutes of work in the New Mexico uranium mine corresponding to 0.0129 WLM exposure. A numerical epithelium model based on experimental data has been utilized in order to quantify cellular hits and doses. Finally, a carcinogenesis model considering cell death induced cell cycle shortening has been applied to assess the biological responses. Computations present, that cellular dose may reach 1.5 Gy, which is several orders of magnitude higher than tissue dose. The results are in agreement with the histological finding that the uneven deposition distribution of radon progenies may lead to inhomogeneous spatial distribution of tumours in the bronchial airways. In addition, on macroscopic level, the relationship between cancer risk and radiation burden seems to be non-linear.