Radon induced hyperplasia: effective adaptation reducing the local doses in the bronchial epithelium

TL;DR

This study investigates how radon-induced hyperplasia in bronchial epithelium acts as an adaptive response, reducing local doses and shielding basal cells from alpha radiation, which impacts dose assessment models.

Contribution

It quantifies the microdosimetric effects of hyperplasia on radon exposure, showing tissue adaptation alters dose distribution and challenges existing dose rate effectiveness assumptions.

Findings

Hyperplasia decreases average tissue dose and basal cell hits.

Induction of hyperplasia shields basal cells from alpha radiation.

Tissue adaptation influences dose assessment in chronic radon exposure.

Abstract

There is experimental and histological evidence that chronic irritation and cell death may cause hyperplasia in the exposed tissue. As the heterogeneous deposition of inhaled radon progeny results in high local doses at the peak of the bronchial bifurcations, it was proposed earlier that hyperplasia occurs in these deposition hot spots upon chronic radon exposure. The objective of the present study is to quantify how the induction of basal cell hyperplasia modulates the microdosimetric consequences of a given radon exposure. For this purpose, numerical epithelium models were generated with spherical cell nuclei of six different cell types based on histological data. Basal cell hyperplasia was modelled by epithelium models with additional basal cells and increased epithelium thickness. Microdosimetry for alpha-particles was performed by an own-developed Monte-Carlo code. Results show that the average tissue dose, and the average hit number and dose of basal cells decrease by the increase of the measure of hyperplasia. Hit and dose distribution reveal that the induction of hyperplasia may result in a basal cell pool which is shielded from alpha radiation. It highlights that the exposure history affects the microdosimetric consequences of a present exposure, while the biological and health effects may also depend on previous exposures. The induction of hyperplasia can be considered as a radioadaptive response at the tissue level. Such an adaptation of the tissue challenges the validity of the application of the dose dose rate effectiveness factor from a mechanistic point of view. As the location of radiosensitive target cells may change due to previous exposures, dosimetry models considering the tissue geometry characteristic of normal conditions may be inappropriate for dose estimation in case of protracted exposures. As internal exposures are frequently chronic, such changes in tissue...