  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...
