RESUMO
After smoking, exposure to radon and its progeny is the second leading cause of lung cancer. The probability of inducing lung carcinomas by inhaled radon progeny depends on the deposited radiation dose, and is significantly affected by physiological and morphometric changes induced by smoking. Due to irritation of the airways, the inhalation of cigarette smoke leads to the hyperproduction of mucus. Two concurrent processes occur: on one hand, increased production of mucus protects the target cells against radiation damage; on the other hand, in the case of long-term smokers, a chronic lung obstruction develops, causing an increase in the radiation dose to the lungs. Depending on the duration and intensity of smoking, these processes contribute to the final radiation dose with different weights. The primary objective of this study was to investigate to what extent these smoke-induced changes can modify the resulting absorbed dose of inhaled radon progeny relative to healthy nonsmokers. Since the bronchial dose depends on the degree of lung tissue damage, we have used this dose as a tool for detecting the effects of smoking on the lung epithelium. In other words, the biological effect of radon served as a tracer of changes induced by smoking.
Assuntos
Pneumopatias/induzido quimicamente , Neoplasias Pulmonares/induzido quimicamente , Radônio/efeitos adversos , Fumar , Administração por Inalação , Humanos , Pulmão/efeitos da radiação , Neoplasias Induzidas por Radiação , Probabilidade , Doses de Radiação , Radiometria , Medição de Risco , Produtos do TabacoRESUMO
Smoking modifies morphological and physiological parameters of the lungs. Due to the irritation of airways, the natural self-cleaning ability of the lungs is impaired. The mucus accumulates in the airways and various infections develop, leading to chronic bronchitis. After the cessation of smoking, the lungs of the smoker start to heal and regenerate. Cilia in the lungs start to grow again and cleanse the lungs, thus reducing the risk of infection. The regeneration of the lungs takes a long time and depends on the degree of lung damage due to smoking. The aim of this study was to reconstruct the evolution of this regeneration process in chronic smokers by using the biological effects of radon and its decay products. Thus, radon in this study served as a tracer of changes induced by smoking.
