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L ung cancer is the leading cause of cancer deaths (1). Its early detection and treatment are important to reduce the mortality rate. According to the National Lung Screening Trial, annual lung cancer screening by using low-dose (LD) chest CT reduced the number of deaths in patients at high risk (2). LD CT screening is not without risk and although the associated radiation dose is about one-fourth that of standard-dose (SD) CT (3), on the basis of the linear nonthreshold theory, the cancer risk from radiation exposure at LD CT cannot be ignored. Annual screening has been suggested to increase the risk for lung cancer (4,5), although the radiation-induced cancer risk from exposure to less than 100 mSv remains unclear (6,7).g-H2AX analysis to evaluate the biologic effects of lowdose radiation including CT revealed that exposure even at the diagnostic level induces DNA damage (8-14). Dicentric and ring chromosome analyses are the reference standard in biodosimetry. Immunofluorescence analysis of nuclear foci formed by the phosphorylated histone H2AX (g-H2AX), a technically simple and highly sensitive method, yields a marker of DNA double-strand breaks (15). The effects of LD CT on DNA damage and chromosome aberrations (CAs) in adults remain to be clarified before the implementation of

D and D were significantly smaller in NOMI patients than in the controls and D is a more significant parameter than D.

The radiation dose for CACS can be reduced at a low tube current and hIR without affecting the calcium score.

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