目前了解低劑量輻射誘發罹癌的風險，是從日本原子彈爆炸生還者由較高劑量和高劑量率外插到低 劑量區域。為了輻射防護的目的，目前人類游離輻射暴露限制準則，在輻射致癌是基於線性無閾值 (linear-no-threshold, LNT)的假說，即罹癌的風險會隨著輻射劑量的增加而呈線性增加。在LNT 模式下即使 是非常小的劑量都可能造成癌症，因此被用來建立人類輻射暴露限制的準則。輻射生物學的研究支持了LNT 的模式，但是這些大多是被限制在相對高劑量的研究。最近，隨著低劑量曝露效應的實驗模式與在分子、 細胞生物學的新進展，一系列新的輻射生物效應已經被觀察到。這些效應包括:基因組不穩定性(genomic instability)、適應反應(adaptive response)和旁觀者效應(bystander effect)，這些效應在低劑量時是顯著非線性 反應是它們共同的特點。這些新的觀察讓我們對低劑量暴露的生物效應提出一個重大的質疑，需要進一步 研究來說明它的機制，並確定它們的相關性。

Current understandings of low dose radiation risk for cancer induction in humans are extrapolated from the Japanese atomic bomb survivors, who were exposed to relatively high dose and high dose rates. For radiation protection purposes, current guidelines for limiting exposure of humans to ionizing radiation are based on the linear-no-threshold (LNT) hypothesis for radiation carcinogenesis under which cancer risk increases linearly as the radiation dose increases. With the LNT model even a very small dose could cause cancer and the model is used in establishing guidelines for limiting radiation exposure of humans. Recently, with new advances for studying effects of low-dose exposure in experimental models and advances in molecular and cellular biology, a range of new effects of biological responses to radiation has been observed. These include genomic instability, adaptive responses and bystander effects. Most have one feature in common in that they are observed at low doses and suggest significant non-linear responses. These new observations pose a significant challenge to our understanding of low-dose exposure and require further study to elucidate mechanisms and determine their relevance.