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<blockquote>Most adverse health effects of radiation exposure may be grouped in two general categories:

*stochastic effects, i.e., cancer and heritable effects involving either cancer development in exposed individuals owing to mutation of somatic cells or heritable disease in their offspring owing to mutation of reproductive (germ) cells.</blockquote>

<blockquote>The induction of tissue reactions is generally characterised by a threshold dose. The reason for the presence of this threshold dose is that radiation damage (serious malfunction or death) of a critical population of cells in a given tissue needs to be sustained before injury is expressed in a clinically relevant form. Above the threshold dose the severity of the injury, including impairment of the capacity for tissue recovery, increases with dose.

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<blockquote> The manifestations of tissue injury vary from one tissue to another depending on cellular composition, proliferation rate, and mechanisms of response to radiation, which may be highly tissue specific. Examples ... include cataracts of the lens of the eye, non-malignant damage to the skin, cell depletion in the bone marrow causing haematological deficiencies, and gonadal cell damage leading to impairment of fertility. Tissue reactions, especially late reactions, also depend on damage to blood vessels or elements of the extracellular matrix, which are common to most organs of the body. </blockquote>

<blockquote> In the case of cancer, epidemiological and experimental studies provide evidence of radiation risk albeit with uncertainties at doses about 100 mSv or less. In the case of heritable diseases, even though there is no direct evidence of radiation risks to humans, experimental observations argue convincingly that such risks for future generations should be included in the system of protection. </blockquote>

<blockquote>... the practical system of radiological protection ... will continue to be based upon the assumption that at doses below about 100 mSv a given increment in dose will produce a directly proportionate increment in the probability of incurring cancer or heritable effects attributable to radiation. This dose-response model is generally known as ‘linear-non-threshold’ or LNT. ... the adoption of the LNT model ... provides a prudent basis for the practical purposes of radiological protection, i.e., the management of risks from low-dose radiation exposure.

... whilst the LNT model remains a scientifically plausible element in its practical system of radiological protection, biological/epidemiological information that would unambiguously verify the hypothesis that underpins the model is unlikely to be forthcoming ... Because of this uncertainty on health effects at low doses, ... it is not appropriate, for the purposes of public health planning, to calculate the hypothetical number of cases of cancer or heritable disease that might be associated with very small radiation doses received by large numbers of people over very long periods of time ... </blockquote>

<blockquote> There continues to be no direct evidence that exposure of parents to radiation leads to excess heritable disease in offspring. However, ... there is compelling evidence that radiation causes heritable effects in experimental animals. Therefore, the Commission prudently continues to include the risk of heritable effects in its system of radiological protection. </blockquote>

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