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Age at exposure.
Cancer risk is determined by the age at exposure and concentration of radioisotopes in particular tissues.
It's important to remember that dose, duration and age at exposure all play a role, but there is mounting evidence that these chemicals may be a factor in early puberty.
The gender and the age at exposure are additional modifiers of the individual biological risk.
Thus, we might postulate an approach adapted to the cancer risk, i.e. based on organ doses, the age at exposure and gender.
Time-Since-Exposure = mean attained age – mean age at exposure.
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Gender, log mean attained age, and 14 indicator variables defined by 0 ≤ age-at-exposure < 5, 5 ≤ age-at-exposure < 10,... and 65 ≤ age-at-exposure < 70 were used as controls.
Indicator variables defined from mean age-at-exposure (cell data) are identical to those defined from the age-at-exposure stratification of the dataset.
The age-at-exposure effect is shown by a 20% decrease in attained-age-specific ERRs per decade increase in age at exposure.
An indicator defined by 70 ≤ age-at-exposure would be redundant.
The random-effects model, based on aggregate ERR data from individual studies without age-at-exposure information, predicts that population circulatory disease EAR (i.e., REID) in the United Kingdom varies minimally with age at exposure (Table 5).
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