Introduction to Health Physics: Fourth Edition - Ruang Baca FMIPA UB

BIOLOGICAL BASIS FOR R ADIATION SAFETY 285
most probable fate is determined chiefly by the LET of the radiation. In the case of a
high rate of LET, such as that which results from passage of an alpha particle or other
particle of high specific ionization, the free OH radicals are formed close enough
together to enable them to combine with each other before they can recombine
with free H radicals, which leads to the production of hydrogen peroxide,
OH + OH → H2O2, (7.5)
while the free H radicals combine to form gaseous hydrogen. Whereas the products
of the primary reactions of Eqs. (7.1) through (7.4) have very short lifetimes, on the
order of a microsecond, the hydrogen peroxide, being a relatively stable compound,
persists long enough to diffuse to points quite remote from their point of origin.
The hydrogen peroxide, which is a very powerful oxidizing agent, can thus affect
molecules or cells that did not suffer radiation damage directly. If the irradiated water
contains dissolved oxygen, the free hydrogen radical may combine with oxygen to
form the hydroperoxyl radical as follows:
H + O2 → HO2. (7.6)
The hydroperoxyl radical is not as reactive as the free OH radical and therefore
has a longer lifetime than it. This greater stability allows the hydroperoxyl radical to
combine with a free hydrogen radical to form hydrogen peroxide, thereby further
enhancing the toxicity of the radiation.
Radiation is thus seen to produce biological effects by two mechanisms, namely,
directly by dissociating molecules following their excitation and ionization and indirectly
by the production of free radicals and hydrogen peroxide in the water of the
body fluids. The greatest gap in our knowledge of radiobiology is the sequence of
events between the primary initiating events on the molecular level described above
and the gross biological effects that may be observed long after irradiation.
THE PHYSIOLOGICAL BASIS FOR INTERNAL DOSIMETRY
The determination of radiation dose from radionuclides within the body and the
calculation of amounts that may be safely inhaled or ingested depend on the knowledge
of the fate of these radionuclides within the body. Specifically, we need to know
the pathways that the radionuclides follow, the organs and systems that make up
these pathways, the rates at which they travel along these pathways, and the rates at
which they are eliminated from the body.
Physiologically based pharmacokinetic models are used to mathematically describe
the kinetics of metabolism of a radionuclide. If we know the quantitative
relationships among exposure, intake, uptake, deposition, and excretion of a radionuclide,
we can calculate the radiation dose from a given exposure. Knowledge
of the kinetics of metabolism can also be used to infer the radiation dose from
bioassay measurements and to set maximum acceptable concentrations in the environment.
The same methodology is also used for the control of nonradioactive
environmental contaminants. These underlying quantitative relationships are based
on the biochemical and biophysical principles that govern physiological processes.