The deterministic effects occur when above a certain “threshold”
an appropriately high dose (above 500–1000 mSv) is absorbed in the
tissues and organs to cause the death of a large number of cells and consequently
to impair tissue or organ functions early after exposure. The severity
of injury depending on the absorbed dose according to an s-shaped dose-response
curve might be manifested in the various syndromes of radiation illness,
i.e. the bone marrow, the gastro-intestinal and the central nervous system-vascular
syndromes. The effects can be detected by laboratory and clinical techniques.
The stochastic effects might occur following low doses (below several tens or 100–200 mSv). The probability of consequences increases with the dose and the relationship between dose and effect is assumed to be linear. Accordingly, not having a “threshold” dose a certain risk – albeit very small – can be attributed to any low dose.
Such late effects might be the development of malignant (cancerous) diseases and of the hereditary consequences. Here, it has to be mentioned that in human populations hereditary effects could not be detected even in the offsprings of the large population of A-bomb survivors in the first two generations. The possibility of hereditary alterations is known only from experimental observations in radiation biology.
The model for assessing the detrimental health effects used for the deterministic effects is the non-linear-threshold (NL-T) model, while for the stochastic effects the linear-non-threshold “L-NT” one. In the low dose dilemma the problem raised is whether the use of the L-NT model is justified to attach any health risks to low doses.
|For stochastic effects
for gamma and x-rays
For cellular reactions
when less than 20 % of “gross sensitive volume – GSV”
(F target) will be hit once
See Table 2
The avarage natural background
in a year
in the life-time of a person
“Insignificant individual dose”
“De minimis” dose
Webb and McLean 1977
granulocyte oxidant production increases
superoxide dismutase in spleen increases
oxidative stress increases
Lymphocyte mitogenic stimulation by lectins
Thymidin kinase activity
CHO-CD2+ fenotype alteration
Spleen colony formation stimulation
Cell membrane stucture and function
Adaptive response develops
Vicker et al. 1991
Yamaoka et al. 1990
Makinodan and James 1990
Nogami et al. 1994
Feinendegen et al. 1988
Krymskx-Ruda et al. 1992
Kitsiou et al. 1993
Rozhdestvensky and Fomicheva 1995
Grosovsky and Little 1985
Belyaev and Harms-Ringdahl 1996
Köteles et al. 1997
Petcu et al. 1997
Bojtor and Köteles 1998
Kubasova et al. 1981 a,b
Mosoi and Sakamoto 1990
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