With the above digression, we can uow ceturn to Fig. 3.
from the figure that it is

incomplete and misleading to present the data

terms of a “linear-no-threshold”
Fig.

2

It is clear

relationship.

Rather,

as shown also in

the data should be presented as distributions of hit cells,

the

area of the distribution representing the total amount of exposure.

It

then becomes clear

that what ts needed

that will respond quantally is
response curve,

to evaluate

the number of hit cells

the cell equivalent of an organ-dose

1.,¢@., a relationship

that will provide the probability of

a cell quantal response, as a function of iucreasing cell dose.
function,
-

termed a hit-size effectiveness

developed (11-14).
curve In Fig. 2,

in

One such curve

function (HSEF),

Such a

has heen

is shown schematically as

the S-shaped

An actual curve for chromosome abnormalities, derived

From the data in Fig. 1, is shown in Fig. 5.(3).

The use of these curves

is now discussed, following which thetr derivation is summarized.

.
&3
ca
2

1.0

T

T

oF ot

ae:

PROBABILITY OF QUANTAL EFFECT

CH26, CELLS
chromosome abnomalities

0.8}

(Skarsgard}

4

abnormal metaphases

0.6

o 8215p m*

4

O4F

4

0.2 5+

4
chromatid exchange

F = 10.4 pm?
oO

10

20

L

30

ai.

id

50 70 100
iiiJ

y/ kev m'

Fig. 5
Ref.

3}.

1

200 300

An HSEF derived from the data shown in Fig. 1 (from
The two curves are for different chromosome aberrations.
Use of the HSEF

The use of the liSEF is shown schematically in Fig. 2.

For any one or

combination of cell hit size distributions shown, one simply multiplies theja

distribution by the HSEF, ise.,

the number of hit cells at each hit size 1s

multiplied by the corresponding point on the HSEF.

-216-

20129 16

The resulting products egy

r
ai

ne
af,

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