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373
T, = L + k CDT - DR>
where
FIG. 2. Scanning radiometer. A = glass back plate; B = metal
Ts = skin temperature (“C) frame support for thermo-receiver worm-drive, C, for adjusting
Tc = chopper temperature (“C) position of receiver D ; E = leads from receiver; F = millimeter
DT = total deflection in millimeters at time t rule for receiver position indication ; G = glass front plate; H =
DR = deflection in millimeters due to reflected radiation metal plate for rotating frame and receiver; Z = metal mounting
k = calibration constant = ‘C/mm deflection/o.94 plate.
INTENSITY CONTOURS IN minus 32.5OC. These values were then substituted in the
IRRADIATED AREAt% of MAXItim equation which was solved for t :
t =- (aT> 2kw
I .13Q2
where
1.13 = 4a2/r
kpc = product of therm al conductivity, k, density, p, and TABLE I. Thermal Inertia (kpc) of Skin at Pain Threshold
-.__ -----.- -
specific heat, c, in mcal/cm4 “C sec.
(A7*) = rise in skin temperature in “C = final skin tempera- kpc (X10-j) caP/cm4/“C/sec.
ture - initial skin temperature Irradiance mc/cm2 sec.
=
fl absorptivity of India-inked skin = 0.94 Average Range
Q = radiation intensity in Cal/cm2 set -..~._ -- ------
1 = time in seconds 100
96 75-I 17
150 I IO 89-142
Then, when the initial temperatu re w as differen t from 200 127 95-158
3oo ‘39 I15-168
‘32.5OC,
c . kpc was determ ined from the measured values
400 I59 144-181
and (AT) was set equal to the observed final temperature
threshold pain occurs at a skin temperature of about Here are shown two heating curves at different irradi-
45OC and ceiling pain at about 6o”C, almost indepen- antes. The left ordinate indicates temperature and the
dently of the time required to attain these levels. Blister- right ordinate the corresponding rate of protein denatu-
ing, however, depends strongly on both temperature and ration as determined by Henriques and Moritz. In the
time. Thus, with an irradiance of IOO mcal/cm%ec., temperature curves ‘skin temperature’ refers to the sur-
threshold blisters were produced at a skin temperature face of the skin and ‘tissue temperature’ to the computed
of 52.g°C attained after 33.8 seconds of exposure; temperature at a depth of 80 p below the surface, or
whereas, at 300 mcal/cm2sec., threshold blistering oc- approximately the basal layer. The damage integral is
curred at a skin temperature of 56.7OC attained after obtained by plotting the rate of denaturation corre-
7.8 seconds of exposure, while heating the skin to 53OC sponding to the tissue temperature against the time at
with radiation of this higher intensity produced only a which the temperature occurred during the exposure and
transient erythema. On the other hand, even slight pro- then, by planimetry, measuring the area under the
longation of the exposure, such that the peak skin tem- resultant curve. Thus, it is seen that for the production
perature exceeds the values corresponding to threshold of threshold blisters in these instances, the damage
blisters by as little as I “C, results in a full blister, i.e. integral, 0, was 0.15 and 0.27, or about two-tenths of
a single blister involving the entire irradiated area formed the value obtained by Henriques and Moritz for the
within a few hours after the exposure and often raised to same injury using constant temperatures.
a height of 3-5 mm within 24 hours. These data, which Table 3 shows irradiances, temperatures and the
are represented by the third curve (fig. 4), resulted from corresponding average values of Q, as computed by the
overshooting the desired end point and are not intended method above for the threshold blisters. The full blister
to delineate the lower limit of full blistering. data are also shown, but are fragmentary and are in-
Henriques and Moritz (3, 4), using constant tempera- cluded only incidentally since they do not delineate the
ture levels, have derived the equation below for the lower limit of exposure time for full blisters. Not in-
evaluation of tissue damage, whereby damage is related cluded in this table, but worthy of mention as an illustra-
to the rate of protein denaturation and the exposure time tion of the great importance of initial skin temperature,
at a given temperature: is one burning episode at 150 mcal/cm2sec. which re-
sulted in an Q value of 2.0. This exposure was made for
a time (22.15 sec.) expected to produce blistering with
an initial skin temperature of about 32.o”C but, instead,
where produced a white burn with immediate destruction of
62 = tissue damage TABLE 2. Irradiance, Time and Tmjerature for Pain Threshold and
P = integration constant Blister Production
AE = energy of inactivation ----- ~.-
-- -~.___-- -~-
R = gas constant Pain Threshold
Pain Threshold
TI* = tissue temperature Controls Threshold Blister Full Blister
Radia- (During Burning)
(Nonburn)
t = exposure time tion
tensi ty
In-
meal/
cm2 sec. No .
I, 1 Ts,
Thus, the symbol Q was chosen to represent damage. It of
sec. “C
obs.
was defined as the integral of the damage rate (&/dt)
for the exposure time noted and was given the value of 100 6 /12.4;45.8: r2 i33.852.g I 37k53.4
49 ‘3.5145.’
I .o when complete transepidermal necrosis in pig skin, 125 3’ I0.1145.3 I I I I
or blistering in human skin, was produced. Using the 150 67 7-845-9
200 22 5.5 46.5
damage rates determined by these authors for various
300 36 Q-9,47- I
tissue temperatures, the computation of Q was applied to
400 ‘3
the present experimental data as illustrated in figure 5.
mc/Cm*/sec fiti-
fi
Fig. 5
lc
--
56-
do
701
RADIATION
t
= 300 mc/cmVsec dt
x lo-’
x10-=
RADIATION = 100 mc/cm%ec 16
FIG. 4. Irradiance and ex- 2.5
time to threshold pain -5
posure
and blistering.
-4
FIG. 5. Temperatures at skin
surface and those calculated at
-3
80 p beneath surface during ther-
mal exposure, and resultant /
-2 a=0 27
damage integrated at damage Threshold
Blister
rates from Henriques’ study.
-I
cc--J, !\ -0
I I, I I I I I, I, I, 1, t * I C&--l ’
4 8 12 16 20 24 28 32 36 0 IO 20 30 40 50 s,ec set
TIME (SECONDS) TIME
TAHLK 3. h-radiance, 0 bserved Temperatures and Damage rate at which heat is conducted away from the surface.
Thus, the flow of heat through the surface layers, i.e. the
Skin Temp., “C India ink and the epidermis, must be enhanced, effecting
Threshold Blister
(I, mcal,/c-m2 sec. Full Blister f2
-_ sz a change in the value of kpc as derived from the observed
T, Tt quantities, irradiance, surface temperature and expo-
-__--.-- (- 1-----__I ---1
sure time. It is well known that the thermal conductivity
100 52.9 52.3 0.15 0.20
of water and certain aqueous solutions (in direct con-
150 54-o 53.2 0. ‘7 0.54
300 56.7 55.2 0.27 0.91 trast to most materials) increases with an increase in
40” 59.’ 57-2 0.83 temperature. It may be that the engorged tissue under-
lying the epidermis behaves in the same manner with
respect to thermal conductivity, effecting a real increase
the epidermis, completely bypassing blister formation in k of this tissue and further enhancing heat loss from
and deeply involving the dermis. On analysis of the the surface. As the level of irradiance is increased, higher
record it was found that the initial skin temperature had temperatures are produced within the same exposure
been ~~~+5°C, considerably higher than expected; there- time so that this k may attain increasingly high values,
fort, Ke exposure of 22. I 5 seconds was equivalent to an thus contributing to increasingly high values for kpc.
exposure of 24.0 seconds if the initial skin temperature From the data on pain threshold presented in table 2
had tIeen 32.5”C. Also, the final skin temperature was it is possible to estimate the firing temperature and the
58.2”C, whereas a skin temperature of 55OC (table I) average depth of the pain receptors, assuming that the
attained at this radiation intensity is sufficient to produce receptors fire at some definite temperature, from the
a full blister. Thus, the importance of skin temperature, mathematical formulations for heat transfer as used by
both initial and final, cannot be overemphasized in this Henriques (3). Although this equation was derived for
type of heating, in which far different histological results use in the unsteady state when the surface is immedi-
can be achieved with the same intensity-time dosages ately brought to and maintained at a constant tempera-
when the initial temperature is only I “C or so different. ture, it is equally valid when the surface temperature,
Empirically it is found from the accumulated data although not constant, is known at every instant in time,
that, because of the similarity in form of the curves for the radiation is nonpenetrating, and heat transfer in-
threshold pain and threshold blisters, the time to pro- ward is conductive. Thus, the receptor temperature at
duce blistering may be predicted simply by multiplying the time pain threshold is reached is the same at all
the exposure time to pain threshold by a constant, in this irradiances and may be expressed as:
instance 2.52. However, the value of the constant, just
as the exposure time itself, depends strongly upon the
initial skin temperature. Nevertheless, in any standard- 02
ized irradiation procedure a factor such as this one may
be determined approximately from a very few experi-
ments and thereafter serve as a useful rule-of-thumb where
throughout the range of irradiances to be used. The
TR = temperature of receptors (“C)
fundamental significance of the relationship shown here
Ts = skin temperature (“C) at pain threshold
is treated in the later part of the discussion which follows. 7-O = initial skin temperature at start of radiation
t = time to pain threshold
DISCUSSION
Y=
D
-
k where D is the depth of the receptors in cm;
Considering first the data on kpc values presented in 2 -
table I, it is seen that the value of kpc increases with ir- d
k/pc =
PC
thermal diffusivity where k is the conductivity
radiance and reaches a maximum of about 160 X IO-~
(Cal/cm sec. “C); p is the density (gm/cc) and c is the
ca12/cm4/‘C/sec. at the 400 mc/cm2 sec. level. It has specific heat (cal/gm “C)
been pointed out (9) that, for exposure times of less than
20 seconds the kpc of normal living skin was about go-100 and
x 10-5, while, on prolonged heating, this value in-
A
s
creased to as much as 400 X IO-~, which was at-
2 4t
trihuted to local passive vasodilation. However, in the - e--y2 dy = probability integral.
d = 0
measurements cited, the irradiance was not more than
55 mc/cm2sec. and the increase in skin temperature
(forearm) was about 7OC in 20 seconds, therefore, well Then, assuming as a first approximation that the
below pain threshold and well below the temperature thermal diffusivity of the skin from the surface inward is
elevation at pain threshold (I 2.5OC or greater) experi- a constant, the observed values for T,, & and t at each
enced in the present study. Since the epidermis is avas- irradiance are introduced and the equation solved for
cular it is unlikely that p and c of the surface vary greatly Tn through a series of increasing values for 7 until TR
during irradiation; however, the blood content of the is found to be the same at all irradiances. The value for
underlying tissue must certainly increase, affecting the y found by this method was 0.45 and that of TR, the
pain receptor temperature at pain threshold, was not likely to affect the computation significantly. Of the
43.2 & 0.4”C throughout the range of irradiances em- other factors, certainly p and c cannot be far different
ployed. In order to solve for D in the equation from I .o. Thus, the figure of least confidence is the value
of k; the fact that this has a large effect is obvious. If,
D to circumvent the uncertainties of applying porcine skin
0.45 = y = ~
k constants, the value for thermal diffusivity, as deter-
2 - mined by Hensel (I 3), for the most superficial ‘layer’ of
^J PC
human skin (o to 0.26 mm) is used, the depth becomes
it becomes necessary to adopt reasonable values for k, p
and c. Dealing first with the most superficial 1ayer, epi-
dermis, a value of 0.0005 ca .l cm/cm2 sec.OC has been
determined for k of porcine epidermis (I o), which may
be expected to be quite similar to human epidermis. Al- where
though Henriques worked with an assumed value of
0.8 gm/cc for p, such data as are available in the litera- k/w = 4 x 10-1
\gradient through the skin is such that the basal layer is ble without producing complete transepidermal necrosis
maintained at an injurious temperature level while the in porcine tissue) was assumed with the expectation that
pain receptors are maintained at a subthreshold level. additional damage at a submaximal rate would proceed
Considering now the threshold blister data, it is possi- after the end of the exposure during the return of the
ble to apply the rate process equation to these and to skin temperature to the initial level. With the exception
predict the exposure time to blister formation applicable of the instance of the lowest intensity radiation used,
to the dynamic type of heating, used here in a manner which will be discussed later, the exposure times pre-
similar to that used by Henriques and Moritz for steady dicted in this manner were remarkably accurate
states. To arrive at an approximate exposure time pro- (table 4). H owever, despite the agreement in exposure
ductive of blistering, the procedure used was to deter- time, the values for Q (table 3) obtained by planimetry
mine the theoretical temperature rise during a given ex- from the observed data and the corresponding damage
posure to radiation intensity according to equation I, then rates were much smaller than the predicted values of
to find the corresponding tissue temperature at a depth from 0.5 to LO, except for the exposures at the highest
of 8o p, according to the method of Henriques and intensity (table 5, col. 8). The reasons for the discrepan-
Moritz, and assign the damage rate associated with each cies noted become clear on consideration of the data pre-
tissue temperature to the instant in time at which the sented in table 5. It should be recalled that the assump-
tcmpcrature was attained. Thus, a log plot of d&G&, the tions made in predicting the exposure time were: a) that
damage rate, with respect to t, the exposure time, was the temperature rise with respect to exposure time was
obtained, and the slope of this line was used to find the described adequately by equation I; 6) that the damage
time at which a given value for a, the total damage, performed during cooling would be approximately equal
could bc expected. Thus, to that performed during heating and c) that the damage
rate derived from the data of Henriques and Moritz,
I/ =
sc 2iyo3K(tz- to)- e2*303Jwl-t~)
t2 du
- dt =
t1 dt s t1
t2
Ce2.303K(+-to) dt
(3)
dfi/dt = PeAE”RTt
(,1=
1 2.303K
1 where
100 55.5 54.9 I.42 X 10-l 52.9 52.3 2.4 X Iow2 0.15 20.1 14.0
150 56.5 55.5 I .8 X 10-l 54.0 53.2 4.4 x 10-2 0.17 ‘3.4 8-4
300 58.8 57.2 6.4 X 10-l 56.7 55.2 1.7 X 10-l 0.27 4.8 5-o
4oo 62.4 59.3 3-o 59-I 57.2 6.9 x IO-’ 0.83 3.4 3.5
common observation that less total heat is required to This finding leads to a consideration of the second
produce equivalent damage at high levels of radiation alternative, that of attributing the difference to inaccu-
intensity than at low levels. The third assumption, that racies in measurement of the surface temperatures or
the damage rate relationship is accurate, is borne out inappropriateness of method in obtaining tissue tem-
approximately at the highest intensity exposures, but peratures. The difference in damage rates at 45°C is
becomes progressively inapplicable at the lower intensi- equivalent to a temperature difference of almost 6°C. It
ties. Thus, the agreement, or lack of agreement, in pre- is not possible, even by accumulating all reasonable
dicted and observed exposure times reflects the degree to possible errors of measurement of both methods in addi-
which the necessary conditions were fulfilled. tion to those of the method of computation, to approach
In reconciling the experimental findings of this study a difference of 6OC, particularly at the lower levels of
with those obtained by conductive heating, at least three temperature where the greatest accuracy is achieved in
alternatives present themselves : either the damage rate both methods. Thus, an error in tissue temperature as
associated with each temperature is not accurate, or the great as even 2OC is inconceivable with the conductive
surface or tissue temperatures obtained by one or the method of heating where the heating is maintained for
other methods are not accurate, or there is a disconti- 2-3 hours. Similarly, in the radiative method, even if
nuity in the relationship between damage rate and other methods of computation of tissue temperature are
temperature which is obscured by the transition from used (7, Ig), the accumulated possible error does not
the steady state to the unsteady state conditions. approach 2OC. In fact, if the measured surface tempera-
Considering these alternatives in order, it was possible ture itself is used as the damage-effecting temperature,
to adjust the damage rate with respect to tissue tempera- the damage integral Q increases to only 0.28 at the IOO
ture empirically to yield Q = I .o for each level of radia- mcal/cm2sec. level and to 0.38 at the 150 meal cm2sec.
tion intensity. This adjustment resulted in a change of level, both far less than 1.0. Thus, it appears that the
slope of log dQ/dt vs. T, from 0.297 for the conductive discrepancy cannot be attributed to this source.
heat data to o. 166 for the radiative heating. The two The third alternative remains, i.e. there is a discon-
curves then intersected at 57.4OC, indicating that with tinuity in the damage rate function which is obscured
radiative heating the damage proceeded more rapidly at in passing from the steady to the unsteady temperature
lower temperatures and more slowly at temperatures state. In evaluating this possibility, careful consideration
above 57.4OC than it did with conductive heating. How- must be given to the special features applicable to each
ever, on substituting the new rates in the original equa- method of producing the tissue damage, as well as to
tion of the rate process and solving for the exposure time the handling of the experimental facts. Enumeration and
when the temperature is maintained constant, it was comparison of these features reveals that, in the con-
found that the exposure time at a tissue temperature of ductive method: I) experimental data are most de-
57.2OC was practically unaffected, while at 45OC the pendable at the relatively low-temperature, long-term
exposure time was reduced by a factor of about 60. exposures, i.e. up to a surface temperature of 5oOC.
However, the finding of a pain threshold at 47.5’- TABLE 6. Pain, Tissue Temperatures and DarnaS” Rates
Established Herein
48.5OC (4), with exposures of 40 minutes duration, is
puzzling, since direct skin temperature measurements, Observed Tissue Damage Ratios of Predicted
whether on blackened or unblackened skin, yield a pain Pain Temp., Rate, Stimulus Time to
Intensity, “C dQ/dt Intensity, Threshold
threshold of about 45OC when heating time to pain
threshold is not shorter than IO seconds.
JND s/so = dfj/dt/ Blister When
du/dt (1 512= I, see.
2) The inactivation energy value was derived from I 3.3x10-4 I .o 3300.0
45
the data pertaining to low temperatures only and was 2 4.7X IO-~ I -4 2130.0
applied subsequently to observations at higher temper- 4 46 9.7x 10-J 2.9 1030.0
8 4.2X 10~~ 12.4 228.0
a tures.
IO 48 8.4X IO-~ 25.4 I 18.0
7) At temperatures above 5o°C, the steady state was I2 I .8x IO-~ 56.0
54.5
never achieved and the exposure time noted did not ‘4 50 3.6x 10~~ 109.0 28.0
include the cooling time. The latter becomes progres- 16 8.3x 10-l 252 .o 12.0
18 I .5x 10-l 6.7
sively longer the higher the final temperature. Thus, the 53 456-o
20 3.0X 10-l 912 .o
3.3
observed time was shorter than the actual time through
21 56 4.7X 10-l 1430.0 2.1
which damage was inflicted and became progressively
so as the applied temperature level was elevated.
Similarly, with respect to the radiative method, it is rates at lower temperatures may possibly be indicative
found that: a) the measurements at the lowest radiation of higher temperature at the basal layer for the same sur-
intensities and, therefore, the longest times, are least face temperatures when heating is produced by radi-
critical and therefore technically most dependable. ation on blackened skin. The blackening may result in
!I) Temperature and time vary simultaneously greater
c localization of heat near the surface as compared
throughout the range of experimentation; therefore, with conductive heating where a flatter temperature
assumptions with respect to inactivation energy, etc. gradient to the interior might be expected. On the other
apply equally throughout and the steady state condition hand, it should be pointed out that the application of
does not apply at all. However, damage inflicted during cgraphical integration to the experimental data of
both heating and cooling is taken into account in the Henriques results in Q’s well over I .o and as much as I .5
determination of total damage. when damage during temperature fall is included.
c) In the original series, no experiments were per- It appears also that the change in rates of damage with
formed at levels of irradiation productive of peak temperature decelerates above the pain threshold tem-
temperatures less than 52 “C; therefore, inferences con- perature, rather than accelerating as might be expected.
cerning relatively low temperature exposures were ex- It is possible that this effect may be brought about
trapolative in nature. through alterations, chemical, physical, or both, in the
In order to overcome the latter deficiency and to pro- more superficial cells of the epidermis so that these cells
vide a common ground for direct comparison, a few then provide an insulating layer with respect to the
experiments were performed in which the radiative tech- deeper layers of the tissue. Fugitt (20) and Mixter (29,
nique was modified to provide a ‘steady state’ at rela- from considerations of Henriques’ and Moritz’ data,
tively low temperature. This end was accomplished by have suggested that a two-process system may be in-
producing a constant skin temperature reported as just volved in the relation of damage rates to temperature.
above the Pain threshold and maintained long enough to The present data neither support nor refute such a pos-
yield the desired end point of blistering. This procedure sibility. In this type of procedure, however, inferences
required adjustment of the radiation intensity after the with respect to intracellular mechanisms and molecular
initial heating to pain threshold (I o sec.) and resulted in changes must be considered as highly speculative at
an average temperature level of 46. I “C =t 0.5OC main- best. It would appear to be preferable to confine such
tained for 1050 seconds. The time required was much inferences to mechanisms in the physiological sense, each
longer than that predicted by extrapolation of the encompassing perhaps myriad chemical systems, and
damage rate curve appropriate to the higher temper- each related to a feature of the organism as a whole, in
ature burns (IOO sec.) and much smaller than that ob- the present instance, the production of pain and the
served by Henriques and Moritz with conductive heat- destruction of a portion of the integument. From this
ing at the same temperature (5000 sec.). However, the point of view it should be possible to show a relationship
application of the graphical integration method so that between these two phenomena, inasmuch as they have in
f-2 = I at the blister threshold provided a damage rate common the same stimulus, approximately the same
such that the log plot of the curve &/dt vs. T has a slope threshold and the same culmination in the sense that
of 0.421 and intersects the damage rate curve appro- sensation from the tissue stimulated ceases when the
priate to the higher temperature burns at about 5oOC. tissue is destroyed. It has been shown by Hardy, Wolff
Thus, all the data could be fitted to the composite and Goode11 (8) that there are 21 just noticeable differ-
damage rate curve shown in figure 6. The displacement ences (JND) in the discrimination of pain intensity.
of the curve for the present data toward higher damage It was possible also to correlate the temperature of the
basal layer of the skin with JND’s of pain (22). Drawing intensity and, where S and So are expressed in terms of
upon these data and plotting the rate of injury, as de- the damage rate corresponding to the appropriate tissue
termined for the present thermal burn data (fig. 6), temperature as shown in table 6. Since it has been dem-
corresponding to the tissue temperature productive of onstrated here that at the same damage rates, threshold
a given level of pain sensation measured in JND’s, the blistering is produced within 24 hours when exposure
relationship shown in figure 7 was found. This relation- is such that Q = I, then it follows that under the same
ship indicates that pain intensity is linearly related to conditions the time to blistering at a constant pain in-
the log of the damage rate throughout the entire range tensity can also be predicted and is the reciprocal of the
of pain sensation. Previous attempts (I) to establish this damage rate obtained at the corresponding tissue tem-
correlation by use of the damage rates as determined perature (table 6, col. 5). Of more importance than the
by Henriques and Moritz failed at pain intensities above actual prediction of the stimulus duration, however, is
I 7 JND’s. The present data establish that pain intensity, the fact that the excellent correlation of the psycho-
like other sensations, quantitatively bears out the rela- physical data with the empirically derived physiological
damage rates constitutes strong support for the hy-
pothesis (I, 22) that noxious stimulation depends upon
P= the instantaneous rate at which certain reactions are
PO (I + K log S/So)
occurring, rather than upon the amount of effect or
extent of damage existing at any moment.
where P = pain intensity (JND), PO = threshold sensa-
tion, EC = (~/slope) of log &/dt vs. JND = constant = The authors express thanks to Mr. Richard J. Crosbie for the
6.4, S = stimulus intensity and So = threshold stimulus sol ution of equation 3.
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