TEMPERATURE VERSUS TIME TO INCAPACITATION
FOR CARBON MONOXIDE CONCENTRATIONS

50+ x = 0 PPM
4s + = 1000 PPM

154

TIME TO INCAPACITATION IN MINUTES
3

0. , 1 : 7 1
20 25 30 35 40 45 50 35 60

TEMPERATURE IN DEGREES CELSIUS

Figure 6, Variation in time-to-incapacitation with temperature
at 3 carbon monoxide concentrations.

CARBON MONOXIDE CONCENTRATION VERSUS TIME TO {NCAPACITATION

604

20 DEG. C.

TIME TO INCAPACITATION IN MINUTES
3

0 500 1000 1500 2000 2500 3000
CARBON MONOXIDE CONCENTRATION IN PARTS / MILLION

Figure 7, Variation in time-to-incapacitation with carbon
monoxide concentration at 5 temperatures.

12


Gas Handling Equipment: Carbon monoxide (research grade) and
breathing air were mixed by passage through a baffled cylindrical
mixing tube before entering the animal exposure chamber. The CO
flow rate was regulated automatically by a Matheson model 8240
mass flow controller; air flow rates were controlled manually by
use of a simple, tank-mounted, two-stage pressure regulator and
needle valve assembly. Gas input into the chamber was through a
port in the top near the heated air inlet; the exhaust port was
located in the rear panel. The entire chamber was installed
inside a fume hood into which the chamber exhaust was vented.

Temperature Control Equipment: To provide a regulated
temperature in the 40-60°C range, we mounted a modified heat gun
in the upper end of the chamber with the heated airflow in the
direction of the cage rotation. Modifications included
connecting the air intake to a return tube so that chamber
atmosphere was recirculated through the heating coils in a closed
cycle, and sealing the entire blower housing. The unit was
rewired to allow constant blower operation with the heating coils
controlled by thermistor input to a temperature controller, and
with in-line heater voltage controlled by a'variable transformer.
This arrangement allowed the initial chamber temperature to be
established quickly (at high voltage) and maintained with minimal
fluctuation (at low voltage) due to the on/off application of
power by the temperature controller.

Gas Analysis: The chamber atmosphere was analyzed for CO by gas
chromatography, using a Carle series 100 gas chromatograph (GC)
equipped with 1/8-inch packed columns and a thermistor detector.
A continuous stream of chamber atmosphere was pumped from a
sampling port about 2 cm above the head of the walking rat,
routed through the GC sample loop, then back to the chamber. The
flow rate of 55 mL/min was maintained by a ceramic piston pump
(FMI model RRP, Fluid Metering, Inc., Oyster Bay, NY).

Injections were accomplished automatically by activating the
sample injector valve with an interval timer. The initial sample
(after rat insertion) was injected at 1 min; additional samples
were injected at 1.5-min intervals, the minimum allowed by the Co
retention time. Concentrations were determined by comparison of
peak height to a standard curve prepared by operating the
injector valve while flowing syringe dilutions of tank CO and air
through the sample loop at the same 55 mL/min rate used in the
automatic sampling system. Initial tests indicated that a 4
L/min airflow was adequate to insure the maintenance of the
ambient oxygen:level with single rat exposures; therefore,
chamber oxygen was not monitored during subsequent analyses.

Test Atmosphere Generation: With the chamber assembled and the
vent open, compressed air flow was adjusted to 4 L/min with the
in-line needle valve. The temperature controller was set at the
required chamber temperature and the blower, mixing fans, and
cage rotation motor were turned on. Carbon monoxide flow was set

3


TIME TO INCAPACITATION VERSUS TEMPERATURE
UNE FITTED FROM EQUATION 4

al

4 .

> 50

Zz Y=k(1)/(x—K(2))

5 K(1)= 252

2 go . K(2)= 35.1

z

9

E

& 304

oo

<

a x

Oo 204

z

e

w 104

=

=
0 a ee 7, hn eee T —>
35 40 45 50 55 60 65

TEMPERATURE IN DEGREES CELSiuS

Figure 4, Scatter Plot of time~to~incanacitation vs temperature,

TABLE 2
TIME TO INCAPACITATION FOR WHOLE BODY
EXPOSURE AT ELEVATED TEMPERATURES

TEMP °C OBSERVED ti (min) No. TEMP o¢ OBSERVED ti (min)

1 40 50.5 17 50 15.8
2 40 53.0 i 18 50 16.0
3 40 39.9 1 19 50 18.0
4 40 51.4 rs) 50 20.1
5 40 57.6 1 21 55 13.7
6 40 58.4 f 22 55 11.5
7 40 49.5 1 23 55 11.7
8 45 25.9 1 24 SS 12.2
9 45 26.5 1 25 55 12.8
10 45 24,1 i 26 55 12.4
11 45 23.5 1 27 60 10.0
12 45 26.0 i 28 60 10.8
13 45 29.0 ' 29 60 10.0
14 50 16.2 i 30 60 9.2
15 50 14.8 + 31 60 9.1
16 50 16.6 t 32 60 11.0

t,(CO) or tj (temperature) , an incapacitating "dose" had been
reached; for any specific time less than these, a fractional dose


1000 ppm CO at 40°C, 1600 ppm CO at 40°C...3100 ppm CO at 60°C.
Sixty-three rats were exposed to these combinations of co
concentrations and elevated temperatures; t; was recorded for
each exposure.

ag QO | cootrotser

Gas Mixing Assembly

Animal Exposure Chamber
with Rotating Cage Assembly
‘

(Fes) fTneenocounte

Heater-blover Assenbly econ

Variable
Transformer

enperacure Sanpte
Coneretler oer My valve LA

Recorder

‘Thermistor

Air Pump

Figure 2. Animal Exposure System

RESULTS AND DISCUSSION

Continuous walking in the rotating cage limited the saliva
spreading activity that is critical to body-temperature
regulation in the rat (5), and the use of male rats may have
indicated a higher degree of thermal resistance than would have
been shown with female rat subjects. Actual physical activity
was moderate; the walking speed of 8.5 cm/s (0.19 mph) was well
below the 1 mph required by Gollnick and Ianuzzo (6) to reach a
plateau core temperature of 40.2°C. The rectal temperatures, for
rats exposed to elevated temperatures only, averaged 43.5°C
(s.d.= 0.80) at incapacitation, which corresponded well with the
40.4 to 43.0°C temperature range recorded at exhaustion by
Hubbard et.al. (7).

The average CO concentration to which each rat was exposed was
calculated by integrating the area under a concentration vs time
curve from time=0 to time=t, and dividing the c*t, j7product by t,
[average concentration = (fe dt)/t,;]. The average temperature,

5


on the mass flow controller at the levels calculated to produce
the desired concentration when diluted by the 4 L/min airflow.
Pure CO was manually injected into the chamber in a volume
slightly less than that required to quickly adjust the
concentration to the experimental level. When an equilibrium
concentration was reached (as indicated by the 1.5-min interval
monitoring), any minor concentration adjustments were made by
adjusting the CO volume input with the mass flow controller.

Test Procedure: When gas concentration and/or chamber
temperature reached the desired equilibriun conditions, a final
pre-insertion sample was injected into the GC; the fans and cage
motor were turned off. The sampling timer was reset to zero and
the retaining screws on the chamber access door were removed in
preparation for rat insertion. In rapid sequence, the door was
opened, one rat was inserted, the door was closed, and the timer,
fans, and cage motor were activated. A chromel-alumel
thermocouple, suspended 2 inches above the nose of the walking
rat, provided continuous recording of chamber temperatures; GC
peak traces and the associated chamber temperatures were recorded
synchronously using a multichannel strip recorder. Sampling was
continued at 1.5-min intervals until the rat could no longer
continue walking in the rotating cage and began to tumble or
Slide. Time-to-incapacitation (t;) was then recorded and one
additional gas sample was taken to provide a continuous
concentration record from insertion through t,. At this point,
the fan, sampling timer, and cage motor were turned off. The rat
was removed from the exposure chamber and placed in a small
chamber containing a high concentration of CO, and was left until
respiration ceased. The animal exposure system is depicted
schematically in Figure 2.

Relative humidity (RH) inside the chamber was noted, but not
controlled. The 4 L/min airflow provided an 8 to 10% RH at the
beginning of each experiment; maximum RH was 28% {at t;) for the
60°C studies and 58% for the 40°C studies for temperature effects
alone (i.e., without CO). Humidity remained well above the <5%
level at which dehydration normally occurs (3,4).

The temperature/response relationship was determined by exposing
32 rats, individually, to environmental temperatures of 40 to
60°c, in 5° increments, and measuring t, with continuous
temperature monitoring. The concentration/response for CO alone
was determined in the same system by exposing 43 rats,
individually, to mean CO concentrations over the range of 995 to
9111 ppm (v/v).

The effects of elevated temperature on CO response were measured
by exposing rats to nominal CO concentration levels of 1000,
1600, and 3100 ppm (that normally result in 43, 23, and 11 min
t,;'s respectively at ambient temperature) combined with elevated
chamber temperatures from 40 to 60°C (using 5° intervals), i.e.,

4


TIME TO INCAPACITATION IN MINUTES

TIME TO INCAPACITATION VERSUS CARBON MONOXIDE

60- UNE FITTED FROM EQUATION 3

504 Yeek(1)/(X-K(2))
Ld K(1)= 29995

40-4 K(2)= 302

30-4

204

104

0 T T T 1
0 2000 4000 6000 8000 10000

CARBON MONOXIDE IN PARTS PER MILLION

Figure 3. Scatter plot of time-to-incapacitation vs carbon
monoxide concentration,

TABLE 1
TIME TO INCAPACITATION FOR CARBON MONOXIDE
AT AMBIENT TEMPERATURE (20°C)

2
3

eornnsunn|

co OBSERVED co OBSERVED
PPM ti (min) No. PPM ti (min)

1 23 3135 10.3
1005 30.8 ' 24 3135 10.0
1013 50.8 1 25 5429 6.9
1016 43.1 ‘ 26 5465 6.8
1016 45.5 ' 27 5542 6.2
1021 45.0 t 28 5600 7.2
1449 23.5 H 29 5616 4.9
1467 21.9 H 30 5616 5.8
1473 34.8 H 31 $677 4.9
1475 26.4 H 32 5804 5.4
1504 26.0 ' 33 6066 4.9
1510 22.1 H 34 6091 4.7
2974 10.3 ' 35 6091 4.7
3026 11.1 i 36 6130 4.7
3052 11.0 H 37 6185 4.7
3053 10.8 H 38 6189 5.0
3072 9.9 : 39 7890 2.9
3083 10.5 Hl 40 8583 2.8
3088 12,0 : 41 8907 2.8
3103 11.4 Hl 42 8992 3.1
3130 11.3 H 43 9111 3.2
3134 7.9


Doc
FAA

16

Doc



TABLE 3
COMBINED EFFECTS OF CARBON MONOXIDE AND ELEVATED TEMPERATURE
ON TIME TO INCAPACITATION

cO.ppm Temp,°c

986
1001
1002
1010
1013
1017
1505
1509
1531
1567
1568
1592
3118
3141
3212
1003
1005
1009
1014
1015
1026
1484
1488
1493
1497
1500
1512
1866
1878
1906
3262
3275
3288

961
1004
1098
1537
1538
1563
3170
3192
3218

996
1006
1033
1589
1592
1599
3119
3193
3274
1033
1044
1044
1602
1612
1613
3008
3037
3047
3072
3121
3130

40.0
40.0
40.0
40.0
40.0
40.0
40.0
40.0
40.0
40.0
40.0
40.0
40.0
40.0
40.0
45.0
45.0
45.0
45.0
45.0
45.0
45.0
45.0
45.0
45.0
45.0
45.0
44.6
45.0
45.0
45.0
45.0
45.0
50.0
50.0
50.0
50.0
$0.0
50.0
50.0
50.0
50.0
55.0
55.0
55.0
55.0
55.0
55.0
55.0
55.0
55.0
60.0
60.0
60.0
59.8
60.0
59.8
58.9
Ss9.1
58.5
59.2
59.5
59.5

CALC ti

44.2
43.2
43.2
42.7
42.5
42.2
24.7
24.6
24.2
23.5
23.5
23.0
10.5
10.4
10.2
43.1
43.0
42.7
42.4

22.9

10.2

9.9
41.3
40.6
40.6
22.9
22.7
22.7
10.9
10.8
10.7
10.7
10.5
10.4

from ¢Q

10

CALC ti
from temp
51.8
51.8
51.8
5i.8
51.8
51.8
51.8
$1.8
51.8
51.8
$1.8
51.8
51.8
51.8
51.8
24.2
24.2
24.2
24.2
24.2
24.2
24.2
24.2
24.2
24.2
24.2
24.2
25.2
24.2
24.2
24.2
24.2
24.2
16.3
16.3
16.3
16.3
16.3
16.3
16.3
16.3
16.3
12.5
12.5
12.5
12.5
12.5
12.5
12.5
12.5
12.5
10.4
10.4
10.4
10.4
10.4
10.4
10.8
10.7
1lo.9
10.7
10.6
10.6

OBSERVED CALC ti

tismin

33
37
36
41
32
31

12.

. bee
MOMISMSOOVwO MDH

+2
.0
al
17
8
0

3

WOhUNNOKACAOMON

CO _+ TEMP
33.2
32.8
32.7
32.5
32.4
32.3
22.9
22.8
22.5
22.1
22.1
21.8
11.7
11.6
11.4
22.0
22.0
22.0
21.9
21.9
21.8
17.3
17.2
17.2
17.2
17.1


a

was assumed to have been absorbed, and the magnitude of this dose
was proportional to time and to the CO concentration (or
temperature). Since t, was inversely proportional to both co
concentration and elevated temperature, the simultaneous
application of both was expected to drive the observed t, in the
same direction, i.e., toward a shorter time than was observed for
either single condition. This trend was supported by inspection
of the combined exposure data.

Although the mechanisms for incapacitation from heat exhaustion
and from carbon monoxide inhalation are surely different, we felt
that an empirical equation derived from the observed times-to-
incapacitation of rats responding to the combined effects of
defined temperature and CO concentration would be useful in
estimating the effect of the thermal contribution when the test
temperature exceeds the calculated t, of 35.1°C (if only for the
narrow range of temperatures in this’ study). For an exactly
additive effect, we reasoned that the sum of the reciprocal t,

for CO and temperature would equal the reciprocal of the observed
t,, that is,

1/t; (for coy + 1/t;Cfor tem) = 1/+t,; (observed) Eq. 5

Since an “exactly additive" effect was unlikely for two
dissimilar mechanisms, we judged that a more likely form for the
equation might be,

K,/t,¢for coy + K3/t,Cfor. tem) = 1/t, (observed) Eq. 6

where K, and K, are weighting factors for the two effects.

By performing "a multiple linear regression relating the
calculated t;'s for Co and temperature to the observed t,'s for
the combined’ effects, and using the algorithm that forces the
intercept to equal zero, the least-squares estimates for K, and
K, were 0.78 and 0.66, respectively. The working equation ‘gor
predicting the combined effects of CO toxicity and elevated air
temperature became,

1/t, = (0.78*([CO-302]/29995)] + [0.66*([T°C-35.1]/252)] Eq. 7

The relationship presented as equation 7 can be used to predict
response time to CO concentrations and whole-body thermal
environments within the limits used in the original exposures.
Table 3 lists the numerical values for observed t,;'s and
predicted t;'s (from Eq. 7) for the 63 combined exposures.


for those experiments involving elevated temperatures, was
similarly determined, i.e., average temperature = (ft at) /t,.

A scatter plot was constructed for the ambient-temperature co
exposures by plotting t, as a function of the average CO
concentration. A line fitted to these points had the general
shape of a rectangular hyperbola with non-zero asymptotes. When
an equation of that form was fitted to the data, a negative value
was obtained for the t, asymptote, i.e.,

(t; -[--604])*([Co] - 259) = 32,233 Eq. 1

This would indicate that t; could be reduced to less than zero by
an infinite concentration of co, which is biologically unlikely,
or simply that ‘the form of the equation is inappropriate for
describing the concentration-vs-time relationship beyond the
experimental limits of this study. A simplified 2-parameter
equation of the form,

(t,; - 0)*(([CO] - K1) = K2 Eq. 2

where Kl and K2 are constants, was derived using a standard
nonlinear regression technique to obtain

t, = (29995/([CO] - 302)) Eq. 3

A scatter plot of the data with the fitted-equation line is
depicted in Figure 3. Table 1 lists the t; vs CO concentration
data.

In a similar fashion, a scatter plot was constructed from data
relating t, to elevated-temperature exposures (at zero CO
concentration) by plotting t; as a function of the exposure
temperature. A simplified 2-parameter equation was derived by
the technique used in deriving equation 3 to obtain

t, = 252/((T°c] - 35.1) Eq. 4
A plot of these data, with the fitted-equation line, is depicted
in Figure 4. Table 2 lists the corresponding raw data used to
derive Eq. 4.

Initial inspection of the combined exposure data indicated that
over 90% of the observed t;'s were less than either of the
predicted t,'s (from Equations 3 and 4) for the respective
temperatures and co concentrations, indicating that the combined
effect was toward a shorter t, than would be obtained from either
exposure condition by itself; exceptions were near the "no-
effect" level for one of the parameters. We reasoned that the
product (time x temperature) at t; represented a "dose" analogous
to the (time x concentration) value for carbon monoxide. At


the test animals. The rotating cage was driven by a 4-rpm geared
motor providing a circumferential velocity of 8.5 cm/s. Two
Plastic-bladed fans mounted on opposite ends of the chamber
provided uniform thermal mixing and gas distribution.

1 Ye

|} _—5

| >6
TNS li
em! ot _
BEL 12

Figure 1. Animal. Exposure Chamber

1, Modified heat gun (Master- Appliance Corp., Racine, Wisconsin
model HG301).

2. Mixing fan assembly (1/15 hp motor, 5,000 rpm, fitted with
7-cm, 4-bladed Nylon fan).

3. Ventilation holes, 12-mm dia, cut through center divider of
rotating cage.

4, Exposure chamber walls constructed from 1/2-inch (12-mm) thick
polymethyImethacrylate.

5. Rotating cage assembly (divider and outer rim are 1/4-inch
(6-mm) thick polymethylmethacrylate; surface is polyethylene

mesh).
6. Gas sampling ports sealed with serum vial stoppers.
7. Chamber access port for animal insertion and removal.
8. Thumbscrew fasteners.
9. Polyethylene mesh cover, mesh openings are approximately

J-mm square.
10. Center divider and support for rotating cage.
ll. Cage drive motor (4-rpm).
12. Cross supports for chamber rims and plastic mesh cover.

Animals: Male albino rats of Sprague-Dawley origin were obtained
from Charles River Breeding Laboratories, Wilmington, MA, ina
100-200g weight range. They were inspected by a veterinarian
upon arrival and held in isolation for 8 days prior to use. All
rats were fasted overnight before testing to establish equivalent
metabolic states.


SUMMARY AND CONCLUSTONS

Laboratory rats were exposed to CO in air, to whole-body thermal
environments from 40-60°C, and to selected CO concentrations in
elevated temperature environments. For each animal, and for each
exposure condition, the time to physical incapacitation (t;) was
measured using a motor-driven rotating cage assembly.

The response times for experiménts using CO exposures alone, and
for those using elevated temperatures alone, were plotted against
the respective concentrations or temperatures, and equations were
derived by nonlinear regression techniques to mathematically
describe these relationships. The resulting equations, for time-
to-incapacitation, are:

t, = 29995/((CO] - 302) for carbon monoxide)

and

t, = 252/((T°C] - 35.1) (for elevated temperatures of 40-60°C)

where t; is in minutes, [CO] is the carbon monoxide concentration
in parts- per-million by volume, and [T°C] is the whole-body
exposure temperature in degrees Celsius. The observed response
times obtained at selected concentrations of CO at elevated
temperatures were analyzed with respect to the predicted response
times for individual CO and temperature effects.

We concluded from this analysis that incapacitation occurs
earlier when CO inhalation is combined with elevated whole-body
temperatures than is observed in exposures to the same CO
concentrations and thermal parameters individually. Response
deviations are more prominent for elevated temperatures combined
with low CO concentrations, and for low temperature exposures
combined with higher CO concentrations, that is, when one
parameter becomes the controlling factor in mediating the animal
response. The mechanistic hypothesis that is supperted by the
data is that the incapacitating effects of CO and of elevated
temperatures are fractionally additive when simultaneously
applied. This reaffirms the need for adequate temperature control
in experiments where the rat model is used to integrate the toxic
effects of combustion gases. With the caveat that estimates be
limited to the CO and temperature ranges of the original data, we
offer an equation that may be useful in estimating the time-to-
incapacitation produced by the inhalation of CO in an elevated
temperature environment:

t, = 1
' [0.78*([CO]-302)/29995] + [0.66*([T°C]-35.1)/252]

13


INHALATION TOXICOLOGY: XI. THE EFFECT OF ELEVATED TEMPERATURE
ON CARBON MONOXIDE TOXICITY

INTRODUCTION

The use of the laboratory rat as an animal model for determining
the toxicity of combustion gases is well established. Nearly all
of the current assay methods in combustion toxicology utilize
some physiological response of an experimental animal as a
measure of the total toxicity of the inhaled gases. Although the
rat conveniently integrates the effects of the multiple toxic
gases produced from burning materials, other combustion-induced
conditions of elevated temperatures and oxygen depletion can
alter the degree of observed response unless these parameters are
carefully controlled.

Previous work in this laboratory determined the time and
temperature conditions required for heat incapacitation in rats
and mice (1), and earlier work by Robinson (2) defined survival
times in resting and exercising conditions at elevated
temperatures. Although the commonly-observed animal responses
(physical incapacitation, shock avoidance failure, and death) can
be caused by hyperthermia alone, either from exposure to elevated
ambient temperatures or from exhaustion-induced heatstroke, the
more subtle effects of moderately elevated temperatures on the
response to known concentrations of a single gas have not been
quantitatively described. As part of our continuing program to
study the effects of combinations of combustion products, this
report explores the effects of whole body exposure to moderately
elevated air temperatures (40 to 60° C) on carbon monoxide (CO)
toxicity.

MATERIALS AND METHODS

Chamber Design: The exposure chamber used for this study was
constructed by the authors from 1/2-inch polymethylmethacrylate
(PMMA) sheets as shown in Figure 1; internal dimensions are 50.8-
em long by 26.6-cm wide by 50.6-cm high. The cylindrical
rotating cage assembly (40.6-cm dia) has a plastic mesh floor
(perimeter) and a perforated PMMA internal divider that acts as a
central support. The cage was suspended across the width of the
chamber by an axle passing through the central divider and
connected to an external geared motor; the walls of the chamber
functioned as exterior sidewalls for the cage. A gasketed door
(10 by 10 cm) was installed in the side of the chamber at the
level of the cage floor to allow rapid insertion and removal of


Technical Report Documentation Page

T. Report No. 2. Government Accession No. J, Recipient's Caraleg No.

DOT/FAA/AM-90/ 16

a. Title and Subtitle 3, Report Date
December 1990

6. Performing Organization Code

INHALATION TOXICOLOGY: XI. THE EFFECT OF ELEVATED
TEMPERATURE ON CARBON MONOXIDE TOXICITY

G. Performing Organization Report No.

7, Author's) ,
DONALD C. SANDERS and BOYD R. ENDECOTT

9. Perlorming Organization Name ond Address 10, Work Unit No. (TRAIS)
FAA Civil Aeromedical Institute
P. 0. Box 25082 TT. Contract er Grant No.

Oklahoma City, OK 73125

TS. Type of Report and Period Covered

12. Sponsoring Agency Name ond Address
Office of Aviation Medicine
Federal Aviation Administration
800 Independence Avenue SW 14. Sponsoring Agency Code
Washington, D.C. 20591

15. Supplementary Notes

This work was performed under task AM-B-88-TOX-56.

16, Abstract

Laboratory rats were exposed (a) to experimental concentrations of carbon monoxide
in air at ambient temperature, (b) to elevated temperature atmospheres from 40°C
to 60° C, and (c) to selected carbon monoxide (CO) concentrations at the elevated
temperatures in (b). The incapacitating potency of each of the environments was
evaluated by measurement of time-to~incapacitation (t,) as a function of CO
concentration and/or temperature; incapacitation was defined operationally as loss
of ability to walk inside a motor-driven, rotating cage enclosed in an exposure
chamber. Comparison of data from the combined (CO + elevated temperature)
exposures and exposures to CO and elevated temperatures alone indicated that
incapacitation occurred earlier when CO inhalation was combined with a whole-body,
elevated temperature environment than was observed for the same exposure parameters
applied individually. No evidence for a synergistic effect was noted. An
empirical equation was derived that allows the calculation of a predicted t, for
combinations of CO and temperature within the ranges utilized in the experimental

exposures.

17. Key Words V 18. Distibution Statement

Combustion toxicology,” carbon monoxide, | This document is available to the public
heat, thermal effects, time-to- through the National Technical
incapacitation Information Service, Springfield, VA 22161
19. Security Classif, (of this report) 20, Security Classil. (ol this poge Zhe No. of Poges | 22. Price
Unclassified Unclassified 18

Form DOT F 1700.7 (8-72) Reproduction of completed poge outhorized


Figure 5 is a plot of the correspondence between the two sets
of values; a least squares regression line to fit the data is
described by the equation,

tipredicted) = [2.6 + (0.84) *t i cobserved)] .

OBSERVED TIME TO INCAPACITATION VERSUS
CALCULATED TIME TO INCAPACITATION

404

OBSERVED TIME TO INCAPACITATION IN MINUTES

Figure 5, Observed vs predicted time-to-incapacitation for
rats exposed to CO at elevated temperatures

n

Ld

=

2

Z

=

z

Zz

2 30
= 30-4
=

oO

<=

Qa

& 20-4
Z

e

¥ 104
i

a

Ld

=

3 o t ’ 1 1 1
Ba 0 10 20 30 40 50
a

&

To graphically display the variation of t,; to changes in the
thermal environment at the nominal co concentrations of 0, 1000,
1500, and 3000 ppm, we plotted the mean observed t,'s at each
temperature and concentration, as shown in Figure 6. A similar
treatment of the data was employed for Figure 7 to show the
variation in t, with Co concentration for each temperature. In
both graphs, lines between points are drawn to differentiate
treatments, and do not indicate continuous values between points;
vertical bars indicate the standard error of the mean (s/¥n) for
all observed t,'s at each point.

11



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*U.S.GOVERNMENT PRINTING OFFICE;1991-561-020/20592

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