NBSIR 77-1234

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Hazard Characteristics of

Combustion Products in Fires:

The State-of-the-Art Review

Merritt M. Birky

Center for Fire Research

Institute for Applied Technology

National Bureau of Standards

Washington, D.C. 20234

May 1 977

Final Report

Sponsored by;

National Aeronautics and Space Administration

Lewis Research Center

Cleveland, Ohio 44135

(NASA-CR- 135088)

NBSIR

HAZARD CHARACTERISTICS OF

COMBUSTION PRODUCTS IN FIRES:

THE STATE-OF-THE-ART REVIEW

Merritt M. Birky

Center for Fire Research

institute for Applied Technology

National Bureau of Standards

Washington, D C. 20234

May 1977

Final Report

Sponsored by:

National Aeronautics and Space Administration

Lewis Research Center

Cleveland, Ohio 44135

(NASA-CR- 135088)

O/ H.- X'i'

U S. DEPARTMENT OF COMMERCE, Juanita M. Kreps, Secretary

Dr. Sidney Harman, Under Secretary

Jordan J. Baruch, Assistant Secretary for Science and Technology

NATIONAL BUREAU OF STANDARDS, Ernest Ambler, Acting Director
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CONTENTS

Page

LIST OF TABLES iv

Abstract 1

1. INTRODUCTION 1 1.1. Clinical Definition of Problem 1 1.2. Limitations of Clinical Data 3 1.3. Role of Synthetic Materials and Fire Retardants 4

2. METHODOLOGY FOR ASSESSMENT OF SMOKE AND TOXICOLOGICAL HAZARD

IN FIRE 5 2.1. Background 5 2.2. Measurement of Particulate Combustion Products 5 2.3. Analysis of Gaseous Products 7 2.3.1. Detailed Chemical Analysis of Gases 7 2.3.2. Selected Gas Analysis — Small Scale 8 2.3.3. Selected Gas Analysis — Large Scale 9 2.4. Toxicity of Multi-Component Gas Mixtures 10

2.5. Limitations of Smoke and Toxic Gas Measurements 11

3. BIOLOGICAL ASSESSMENT OF TOXICITY 12

3.1. Background 12

3.2. System for Biological Assessment of Toxicity 14

3.2.1. Combustion Systems 14

3.2.2. Animal Exposure System 15

3.2.3. Chemical Analysis Systems 16

4. MECHANISMS AND MODELS 17

4.1. Carbon Monoxide 17

4.2. Hydrogen Cyanide 18

4.3. Synergism 19

4.3.1. Mathematical Analysis for Synergism 20

4.4. Sensory and Respiratory Irritants 21

4.5. Organophosphate Ester Toxicity 22

4.5.1. Neurotoxicity of Organophosphates 22

4.5.2. Carcinogensis of Organophosphate Fire Retardants . . 25

5. PREVENTIVE MEASURES THROUGH CODES AND STANDARDS 25

5.1. Building Codes 26

5.2. Code Requirements for Detection and Suppression System ... 27

5.2.1.

Fire Detection Devices 27

5.3. Automatic Sprinkler Systems 27

5.4. Smoke Control Systems 28

6. CONCLUSIONS 28

7. ACKNOWLEDGMENTS 29

8. REFERENCES 29

9. BIBLIOGRAPHY 3 9

iii
LIST OF TABLES

Page

Table 1. Summary of Combustion Toxicology Systems 36

Table 2. Effects in Rats Exposed 30 Minutes to Combinations

of Hydrogen Cyanide and Carbon Monoxide [51] 38

Table 3. Speculations on the Level of Response Which Would Occur

in Humans from Results Obtained in Mice [75] 38

IV
HAZARD CHARACTERISTICS OF COMBUSTION

PRODUCTS IN FIRES: THE STATE-OF-THE-ART REVIEW

Merritt M. Birky

Abstract

The purpose of this effort is to review what is known about

the " smoke inhalation" hazard as related to human fatalities, the

limitations of the fire fatality data and the methods that have

been and are being used to assess the inhalation toxicity hazard.

Fire statistics indicate that 70 to 80% of the fire fatalities

are attributed to smoke inhalation. In depth autopsy studies of some of these fatalities show that carbon monoxide is the predominant toxicant produced from fires. The role of new synthetic

polymers and other additives is unknown as is the role of hydrogen cyanide in fire fatalities.

Chemical analysis of combustion products has been used extensively to assess the toxicological hazard in fire research. The

limitations of such measurements are addressed and a combination

of toxicology (animal exposures) and analytical chemistry is

recommended. Recent combined biological and selected analytical

measurements are critically reviewed.

The mechanism of toxic action of a few well known combustion

products is discussed. Due to the extensive use of organophosphates as fire retardants in polymeric materials, the toxicity of

this class of compounds is reviewed in some detail.

The role of building codes and standards and early detection

and suppression of fire are discussed as a means of reducing human

exposure to toxic combustion products. For example, the 1976

French regulation that limits the use of flammable materials that

contain chlorine and nitrogen in their molecular structure is

presented

Key words: Biological assessment; chemical analysis; combustion

products; fire fatalities; smoke inhalation; toxicity.

1 . INTRODUCTION

1.1. Clinical Definition of Problem

Statement of problem: Approximately 80% of the fire

fatalities reportedly result

from "smoke inhalation."-^

What does this mean?

In the fire literature the term "smoke inhalation" usually refers to the

inhalation of the undifferentiated air-borne products of combustion, including

gases, vapors, liquid droplets, and solid particles. More precise identification of the causative agent is rarely made. In this report we consider

the hazard characteristics of all forms of combustion products.

1
The U.S. National Commission on Fire Prevention and Control reported that

the United States holds the dubious honor of being the leader of all major

industrialized countries in per capita deaths and property loss from fire [1]^.-

The deaths-per-million population rate in the United States is nearly twice

that of second-ranking Canada (57.1 vs 29.7). This leaves little doubt that

the United States leads the other industrialized nations even though different

reporting procedures make international comparisons imprecise.

A comparison of 1974 international fire losses for various nations was assembled by the National Fire Prevention Association (NFPA) [ 2 ] . The NFPA

[3] breakdown of these fire losses for U.S. shows that 62% of the deaths

occurred in residential occupancies. Bowes [4] reported similar findings for

the United Kingdom.

In a further breakdown of fire statistics, Clarke and Ottoson [5] sur- veyed NFPA fire data to identify and rank what appear to be the most frequent

scenarios for fire death in the United States. They found that the most

common fire death scenario is the residential furnishings fire caused by

smoking materials. This scenario was estimated to account for 27% of the

fire deaths.

Bowes [4] prepared a survey of the United Kingdom fire casualties based

on reports of the fire brigades for the period 1955 to 1971. He concluded

that the proportion of fatalities attributed to smoke and gas during this

period increased by a factor of about three (3) while the number of fatal

casualties from all causes in fires showed only a small upward trend.

According to Thomas [6] approximately 80% of the victims of fire are not

touched by flames, but die as a result of "smoke inhalation." Smoke inhalation represents one of the major hazards of fire, both to civilian and to

firefighters. Two detailed autopsy studies of fire fatalities [7,8] indicate

the nature of the smoke inhalation problem.

First, Zikria's [7] analysis of autopsies performed on fire victims in

New York City during 1966 and 1967 confirm Thomas' conclusions. Zikria found

that of the 311 victims that were autopsied, 185 survived less than 12 hours.

Carbon monoxide poisoning was the probable primary cause of death [carboxyhemoglobin (COHb) greater than 50%)] in 24.3% of these fatalities. In another

34.5%, CO was believed to be a significant factor. In 11.4%, or 21 cases,

the COHb level was 10% or less and in the remainder of the cases [55] carboxyhemoglobin measurements were not made. Very little data was obtained on COHb

levels in the victims that lived longer than 12 hours.

In the second study by the Johns Hopkins University, detailed autopsies

were performed on 129 Maryland fire fatalities for the period October 1971 to

January 1974. In this study reported by Halpin et al . [8], blood carboxyhemoglobin and blood alcohol measurements and a careful dissection of the coronary

artery were performed in all cases. Analysis of the results indicated the

following: a) carbon monoxide was the primary cause of death in 50% of the cases and b) in another 30% of the cases carbon monoxide plus the presence of

pre-existing heart disease, alcohol and burns (including respiratory) were contributing factors. Approximately 10% of the fatalities were due to burns

and 10% remain unexplained. The role of other toxicants, including HCN, in

the above fatalities has not been established (368 autopsies have been performed to data with the same findings)

Numbers in brackets refer to the literature references listed at the end

of this paper.

2
A third fire fatality autopsy study has been initiated by the Fire

Research Station in England [9] . This study is being done at the University

of Glasgow, Scotland and should give additional information as to the nature

of inhalation toxicity resulting from fire exposure.

The role of particulates in causing casualties has not been adequately

defined in past studies. Obscuration of vision which interferes with escape

and hinders firefighting and rescue operations, is generally believed to be a significant factor, but no quantitative measure can be placed on its effect.

Indeed, the victim who fails to escape due to obscuration of vision will

appear in the record as a burn or toxic gas casualty and there is no way of

knowing whether they would have survived had good visibility been maintained.

Particulate matter may also provide a means of transport and deposition

of toxic products into the respiratory tract [10-12] . In the past such

effects have seldom been differentiated from those of toxic gas inhalation.

The fire casualty study at the Johns Hopkins University is now beginning to

investigate this problem [8]. In addition to acute toxicity effects, chronic

effects due to deposition of heavy metals and other unidentified toxicants

may be significant, particularly in the case of firefighters and others

subjected to repeated exposures.

Despite the lack of definitive information on the importance of particulates, a considerable effort is being devoted to the development of methods

of measuring particulate formation, the characterization of particulates, and

the development of materials with decreased potential for obscuration of

vision. A few standards which set limits on the smoke producing properties

of materials have been adopted or proposed (see section 2.2.). It would be

highly desirable to be able to relate these efforts to the hazard they seek

to address in a quantitative manner.

1.2. Limitations of Clinical Data

Statement of problem: Is the inhalation hazard of

past fires predictive of

future problems?

The above clinical data illustrate the nature of the inhalation toxicity

hazard associated with the fire environment. Carbon monoxide appears as the

single major cause of death in the above fatalities. However, the limitations

of these findings should be recognized. In the Hopkins study, on-the-scene

fire investigations are carried out to determine the type of materials

involved in the fire in order to determine if certain materials present an unusual toxicological hazard. To date most of the fires involved rather

conventional materials. That is, there does not appear to be a significant

involvement of new synthetic materials. As a result the hazard of new materials remains unknown. The retrospective nature of these data must be recognized and as more and newer synthetic materials are introduced into commerce

the nature of the hazard may change. Past problems may not be future problems.

The significance of hydrogen cyanide and other toxicants besides CO in

fire fatalities and casualties is still unknown. Similarly the effects of

sub-lethal concentrations of toxic combustion products, especially on those

exposed repeatedly such as firefighters, have not been delineated.

3
1.3. Role of Synthetic Materials and Fire Retardants

Statement of problem: Is the technological fix

for flammability creating

a worse toxicological hazard?

It is frequently suggested that the new materials being introduced into

the built environment have the potential for creating an unrecognized toxicological hazard. Some new synthetic materials tend to increase the amount

of smoke during a fire and the potential of changing the toxic gas hazard

exists. At the present time, there are no statistics to prove that the toxicity hazard is worse as a result of the use of synthetic materials. However,

it is recognized that many synthetic materials ignite more readily and the

surface flame spread rate may be greater than for some of the natural materials.

In an attempt to reduce the fire hazard, mandatory standards have been

instituted to reduce the ignitability and flame spread rates of certain

materials depending on the end use. One of the ways technology has responded

to this demand is by the incorporation of fire retardant additives [13] . The

effect of these retardants on the toxicity of the combustion products is now

becoming a cause for concern, due in part to the type of compounds that are being added: i.e., organic compounds containing phosphorus and halogens.

The toxicity of organophosphate compounds with and without halogens, such as chlorine and bromine, will be discussed in section 4. At the University of

Utah [14,15] a toxic bicyclic phosphorus containing ester has been identified

as a combustion product from a fire retarded rigid polyurethane foam based on

a low molecular weight propoxylated trimethylolpropane . This example serves only to illustrate the concern caused by the use of fire retardants based on organophosphorus compounds. However, this single finding should not be used

to indict all fire retarded polymeric materials.

Some of the additives that are proposed for fire retardants may be

inherently toxic even when a fire does not occur. For example, a recent

article by Bellett and Casida [16] on the high toxicity of bicyclic phosphorus

esters should be noted since the authors suggest that these compounds are candidates for flame retardants, vinyl stabilizers and antioxidants and thus

may find their way into polymeric materials. A perchlorinated , cage-structured

hydrocarbon (C 10 CI 12 ) has been identified as an environmental pollutant and

the author, Kaiser, [17] states this compound has been promoted as a flame

retardant additive for polymers. Similarly, the brominated biphenyls are being used as fire retardants [18] . Their structural similarity to the

restricted chlorinated biphenyl suggests that similar environmental and

toxicity problems may exist and raises some serious questions about the

advisability of such usage.

It should however by recognized that the use of fire retardants based on today's technology has the potential for creating two rather distinct toxicological problems. The first is the toxicity of the fire retardant (FR)

itself, e.g., without thermal modification of the material. Exposure may

result from normal usage by leaching out, or accidental loss of the fire

retardant or during disposal. This type of exposure is likely to be a longterm chronic exposure, perhaps by way of contamination of the environment.

Leaching out of the monomer and plasticizers from polymeric materials,

especially food and drink containers, may also create a similar toxicological

problem. The second toxicological problem, which is exemplified by the

bicyclic phosphate ester, occurs only during a fire. This exposure is likely

to be a single acute dose, except perhaps for the firefighter in which case repeated acute exposures could occur. Depending on the biological activity

of the toxicants, the toxicological effects of the two different types of

exposure will be quite different.

4
A symposium sponsored by the National Academy of Sciences and the

University of Utah [19] on the toxicology of products produced from the

thermal decomposition of polymeric materials indicates the world-wide concern

with combustion product toxicity.

2. METHODOLOGY FOR ASSESSMENT OF SMOKE

AND TOXICOLOGICAL HAZARD IN FIRE

Statement of problem: How does one realistically assess

these hazards? Can small scale

laboratory measurements be made?

If so, what are these measurements?

2.1. Background

Except for limited autopsies of fire victims discussed in section 1, the

world effort in the past to assess the toxicological hazard associated with

fire has been confined to laboratory measurements that fall into three broad

categories

1. analytical assessment

2. biological or bioassay assessment

3. combined analytical and biological assessment.

Of the three categories, major emphasis has been placed in the first category.

This includes smoke obscuration measurements and chemical analyses for specific toxicants in small scale laboratory experiments and in large scale fire

tests. The analytical measurements are usually further divided into two

major types of determinations: the particulate fraction (smoke) and gaseous

fraction. The separation of the smoke (particulates and aerosols) measurement from the gases is usually done by necessity due to the fact that these

two components have quite different properties that require different measurement techniques for their quantification.

2.2. Measurement of Particulate Combustion Products

Standard methods for the measurement of the concentration of particulates

in combustion products are further advanced than are methods for measuring

toxicity. This is undoubtedly due to the greater ease of making measurements

of the first type rather than to their relative importance. It has generally

been assumed that toxic gas formation will parallel smoke production, and thus

control of the latter will provide a measure of control over the former. This

assumption has been rationalized since both are products of incomplete com- bustion and the conditions which favor incomplete combustion, low temperatures

and limited oxygen supply, should favor the formation of both particulates and

toxic gaseous products. Recently, King [20] has examined this assumption

experimentally. He found that smoke formation was accompanied by carbon

monoxide formation but he was unable to establish any quantitative correlation

between the two. His work illustrates the well-known fact that the production

of both CO' and particulates is strongly dependent on oxygen concentration,

incident energy flux to the sample, and other experimental variables. One

concludes that there is no established relationship between a smoke standard

or measurement and the toxicity problem.

5
Two basic techniques have been used for the measurement of particulates

in combustion products: the optical measurement of light attenuation in the

gaseous suspension, and collection by filtration or impingement and subsequent

gravimetric or optical measurement. Since obscuration of vision has been

considered to be the principal hazard, the optical attenuation methods have

been favored for product development and regulatory purposes. If the transport

and deposition of toxic agents by particulates proves to be a serious problem,

collection methods may prove useful. They have the advantage of providing

samples for analysis and physical characterization.

Smoke test methods have been reviewed recently by an ASTM Task Group [21]

Three standard test methods have been used extensively in the United States

for the measurement of the smoke producing potential of materials for regulatory purposes. These are the ASTM E 84 (Tunnel) Test, the ASTM D 2843 (XP-2

chamber) Test, and the NFPA 258 (Smoke Density Chamber) Test. Other methods

are used in various laboratories for research and development purposes, but

they have not been developed to the point where they are suitable for regulatory purposes.

The E 84 method is applicable to wall and ceiling finishing materials.

It has also been used for floor coverings although this usage is not covered

by the standard. The sample is burned on the tunnel ceiling under a single

set of exposure conditions in a well ventilated, intense gas flame. The percent light obscuration is measured in the exhaust stack over a period of ten

minutes. This allows some estimate of the rate of smoke formation as a function of time, but apparently no attenpt has been made to use this feature

of the test for regulatory purposes. Instead, the percent light attenuation

is integrated over the 10-minute test period and this figure is compared to

that obtained when a red oak standard is burned under similar conditions.

Since the light attenuation is not a linear function of the quantity of

smoke, it is not possible to attach any quantitative physical meaning to the

value of the integral and there is no way to scale the results to larger

fires

In some cases the rate of smoke production is still increasing at the

end of the 10-minute measurement period. The reproducibility of smoke measurements by the E-84 is less than is desirable for a standard test method

[ 22 ] . The D2843 test method is applicable to the measurement of the smoke

producing properties of plastics. The sample is burned under strong heat

exposure conditions with limited ventilation. The percent light attenuation

in the test chamber is measured by means of a horizontal photometer located

about two-thirds of the height of the chamber from the floor. Since smoke

mixing takes place through thermal convection considerable layering occurs

and the smoke density at an arbitrary height is of questionable significance.

The maximum smoke density is recorded as percent light absorption and the

light absorption curve is integrated over a four-minute time interval to give

a "smoke density rating." Again, the percent light absorption is not a measure of the amount of smoke produced and since the smoke accumulates in

the chamber during the period of the test the practice of integrating the

absorption curve over a time interval has even less justification than in the case of the E 84 test method.

6
The NFPA 258 test method measures the total

from a material in terms of the specific optical

amount of smoke released

density, D^, defined as

D

s Kl 'o''*'

where V

A

L

F

o

volume of test chamber

surface area of specimen

length of light path

incident light flux

F = transmitted light flux.

The specific optical density is a non-dimensional quantity that provides

a quantitative measure of smoke formation. By applying appropriate dimensional

relationships, the optical density to be expected under the conditions of a specific fire situation can be estimated.

The smoke density chamber has the photometer light beam oriented vertically, so it measures an average optical density through any layering of the

smoke. The sample is oriented vertically and exposed on one surface (wall

position) . Some thermoplastic materials melt and flow out of the sample

holder, producing erratic results. A recently developed modification using

a horizontal sample holder should help to correct this problem [23]

The smoke density chamber method recognizes that the smoke producing

properties of materials may depend strongly on the conditions under which

they are burned. While no test method can simulate the entire range of

conditions that may be encountered in real fires, the method measures smoke

formation under two different well-defined sets of conditions representative

of typical fire environments. Thus it provides a better indication of material

performance than measurements made under a single set of conditions. The

sample is exposed to a radiant energy flux of 2.5 W/cm^ . Measurements are made in the absence of open flaming (smoldering combustion) or in the presence

of a pilot flame (flaming combustion) . Materials may give quite different

results under these different conditions. Cellulosic products tend to produce more smoke under conditions of smoldering combustion while many synthetics

produce more smoke during flaming combustion [24]

2.3. Analysis of Gaseous Products

A review of the literature suggests that the efforts to assess the

toxicological hazard in the fire environment by analytical methods can be

divided into two types of measurements. The first is a detailed analysis of

the products of pyrolysis, and in some cases combustion, using such methods

as gas chromatography and mass spectrometry. The second type of measurement

assumes the hazard is due to a few selected gases and analyzes only for these

products. These measurements are limited to the gaseous fraction with the

smoke (particulates) being treated separately.

2.3.1. Detailed Chemical Analysis of Gases

Early efforts to identify the products of thermal degradation were not

tailored toward toxic product assessment. The work of Madorsky [25] , for

example, was designed to elucidate the mechanism and kinetics of polymer

7
degradation. Nonetheless, product identification as a function of temperature was an important aspect of his efforts. A wide range of polymers was studied including cellulosics, polyolefins, fluorocarbons, sytrene , acrylates,

natural rubber, polyoxides, polyamides, etc.

Woolley et al. [26] analyzed the degradation products from flexible polyester and polyether polyurethane foaims based on toluene diisocyanate (TDI) . The degradation products of the yellow smoke that is produced from urethane

were also studied. The experiments were carried out in nitrogen, and the

product identification was done with a gas chromatograph and mass spectrometer. At least 30 products were separated on one chromatographic column

from the polyester smoke produced at 850 °C. Subsequent efforts by Woolley

and Wadley [27] showed that TDI is also produced during the degradation.

Hileman et al. [28] analyzed the products resulting from the thermal

degradation of a commercial flexible polyurethane based on TDI. They con- firmed that TDI is produced during the thermal degradation of the material

and suggested a mechanism for the degradation. Numerous products were

identified

Similar efforts to analyze the degradation products of polyvinylchloride

(PVC) have identified a large number of products. An extensive review of the

literature on the pyrolysis and combustion of PVC and the effects of plasticizers, stabilizers, etc., on the decomposition products was given by Wagner

[29]. O'Mara [30] analyzed the products from PVC resin and plastisols.

Polyvinylchloride was studied extensively at Boreham Wood by Woolley

[31] to assess the "real-life" fire hazard from this material. He examined

the pyrolysis products from a commercial rigid PVC decomposed in nitrogen and

in air between 300 °C and 600 °C. Approximately 75 organic materials were separated by gas chromatography and identified by mass spectrometry. Special

care was taken to analyze for phosgene and vinyl chloride. Vinyl chloride

was detected and quantified. No phosgene was found at the detection limit of

the instrumentation (50 ppm) . An evaluation of the toxicity of the products

from PVC was obtained by Woolley [31] based on the toxicity index introduced

by Tsuchiya and Sumi [32]

He concluded that the main toxic risks from the

decomposition products of PVC are hydrogen chloride and carbon monoxide.

This index will be discussed in section 2.4.

The pyrolysis gas from an impressive list of polymer systems, including

PVC samples, has been analyzed both qualitatively and quantitatively by

Boettner et al. [33]. Some 50 compounds have been identified qualitatively

from PVC. In addition to PVC, Boettner et al . [33] studied polysulfone,

polyurethanes, polyimides, phenol formaldehyde, urea formaldehyde, polystyrene,

polyethylene, polypropylene, polyester, polycarbonate, polyphenylene oxide,

synthetic fabrics and certain natural materials such as wood and wool.

2.3.2. Selected Gas Analysis — Small Scale

Statement of problem: Can chemical analysis of selected gases in

small scale laboratory tests determine the

nature of toxicity of combustion products?

The second approach of assuming what toxic species are produced and only

analyzing for these products has been used extensively in the. assessment of

toxic risk due to fire. This philosophy was used in the extensive work

reported by Gross et al . [34] involving aircraft interior materials. In this

study 141 materials were evaluated in the NBS smoke chamber for smoke production, quantities of CO, HCl , HCN, and in some cases NO^, HF , SO 2 , NH 3

, COCL depending on the polymer being decomposed. The gases were measured

mainly with gas detector tubes and smoke was measured by optical attenuation.

8
The data accumulated by Gross et al. were presented in a comparative

fashion, with various material types such as carpets, fabrics, sheets (panels),

laminates, and foams separated into groups for comparison. Parts et al . [35]

went one step further and instrumented the NBS smoke chamber for on-line

continuous analyses for CO, CO 2 , total hydrocarbon, oxides of nitrogen,

oxygen, and hydrogen chloride. Hydrogen cyanide was measured at the end of some experiments.

O' Mara [36] carried out similar experiments in an instrumented smoke

chamber, also selecting various toxic products for analysis. He studied the

rate of formation of CO and CO 2 from various natural materials (mainly wood

products) . Analysis of various organic species were also carried out using

gas chromatographic procedures.

The selected gas analysis approach has been used most extensively for

fire toxicological hazard assessment. This approach assumes the hazard is

due to a few selected toxic products and measures only these.

2.3.3. Selected Gas Analysis — Large Scale

A fairly sizable number of large scale fire tests have been carried out

in the last few years only a few of which will be considered here [37-41]

The objective of most of these experiments was to determine the burning

characteristics of materials under simulated-end use conditions and not

necessarily toxic product hazard assessment. Certainly, toxicity hazard

assessment was not the primary goal. However, selective gas (CO, CO 2 , and O 2 and smoke measurements were made in most of the large scale experiments

The Battelle [37] studies are most interesting since four different

types of bedroom furnishings ranging from conventional to extensively fire

resistive furnishings were used. These studies illustrate the effects of

improved commercially available fire-resistive furnishings and "space-age"

room furnishings over conventional materials in terms of fire spread and

combustion product generation. Gas analyses show significant differences

among the combustion products that were measured for the different types of

furnishings. From the gas data the authors concluded that the products of

major importance from a toxicological view appear to be HCN , CO, CO 2

. The

high aldehyde concentration in the "improved" room fire study, and the peak

NO concentrations in all but the space-age room fire were recognized as significant hazards.

The goal of Southwest Research Institute [38] large scale fire tests was

to determine the burning characteristics of upholstered furniture. Cigarettes

were used as the ignition source. Combustion product measurements included

CO, CO2 , and light obscuration at the 5-ft level. Oxygen depletion and temperature were measured in six locations.

Factory Mutual and Harvard [39] carried out bedroom fires to determine

the sequence of events of such fires to guide other fire research efforts.

Methenamine pills on a urethane mattress were used for an ignition source. Measurements of smoke (optically), oxygen, carbon dioxide, carbon monoxide

and total hydrocarbon were made. Croce and Emmons [39] concluded that the

gas concentrations in the lower half of the enclosure were such that escape

was possible at any time prior to flashover.

Palmer et al. [40] carried out full-scale fire experiments to determine

the burning characteristics of a variety of upholstered furniture and floor

coverings arranged in a typical sitting/dining room. The upholstered furniture

included traditional (wooden framing with mainly natural fibers) , semi-modern

(latex foam on wood) , and modern (polyether based polyurethane foam on wood

9
and molded plastic) items. The conclusions that the authors reached are:

1. The peak concentrations of CO, CO 2 , NO , and HCN were comparable for each furnished room.

^

2. The time required to reach maximum toxic gas concentrations

decreased as furniture was changed from traditional to modern.

3. The rate of oxygen depletion was greater and the minimum con- centration lower for modern furniture.

4. Of the 3 types of furniture, the rate of smoke production was least for polyether foam on wood, with the latex unit

producing the most rapid smoke build-up.

5. Less time was available for escape in fires involving modern

furniture than with the traditional furniture.

In the NBS floor covering studies [41] , a 30-foot corridor 8 feet wide

was used to assess the contribution of floor covering materials to the

flame spread problem. Gas and smoke measurements were reported. Continuous

measurements of CO, CO 2 , O 2 depletion and smoke optical density were made.

Samples of combustion products were analyzed. Extremely high levels of smoke

and carbon monoxide were encountered in all the carpet fires. Extensive

light attenuation occurred within five minutes after ignition. Carbon

monoxide levels rose rapidly along with oxygen depletion in most cases so that it was difficult to determine which was the primary or most immediate

hazard

In view of the state-of-the-art, the large scale fire tests reported

above are not very conclusive in terms of toxicological hazard. In a large

scale fire the concentrations of the various toxicant species that one selects

for analysis will be different depending on the sampling location. In addition

the effects of multi-component toxicants on biological systems cannot be predicted at this time. The latter criticism can be applied to the extensive

chemical analysis of small scale experiments.

2.4. Toxicity of Multi-Component Gas Mixtures

Statement of problem: What does one do with the large amount

of analytical data?

Tsuchiya and Sumi [32] suggested that the toxicity of multi-component

combustion products can be evaluated from quantitative data using the

toxicity index (T) given by the relationship

T - I.(C /C.), . (1)

1 e f 1 In this relationship C is the concentration of a volatile or gaseous product

evolved from one gram §f material undergoing thermal degradation into a volume of 1 m^. The term is defined as the concentration of the gas that

is fatal to man in 30 minutes.

The above relationship has been used for toxicological assessment.

Woolley [31] calculated the toxicity index for the decomposition products from

PVC. His chemical analytical efforts yielded approximately 75 products from

the thermal degradation of a commercial polyvinylchloride sample.

10
Based on his chemical analysis, seven compounds were selected for calculating the toxicity index. These compounds were hydrogen chloride, benzene,

toluene, total xylene, napthalene , vinyl chloride, and phosgene (used detection limit value) . For these toxicants the values were taken from the

American Industrial Hygiene Association [42] . Estimated values were used when

values were not available. Rashbash [43] suggested that one use twenty times

the maximum allowable concentration (MAC) for the C_ values in the fire environment for a thirty-minute exposure. ^

Based on the above assumptions, Woolley [31] concluded that CO and HCl are the main toxic risks from decomposition products of PVC . However,

information obtained by exposing animals to PVC decomposition products suggest

more complex plenomena may be involved that cannot be explained by HCl and CO

alone [76]. This will be discussed further in section 4.4.

It should be recognized that the above relationship is limited to the

gaseous toxicants. The effects of smoke (particulates and aerosols) may

modify any conclusions based on this index. In addition, the combustion gas

mixture is so complex that minor products that are extremely toxic may remain

unidentified and be the primary toxicological hazard or contribute to the

toxicity in a significant way.

2.5. Limitations of Smoke and Toxic Gas Measurements

Statement of problem: Can one separate the smoke and gas

measurements and determine the

hazard?

As a result of the separation of the analysis of combustion products

into two fractions (solid and gas) the inhalation or toxicological hazard has

been separated in the same fashion leading to an over-simplification of the

problem. Obviously the presence of smoke will reduce visibility (optical

attenuation) , but the irritant effects of the smoke resulting in tearing and

burning of the eyes is most likely the primary limitation in escaping from a fire rather than light attenuation. An optical attenuation measurement cannot assess this problem. In addition, the adsorption of toxic species on the

smoke particulates may be a primary mode of entry of toxic species into the

respiratory tract. Desorption from the inhaled particulates is required, and

the degree of toxicity from the desorption process is critical to the degree

of toxicity. Obviously, an optical measurement and a strict chemical analysis

of gases cannot assess this problem and one should be aware of this in assessing the toxicity hazard of combustion products.

A further word of caution is in order regarding the literature on the

analytical assessment of the toxicity hazard. A number of the efforts to assess the toxicological hazard due to fire gases assumed that the hazard is

due to CO, CO 2 , O 2 depletion, HCl and HCN. Most of these gases are relatively

easy to measure, except perhaps HCN. Based on this assumption, the approach

to the toxicity hazard assessment has been to analyze only for these products

and base the potential hazard on such measurements. This type of measurement

neglects the possibility that other compounds may play a role in toxicity of

environment. A hazard assessment derived from measurements founded on a questionable assumption is unreliable.

Some workers in the combustion field have not only assumed that these

are the important gases but have gone one step further to assess the synergistic effect of a synthetic combination of these products [44]

This is

being done even before effects of individual components are known to sufficient degree to allow recognition of the effects of multiple components.

11
It is interesting to note that Boettner et al. [33] concluded, after the

analysis of the products from phenol formaldehyde, that no conclusions as to

toxicity can be drawn pending further analytical work. After the analysis of

the products from polyurethanes they conclude that carbon monoxide and hydrogen cyanide are the only acutely toxic compounds identified. Since carbon

monoxide disrupts the ability of the blood to carry oxygen and cyanide disrupts

the cell's ability to utilize oxygen, there is a toxicological synergism

between the two. Is this a valid method of toxicity assessment and determination of synergism? What about the effects of nitriles and TDI identified

by Woolley and Wadley [27] and Hileman et al . [28]?

Each of the materials that have been studied has an impressive list of

products which depend on temperature and the environment of thermal decomposition. The relevance of these data to the toxicity hazard remains to be seen.

3. BIOLOGICAL ASSESSMENT OF TOXICITY

Statement of problem: How does one determine the

effects of a complex mixture

of toxicants on a complex

biological system?

3.1. Background

Inhalation toxicity of combustion products is a complex problem involving

a biological system, a combustion process, and analytical chemistry. This

suggests that the problems associated with an investigation of the inhalation

toxicity of combustion products can be divided into three major areas of

expertise. A concerted effort to solve the problem must involve all three:

1. the methodology for the generation of the products;

2. the methodology for determining the biological response

elicited from the exposure to the products;

3. chemical analyses (identification and quantification) of the

products responsible for that response.

Some of the problems associated with determining the toxicology of

combustion products have been discussed by MacFarland [45] . He compares

conventional toxicology experiments to experiments on the inhalation toxicology of combustion products. In conventional inhalation toxicology, an organism is exposed to a known quantity of a single agent and the organism's

responses are noted as a function of time and concentration (dose-response

relationship). In combustion product inhalation toxicology, by contrast, the

agents and dosage usually remain unknown due to the difficulty of measuring

the amount of toxicants produced and inhaled , due to the large number of

products produced, and due to the fact that the composition and concentration

of products change with time and combustion conditions. In addition, as pointed out by MacFarland [45] and Amdur [46] , particulates are also present

and may play a significant role in the toxicity of the products that is

difficult to assess analytically.

The toxicological studies on the thermal decomposition products of

polytetraf luoroethylene (PTFE) as reported by Clayton et al . [11] and Waritz

and Kwon [12] represent some of the most definitive work on toxicological

assessment of theirmal decomposition products of a polymeric material in which

animals were used. These studies on PTFE are classic and illustrate the value

of using animals as detectors for assessment along with some chemical analyses

of products for correlation with the biological results. The chemical analysis

was also used to verify the conclusion of the bioassay experiments. The

importance of particulates in inhalation toxicity is also dramatically illustrated . , _
Zapp et al. [47] reported the pyrolysis products from PTFE decomposed at

300 °C in air to be tetraf luoroethylene , hexaf luoroethane , hexf luoropropylene

,

octaf luorocyclobutane , and octaf luoroisobutylene . Clayton et al . [11] showed

that a particulate material was responsible for the toxicity of PTFE at certain

temperatures. Further work by Waritz and Kwon [12] showed that at a sample

pyrolysis temperature of 450 °C , a 100% mortality was obtained on rats. By

passing the effluent through microporous filters to remove particulates before

exposing the animals to the products, the mortality was reduced to zero. This

result suggested that the major toxicants reside in or with the particulate

phase: at least at 450 °C. It was also noted that hydrolyzable fluoride was decreased by filtration. In addition, it was determined that the toxicity was strongly dependent on temperature and the atmosphere in which the material was decomposed, the toxicity being significantly reduced when decomposition occurred

in a nitrogen atmosphere. When the rats were exposed to the degradation

products generated at 450 °C in air, gross pathology showed microscopic focal

hemorrhagic lungs. When pyrolysis was done in nitrogen no hemorrhages were observed in animals sacrificed after exposure.

Scheel, McMillan and Phipps [48] exposed rats to the pyrolysis products

of PTFE containing hydrolyzable fluoride equivalent to 50 ppm COF 2 for one hour daily. Urine excretion of fluoride correlated with the measured changes

in the succinic dehydrogenase activity as expected from fluoride poisoning.

The authors concluded that COF 2 is generated during the pyrolysis of PTFE and

hydrolyzed in the body fluids to produce fluoride toxicity in the exposed

rats

Scheel, Lane, and Coleman [49] exposed dogs, rabbits, guinea pigs, cats

and mice to the pyrolysis products of PTFE. They also concluded that the

principal toxic effects are due to the hydrolyzable fluoride produced when

carbonyl fluoride and other hydrolyzable products are absorbed into the

tissue. The lesions associated with the particulate material observed in the

lungs of exposed animals prove that the particulate is irritating for at

least seven to ten days following inhalation.

Various air pollution studies have also demonstrated the role of particulates in the inhalation toxicology of various materials and deserve some attention in fire gas research.

The role of an inert aerosol on the irritant properties of sulfur

dioxide and formaldehyde has been studied in some detail by Amdur [46] using

guinea pigs and deserves some attention in the fire gas problem. She found

that 0.04 y NaCl aerosol had a definite potentiating effect on the irritant

properties of SO 2 , where 2.5 y aerosol did not. The effect increased as the

aerosol concentration increased from 4 to 30 yg/ml at the same concentration

of formaldehyde. The potentiating effect of the inert aerosol on the formaldehyde exposure was also particulate size dependent. This is consistent

with the fact that the small aerosol with the absorbed gas will pass through

the upper respiratory tract and reach the alveoli of the lungs where it is

retained as an irritant and released causing deeper involvement of the lower

respiratory tract. She also noted that the presence of the aerosol with

irritant gas delays the recovery of the animal as compared to the exposure to

the irritant gas without the aerosol. In the non-aerosol exposure, pulmonary

resistance returns to pre-exposure value (level) in about two hours (depending

on the concentration) whereas the recovery from the aerosol-irritant required

a considerably longer time up to 24 hours. Amdur speculates that two physiological phenomena occur: 1) the low level irritant produces mechanical

constriction which is reversible once the irritant is removed and 2) the

combination of aerosol-irritant may be the beginning of tissue damage in the

alveolar region of the lungs.

From the foregoing discussion it should be clear that particulates may

affect the toxicological effects of combustion products on a biological

system. It should be realized that the rate of desorption of any toxic

13
product adsorbed on particulates is critical. In turn, a number of factors

will affect the products that are produced during thermal degradation. These

include shape and weight of material, temperature of degradation, combustion

equipment, air supply, and exposure chamber. In addition, the mode of degradation, flaming, smoldering, or pyrolysis will affect the composition and

concentration of the products that are generated. Since the methodology for

exposing the animals and assessing the effects on the animals will affect the

conclusions, it is extremely difficult to compare the results found by various

experimentalists who use different techniques. However, from a practical

point of view, it may only be necessary to show that one material is more or less toxic than another under certain specified conditions.

3.2. System for Biological Assessment of Toxicity

Statement of problem; How does one generate combustion

products reproducibly and expose

animals to these products?

The last two years have produced a rapid increase in the number of laboratories that are doing biological testing of combustion products and the

field is in a rapid state of flux. Table 1 is a summary of these systems

presently being used for such purpose. Much of this work was reviewed at the

Symposium on Toxicity and Physiology of Combustion Products [50] . Rather

than reviewing and critiquing all of these experiments in detail, there are some general comments that are applicable to most of the systems that indicate the advantages and disadvantages of the various methodologies.

3.2.1. Combustion Systems

The nature and concentration of combustion products will depend on the

(1) mass of the sample; (2) volume of the chamber; (3) heat flux or temperature to which the sample is exposed; (4) time of heat exposure; (5) sample

formulation; (6) flaming or nonflaming mode; (7) atmosphere surrounding the

sample; and (8) orientation and physical structure of the sample. Specification of these parameters is a minimum requirement if data are to be reproduced in the laboratory. This is not to suggest that other parameters will

not become important as animal experiments are coupled with combustion

experiments

Various thermal decomposition techniques have been used to generate

products for animal exposure in order to assess the toxicity of the gaseous

products. The thermal decomposition systems fall into two broad classes:

(1) those that generate the products external to the animal chamber with the

products transferred to the animals (flow-through system) ; and (2) those

that generate the products inside the animal chamber. Both have advantages

and disadvantages that may affect the overall toxicological results.

An example of the first type of system is that being used in West Germany

by Kimmerle [51] and Hofmann and Oettel [52]. This system has prO|duced the

most information since a wide variety of materials have been intercompared

and evaluated on an equal volume basis and on an equal mass basis. According

to Kimmerle [51] , the German toxicologists have agreed on the methodology for

the generation of pyrolysis products for the exposure. The thermal degradation system consists of a short tube furnace with the samples enclosed in a quartz tube. The furnace travels along the quartz tube — sample, with air

flowing in the direction of furnace travel or counter to it. Using this

system the toxicity of the products can be compared by sample weight or sample volume. Kimmerle states that "for an evaluation of combustion processes, the second approach (volume) seems to be more in line with actual

conditions" and, furthermore, that in Germany "it was agreed that only

14
smoldering conditions are of interest." It would appear to this author that

the decision on smoldering combustion is a bit premature until more inforroation on the relative toxicity of the products of smoldering combustion as compared to flaming combustion is available as determined by careful bioassay

experiments

The efforts in France [53] and Belgium [54] summarized in Table 1 use

the German system for combustion product generation . The work in France

was reported in some detail at the International Symposium on Physiological

and Toxicological Aspects of Combustion Products in March 1976 [53]

The second type of system is used at the University of Utah in which

animals have been placed directly in a smoke density chamber [14]. This

system specifies many of the parameters that influence the quality and

quantity of products. Moreover, with recent modifications reported by Seader

,

Chien, and Birky [55], it is possible to change heat flux from 2 to 7.5 W/cm^

and monitor scimple mass on a continuous basis. The chamber, however, is not

the most convenient for animal exposures in terms of observations of the

animals and monitoring animal physiological functions. These limitations

will be discussed later.

3.2.2. Animal Exposure System

Even though it may not be possible to determine a true dose in fire

experiments, the time of exposure must be specified. Whether or not the

animals are restrained or allowed to move about during the exposure may have

a significant effect on the outcome of the experiment. Animals that are free

to move about in a cage generally will huddle together causing variations in

exposure.

Placing the animals directly in the chamber where combustion occurs or transferring the combustion products to the animal chcimber may also cause significant differences in the results. If the products are transferred into

the animal chcunber then the temperature, diameter and length of the transfer

lines can play a role in the dosage received by the animals. In this case,

it may be very difficult to intercompare biological results with other experiments and to intercompare the toxicity of products from different materials

due to the preferential trapping of different constituents. If the aerosol or particulates play a significant role in the toxicity of PVC then the assessment of the toxicity of PVC relative to the toxicity of some other product

that does not involve particulates will be misleading. For example, the

studies on the fire retarded rigid polyurethane foam [14,15] mentioned earlier

indicate that the highly toxic bicyclic phosphate ester may be concentrated

in the smoke (particulate) phase of the pyrolysis products.

In the flow-through or product transfer system, a toxic product that has

a relatively low vapor pressure may be trapped out on the walls of the

I transfer tube unless the walls are heated. This differential trapping can make a significant difference in the ranking of materials for toxicity hazard.

)l If the material produces low levels of a highly toxic agent it may not appear

to be hazardous when the products are transferred through a cold tube.

’ In the systems that place animals directly in a combustion atmosphere

,

I such as the smoke density chamber, one must be aware of the potential for

' producing a decreased oxygen atmosphere and elevated temperatures. This, of

j course, depends on the ratio of chamber volume to the sample mass. Both

oxygen concentration and air temperature should be measured in order to avoid

placing these stresses on the animal. In addition, animal monitoring for EEG

and EKG is difficult in the smoke density chamber as presently designed since

it was not made for this purpose. As a result of this new application of the

smoke density chamber, modifications for animal exposures are being developed.

15
In the German system, large amounts of air are mixed with the combustion

products so that decreased oxygen content is not likely to occur and elevated

temperatures are not likely to be a problem. Both of these stresses (high

temperature and low oxygen) will cause major differences in toxicological

results

Cornish [56] in a corollary study to that of Boettner et al. [33] ranked

materials according to material LD 50 (lethal dose of thermal degradation

products resulting in 50% mortality) using two different systems for product

generation and exposing the rats. He referred to the two systems as a "flowthrough chamber" and a "static chamber." He concluded that the relative

toxicity of the thermal decomposition products of a number of materials is

significantly different as determined by the two systems. This is not a surprising result when one reviews the two systems.

In his flow-through system, a pyrolysis mode of thermal decomposition

was used; and in the static chamber, a combustion mode was used. It is not

entirely clear if combustion occurred in the flow-through technique; but at

a heating rate of 3 degrees per minute, it is unlikely. In the static

system, the sample combustion temperature was reached in one or two minutes.

In addition to this rather fundamental difference, exposure time and

product concentrations were also different. Pyrolysis in the flow-through

system was continued for 140 minutes with an airflow over the sample of 1 liter

per minute diluted with 2 liters of air per minute before exposure. This gives

a total voliame of approximately 420 liters and an animal exposure time of 140

minutes. In the static chamber the total volume was 1500 liters and the

exposure time was four hours.

Both exposure times are unrealistic for exposure to combustion products.

For the fire environment, a maximum exposure time of 30 minutes is reasonable.

In addition, if the rate of intoxication is an important parameter, then, of

course, the exposure time and sample mass to air volume ratio (fuel loading)

and heating rate and combustion rate become important parameters.

If the goal is to compare the two types of animal exposure techniques then

the products should be generated in the same fashion. If the goal is to com- pare pyrolysis products with combustion products, then of course the same animal exposure conditions must be used. But when both the thermodegradation

conditions and animal exposure conditions have been changed simultaneously,

one cannot determine what effect is related to which variable. As a result

of measurement with two entirely different systems, the fact that Cornish

[56] ranked various materials in a different order based on a lethal dose per

gram of material undergoing thermal decomposition means only that the results

depend on the system as pointed out previously.

3.2.3. Chemical Analysis Systems

The analytical measurements can be divided in two categories: (1)

analysis of combustion products (environmental) to which the animals are exposed and (2) biochemical analysis, predominately blood chemistry. Measurements and correlation of toxicants in environment and in the biosystem

have not been done to any great extent in the biological assessments. This

approach was used in studies on polytetraf luoroethylene [47-49] . The various degrees of chemical analysis of combustion products were

discussed in earlier sections. Measurements of selected products discussed

in these sections are extremely valuable in animal experiments. Oxygen

measurements are necessary to determining if oxygen depletion is a significant factor or in order to avoid this condition. Carbon monoxide, a toxicant

produced in most if not all fires, should be measured and correlated with the

COHb levels in the animals. Carbon dioxide is also common to the combustion

16
process and should be monitored. If hydrogen cyanide is considered to be a product in the degradation of a material, then one may wish to monitor this

toxicant

In some of the systems that have been reviewed in the previous sections

[51,53,54], carboxyhemoglobin data is reported either at the point of death,

incapacitation or at the end of the exposure period. This data is extremely

valuable in determining the significance of carbon monoxide relative to some other toxicants. That is, if the value of COHb is significantly less than

that required to cause incapacitation or death and the animals were either

incapacitated or dead, then some other toxicant should be considered. This

approach was used in the study reported by Petajan, et al . [14].

The chemical make up of the polymer system being studied can be used to

determine what other toxicants should be measured in the biological system.

For example, blood cyanide can be measured when the animals are exposed to

degradation products from polymers containing nitrogen in their chemical

structure. This measurement may cause some difficulties which are discussed

below (section 4.2). In any event, COHb measurements appear to be minimal

biochemical measurements.

4. MECHANISMS AND MODELS

Statement of problem: Very little is known about the mechanism

of action of most toxicants found in fire

environment except CO and perhaps HCN.

Most toxicity studies have been directed

to chronic (long term, low level)

exposures to single toxicants. Virtually nothing is known about the effects

of complex mixtures of toxicants found

in the fire environment or about the

effects of short exposures to high con- centrations or single toxicants.

Various reviews on toxic products in the fire environment have included

reviews that describe the expected physiological effects of individual toxicants at various levels on humans [51,57]. Some animal reponse data is also

included in Kimmerle's review [51]. All of the information presented in

these reviews is limited to a description of physiological symptoms and does

not consider mechanisms. The effects of multiple components have not been

investigated and it is clear that multiple component effects cannot be determined without a clear understanding of the effects of individual toxicants.

4.1. Carbon Monoxide

The physiological effects of low levels of carbon monoxide on man and

animals have been studied extensively [58,59]. The mechanism of intoxication

is well documented and is primarily the result of tissue hypoxia caused by

the inability of the blood to carry sufficient oxygen to the cells [60]

The

inability of the blood to transport oxygen is due to the fact that the affinity

of hemoglobin for carbon monoxide is 300 times greater than that for oxygen

so that the CO preferentially ties up the hemoglobin to produce carboxyhemoglobin (COHb) .

17
R. Stev/art et al. [61] exposed humans to high concentrations of CO for

short periods of time and monitored EEC, EKG, cardiac output, COHb , visual

evoked response, etc. The main objective of this study was to accurately

determine the rate of CO absorption during brief exposures to the gas in

concentrations found in automobile exhaust and in burning buildings. Since

COHb levels were not allowed to exceed 16%, significant changes in the

measured physiological parameters did not occur. As a result of these and other studies on carbon monoxide it is well

known at relative low concentrations what level of carbon monoxide in the

environment will produce a given level of COHb and furthermore what the

physiological response is likely to be. It is not as well known what happens

on exposure to high concentrations of CO that result in corresponding high

carboxyhemoglobin concentrations in human subjects. Likewise, it is not

known if individuals with cardiovascular disease are more susceptible to the

effects of carbon monoxide. In addition it is not known what the effects of

CO are on an individual who has a high level of blood alcohol.

Based on the information on the toxicity of carbon monoxide, the toxicity

of combustion products from wood was compared to that of CO by Edginton and

Lynch [62], and Zikria [63]. Edginton and Lynch concluded that the sole

toxic principle released in hazardous amounts by burning plywood or flame

retardant treated plywood is carbon monoxide.

Zikria noted that when test animals were exposed to the combustion

products from wood, carbon monoxide alone did not account for the deaths. By

combining gas analysis with bioassay experiments and with clinical data that

showed many deaths involved respiratory tract damage , he concluded that

aldehydes in combination with the CO could explain the deaths.

Carbon monoxide has become the toxicant of choice for use in the development of an animal model for toxicity assessment of combustion products

[64]. This is due to various reasons. First, CO is believed to be produced

in virtually all fires. Secondly, it is probably the most studied and understood toxicant and consequently its effects on many species is well documented making it relatively easy to compare CO toxic response to the response

from combustion products.

4.2. Hydrogen Cyanide

Statement of problem: What is known about role

of HCN in fire deaths?

Hydrogen cyanide is a good example of a toxicant about which there is a lot of speculation in fire literature and not much factual information. It

has become a major concern in fire fatalities since (1) it is known to be a product resulting from the thermodegradation of some polymers containing

nitrogen, (2) because it has a relatively high toxicity, and (3) there is a strong public reaction to this toxicant. The role of hydrogen cyanide in

fire fatality studies raises some interesting questions since most of the

data on cyanide in these studies are questionable due to questionable sample

treatment and analytical procedures. At this time there is little clinical

information or data from animal studies to determine the validity of this concern. The data that are available raise more questions than they answer.

For a detailed discussion of the mechanism of action of cyanide on biological systems the reader is referred to Goodman and Gilman [65]

Hydrogen cyanide reacts readily with trivalent iron of cytochrome oxidase in mitochondria to form the cytochrome oxidase-CN complex which inhibits cellular

respiration, an action referred to as cytotoxic hypoxia. In low concentrations,

cyanide stimulates respiration. Its activity on the brain electrical activity

18
is one of depression. Lethal concentrations result in progressive slowing of

the heart and the heart continues to beat several minutes after the last

respiration

The physiological effects of cyanide on the central nervous system and

the cardiovascular system have also been delineated. The route of detoxification is through the formation of thiocyanate by the action of rhodanese.

Detoxification is limited by the endogenous supply of thiosulfate.

What does not appear to be well known is the level of environmental

cyanide that will produce a given biological or blood level, and what will be

the corresponding physiological effects in humans or animals at a given level.

A great deal of the difficulty appears to be due to the lack of accurate and

reproducible analytical techniques for the measurement of hydrogen cyanide in

air and in biological systems.

Wetherell [66] determined blood cyanide levels in 53 fire victims in

Michigan and found that 39 of the victims had blood cyanide levels that

ranged from 17 yg/100 ml to 200 yg/100 ml. The minimum lethal level is

reported to be 300 yg/100 ml [67]All measurements were performed within

24 hours on refrigerated samples so that cyanide from decomposition was supposedly ruled out. Also stomach cyanide levels were determined to rule out

ingestion.

Post mortem analysis of 26 victims of cyanide poisoning by Sunshine and

Finkel [68] shows that the brain has the lowest cyanide levels and the spleen

the highest. They found that in some refrigerated samples, blood cyanide

concentrations rose to 500 to 700 yg/100 ml in 14 days. They also demonstrated that blood samples incubated at 37 °C did not show cyanide. The

source of the cyanide in the refrigerated samples was believed to be from

bacteria. This information raises some questions about the significance of

Wetherell 's data and conclusions.

The problems of sample handling and other questions concerning the

analvsis of HCN in biological samples need to be answered before significance

car. be attached to clinical cyanide measurements. Not only is the treatment

of biological samples for cyanide analysis important, but the time elapsed

between death and sample collection must also be considered. Obviously even

before these questions can be answered, a good reliable analytical procedure

must be available for cyanide analysis of biological samples.

In summary, the role of hydrogen cyanide in fire fatalities or casualties

is not clear. It is known that some hydrogen cyanide is produced when

nitrogen containing polymeric materials are exposed to or involved in fires,

but until more is known about its significance in human casualties, its

hazard in fires cannot be stated.

4.3. Synergism

Statement of problem: What do we know about the synergistic

effect of two or more toxic gases in

fire deaths?

The possibility of synergistic action between two or more toxicants in

the fire environment has been suggested by a number of individuals in the

fire literature. Synergism in the toxicological sense is defined as a toxicological response from a mixture that is greater than the siammation of the

individual toxicities of the components. For example Boettner et al. [33]

19
concluded that carbon monoxide and hydrogen cyanide are the only acutely

toxic compounds identified from the analytical studies on polyurethane; and

since carbon monoxide disrupts the ability of the blood to carry oxygen and

cyanide disrupts the cell's ability to utilize oxygen, there is a toxicological synergism between the two.

Moss et al . [69] exposed rats to CO and HCN alone and in combination to

determine if synergism exists between the two toxicants. Although they

avoided the term synergism, their descriptive conclusions are suggestive of

the fact that they considered the toxicological interaction between CO and

HCN to be more than additive.

Based on exposure of rats to CO and HCN, Kimmerle [51] concluded that

there was a synergistic action between the two toxicants. Birky [70] analyzed

the data obtained by Kimmerle and concluded that synergism was not demonstrated.

In an effort to determine if toxicological synergism does occur between

CO and HCN, Lynch [71] exposed rats to CO and HCN singly and in combination.

Death was used as the endpoint. Based on this work. Lynch reported that

synergism did not occur between these two gases.

Pryor and coworkers [72] investigated the combined actions of various

factors related to the fire environment. They exposed mice to the combined

actions of oxygen depletion, carbon dioxide, carbon monoxide, and heat as the primary variables. Low levels of hydrogen cyanide, nitrogen dioxide and

sulfur dioxide v?ere added singly to the above constituents to study the com- bined action.

It is difficult to assess the data presented by Pryor and coworkers on the effects of these combinations of noxious gases due to the large variability

of the data. For example, in their table 4, three mice died as a result of a four-hour exposure to 16% O 2 , 0.075% CO, and 30% CO; at 85 °F, while in their

table 7, no mice died when exposed to the same atmosphere at a temperature of

100 °F for 4-hour and 24-hour exposure times. The authors suggest at one point that a new batch of animals gave different results. However, it is not

clear why this should be so, or whether the data in table 7 are comparable

with the data in table 4. In any event, the large variability shown by these

data suggests that the conclusion regarding synergism due to low levels of

irritant gases is highly questionable. In addition, an exposure time of four

hours is excessive for relevance to the fire problem.

It is not entirely clear that the final answer is available concerning

the question of synergism between CO and HCN. Data that are available suggest

that synergism does not occur between these 2 toxicants, at least in rats.

In one sense synergism has become a catchword to explain many unanswered

questions regarding fire fatalities.

4.3.1. Mathematical Analysis for Synergism

A mathematical equation was defined in section 2.4.3 as a means of

estimating the additive effects of a mixture of toxicants. It has been proposed [70] that this equation can be used to determine if two or more toxicants

are additive or synergistic in nature. In equation (1) , if C, is defined as the concentration that is fatal to 50% of the animals (LC^q) for the individual

toxic components and C is the concentration of the individual components to

which the animal is exposed in a mixture, then the Siam of toxicity indices (T)

should be approximately 1 at the LC 5

0

concentration of the combination if no synergism exists; that is, the toxicity of two or more agents is additive.

T Z . X (Ce/Cf)i 1

20
If the summation is less than 1, then it can be assumed that synergism exists

and in the summation above an interaction term is required. On the other

hand, if T is significantly greater than 1, then one should look for antagonism.

Kimmerle [51] has some data on the toxicity of carbon monoxide and

hydrogen cyanide that served to illustrate the use of the above relationship.

According to Kimmerle, the 30-minute LC 50 rats exposed to carbon

monoxide and hydrogen cyanide individually are 5500 ppm and 200 ppm, res- pectively. In table 2 reproduced from Kimmerle [51] , 3300 ppm of 30 and 45

ppm of HCN resulted in 50% mortality again for 30 minutes. The toxicity

index for this combination is

T = 3300/5500 + 45/200 = 0.83

Similarly, 4400 ppm of CO and 38 ppm of HCN gave a 45% mortality, not quite

50% but probably within experimental error. These concentrations give a toxicity index of 0.99.

By the above stated criteria, one might expect that some synergism

exists in the first case since T < 1 (0.83). However, the uncertainty in

the overall measurement, while not stated, is expected to be in the order of

+0.2. This would include the errors in HCN and CO measurements and variability in animal response. The conclusion of this author is that no synergism has been proven to exist between HCN and CO, at least by these data,

contrary to Kimmerle 's conclusion. Certainly the second set of data where

T = 0.99 shows no synergism by the above criterion.

4.4. Sensory and Respiratory Irritants

Statement of Problem: What is the relative role of eye and

nasal irritation as compared to light

obscuration during fire?

As indicated in earlier sections, light attenuation measurements have

been used exclusively as a measure of the hazard of smoke from combustion

products. While it is true that light attenuation is a problem for the

firefighter both in fire fighting and rescue operations, inability to find

an exit due to impairment of vision caused by irritants may be the primary

problem for the individual caught in a fire.

The effects of irritants in smoke on visual acuity was investigated by

Lopez [73] . He studies smoke emission from burning aircraft cabin materials

to determine: (a) the degree of correlation between NBS smoke chamber data

for various cabin materials and similarly acquired data from large-scale tests

conducted in a cabin mock-up representative of a wide-bodied transport, and

(b) the effect of smoke on human visual acuity and the relationship of this

visual acuity to optical attenuation measurements. For the second objective,

two sets of human subjects were used: ( 1 ) individuals outside the mock-up

viewing a sign through a window and ( 2 ) the second set in which the window

was removed so that their eyes alone were exposed to the smoke.

Ten classes of cabin materials were tested with two different compositions of each class. For example, a wool carpet and a 50/50 cotton-rayon

carpet were tested. Likewise two Tedlar coated ceiling panels were tested.

The major conclusions of the study were that; (a) fair to good correlation exists between laboratory chamber and mock-up smoke measurement results,

and (b) that the dominating factor on human visibility is the irritating

effects of combustion products as opposed to light obscuration.

21
An extensive review of the mechanisms of sensory irritation in the upper

respiratory tract was prepared by Alarie [74] . The nasal respiratory epithelium, as well as the cornea, receive their sensory innervation from the

afferent trigeminal nerve. As pointed out in this review there are some important differences between the sensory nerve endings of the nasal respiratory mucosa, the cornea, the skin and other mucous membranes. "However, all

represent the common chemical sense receptor in mammals and in general can be

stimulated by the same chemicals."

Based on this knowledge of the basic physiological similarities between

the sensory nerves, Alarie reported on the irritant properties of combustion

products from a polyurethane using mice as experimental animals. Change in

respiratory rate and tidal volume was measured and expected human responses

proposed [75]. Table 3 taken from Alarie's results, is the proposed relationship between results obtained with mice and the proposed human response to

sensory irritants. In a comparison of the sensory irritation response in mice

to HCl and Cl^ and the thermal degradation products of PVC , Alarie concluded

that the decomposition products of PVC were somewhat more potent than HCl [76]

No explanation of this fact has been obtained at this time, but this fact

would tend to be born out by experience of the fire services in fighting

electrical fires. Fires involving PVC electrical insulation, as reported by

Dyer and Esch [77], appear to be deceptively hazardous.

4.5. Organophosphate Ester Toxicity

Statement of problem: Is the identification of the

highly toxic phosphate ester in

the combustion products of a fire

retarded polyurethane foam predictive of future problems with

fire retarded materials?

Since many of the fire retardants used in polymeric materials are organophosphates or halogenated organophosphates , this raised the obvious question

of the toxicity of these compounds, both in the environment and of their com- bustion products during a fire.

4.5.1. Neurotoxicity of Organophosphates

Two extensive reviews on the mechanism of neurotoxicity of chemical agents

and in particular on organophosphorus esters have been prepared in the last

couple of years [78,79]. This most recent review is oriented to the biochemical mechanism of neurotoxicants [79] . The subject is extremely complex and

in some cases the mechanisms are not clearly understood. For an understanding of what is known about the mechanism of action, the serious reader is

referred to the above references.

In summary, the toxic actions of organophosphorus compounds are of three

known types: (a) acetycholinesterace inhibitor, (b) delayed neurotoxic action

and (c) Y-aminobutyrate antagonism (GABA) . The first two types are well

documented in terms of clinical manifestations, but it is only the first type

in which the biochemical mechanism is well understood. In those compounds

that show delayed neurotoxic activity, the action is postulated to be by

inhibition of esterases. The esterase activity is referred to as "neurotoxic

esterase" for which the physiological function and biochemical mechanism are unknown. The third type of action, GABA antagonism, is not discussed in the

above reviews and very little exists in the literature on this type of toxic

action

22
The review of the neurotoxicity of organophosphorus esters cover the

first two types of neuropathies [79] . The first is a selective effect upon

certain hydrolytic enzymes, notably pseudo (or serum) cholinesterase. This

type of action is most commonly referred to as acetycholinesterase inhibition.

As mentioned, the biochemical mechanism is well understood and the clinical

symptoms are quite characteristic.

The second type produces a delayed neurotoxic sequelae in which the

clinical effects are not seen until 8 to 14 days after ingestion of the toxic

agent. The clinical manifestations of the intoxication are well known and

these will be described. However, as indicated, the biochemical mechanism

is not well understood.

A comparison of a number of organophosphates shows, however, that there

is no correlation between the neurotoxicity with inhibitory power against the

esterases, an enzyme in the brain and spinal cord that is the target for

neurotoxic agents. The biochemical mechanism is believed to be by inhibition

of neurotoxic esterase even though it is known that young hens do not develop

neuropathy after single doses of neurotoxic agents; though their neurotoxic

esterase is inhibited. This is apparently an unresolved problem and possible

suggestions for the lack of neurotoxic response have been made in young

chicken^ . In general, the young in most species seem to be more resistant

than the adults to the effects of delayed neurotoxicants.

By way of physiological mechanism of the delayed neurotoxicants, the

following observations have been made. By far the largest number of chemicals

with selective neurotoxic activity appear to act upon the neurons. The

neuron has two properties not found with other tissues that render it more

sensitive to outside influences. First, neurons that are irrepairably

damaged and die cannot be replaced in mature animals. Any "recovery" from

loss of neurons can only be effected by establishing new neuronal circuits

or by greater use of those remaining. Secondly, if the structural maintenance

program of a neuron is interfered with so that it is unable to maintain its

long axon, and consequently degeneration of a distal part of the axon occurs,

a break in communication system takes place leading to a loss of function of

the signaling unit. By comparison, if a break occurs in the peripheral nerve

fibers regardless of the extent, the potential for regeneration is very great

and contact is re-established although the growth rate is limited to about

1 mm/day. Repair of damaged central nervous system fiber does not occur.

It is observed that while the initial attack on neurotoxic esterase occurs throughout the nervous system, only certain axons degenerate. This is believed

to be related to the length and diameter of the axon, the longer axon being

affected to a higher degree.

One can summarize by saying that "at present no clear metabolic disturbance has been proven to be associated with the inhibition of neurotoxic

esterase and the genesis of the delayed neurotoxic response." As a warning,

delayed neurotoxicity is an irreversible effect, and the fullest possible

measures should be made of the hazard associated with a new compound.

There is another class of compounds that compete for the active site of

the neurotoxic esterase that are not only non-neurotoxic but actively protect

test animals from the neurotoxic phosphate esters. Carbamate, phosphinate

and sulphonate produce inhibited enzyme in which there is no toxic effect

and protection occurs since the enzyme is not available for attack by neurotoxic compounds. These compounds can be used as blocking agents.

In the delayed neuropathy, the onset of paralysis in man is signaled by

abnormal sensory experience such as burning or tingling, particularly in the

feet and hands. Motor weakness is the cardinal symptom that begins in the

feet and later involves the legs more generally and the hands. Ataxia may

develop depending on the degree on intoxication. Sensory nerves may also

23
show degeneration, again particularly in distal limb regions; the most widely

affected end-organ being the annulospiral formation of the muscle spindle.

Man and the chicken appear to be equally susceptible to the neurotoxicity

of organophosphate esters and the latter has become the standard test animal.

As noted earlier, the young of a sensitive species are usually much less

susceptible and the reason for this is not known. Consequently, adult hens

more than 100 days old are used for screening of 0-P compounds. Rats and

guinea pigs seem to be insusceptible or respond only poorly.

Tri-o-cresyl phosphate (TOCP) is the classical example of a phosphate

ester that produces a delayed neurotoxic response, and it has been studied

in some detail. Cresyl and related phosphates have been used as hydraulic

fluids, lubricants, plasticizers and flame retardants. Studies on these

types of compounds show that a large number of triaryl phosphates possess

neurotoxic potential, although only a few limited correlations could be made

between structure and activity.

Biochemical studies on TOCP show that a liver metabolite of TOCP is

30 to 60 times more neurotoxic than TOCP itself. Based on this finding it was suggested that, as far as aryl phosphates are concerned, the liver plays

an essential role in producing the toxic substance. It is believed that this

process helps to explain the longer delay period between the administration

of an aryl phosphate and the onset of symptoms of paralysis as compared to

the alkyl phosphates.

Extensive studies on a wide range of alkyl and aryl-substituted analogues

have shown that the only thing common to the neurotoxic and anti-esterase

compounds is possession of a phosphate group. There is thus at present no certain way of predicting on the basis of its chemical structure whether a compound will be neurotoxic or not until tested.

It was reported that triphenyl phosphate was neurotoxic in cats, producing an effect like TOCP. It has since been shown that pure triphenyl

phosphate is totally non-neurotoxic in the hen. Samples of "pure" triphenyl

phosphate prepared from coal-tar phenol have been shown to contain neurotoxic

impurities, as have other triaryl phosphates.

This type of information should serve as a warning to those laboratories

doing research on existing and potential fire retardants that are organophosphates that may in themselves be non-neurotoxic but may contain impurities

that can be very neurotoxic.

Two organophosphate compounds used for fire retarding textiles have

been reported to possess anticholinesterase activity [80] . In this study

anticholinesterase activity of tris (2,3 dibromopropyl) phosphate (I),

N-methylol dimethyl phosphonopropionamide (Pyrovatex CP) (II) , and THPOH

[ (Tetrakis (hydroxymethyl) phosphonium hydroxide] (III) were compared to the

insecticide, Tetram S- [2- (diethylamino) ethyl] (0,0-dithyl phosphorodithioate

hydrogen oxalate) . The first compound (I) was found to produce about 16% of

the inhibition of the insecticide whereas compound II produced 25% of the

inhibition of the insecticide on a equimolar basis. The anticholinesterase

activity of compound III could not be determined due to measurement interferences .

In the same study goldfish were exposed to 1 ppm in 30 gallons of water

of each of these three compounds individually. All the fish died within five

days from compound I, none died from the second fire retardant in a 30-day

exposure, and 5 of the 6 fish died within 16 days from compound III.

24
Skin absorption of fire retardants as a result of wearing flame resistant

treated fabric has been a concern for a number of years, although there appears

to be little information available on this subject. Tris (2,3 dibromopropyl)

phosphate (TBPP) has been studied to a limited degree [81] . Chromatographic

analysis of treated urine from rats exposed to dermal applications of TBPP

yielded a 2,3 dibromopropanol free and conjugated (DBP) that was believed to

be a metabolite of TBPP. This compound was not found in the urine of individuals wearing clothing treated with the fire retardant although a rat allowed

to chew on such a fabric did have low levels of DBP.

4.5.2. Carcinogensis of Organophosphate Fire Retardants

Tris (2,3 dibromopropyl) phosphate was tested [82] for mutagenicity in

the histidine deficient strains of Salmonella typhimurium according to the

Ames procedure [83]Preliminary results of this testing indicate that this

compound is mutagenic and that metabolic activation by rat liver enhanced

the mutagenic activity. The Salmonella/microsome test shows that 90% of the

known carcinogens were detected as mutagens. The reverse correlation has not

been established. Carcinogenicity studies on rats and mice are in progress

at the National Cancer Institute to validate the above findings.

The first indication of a potentially serious problem in the fire

environment due to organophosphate compounds was reported by Petajan et al

[14] . It was shown that a highly toxic bicyclic phosphorus ester (4-ethyll-phospha-2 ,6 , 7-trioxabicyclo (2,2,2) octane-l-oxide) was produced when a phosphorus fire retarded rigid polyurethane foam based on a low molecular

weight propoxylated trimethylolpropane was exposed to a high heat source and

thermally degraded. It was reported that the rats exposed to the combustion

products from this foam exhibited major motor seizures and died of status

epiliptus

The toxicity of the 4-alkyl bicyclic phosphorus esters was previously

reported [16] at which time it was noted that the toxicity syndrome in mice

and rats from an acute exposure do not resemble the characteristic poisoning

by acetylcholinesterase inhibition. The mechanism was not defined.

These data suggested that a third type of neuropathy attributed to

organophosphates that was not addressed in the review articles above may

occur. The mode of action of the third type was defined by Bowery et al

[84] as y^inobutyrate antagonism.

The above limited data on the toxicity of organophosphorus compounds

used as fire retardants should not be interpreted or extrapolated to the

point of suggesting that all fire retardants enhance the toxicity of com- bustion products or of the materials in which they are included. In fact,

quite to the contrary, preliminary results from a bioscreening program at

the University of Utah in which thermal degradation products from polymeric

materials with and without fire retardants are compared do not show any

significant change in the toxicity of the combustion products from these

materials. This is not to suggest that there will not be materials in which

the toxicity of the fire retardant is unacceptable or that the combustion

products of a polymer with a fire retardant will not be increased as compared

! to the material without the fire retardant.

5. PREVENTIVE MEASURES THROUGH CODES AND STANDARDS

Statement of problem; Can building codes and standards be

used to limit smoke and toxic products?

25
5.1. Building Codes

Combustion toxicity requirements for cellular plastics appeared first

in the 1958 Uniform Building Code. In the 1961 Code the toxicity requirement was extended to other interior finish materials. The requirement

states: "The products of combustion shall be no more toxic that the burning

of untreated wood under similar conditions." This requirement has remained

unchanged at this time.

The toxicity code creates an interesting situation since at the time it was written the toxicity of wood was basically unknown and there existed no recognized test method for its determination or for the comparison of wood

with a plastic material. This situation is still true. As a result the

requirement has not been enforced or perhaps it is more appropriate to state

the requirement is unenforceable.

As a result of this situation the International Conference of Building

Officials research committee proposed an acceptance criteria for foamed

plastics under Section 1717 of the 1976 Uniform Building Code that included

a biological test method using rats by which wood combustion products are to

be compared to the plastic material [85] . This toxicity requirement was

dropped. This is the status of toxicity requirement in the building codes

today

Smoke density requirements were introduced in the 1961 edition and were

also related to the burning of untreated wood under similar burning con- ditions. Methods are available however for smoke measurements based on light attenuation. The relevance of such a measurement to physiological

hazard is however open to considerable question.

The French government recently passed a toxicity regulation limiting

the use of synthetic materials containing chlorine and nitrogen in their

polymeric structure [ 86 ] . The limitation applies to synthetic materials for use in public establishments that do not receive M and Mj flammability

ratings. The toxicity requirement applies only to^the M 2 , M 3 , M4 and M 5 classification as determined by the fire test "a'l' epiradieur" or radiant

heat exposure. Materials included in the regulation are: decorative

elements, wall hangings, door hanging, curtains, wall coverings, partitions,

ceiling, ducts and pipes not built in, built in furniture, and furniture

fixed in place.

Only two toxic gases, HCN and HCl , are considered in the regulation.

The total quantity of nitrogen in the synthetic material is limited to 5 grams per m^ of the volume of the buildings, while the chlorine in a synthetic material is limited to 25 grams per m^ of the volume of the buildings.

Permissible quantities of the materials were determined by the following

criteria or assumptions:

1 . one third of the material will be exposed to degradation

temperature prior to evacuation during fire,

2 . one third of this fraction will give rise to an emission

of nitrogen as HCN and chloride as HCl,

3. toxicity limits for fatality were set at 450 ppm for HCN and

1500 ppm for HCl, and

4. HCl concentration limit doubled due to its early detection

as a result of the fact that its irritant properties will warn people of the hazard.

This legislation went into effect in March 1976. This appears to be

the first attempt at integrating toxicity hazard with flammability criteria.

26
5.2. Code Requirements for Detection and Suppression System

The use of various fire protection systems in buildings can substantially reduce or eliminate the exposure of the building occupants to the toxic

products of combustion. For this reason many codes require the installation

of detection, fire suppression and smoke control systems in buildings. The

National Fire Protection Association Life Safety Code [87] for example,

requires the use of detection and extinguishing systems in such occupancies

as newly constructed hospitals and nursing homes. The model building codes

such as the BOCA Basic Building Code [88] require complete automatic sprinklers in high-rise buildings. Many state authorities such as Maryland and

Massachussetts , currently require the installation of smoke detectors in all new one- and two-family dwelling construction.

5.2.1. Fire Detection Devices

From the moment of its initiation, fire produces a variety of changes

in the surrounding environment. Any product of a fire which changes the

ambient condition is referred to as a "fire signature" and has the potential

for use in detection [89] . The production of smoke for example will result

in a decrease in visibility. Not all fire signatures however, are practical

for detection purposes. To be useful, a fire signature should generate a measurable change in some ambient condition. The magnitude of that change

must be greater than the normal background variations for the condition.

The fire signatures currently most practical for use in detecting fire in

non-industrial occupancies are the aerosol signatures and the convective

thermal energy signature. The aerosol material released during fire is

generally referred to as smoke. Smoke appears in detectable amounts early

in the history of a fire. Work on the siting of smoke detectors for residential applications by Illinois Institute of Technology Research Institute

[90] has indicated that properly placed smoke detectors in a dwelling can provide the occupants with sufficient time to leave the building prior to

the accumulation of untenable amounts of smoke or toxic gases.

The convective thermal energy signature is commonly detected by the use

of heat sensors. Although heat is also generated in the early stages of the

fire growth scenario, considerable time is often required before detectable

heat levels are present, even in the room of fire origin. In several fullscale fire experiments it was shown that untenable conditions were reached

in exit passageways prior to an alarm from heat detectors located in the

room of fire origin [91]. The use of early warning detection devices -to

provide time for building occupants to escape the effects of smoke and toxic

products offers one possible supplement to the control of toxic gases by

materials standards. It must be remembered however, that detection systems

simply provide a warning of potential hazard and it is therefore incumbent

upon the occupants themselves to take some positive action to reduce their

exposure to toxic products once the alarm has sounded.

5.3. Automatic Sprinkler Systems

Automatic sprinkler systems can reduce the occupant exposure to toxic

products of a fire by eliminating or substantially reducing the fire at its

source. The overall sprinkler performance record to the United States [93]

indicated that they are 96.2% effective across the total range of occupancies.

Similar information obtained in Australia and New Zealand [94] shows an overall performance record of 99.76% satisfactory. The reason for the discrepancy lies in the fact that in the United States, fire controlled by one

or two sprinklers are seldom reported to the National Fire Protection Association. In Australia and New Zealand it is required that all sprinkler

systems be connected to the fire department and therefore even single head

27
operations are reported in their data bank. It should be noted however that

the typical sprinkler system is heat actuated and therefore will be subject

to the same delays and reponse to a fire that are noted with typical heat

detectors. Response can be speeded up considerably by using a smoke detector

to initiate waterflow but this poses problems with false alarms [95]. Work

is currently underway, however, to develop automatic sprinklers with a more rapid response to heat. A series of test methods and performance criteria

is currently under development for such devices by Underwriters' Laboratories.

5.4. Smoke Control Systems

Under some circumstances, in high-rise buildings for example, the use

of smoke detection devices may not provide sufficient advance warning for

complete evacuation of the occupants. In high-rise buildings smoke generated by a fire may move throughout the building either through the air handling

system or by stack effect generated due to differences in temperature between

the inside and the outside of the building. In order to minimize the exposure

of occupants to the toxic products of a fire in high-rise buildings, methods

have been developed that use the building air handling system for the control

of smoke movement within the building [96]. A typical smoke control system

for a high-rise building would, in the event of a fire, place the air handling

zone servicing the fire f].oor in a 100% exhaust mode. The air handling zones above and below the zone of fire origin are placed in a 100% supply mode such

that the resulting pressure differentials will restrict the movement of smoke

beyond the fire zone. The use of smoke control systems described above can maintain major portions of a high-rise building under essentially smoke free

conditions and thus allow the occupants to remain in the building for the

duration of the fire. It should be noted however that it is still necessary

to evaluate those persons within the air handling zone where the fire

originates

6. CONCLUSIONS

The present state-of-the-art in combustion toxicology is in a state of

rapid change. For a number of years it was assumed that the toxicological

hazard of combustion products would be determined with a chemical analysis of

selected toxic products. Due to the complexity of the product mixture and

possible interaction of toxicants, this is no longer considered feasible and

within the last few years an increasing number of laboratories have been

using biological methods.

The predominant animal model being used to develop combustion toxicity

data is the rat. The toxicological results or relative toxicity of combustion

products from various materials will depend strongly on the method used to

generate the products. Consequently, the relative ranking of materials

between various laboratories are likely to be highly variable and appear to

be inconsistent. The biological endpoint, that is, death or incapacitation,

may also affect the relative ranking or toxicological hazard believed to be

associated with combustion products from various materials.

Until more data and experience has been accumulated in this type of

hazard assessment, it will be difficult to assess small differences in

materials. However, orders of magnitude in relative toxicity can be determined using a bioassay technique.

The reader should

of combustion products

other factors, such as

in question.

recognize that the emphasis of this review is

and any fire hazard assessment must take into ease of ignition and flame spread rate of the

toxicity

account

material

28
7 . ACKNOWLEDGMENTS

The author gratefully acknowledges the contributions of Dr. Clayton

Huggett and Mr. Richard Custer. Assistance from Ms. Nora Jason and the staff

of the Fire Research Information Services of the National Bureau of Standards

for their aid in procurement and compilation of references and bibliographic

materials is gratefully acknowledged.

8 . REFERENCES

[1] National Commission on Fire Prevention and Control, America Burning,

U.S. Government Printing Office, Washington, D.C. (1973).

[2] Harlow, D.W. , International Fire Losses, 1974, Fire Journal, Vol. 69,

No. 6, 43 (November 1975).

[3] Fires and Fire Losses Classified, 1974, Fire Journal, Vol. 69. No. 5,

43-45 (September 1975)

[4] Bowes, P.C., Smoke and Toxicity Hazards of Plastics in Fire, Annals

of Occupational Hygiene, Vol. 17, 143-157 (1974).

[5] Clarke, III, F.B. and Ottoson, J. , Fire Death Scenarios and Fire Safety

Planning, Fire Journal, Vol. 70, No. 3 (May 1976).

[6] Thomas, D.M. , The Smoke Inhalation Problem, Symposium on Occupational

Health and Hazards of the Fire Service, Proceedings, Notre Dame

University, South Bend, Indiana, January 11-13, 1971.

[7] Zikria, B.A. , Weston, G.C., Chodoff, M. and Ferrer, J.M. , Smoke and

Carbon Monoxide Poisoning in Fire Victims, Journal of Traxima , Vol. 12,

No. 6, 641-645 (1972).

[8] Halpin, B.M. , Radford, E.P., Fisher, R. and Kaplin, Y. , A Fire

Fatality Study, Fire Journal, Vol. 69, No. 3, 11-13,99 (May 1975).

[9] Woolley, W.A. and Fardell, P. J. , The Prediction of Combustion Products,

International Symposium on Toxicity and Physiology of Combustion Products,

Proceedings, Salt Lake City, Utah, March 22-26, 1976.

[10] Stone, J.P., Hazlett, R.N. , Johnson, J. and Corhart, H. , The Transport

of Hydrogen Chloride by Soot from Burning Polyvinyl Chloride, Journal

of Fire and Flammability, Vol. 4, No. 1, 42-50 (January 1973).

[11] Clayton, J.W. , Hood, D.B. and Raynesford, G.E., The Toxicity of the

Pyrolysis Products of Teflon TFE-Fluoro-Carbon Resins, American

Industrial Hygiene Association, Annual Meeting, Proceedings, May 1959.

[12] Waritz, R.S., and Kwon, B.K. , The Inhalation Toxicity of Pyrolysis

Products of Polytetraf luoro-ethylene Heated Below 500° Centigrade.

American Industrial Hygiene Association Journal, Vol. 29, 19-26

( January-February 1968)

[13] Lyons, J.W. , The Chemistry of and Uses of Fire Retardants, WileyInterscience , New York (1970).

[14] Petajan, J.H. , Voorhees, K. J. , Packham, S.C., Baldwin, R.C., Einhorn,

I.N. , Grunnett, M.L. , Dinger, B.G. and Birky, M.M. , Extreme Toxicity

from Combustion Products of a Fire-Retarded Polyurethane Foam, Science,

Vol. 187, No. 4178, 742-744 (February 28, 1975).

29
[15] Voorhees, K. J. , Einhorn , I.N. and Wojeik, L.N. , The Identification

of a Highly Toxic Bicyclophosphate in the Combustion Products of a Fire Retardant Urethane Foam, Polymer Letters Edition, Vol. 13,

293-297 (1975).

[16] Bellet, E.M. and Casida, J.E., Bicyclic Phosphorus Esters; High

Toxicity Without Cholinesterase Inhibition, Science, Vol. 182,

1135-1136 (December 14, 1973).

[17] Kaiser, L.E.K., Mirex: An Unrecognized Contaminant of Fishes from

Lake Ontario, Science, Vol. 185, 532-535 (August 9, 1974).

[18] Norris, J.M. , Kociba, R.J., Schwetz , B.A. , Rose, J.Q., Humiston,

C.G., Jewett, G.L., Gehring, P.J. and Mailhes, J.B., Toxicity of

Oxtabromobiphenyl and Decabromodiphenyl Oxide, Environmental Health

Perspectives, Vol. 11, 153-161 (1975).

[19] National Academy of Sciences, International Symposium on Physiology and

Toxicological Aspects of Combustion Products, Proceedings, Salt Lake

City, Utah, March 18-20, 1974.

[20] King, T.Y. , Smoke and Carbon Monoxide Formation from Materials Tested

in the Smoke Density Chamber, Final Report, Nat. Bur. Stand. (U.S.),

NBSIR 75-901 (October 1975); PB-246860.

[21] A Report on Smoke Test Methods, ASTM Standardization News, Vol. 4,

No. 8, 18-25 (August 1976).

[22] Lee, T.G. and Huggett, C., Interlaboratory Evaluation of ASTM E84-70

Tunnel Test Applied to Floor Coverings, Journal of Testing and

Evaluation, Vol. 3, No. 1, 3-14 (January 1975).

[23] Breden, L. and Meisters, M. , The Effect of Sample Orientation in the

Smoke Density Chamber, Journal of Fire and Flammability, Vol. 7,

234-247 (April 1976)

[24] Robertson, A.F., Two Smoke Test Methods - A Comparison of Data,

Fire Technolgoy, Vol. 10, No. 4, 282-286 (November 1974).

[25] Madorsky, S.L., Thermal Degradation of Organic Polymers, Interscience

Publishers (1964)

[26] Woolley, W.D., Wadley, A. I. and Fields, D. , The Formation of NitrogenContaining Products from the Thermal Decomposition of Flexible

Polyurethane Foams, F.R. Note 881 (August 1971).

[27] Woolley, W.P. and Wadley, A. I., The Production of Free Tolylene

Diisocyanate from the Thermal and Thermal-Oxidative Decomposition of

Flexible Polyurethane Foams, Journal of Fire and Flammability/

Combustion Toxicology, Vol. 1, 259-267 (November 1974).

[28] Hileman, F.D. , Voorhees, K.J., Wojeik, L.H., Birky, M.M. , Ryan, D.W.

and Einhorn, I.N., Pyrolysis of a Flexible-Urethane Foam, Journal

of Polymer Science: Polymer Chemistry Edition, Vol. 13, 571-584 (1975).

[29] Wagner, J.P., Survey of Toxic Species Evolved in the Pyrolysis and

Combustion of Polymers, Fire Research Abstracts and Reviews, Vol. 14,

No. 1, 1-23 (1972).

[30] O'Mara, M.M. , High Temperature Pyrolysis of Poly (vinyl chloride):

Gas Chromatographic-Mass Spectrometric Analysis of Pyrolysis Products

from PVC Resin and Plastisols, Journal of Polymer Science: Part A-1,

Vol. 8, 1887-1889 (1970).

30
/

[31] Woolley, W.D., Decomposition Products of PVC for Studies of Fires,

British Polymer Journal, Vol. 3, 186-193 (July 1971).

[32] Tsuchiya, Y. and Sumi , K.J., Evaluation of the Toxicity of Combustion

Products, Journal of Fire and Flammability, Vol. 3, No. 1 (January 1972).

[33] Boettner, E.A. , Ball, G.L. and Weiss, B., Combustion Products from the

Incineration of Plastics, Final Report on EPA Grant No. 00386,

Environmental Protection Agency (U.S.) EPA-670/2-73-049 (February 1973);

PB-222001.

[34] Gross, D., Loftus, J.J., Lee, T.G. and Gray, V.E., Smoke and Gases

Produced by Burning Aircraft Interior Materials, Nat. Bur. Stand. (U.S.),

Building Science Series 18 (February 1969); PB-193736.

[35] Parts, L. , Olt, R.G., Miller, J.T. and Wooten, G.W. , Products Resulting

from Polymer Combustion, Polymer Conference Series, Flammability of

Materials, Proceedings, University of Utah, Salt Lake City, July 11, 1974.

[36] O'Mara, M.M. , The Combustion Products from Synthetic and Natural

Products-Part I: Wood, Journal of Fire and Flammability, Vol. 5,

No. 1, 34-53 (January 1974).

[37] Hillenbrand, L.J. and Wray, J.R., Full Scale Fire Program to Evaluate

New Furnishings and Textile Materials Developed by NASA, Battelle

Columbus Laboratories, Contract No. NASW-1948; NASA Technical Note

B70-10450; N74-35350; NASACR-2468 (July 1973).

[38] Yuill, C.J., The Life Hazard of Bedding and Upholstered Fires, Journal

of Fire and Flammability, Vol. 1, 312-323 (October 1970).

[39] Croce, P.A. and Emmons, H.W. , The Large Scale Bedroom Fire Test, July 11,

1973, Prepared for the Home Fire Project, NSF-RANN Final Technical

Report, National Science Foundation (July 1974)

[40] Palmer, K.M. , Taylor, W. and Paul, K.T., Fire Hazards of Plastics in

Furniture and Furnishings; Characteristics of the Burning, Joint Fire

Research Organization, Fire Research Station, Borehamwood, England,

Current Paper 3/75 (January 1975)

[41] Birky, M.M. and Manka , M. , The Use of Room and Corridor Tests in

Predicting Fire Parameters, Polymer Conference Series, Fire Prevention

and Control — A Major Societal Problem, Proceedings, University of Utah,

Salt Lake City, June 4-9, 1973.

[42] Threshold Limit Values of Airborne Contaminants Adopted by ACGIH for

1973, American Conference of Governmental Industrial Hygienists,

Cincinnati, Ohio (1973).

[43] Rashbash, D.J., Smoke and Toxic Products Produced at Fires, Transactions

of the Journal of the Plastics Institute Supplement, 55-61 (January

1967)

[44] Higgins, E.A. , Fiorica, V., Thomas, A. A. and Davis, H.V. , Acute Toxicity

of Brief Exposure to HF , HCl , NO 2 and HCN With and Without CO,

Fire Technology, Vol. 8, No. 2, 120-130 (May 1972).

[45] MacFarland, H.N. , The Pyrolysis Products of Plastics-Problems in Defining

Toxicity, American Industrial Hygiene Association Journal, Vol. 29,

7-9 ( January-February 1968)

[46] Amdur, M.O., The Effect of Aerosols on the Response to Irritant Gases

In: Inhaled Particles and Vapors, Edited by C.N. Davies, Pergamon

Press, 281-292 (1961).

31
[ 47 ] Zapp, Jr., J.A. , Limperos, G. and Brinker, K.C., Toxicity of Pyrolysis

Products of Polytetraf luoro-ethylene Heated Below 500° Centigrade,

American Industrial Hygiene Assocation, Annual Meeting (May 1955) .

[48] Scheel, L.D., McMillan, L. and Phipps, F.C., Biochemical Changes

Associated with Toxic Exposures to Polytetraf luorethylene Pyrolysis

Products, American Industrial Hygiene Association Journal, Vol. 29,

49-53 (January-February 1968)

[49] Scheel, L.D., Lane, W.C. and Coleman, W.E. , The Toxicity of Polytetraf luoroethylene Pyrolysis Products-Including Carbonyl Fluoride and a Reaction Product Silicon Tetraf luoride , American Industrial Hygiene

Association Journal, Vol. 29, 41-48 (January-February 1968).

[50] National Academy of Sciences, International Symposium on Toxicity and

Physiology of Combustion Products, Proceedings, University of Utah,

Salt Lake City, March 22-26, 1976.

[51] Kimmerle, G. , Aspects and Methodology for the Evaluation of Toxicological Parameter During Fire Exposure, Journal of Fire and Flammability/

Combustion Toxicology, Vol. 1, No. 1, 4-51 (February 1974).

[52] Hofmann, H.T. and Oettel, H. , Comparative Toxicity of Thermal Decomposition Products, Modern Plastics, Vol. 46, No. 10, 84, 90-100

(October 1969)

[53] Jouany, J.M. , Boudene, C. and Truhaut, R. , The Physiogram as a Method

for the Evaluation of Toxicity of Combustion Products in Controlled

Ventilation Experiments, International Symposium on Toxicity and

Physiology of Combustion Products, Proceedings, Salt Lake City, Utah,

March 22-26, 1969.

[54] Herpol, C. , Biological Evaluation of Toxicity of Products of Pyrolysis

and Combustion of Materials, Fire and Materials, Vol. 1, No. 1, 29-35

(1976) .

[55] Chien, W.P. and Seader, J.D. , Smoke Development at Different Energy

Flux Levels in NBS Smoke Density Chamber, Fire Technology, Vol. 10,

No. 3, 187-196 (August 1974).

[56] Cornish, H. , Toxicity of Thermal-Degradation Products of Plastics,

Symposium on Products of Combustion of (Plastics) Building Materials,

Proceedings, Armstrong Cork Company, Lancaster, Pa., March 26-27, 1973.

[57] Autian, J. , Toxicologic Aspects of Flammability and Combustion of

Polymeric Materials, Journal of Fire and Flammability, Vol. 1, 239-269

(July 1970)

[58] Stewart, R.D. , Peterson, J.E., Baretta, E.D. , Bachand, R.T. , Hosko,

M.J. and Herrmann, A.A. , Experimental Human Exposure to Carbon Monoxide,

Archives of Environmental Health, Vol. 21, 154-164 (August 1970).

[59] Eckardt, R.E., MacFarland, H.N. , Alarie, Y.C.E. and Busey, W.M. , The

Biologic Effect from Long-Term Exposure to Carbon Monoxide, Archives of

Environmental Health, Vol. 25, 381-387 (December 1972).

[60] Goodman, L.S. and Gilman, A., The Pharmacological Basis of Therapeutics,

5th Edition, 900-904, Macmillan Publishing Co., Inc. (June 1975).

[61] Stewart, R.D. , Peterson, J.E., Fisher, T.M. , Hosko, M. J. , Baretta, E.D.,

Todd, H.C. and Herrmann, A.A.

,

Experimental Human Exposure to High

Concentrations of Carbon Monoxide, Archives Environmental Health,

Vol. 26, 1-7 (January 1973).

32
[62] Edginton, J.A.G., and Lynch, R.D. , The Acute Inhalation Toxicity of

Carbon Monoxide from Burning Wood, Joint Fire Research Organization,

Fire Research Station, Borehamwood, England, F.R. Note 1040 (August 1970).

[63] Zikria, B.A. , Ferrer, J.M. and Floch, H. , The Chemical Factors

Contributing to Pulmonary Damage in "Smoke Poisoning," Vol. 71, No. 5,

704-709 (May 1972)

[64] Packham, S.C., Behavior and Physiology: Tools for the Assessment of

Relative Toxicity, National Cellular Plastics Conference on Safety

and Product Liability, 19th, Society of the Plastics Industries,

Washington, D.C., November 18-20, 1974.

[65] Goodman, L.S. and Gilman, A., The Pharmacological Basis of Therapeutics,

5th Edition, 904-905, Macmillan Publishing Company, Inc. (1970).

[66] Wetherell, H.R. , The Occurrence of Cyanide in Blood of Fire Victims,

Journal of Forensic Science, Vol. 11, No. 2, 167-173 (April 1966).

[67] Gettler , L.A. , Linn, R.A. and Zak, B. , The Toxicology of Cyanide,

American Journal of Medical Sciences, Vol. 195, 182-198 (1938).

[68] Sunshine, I. and Finkle, B. , The Necessity for Tissue Studies in Fatal

Cyanide Poisonings, Int. Archiv fur Gewerbepathologic Gewerbehvg.,

Vol. 20, 558-561 (1964)

[69] Moss, R.H., Jackson, C.F. and Seiberlich, J. , Toxicity of Carbon

Monoxide and Hydrogen Cyanide Gas Mixtures, Industrial Hygiene and

Occupational Medicine, Vol. 4, 53-64 (1951).

[70] Birky, M.M. , Philosophy of Testing for Assessment of Toxicological

Aspects of Fire Exposure, Journal of Fire and Flairanability/

Combustion Toxicology, Vol. 3, No. 1, 5-23 (February 1976).

[71] Lynch, R.D. , On the Non-existence of Synergism Between Inhaled Hydrogen

Cyanide and Carbon Monoxide, Joint Fire Research Organization, Fire

Research Station, Borehamwood, England, F.R. Note 1035 (May 1975).

[72] Pryor, A.J., Johnson, D.E. and Jackson, N.N. , Hazards of Smoke and

Toxic Gases Produced in Urban Fire, DAHC20-70-C-0212 , AD 697839

(September 1975) .

[73] Lopez, E.C., Smoke Emission from Burning Cabin Materials and the Effect

on Visibility in Wide-Bodied Jet Transport, Journal of Fire and

Flammability, Vol. 6, 405-450 (October 1975).

[74] Alarie, Y. , Sensory Irritation by Airborne Chemical Agents, Critical

Reviews in Toxicology, Vol. 2, No. 3, 299-363 (November 1973).

[75] Alarie, Y. , Wilson, E., Civic, T. , Magill, J. , Funt, J. , Barrow, C.,

and Frohliger, J. , Sensory Irritation Evoked by Polyurethane Decomposition Products, Journal of Fire and Flammability, Vol. 2, 139-150

(May 1975) .

[76] Barrow, C.S., Alarie, Y. and Stock, M.F. , Sensory Irritation Evoked by

the Thermal Decomposition Products of Plasticized Polyvinyl Chloride,

International Symposium on Toxicity and Physiology of Combustion

Products, University of Utah, Salt Lake City, Utah, March 22-26, 1976.

[77] Dyer, R.F. and Esch, V.N., Polyvinyl Chloride Toxicity in Fires:

Hydrogen Chloride Toxicity in Fire Fighters, Journal of the American

Medical Association, Vol. 235, No. 4, 393-397 (January 26, 1976).

33
[ 78 ] Cavanagh, J.B., Peripheral Neuropathy Caused by Chemical Agents,

Critical Reviews in Toxicology, Vol. 2, No. 3, 365-417 (November

1973)

[79] Johnson, M.K., The Delayed Neuropathy Caused by Some Organophosphorus

Esters: Mechanism and Challenge, Critical Reviews in Toxicology,

Vol. 3, Issue 3, 289-316 (June 1975).

[80] Gutenmann, W.H. and Lisle, D.J., Flame Retardant Release from Fabrics

During Laundering and Their Toxicity to Fish, Bulletin of Environmental

Contamination and Toxicology, Vol. 14, No. 1, 61-64 (1975).

[81] St. John Jr., L.S., Elderfrawi, M.E. and Lisk, D.J., Studies of Possible

Absorption of a Flame Retardant from Treated Fabrics Worn by Rats and

Humans, Bulletin of Environmental Contamination and Toxicology, Vol. 15

No. 2, 192-197 (1976)

[82] Prival, M.J., McCoy, E.C., Gutter, B. and Rosenkrunz, H.S., Tris

(2 , 3-dibromopropyl) Phosphate: Mutagenicity of a Widely Used Flame

Retardant, Science, Vol. 195, No. 4273, 76-78 (1977).

[83] McCann, J. , Choi, E., Yamasaki, E. and Ames, B.N. , Detection of

Carcinogens as Mutagens in the Sammonells/Microsome Test: Assay of

300 Chemicals, Proceedings of the National Academy of Sciences,

Vol. 72, No. 12, 5135-5139 (1975).

[84] Bowery, N.G., Collins, J.F. and Hill, R.G. , Bicyclic Phosphorus

Esters That are Potent Convulsants and GABA Antagonists, Nature,

Vol. 261, 601-603 (June 17, 1976).

[85] Nosse, J.H., A Toxicity Standard for Cellular Plastics Used in

Construction, International Symposium on Toxicity and Physiology of

Combustion Products, University of Utah, Salt Lake City, March 22-26

1976.

[86] Brisson, Y. , Regulations with the Aim of Limiting the Risks of

Poisoning by the Combustion Products of Certain Synthetic Materials,

International Symposium on Toxicity and Physiology of Combustion

Products, Univerisity of Utah, Salt Lake City, March 22-26, 1976.

[87] Code for Safety to Life from Fire in Buildings and Structures, NFPA

101-1973, Boston, Massachusetts.

[88] BOCA Basic Building Code, 1975; 6th Edition, Building Officials and

Code Administrators International, Inc., Chicago (1975).

[89] Custer, R.L.R. and Bright, R.G., Fire Detection: The State-of-the-Art

,

Nat. Bur. Stand. (U.S.) Technical Note 839 (June 1974); U.S. Government

Printing Office, Wash., D.C. , SD Catalog No. C13. 46:839; NASA CR-134642

[90] Bukowski, R. , Waterman, T.E. and Christian, W. J. , Detector Sensitivity

and Siting Requirements for Dwellings, Final Technical Report, NBS

Contract No. 4-36092, IIT Research Institute, NBS-GCR-75-51 (1975);

PB-247483.

[91] McKinnon, G.P. and Tower, K. , Eds., Fire Protection Handbook, 14th

Edition, National Fire Protection Association, Boston, Massachusetts

(1976).

34
I 92] iMarryatt, H. , Automatic Sprinkler Performance in Australia and New

Zealand 1886-1968, Australian Fire Protection Association, Melbourne,

Australia (1971).

[93] Custer, R.L.P., Detector Activated Sprinkler Systems — A Preliminary

Evaluation, Nat. Bur. Stand. (U.S.) Technical Note 836 (July 1974);

U.S. Government Printing Office, Wash., D.C., SD Catalog No. C13. 46:836.

[94] Fung, F.C.W. , Smoke Control by Systematic Pressurization, Fire Tech.

Vol. 11, No. 4, 261-269 (November 1975).

[95] Kishitani, K. , and Nakamura, K. , Toxicities of Combustion Products,

Journal of Fire and Flammability/Combustion Toxicology, Vol. 1, 104-123

(May 1974 ) .

[96] Bowes, P.C., Edgington, J.A.G., and Lynch, R.D., The Inhalation Toxicity

of Polyvinylchloride Pyrolysis Products, Joint Fire Research Organization,

Fire Research Station, Borehamwood, England, F.R. Note 1048 (February

1976)

[97] Birky, M.M. , Coats, A.W. , Alderson, S.E., Brown, J.E., Paabo, M. and

Pitt, B. , New Measurements and Observations of the Toxicological

Hazard of Fire in a Metrorail Interior Mock-Up, Fire Line, 9-16

(October 26 )

\

35
Table

1,

Summary

of

Combustion

Toxicology

Systems

Measurements Analytical & Bioloelcal oau ooo^

CN o O J= - CO z o. o» CO

blood

chemistry

(pH

COHb. 0.

Hb, *

**

ECG,

EEG,

etc.)

CLeH .oZ - o CN U o CO,

HCN,

T,

COHb

H Ht O -K z • o X Cd

«-

au o

(j . • , Z CN Ht “ u o o CN X u O o a u

CJ

*• CN 40 o

CN OXa ou

X ozz

CJX

paX rH O X CJ

CJoo

>v

60oHOcda

to

(0o

60 0 rH0 - X CN X AJ 0 td U 0 CL

CJ 0 oc 0 O! o fH

AJ 4= (0 OJ c

•H 4J ^ <0 nH

0)

O T3 0) o 4= (d

X o o 2 X c T3 JZ -H a flj •H T3 o o o> (d U (0 (0 tJ O M •H *0 H TD cM

JZ

y

V) co

•H i~t 3 (U

U

X T3

iH o

0) •H <0 IV 60 AJ 4-1 3 U 3 60

(V n) <0 3

rH sO 1 u

to to 0 o oi IT 0 p

H

•o ii 60

q CN

a uo 00

"w) « 3

JZ

b

AJ -O -H

C/5 S-2 o ' o y-i w ^ ^ QJ 3 U (0 OO 3O 0) o> 3

a>w oo OJ o M M Z flJ

O CN o C m c orH

O

tM tM - o

rH

4HOc 0 X C tM

a

tj §

01

O 43

O 43 o o •H 3 U P. -H Li CL -H 43 < cfl — C _

<u ^

-C.

<y ^

oi'

M ^ *D

X T3

m 3 AJ 3 AJ o Td -a '^0

•H 3 O

'U 'U CN (d 0 (d CN

a §1

CO o •H

O (0

•rl (0 en to ^ CN to 4-1 CO Cd

<u CO 1 2 1 2

45 td AJ AJ c^ o to o <d M Cd

X

I—

cO i-N to3

43 s ^ (0 CO •o .-1 co’ TJ 9 a o o o u O o (0 H

0) <H cn

X 5 a ^ +

tim(

X

(0 to T3 •H

01

C

O z o 9 a. cn o CO o

rH o 0 e 01 *o * rH m

•H

T» *s

IS T3 O. V O fH c rH Li o 1—( rH O s 4= 4= 2 X X

•H

n T3 a< 60 cri c <»4

C < C CO o o U

x£> nH

O

O rH 0

CJ 3

iH 3

•H in

u

U '-'

u «> o a * 0

ffl • ® i^CN s o a

O CJ c AJ CJ c 0 c § o T i

CJ 3 C 3 3

E-t \0 ' ^ B

O ' ' o ^ o O «d 0 Cd m 0 Cd NT

a,

X

eO

u (V

V

•S

C

M C43

C 3 0> 0) d) 3 O M-( c ^ c •H 3 (d o (d 01 Cd

U

lU •H <0

b c u 3 W 3^ C 3 3 CO 40 > tM ^ t2 " i2 > 3 a <N B

JZ 60 tM c O 0> o

4J c S''

0> A4 >.

C

X AJ <0 q 0 X0

OJ sas

O 4=

O c m

H 0»

O T3 m • *H ^Oi rH

O CdO 3 in . o —

(0 -H c

L- 43L 0m 0 Li

X

•H

CO z w > n > >H CJ

•H S > ^ X

O _E o X _2 ^

36

ECGElectrocardiogramEEGElectroencephalogram

RRRespiratory

rate
Table

1,

continued

37

ECG

-

Electrocardiogram

EEG

“

Electroencephalogram

RR

-

Respiratory

rate
Table 2. Effects in Rats Exposed 30 Minutes to Combinations

of Hydrogen Cyanide and Carbon Monoxide [51]

Carbon Monoxide

(ppm)

Hydrogen Cyanide

(ppm)

Mortality

(%)

3,300 107 100

3,300 57 65

3,300 45 50

3,300 27 20

3,300 14 0

4,400 53 100

4,400 44 75

4,400 38 45

4,400 30 40

4,400 21 30

4,400 12 20

Table 3. Speculations on the Level of Response Which Would

Occur in Humans from Results Obtained in Mice [75]

Results Obtained in Mice Predicted Reactions in Humans

Concentration =

Concentration = 1/10 RD^_

D U

Concentration = 1/100 RD_.

DU

Intolerable and rapidly

incapacitating

Slightly irritating with

burning sensation of the

eye-nose- throat

Tolerable with very slight

or no irritating sensation

38
9. BIBLIOGRAPHY

Alarie, Y. , Sensory Irritation by Airborne Chemical Agents, Critical Reviews

in Toxicology, Volume 2, No. 3, 299-363 (November 1973).

Alarie, Y. , Wilson, E., Civic, T., Magill, J., Funt , J. , Barrow, C. and

Frohliger, J. , Sensory Irritation Evoked by Polyurethane Decomposition

Products, Journal of Fire and Flammability, Voliame 2 , 139-150 (May 1975)

Amdur , M.O. , The Effect of Aerosols on the Response to Irritant Gases, In:

Inhaled Particles and Vapors, Edited by C.N. Davies, Pergamon Press,

281-292 (1961)

Autian, J. , Toxicologic Aspects of Flammability and Combustion of Polymeric

Materials, Journal of Fire and Flammability, Volume 1, 239-269

(July 1970) . Barrow, C.S., Alarie, Y. and Stock, M.F., Sensory Irritation Evoked by the

Thermal Decomposition Products of Plasticized Polyvinyl Chloride,

International Symposium on Toxicity and Physiology of Combustion

Products, University of Utah, Salt Lake City, March 22-26, 1976.

Bellet, E.M. and Casida, J.E., Bicyclic Phosphorus Esters: High Toxicity

Without Cholinesterase Inhibition, Science, Volume 182, 1135-1136

(December 14, 1973).

Birky, M.M. , Philosophy of Testing for Assessment of Toxicological Aspects

of Fire Exposure, Journal of Fire and Flammability/Combustion Toxicology

Volume 3, No. 1, 5-23 (February 1976).

Birky, M.M. and Manka, M. , The Use of Room and Corridor Tests in Predicting

Fire Parameters, Polymer Conference Series, Fire Prevention and Control

A Major Societal Problem, Proceedings, University of Utah, Salt Lake

City, June 4-9, 1973.

BOCA Basic Building Code, 1975; 6th Edition, Building Officials and Code

Administrators International, Inc., Chicago (1975).

Boettner , E.A. , Ball, G.L. and Weiss, B. , Combustion Products from the

Incineration of Plastics, Final Report on EPA Grant No. 00386,

Environmental Protection Agency, Washington, D.C., EPA-670/2-73-049

PB-222001 (February 1973) . Bowery, N.G. , Collins, J.F. and Hill, R.G., Bicyclic Phosphorus Esters That

Are Potent Convulsants and GABA Antagonists, Nature, Volume 261,

601-603 (June 17, 1976) .

Bowes, P.C. , Smoke and Toxicity Hazards of Plastics in Fire, Annals of

Occupational Hygiene, Volume 17, 143-157 (1974).

Bowes, P.C., Edgington, J.A.G. and Lynch, R.D. , The Inhalation Toxicity of

Polyvinylchloride Pyrolysis Products, Joint Fire Research Organization,

Fire Research Station, Borehamwood, England, F.R. Note 1048

(February 1976)

Breden, L. and Meisters, M. , The Effect of Sample Orientation in the Smoke

Density Chamber, Journal of Fire and Flammabiltiy , Volume 7, 234-247

(April 1976)

39
Brisson, Y. , Regulations with the Aim of Limiting the Risks of Poisoning by

the Combustion Products of Certain Synthetic Materials, International

Symposium on Toxicity and Physiology of Combustion Products,

University of Utah, Salt Lake City, March 22-26, 1976.

Bukowski, R. , Waterman, T.E. and Christian, W. J. , Detector Sensitivity and

Siting Requirements for Dwellings, Final Technical Report, NBS Contract

No. 4-36092, IIT Research Institute, NBS-GCR-75-51 , PB-247483 (1975).

Cavanagh, J.B., Peripheral Neuropathy Caused by Chemical Agents, Critical

Reviews in Toxicology, Volume 2, No. 3, 365-417 (November 1973).

Chien, W.P. and Seader , J.D., Smoke Development at Different Energy Flux

Levels in NBS Smoke Density Chamber, Fire Technology, Voliame 10, No. 3,

187-196 (August 1974) . Clarke, III, F.B. and Ottoson, J. , Fire Death Scenarios and Fire Safety

Planning, Fire Journal, Volume 70, No. 3 (May 1976).

Clayton, J.W. , Hood, D.B. and Raynesford, G.E., The Toxicity of the Pyrolysis

Products of Teflon TFE-Fluoro-Carbon Resins, American Industrial Hygiene

Association, Annual Meeting, Proceedings, May 1959.

Code for Safety to Life from Fire in Buildings and Structures, NFPA 101-1973,

National Fire Protection Association, Boston, Massachusetts.

Cornish, H. , Toxicity of Thermal-Degradation Products of Plastics, Symposium

on Products of Combustion of (Plastics) Building Materials, Proceedings,

Armstrong Cork Company, Lancaster, Pa., March 26-27, 1973.

Croce, P.A. and Emmons, H.W. , The Large Scale Bedroom Fire Test, July 11, 1973,

Prepared for The Home Fire Project, NSF-RANN Final Technical Report,

National Science Foundation (July 1974)

Custer, R.L.P., Detector Activated Sprinkler Systems - A Preliminary Evaluation,

National Bureau of Standards Technical Note 836, U.S. Government Printing

Office, Washington, D.C., SD Catalog No. C13. 46:836 (July 1974).

Custer, R.L.P. and Bright, R.G., Fire Detection: The State-of-the-Art

,

National Bureau of Standards Technical Note 839, U.S. Government

Printing Office, Washington, D.C. , SD Catalog No. C13. 46:839; NASA

CR-134642 (June 1974).

Dyer, R.F. and Esch, V.N. , Polyvinyl Chloride Toxicity in Fires: Hydrogen

Chloride Toxicity in Fire Fighters, Journal of the Americal Medical

Association, Volume 235, No. 4, 393-397 (January 26, 1976).

Eckardt, R.E., MacFarland, H.N. , Alarie, Y.C.E. and Busey, W.M. , The

Biologic Effect from Long-Term Exposure to Carbon Monoxide, Archives

of Environmental Health, Volume 25, 381-387 (December 1972).

Edginton, J.A.G. and Lynch, R.D., The Acute Inhalation Toxicity of Carbon

Monoxide from Burning Wood, Joint Fire Research Organization, Fire

Research Station, Borehamwood , England, F.R. Note 1040 (August 1970).

Fires and Fire Losses Classified, 1974, Fire Journal, Volume 69, No. 5,

43-45 (September 1975) . Fung, F.C.W. , Smoke Control by Systematic Pressurization, Fire Technology,

Volume 11, No. 4, 261-269 (November 1975).

40
Gettler, L.A. , Linn, R.A. and Zak, B., The Toxicology of Cyanide, American

Journal of Medical Sciences, Volume 195, 182-198 (1938).

Goodman, L.S. and Gilman, A., The Pharmacological Basis of Therapeutics,

5th Edition, Macmillan Publishing Company, Inc. (June 1975).

Gross, D. , Loftus, J.J., Lee, T.G. and Gray, V.E. , Smoke and Gases Produced

by Burning Aircraft Interior Materials, National Bureau of Standards,

Building Science Series 18, PB-193736 (February 1969).

Gutenmann, W.H. and Lisk, D.J., Flame Retardant Release from Fabrics During

Laundering and Their Toxicity to Fish, Bulletin of Environmental

Contamination and Toxicology, Volume 14, No. 1, 61-64 (1975).

i

j Halpin, B.M. , Radford, E.P., Fisher, R. and Kaplin, Y. , A Fire Fatality

I Study, Fire Journal, Volume 69, No. 3, 11-13, 99 (May 1975).

i Harlow, D.W. , International Fire Losses, 1974, Fire Journal, Volume 69,

' No. 6, 43 (November 1975).

i Herpol , C., Biological Evaluation of Toxicity of Products of Pyrolysis and

Combustion of Materials, Fire and Materials, Volume 1, No. 1, 29-35

(1976).

Herpol, C. and Minne , R. , Biological Evaluation of Toxicity of Gases Produced

Under Fire Conditions by Synthetic Materials; Part 2: Behaviour of

synthetic materials in definite combustion conditions as compared to

the behaviour of traditional materials in same conditions. Combustion

I Science and Technology, Volume 12, 229-244 (1976).

I Herpol, C., Minne, R. and Van Outryve , E., Biological Evaluation of the

Toxicity of Gases Produced Under Fire Conditions by Synthetic Materials;

I Part 1: Methods and preliminary experiments concerning the reaction of

' animals to simple mixtures of air and carbondioxide or carbonmonoxide

,

' Combustion Science and Technology, Volume 12, 217-228 (1976).

I, Higgins, E.A. , Fiorica, V., Thomas, A. A. and Davis, H.V. , Acute Toxicity of

ij Brief Exposure to HF, HCl , NO 2 and HCN With and Without CO, Fire

Technology, Volume 8, No. 2, 120-130 (May 1972).

’Hileman, F.D., Voorhees, K.J., Wojcik, L.H., Birky, M.M. , Ryan, D.W. and

( Einhorn, I.N., Pyrolysis of a Flexible-Urethane Foam, Journal of

i Polymer Science: Polymer Chemistry Edition, Volume 13, 571-584 (1975).

li Hillenbrand, L.J. and Wray, J.R. , Full Scale Fire Program to Evaluate New

Furnishings and Textile Materials Developed by NASA, Battelle Columbus

i Laboratories, Contract No. NASW-1948; NASA Technical Note B70-10450;

N74-35350; NASACR-2468 (July 1973).

[Hofmann, H.T. and Oettel, H. , Comparative Toxicity of Thermal Decomposition

I

I Products, Modern Plastics, Volume 46, No. 10, 84 , 90-100 (October 1969).

[Johnson, M.K., The Delayed Neuropathy Caused by Some Organophosphorus Esters:

j Mechanism and Challenge. Critical Reviews in Toxicology, Volume 3,

I Issue 3, 289-316 (June 1975).

I

iJouany, J.M. , Boudene , C. and Truhaut , R. , The Physiogram as a Method for the

Evaluation of Toxicity of Combustion Products in Controlled Ventilation

' Experiments, International Symposium on Toxicity and Physiology of

Combustion Products, Proceedings, University of Utah, Salt Lake City,

i March 22-26, 1969.

41
Kaiser, L.E.K., Mirex: An Unrecognized Contaminant of Fishes from Lake

Ontario, Science, Volume 185, 532-535 (August 9, 1974).

Kimmerle, G. , Aspects and Methodology for the Evaluation of Toxicological

Parameter During Fire Exposure, Journal of Fire and Flammability/

Combustion Toxicology, Volume 1, No. 1, 4-51 (February 1974).

King T.Y. , Smoke and Carbon Monoxide Formation from Materials Tested in the

Smoke Density Chamber, Final Report, National Bureau of Standards,

Washington, D.C., NBSIR 75-901, PB-246860 (October 1975).

Kishitani, K. , Research In Japan on Toxicities of Combustion Gases Produced

During Fire, Second Joint Meeting, U.S. Japan Panel on Fire Research

and Safety, 1-32, UJNR, Tokyo, October 19-22, 1976.

Kishitani, K. and Nakamura, K. , Study on Toxicities of Combustion Products

of Buildings Materials at Initial Stage of Fire, Second Joint Meeting,

U.S. Japan Panel on Fire Research and Safety, 1-31, UJNR, Tokyo,

October 19-22, 1976.

Kishitani, K. and Nakamura, K. , Toxicities of Combustion Products, Journal of

Fire and Flammability/Combustion Toxicology, Volume 1, 104-123 (May 1974)

Kishitani, K. and Saito, F., Study and Proposals Concerning Method of Test

for Toxicities of Combustion Gases of Building Materials, Second Joint

Meeting, U.S. -Japan Panel on Fire Research and Safety, 1-34, UJNR, Tokyo,

October 19-22, 1976.

Lee, T.G. and Huggett , C., Interlaboratory Evaluation of ASTM E84-70 Tunnel

Test Applied to Floor Coverings, Journal of Testing and Evaluation,

Volume 3, No. 1, 3-14 (January 1975).

Lopez, E.C., Smoke Emission from Burning Cabin Materials and the Effect on Visibility in Wide-Bidied Jet Transport, Journal of Fire and Flammability

Volume 6, 405-450 (October 1975).

Lynch, R.D., On the Non-ex3.stence of Symergism Between Inhaled Hydrogen

Cyanide and Carbon Monoxide, Joint Fire Research Organization, Fire

Research Station, Borehamwood , England, F.R. Note 1035 (May 1975).

Lyons, J.W. , The Chemistry of and Uses of Fire Retardants, Wiley-Interscience

,

New York (1970)

Madorsky, S.L., Thermal Degradation of Organic Polymers, Interscience

Publishers (1964)

Marryatt, H. , Automatic Sprinkler Performance in Australia and New Zealand

1886-1968, Australian Fire Protection Association, Melbourne,

Australia (1971)

Moss, R.H., Jackson, C.F. and Seiberlich, J. , Toxicity of Carbon Monoxide

and Hydrogen Cyanide Gas Mixtures, Industrial Hygiene and Occupational

Medicine, Volume 4, 53-64 (1951).

MacFarland, H.N. , The Pyrolysis Products of Plastics-Problems in Defining

Toxicity, American Industrial Hygiene Association Journal, Volume 29,

7-9 (January/February 1968)

McCann, J., Choi, E., Yamasaki, E. and Ames, B.N., Detection of Carcinogens

as Mutagens in the Sammonells/Microsome Test: Assay of 300 Chemicals,

Proceedings of the National Academy of Sciences, Volume 72, No. 12,

5135-5139 (1975).

42
McKinnon, G.P. and Tower, K. , Eds., Fire Protection Handbook, 14th Edition,

National Fire Protection Association, Boston, Massachusetts (1976).

National Academy of Sciences, International Symposium on Physiology and Toxicological Aspects of Combustion Products, Proceedings, University of

Utah, Salt Lake City, March 18-20, 1974.

National Academy of Sciences, International Symposium on Toxicity and Physiology of Combustion Products, Proceedings, University of Utah, Salt Lake

City, March 22-26, 1976.

National Commission on Fire Prevention and Control, America Burning, U.S.

Government Printing Office, Washington, D.C. (1973).

Norris, J.M. , Kociba, R.J., Schwetz, B.A. , Rose, J.Q., Humiston, C.G.,

Jewett, G.L., Gehring, P.J. and Mailhes, J.B., Toxicity of

Oxtabromobiphenyl and Decabromodiphenyl Oxide, Environmental Health

Perspectives, Volume 11, 153-161 (1975).

Nosse, J.H., A Toxicity Standard for Cellular Plastics Used in Construction,

International Symposium on Toxicity and Physiology of Combustion

Products, University of Utah, Salt Lake City, March 22-26, 1976.

O'Mara, M.M. , High Temperature Pyrolysis of Poly (vinyl chloride): Gas

Chromatographic-Mass Spectrometric Analysis of Pyrolysis Products from

PVC Resin and Plastisols, Journal of Polymer Science: Part A-1, Volume 8,

1887-1889 (1970)

O'Mara, M.M. , The Combustion Products from Synthetic and Natural ProductsPart I: Wood, Journal of Fire and Flammabiltiy , Volume 5, No. 1, 34-53

(January 1974)

Packham, S.C., Behavior and Physiology: Tools for the Assessment of Relative

Toxicity, National Cellular Plastics Conference on Safety and Product

Liability, 19th, Society of the Plastics Industries, Washington, D.C.,

November 18-20, 1974.

Palmer, K.M. , Taylor, W. and Paul, K.T., Fire Hazards of Plastics in

Furniture and Furnishings; Characteristics of the Burning, Joint Fire

Research Organization, Fire Research Station, Borehamwood , England,

Current Paper 3/75 (January 1975).

Parts, L. , Olt, R.G. , Miller, J.T. and Wooten, G.W. , Products Resulting from

Polymer Combustion, Polymer Conference Series, Flammability of Materials,

Proceedings, University of Utah, Salt Lake City, July 11, 1974.

Petajan, J.H., Voorhees, K. J. , Packham, S.C., Baldwin, R.C., Einhorn, I.N.,

Grunnett, M.L., Dinger, B.G. and Birky, M.M. , Extreme Toxicity from

Combustion Products of a Fire Retarded Polyurethane Foam, Science,

Volume 187, No. 4178, 742-744 (February 28, 1975).

Thomas, D.M., The Smoke Inhalation Problem, Symposium on Occupational Health

and Hazards of the Fire Service, Proceedings, Notre Dame, University,

South Bend, Indiana, January 11-13, 1971.

Threshold Limit Values of Airborne Contaminants Adopted by ACGIH for 1973.

American Conference of Governmental Industrial Hygienists, Cincinnati,

Ohio (1973).

43
Tsuchiya, Y. and Sumi , K.J., Evaluation of the Toxicity of Combustion Products,

Journal of Fire and Flammability, Volume 3, IIo. 1, 46-"0 (January 1972).

Voorhees, K.J., Einhorn, I.N. and Wojeik, L.N., The Identification of a Highly

Toxic Bicyclophosphate in the Combustion Products of a Fire Retardant

Urethane Foam, Polymer Letters Edition, Volume 13, 293-297 (1975).

Wagner, J.P., Survey of Toxic Species Evolved in the Pyrolysis and Combustion

of Polymers, Fire Research Abstracts and Reviews, Volume 14, No. 1,

1-23 (1972)

Waritz , R.S. and Kwon , B.K., The Inhalation Toxicity of Pyrolysis Products

of Polytetraf luoro-ethylene Heated Below 500° Centigrade, American

Industrial Hygiene Association Journal, Volume 29, 19-26 (January/

February 1968)

Wetherell, H.R., The Occurrence of Cyanide in Blood of Fire Victims,

Journal of Forensic Science, Volume 11, No. 2, 167-173 (April 1966).

Woolley, W.D., Decomposition Products of PVC for Studies of Fires, British

Polymer Journal, Volume 3, 186-193 (July 1971).

Woolley, W.D. and Fardell, P.J., The Prediction of Combustion Products,

International Symposium on Toxicity and Physiology of Combustion

Products, Proceedings, University of Utah, Salt Lake City,

March 22-26, 1976.

Woolley, W.D. and Wadley, A. I., The Production of Free Tolylene Diisocyanate

from the Thermal and Thermal-Oxidative Decomposition of Flexible

Polyurethane Foams, Journal of Fire and Flammability/Combustion

Toxicology, Volume 1, 259-267 (November 1974).

Woolley, W.D., A. I. and Fields, D., The Formation of Nitrogen-Containing

Products from the Thermal Decomposition of Flexible Polyurethane Foams,

Joint Fire Research Organization, Fire Research Station, Borehamwood

,

England, F.R. Note 881 (August 1971).

Yuill, C.J., The Life Hazard of Bedding and Upholstered Fires, Journal of

Fire and Flammability, Volume 1, 312-323 (October 1970).

Zapp, Jr., J.A., Limperos, G. and Brinker, K.C., Toxicity of Pyrolysis

Products of Polytetraf luoro-ethylene Heated Below 500° Centigrade,

American Industrial Hygiene Association, Annual Meeting (May 1955).

Zikria, B.A. , Ferrer, J.M. and Floch, H. , The Chemical Factors Contributing

to Pulmonary Damage in "Smoke Poisoning," Surgery, Volume 71, No. 5,

704-709 (May 1972)

Zikria, B.A. , Weston, G.C., Chodoff, M. and Ferrer, J.M. , Smoke and

Carbon Monoxide Poisoning in Fire Victims, Journal of Trauma, Volume 12,

No. 6, 641-645 (1972)

44
NBS-114A (REV. 7-7a)

U S. OE^T. OF COMM. 1. publication or report no. 2. Gov’t Accession

BIBLIOGRAPHIC DATA

sheet NBSIR 77-1234 No.

Hazard Characteristics of Combustion Products

in Fires; The State-of-the-Art Review

3. Recipient’s Accession No.

5. Publication Date May 1977

6. Performing Organization Code

7. AUTHOR(S)

Dr. Merritt Birky

8. Performing Organ. Report No. NASA-CR-135088

9. PERFORMING ORGANIZATION NAME AND ADDRESS

NATIONAL BUREAU OF STANDARDS

DEPARTMENT OF COMMERCE

WASHINGTON, D.C. 20234

10. Project/Task/Work Unit No. 491 1677

11. Contract/Grant No. Order C-97823-B

12. Sponsoring Organization Name and Complete Address (Street, City, State, ZIP)

National Aeronautics and Space Administration

Lewis Research Center

Cleveland, Ohio 44135

13. Type of Report & Period Covered

Final Report

14. Sponsoring Agency Code

NASA

15. SUPPLEMENTARY NOTES

j 16. ABSTRACT (A 200-word or less factual summary of most si^ificant information. If document includes a significant

bibliography or literature survey, mention it here.)

! The purpose of this effort is to review what is known about the "smoke inhalation"

|. hazard as related to human fatalities, the limitations of the fire fatality data and the

methods that have been and are being used to assess the inhalation toxicity hazard.

|i Fire statistics indicate that 70 to 80% of the fire fatalities are attributed to smoke

I Inhalation. In depth autopsy studies of some of these fatalities show that carbon monoxide is the predominant toxicant produced from fires. The role of new synthetic polymers

I and other additives is unknown as is the role of hydrogen cyanide in fire fatalities.

. Chemical analysis of combustion products has been used extensively to assess the toxlj cological hazard in fire research. The limitations of such measurements are addressed anc

' a combination of toxicology (animal exposures) and analytical chemistry is recommended.

Recent combined biological and selected analytical measurements are critically reviewed.

The mechanism of toxic action of a few well known combustion products is discussed.

Due to the extensive use of organophosphates as fire retardants in polymeric materials,

the toxicity of this class of compounds is reviewed in some detail.

The role of building codes and standards and early detection and suppression of fire

^ are discussed as a means of reducing human exposure to toxic combustion products. For

example, the 1976 French regulation that limits the use of flammable materials that contain chlorine and nitrogen in their molecular structure is presented.

17. KEY WORDS (six to twelve entries; alphabetical order; capitalize only the first tetter of the first key word unless a proper name; separated by semicolons) giological assessment; chemlcal analysis; combustion products;

fire fatalities; smoke inhalation; toxicity.

18. AVAILABILITY FT Unlimited

I

' For Official Distribution. Do Not Release to NTIS

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I Order From Sup. of Doc., U.S. Government Printing Office Washington, D.C. 20402, SD Cat. No. C13

IX I Order From National Technical Information Service (NTIS)

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