NIST Technical Note 1644 

Compilation of Data on the 

Sublethal Effects of Fire Effluent 

Erica D. Kuligowski 
NIST Technical Note 1644 

Compilation of Data on the 

Sublethal Effects of Fire Effluent 

Erica D. Kuligowski 

Fire Research Division 

Building and Fire Research Laboratory 

August 2009 

U.S. Department of Commerce 

Gary Locke, Secretary 

National Institute of Standards and Technology 

Patrick D. Gallagher, Acting Director 
Certain commercial entities, equipment, or materials may be identified in this 

 document in order to describe an experimental procedure or concept adequately. Such 

identification is not intended to imply recommendation or endorsement by the 

National Institute of Standards and Technology, nor is it intended to imply that the 

entities, materials, or equipment are necessarily the best available for the purpose. 

National Institute of Standards and Technology Technical Note 1644 

Natl. Inst. Stand. Technol. Tech. Note 1644, 47 pages (August 2009) 

CODEN: NSPUE2 

Abstract 

The Nuclear Regulatory Commission (NRC) is developing guidance for performing 

quantitative human reliability analysis for post-fire mitigative human actions. In some of 

the scenarios, operators may be exposed to fire effluent as they perform critical tasks. 

In this report, the National Institute of Standards and Technology (NIST) provides a 

review of the state-of-the-art on how fire effluent might affect people. The available 

scientific literature on the effects of narcotic and irritant gases, smoke obscuration, and 

heat on humans and animals were reviewed. The fire effluent data presented in this report 

are categorized by levels of effect on humans; specifically 1) minor physiological effects 

that are unlikely affect job performance or duties, 2) moderate to major physiological 

effects that may negatively influence job performance or duties, and 3) major 

physiological effects that may render an individual unable to perform his/her job duties. 

Where possible, NIST has identified groupings and/or contradictions for the compiled 

exposure data. With this information, one can estimate how exposure to various fire 

effluent might affect the operators’ ability to perform critical procedures during a fire 

event. 

Keywords 

fire, fire research, smoke, heat, fire toxicity, smoke toxicity
iii 

Contents 

1. Introduction............................................................................................................................. 2 

2. Data Collection ....................................................................................................................... 2 

3. Data Grouping......................................................................................................................... 4 

4. Report Limitations .................................................................................................................. 5 

5. Data Tables and Summaries.................................................................................................... 6 

5.1. Narcotic Gases – Tables and Summaries........................................................................ 7 

5.1.1. Carbon monoxide (CO)........................................................................................... 8 

5.1.2. Hydrogen Cyanide (HCN) .................................................................................... 11 

5.2. Irritant Gases – Tables and Summaries ........................................................................ 13 

5.2.1. Hydrogen Chloride (HCl) ..................................................................................... 14 

5.2.2. Hydrogen Fluoride (HF) ....................................................................................... 17 

5.2.3. Hydrogen Bromide (HBr)..................................................................................... 19 

5.2.4. Acrolein (C3H4O).................................................................................................. 21 

5.2.5. Formaldehyde (CH2O).......................................................................................... 22 

5.2.6. Nitrogen Dioxide (NO2)........................................................................................ 24 

5.3. Heat – Tables and Summaries....................................................................................... 27 

5.4. Smoke – Tables and Summaries................................................................................... 31 

6. Conclusion ............................................................................................................................ 34 

7. References............................................................................................................................. 35 
iv 

Tables

Table 1. Carbon Monoxide ............................................................................................................. 9 

Table 2. Summary of Data on Carbon Monoxide......................................................................... 10 

Table 3. Hydrogen Cyanide .......................................................................................................... 12 

Table 4. Summary of Data on Hydrogen Cyanide........................................................................ 13 

Table 5. Hydrogen Chloride ......................................................................................................... 15 

Table 6. Summary of Data on Hydrogen Chloride....................................................................... 16 

Table 7. Hydrogen Fluoride.......................................................................................................... 18 

Table 8. Summary of Data on Hydrogen Fluoride ....................................................................... 19 

Table 9. Hydrogen Bromide ......................................................................................................... 20 

Table 10. Summary of Data on Hydrogen Bromide..................................................................... 20 

Table 11. Acrolein ........................................................................................................................ 21 

Table 12. Summary of Data on Acrolein...................................................................................... 22 

Table 13. Formaldehyde ............................................................................................................... 23 

Table 14. Summary of Data on Formaldehyde............................................................................. 24 

Table 15. Nitrogen Dioxide .......................................................................................................... 25 

Table 16. Summary of Data on Nitrogen Dioxide........................................................................ 26 

Table 17. Heat............................................................................................................................... 29 

Table 18. Summary of Data on Heat ............................................................................................ 31

Table 19. Smoke Density.............................................................................................................. 32 

Table 20. Summary of Data on Smoke Density ........................................................................... 34 
Acknowledgements 

Support for the compilation of data on the sublethal effects of fire effluent has been provided by 

the Office of Nuclear Regulatory Research at the U.S. Nuclear Regulatory Commission. Thanks 

to Susan Cooper, Kendra Hill, Mark Salley, and Jason Dreisbach for their efforts. My 

appreciation to Richard Gann, Richard Peacock, Nathan Marsh, Jason Averill, and Nelson 

Bryner for providing detailed and insightful suggestions. 
Compilation of Data on the Sublethal Effects 

of Fire Effluent 

Erica D. Kuligowski 

Fire Research Division; Building and Fire Research Laboratory 

1. Introduction 

The burning of materials produces toxic gases (narcotic and irritant gases), smoke aerosols, and 

heat. The quantity and type of materials burning and the ventilation available influences what 

types of fire products (effluent) are produced [1,2]. For example, nonflaming, ventilation-limited 

and/or large, post-flashover fires are the prime conditions for producing toxic products, 

specifically narcotic and irritant gases, and heavy, dark smoke. 

Fires can spread smoke and hot gases throughout a building. An individual’s location relative to 

the fire is a good predictor of whether he/she is likely to encounter harmful fire products and 

what types of products he/she is most likely to encounter first. This is known as the limited 

hazard [3]. For example, if an individual is located close to the fire source, he/she is more likely 

to encounter and be affected by the heat from the fire first, but if an individual is located farther 

away from the fire, he/she is more likely to initially encounter spreading smoke and gases. 

If individuals are exposed to one or more fire products at sufficient concentrations over time, 

they can develop potentially serious physiological effects. Physiological effects from narcotic 

gases can include headaches, dizziness, and depression of the central nervous system; effects 

from irritant gases can include minor to severe irritation of the eyes, the upper respiratory tract 

(e.g., the nose, throat, and mouth), and/or lower respiratory tract (e.g., the trachea, bronchi, and 

lungs); and thermal effects can include hyperthermia, skin burns, and burns to the respiratory 

tract. These effects can lead to an inability to perform job duties, an inability to escape from a 

building, unconsciousness, and/or death. In addition to the effects during exposure, people can 

develop harmful symptoms after exposure that can lead to health problems and/or death [2]. 

The purpose of this report is to summarize data on the amount of fire effluent (narcotic gases, 

irritant gases, heat and smoke) necessary to produce sublethal effects to humans. Sublethal 

effects are important because they reduce the effectiveness of people performing critical tasks 

and also inhibits people’s abilities to move to safety such that they may ultimately be exposed to 

lethal conditions. 

2. Data Collection 

Although fires can produce a variety of different harmful products, this report features the fire 

products most often identified as likely products that are toxic or irritant to humans (not limited 
3

to nuclear power plants). This report focuses on effects to humans from exposures to heat; 

smoke; narcotic gases, specifically carbon monoxide (CO) and hydrogen cyanide (HCN); and 

irritant gases, specifically hydrogen chloride (HCl), hydrogen fluoride (HF), hydrogen bromide 

(HBr), acrolein (C3H4O), formaldehyde (CH2O), and nitrogen dioxide (NO2). 

The bibliography of research studies compiled in this report was developed using the following 

major sources: the relevant National Fire Protection Association and Society of Fire Protection 

Engineers handbook chapters [1,2,4], Acute Exposure Guideline Levels (AEGL) documents [5] 

and the SFPE Engineering Guide Predicting 1st and 2nd Degree Skin Burns from Thermal 

Radiation [6]. These documents were seminal in identifying those studies where humans and 

animals developed sublethal effects to various gas, heat and smoke exposures. As much as 

possible, data found in the NFPA, SFPE, and AEGL resources were traced back to the original 

primary (or barring that, secondary) source. 

The AEGL documents provided the majority of the references for the toxicological studies 

(narcotic and irritant gas studies) included in this report. The AEGL draft reports are developed 

by the Environmental Protection Agency (EPA)-sponsored*

 National Advisory Committee for 

Acute Exposure Guideline Levels for Hazardous Substances (NAC/AEGL), which are 

subsequently reviewed, modified, and published by the National Research Council’s (NRC) 

Committee on Toxicology. The NAC/AEGL consists of members from the EPA, the Department 

of Defense (DOD), the Department of Energy (DOE), the Department of Transportation (DOT), 

other federal and state governments, the chemical industry, academia, and organizations from the 

private sector. In the AEGL reports, members of NAC/AEGL identified, reviewed, and 

interpreted data from relevant toxicological studies on humans and animals to develop acute 

exposure guideline levels (AEGLs) for the general public†. An AEGL document was available 

for each narcotic and irritant gas included in this report. 

For narcotic fire effluent, toxicity (physiological effects) depends on the accumulated dose by the 

human or animal; namely the concentration of the effluent (in microliters per liter –μl/l)‡ and the 

time of exposure. Therefore, for each human or animal study, the concentration of the fire 

product, the time duration of the exposure (if applicable), and a description of the sublethal effect 

was noted as one data point. In some studies, more than one test was performed, which led to 

multiple data points from the same study. Data were collected from toxicological studies of 

animals exposures because data on humans, especially near-lethal effects, are understandably 

 

*

 The EPA’s Office of Pollution Prevention and Toxics (OPPT) 

† AEGL exposures levels: The first level provides the threshold concentration (in parts per million – ppm) above 

which the general public, including susceptible populations (such as children, elderly, and people with pre-existing 

heart or respiratory diseases), could experience notable discomfort. The second level provides the threshold value 

above which the general public, including susceptible populations, could experience irreversible or other serious 

health effects and/or inability to escape. The third level provides the threshold value above which the general public, 

including susceptible populations, could experience life-threatening health effects or death. 

‡

 Historically, toxicological publications have used parts per million by volume (ppm) as the units for toxic gas 

concentrations. According to ISO [26:2], “the typical units for the concentration of a toxic gas are microliters per 

liter (μl/l).” Therefore, this report uses μl/l. Please note that the units of μl/l are numerically equivalent to ppm by 

volume [26]. Also, the term “concentration” will be used throughout the report to refer to the amount of a 

contaminant (gas) in the atmosphere per unit volume of the atmosphere (μl/l) rather than “volume fraction” to 

follow ISO 13571 [26].
4

limited. Animal studies have no one-to-one correspondence to human effects, but can provide 

some insight on human effects. 

There were data found that are not included in this report. First, per request from the NRC, no 

data on susceptible populations are provided in this report. For example, susceptible populations 

can include fetuses, children, coronary artery disease patients, and asthmatics to narcotic or 

irritant gases. The AEGL threshold values† are also omitted from this report because they 

include data that account for susceptible populations in the threshold concentrations. Last, data 

for compounds that produce no effect on humans or animals and data for compounds that 

produce lethal effects on humans or animals are not included in this report. These two categories 

are outside of the scope of this report. 

3. Data Grouping 

The data points, consisting of the fire product concentration or dose and the description of the 

sublethal effect, were categorized into three main groupings. The following three categories, 

derived as part of this project, characterize the ability of the operator to perform work-related 

functions during exposure to fire products: 

Category 1: Minor physiological effects that are unlikely to affect job performance or duties 

Category 2: Moderate to major physiological effects that may negatively influence job 

performance or duties 

Category 3: Major physiological effects that may render an individual unable to perform his/her 

job duties. 

Category 1 groups all concentrations or doses that produce only minor physiological effects. 

These effects are unlikely to affect job performance or duties. For narcotic gases, these effects 

can include occasional or slight headaches or other mild central nervous system effects. For 

irritant gases, this can include mild irritation to the eyes or nose. In the case of heat, this can 

include mild discomfort to the individual. For smoke, this can include a slight decrease in an 

individual’s walking speed or steadiness of movement. Concentrations or doses listed in 

Category 1 are likely to produce only slight discomfort that is unlikely to affect job performance 

or duties. 

Category 2 groups all concentrations or doses that produce moderate to major physiological 

effects that may negatively influence job performance or duties. Effects from narcotic gases in 

Category 2 can include decided headaches, dizziness, and vomiting. The effects from irritant 

gases can include moderate to severe eye, nose, and throat irritation with possible developments 

of mild pulmonary effects. In the case of heat, this can include the initiation of pain to the skin. 

In the case of smoke, this can include a more significant decrease in walking speeds or visibility 

distance. 

Category 3 groups all concentrations or doses that produce effects that render an individual 

unable to function and/or perform his/her job duties but are less than those concentrations or 

doses which may result in death. At this level, concentrations or doses of narcotic gases, irritant 

gases, heat, or smoke are so high that incapacitation potentially to loss of consciousness occurs. 

Irritant gases (except at doses likely to cause pulmonary effects), heat, and smoke are unlikely to 
5

cause an individual to lose consciousness. For these fire products, incapacitation is defined as the 

inability of an individual to take constructive action to effect one’s own escape. In this category, 

the irritant gases, heat, and smoke levels are such that the person is no longer able to see or move 

to effect his/her own escape. For example, heat effects at this level include the onset of pain and 

blistering to exposed skin and hyperthermia. In conclusion, Category 3 exposure levels represent 

significant danger to the individual exposed and a major threat to task completion. 

In addition to the judgment of the author, two experts in the fields of 1) occupational medicine 

and internal medicine and 2) inhalation toxicology and fire science were consulted on the 

categorization of specific data points. For data points where experts did not agree, the data point 

was categorized using the more severe (or conservative) category chosen by one of the experts. 

4. Report Limitations 

There are several limitations regarding the potential use of this report and the data used within 

the report. First, this report is not a toxicological study, but rather an exercise of applied 

engineering judgment. As with most engineering judgment, legitimate differences of 

interpretation may exist given the uncertainty in the baseline of available data and the current 

state of scientific understanding of the toxicological effects of fire effluent. The data are 

presented in such a way that the categorization is transparent and may be re-categorized using 

other methods more appropriate to a particular engineering problem. Second, any assessment as 

to why one data point is higher or lower than another from the same study or different studies is 

outside of the scope of this report.

Third, this report provides data on each fire product as if it was the sole product in the fire 

scenario, although this is typically not the case in a real fire. The source data on exposures to 

gases, smoke, and heat are primarily based on studies that expose the subject to only a single fire 

product. Multiple toxic products may interact in three ways: 1) no interaction, in that the 

presence of other products has no effect on the symptoms caused by any particular product, 2) 

additive, in that each product contributes to the overall toxic level such that their contributions 

“add up” and are linear with the concentration of each product, and 3) synergistic, in that one 

particular product enhances the toxic hazard of one or more other products. There are studies that 

have found no measurable interaction between CO and HCN [7,8,9] and between carbon dioxide 

(CO2) and CO [10,11]. Contradictory to this, studies have shown that there is at least some 

additive effect between CO and HCN [1,12,13,14,15,16] and CO and HCl [17]. Narcotic and/or 

irritant gases are additive when the fraction of the toxic dose of each gas (e.g., for incapacitation) 

adds up to unity [1,18]§

. In the case of synergism, some studies have found synergism between 

 

§ Fractional effective dose (FED) models can be used for predicting toxic hazards from toxicological and flammability data. A 

fractional effective dose for a fire product can be calculated by dividing the incremental exposure dose (concentration multiplied 

by time increment) by the total exposure dose required to produce a given toxicological effect (i.e., incapacitation or lethality). 

For irritants, the fractional effective concentration can be calculated by dividing the concentration of the irritant at a certain time 

by the concentration of irritant required to cause a specific effect (e.g., incapacitation). The fractional effective doses (or

concentrations) for one or more toxic products are summed until a time is reached at which the sum become unity. At this time, 

the exposed subjects are expected to succumb to the effect (i.e., incapacitation or lethality). FED models and equations are not 

included in this report per request of the NRC and due to the fact that these models are used to predict very serious effects, such 

as incapacitation and lethality (lethality is not included in this report).
6

HCN and CO [1,19] and CO and CO2 [16,20,21], with HCN and/or CO2 increasing the 

respiration rate of an individual and in turn, producing a more rapid uptake of the toxicants 

present in the atmosphere. Purser [1] states that even though CO2 is not toxic at concentrations 

below 5 %, at 3 % of CO2, the respiratory minute volume (RMV) (or volume of air breathed) of 

an individual is approximately doubled and at 5 % CO2, the RMV is approximately tripled. 

Overall, Purser [1] suggests the following: assume that CO and HCN are directly additive, 

assume that the rates of CO and HCN increase in proportion to any increase in ventilation caused 

by CO2, and assume that irritancy is independent of asphyxia, however, the uptake of irritants is 

increased by CO2. 

Fourth, there are limited toxicological data on humans and even less data on more sensitive 

individuals. Not all humans exposed to the same amount of fire product for the same time period 

will experience similar effects. Some people are more sensitive than the general public and there 

are others that are more resistant. Those members of the subpopulations who are more sensitive 

to acute exposures of smoke gases include fetuses, children, the elderly, and individuals with 

pre-existing diseases that decrease the availability of oxygen to critical body tissues (e.g., 

coronary artery disease) for narcotic gases [5] and people with pre-existing respiratory diseases 

(e.g., asthma) for irritant gases [5]. Also, the activity level of the individual during exposure 

affects the uptake of the particular gas into the body, which influences the severity level of the 

effect(s) experienced by the person. Those individuals more susceptible to heat effects are people 

with higher skin temperatures (in the case of skin burns) and thinner skin thickness (in the case 

of skin blisters) [22]. An individual’s initial skin temperature can vary significantly (between 27 

to 38 °C) among people based on attributes such as age, sex, occupation, physical activity, and 

pregnancy [22]. Data on susceptible populations are outside of the scope of this report. 

Finally, there are also uncertainties associated with the methods, data collection, and analysis of 

the human and animal studies collected for this report. In some cases, data are presented in 

secondary sources with no possibility of obtaining the original source. The reader should 

evaluate each value cited in this report to assess whether the data are appropriate to his/her 

analysis, taking into account the scientific measurement methods, experimental protocols, range 

of data, and purpose of the study. With these limitations in mind, readers of this report should 

use the provided data with caution and with complete understanding of the uncertainties 

associated with its collection and presentation. 

5. Data Tables and Summaries 

In the following sections of this report, data from a variety of different human and animal studies 

are categorized, including concentrations or dose and description of the sublethal effect. Data are 

provided first for narcotic gases, then irritant gases, and then for heat and smoke. In each section, 

a description of the fire product is provided, then all data points are presented in a compilation 

table, and finally data summaries are displayed based on the three severity categories described 

in the Data Grouping section of this report. 
7

The compilation tables consist of all of the data points collected for each of the fire products that 

are categorized into the three main severity level categories. Data from studies performed on 

both humans and animals are included in each compilation table. Animal data are included in the 

compilation tables to provide additional information to support the more limited human data; 

however a larger uncertainty exists in their relation to human effects. In some cases, a factor of 

three difference is found between human and animal data. To the extent that animal studies 

provide data points that are the same or different from other data point/results, explanations for 

these results are outside of the scope of this report. For these kinds of interpretations, the reader 

would need to consult experts in human and animal physiology for further clarification. 

Following the compilation table in each section, a data summary table is provided to summarize 

the data from the compilation tables. For each fire product, the range of concentration or dose 

data from the human and primate (if any) studies is provided for each of the severity categories, 

specifically identifying those concentrations or doses that caused minor, moderate, or severe 

effects on humans. Primate data are included because experts have found that primates are 

appropriate models for humans due to the similarity in both gross anatomy and respiration 

patterns [23,24]. In some circumstances, it would have been possible to extrapolate and/or 

interpolate from the compilation data to produce more complete data ranges for categories for 

which there were little or no data. However, due to uncertainty in the data on sublethal effects, 

the decision was made for the summary data tables to include only the data available in the 

literature. By using only the available data, data ranges for different categories sometimes 

overlap and other times, there are data gaps in between categories. 

5.1. Narcotic Gases – Tables and Summaries 

Narcotic gases produce effects on an individual by depressing the body’s central nervous system. 

Normal body function is possible up to a certain concentration of narcotic gas for a period of 

time, then deterioration of the body functions are quick and severe. Effects can begin with slight 

headaches, dizziness, lethargy and then rapidly progress to incapacitation and death if the 

exposure continues. 

The effects of narcotic gases on humans depend on the concentration of gas accumulated over a 

period of time. This is known as the accumulated dose. An individual can sustain a low 

concentration for a longer time or a high concentration for a shorter time and experience the 

same symptoms. 

The principal narcotic gases produced in a typical fire are carbon monoxide (CO) and hydrogen 

cyanide (HCN). Although lower concentrations of oxygen (O2) (less than 15 % from 21 %) and 

very high concentrations of CO2 (greater than 5 %) can produce toxic effects, compiled and 

summarized data for these toxicants are not included in this report [1,25, 45]. At levels of O2 and 

CO2 where toxic effects can begin, the principal narcotic gases (CO and HCN) are likely to be 

present in doses that can cause harmful effects to humans. Therefore, this report focuses on those 

narcotic products most often identified as likely products that are toxic to humans (CO and 

HCN). In cases where additional information is required on the effects of O2 depletion and CO2

on humans, literature is available [1]. 
8

Data are presented on the accumulated doses of CO and HCN that produce three levels of 

severity effects in humans and animals. Each section describes the narcotic gas, presents the 

compiled data on the effects of the accumulated dose of the narcotic gas on humans and animals, 

and provides a data summary on human and/or primate data for each severity category. 

5.1.1. Carbon monoxide (CO) 

Carbon monoxide (CO) is a tasteless, nonirritating, odorless, and colorless gas. CO binds to 

hemoglobin in the blood forming carboxyhemoglobin (COHb), which renders hemoglobin 

molecules in the body less able to bind oxygen. By blocking the oxygen, CO lowers the blood’s 

oxygen delivery capacity, thereby depriving the body’s tissues, especially brain tissue, of oxygen 

[1,26,27]. The effects or symptoms produced by CO exposure are directly correlated to the 

percentage of blood hemoglobin that is converted to COHb during exposure. 

For that reason many of the toxicological studies of CO on humans and animals report the 

percentage of COHb that causes specific physiological symptoms/effects on humans and 

animals. COHb is defined as the amount of CO (in ml) per ml of blood at a specific exposure 

time. COHb can be presented as a percentage by multiplying this concentration by 100 and then 

dividing by the concentration of oxyhemoglobin (OHb), i.e., the ml of oxygen per ml of blood 

under normal conditions [27]. COHb, as a percentage, can be converted to a specific 

concentration of CO (μl/l) over a time period (and vice versa) by using a mathematical model 

known as the Coburn Foster Kane equation (CFK) [27,28]. 

Table 1 includes data points from both human and animal exposures to CO categorized by the 

three main groupings. Note that only data on healthy adults and animals are included in this 

compilation table. In some studies or secondary sources, the accumulated dose is presented as a 

percentage of COHb, whereas in others, the dose is presented as a concentration of CO (μl/l) 

over time. Both types of data are presented in the compilation table for CO. 
9

Table 1. Carbon Monoxide 

Category 1: Minor effects unlikely to affect job performance 

μl/l COHb 

(%) 

Time 

(min) Subject Notes References 

 5 NA Human Subtle, nonadverse effects; decrements in 

neurobehavioral function begin at this percentage 

[29,30,31] 

 15 to 20 NA Human No effects observed during submaximal exercise in 

healthy individuals 

[32] 

 10 NA Human No appreciable effect [31] 

 20 NA Human Shortness of breath on moderate exertion, occasional 

headaches with throbbing temples 

[31] 

600 60 Human 2 out of 9 subjects reported slight headache [33] 

200 240 Human Mild sinus headache in final hour (sedentary) [34] 

500 20, 60, 

90 

Human Lightheadedness and frontal headache [34] 

524 10 Human Lowest value to cause an effect [35] 

Category 2: Moderate to major effects that may negatively affect job performance 

 30 Human Decided headache, irritable, easily fatigued, 

judgment disturbed, possible dizziness, dimness of 

vision 

[31] 

 20.7 ± 

7.0 

 Human Majority complained of headaches, dizziness, 

weakness, nausea, trouble thinking, (6 % lost 

consciousness) 

[36] 

 21 ± 

0.7 

 Human Majority complained of severe headaches, dizziness, 

weakness, nausea, chest pain/tightness, shortness of 

breath 

[37] 

5 000 11.5 Human Increased breathing after running upstairs [38] 

3 600, 

3 900 

 30 Human On walking, throbbing in head, palpitations; on 

running, out of breath, slightly impaired vision 

[38] 

2 100 60 Human Increased breathing more distinct; beginning to look 

pale/yellowish 

[38] 

1 200 120 Human Increased breathing distinct, feeling uneasy; on 

running – weak in the legs, impaired vision and 

hearing 

[38] 

460 240 Human Unusual shortness of breath, slight palpitations [38] 

 16 to 21 Monkey Deficits in behavioral task performance started – 

momentary closure of eyes, yawning, shaking of 

head, occasional sitting down, less active 

[39] 

Category 3: Major effects that are likely to render an individual unable to complete job tasks 

 21 Human Fullness of head and precordial pain, transient 

unconsciousness 

[40] 

 28 to 32 Human Throbbing headaches, vomiting, vertigo; passed out 

several times 

[41] 

 40 to 50 Human Headache, confusion, collapse, fainting on exertion [31] 

 27 ± 12 Human Loss of consciousness at higher percentages [42] 

800- 

900 

 60 Human Decided frontal headaches, insomnia, irritability, 

marked loss of equilibrium 

[33] 

 30 Baboons Incapacitation [43] 

2 700 10 Primates Incapacitation [1] 

900 30 Primates Incapacitation [1] 

2 738-

2 968 

 10 Rats Incapacitation [12] 
10

With the exception of one set of data [38], these data converge to create data ranges for each 

category for healthy adults. A summary data table (Table 2) was developed from the data on 

healthy adults. The summary data ranges were formed by examining the human data within each 

category and forming a range around which all or most of the data converge. 

Most of the data on healthy adults can be placed within a range of COHb percentages, which can 

then be converted to concentrations of CO (μl/l) for specific time periods. For Category 1, the 

literature values converged between 5 % to 20 % of COHb by using the data from WHO [31] as 

the upper and lower bounds for the range. For Category 2, the literature values converged to 

form a range of 13 % to 30 % COHb by using Burney et al. [36] for the lower end of the range 

and WHO [31] to create the upper bound. Even though unconsciousness (6 %) was found in the 

Burney et al. [36] study, the lower bound of COHb from this study (13 %) is used as a lower 

bound for Category 2. For Category 3, data converged around a range of 21 % to 40 % COHb by 

using the Ebisuno et al. [40] study as the lower bound for incapacitating effects and the WHO 

[31] data as the upper bound. These data were even supported by the animal data presented in 

Table 1, however only human data were used to create the data ranges for each category. The 

Haldane study [38] was the only outlier in Table 1 that did not support this data range. 

Table 2 shows the data ranges for each category from exposures to CO. The COHb percentages 

listed above were converted to concentrations of CO (μl/l) for each time interval using the CFK 

equation [27,28] with the Peterson and Stewart correction [44]**. Where values fell slightly 

outside of the COHb range but still converged to the data range, these were listed in the table 

(see [33,34,35] in Table 2). However, when they fell inside the data range, they were listed in the 

reference list (see a, b, and c in Table 2). 

Table 2. Summary of Data on Carbon Monoxide 

 10 min 30 min 60 min 120 min 240 min 

Category 1 (μl/l) 550 to 2 500 a

524 [35]

195 to 880 a 105 to 475a

500 [34] 

600 [33]

60 to 275 a 42 to 190 a

200 [34]

Category 2b (μl/l) 1 590 to 3 800 560 to 1 330 300 to 730 175 to 430 115 to 300 

Category 3c (μl/l) 2 630 to 5 110 920 to 1 800 500 to 1 000 290 to 600 200 to 440 a

 The Category 1 concentrations were constructed based on the following studies that suggested minor effects from 5 

% to 20 % COHb: WHO [31]; EPA [29]; Ely et al. [37]; Kimmerle [45]; Stewart et al. [34] 

b

 The Category 2 concentrations were constructed based on the following studies that suggested major effects from 

13 % to 30 % COHb: WHO [31], Burney et al. [36]; Ely et al. [37]; Kimmerle [45]; Stewart et al. [34]. These values 

were supported by Purser and Berrill [39].

c

 The Category 3 concentrations were constructed based on the following studies that suggested human 

incapacitation from 21 % to 40 % COHb: WHO [31]; Ebisuno et al. [40]; Grace and Platt [41]; Burney et al. [36]; 

Sokal and Kralkowska [42]; Henderson et al. [33]; Stewart [46]. These values were supported by Kaplan et al. [43]; 

Purser [1]; Crane et al. [12]. 

The data presented in Table 2 can be used to predict what effects are likely when/if an individual 

is exposed to a specific concentration of CO over a period of time. For some accumulated dose 

 

** This calculation was done assuming a 70-kg man, a blood volume of 5 500 ml [28] and a daily inhalation volume 

(VE) of 22 m3 (this assumes 8 hours resting and 16 hours light/non occupational activity), a respiration rate of 18-

min-1 and a dead space (VD) of 2.2 ml/kg. These are the same assumptions used the CO AEGL document [27]. 
11

values (e.g., 2 500 μl/l for 10 min), Table 2 shows that an individual can experience Category 1 

effects or Category 2 effects. This overlap occurs because humans react to CO exposure in 

different ways. The concentration that may cause considerable effects in one person may cause 

almost no effects in another. 

5.1.2. Hydrogen Cyanide (HCN) 

Hydrogen cyanide (HCN) is a colorless, highly poisonous gas with an odor of bitter almonds 

[47,48]. The lethal dose is 25 times smaller than CO and it is a fast-acting narcotic. HCN 

prevents the utilization of oxygen by the cells of the body, which can lead to loss of 

consciousness, respiratory arrest, and death [26,47]. 

The compilation data for HCN are presented in Table 3, which includes both human and animal 

exposure studies. In each study or secondary source, the accumulated dose is presented as a 

concentration of HCN (μl/l) over time. Only data involving healthy subjects and animals were 

found for HCN, therefore people with health problems (e.g., asthma) or other susceptibilities are 

not represented in this data compilation. 
12

Table 3. Hydrogen Cyanide 

Category 1: Minor effects unlikely to affect job performance 

μl/l Time 

(min) Subject Notes References 

8 60 Human No more than mild central nervous system 

effects (e.g., mild headaches) 

[49] by 

interpreting [50] 

4 to 12 years Human Headache, weakness and objectionable 

changes in taste and smell 

[50] 

18 to 36 120+ Human Slight headaches after several hours [45] 

Category 2: Moderate to major effects that may negatively affect job performance 

>15 Unknown Human Headache, dizziness, nausea or vomiting, loss 

of appetite 

[51] 

25 to 75 60 Human Numbness, weakness, vertigo, nausea, rapid 

pulse, and flushing of the face 

[52] 

45 to 54 30 to 60 Human Could be tolerated for 1⁄2 to 1 hour [45] 

500 to 625 1.5 Human No immediate effects; postexposure - feelings 

of nausea, inability to concentrate in 

conversation 

[53] 

60 30 Monkey Slight depressive effect on nervous system; 

changes in brain wave activity at end of 

exposure 

[54] 

55 30 Rat No toxic signs, changes in lung dynamics [55] 

200 12.5 Rat Possible changes in blood enzymes attributed 

to cardiac effects 

[56] 

63 30 Mouse Respiratory depression by 50 % [57] 

Category 3: Major effects that are likely to render an individual unable to complete job tasks 

450 3 Human Collapsed and unconscious [58] 

125 12 Monkey Distinctly toxic [59] 

100, 102, 

123, 140, 

147, 156 

19, 16, 

15, 10, 8, 

8 

Monkey Incapacitation [60] 

80 to 180 Up to 30 Monkey Episode of hyperventilation with subsequent 

unconsciousness some time during 30-min 

period 

[54] 

94 30 Monkey Incapacitation [60] 

99 to 119 10 Rats Incapacitation [12] 

124, 74, 

50, 42 

5, 10, 20, 

30 

Mouse Lack of movement for 5 min in a rotating cage 

after exercise 

[61] 

150 11 Mouse Incapacitation [57] 

Although most of the human studies available on HCN exposure were limited to occupational 

reports and short-term exposures, data summaries can still be created from the data compilation. 

Table 4 shows the summary data for human and primate exposures to HCN. Data summary 

ranges are only provided for the exposure time on which data was available. 

There are limited human data presented in Category 1. El Ghawabi et al. [50] found that 

individuals experienced headaches, weakness and changes in taste and smell after years of 

occupational exposure to 4 μl/l to 12 μl/l of HCN. From this data, the NRC Subcommittee on 
13

Spacecraft Maximum Allowable Concentrations concluded that 8 μl/l of HCN would likely 

produce only mild central nervous system effects (e.g., slight headaches) after a 60-min exposure 

[49]. Therefore, the range chosen to produce only minor effects on humans after a 60-min 

exposure to HCN is 4 μl/l to 12 μl/l of HCN. Kimmerle [45] (secondary source) reports that 

individuals can be exposed to even higher concentrations for longer periods of time, which is 

considered to be an outlier for Category 1. These are the only data points found where the 

concentration produced only minor effects in healthy humans. 

Table 4. Summary of Data on Hydrogen Cyanide 

 10 min Subject 30 min Subject 60 min Subject 

Category 1 

(μl/l) 

-- -- -- -- 4 to 12 Human [49,50] 

Category 2 

(μl/l) 

-- -- 45 to 54 Human [45,59,62]a

 25 to 54 Human [45,52,62] 

Category 3 

(μl/l) 

125 to 140 Monkey [59,60] 80 to 94 Monkey [54,60] --- --- 

a supported by Purser [54] 

In Category 2, data on HCN concentrations are provided mainly for exposure times ranging from 

30 min to 60 min. As a result, summary data for Category 2 are provided only for 30-min and 

60-min exposure times (see Table 4). Kimmerle [45] and Dudley et al. [59], from Flury and 

Zernik [62], state that humans can tolerate 45 μl/l to 54 μl/l of HCN without too many 

difficulties for 30 min to 60 min. These data are supported by Purser [54] who found that 

monkeys experienced only moderate effects to brain wave activity at concentrations of 60 μl/l 

for 30 min. Therefore, Table 4 suggests that the 30-min dose of HCN that is likely to cause 

Category 2 effects in humans is 45 μl/l to 54 μl/l. For 60-min exposures, Parameter [52] found 

that humans experienced moderate to major effects between 25 μl/l and 75 μl/l and Kimmerle 

[45] suggests the same range of HCN (45 μl/l to 54 μl/l) as for 30-min exposures. In an attempt 

to conservatively mesh the two data ranges together, the 60-min exposure of HCN in Table 4 

uses the lower bound of Parameter’s [52] range and the upper bound of Kimmerle’s [45] range. 

Therefore, a 60-min dose of HCN likely to cause Category 2 effects in humans is 25 μl/l to 54 

μl/l. 

For Category 3, the data summary was constructed of primate data since there was only one data 

point from a human study available (and this study provided a very short exposure time to HCN). 

At ten min, the primate data in Table 3 show that major effects can occur between 125 μl/l and 

140 μl/l of HCN [59,60]. Additionally, primate data show that incapacitation can begin 

anywhere from 80 μl/l to 180 μl/l during a 30-min exposure to HCN [54] and another study 

notes the incapacitation of a monkey after 30 min of exposure to 94 μl/l of HCN [60]. Since 

there is an actual exposure time associated with 94 μl/l (and incapacitation can occur almost 

immediately at 180 μl/l), 94 μl/l was used as the upper limit for a 30-min exposure to HCN. 

5.2. Irritant Gases – Tables and Summaries 

Irritant gases cause physiological effects on people in two different ways: irritation to the upper 

respiratory tract (referred to as sensory irritation) and effects to the lungs. Irritant gases can affect 
14

the upper respiratory tract and eyes of an individual almost instantaneously [1,2,26]. These 

sensory effects can range from eye irritation to pain in the respiratory tract. Although pain may 

be considered as functionally incapacitating, unconsciousness or even lethality is not likely to 

result from irritant gases, except at higher concentrations, where they are likely to penetrate the 

lungs and lead to pulmonary inflammation and edema (i.e., swelling or fluid accumulation in the 

lungs). Inflammation and edema can cause respiratory difficulties and ultimately lead to death 

hours after exposure. Whereas sensory effects are likely to occur immediately in response to 

certain concentrations of irritant gas, pulmonary effects depend on an accumulated dose. 

Data are presented on the concentrations of irritant gases that produce three levels of severity 

effects in humans and animals. The irritant gases that are tabulated are hydrogen chloride (HCl), 

hydrogen fluoride (HF), hydrogen bromide (HBr), acrolein (C3H4O), formaldehyde (CH2O), and 

nitrogen dioxide (NO2). Each section describes the irritant gas, presents the compiled data on the 

effects of the concentration and/or accumulated dose of the irritant gas on humans (and animals), 

and provides a data summary on human and/or primate data for each severity category. 

In the irritant gas data compilation tables presented in this report, many of the data points for 

humans include only the concentration rather than an accumulated dose. This is because much of 

the data available from human studies involve only sensory irritation, which is almost 

immediate, making the inclusion of a time period unnecessary. In the instances where an 

exposure time is listed for a human study, this is included in the summary table. It is more 

conservative to assume an immediate response for all sensory irritation effects. Also, when a 

concentration for incapacitation of humans is listed for each irritant gas, an immediate effect 

should also be assumed [26]. 

For all of the animal studies, a time of exposure is provided in the study in addition to the 

concentration of irritant gas for both sensory and pulmonary irritant effects. Therefore, the 

irritant gas compilation tables will always provide the exposure time for each concentration 

value or range of values. Again, with sensory irritation, an immediate effect should be assumed. 

For all cases, any evidence of concentrations that result in pulmonary effects (to both humans 

and animals) will be placed in the serious category (Category 3) unless the pulmonary effects are 

labeled by experts as mild or transient, in which case the concentrations are categorized as 

moderate to serious (Category 2). 

5.2.1. Hydrogen Chloride (HCl) 

Hydrogen chloride (HCl) is a colorless gas with a pungent, even suffocating odor, which is the 

product of the decomposition of any chloride-containing product, e.g., polyvinyl chloride. HCl is 

a sensory irritant as well as a pulmonary irritant [2,63]. 

The compilation data for HCl are presented in Table 5, which includes both human and animal 

exposure studies. From each study or secondary source, the concentration of HCl is presented 

and where known, the exposure time is also listed. Exposure times are only relevant when 

pulmonary effects are a consequence of the exposure. The data presented in the compilation data 

are taken from studies of healthy subjects and animals only. 
15

Table 5. Hydrogen Chloride 

Category 1: Minor effects unlikely to affect job performance 

μl/l Time 

(min) Subject Notes References 

≥ 5 to 10 NA Human Immediately irritating; adaptation can occur [64] 

5 to 10 NA Human Mild irritants of the mucous membranes [45] 

107 30 Guinea pig Exercising; mild irritation [65] 

Category 2: Moderate to major effects that may negatively affect job performance 

10 to 50 NA Human Irritation of the throat (35 μl/l); serious 

sensory irritation at end of range; can 

tolerate range for a few hours 

[1,45,64,66] 

500 15 Baboon No impairment of pulmonary functions; 

however some moderate irritation effects 

[67] 

520 15 Guinea pig Decrease in respiratory rate in moderate 

irritation range 

[68] 

120 10 Mouse Mild to moderate nasal effects [69] 

200, 295 15 Rat Decrease in respiratory rate in moderate 

irritation range 

[17] 

Category 3: Major effects that are likely to render an individual unable to complete job tasks 

50 to 100 NA Human Barely tolerable, severe sensory irritation [1,45,66,70,71] 

1 000 NA Human Incapacitation [26] 

5 000; 10 000 15 Baboon Severe effects during exposure; (pulmonary 

hemorrhages) 

[67] 

11 400 5 Baboon Able to perform escape task after 5 min 

exposure (permanent lung damage after 

exposure) 

[43] 

16 570; 

17 290 

5 Baboon Able to perform task but died several weeks 

after exposure 

[43] 

140; 162 16.5; 

1.3 

Guinea pig ‘E-Incapacitation’ – during exercise, the 

trained guinea pig collapsed and could no 

longer run 

[65] 

3 940 15 Guinea pig Deaths shortly after exposure (lung damage 

observed postexposure) 

[68] 

475 15 Mouse Only moderate sensory irritation; however, 

4/9 died postexposure (contradicts with 

other data) 

[68] 

2 550 15 Mouse Died days after exposures (moderate lung 

edema found in one animal) 

[68] 

3 890 15 Rats Moderate to severe sensory effects; no 

deaths postexposure 

[68] 

Due to the spread and difference in the data displayed in the compilation table (Table 5), it is 

imperative to summarize these data. Therefore, a data summary table (Table 6) is presented to 

provide ranges of healthy human (and primate) data for each severity category. Even though 

animal data are included in the compilation table, only human and primate data will be 

summarized due to the uncertainty in species differences between human/primates and other 

animals. Almost all of the human data from HCl exposures are collected from secondary sources. 
16

Table 6. Summary of Data on Hydrogen Chloride 

 Concentration (μl/l) Time (min) Subject 

5 to 10 NA Human Category 1 (μl/l) --- --- Baboon 

10 to 50 NA Human Category 2 (μl/l) 500 (one data point) 15 Baboon 

50 to 1 000 NA Human Category 3 (μl/l) 5 000 to 17 290 5 to 15 Baboon 

There are limited data presented on those effects that are unlikely to affect job performance 

(Category 1). Elkins [64] found that greater than and equal to 5 μl/l of HCl is immediately 

irritating and at concentrations up to 10 μl/l of HCl, workers developed some tolerance to the 

exposure. Therefore, a range of 5 μl/l to 10 μl/l is provided for Category 1. This range is also 

supported by data from Kimmerle [45]. 

Secondary sources have identified that 10 μl/l to 50 μl/l of HCl can negatively affect job 

performance (Category 2) [1,45,64,66]. While some of these sources mention that irritation can 

be immediate at these levels, especially throat irritation around 35 μl/l, Henderson and Haggard 

[66] state that 10 μl/l to 50 μl/l is maximum concentration tolerable for one hour. It is always 

more conservative to assume that effects begin immediately at these levels. 

In Category 2, data are also provided for primates exposed to HCl. Kaplan et al. [67] found that 

baboons could withstand 500 μl/l of HCl for 15 min with only moderate sensory impairments 

and no impairment to pulmonary functions. This concentration of 500 μl/l is significantly higher 

than the suggested concentrations for humans that will produce the same physiological effects. 

While data from Kaplan et al. [67] are outliers in relation to the human data from secondary 

sources, it is important to report it since a baboon is considered a good model for human 

exposure to smoke gases. 

Secondary sources also provide the range of HCl that can produce major effects in humans 

rendering them unable to perform job duties [1,45,66,70,71]. From 50 μl/l to 100 μl/l of HCl, it 

is suggested that humans encounter severe sensory irritation. Also, the data range for humans in 

Category 3 is bounded by the concentration likely to cause incapacitation in humans provided by 

the ISO [26]. At this concentration, humans are unable to take constructive action to effect their 

own escape. Therefore, this concentration (1 000 μl/l for HCl) was placed as the upper bound for 

the third category. 

Also listed in Category 3, are data from baboon studies [43,67]. Kaplan et al. [67] found that 

baboons could withstand up to 17 290 μl/l of HCl and still perform the task assigned to them. 

Baboons exposed to 16 570 μl/l and 17 290 μl/l did perish after exposure. Baboons at other 

concentrations (5 000 μl/l, 10 000 μl/l, and 11 400 μl/l) survived at these concentration but 

experienced symptoms of pulmonary damage postexposure. 
17

5.2.2. Hydrogen Fluoride (HF) 

Hydrogen fluoride (HF) is a colorless, highly irritating and corrosive gas. HF is severely 

irritating to the eyes and nasal passages and at low concentrations, can be effectively scrubbed 

from the inhaled air, remaining in the anterior nasal passage. However, like other irritants, at 

higher concentrations, HF is likely to penetrate the lower respiratory tract and cause damage to 

the lungs [72]. In comparison with HCl, it is more likely that the body can effectively scrub a 

larger amount of HF in the nasal cavity, resulting in less penetration of HF into the lungs and less 

damage to the lower respiratory tract. Humans may experience effects to the lower respiratory 

tract especially during heavy exercise or physical exertion [72]. 

The compilation data for HF are presented in Table 7, which includes both human and animal 

exposure studies. From each study or secondary source, the concentration of HF is presented and 

where known, the exposure time is also listed. Exposure times are only relevant when pulmonary 

effects are a consequence of the exposure. The data presented in the compilation data are taken 

from studies of healthy subjects and animals only. 
18

Table 7. Hydrogen Fluoride 

Category 1: Minor effects unlikely to affect job performance 

μl/l Time 

(min) Subject Notes References 

2.6 to 4.7 Days Human Slight irritation to skin, nose, and eyes [73,74] 

3 to 6.3 60 Human Few experienced upper respiratory 

irritation; potential overreporting (1) of 

tightness in chest 

[75] 

32 3 Human Mild irritation to eyes and nose; discomfort 

experienced 

[76]; supported 

by [45] 

460 15 Dog Mild eye, nasal and respiratory irritation [77] 

157 60 Dog Mild eye, nasal and respiratory irritation [77] 

61 300 Guinea pig 

Rabbit 

Mild irritation to respiratory tract [76] 

103, 126 15 Rat Occasional to mild eye, nasal irritation [77] 

307, 376 15 Rat Slight to mild eye, nasal irritation [77] 

Category 2: Moderate to major effects that may negatively affect job performance 

61 1 Human Eye and nasal irritation; irritation of 

breathing tracts 

[76]; supported 

by [45] 

666, 243 15, 60 Dog Moderate eye, nasal and respiratory 

irritation, signs of discomfort 

[77] 

749, 590, 291 5, 15, 60 Rat Moderate eye, nasal irritation [77] 

1 669 10 Rat Inflammation, hemorrhage of the nasal area 

(moderate to severe ratings by experts) 

[78,79] 

100 to 1 000, 

1 300 

30, 30 Rat Inflammation, hemorrhage of the nasal area; 

no damage to lungs; moderate irritation 

shown by respiratory rate 

[80,81] 

Category 3: Major effects that are likely to render an individual unable to complete job tasks 

50 to 100 NA Human Dangerous to life after a few minutes [45,66] 

120 NA Human Severe sensory [1,70] supported 

by [45] 

122 1 Human Highest concentration that can be 

voluntarily tolerated for > 1 min 

[76] 

500 NA Human Incapacitation [26] 

18.5 6hr/days Primate Exposure tolerable; damage to kidneys [82] 

54 360 Guinea pig Some liver and kidney damage [76] 

54 360 Rabbit Some liver and kidney damage [76] 

854 15 Rabbit Moderate sensory and lung hemorrhage [77] 

1247 15 Rabbit Severe sensory and respiratory distress [77] 

1438 5 Rat Severe sensory irritation only [77] 

2 432, 1 410, 

1 377, 489 

5, 15, 30, 

60 

Rat Severe sensory irritation and respiratory 

distress 

[77] 

6 392 2 Rat Moderate to severe damage to nasal 

passage; acute lung inflammation 

[78,79] 

7 014, 3 847, 

1 224 

10,10, 60 Rat Moderate to severe sensory irritation; 

respiratory distress 

[78,79] 
19

A data summary table (Table 8) is presented to provide ranges of healthy human data for each 

severity level category. Even though most of the compilation table data are provided by animal 

studies, only data on human exposures will be summarized in the summary table. The human 

data on HF exposures are collected from experimental studies and secondary sources. 

Table 8. Summary of Data on Hydrogen Fluoride 

 Concentration (μl/l) Time (min) Subject 

2.6 to 32 NA Human Category 1 (μl/l) --- --- Primate 

61 (one data point) 1 Human Category 2 (μl/l) --- --- Primate 

50 to 500 NA Human Category 3 (μl/l) --- --- Primate 

The data presented in Category 1 can be grouped into a HF range of 2.6 μl/l to 32 μl/l. Humans 

exposed to this range have experienced effects that are unlikely to affect job performance. Data 

from longer exposures of one hour or even over days show that humans exposed to 2.6 μl/l to 6.3 

μl/l have experienced mild irritation to the upper respiratory tract [73,74,75]. More immediate 

effects have been experienced by humans exposed to approximately 32 μl/l of HF [76]. This 

range is supported by Kimmerle [45]. Therefore, a range of 2.6 μl/l to 32 μl/l is provided for a 

concentration range that can produce mild effects unlikely to affect job performance in healthy 

adults. 

Only one data point from a human study could be found for a Category 2. Machle et al. [76] 

found that humans exposed to 61 μl/l immediately developed eye and nose irritation and 

irritation of the breathing tracts. Although this information is important, it is not enough to 

produce a summary range for Category 2. 

The data in Category 3 can be grouped into a range of HF concentrations from 50 μl/l to 500 μl/l. 

First, secondary sources suggest that 50 μl/l to 100 μl/l of HF is dangerous to life after a few 

minutes and that 120 μl/l can produce severe sensory irritation in humans [1,45,66,70]. 

Supported by these data, Michle et al. [76] found that 122 μl/l was the highest concentration that 

could be voluntary tolerated by humans for greater than one min. While these concentrations are 

at the lower end of the data range for Category 3, this range is bounded by the concentration 

likely to cause incapacitation in humans provided by the ISO [26]. At this concentration, humans 

are unable to take constructive action to effect their own escape. Therefore, this concentration 

(500 μl/l for HCl) was placed as the upper bound for the third category. 

 

5.2.3. Hydrogen Bromide (HBr) 

Hydrogen Bromide (HBr) is a colorless, corrosive gas that is severely irritating to the eyes, skin 

and nasal passages. Like many other irritants, at high concentrations, HBr may penetrate to the 

lower respiratory tract, possibly causing serious effects such as edema or hemorrhage [83]. 
20

The compilation data for HBr are presented in Table 9, which includes both human and animal 

exposure studies. From each study or secondary source, the concentration of HBr is presented 

and where known, the exposure time is also listed. Exposure times are only relevant when 

pulmonary effects are a consequence of the exposure. The data presented in the compilation data 

are taken from studies of healthy subjects and animals only. Also, since there are limited data 

available for human or animal exposure to HBr, data are provided in Table 9 for categories two 

and three only. No exposure data to HBr were found for Category 1. 

Table 9. Hydrogen Bromide 

Category 1: Minor effects unlikely to affect job performance 

μl/l Time 

(min) Subject Notes References 

--- --- --- No data are provided for Category 1 --- 

Category 2: Moderate to major effects that may negatively affect job performance 

3 to 6 NA Human Nose and throat irritation (no eye irritation) [84] 

Category 3: Major effects that are likely to render an individual unable to complete job tasks 

100 NA Human Severe sensory irritation [1,70] 

1 000 NA Human Incapacitation [26] 

100 to 1 000 30 Rat Moderate to severe nasal damage; no 

damage to the lungs; no deaths 

[80,81] 

1 300 30 Rat Moderate to severe nasal damage; no 

damage to the lungs; 8 % mortality 

[80] 

A data summary table (Table 10) is presented to provide ranges of healthy human data for 

severity levels two and three. Only human data are reviewed in the summary table. The human 

data of HBr exposures are collected from experimental studies and secondary sources. 

Table 10. Summary of Data on Hydrogen Bromide 

 Concentration (μl/l) Time (min) Subject 

--- --- Human Category 1 (μl/l) --- --- Primate 

3 to 6 NA Human Category 2 (μl/l) --- --- Primate 

100 to 1 000 NA Human Category 3 (μl/l) --- --- Primate 

Only one human study (with multiple data points) is provided for Category 2. Connecticut State 

Department of Health [84] found that humans exposed 3 μl/l to 6 μl/l of HBr experienced nose 

and throat irritation (without reports of eye irritation). This study neglected to mention the 

severity of the irritation; therefore, the reader should know that mild irritation is possible at these 

levels. As the data are unclear, the data were placed in Category 2 rather than Category 1. 
21

The data in Category 3 are provided only by secondary sources. Secondary sources suggest that 

100 μl/l of HF can produce severe sensory irritation in humans [1,70]. This concentration is used 

as the lower bound of the data summary for Category 3. The upper bound of this range is 

provided by the concentration likely to cause incapacitation in humans provided by the ISO [26]. 

At this concentration, humans are unable to take constructive action to effect their own escape. 

Therefore, the data summary provided for Category 3 is 100 μl/l to 1 000 μl/l. 

5.2.4. Acrolein (C3H4O) 

Acrolein (C3H4O) is a colorless or yellowish liquid at ambient temperature and pressure that has 

a strong, acrid, pungent odor. Acrolein is highly irritating to the upper respiratory tract and eyes 

and is a potent irritant at low concentrations and short exposure durations [85]. At higher 

concentrations and longer exposure times, pulmonary edema is possible. 

The compilation data for acrolein are presented in Table 11, which includes both human and 

animal exposure studies. From each study or secondary source, the concentration of acrolein is 

presented and where known, the exposure time is also listed. Exposure times are only relevant 

when pulmonary effects are a consequence of the exposure. The data presented in the 

compilation data are taken from studies of healthy subjects and animals only. 

Table 11. Acrolein 

Category 1: Minor effects unlikely to affect job performance 

μl/l Time 

(min) Subject Notes References 

0.1 to 0.3 NA Human Eye irritation, nose irritation, mild decrease in 

respiratory rate 

[86] 

Category 2: Moderate to major effects that may negatively affect job performance 

0.4 to 0.6 NA Human Throat irritation at 0.43 μl/l, moderate 

decrease in respiratory rate 

[86] 

0.8 NA Human Lacrimation, irritation of mucous membranes [45,87] 

<200 10 Dog Mild pulmonary edema developed 

postexposure 

[88] 

Category 3: Major effects that are likely to render an individual unable to complete job tasks 

1.0 to 5.5 NA Human Severe sensory irritation [1,45,66,70,71,89] 

30 NA Human Incapacitation [26] 

1 025, 2 780 5 Baboon Baboons can escape chamber; not 

incapacitating, however, pulmonary 

complications and some deaths after exposure 

(some survived) 

[43] 

200 to 300 10 Dog Pulmonary edema consistently found 

postexposure 

[88] 
22

A data summary table (Table 12) is presented to provide ranges of healthy human (and primate) 

data for each severity level category. The human data on acrolein exposures are collected from 

experimental studies and secondary sources. 

Table 12. Summary of Data on Acrolein 

 Concentration (μl/l) Time (min) Subject 

0.1 to 0.3 NA Human Category 1 (μl/l) --- --- Baboon 

0.4 to 0.8 NA Human Category 2 (μl/l) --- --- Baboon 

1 to 30 NA Human Category 3 (μl/l) 1 025 to 2 780 5 Baboon 

There are limited data presented on those effects that are unlikely to affect job performance 

(Category 1). Weber-Tschopp et al. [86] found that concentrations between 0.1 μl/l and 0.3 μl/l 

of acrolein caused healthy adults to experience mild eye and nose irritation and a small decrease 

in respiratory rate. With no other data available in this category, a range of 0.1 μl/l to 0.3 μl/l is 

provided. This range of data is provided from the same experimental study. 

For Category 2, experimental studies on humans [86,87] supported by secondary sources [45] 

provide a range of 0.4 μl/l to 0.8 μl/l of acrolein. In this range, healthy adults experienced throat 

irritation (0.43 μl/l), a decrease in respiratory rate that signifies moderate sensory irritation, and 

lacrimation (or tearing of the eyes). Therefore, between 0.4 μl/l and 0.8 μl/l of acrolein, humans 

experienced effects that may negatively influence their job performance. 

An experimental study [89] and secondary sources [1,45,66,70,71] also provide the range of 

acrolein that can produce major effects in humans rendering them unable to perform job duties. 

From 1.0 μl/l to 5.5 μl/l of acrolein, it is suggested that humans encounter severe sensory 

irritation. Also, the data range for humans in Category 3 is bounded by the concentration likely 

to cause incapacitation in humans provided by the ISO [26]. At this concentration, humans are 

unable to take constructive action to effect their own escape. Therefore, this concentration (30 

μl/l for acrolein) was placed as the upper bound for the third category. 

However, also listed in Category 3, are data from a study on the effects of acrolein on baboons 

[43]. Kaplan et al. [43] found that baboons could still perform an “escape task” without 

succumbing to incapacitation at acrolein concentrations of 1 025 μl/l and 2 780 μl/l. Baboons 

exposed to these concentrations did experience pulmonary complications postexposure and some 

died. 

5.2.5. Formaldehyde (CH2O) 

Formaldehyde (CH2O) is a colorless, flammable gas with a pungent, even suffocating odor [90]. 

At low concentrations, formaldehyde primarily affects the upper respiratory tract. Due to its 

solubility in water, formaldehyde becomes scrubbed by the nasal passages of humans and 
23

rodents preventing it from reaching the lower respiratory tract. At higher concentrations 

formaldehyde becomes extremely irritating, affecting both the upper and lower respiratory tract 

[90]. 

The compilation data for formaldehyde are presented in Table 13, which includes both human 

and animal exposure studies. From each study or secondary source, the concentration of 

formaldehyde is presented and where known, the exposure time is also listed. Exposure times are 

only relevant when pulmonary effects are a consequence of the exposure. The data presented in 

the compilation data are taken from studies of healthy subjects and animals only. 

Table 13. Formaldehyde 

Category 1: Minor effects unlikely to affect job performance 

μl/l Time 

(min) Subject Notes References 

>0.3 NA Human Eye irritation [91,92] 

0.9 to 1 NA Human Slight irritation, no pulmonary effects [92,93,94] 

0.1 to 1.6 NA Human Slight irritation of eyes and nose; no 

effect on performance of math tests or 

number transfer tasks 

[45,95,96] 

2.0 to 2.1 NA Human Mild nose and throat irritation during 

exercise 

[96,97,98] 

6; 15 360 Rat Mild decrease in respiratory rate [99,100] 

20; 30 360 Rat Mild effects [101] 

Category 2: Moderate to major effects that may negatively affect job performance 

2 40 Human Moderate sensory irritant effects (at rest 

and exercising subjects) 

[102,103,104,105] 

3a 60 to 

180 

Human Moderate sensory irritation; small, 

transient decrements in pulmonary 

function in exercising healthy subjects 

[97,98,106,107,108] 

13.8 30 Human Eye irritation with mild lacrimation, then 

adaptation 

[87]; supported by 

[109] 

6 360 Monkey Eye irritation, mild lacrimation [110] 

Category 3: Major effects that are likely to render an individual unable to complete job tasks 

5 5 Human Severe eye irritation [111] 

5 to 10 NA Human Severe sensory irritation [1,45,70,71] 

20 NA Human Lacrimation within seconds; eye, nose 

and throat irritation intolerable 

[112] 

250 NA Human Incapacitation [26] 

a

 Without exercise, no decrease in pulmonary functions 

A data summary table (Table 14) is presented to provide ranges of healthy human (and primate) 

data for each severity level category. The human data on formaldehyde exposures are collected 

from experimental studies and secondary sources. 
24

Table 14. Summary of Data on Formaldehyde 

 Concentration (μl/l) Time (min) Subject 

0.3 to 2.1 NA Human Category 1 (μl/l) --- --- Monkey 

2 to 13.8 + 30 (to 180)a Human Category 2 (μl/l) 6 (one data point) 360 Monkey 

5 to 250 NA Human Category 3 (μl/l) --- --- Monkey a

 2 μl/l for 40 min, 3 μl/l for 60 to 180 min, and 13.8 μl/l for 30 min 

Formaldehyde is the one gas presented in this report that has had a great deal of human-subject 

clinical studies performed. The studies presented in the compilation table (Table 13) conform to 

a range of 0.3 μl/l to 2.1 μl/l of formaldehyde for Category 1. Clinical studies have shown that 

concentrations of formaldehyde in this range have produced only mild effects in humans, 

including slight sensory irritation [45,91,92,93,94, 95,96], and mild nose and throat irritation 

during exercise [96,97,98]. One study demonstrated that 1.6 μl/l of formaldehyde did not affect 

performance of math tests or number transfer tasks [95]. Therefore, this range of concentrations 

has produced minor effects in healthy adults that are unlikely to affect job performance. 

Clinical studies were used to create a formaldehyde range of 2 μl/l to 13.8 μl/l for Category 2. At 

the lower level of this range, exposures of 2 μl/l or 3 μl/l of formaldehyde caused moderate 

sensory irritation and even slight decrements in pulmonary function in exercising healthy adults 

[97,98,102,103,104,105,106,107,108]. At the upper bound of this range Sims and Pattle [87] and 

Douglas [109] found that 13.8 μl/l of formaldehyde led to eye irritation and tearing of the eyes. 

Therefore, the range of 2 μl/l to 13.8 μl/l of formaldehyde has produced major effects that may 

negatively influence job performance. 

Clinical studies [111,112] and secondary sources [1,45,66,70,71] provide evidence for the range 

of formaldehyde that can produce major effects in humans rendering them unable to perform job 

duties. From 5 μl/l to 10 μl/l of formaldehyde, it is suggested that humans encounter severe 

sensory irritation. Also, Barnes and Speicher [112] found that humans experienced intolerable 

eye, nose and throat irritation at 20 μl/l of formaldehyde. The data range for humans in Category 

3 is bounded by the concentration likely to cause incapacitation in humans provided by the ISO 

[26]. At this concentration, humans are unable to take constructive action to effect their own 

escape. Therefore, this concentration (250 μl/l for formaldehyde) was placed as the upper bound 

for the third category. 

5.2.6. Nitrogen Dioxide (NO2) 

Nitrogen dioxide (NO2) is a reddish-brown gas with a sweet odor. NO2 irritates the mucous 

membranes and with more severe exposures, can cause pulmonary edema represented by signs of 

chest pain, cough, dyspnea, and other serious symptoms [113]. 
25

The compilation data for NO2 are presented in Table 15, which includes both human and animal 

exposure studies. From each study or secondary source, the concentration of NO2 is presented 

and where known, the exposure time is also listed. Exposure times are only relevant when 

pulmonary effects are a consequence of the exposure. The data presented in the compilation data 

are taken from studies of healthy subjects and animals only. 

Table 15. Nitrogen Dioxide 

Category 1: Minor effects unlikely to affect job performance 

μl/l Time 

(min) Subject Notes References 

10 to 20 NA Human Mild irritation to eyes, nose and upper 

respiratory tract 

[45] 

125, 52, 39 5, 15, 60 Dog Mild sensory effects [114] 

20 24 hours Dog, Rabbit, 

Guinea pig 

Minimal signs of irritation [115] 

Category 2: Moderate to major effects that may negatively affect job performance 

5 120 Human Moderate effects on airway and O2 partial 

pressure 

[116] 

10, 15 120 Monkey Only mild respiratory effects; mild 

changes to the lung 

[117] 

164, 85, 53 5, 15, 60 Dog Mild sensory effects, but some respiratory 

distress 

[114] 

9, 13 120 Guinea pig Moderate respiratory effects [118] 

5.2, 6.5 240 Guinea pig Moderate respiratory effects [118] 

Category 3: Major effects that are likely to render an individual unable to complete job tasks 

30 120 Human Mild effects after 30 min; Burning 

sensations in chest, severe cough after 70 

min; barely tolerable at 120 min 

[119] 

50 NA Human Distinct irritation [45] 

80 NA Human Severe sensory irritation [1,70,71] 

80 3 to 5 Human Tightness of chest [45] 

250 NA Human Incapacitation [26] 

35 120 Monkey Portion of lung collapsed, bronchi 

inflamed 

[117] 

Aside from what is presented in the compilation table (Table 15), there are other data available 

that provide some context for the data points in the table. The AEGL document for NO2 suggests 

that there is a threshold level for NO2 before which pulmonary functions are found to affect 

healthy adults [113]. 

Data show that no changes in pulmonary functions were found at concentrations of 1 μl/l (2 

hours), 2 μl/l (3 hours), 2 μl/l (4 hours), 3 μl/l (2 hours), or 2.3 μl/l (5 hours) for healthy subjects 

[120,121,122,123]. Additionally, no pulmonary effects were found in healthy adults engaging in 

intermittent light or heavy exercise at 4 μl/l (1 hour) [124]. However, moderate irritation to the 

respiratory tract were found at 5 μl/l (2 hours) [116], which is listed in Table 15. 
26

Table 15 also does not show any data on exposures of rats and mice to NO2. Many of these 

studies discussed here performed experiments on rats to discover those concentrations of NO2

over certain time durations at which serious pulmonary effects would occur (e.g., pulmonary 

edema, increased lung wet weights, etc.). These pulmonary effects can be more serious than the 

three categories listed in Table 15. Therefore, instead of listing data from rat and mice studies in 

Table 15, a list of concentrations of NO2 (with time durations) that did not produce serious 

pulmonary effects on rats and mice are provided here: 

10 μl/l (30 min); 25 μl/l to 50 μl/l (up to15 min) for rats [125] 

74 μl/l (5 min); 33 μl/l (15 min) for rats [114] 

20 μl/l (up to 24 hours) for rats and mice [115] 

A data summary table (Table 16) is presented to provide ranges of healthy human and primate 

concentration data for each severity level category. The human data on NO2 exposures are 

collected from experimental studies and secondary sources. 

Table 16. Summary of Data on Nitrogen Dioxide 

 Concentration (μl/l) Time (min) Subject 

10 to 20 NA Human Category 1 (μl/l) --- --- Monkey 

5 (one data point) 120 Human Category 2 (μl/l) 10 to 15 120 Monkey 

30 to 250 NA Human Category 3 (μl/l) 35 (one data point) 120 Monkey 

For Category 1, a secondary source [45] suggests a concentration range for healthy adults that is 

likely only to produce mild irritation to the upper respiratory tract. Unfortunately, these are the 

only data available for Category 1. Therefore, 10 μl/l to 20 μl/l of NO2 is listed as causing only 

minor effects in healthy adults that are unlikely to affect job performance. 

Only one human data point is provided in Category 2 (5 μl/l for 120 min). At this concentration, 

von Neiding et al. [116] found that exposure to NO2 produced moderate irritation to the 

respiratory tract. However, this concentration actually falls below the range of data provided in 

Category 1. This is likely the result of the long exposure time because breathing NO2 for long 

periods of time at lower concentrations will cause a buildup of nitric acid throughout the 

respiratory system (primarily in the upper respiratory tract). 

On the other hand, a study performed by Henry et al. [117] found that monkeys experienced mild 

respiratory effects and mild changes to the lung (which is why this is grouped in Category 2) 

after 120 min of 10-15 μl/l of NO2. This provides support for the concentration data range listed 

in Category 1 as well as provides another viable data point for the range presented in Category 2. 

Both experimental and secondary data provide evidence for the data range presented for 

Category 3 (30 μl/l to 250 μl/l of NO2). Henschler et al. [119] exposed humans to 30 μl/l of NO2

for 120 min and found that while only mild effects were experienced 30 min into the exposure, 

subjects eventually found the concentration barely tolerable after 120 min. Also, secondary 
27

sources suggest that humans experience distinct irritation at 50 μl/l [45] and severe sensory 

irritation and even tightness in the chest area at 80 μl/l [1,45,70,71]. Therefore, these values 

provide the lower bounds for the Category 3 range of NO2 concentrations. This data range is also 

bounded by the concentration likely to cause incapacitation in humans provided by the ISO [26]. 

At this concentration, humans are unable to take constructive action to effect their own escape. 

Therefore, this concentration (250 μl/l for NO2) was placed as the upper bound for the third 

category. 

5.3. Heat – Tables and Summaries 

During a fire, individuals can be exposed to heat in the form of conductive heat (the temperature 

of the hot object in °C), convective heating (hot gases in °C) and radiative heating (heat flux in 

kW/m2

). Exposure to conductive, convective and radiative heat can cause very serious effects on 

humans. Harmful effects on people due to heat depend on both the level of the heat (temperature 

or heat flux) and the period of time over which exposure to heat has taken place. 

The three ways in which people can develop serious effects due to heat are hyperthermia (i.e., 

heat stroke), body surface burns, and burns of the respiratory tract. Hyperthermia occurs when 

people are exposed to heated environments at temperatures too low to cause burns, for an 

extended period of time (15 min or more) [1]. Exposure to these conditions gradually increases 

the individual’s core body temperature to unhealthy levels [126], which can lead to 

unconsciousness or even death. 

Skin burns can occur due to conducted, convective, and radiant heat [1,26]. Skin burns occur 

from a rise in skin temperature to a point where damage to the skin occurs [6]. Skin burns from 

conducted heat can occur anytime an individual comes in contact with a hot surface. Unless an 

individual is near to the fire and actually comes in contact with hot materials or the fire itself, 

these types of burns are unlikely to occur. Skin burns can also occur from convective heat, where 

any surface of the person comes in contact with hot gases from the fire. Last, radiant energy from 

a fire can travel from the source of the heat and be absorbed by any surface that it encounters, 

including human beings. 

The last effect of heat on people is thermal damage or burns to the respiratory tract. If hot gases 

(at certain levels and humidity) are inhaled by an individual, burns to the larynx are possible, 

which may result in edema of the larynx and even damage to the lungs if not treated. However, 

thermal burns to the respiratory tract will not occur unless the temperatures and/or humidity are 

such that facial burns are likely to occur first [1]. Therefore, this report will focus on heat levels 

likely to cause skin burns, since these are likely to happen before any thermal damage to the 

respiratory tract. 

The compilation data for heat are presented in Table 17. Data from studies of human exposure 

(exposed skin) to both radiant heat and convective heat are included in the compilation table. The 

table organizes data from heat studies into those levels of heat (heat flux and temperature) that 

produce only minor effects, moderate to major effects the may negatively interfere with job 
28

performance, and major effects likely to render an individual unable to complete job tasks. When 

using temperatures listed in either the compilation data or the summary table for convective heat, 

the reader should know that the effects depend not only on the temperature of the air but also the 

amount of humidity or volume of water vapor present in the air. Hot air at lower temperatures 

with higher humidity can cause the same kinds of effects as higher temperature with lower 

humidity. 
29

Table 17. Heat 

Category 1: Minor effects unlikely to affect job performance 

kW/m2 °C Time 

(min) Subject Notes References 

<2.5 30 min Humans Can be tolerated without significant 

consequences 

[1,26,127] 

<1.7 Any Humans No pain experienced by any test subject 

below this incident heat flux 

[128] 

<1.1 Any Threshold below which individuals can 

tolerate for a time without pain 

[129] 

 +27 Humans If higher temperatures, or higher humidity 

(higher than 35 % to 60 % at 27 °C), people 

are uncomfortable 

[130] 

Category 2: Moderate to major effects that may negatively affect job performance 

--- --- --- --- No data are provided for Category 2 --- 

Category 3: Major effects that are likely to render an individual unable to complete job tasks 

16.7 

12.6 

8.4 

6.2 

5.2 

4.1 

 2 s 

2.5 s 

5.5 s 

8 s 

10 s 

13 s 

Humans Onset of pain to exposed skin [131] 

23.5 

10.5 

2.5 

 1.6 s 

5 s 

40 s 

Humans Onset of pain to exposed skin [132] 

16.7 

12.6 

8.4 

6.2 

4.1 

 6 s 

8 s 

13 s 

21 s 

34 s 

Humans Onset of blistering to exposed skin [131,133] 

21 

12.5 

8.4 

3.3 

2 

 2 s 

5 s 

10 s 

30 s 

50 s 

Humans Unbearable pain [129] 

 146 NA Humans Without moisture in air, this is the maximum 

survivable breathing air temperature 

[26] 

 120 dry 

80 sat.a

15+ min Humans Below this threshold, hyperthermia possible 

over longer exposures (15+ min) 

[1] 

 100 dry 

120 

140 

160 

180 

12 min 

7 min 

4 min 

2 min 

1 min 

Humans Above this, onset of considerable pain in 

minutes along with production of burns 

[1,26,126] 

a

 Saturated air

As the Table 17 shows, Category 1 included those levels of heat that could be tolerated for a 

specific amount of time without significant consequences. There are little data on this level; 
30

therefore, the author also included information on temperatures that cause discomfort in humans 

(Category 1). 

No data are provided for Category 2. Research studies on the effects of heat consistently report 

heat levels likely to cause pain, burns, and blisters to exposed skin. Heat levels high enough to 

cause the onset of pain, which could be included Category 2, occur within seconds and are 

quickly followed (again in seconds) by burns, blistering, and severe pain. Due to the small time 

frame within which these effects occur, all data on pain and burns are included in Category 3. 

Category 3 includes those levels of heat that initiate considerable pain, burning and blistering of 

the skin, and the threshold temperature for hyperthermia to occur. There is no specific listing for 

incapacitation for this category, although the levels of heat included in this category are very 

painful and could be considered incapacitating. 

In order to make sense of the data included in the compilation table, a summary table for radiant 

heat and convective heat is included below as Table 18. If the level of heat is known for certain 

spaces of the building where people are expected to be, these data can assist with assessments 

made on how long an individual can withstand the effects of heat until minor or even major 

effects are likely to occur. 

The data summary for radiant heat provides the range of heat flux (kW/m2

) that, if sustained for 

less than 30 min, is likely to produce only minor effects (if any at all) (Category 1) and the 

threshold for heat flux above which considerable pain can begin in a matter of seconds (Category 

3). There are not enough data provided on radiant heat to establish a range of data for Category 2 

with any confidence. The research on radiant heat can be summarized in the following way: 

Category 1: Humans can be exposed to radiant heat between 1.1 and 2.5 kW/m2 for up to 

30 min and experience minor effects which are unlikely to affect job performance 

[1,26,127,129]. 

Category 3: Humans exposed to radiant heat at or above 2.5 kW/m2

 are likely to 

experience burning of the skin and blistering within 30 s or less [1,129,131,132,133]. 

Therefore, a radiant heat flux at or greater than 2.5 kW/m2

 can cause very serious effects to 

individuals that may render them unlikely to complete job tasks (Category 3). 

Summary data are also provided for convective heat. The data summary provides a threshold 

value (°C) for Category 1 that, if exceeded, is likely to produce only minor effects and 

discomfort to the individual. Also a threshold value (°C) is provided for Category 3 to predict 

considerable pain and hyperthermia. There are not enough data provided on convective heat to 

establish a range of data for Category 2 with any confidence. The research on convective heat 

can be summarized in the following way: 

Category 1: Temperatures above 27 °C (35 % to 60 % humidity) or higher humidity at 

27 °C can cause humans to experience discomfort [130]. 
31

Category 3: Humans exposed to dry air temperatures above 120 °C are likely to 

experience the onset of considerable pain along with the production of burns within 

minutes [1,26,126].

Category 3: Humans exposed to dry air temperatures below 120 °C (80 °C in saturated 

air) for longer than 15 min can develop hyperthermia [1]. 

Therefore, convective heat greater than 120 °C (within minutes) and below 120 °C (for a 

prolonged exposure greater than 15 min) can cause very serious effects to individuals that may 

render them unlikely to complete job tasks (Category 3). 

Table 18. Summary of Data on Heat 

Categories Heat Time (min) 

Radiant Heat (kW/m2) 1.1 to 2.5 Up to 30 min Category 1 Convective Heat (°C) + 27 (lower limit) NA 

Radiant Heat (kW/m2) --- --- Category 2 Convective Heat (°C) --- --- 

Radiant Heat (kW/m2) + 2.5 NA 

Category 3 Convective Heat (°C) + 120 

- 120 

Within minutes 

For greater than 15 min 

Clothing has been shown to provide some protection against skin pain and blistering. Its effect, 

however, is difficult to quantify due to the range of clothing available, its thickness, its 

construction and materials, and how tight it fits against the skin [1,133,134,135,136]. While 

clothing does slow the process of skin burns, any exposed skin is susceptible to skin burns. 

5.4. Smoke – Tables and Summaries 

From the burning of materials, smoke contains fire gases as well as particulate matter and 

aerosols (suspended liquid droplets). Due to the fact that the wavelength of visible light is similar 

to the average size of the smoke particulates and aerosols, the passage of light through the smoke 

is obscured, also obscuring an individual’s vision through the smoke [2]. Smoke obscuration (or 

optical density of smoke) is related to its concentration and usually expressed as optical density 

per meter (m-1) [4]. 

A high smoke obscuration is likely to affect an individual’s safety in a building. Exposures to 

thick, dense smoke can negatively affect an individual’s ability to see their surrounding 

environment, and in turn, affect their speed of movement throughout a smoke-filled space and 

their concentration on a job task [1,137]. The density of the smoke itself affects visibility as well 

as the irritancy of the smoke. In some cases, irritants can be so potent that individuals cannot 

open their eyes to see. For people wearing smoke masks, the density or thickness of the smoke is 

the main problem. 
32

Table 19 is the compilation data table for research on the effects of smoke density. There are data 

from two main research studies presented in the table and the threshold values for safe escape are 

presented from other research in the field. The research results have been grouped into the three 

main categories by relating job performance to impairments to visibility, walking speed and 

steadiness and concentration. 

Table 19. Smoke Density 

Category 1: Minor effects unlikely to affect job performance 

Optical 

density (m-1) 

Visibility 

(m) Subject Notes References 

0.087 to 0.13 6.7 to 10 Human Walking speeds begin to be negatively affected at 

these densities 

[4,137,138] 

0.04 to 0.17 5 to 20 Human Steadiness of subject (steadiness tester) begins to 

degrade - irritant smoke 

[4,137,139] 

Category 2: Moderate to major effects that may negatively affect job performance 

0.04 20 Human Threshold for safe escape [140] 

0.065 

0.22 

13 

4 

Human Threshold for safe escape – unfamiliar 

Threshold for safe escape – familiar 

 [4] 

0.08 

0.2 

10 

4.3 

Human Threshold for safe escape – unfamiliar 

Threshold for safe escape – familiar 

[1] 

0.087 10 Human Threshold for safe escape [141,142] 

0.19 4.5 Human Threshold for safe escape [143] 

0.72 1.2 Human Threshold for safe escape [144] 

0.17 to 0.22 4 to 5 Human Walking speeds are decreased by 50 % in irritant 

smoke 

[4,137,138] 

0.22 to 0.41 2.1 to 4 Human Walking speeds are decreased by 50 % in 

nonirritant smoke 

[4,137,138] 

0.15 to 0.24 3.6 to 5.7 Human Steadiness of the expert researcher (steadiness test) 

begins to degrade – irritant smoke 

[4,137,139] 

Category 3: Major effects that are likely to render an individual unable to complete job tasks 

0.22 4 Human Walking speeds are decreased as if individual is 

walking in the dark – irritant smoke 

[4,137,138] 

0.43 2 Human Walking speeds are decreased as if individual is 

walking in the dark – nonirritant smoke 

[4,137,138] 

1.7 0.5 Human Incapacitation [26] 

Research has shown that smoke optical density has an effect on how far people can see through 

the smoke (visibility), how fast people can walk or move (walking speed), and how steady an 

individual can remain during a steadiness test††. Results from these studies can be categorized 

into the three main categories using the following assumptions: 1) visibility can affect both an 

individual’s ability to escape a building and his/her ability to perform work function or tasks; 2) 

a decrease in walking speed can affect both an individual’s ability to escape and his/her ability to 

 

†† Subjects, one at a time, sat at a table and manipulated a steadiness tester in a room filled with smoke. The subject 

was told to place a metal stylus into holes in a specific order without touching the hole edges with the stylus. The 

holes ranged in size from large to small, taking more concentration to place the stylus in the smaller holes without 

contact. 
33

move around a building to perform a work task or tasks; and 3) a decrease in steadiness and 

concentration can affect an individual’s ability to perform certain work tasks efficiently and 

correctly. Each research result has been categorized with this logic to identify the smoke optical 

density ranges that are likely to produce minor, moderate, and serious effects on an individual’s 

job performance. 

The data grouped into Category 1 show that smoke optical densities of 0.087 m-1 to 0.13 m-1 (6.7 

m to 10 m visibility) begin to slow walking speeds of individuals and smoke optical densities of 

0.04 m-1 to 0.17 m-1 in irritant smoke (5 m to 20 m visibility) begin to affect one’s ability to 

concentrate on a steadiness task [137]. These values were grouped into Category 1 because at 

these smoke optical densities, the effects of smoke on functioning (speed and steadiness) were 

just beginning. It is assumed that at this level, smoke density will only produce minor effects on 

individuals that are unlikely to affect job performance. 

The data grouped in Category 2 include threshold smoke density levels for safe escape for 

familiar and unfamiliar occupants, smoke optical densities that are reported to reduce walking 

speeds by 50 %, and smoke optical densities that are reported to reduce the steadiness or 

concentration of expert researchers of the steadiness tester study. The thresholds for safe escape 

were grouped into Category 2 because these densities specify the limit at which people can still 

safely escape a building. At these levels, it is assumed that people can still function enough to 

escape a building, however their escape (and therefore, their job performance) may be negatively 

affected. The data presented in Table 19 show a large spread of threshold values ranging from 

0.04 m-1 (20 m visibility) to 0.72 m-1 (1.2 m visibility). There is no indication from any of the 

research which value(s) are more appropriate than the others. Other data presented in Category 2 

show that smoke optical densities of 0.17 m-1 to 0.22 m-1 (4 m to 5 m visibility) for irritant 

smoke and 0.22 m-1 to 0.41 m-1 (2.1 m to 4 m visibility) for nonirritant smoke slow walking 

speeds of individuals by 50 % and smoke optical densities of 0.15 m-1 to 0.24 m-1 in irritant 

smoke (3.6 m to 5.7 m visibility) begin to affect an expert’s ability to concentrate on a steadiness 

task [137]. At these lower visibility conditions (2.1 m to 5.7 m visibility), job performance may 

be negatively affected. 

The data grouped in Category 3 include smoke optical densities that significantly decrease 

speeds and the value provided by ISO [26] for incapacitation due to smoke density. At specific 

values of smoke optical density, namely 0.22 m-1 (4 m visibility) for irritant smoke and 0.43 m-1

(2 m visibility) for nonirritant smoke, individuals’ walking speeds are decreased to a value (0.3 

m/s) as if they were walking in the dark [137]. At these levels of smoke density, individuals did 

not walk in a straight line and guided their hands along the wall for support during movement, 

therefore individuals cannot be relied upon to complete work tasks. This category is bounded by 

the ISO level of smoke optical density likely to produce incapacitation. Incapacitation for smoke 

density is defined as the inability of an individual to effect his/her own escape. At an optical 

density of 1.7 m-1 (i.e., a visibility of 0.5 m), an individual is no longer able to see one’s hand in 

front of one’s face. Therefore, an individual subjected to smoke at an optical density of 1.7 m-1 is 

considered unlikely to be able to complete job tasks. 

Data from the smoke density compilation table are summarized in Table 20. Ranges of smoke 

optical densities (m-1) and corresponding visibility distances (m) likely to produce Category 1, 2, 
34

and 3 effects are found in the table for both nonirritant and irritant smoke. For all three 

categories, data ranges are taken directly out of the compilation table and listed in summary form 

in Table 20. The data that are not included in the summary table are the thresholds for safe 

escape due to the large spread in data with little indication of the value of one set of data over the 

other. Table 20 shows that lower smoke density values (higher visibility distances) are listed for 

irritant smoke due to the fact that the irritants negatively affect the eyes before the thickness of 

the smoke can influence visibility. 

Table 20. Summary of Data on Smoke Density 

Categories Optical Density (m-1) Visibility (m) 

Nonirritant smoke 0.087 to 0.13 6.7 to 10 Category 1 Irritant smoke 0.04 to 0.17 5 to 20 

Nonirritant smoke 0.22 to 0.41 2.1 to 4 Category 2 Irritant smoke 0.15 to 0.24 3.6 to 5.7 

Nonirritant smoke 1.7 to 0.43 0.5 to 2 Category 3 Irritant smoke 1.7 to 0.22 0.5 to 4 

6. Conclusion 

The purpose of this report is to summarize data on the amount of fire effluent (namely narcotic 

gases, irritant gases, heat and smoke) necessary to produce sublethal effects to humans. This 

study first identified and collected research studies that documented sublethal effects to humans 

and animals from exposures to the more common fire products. Once research studies were 

collected, each was reviewed and data on concentrations of fire product (gas, heat, or smoke) that 

produced sublethal effects on humans or animals were tabulated. Then, the data were categorized 

into three main severity levels. For each fire product, consistencies in the human and primate 

data were identified as well as any data that were inconsistent with the rest. To resolve any of 

these inconsistencies would require a more in-depth physiological analysis, which is outside of 

the scope of this report. 
35

7. References 

1 Purser, D.A.. 2008. “Toxicity assessment of combustion products,” in The SFPE Handbook of Fire Protection 

Engineering, 3rd edition. National Fire Protection Association, Quincy, MA. 

2 Gann, R.G. and N.P. Bryner. 2008. “Combustion products and their effects on life safety,” in The Fire Protection 

Handbook, 20th edition, National Fire Protection Association, Quincy, MA. 

3 Gann, R.G., V. Babrauskas, R.D. Peacock, and J.R. Hall. 1994. “Fire conditions for smoke toxicity measurement.” 

Fire and Materials 18:193-199. 

4 Jin, T. 2002. “Visibility and human behavior in fire smoke,” in The SFPE Handbook of Fire Protection 

Engineering, 3rd edition. National Fire Protection Association, Quincy, MA. 

5 U.S. Environmental Protection Agency Acute Exposure Guideline Levels. 2008. “Chemicals,” 

http://www.epa.gov/oppt/aegl/pubs/chemlist.htm 

6 Engineering Guide: Predicting 1st and 2nd Degree Skin Burns from Thermal Radiation, Society of Fire Protection 

Engineers, Bethesda, MD: 2000. 

7 Anderson, R.A., K.N. Willetss, K.N. Cheng, and W.A. Harland. 1983. “Fire deaths in the United Kingdom 1976-

82. Fire Mater. 7:67-72. 

8 Yamamoto, D. 1976. “Acute combined effects of HCN and CO with the use of the combustion products from 

PAN (polyacrylonitrile)-gauze mixtures. Z. Rechtsmed. 78:303-311. 

9 Higgins, E.A., V. Fiorca, A.A. Thomas, and H.V. Davis. 1972. “Acute toxicity of brief exposures to HF, HCl, 

NO2, and HCN with and without CO.” Fire Technology 8:120-130. 

10 Crane, C.R. 1985. “Are the combined toxicities of CO and CO2 synergistic?” Journal of Fire Sciences 3:143-144. 

11 Edginton, J.A.G. and R.D. Lynch. 1975. The Acute Inhalation Toxicity of CO from Burning Wood. Fire Research 

Note NO. 1040, Fire Research Station, Salisbury, Wiltshire, England. 

12 Crane, C.R., D.C. Sanders, and B.R. Endecott. 1989. “Inhalation Toxicology: IX. Times-to incapacitation for rats 

exposed to carbon monoxide alone, to hydrogen cyanide alone, and to mixtures of carbon monoxide and 

hydrogen cyanide.” Technical Report DOT/FAA/AM-89/4. 

13 Hartzell, G.E., H.W. Stacy, W.G. Switzer, D.N. Priest, and S.C. Packham. 1985. “Modeling of toxicological 

effects of fire gases: V. Mathematical modeling of intoxication of rats by combined carbon monoxide and 

hydrogen cyanide atmospheres.” Journal of Fire Sciences 3:330-342. 

14 Purser, D.A. and P. Grimshaw. 1984. “The incapacitative effects of exposure to thermal decomposition products 

of polyurethane foams.” Fire and Materials 8:10-16.. 

15 Pitt, B.R., E.P Radford, G.H. Gurtner, and R.J. Traystman. 1979. “Interaction of carbon monoxide and cyanide 

on cerebral circulation and metabolism.” Arch. Environ. Health 24: 354-359. 

16 Levin, B.C., M. Paabo, J.L. Gurman, and S.E. Harris. 1987. “Effects of exposure to single or multiple 

combinations of the predominant toxic gases and low oxygen atmospheres produced in fires.” Fundamental 

and Applied Toxicity 9:236-250.

17 Hartzell, G.E., H.W. Stacy, W.G. Switzer, D.N. Priest, and S.C. Packham. 1985. “Modeling of toxicological 

effects of fire gases: IV. Intoxication of rats by carbon monoxide in the presence of an irritant.” Journal of 

Fire Sciences 3:263-279. 

18 Hartzell, G.E. and H.W. Emmons. 1988. “The fractional effective dose model for assessment of toxic hazards in 

fires.” Journal of Fire Sciences 6:356-362. 

19 Moss, R.H., C.F. Jackson, and J. Seiberlich. 1951. “Toxicity of carbon monoxide and hydrogen cyanide gas 

mixtures.” Arch. Ind. Hyg. Occup. Med. 4:53-64. 

20 Rodkey, F.L. and H.A. Collison. 1979. “Effects of oxygen and carbon dioxide on carbon monoxide toxicity.” 

Journal of Combustion Toxicology 1:191-235. 

21 Nelson, G.L., E.J. Hixon, and E.P. Denine. 1978. “Combustion product toxicity studies of engineering plastics.” 

Journal of Combustion Toxicity 5:222-238. 

22 Wieczorek, C.J. and N.A. Dembsey. 2001. “Human variability correction factors for use with simplified 

engineering tools for predicting pain and second degree skin burns,” Journal of Fire Protection 

Engineering 11:88-111. 

23 Barrow, C.S. 1986. Toxicology of the Nasal Passages. New York: Hemisphere Publishing Corporation. 

24 Jones, T.C., D.L. Dungworth, and U. Mohr, eds. 1996. Monographs on Pathology of Laboratory Animals: 

Respiratory System. New York:Springer Verlag. 
36

25 Haldane, J.S. 1922. Respiration. New Haven, CT: Yale University Press.

26 ISO 1357l. 2007. Life-Threatening Components of Fire—Guidelines for the Estimation of Time Available for 

Escape Using Fire Data, International Organization for Standardization, Geneva, Switzerland. 

27 AEGL. 2005. “Interim acute exposure guideline levels: Carbon monoxide.” For NAS/COT Subcommittee for 

AEGLs. http://www.epa.gov/oppt/aegl/pubs/tsd306.pdf 

28 Coburn, R.F., R.E. Forster and P.B. Kane. 1965. “Considerations of the physiological variables that determine 

the blood carboxyhemoglobin concentration in man.” Journal of Clinical Investigation 44:1899-1910. 

29 EPA, U. S. Environmental Protection Agency, 2000. Air quality criteria for carbon monoxide. EPA 600/P99/001F, U.S. Environmental Protection Agency, Office of Research and Development, Washington, D.C. 

30 Hazucha, M.J. 2000. “Effect of carbon monoxide on work and exercise capacity in humans.” Chapter 5 in: 

Carbon Monoxide Toxicity. D.G. Penney (Ed.). CRC Press, Boca Raton, London, New York, Washington 

D.C., pp. 101-134. 

31 WHO, World Health Organization. 1999. Environmental Health Criteria 213, Carbon Monoxide (Second 

Edition), IPCS, International Programme on Chemical Safety; World Health Organization, Geneva, 

Switzerland. 

32 Kizakevich, P.N., M.L. McCartney, M.J. Hazucha, L.H. Sleet, W.J. Jochem, A.C. Hackney and K. Bolick. 2000. 

“Noninvasive ambulatory assessment of cardiac function in healthy men exposed to carbon monoxide 

during upper and lower body exercise.” Eur. J. Appl. Physiol. 83:7-16. 

33 Henderson, Y., H.W. Haggard, M.C. Teague, A.L. Prince and R.M. Wunderlich. 1921. “Physiological effects of 

automobile exhaust gas and standards of ventilation for brief exposures.” Journal of Industrial Hygiene 3: 

79-92. 

34 Stewart, R.D., J.E. Peterson, E.D. Baretta, R.T. Bachand, M.J. Hosko and A.A. Herrmann. 1970. “Experimental 

human exposure to carbon monoxide.” Archives of Environmental Health 21:154-164. 

35 Gigiena Truda i Professional'nye Zabolevaniia. 1987. Labor Hygiene and Occupational Diseases. 31. 

36 Burney, R.E., Wu, S.C., Nemiroff, M.J. 1982. “Mass carbon monoxide poisoning: Clinical effects and results of 

the treatment of 184 victims.” Ann Emerg Med 11:394-399. 

37 Ely, E.W., B. Moorehead, and E.F. Haponik. 1995. “Warehouse workers’ headache: emergency evaluation and 

management of 30 patients with carbon monoxide poisoning.” Am. J. Med 98:145-155. 

38 Haldane, J. 1895. “The action of carbonic acid on man.” J. Physiol. 18:430-462. 

39 Purser, D.A. and K.R. Berrill. 1983. “Effects of carbon monoxide on behavior in monkeys in relation to human 

fire hazard.” Arch. Environ. Health 38:308-315. 

40 Ebisuno, S., M. Yasuno, Y. Yamada, Y. Nishino, M. Hori, M. Inoue and T. Kamada. 1972. “Myocardial 

infarction after acute carbon monoxide poisoning: Case report.” Angiology 37:621-624. 

41 Grace, T.W. and F.W. Platt. 1981. “Subacute carbon monoxide poisoning.” J. Am. Med. Assoc. 246:1698-1700. 

42 Sokal, J.A. and E. Kralkowska. 1985. “The relationship between exposure duration, carboxyhemoglobin, blood 

glucose, pyruvate and lactate and the severity of intoxication in 39 cases of acute carbon monoxide 

poisoning in man.” Arch. Toxicol. 57:196-199. 

43 Kaplan, H.L., Grand, A.F., Switzer, W.G., Mitchell, D.S., Rogers, W. R., and Hartzell, G.E. 1985. “Effects of 

combustion gases on escape performance of the baboon and the rat.” Journal of Fire Sciences 3:228-244. 

44 Peterson, J.E. and R.D. Stewart. 1975. “Predicting the carboxyhemoglobin levels resulting from carbon 

monoxide exposures.” J. Appl. Physiol. 39:633-638. 

45 Kimmerle, G. 1974. “Aspects and methodology for the evaluation of toxicological parameters during fire 

exposure.” Combust. Toxicol. 1:4-51. 

46 R.D. Stewart. 1974. “The effects of carbon monoxide on man.” JFF/ Combustion Toxicology 1:167. 

47 AEGL - Subcommittee on Acute Exposure Guideline Levels Committee on Toxicology. 2002. “Acute exposure 

guideline levels for selected airborne chemicals, Volume 2: Appendix 5. Hydrogen cyanide acute exposure 

guideline levels.” National Research Council of the National Academies. National Academies Press, 

Washington, DC. http://www.epa.gov/oppt/aegl/pubs/tsd6.pdf 

48 Hartung, R. 1994. Cyanides and nitriles. In Patty's Industrial Hygiene and Toxicology, 4th ed., vol. II, Part D. 

John Wiley & Sons, pp. 3119-3172. 

49 NRC (National Research Council). 2000. Hydrogen cyanide. In Spacecraft Maximum Allowable Concentrations 

for Selected Airborne Contaminants, Volume 4. Washington, DC; National Academy Press, pp. 330-365. 
37

50 El Ghawabi, S.H., M.A. Gaafar, A.A. El-Saharti, S.H. Ahmed, K.K. Malash and R. Fares. 1975. “Chronic 

cyanide exposure: A clinical, radioisotope, and laboratory study.” Brit. J. Ind. Med. 32:215-219. 

51 Blanc, P., M. Hogan and M. Mallin. 1985. “Cyanide intoxication among silver-reclaiming workers.” J. Amer. 

Med. Assoc. 253:367-371. 

52 Parmenter, D.C. 1926. “Observations on mild cyanide poisoning: Report of a case.” J. Indust. Hyg. 8:280-282. 

53 Barcroft, J. 1931. “The toxicity of atmospheres containing hydrocyanic acid gas.” J. Hyg. 31:1-34. 

54 Purser, D.A. 1984. “A bioassay model for testing the incapacitating effects of exposure to combustion product 

atmospheres using cynomolgus monkeys.” Journal of Fire Sciences 2:20-36. 

55 Bhattacharya, R., P. Kumar, and A.S. Sachan. 1994. “Cyanide induced changes in dynamic pulmonary 

mechanics in rats.” Indian J. Pharmacol. 38:281-284. 

56 O'Flaherty, E.J. and W.C. Thomas. 1982. “The cardiotoxicity of hydrogen cyanide as a component of polymer 

pyrolysis smokes.” Toxicol. Appl. Pharmacol. 63:373-381.

57 Matijak-Schaper, M., and Y. Alarie. 1982. “Toxicity of carbon monoxide, hydrogen cyanide and low oxygen.” 

Combust. Technol. 9:21-61. 

58 Bonsall, J.L. 1984. “Survival without sequelae following exposure to 500 mg/m3

 of hydrogen cyanide.” Human 

Toxicol. 3:57-60. 

59 Dudley, H.C., T.R. Sweeney, and J.W. Miller. 1942. “Toxicology of acrylonitrile (vinyl cyanide). II. Studies of 

effects of daily inhalation.” J. Ind. Hyg. Toxicol. 24:255-258. 

60 Purser, D.A., P. Grimshaw, and K.R. Berrill. 1984. “Intoxication by cyanide in fires: A study in monkeys using 

polyacrylonitrile.” Arch. Environ. Health 39:394-400. 

61 Sakurai, T. 1989. “Toxic gas tests with several pure and mixed gases using mice.” J. Fire Sci. 7:22-77. 

62 Flury F. and F. Zernik. 1931. Schädliche gase dämpfe, nebel, rauch und staubarten. Berlin, Germany: Verlag von 

Julius Springer, p. 337 (in German). 

63 AEGL - Subcommittee on Acute Exposure Guideline Levels Committee on Toxicology. 2004. “Acute exposure 

guideline levels for selected airborne chemicals, Volume 4: Appendix 2. Hydrogen chloride acute exposure 

guideline levels.” National Research Council of the National Academies. National Academies Press, 

Washington, DC. http://www.epa.gov/oppt/aegl/pubs/tsd52.pdf 

64 Elkins, H.B. 1959. The Chemistry of Industrial Toxicology, 2nd Ed. New York, NY: John Wiley & Sons. Pp. 79-

80. 

65 Malek, D.E., and Y. Alarie. 1989. “Ergometer within a whole-body plethysmograph to evaluate performance of 

guinea pigs under toxic atmospheres.” Toxicol. Appl. Pharmacol. 101:340-355. 

66 Henderson, Y. and H. W. Hagard. 1943. Noxious Gases. New York: Reinhold Publishing Corp. Pp. 126. 

67 Kaplan, H.L., A. Anzeuto, W.G. Switzer, and R.K. Hinderer. 1988. “Effects of hydrogen chloride on respiratory 

response and pulmonary function of the baboon.” J. Toxicol. Environ. Health 23:473-493. 

68 Kaplan, H.L., W.G. Switzer, R.K. Hinderer, and A. Anzeuto. 1993. “Studies of the effects of hydrogen chloride 

and polyvinyl chloride (PVE) smoke in rodents.” J. Fire Sci. 11:512-552. 

69 Barrow, C.S., H. Lucia, and Y.C. Alarie. 1979. “A comparison of the acute inhalation toxicity of hydrogen 

chloride versus the thermal decomposition products of polyvinylchloride.” J. Combust. Toxicol. 6:3-12. 

70 “Documentation of the threshold limit values for substances in workroom air,” American Conference of 

Governmental Industrial Hygienists, Cincinnati (1980). 

71 Kane, L.E., C.S. Barrow, and Y. Alarie. 1979. “A short-term test to predict acceptable levels of exposure to 

airborne sensory irritants.” Am. Ind. Hyg. Assoc. J., 40: 207-229.

72 AEGL - Subcommittee on Acute Exposure Guideline Levels Committee on Toxicology. 2004. “Acute exposure 

guideline levels for selected airborne chemicals, Volume 4: Appendix 3. Hydrogen fluoride acute exposure 

guideline levels.” National Research Council of the National Academies. National Academies Press, 

Washington, DC. http://www.epa.gov/oppt/aegl/pubs/tsd53.pdf 

73 Largent, E.J. 1961. Fluorosis: The Health Aspects of Fluorine Compounds. Columbus, OH: Ohio State 

University Press. Pp. 34-39, 43-48. 

74 Largent, E.J. 1960. “The metabolism of fluorides in man.” AMA Arch. Ind. Health 21:318-323. 

75 Lund, K., J. Ekstrand, J. Boe, P. Sostrand, and J. Kongerud. 1997. “Exposure to hydrogen fluoride: An 

experimental study in humans of concentrations of fluoride in plasma, symptoms, and lung function.” 

Occup. Environ. Med. 54:32-37. 
38

76 Machle, W., F. Thamann, K. Kitzmiller, and J. Cholak. 1934. “The effects of the inhalation of hydrogen fluoride. 

I. The response following exposure to high concentrations.” J. Ind. Hyg. 16:129-145. 

77 Rosenholtz, M.J., T.R. Carson, M.H. Weeks, F. Wilinski, D.F. Ford, and F.W. Oberst. 1963. “A toxicopathologic 

study in animals after brief single exposures to hydrogen fluoride.” Amer. Ind. Hyg. Assoc. J. 24:253-261. 

78 Dalbey, W., B. Dunn, R. Bannister, W. Daughtrey, C. Kirwin, F. Reitman, M. Wells, and J. Bruce. 1998. “Shortterm exposures of rats to airborne hydrogen fluoride.” Toxicol. Environ. Health 55(Part A):241-275. 

79 Dalbey, W. 1996. Evaluation of the Toxicity of Hydrogen Fluoride at Short Exposure Times. Petroleum 

Environmental Research Forum Project 92-09, performed at Stonybrook Laboratories Inc., Pennington, NJ. 

80 Stavert, D.M., D.C. Archuleta, M.J. Behr, and B.E. Lehnert. 1991. “Relative acute toxicities of hydrogen 

fluoride, hydrogen chloride, and hydrogen bromide in nose- and pseudo-mouth-breathing rats.” Fundam. 

Appl. Toxicol. 16:636-655. 

81 Kusewitt, D.F., D.M. Stavert, G. Ripple, T. Mundie, and B.E. Lehnert. 1989. “Relative acute toxicities in the 

respiratory tract of inhaled hydrogen fluoride, hydrogen bromide, and hydrogen chloride.” Toxicologist

9:36. 

82 MacEwen, J.D., and E.H. Vernot. 1970. Toxic Hazards Research Unit Annual Technical Report: 1970. AMRLTR-70-77, AD 714694. Aerospace Medical Research Laboratory, Wright-Patterson AFB, Ohio. 

83 AEGL. 2005. “Proposed acute exposure guideline levels AEGLs for hydrogen bromide / hydrogen iodide.” For 

NAS/COT Subcommittee for AEGLs. 

84 Connecticut State Department of Health. 1955. Unpublished data. Occupational Health Section, Connecticut 

State Department of Health, Hartford, CT. 

85 AEGL. 2005. “Interim acute exposure guideline levels: Acrolein.” For NAS/COT Subcommittee for AEGLs. 

http://www.epa.gov/oppt/aegl/pubs/tsd303.pdf 

86 Weber-Tschopp, A., Fischer, T., Gierer, R., et al. 1977. “Experimentally induced irritating effects of acrolein on 

men.” Int. Arch. Occup. Environ. Health 40:117-130. 

87 Sim, V.M. and Pattle, R.E. 1957. “Effect of possible smog irritants on human subjects.” JAMA 165:1908-1913. 

88 Hales, C. A., Barkin, P. W., Jung, W., et al. 1988. “Synthetic smoke with acrolein but not HCl produces 

pulmonary edema.” J. Appl. Physiol. 64:1121-1133.

89 Darley, E.F., Middleton, J.T., Garber, M.J. 1960. “Plant damage and eye irritation from ozone hydrocarbon 

reactions.” J. Agric. Food. Chem. 8:483-485. 

90 AEGL. 2007. “Interim acute exposure guideline levels for formaldehyde.” For NAS/COT Subcommittee for 

AEGLs. http://www.epa.gov/oppt/aegl/pubs/formaldehydeinterimornl_oct2007c.pdf 

91 Ritchie, I.M. and R.G. Lehnen. 1987. “Formaldehyde-related health complaints of residents living in mobile and 

conventional homes.” Am. J. Public Health 77:323-328. 

92 Bender, J.R., L.S. Mullin, G.J. Grapel, and W.E. Wilson. 1983. “Eye irritation response of humans to 

formaldehyde.” Am. Ind. Hyg. Assoc. J. 44:463-465. 

93 Paustenbach, D., Y. Alarie, T. Kulle, N. Schacter, R. Smith, J. Swenberg, H. Witchi, and S.B. Horowitz. 1997. 

“A recommended occupational exposure limit for formaldehyde based on irritation.” J. Toxicol. Environ. 

Health 50:217-263. 

94 Day, J.H., R.E.M. Lees, R.H. Clark, and P.L. Pattee. 1984. “Respiratory response to formaldehyde and off-gas of 

urea formaldehyde foam insulation.” Can. Med. Assoc. J. 131:1061-1065. 

95 Andersen, I. and L. Molhave. 1983. “Controlled human studies with formaldehyde.” pp. 154-165 in Gibson, J.E., 

ed., Formaldehyde Toxicity. Washington, DC: Hemisphere Publishing Corporation. 

96 Weber-Tschopp, A., T. Fischer, and E. Grandjean. 1977. “Irritating effects of formaldehyde on men.” Int. Arch. 

Occup. Environ. Health 39:207-218. 

97 Kulle, T.J. 1993. “Acute odor and irritation response in healthy nonsmokers with formaldehyde exposure.” Inhal. 

Toxicol. 5:323-332. 

98 Kulle, T.J., L.R. Sauder, J.R. Hebel, and D.J. Green. 1987. “Formaldehyde dose-response in healthy 

nonsmokers.” J. Air Pollut. Control Assoc. 37:919-924. 

99 Morgan, K.T., D.L. Patterson and E.A. Gross. 1986. “Responses of the nasal mucociliary apparatus of F-344 rats 

to formaldehyde gas.” Toxicol. Appl. Pharmacol. 82:1-13. 

100 Chang, J.C.F., E.A. Gross, J.A. Swenberg, and C.S. Barrow. 1983. “Nasal cavity deposition, histopathology, 

and cell proliferation after single or repeated formaldehyde exposures in B6C3F1 ice and F-344 rats.” 

Toxicol. Appl. Pharmacol. 68:161-176. 
39

101 Tobe, M., K. T. Kaneko, Y. Uchida, et al. 1985. Studies of the inhalation toxicity of formaldehyde. U.S. 

Environmental Protection Agency translation, TR-85-0236. Washington, DC: U.S. EPA. 

102 Witek, T.J., E.N. Schacter, T. Tosun, G.J. Beck, and B.P. Leaderer. 1987. “An evaluation of respiratory effects 

following exposure to 2.0 ppm formaldehyde in asthmatics: lung function, symptoms, and airway 

reactivity.” Arch. Environ. Health 42:230-237.

103 Schachter, E.N., T.J. Witek, T. Tosun, B.P. Leaderer, and G.J. Beck. 1986. “A study of respiratory effects from 

exposure to 2.0 ppm formaldehyde in healthy subjects.” Arch. Environ. Health 41:229-239. 

104 Witek, T.J., E.N. Schacter, T. Tosun, B.P. Leaderer, and G.J. Beck. 1986. “Controlled human studies on the 

pulmonary effects of indoor air pollution: Experiences with sulfur dioxide and formaldehyde.” Environ. 

Intl. 12:129-135. 

105 Schachter, E.N., T.J. Witek, T. Tosun, G.J. Beck and B.P. Leaderer. 1985. “Respiratory effects of exposure to 

2.0 ppm of formaldehyde in asthmatic subjects.” Am. Rev. Respir. Dis. 131:A170. 

106 Green, D.J., R. Bascom, E.M. Healey, J.R. Hebel, L.R. Sauder, and T.J. Kulle. 1989. “Acute pulmonary 

response in healthy, nonsmoking adults to inhalation of formaldehyde and carbon.” J. Toxicol. Environ. 

Health 28:261-275. 

107 Green, D.J., L.R. Sauder, T.J. Kulle, and R. Bascom. 1987. “Acute response to 3.0 ppm formaldehyde in 

exercising healthy nonsmokers and asthmatics.” Am. Rev. Respir. Dis. 135:1261-1266. 

108 Sauder, L.R., C.D. Chatham, D.J. Green, and T.J. Kulle. 1986. “Acute pulmonary response to formaldehyde 

exposure in healthy nonsmokers.” J. Occup. Med. 28:420-424. 

109 Douglas, R.B. 1974. “Human reflex bronchoconstriction as an adjunct to conjunctival sensitivity in defining the 

threshold limit values of irritant gases and vapours.” Thesis, TUC Centenary Institute of Occupational 

Health, London School of Hygiene and Tropical Medicine.

110 Monticello, T.M., K.T. Morgan, J.I. Everitt, and J.A. Popp. 1989. “Effects of formaldehyde gas on the 

respiratory tract of rhesus monkeys.” Amer. J. pathol. 134:515-527. 

111 Stephens, E.R., E.R. Darley, O.C. Taylor, and W.E. Scott. 1961. “Photochemical reaction products in air 

pollution.” Int. J. Air Water Pollut. 4:79-100. 

112 Barnes, E.C. and H.W. Speicher. 1942. “The determination of formaldehyde in air.” J. Ind. Hyg. Toxicol. 24:10-

17. 

113 AEGL. 2006. “Interim Acute Exposure Guideline Levels for Nitrogen Dioxide.” For NAS/COT Subcommittee 

for AEGLs. http://www.epa.gov/oppt/aegl/pubs/tsd308.pdf 

114 Carson, T.R., M.S. Rosenholtz, F.T. Wilinski, and M.H. Weeks. 1962. “The responses of animals inhaling 

nitrogen dioxide for single, short-term exposures.” Am. Ind. Hyg. Assoc. J. 23:457-462. 

115 Hine, C.H., F.H. Meyers, and R.W. Wright. 1970. “Pulmonary changes in animals exposed to nitrogen dioxide, 

effects of acute exposures.” Toxicol. Appl. Pharmacol. 16:201-213.

116 von Nieding, G., H.M. Wagner, H. Krekeler, H. Löllgen, W. Fries, and A. Beuthan. 1979. “Controlled studies of 

human exposure to single and combined action of NO2, O3, and SO2.” Int. Arch. Occup. Environ. Health

43:195-210.

117 Henry, M.C., R. Ehrlich, and W.H. Blair. 1969. “Effect of nitrogen dioxide on resistance of squirrel monkeys to 

Klebsiella pneumoniae infection.” Arch. Environ. Health 18:580-587.

118 Murphy, S.D., C.E. Ulrich, S.H. Frankowitz, and C. Xintaras. 1964. “Altered function in animals inhaling low 

concentrations of ozone and nitrogen dioxide.” Am. Ind. Hyg. Assoc. J. 25:246-253. 

119 Henschler, D., A. Stier, H. Beck, and W. Neuman. 1960. “Odor threshold of a few important irritant gases 

(sulfur dioxide, ozone, nitrogen dioxide) and observations in humans exposed to low concentrations.” 

Archiv für Gewerbepathologie und Gewerbehygiene 17:547-570. (translated from German). 

120 Devlin, R., D. Horstman, S. Becker, T. Gerrity, M. Madden, and H. Koren. 1992. “Inflammatory response in 

humans exposed to 2.0 ppm NO2.” Am. Rev. Respir. Dis. 145:A456. 

121 Rasmussen, T.R., S.K. Kjaergaard, U. Tarp, and O.F. Pedersen. 1992. “Delayed effects of NO2 exposure on 

alveolar permeability and glutathione peroxidase in healthy humans.” Am. Rev. Respir. Dis. 146:654-659. 

122 Goings, S.A.J., T.J. Kulle, R. Bascom, L.R. Sauder, D.J. Green, J.R. Hebel, M.L. Clements. 1989. “Effect of 

nitrogen dioxide exposure on susceptibility to influenza A virus infection in healthy adults.” Am. Rev. 

Respir. Dis.139:1075-1081.
40

123 Hackney, J.D., F.C. Thiede, W.S. Linn, E.E. Pedersen, C.E. Spier, D.C. Law, and D.A. Fischer. 1978. 

“Experimental studies on human health effects of air pollutants. IV. Short-term physiological and clinical 

effects of nitrogen dioxide exposure.” Arch. Environ. Health 33:176-181. 

124 Linn, W.S. and J.D. Hackney. 1983. Short-term human respiratory effects of nitrogen dioxide: Determination of 

quantitative dose-response profiles. Phase 1. Exposure of healthy volunteers to 4 ppm NO2. NTIS order no. 

PB84-132299. 30 pp. 

125 Stavert, D.M. and B.E. Lehnert. 1990. “Nitric oxide and nitrogen dioxide as inducers of acute pulmonary injury 

when inhaled at relatively high concentrations for brief periods.” Inhal. Toxicol. 2:53-67.

126 Blockley, W.V. 1973. Biology Data Book, Federation of American Societies for Experimental Biology, 

Bethesda, MD. 

127 Babrauskas, V., 1979. Full-Scale Burning Behavior of Upholstered Chairs (Technical Note 1103), National 

Bureau of Standards, Washington, DC. 

128 Mudan, K.S. and P.A. Croce. 1995. “Fire hazard calculations for large open hydrocarbon fires,” in The SFPE 

Handbook of Fire Protection Engineering, 2nd edition. National Fire Protection Association, Quincy, MA. 

129 D.L. Simms and P.L. Hinkley. 1963. Fire Research Special Report No. 3, Her Majesty’s Stationary Office, 

London, UK.

130 Canadian Centre for Occupational Health and Safety (CCOHS). 

http://www.ccohs.ca/oshanswers/phys_agents/heat_health.html. 

131 Stoll, A.M. and L.C. Greene. 1959. “Relationship between pain and tissue damage due to thermal radiation,” 

Journal of Applied Physiology, 14:373-383. 

132 Buettner, K. 1951. “Effects of extreme heat and cold on human skin. II. Surface temperature, pain and heat 

conductivity in experiments with radiant heat.” J. Appl. Physiol., 3: 703-713. 

133 Veghte, J.H. 1982. “Designing protective clothing, Part 2.” F. Service Today, 49:16-18. 

134 Veghte, J.H. 1973. “Human exposure to high radiant environments.” Aerospace Medicine, October:1147-1151. 

135 Stoll, A.M. and M.A. Chianta. 1971. “Heat transfer through fabrics as related to thermal injury.” Transactions 

of the New York Academy of Sciences 33:649-670. 

136 Stoll, A.M. and M.A. Chianta. 1969. “Method of rating system for evaluation of thermal protection.” Aerospace 

Medicine November: 1232-1237. 

137 Jin, T. 1997. “Studies on human behavior and tenability in fire smoke.” Fire Safety Science – Proceedings of the 

Fifth International Symposium, Hasemi,Y., ed. London, England: Interscience Communications Ltd: 3-21. 

138 Jin, T. 1976. “Visibility through fire smoke (Part 5: Allowable smoke density for escape from fire),” Report of 

Fire Research Institute of Japan, 12-18. 

139 Jin, T. 1979. “Human behavior in fire smoke – Experiments on emotional instability under increasing smoke 

density – Preliminary report.” In U.S./Japan Government Cooperative Program on Natural Resources 

(UJNR). Fire Research and Safety. 4th Joint Panel Meeting. Tokyo, Japan, 323-339 pp.

140 Kawagoe, K. and F. Saito. 1967. “Measures to deal with smoke problems caused by fire.” Journal of Japanese 

Society for Safety Engineering, 6:108-114. 

141 Rasbash, D.J. 1975. “Sensitivity criteria for detectors used to protect life.” 7th International Seminar on 

Automatic Fire Detection, Aachen, Germany. 

142 Shern, J.H. 1966. “Smoke contribution factor in fire hazards classification of building materials.” Sixty-ninth 

Annual Meeting of the American Society for Testing and Materials, American Society for Testing and 

Materials: Philadelphia, PA:93-105. 

143 Rasbash, D.J. 1966. “Smoke and toxic gas.” Fire, 59:175-179. 

144 Kingman, F.E.T. 1953. “The products of combustion in burning buildings.” Journal of Applied Chem, 3: 463-

468.