7

Tear Gas (CS)1

Acute Exposure Guideline Levels

 

 

PREFACE

Under the authority of the Federal Advisory Committee Act (FACA) P.L. 92-463 of 1972, the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances (NAC/AEGL Committee) has been established to identify, review, and interpret relevant toxicologic and other scientific data and develop AEGLs for high-priority, acutely toxic chemicals.

AEGLs represent threshold exposure limits for the general public and are applicable to emergency exposure periods ranging from 10 minutes (min) to 8 hours (h). Three levels—AEGL-1, AEGL-2, and AEGL-3—are developed for each of five exposure periods (10 and 30 min and 1, 4, and 8 h) and are distinguished by varying degrees of severity of toxic effects. The three AEGLs are defined as follows:

AEGL-1 is the airborne concentration (expressed as parts per million or milligrams per cubic meter [ppm or mg/m3]) of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic, nonsensory

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1This document was prepared by the AEGL Development Team composed of Cheryl Bast (Oak Ridge National Laboratory), Lisa Ingerman (SRC, Inc.), Chemical Manager Glenn Leach (National Advisory Committee [NAC] on Acute Exposure Guideline Levels for Hazardous Substances), and Ernest V. Falke (US Environmental Protection Agency). The NAC reviewed and revised the document and AEGLs as deemed necessary. Both the document and the AEGL values were then reviewed by the National Research Council (NRC) Committee on Acute Exposure Guideline Levels. The NRC committee has concluded that the AEGLs developed in this document are scientifically valid conclusions based on the data reviewed by the NRC and are consistent with the NRC guidelines reports (NRC 1993, 2001).



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7 Tear Gas (CS)1 Acute Exposure Guideline Levels PREFACE Under the authority of the Federal Advisory Committee Act (FACA) P.L. 92-463 of 1972, the National Advisory Committee for Acute Exposure Guide- line Levels for Hazardous Substances (NAC/AEGL Committee) has been estab- lished to identify, review, and interpret relevant toxicologic and other scientific data and develop AEGLs for high-priority, acutely toxic chemicals. AEGLs represent threshold exposure limits for the general public and are applicable to emergency exposure periods ranging from 10 minutes (min) to 8 hours (h). Three levels—AEGL-1, AEGL-2, and AEGL-3—are developed for each of five exposure periods (10 and 30 min and 1, 4, and 8 h) and are distin- guished by varying degrees of severity of toxic effects. The three AEGLs are defined as follows: AEGL-1 is the airborne concentration (expressed as parts per million or milligrams per cubic meter [ppm or mg/m3]) of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic, nonsensory 1 This document was prepared by the AEGL Development Team composed of Cheryl Bast (Oak Ridge National Laboratory), Lisa Ingerman (SRC, Inc.), Chemical Manager Glenn Leach (National Advisory Committee [NAC] on Acute Exposure Guideline Levels for Hazardous Substances), and Ernest V. Falke (US Environmental Protection Agency). The NAC reviewed and revised the document and AEGLs as deemed necessary. Both the document and the AEGL values were then reviewed by the National Research Council (NRC) Committee on Acute Exposure Guideline Levels. The NRC committee has con- cluded that the AEGLs developed in this document are scientifically valid conclusions based on the data reviewed by the NRC and are consistent with the NRC guidelines re- ports (NRC 1993, 2001). 309

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310 Acute Exposure Guideline Levels effects. However, the effects are not disabling and are transient and reversible upon cessation of exposure. AEGL-2 is the airborne concentration (expressed as ppm or mg/m3) of a substance above which it is predicted that the general population, including sus- ceptible individuals, could experience irreversible or other serious, long-lasting adverse health effects or an impaired ability to escape. AEGL-3 is the airborne concentration (expressed as ppm or mg/m3) of a substance above which it is predicted that the general population, including sus- ceptible individuals, could experience life-threatening health effects or death. Airborne concentrations below the AEGL-1 represent exposure concentra- tions that could produce mild and progressively increasing but transient and nondisabling odor, taste, and sensory irritation or certain asymptomatic, nonsen- sory effects. With increasing airborne concentrations above each AEGL, there is a progressive increase in the likelihood of occurrence and the severity of effects described for each corresponding AEGL. Although the AEGL values represent threshold concentrations for the general public, including susceptible subpopula- tions, such as infants, children, the elderly, persons with asthma, and those with other illnesses, it is recognized that individuals, subject to idiosyncratic respons- es, could experience the effects described at concentrations below the corre- sponding AEGL. SUMMARY Tear gas is a white crystalline powder with a pepper-like odor. It was first synthesized by Corson and Stoughton in 1928 and is, thus, abbreviated as CS (Corson and Stoughton 1928; US Army Chemical School 2005). CS was devel- oped in the 1950s as a replacement for the chemical incapacitant, 1-chloro- acetophenone (CN), because CS was a much more potent irritant than CN, but was significantly less toxic (WHO 1970; Colgrave and Creasey 1975; Hu et al. 1989). It was adopted for use by the military, and was widely used in the Vi- etnam War (WHO 1970; Hu et al. 1989). It is currently used as an incapacitating agent both by military and law enforcement personnel (HSDB 2005). Upshall (1973) reported that an aerosol concentration of CS at 4 mg/m3 will disperse the majority of rioters within 1 min, and at 10 mg/m3 will deter trained troops. With the exception of more severe cutaneous reactions, recovery from exposure is generally rapid upon exposure to fresh air, generally within 30 min after expo- sure (Ballantyne 1977). CS may be manufactured through carbonyl condensa- tion by combining o-chlorobenzaldehyde and malononitrile (HSDB 2005). Re- cent production data on CS were not found. Human studies did not identify a no-effect level for CS or effects of CS that would be consistent with the definition of AEGL-1. The severity of the ef- fects observed at the lowest tested concentrations in humans (ocular stinging and watering, and nasal, throat, and mouth irritation) exceeded those defined by AEGL-1. Therefore, AEGL-1 values for CS are not recommended. AEGL-2

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Tear Gas (CS) 311 values were based on human exposure to CS at an average concentration of 0.75 mg/m3 for 60 min (Beswick et al. 1972). All five subjects tolerated the exposure, but reported ocular stinging and watering, increased salivation, cough, and face stinging. Some subjects also reported throat irritation (4 subjects), nasal stinging and running (3 subjects), mouth stinging (2 subjects), chest burning (2 subjects), nausea (2 subjects), and headache (2 subjects). An intraspecies uncertainty fac- tor of 3 was applied because contact irritation is a portal-of-entry effect and is not expected to vary widely among individuals. Furthermore, the responses of volunteers with jaundice, hepatitis, or peptic ulcer or who were 50-60 years old were similar to those of “normal” volunteers when exposed at a highly irritating concentration of CS for short durations. The ability to tolerate CS at 14-73 mg/m3 and the recovery time in volunteers with a history of drug allergies, sea- sonal allergies, asthma, or drug sensitivity were similar to normal volunteers; although more severe chest symptoms were reported in the people with pre- existing conditions (Gutentag et al. 1960; Punte et al. 1963). An interspecies uncertainty factor of 1 was applied because the study was conducted in humans. A modifying factor of 3 was also used because the effects observed at 0.75 mg/m3 were considered AEGL-2 effects. Time scaling was not performed be- cause irritation is a function of direct contact with CS and is unlikely to increase with duration of exposure at this level of severity (NRC 2001). AEGL-3 values were based on calculated lethality thresholds for CS at each exposure duration. Rat data from the studies by McNamara et al. (1969), Ballantyne and Callaway (1972), and Ballantyne and Swanston (1978) were used calculate LC01 (lethal concentrations, 1% lethality) values for CS. Calcula- tions were performed using the probit analysis-based dose-response program of ten Berge (2006). Time scaling was performed using the equation Cn × t = k, where the exponent n ranges from 0.8 to 3.5 (ten Berge et al. 1986). An empiri- cal value for n of 0.70 was determined on the basis of the rat data. The 4-h AEGL-3 value was adopted as the 8-h AEGL-3 value because time scaling yielded an 8-h value inconsistent with the AEGL-2 values, which were derived from robust human data. A total uncertainty factor of 10 was applied. A factor of 3 was used to account for interspecies differences, because clinical signs are likely caused by a direct chemical effect on the tissues and this type of portal-of- entry effect is unlikely to vary greatly between species. Furthermore, calculated LCt50 values for different species were all well within a factor of 2 of each other (88,480 mg-min/m3 for rats, 67,200 mg-min/m3 for guinea pigs, 54,090 mg- min/m3 for rabbits, and 50,010 mg-min/m3 for mice) (Ballantyne and Swanston 1978). An uncertainty factor of 3 was used to account for intraindividual varia- bility because contact irritation is a portal-of-entry effect and is not expected to vary widely among individuals. As noted above in support of the AEGL-2 val- ues, a factor of 3 is also supported by the results of studies by Punte et al. (1963) and Gutentag et al. (1960) in subjects with pre-existing conditions. AEGL values for CS are presented in Table 7-1.

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312 Acute Exposure Guideline Levels TABLE 7-1 AEGL Values for Tear Gas Classification 10 min 30 min 1h 4h 8h End Point (Reference) AEGL-1 NRa NRa NRa NRa NRa Insufficient data (nondisabling) AEGL-2 0.083 0.083 0.083 0.083 0.083 Ocular, nasal, and throat (disabling) mg/m3 mg/m3 mg/m3 mg/m3 mg/m3 irritation in humans (Beswick et al. 1972) AEGL-3 140 29 11 1.5 1.5 Threshold for lethality (lethal) mg/m3 mg/m3 mg/m3 mg/m3 mg/m3 (LC01) in rats (McNamara et al. 1969; Ballantyne and Callaway 1972; Ballantyne and Swanston 1978) a Not recommended. Absence of an AEGL-1 value does not imply that exposure below the AEGL-2 value is without adverse effects. The severity of effects observed at the low- est tested concentrations exceeded those defined by AEGL-1. 1. INTRODUCTION CS is a white crystalline powder with a pepper-like odor. It was first syn- thesized by Corson and Stoughton in 1928 (thus, the abbreviation CS) (Corson and Stoughton 1928; US Army Chemical School 2005). It was developed in the 1950s as a replacement for the chemical incapacitant, 1-chloroacetophenone (CN), because CS was a much more potent irritant than CN, but was significant- ly less toxic (WHO 1970; Colgrave and Creasey 1975; Hu et al. 1989). CS was adopted for use by the military, and was widely used during the Vietnam War (WHO 1970; Hu et al. 1989; Smith and Greaves 2002). It is currently used as an incapacitating agent by military and law enforcement personnel (HSDB 2005). It is reported that an aerosol concentration of 4 mg/m3 will disperse the majority of rioters within 1 min, and 10 mg/m3 will deter trained troops (Upshall 1973). With the exception of more severe cutaneous reactions, recovery from exposure is generally rapid upon exposure to fresh air, usually within 30 min after expo- sure (Ballantyne 1977). Because CS is stable when heated and has a low vapor pressure, it requires a means of dispersement (Blain 2003). Different forms of dispersement include the combination of CS with a pyrotechnic compound in a grenade or canister, generating a smoke or fog, and dispersement of a fine powder as an aerosol (WHO 1970; Smith and Greaves 2002). CS1 is a micronized powder formula- tion of CS containing 5% silica gel for dissemination by an explosive burst or dusting apparatus, and CS2 is the same as CS1 except that the CS1 is microen- capsulated with silicone to improve its weather resistance and flow properties (WHO 1970). In controlled studies investigating the toxicologic properties of CS aerosol, CS was disseminated as a 2-10% solution in methylene chloride or acetone by means of a pneumatic atomizing nozzle assembly (Gutentag et al. 1960; Owens and Punte 1963; Punte et al. 1963) or by thermal dispersion by spraying the mol- ten chemical (Gutentag et al. 1960; Punte et al. 1962, 1963).

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Tear Gas (CS) 313 CS may be manufactured through carbonyl condensation by combining o-chlorobenzaldehyde and malononitrile (HSDB 2005). Recent production data of CS were not available. Hydrolysis of CS produces malononitrile and o-chlorobenzaldehyde (NTP 1990). Hydrolysis of CS is relatively rapid, with a half-life of about 15 min at a pH 7, but CS reacts faster with an alkaline solution, having a half-life of about 1 min at a pH of 9 (Blain 2003). CS has a vapor pressure of 3.4 × 10-5 mm Hg; thus, at concentrations greater than 0.35 mg/m3, it will exist in vapor and aerosol forms. CS in the vapor phase will be degraded by reaction with photochemically produced hydroxyl radicals, with an estimated half-life of 110 h. CS in the particulate phase will be removed by wet and dry deposition. The chemical and physical properties of CS are presented in Table 7-2. TABLE 7-2 Chemical and Physical Properties of Tear Gas Parameter Value Reference Common name Tear gas Synonyms CS; o-chlorobenzylidenemalonitrile; HSDB 2005; O’Neil 2-chlorobenzalmalononitrile; et al. 2006 (2-chloro-phenyl)methylene) propanenitrile; 2-chlorobmn; beta, beta-dicyano-o-chlorostyrene CAS registry no. 2698-41-1 O’Neil et al. 2006 Chemical formula C10H5ClN2 O’Neil et al. 2006 Molecular weight 188.6 O’Neil et al. 2006 Physical state White crystalline solid O’Neil et al. 2006 Melting point 95-96°C ACGIH 1991 Boiling point 310-315°C US Army Chemical School 2005 Density (solid) Bulk: 0.24-0.26 g/mL; crystal: 1.04 g/mL US Army Chemical School 2005 Solubility in water (g/L) Sparingly soluble; 2.0 x 10-4 M ACGIH 1991; O’Neil et al. 2006 Vapor density (air =1) 6.5 US Army Chemical School 2005 Vapor pressure 3.4 × 10-5 mm Hg at 20°C US Army Chemical School 2005 Henry’s Law Constant 1.0 × 10-8 atm-m3/mol HSDB 2005 Volatility 0.71 mg/m3 at 25°C US Army Chemical School 2005 Stability/reactivity Combustible material; may burn but does US Army Chemical not ignite readily School 2005 Conversion factors 1 ppm = 7.71 mg/m3 Calculated 1 mg/m3 = 0.13 ppm

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314 Acute Exposure Guideline Levels 2. HUMAN TOXICITY DATA 2.1. Acute Lethality No human acute lethality data on CS were found. 2.2. Nonlethal Acute Toxicity 2.2.1. Experimental Studies In a review article, Blain (2003) reported a TC50 (concentration that caused a perceptible effect on 50% of the population exposed for 1 min) of 0.004 mg/m3 for ocular irritation and 0.023 mg/m3 for airway irritation. An ICT50 (concentration intolerable to 50% of the population exposed for 1 min) was also reported. No further details were presented. A group of male volunteers was exposed to CS aerosol with a mass medi- an diameter (MMD) of 0.9 microns (94 ± 15 mg/m3; 4% larger than 10 microns) or up to 60 microns (85 ± 16 mg/m3; 4% smaller than 20 microns) to assess dif- ferences in ocular and respiratory responses to different particle sizes of CS (Owens and Punte 1963). Six volunteers who had the best ability to tolerate CS were chosen from a group of approximately 50. Subjects wore tightly fitted goggles and a nose and mouth respirator designed to protect against particle sizes less than one micron, and were exposed individually in a wind tunnel with a constant air speed of 5 mph. The exposure protocol was designed to restrict exposure to either the small or large particles to the eyes, to the respiratory sys- tem, or to both the eyes and respiratory system. The wind tunnel was elevated to a height of 5 feet, and a rubber-lined port was installed in the bottom of the duct enabling the subject to insert his head into the airstream of the tunnel and re- move it quickly after the exposure. CS was disseminated from a 2% solution in methylene chloride by means of a pneumatic atomizing nozzle assembly. CS concentrations were determined from air samples collected using filter paper placed on air sampling probes located around the head area (one on top and one on each side at eye level), followed by extraction with ethanol and measurement with ultraviolet spectrophotometry. A modified cascade impactor was used to measure the CS aerosol containing the small particles, while the larger particles were sized microscopically, measuring and counting the various particles in the pre-ground material before dissemination. Tolerance time was defined as the time at which a subject could no longer remain in the atmosphere containing the compound and left the exposure chamber, and recovery time was defined as the time after the exposure when the subjects were able to sort and arrange a series of 24 playing cards from which the corner numbers were removed. Control val- ues were determined before each test. The results indicate that small particles are more effective in rapidly producing ocular irritation (see Table 7-3). The onset of ocular response is hypothesized to be faster with small particles because

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Tear Gas (CS) 315 TABLE 7-3 Tolerance and Recovery Time in Humans Exposed to Tear Gas Particles (1-60 microns) Subjects Tolerating 60-sec Recovery Time (sec) Exposure (%) Exposure Small Particlesa Large Particlesb Small Particlesa Large Particlesb Eyes 40 100 91 280 Respiratory system 0 67 51 9c Eyes and respiratory system 16 85 52 188 a Measured concentration of 94 ± 15 mg/m3. b Measured concentration of 85 ± 16 mg/m3. c 4/6 subjects were able to perform task immediately after exposure. Source: Adapted from Owens and Punte 1963. of they are more soluble than larger particles in ocular fluid. Once begun, how- ever, the irritation process would continue for a longer period with the large particles compared with the small particles. Respiratory effects were more se- vere with small particles (no volunteers could withstand exposure for more than 30 seconds [sec]) and required more time for recovery than the large particles. The difference in response is due to the ability of smaller-sized particles to pene- trate more deeply into the respiratory tract. When both the eyes and the respira- tory system were exposed to CS, the respiratory response predominated with exposure to the small particles, whereas the ocular response predominated with exposure to the large particles. A group of 4-6 volunteers was exposed to CS aerosol in a wind tunnel (8 × 8 × 8 feet; fixed wind speed of 5 mph) (Gutentag et al. 1960; Punte et al. 1963). Volunteers were both military and civilian personnel. Each volunteer’s medical history was recorded, and each was given pre-exposure and post-exposure phys- ical examinations. Volunteers were classified as “normal” or were placed in one of four special categories: those with hypertension (diastolic pressure of 80-110 mm Hg or normal blood pressure reading with a history of hypertension; pre- exposure tests included electrocardiogram, chest X-ray, liver function, and uri- nalysis); those with hay fever, drug sensitivity, or bronchial asthma (volunteers with asthma had normal chest X-ray before exposure); those with a history of jaundice, hepatitis, or peptic ulcers without gastrointestinal bleeding; and those that were 50-60 years of age. Subjects classified as normal were further catego- rized into untrained men with or without protective masks or trained men with or without protective masks. The trained men had previous exposure to CS, whereas the untrained men did not. CS was dispersed as a 10% solution in ace- tone or methylene dichloride with a spray nozzle (MMD 3.0 or 1.0 micron, re- spectively) or by thermal dispersion (spraying the molten chemical; MMD 0.5 micron). Airborne samples of the aerosol were collected at various points in the wind tunnel. Particle size was characterized using a 6-stage modified cascade impactor, and exposure concentrations were measured using ultraviolet spectro- photometry. The subjects did not report any noticeable difference in symptoms from the different dispersion methods.

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316 Acute Exposure Guideline Levels Groups of 3-6 untrained men without masks were exposed to CS in ace- tone, and tolerance times were recorded. Times ranged from 53 to >120 sec at 5 mg/m3, 19-43 sec at 12 mg/m3, and up to 5 sec at 442 mg/m3. When groups of 1- 7 trained men were exposed, tolerance times ranged from 37 to >120 sec at 4 mg/m3, 18-41 sec at 10 mg/m3, and up to 12-25 sec at 141 mg/m3. To compare the effects of hyperventilation on symptoms, untrained subjects ran for approx- imately 100 yards before exposure. Exercising subjects could not tolerate CS as well as normally breathing subjects; groups of three subjects exposed at 10, 13, or 39 mg/m3 could tolerate CS for up to 13, 13, and 9 sec, respectively. While ocular irritation was minimal, chest symptoms were more pronounced and re- covery time was slightly prolonged (by 1-2 min). The reactions of subjects with jaundice, hepatitis, or peptic ulcer or those that were 50-60 years old were simi- lar to those of normal subjects. Subjects with a history of drug allergies or sensi- tivities, hay fever, or asthma also tolerated exposure to CS at concentrations comparable to those tolerated by normal subjects, but the group with pre- existing conditions had a higher percentage of individuals with more severe chest symptoms, with many of them laying prostrate on the ground for several minutes. However, no wheezing or rhonchi were heard, and recovery was as rapid as that seen in other exposure groups. When subjects were exposed to CS at temperatures ranging from 0-95°F, tolerance to the chemical was slightly re- duced at the high temperature of 95°F. Whether the decrease in tolerance was an actual effect of the exposure, the uncomfortable climate, or a combination of both was unclear. An increase in skin-burning symptoms with increased temper- ature was attributed to an increase in perspiration. As part of the study described above, the potential for developing toler- ance to CS was investigated by exposing a group of four subjects to CS at 1.5 mg/m3 for 90 min in a 20,000-L chamber (Punte et al. 1963). No data were pro- vided about the monitoring of the CS aerosol. During exposure, subjects were allowed to smoke, read, and play cards. Only one subject reported nasal irrita- tion (after 2 min), three subjects reported headaches (after 45, 50, and 83 min), and all four subjects reported ocular irritation (after 20, 24, 70, and 75 min). In the second part of the experiment, the four subjects were exposed to CS at 1.5 mg/m3 for 40 min, and then additional CS aerosol was added to the chamber to achieve an airborne concentration of 11 mg/m3 in about 10 min. Although the subjects had not been told of the increase in concentration, they all left within 2 min due to respiratory irritation. The exposure concentration was estimated to be 4.3-6.7 mg/m3 when the subjects left the chamber. In the third part of the exper- iment, the subjects were exposed to CS at 6 mg/m3, which was attained over 10 min. Symptoms reported by the subjects included nasal and throat irritation, chest burning, sneezing, ocular irritation and lacrimation, headache, and dermal irritation. Three of the four subjects reported that the exposure was unbearable after 18, 20, and 29 min, with chest symptoms being the reason the subjects left the chamber. The remaining subject was able to tolerate the agent, and the expo- sure was terminated after 40 min. The investigators attempted to enter the chamber without the benefit of the gradual increase in exposure concentration,

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Tear Gas (CS) 317 and were unable to remain in the chamber. In the fourth experiment, a concen- tration of 6.6 mg/m3 was attained over 30 min. The usual signs and symptoms of CS exposure developed, but to a lesser degree. One of the subjects had to leave after 2 min because of a violent cough, but he returned to the exposure chamber after his cough had ceased upon exposure to fresh air. He remained in the expo- sure chamber for the duration of the 60-min exposure. To assess the potential effect of CS exposure on ventilation, cardiac fre- quency, and breathing pattern, a group of 11 healthy soldier volunteers was ex- posed to CS aerosol (particle diameter of 1 micron) at a concentration that was progressively increased from 0.2 mg/m3 to 1.3 mg/m3 (Cotes et al. 1972; Cole et al. 1977). The exposure duration was not specified, but appeared to be approxi- mately 80 min. CS aerosol was produced by saturating the exposure chamber the evening before the exposure, followed by flushing with air to remove all of the gas except that adsorbed onto the walls and equipment. During exposure, pyro- technic generators were ignited to progressively raise the concentration of CS throughout the exposure session. Subjects wore woolen or denim battle dress covered with cotton coveralls, boots, and gaiters. Electrocardiogram electrodes were applied to the chest, and subjects wore a full respirator into the chamber. For the commencement of exposure, each subject removed his own respirator. During each exposure, each subject completed two 8-min periods of exercise, which consisted of cycling at 20W up to 120W. During exercise, the subjects breathed through an oral-nasal mask and three-way valve box. Inspiration was from the chamber and expiration was through a 6-L capacity mixing bottle into a low resistance gas meter. Cardiac frequency was measured by electrocardio- graph, while a thermister in the valve box recorded respiratory frequency. A control exposure including exercise was conducted the day before and the day after exposure to CS. A major difference between the control and CS exposures was that ventilation was continued throughout the control session but not the CS-exposure session; therefore, the temperature was much higher during the CS-exposure sessions than the control session (~24° vs. 20.5°C for controls). All subjects experienced intense discomfort, including cough, lacrimation, and substernal pain, when first exposed to the CS aerosol. Discomfort was se- vere enough that two subjects withdrew (one before and one after the first period of exercise), and two additional subjects were unable to complete the first period of exercise due to coughing. Coughing coincided with ignition of the CS genera- tors. The discomfort disappeared with continuing exposure. Although cardiac frequency increased during exposure to CS compared with control air, the dif- ference was eliminated when the cardiac frequency was corrected for the in- creased ambient temperature (corrected to the arbitrary temperature of 20°C). The ventilation minute volume was reduced from exposure to CS compared with controls. The reduction appeared to be due to a decrease in respiratory frequen- cy. The exposure was repeated using 17 volunteers (Cole et al. 1975, 1977). Exposure conditions were the same with the following exceptions: the CS can- dles were ignited between and not during periods of exercise, CS concentrations were slightly higher (0.92-2.15 mg/m3), and the subjects were seen on five con-

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318 Acute Exposure Guideline Levels secutive half-day sessions (the first, third, and fifth sessions were for control observations and the other two sessions were allocated one each for exposure to ammonia and to CS [the order of exposure changed between the different weeks of the study]). Results were generally the same as those observed in the first study. The only difference was that the reduction in the ventilation minute vol- ume was the result of a diminution in tidal volume and occurred despite an in- crease in respiratory frequency. To investigate the potential for developing tolerance to CS, 35 healthy male volunteers were exposed for 60 min to increasing concentrations of CS aerosol (Beswick et al. 1972). Exposures were conducted in a 100-m3 chamber. The chamber was generally saturated an hour before the exposure, followed by air being blown through the chamber to remove the CS not absorbed on the walls and equipment. A number of parameters were assessed before and after exposure, including chest radiograph results, hematology and clinical-chemistry analysis, and respiratory-function tests to assess peak flow, tidal volume, and vital capacity. A total of 10 exposure trials were conducted, with no volunteers exposed more than once. Exposure concentrations were kept relatively constant in the first three trials: 0.53-0.86 mg/m3 in trial 1 (three subjects), 0.71-0.78 mg/m3 in trial 2 (five subjects), and 0.31-0.74 mg/m3 in trial 3 (six subjects). For the seven remaining trials, exposure concentrations were increased by a factor of 2, 3, or 4 during the exposure period: 0.8-1.4 mg/m3 in trial 4 (five subjects), 0.84-2.3 mg/m3 in trial 5 (four subjects), 0.7-2 mg/m3 in trial 6 (four subjects), 0.63-2.3 mg/m3 in trial 7 (two subjects), 0.57-2.1 mg/m3 in trial 8 (two subjects); 0.42-1.8 mg/m3 in trial 9 (two subjects), and 0.45-1.7 mg/m3 in trial 10 (two subjects). Chamber concentrations were measured at 10-min intervals. Volun- teers entered the chamber wearing full respirators and protective coveralls. CS was generated and allowed to mix for 3 min before removal of the respirator. Symptoms from all volunteers were reported during individual interviews after exposure. The results of the 10 trials were consolidated into five groups: group I included trial 2 (five subjects), group II included trials 1 and 3 (nine subjects), group III included trial 4 (five subjects), group IV included trials 5 and 6 (eight subjects), and group V included trials 7, 8, 9, and 10 (eight subjects). One of the six subjects in trial 3 left the exposure chamber after 8 min of exposure with complaints of severe stinging of the eyes, throat irritation, cough and dyspnea, salivation, and nausea, and one subject in group IV left after 55 min due to vom- iting. All other subjects remained in the chamber for the entire 60-min exposure period. A summary of the symptoms of the exposed individuals is presented in Table 7-4. The predominant symptoms included excess production of mucus and saliva (34/34 subjects), ocular irritation (stinging in 32/34 subjects and lacrima- tion in 32/34 subjects), runny nose (28/34 subjects), and face stinging (32/34 subjects). Symptoms generally resolved within 10 min of leaving the chamber. Nausea was reported by 11/34 subjects and two vomited, which appeared to follow swallowing of large amounts of saliva. The development of tolerance was assessed in two of the trials (group IV in Table 7-4); in these trials, half of the subjects removed the respirator at the start of the exposure (with the CS concen-

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Tear Gas (CS) 319 tration increasing with time), while the remaining subjects did not remove their respirators until the last 5 min of exposure. The subjects that were exposed to CS throughout the entire exposure period were able to withstand the entire 60- min exposure (concentrations increasing from 0.84 to 2.30 mg/m3 and 0.70 to 2.00 mg/m3) except for the one individual that had to leave the chamber at 55 min because of vomiting. Of the subjects that removed their respirators for the last 5 min of exposure, only one of eight subjects could remain in the chamber for more than 1 min; five left within 30 sec of removing their respirators. No exposure-related changes were observed in hematology or clinical chemistry parameters. Decreases in heart rate after exposure ceased were ascribed to the sense of relief each volunteer felt at the end of an uncomfortable experience, and the increase in systolic blood pressure observed in individuals when exposure commenced was due to the abrupt onset of discomfort; continued exposure re- sulted in normal blood pressure readings. No abnormalities were noted in meas- urements of respiratory function, but the investigator noted that the sample size was small and, thus, may not be representative. It was concluded that the main effects of CS are due to local irritation of exposed nerve endings, and systemic changes noted are due to stress. Three groups of volunteers were exposed to CS aerosol at various concen- trations to investigate potential effects on visual acuity (Rengstorff 1969). The first group was composed of 10 male volunteers exposed to CS2 aerosol (CS treated with Cab-o-Sil® 5 and hexamethyldisilaxane) at concentrations of 0.1 to 1.7 mg/m3. The exposure was conducted in a wind tunnel suspended 4.5 feet above the floor; the volunteer sat on a chair at the end of the wind tunnel and put his head through a rubber aperture in the tunnel until he could no longer tolerate the exposure or for a maximum of 10 min. A powder dispenser disseminated specific concentrations of CS2 (MMD of 0.8 microns) into the air at a wind speed of 4.5 mph. An Orthorater was used to measure the binocular far and near visual acuity of the subjects before and after exposure. The second and third groups were exposed to CS aerosol in a circular steel chamber. CS aerosol (MMD of 0.9 micron) in a methylene dichloride solution was disseminated us- ing a thermal generator, and introduced into the chamber as a uniform cloud. Subjects wore protective masks for the first 5 min in the chamber, and then re- moved their masks for the commencement of exposure. The second group was composed of 34 volunteers, and an Orthorater was again used to measure the binocular far and near visual acuity before and after exposure. A summary of the amount of time volunteers from this group could tolerate exposure to CS is pre- sented in Table 7-5. The third exposure involved 22 volunteers who had a base- line visual acuity of 20/20 and who could remain in the exposure chamber for 10 min. Binocular acuity was measured using a Snellen visual acuity projector be- fore, during, and a few minutes after exposure. The Snellen chart contained a row of 20/30, 20/25, and 20/20 letters. No exposure-related changes in visual acuity were noted except those due to the inability of some subjects to keep their eyes open because of intense ocular irritation. Visual acuity returned to normal in all subjects several minutes after exposure to CS ended.

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370 Acute Exposure Guideline Levels 3 for intraspecies variability. Effects from CS are likely caused by a direct chemical effect on the tissues. This type of portal-of-entry effect is not likely to vary greatly among individuals. Value is also supported by a study that showed that volunteers with a history of jaundice, hepatitis, or peptic ulcer or those that were 50-60 years old had responses similar to those of “normal” volunteers when exposed at a highly irritating concentration of CS for short durations. The ability to tolerate exposure to CS at 14-73 mg/m3 and the recovery time in people with a history of drug allergies, seasonal allergies, asthma, or drug sensitivity was similar to normal volunteers; although more severe chest symptoms were reported in the people with pre-existing conditions (Gutentag et al. 1960; Punte et al. 1963). Calculations: 10-min AEGL-3: 1,385 mg/m3 ÷ 10 = 140 mg/m3 30-min AEGL-3: 290 mg/m3 ÷ 10 = 29 mg/m3 1-h AEGL-3: 109 mg/m3 ÷ 10 = 11 mg/m3 4-h AEGL-3: 15 mg/m3 ÷ 10 =1.5 mg/m3 8-h AEGL-3: Set equal to the 4-h AEGL-3 of 1.5 mg/m3

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Tear Gas (CS) 371 APPENDIX C ACUTE EXPOSURE GUIDELINE LEVELS FOR TEAR GAS Derivation Summary AEGL-1 VALUES AEGL-1 values are not recommended for CS because the effects observed at the lowest tested concentrations exceeded the severity of AEGL-1 effects. AEGL-2 VALUES 10 min 30 min 1h 4h 8h 3 3 3 3 0.083 mg/m 0.083mg/m 0.083 mg/m 0.083 mg/m 0.083 mg/m3 Key reference: Beswick, F.W., P. Holland, and K.H. Kemp. 1972. Acute effects of exposure to orthochlorobenzilidene malononitrile (CS) and the development of tolerance. Br. J. Ind. Med. 29(3):298-306. Test species/Strain/Number: Humans, 5 Exposure route/Concentration/Duration: Inhalation, 0.71-0.78 mg/m3 (average: 0.75 mg/m3) for 60 min Effects: Clinical signs of irritation. Ocular stinging and watering, increased salivation, cough, and face stinging was reported in all subjects. Additional signs of irritation included throat irritation (4 subjects), nasal stinging and running (3 subjects), mouth stinging (2 subjects), chest burning (2 subjects), nausea (2 subjects), and headache (2 subjects). End point/Concentration/Rationale: Ocular, nasal, mouth, and throat irritation, coughing, nausea, and headache at 0.75 mg/m3 for 60 min. Uncertainty factors/Rationale: Total uncertainty factor: 3 Interspecies: 1, because data were from human volunteers Intraspecies: 3, contact irritation is a portal-of-entry effect and is not expected to vary widely between individuals. Value is also supported by a study that showed that volunteers with a history of jaundice, hepatitis, or peptic ulcer and those that were 50-60 years old had responses similar to those of “normal” volunteers when exposed at a highly irritating concentration of CS for short durations. The ability to tolerate the exposure to CS at 14-73 mg/m3 and the recovery time in people with a history of drug allergies, seasonal allergies, asthma, or drug sensitivity was similar to normal volunteers; although more severe chest symptoms were reported in the people with pre-existing conditions (Gutentag et al. 1960; Punte et al. 1963). Modifying factor: 3, because effects at 0.75 mg/m3 were considered AEGL-2 effects. Animal-to-human dosimetric adjustment: Not applicable Time scaling: Not applied. Irritation is a function of direct contact with the CS and is unlikely to increase with duration of exposure at this level of severity (NRC 2001). (Continued)

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372 Acute Exposure Guideline Levels AEGL-2 VALUES Continued Data adequacy: AEGL-2 values are supported by the data of Punte et al. (1963) and Beswick et al. (1972). Exposure of four subjects at 1.5 mg/m3 for 90 min resulted in ocular and nasal irritation in all subjects and headache in 3 subjects (Punte et al. 1963). When a total of 30 subjects were exposed for 60 min to gradually increasing CS concentrations ranging from 0.31-2.3 mg/m3, one subject left at 5 min because of vomiting but returned for the duration of the exposure, and another vomited at 55 min of exposure (vomiting in both cases attributed to swallowing large amounts or saliva). One subject voluntarily left the exposure after 8 min because of irritation; this subject was exposed in the range of 0.56-0.86 mg/m3, and the AEGL-2 values are below this range. AEGL-3 VALUES 10 min 30 min 1h 4h 8h 140 mg/m3 29 mg/m3 11 mg/m3 1.5 mg/m3 1.5 mg/m3 Key references: McNamara, B.P., E.J. Owens, J.T. Weimer, T.A. Ballard, and F.J. Vocci. 1969. Toxicology of Riot Control Chemicals CS, CN, and DM. Edgewood Arsenal Technical Report EATR-4309. US Department of the Army, Edgewood Arsenal Medical Research Laboratory, Edgewood Arsenal, MD. November. Ballantyne, B., and S. Callaway. 1972. Inhalation toxicology and pathology of animals exposed to o chlorobenzylidene malononitrile. Med. Sci. Law 12(1):43-65. Ballantyne, B., and D.W. Swanston. 1978. The comparative acute mammalian toxicity of 1- chloroacetophenone (CN) and 2-chlorobenzylidene malononitrile (CS). Arch. Toxicol. 40(2):75-95. Test species/Strain/Number: Rat, various strains; 8, 10, 20, or 21 per group Exposure route/Concentration/Duration: Inhalation, 37-5,175 mg/m3 for 5-300 min. Effects: Lethality End point/Concentration/Rationale: LC01 for rats calculated using probit-analysis dose- response program of ten Berge (2006). LC01 Point Estimate, mg/m3 Exponent n 10 min 30 min 1h 4h 8h 0.704 1,385 290 109 15 5.6 (0.543-0.865) (477-2,500) (97-496) (32-196) (3.1-35) (-0.93-15) Uncertainty factors/Rationale: Total uncertainty factor: 10 Interspecies: 3, effects from CS are likely caused by a direct chemical effect on the tissues. This type of portal-of-entry effect is unlikely to vary greatly between species. Value is also supported by calculated LCT50 values of 88,480 mg min/m3 for rats, 67,200 mg min/m3 for guinea pigs, 54,090 mg min/m3 for rabbits, and 50,010 mg min/m3 for mice (Ballantyne and Swanston 1978); values are all well within a factor of two of each other. Intraspecies: 3, effects from CS are likely caused by a direct chemical effect on the tissues. This type of portal-of-entry effect is not likely to vary greatly among individuals. Value is also supported by a study that showed that volunteers with a history of jaundice, hepatitis, or peptic ulcer or those that were 50-60 years old had responses similar to those

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Tear Gas (CS) 373 of “normal” volunteers when exposed at a highly irritating concentration of CS for short durations. The ability to tolerate the exposure to CS at 14-73 mg/m3 and the recovery time in people with a history of drug allergies, seasonal allergies, asthma, or drug sensitivity was similar to normal volunteers; although more severe chest symptoms were reported in the people with pre-existing conditions (Gutentag et al. 1960; Punte et al. 1963). Modifying factor: None applied Animal-to-human dosimetric adjustment: Not applicable Time scaling: Cn × t = k, where n = 0.70 based on rat lethality data. The 4-h AEGL-3 value was adopted as the 8-h AEGL-3 value because time scaling yielded an 8-h value inconsistent with the AEGL-2 values that were derived from robust human data. Data adequacy: The AEGL-3 values are considered protective. No mortality was noted in rats exposed to CS at 1,802 mg/m3 for 10 min (Ballantyne and Swanston 1978), in rabbits at 1,434 mg/m3 for 10 min (Ballantyne and Swanston 1978), or in mice and rabbits at 4,250 mg/m3 for 10 min (Ballantyne and Callaway 1972). Dividing these concentrations by a total uncertainty factor of 10, yields values ranging from 140-425 mg/m3, suggesting that the 10-min AEGL-3 is appropriate. No mortality was noted in guinea pigs exposed at 44.7 mg/m3 for 5 h or in mice exposed at 40 mg/m3 for 5 h (Ballantyne and Callaway 1972). Applying a total uncertainty factor of 10 to these concentrations yields a value of approximately 4.0 mg/m3 for 5 h. One of ten rats died when exposed at 37 mg/m3 for 5 h (Ballantyne and Callaway 1972). Dividing 37 mg/m3 by 2 to obtain an approximate threshold for lethality, yields 18.5 mg/m3; application of a total uncertainty factor of 10, yields a value of 1.9 mg/m3 for 5 h. The values derived from the 5-h data show that the AEGL-3 values are protective.

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374 Acute Exposure Guideline Levels APPENDIX D CATEGORY PLOT FOR TEAR GAS FIGURE D-1 Category plot of toxicity data and AEGL values for tear gas.

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TABLE D-1 Data Used in the Category Plot for Tear Gas Source Species Sex No. Exposures mg/m3 Minutes Category Comments AEGL-1 NR 10 AEGL AEGL-1 NR 30 AEGL AEGL-1 NR 60 AEGL AEGL-1 NR 240 AEGL AEGL-1 NR 480 AEGL AEGL-2 0.083 10 AEGL AEGL-2 0.083 30 AEGL AEGL-2 0.083 60 AEGL AEGL-2 0.083 240 AEGL AEGL-2 0.083 480 AEGL AEGL-3 140 10 AEGL AEGL-3 29 30 AEGL AEGL-3 11 60 AEGL AEGL-3 1.5 240 AEGL AEGL-3 1.5 480 AEGL Ballantyne and Calloway 1972 Guinea pig 1 45 300 2 Sneezing Ballantyne and Calloway 1972 Guinea pig 1 3,950 5 SL Mortality: 1/5 Ballantyne and Calloway 1972 Guinea pig 1 4,150 15 SL Mortality: 3/5 Ballantyne and Calloway 1972 Guinea pig 1 4,250 10 3 Mortality: 5/5 Ballantyne and Calloway 1972 Guinea pig 1 4,330 10 SL Mortality: 3/5 Ballantyne and Calloway 1972 Guinea pig 1 4,760 5 2 Mortality: 0/5 Ballantyne and Calloway 1972 Guinea pig 1 5,167 15 3 Mortality: 5/5 (Continued) 375

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376 TABLE D-1 Continued Source Species Sex No. Exposures mg/m3 Minutes Category Comments Ballantyne and Calloway 1972 Mouse 1 40 300 2 Rhinorrhea and lacrimation Ballantyne and Calloway 1972 Mouse 1 3,950 5 SL Mortality: 1/10 Ballantyne and Calloway 1972 Mouse 1 4,150 15 SL Mortality: 3/10 Ballantyne and Calloway 1972 Mouse 1 4,250 10 2 Mortality: 0/10 Ballantyne and Calloway 1972 Mouse 1 4,330 10 SL Mortality: 4/10 Ballantyne and Calloway 1972 Mouse 1 4,760 5 2 Mortality: 0/10 Ballantyne and Calloway 1972 Mouse 1 5,167 15 SL Mortality: 3/10 Ballantyne and Calloway 1972 Rabbit 1 3,950 5 2 Mortality: 0/5 Ballantyne and Calloway 1972 Rabbit 1 4,150 15 SL Mortality: 2/5 Ballantyne and Calloway 1972 Rabbit 1 4,250 10 2 Mortality: 0/5 Ballantyne and Calloway 1972 Rabbit 1 4,330 10 SL Mortality: 2/5 Ballantyne and Calloway 1972 Rabbit 1 4,760 5 2 Mortality: 0/5 Ballantyne and Calloway 1972 Rabbit 1 5,167 15 SL Mortality: 2/5 Ballantyne and Calloway 1972 Rat 1 37 300 SL Rhinorrhea, lacrimation, and mortality (1/10) Ballantyne and Calloway 1972 Rat 1 150 120 2 Mortality: 0/8 Ballantyne and Calloway 1972 Rat 1 3,950 5 2 Mortality: 0/10 Ballantyne and Calloway 1972 Rat 1 4,150 15 2 Mortality: 0/10 Ballantyne and Calloway 1972 Rat 1 4,250 10 SL Mortality: 1/10 Ballantyne and Calloway 1972 Rat 1 4,330 10 SL Mortality: 1/10 Ballantyne and Calloway 1972 Rat 1 4,760 5 2 Mortality: 0/10 Ballantyne and Calloway 1972 Rat 1 5,167 15 SL Mortality: 7/10 Ballantyne and Swanston 1978 Rabbit Female 1 846 5 2 Mortality: 0/10

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Beswick et al. 1972 Human 1 0.31 60 2 Ocular, nasal, throat irritation; nausea, chest discomfort, headaches Beswick et al. 1972 Human 1 0.42 60 2 Ocular, nasal, throat irritation; nausea, chest discomfort, headaches Beswick et al. 1972 Human 1 0.56 8 2 Ocular, nasal, throat irritation; nausea, chest discomfort, headaches Beswick et al. 1972 Human 1 0.57 60 2 Ocular, nasal, throat irritation; nausea, chest discomfort, headaches Beswick et al. 1972 Human 1 0.63 60 2 Ocular, nasal, throat irritation; nausea, chest discomfort, headaches Beswick et al. 1972 Human 1 0.7 60 2 Ocular, nasal, throat irritation; nausea, chest discomfort, headaches Beswick et al. 1972 Human 1 0.78 60 2 Ocular, nasal, throat irritation; nausea, chest discomfort, headaches Beswick et al. 1972 Human 1 0.8 60 2 Ocular, nasal, throat irritation; nausea, chest discomfort, headaches Beswick et al. 1972 Human 1 0.84 60 2 Ocular, nasal, throat irritation; nausea, chest discomfort, headaches Beswick et al. 1972 Human 1 2 60 2 Ocular, nasal, throat irritation; nausea, chest discomfort, headaches Beswick et al. 1972 Human 1 2.1 60 2 Ocular, nasal, throat irritation; nausea, chest discomfort, headaches Beswick et al. 1972 Human 1 2.3 60 2 Ocular, nasal, throat irritation; nausea, chest discomfort, headaches Beswick et al. 1972 Human 1 2.3 60 2 Ocular, nasal, throat irritation; nausea, chest discomfort, headaches McNamara et al. 1969 Dog 1 508 36 SL Mortality: 2/4 McNamara et al. 1969 Dog 1 520 45 SL Mortality: 2/4 (Continued) 377

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378 TABLE D-1 Continued Source Species Sex No. Exposures mg/m3 Minutes Category Comments McNamara et al. 1969 Dog 1 612 45 SL Mortality: 2/4 McNamara et al. 1969 Dog 1 649 30 SL Mortality: 1/4 McNamara et al. 1969 Dog 1 797 60 SL Mortality: 3/4 McNamara et al. 1969 Dog 1 833 20 2 Mortality: 0/4 McNamara et al. 1969 Dog 1 899 40 SL Mortality: 2/4 McNamara et al. 1969 Dog 1 909 60 SL Mortality: 2/4 McNamara et al. 1969 Guinea pig 1 400 5 SL Mortality: 1/10 McNamara et al. 1969 Guinea pig 1 400 10 SL Mortality: 2/10 McNamara et al. 1969 Guinea pig 1 400 15 SL Mortality: 4/10 McNamara et al. 1969 Guinea pig 1 400 25 SL Mortality: 7/10 McNamara et al. 1969 Guinea pig 1 400 30 SL Mortality: 7/10 McNamara et al. 1969 Guinea pig 1 500 20 SL Mortality: 3/10 McNamara et al. 1969 Monkey 1 381 45 SL Mortality: 2/4 McNamara et al. 1969 Monkey 1 469 24 SL Mortality: 1/4 McNamara et al. 1969 Monkey 1 612 45 SL Mortality: 1/4 McNamara et al. 1969 Monkey 1 673 30 SL Mortality: 2/4 McNamara et al. 1969 Monkey 1 699 60 SL Mortality: 1/4 McNamara et al. 1969 Monkey 1 941 60 SL Mortality: 3/4 McNamara et al. 1969 Monkey 1 1,057 60 SL Mortality: 2/4 McNamara et al. 1969 Mouse 1 683 60 SL Mortality: 14/20 McNamara et al. 1969 Mouse 1 740 50 SL Mortality: 5/20 McNamara et al. 1969 Mouse 1 800 40 SL Mortality: 5/20 McNamara et al. 1969 Mouse 1 900 30 SL Mortality: 2/20

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McNamara et al. 1969 Mouse 1 1,100 20 SL Mortality: 7/20 McNamara et al. 1969 Mouse 1 1,200 10 2 Mortality: 0/20 McNamara et al. 1969 Rabbit 1 250 40 2 Mortality: 0/4 McNamara et al. 1969 Rabbit 1 250 80 SL Mortality: 3/4 McNamara et al. 1969 Rabbit 1 267 45 2 Mortality: 0/4 McNamara et al. 1969 Rabbit 1 333 90 3 Mortality: 4/4 McNamara et al. 1969 Rabbit 1 500 30 SL Mortality: 1/4 McNamara et al. 1969 Rat 1 454 55 SL Mortality: 5/10 McNamara et al. 1969 Rat 1 500 60 SL Mortality: 2/10 McNamara et al. 1969 Rat 1 500 80 SL Mortality: 6/10 McNamara et al. 1969 Rat 1 500 90 SL Mortality: 8/10 McNamara et al. 1969 Rat 1 543 35 SL Mortality: 2/10 Owens and Punte 1963 Human 1 1.5 90 2 Nasal and ocular irritation, headache Owens and Punte, 1963 Human 1 6 18 2 Intolerable irritation; escape possible Owens and Punte 1963 Human 1 6.7 2 2 Intolerable irritation; escape possible Owens and Punte 1963 Human 1 85 1 2 Intolerable airway and ocular irritation Owens and Punte 1963 Human 1 94 1 2 Intolerable airway and ocular irritation Rengsdorf 1969 Human 1 1 1 2 Intense ocular irritation Rengsdorf 1969 Human 1 0.4 10 2 Intense ocular irritation Rengsdorf 1969 Human 1 0.6 10 2 Intense ocular irritation Rengsdorf 1969 Human 1 0.9 10 2 Intense ocular irritation Rengsdorf 1969 Human 1 1 1 2 Intense ocular irritation Striker et al. 1967 Monkey 1 900 3 2 Pulmonary congestion, emphysema (Continued) 379

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380 TABLE D-1 Continued Source Species Sex No. Exposures mg/m3 Minutes Category Comments Striker et al. 1967 Monkey 1 1,700 5 2 Pulmonary congestion, emphysema Striker et al. 1967 Monkey 1 2,500 32 SL Severe irritation, pulmonary edema, emphysema, mortality (5/8) Striker et al. 1967 Monkey 1 2,850 10 2 Pulmonary congestion, emphysema, ocular/respiratory irritation For category: 0 = no effect, 1 = discomfort, 2 = disabling, SL = some lethality, 3 = lethal