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Assessment of Exposure-Response Functions for Rocket-Emission Toxicants Appendix E ACUTE TOXICITY OF NITROGEN DIOXIDE BACKGROUND INFORMATION HUMAN and animal data indicate that exposure to nitrogen dioxide (NO2) can produce a variety of toxicological responses of varying degrees of severity depending on the concentration and duration of exposure and on the sensitivity of the population being exposed. Because NO2 is a gas, the primary route of exposure is via inhalation, making the lung the primary target organ; however, extrapulmonary effects also have been reported. There have been numerous reviews on the toxicity of NO2 (NRC 1977; WHO 1977; EPA 1982, 1993). Most have focused on the health effects associated with exposures to low concentrations of NO2, such as those that might occur in the environment or in the workplace. Relatively few studies focused on toxicological responses following shortterm exposures to high concentrations of NO2. PHYSICAL AND CHEMICAL PROPERTIES CAS No.: 10102-44-0 Molecular weight: 46.0 Specific gravity: 1.448 at 20° Boiling point: 21.15°C Melting point: -9.3°C Freezing point: 15°F
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Assessment of Exposure-Response Functions for Rocket-Emission Toxicants Vapor pressure: 720 mm Hg at 20°C Vapor density: 1.58 (air = 1) Flash point: Not applicable Explosive limit: Not applicable Solubility: Soluble in concentrated nitric and sulfuric acids; decomposes in water; and nitric acid. Color: Reddish brown gas Conversion factor: 1 ppm = 1.88 mg/m3 at 20°C 1 mg/m3 = 0.53 ppm at 20°C SOURCES AND OCCURRENCE In the ambient atmosphere, the major sources of NO2 are the combustion of fossil fuels and motor-vehicle emissions. Indoor sources include such appliances as gas stoves, water heaters, and kerosene space heaters. In the workplace, exposures to NO2 have been reported in such occupations as electroplating, acetylene welding, agriculture, space exploration, detonation of explosives, certain military activities, and burning of nitrogen-containing propellants (Mohsenin 1994). In such situations, exposure concentrations can be very high. For example, in armored vehicles during live-fire tests, peak concentrations of NO2 have been measured at over 2,000 parts per million (ppm). That decreases to about 500 ppm after 1 min and decreases to about 20 ppm within 5 min (Mayorga 1994). Of concern to the Air Force is the presence of NOx/HNO3 emissions from rockets that use liquid propellants composed of nitrogen-based compounds. For normal launches, the nitrogen-associated emissions at ground level are negligible. However, in the case of a catastrophic abort, large quantities of nitrogen tetroxide can be released. That gas is rapidly converted to NO2 and HNO3, possibly resulting in production of quantities of NOx/HNO3 as high as 200,000 lb (see Appendix A). PHARMACOKINETICS AND METABOLISM When inhaled, NO2 reacts with the moisture in the respiratory tract, resulting in the formation of nitric acid (HNO3). The nitric acid dissoci-
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Assessment of Exposure-Response Functions for Rocket-Emission Toxicants ates into nitrates and nitrites. At low concentrations, NO2 reacts with moisture in the upper respiratory tract, but as the exposure concentration increases, that reaction penetrates into the lower respiratory tract. An increasing respiratory rate, such as might result from exercise, also results in higher concentrations of NO 2 and its products reaching deeper areas of the lung. Once inhaled, NO2, or its chemical derivatives, can either remain within the lung or be transported to extrapulmonary sites via the bloodstream, where it can react with hemoglobin to form methemoglobin (MetHb). That reaction has important health implications because MetHb is an ineffective oxygen carrier. Transformation of hemoglobin to MetHb can increase health risks to vulnerable individuals who have hypoxia associated with pulmonary and cardiac disease. Increased levels of nitrates have been reported in the blood and urine following exposure to NO2, indicating that NO2 reacts to produce nitrates (EPA 1993). SUMMARY OF TOXICITY INFORMATION In this section, the available data on the toxicity of NO2 to humans and animals are described. EFFECTS IN HUMANS Data on the qualitative and quantitative toxicity of NO2 in humans come from reports of accidental exposures, clinical studies, and epidemiological studies, as described below. Accidental Exposures Accidental exposures to NO2 have been reported in agriculture (1502,000 ppm), mining explosions (500 ppm), space exploration (250 ppm), military activities (500 ppm), and the burning of nitrogen containing propellants (Mohsenin 1994). NO2 has an acrid, ammonia-like odor that is irritating and suffocating to heavily exposed individuals. Such accidental-exposure data, together with relevant animal studies, are most useful in establishing emergency short-term exposure limits.
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Assessment of Exposure-Response Functions for Rocket-Emission Toxicants NO2 can produce a variety of clinical responses, depending on the intensity and duration of the exposure (Lowry and Schuman 1956; Jones et al. 1973). For the most severely exposed, death can occur immediately or be delayed (Mohsenin 1994). Exposure above 150 ppm for 30 min to an hour results in fatal pulmonary edema or asphyxia and can result in rapid death (Lowry and Schuman 1956; NRC 1977; Mayorga 1994). Exposure to NO2 at concentrations of 150-300 ppm can result in bronchiolitis fibrosa obliterans accompanied by restrictive and obstructive ventilatory defects that might lead to death in 2 to 3 weeks (Lowry and Schuman 1956; NRC 1977; Mayorga 1994). Such exposures would likely produce permanent injury in those surviving the exposure. The LC50 (the lethal concentration for 50% of those exposed) for a 1-hr exposure for humans has been estimated to be 174 ppm (Book 1982). Four farmers who entered a freshly filled silo were exposed to high concentrations of NO2, estimated to range from 200 to 4,000 ppm. Two of the individuals died, and the others experienced immediate cough, dyspnea, and fever, which disappeared after several days but reappeared after about 3 weeks (Lowry and Schuman 1956; EPA 1982). Information on lethality from accidental exposures to NO2 is summarized in Table E-1A. At lower exposure concentrations, a variety of nonlethal effects have been observed (see Table E-1B). From 50 to 100 ppm for a 30-min exposure, pulmonary edema and bronchiolitis with focal pneumonitis are likely to develop and last from 6 to 8 weeks; recovery is often spontaneous. Individuals exposed for 30 min at concentrations between 25 and 75 ppm might develop bronchial pneumonia, acute bronchitis, dyspnea, cyanosis, chess pain, rales, headaches, eye irritation, a dry nonproductive cough, and vomiting. Such effects usually are resolved in hours but sometimes are followed by a relapse with shortness of breath, cough, cyanosis, and fever. In addition to its effect on the lung, NO2 can transform hemoglobin to MetHb (Lowry and Schuman 1956; Grayson 1956; Stern 1968; Milne 1969; EPA 1993). Welders exposed to NO2 at 3.9 to 5.4 ppm exhibited 2.3% to 2.6% MetHb in their blood (Patty 1963). In accidental exposures, accurate measurement of exposure concentrations are generally not available. However, during a manned space-flight, three astronauts were exposed to NO2 at concentrations reported to be 250 ppm for about 5 min; the peak was at 750 ppm (Hatton et al. 1977; Table E-1B). They reported immediate breathing difficulties that
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Assessment of Exposure-Response Functions for Rocket-Emission Toxicants TABLE E-1A Summary of NO2 Toxicity in Humans: Mortality from Accidental Exposures Condition Expose Duration Expose Concentration ppm Effect Concentration, ppm End Points References Healthy Minutes 200-400 — 2/4 died Lowry and Schuman 1956 Healthy 30 min >500 >500 Death in less than 2 d due to pulmonary edema Lowry and Schuman 1956; Grayson 1956 >300-400 >300 Fatal edema, bronchopneumonia Lowry and Schuman 1956; Grayson 1956 >150-200 >150 Bronchoiolitis fibrosa obliterans with death in 3-5 weeks Lowry and Schuman 1956; Grayson 1956 50-100 50 Bronciolitis and focal pneumonia with spontaneous recovery Lowry and Schuman 1956; Grayson 1956 Healthy 1 hr 174 — LC50 Book 1982 Table E-1B Summary of NO2 Toxicity to Humans: Nonlethal Effects from Accidental Exposure Condition Exposure Duration Exposure Concentration, ppm Effect Concentration, ppm End Points References Healthy 5 min 250 with peaks to 750 250 with peaks to 750 Chemical pneumonitis, 4.2 increase in MetHb Hatton et al. 1977 Healthy (welders) Daily 3.9-5.4 3.9-5.4 2.3% and 2.6 MetH in the blood Patty 1963 Abbreviation: MetHb, methemoglobin
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Assessment of Exposure-Response Functions for Rocket-Emission Toxicants became more severe within the first 24 hr, and chest radiographs suggested that they suffered diffuse chemical pneumonitis. The MetHb level also increased (4.2%). Several days later, the individuals became asymptomatic (Hatton et al. 1977). Because the exposure was not lethal and recovery was rapid, the exposure concentrations of NO2 might have been overestimated. Human Clinical Studies Human clinical studies of NO2 exposure have been conducted using healthy subjects and volunteer patients with existing pulmonary disease. Although such controlled exposures offer the best data to directly relate cause and effect in humans, few such studies have been conducted. Because the safety of volunteer subjects is of paramount importance, high exposure concentrations cannot be used, and only a few nonevasive end points usually are measured. Normal Subjects Some significant responses, which could be attributed to inhalation of NO2, have been reported at concentrations of more than 1.0 ppm in normal subjects, as described below. Sensory effects. Concentrations of 13.0 ppm or more resulted in complaints of eye and nasal irritation (Stern 1968). Humans can detect the odor of NO2 at low concentrations. At 0.12 ppm, 3 of 9 subjects perceived the odor immediately, and 8 of 13 detected concentrations of 0.22 ppm (Henschler et al. 1960). At a higher concentration (0.42 ppm), 8 of 8 subjects recognized the odor (Henschler et al. 1960). Feldman (1974) reported that 26 of 28 subjects had a perception of NO2 odor at concentrations of 0.11 ppm. Bylin et al. (1985) reported an odor threshold of 0.04 ppm for healthy subjects and 0.08 ppm for asthmatic subjects. However, in another study, exposed subjects were unable to detect the odor at 0.1 ppm (Hazucha et al. 1983). A 5-min exposure to NO2 at 25 ppm caused slight-to-moderate nasal discomfort in 5 of 7 volunteers and chest pain in 3 of the 7 (Meldrum 1992). Threshold values for impairment of dark adaptation was reported to be 0.07 ppm after 5 min inhalation of NO2 by mouth or after 25 min inhalation through the nose only (4 of 4 subjects) (Shalamberidze 1967). However, Bondareva (1963) found no evidence of impairment of dark adaptation. Sensory effects in humans exposed to NO2 for a 0.5 hr or less are summarized in Table E1c.
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Assessment of Exposure-Response Functions for Rocket-Emission Toxicants TABLE E-1c Summary of NO2 Toxicity in Humans: Sensory Effects Condition Exposure Duration Exposure Concentration, ppm Effect Concentration, ppm End Points References Olfactory Healthy Minutes ≥13 ≥13 Complaints of eye and nasal irritation Stern 1968 Healthy Immediate 0.42 0.42 Perception of odor (8/8 Henschler et al. 1960 0.22 0.22 Perception of odor (8/13) 0.12 0.12 Perception of odor (3/9) Healthy Immediate 0.11 0.11 Perception of odor (26/28) Feldman 1974 Healthy Immediate 0.04 0.04 Odor threshold for normal and asthmatic Bylin et al. 1985 0.08 0.08 subjects Healthy Immediate 0.1 — Odor not detected Hazucha et al. 1983 Healthy 5 min 25.0 25.0 Slight nasal discomfort (5/7) and chest pain (3/7) Meldrum 1992 Visual Healthy 5 min, 25 min 0.07 0.07 Impaired dark adaptation Shalamberidze 1967
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Assessment of Exposure-Response Functions for Rocket-Emission Toxicants Effects on lung function. von Nieding and Wagner (1977) and von Nieding et al. (1979) reported that healthy subjects exposed to NO2 for 2 hr at a concentration of 5.0 ppm exhibited increased airway resistance and impaired oxygen exchange in the lung. They also reported a decrease in carbon dioxide diffusion capacity following a 15-min exposure at 5.0 ppm. Other investigators measured increases in airway resistance following a 10-min exposure at 0.7 to 2.0 ppm or at 4 to 5 ppm (Suzuki and Ishikawa 1965; Abe 1967). However, Linn et al. (1985b) and Mohsenin (1988) failed to find any changes in airway resistance or spirometry at concentrations of 4.0 ppm for 75 min or 2.0 ppm for 2 hr. Another investigator found increases in airway resistance in some subjects after a 10- to 120-min exposure to NO2 at 7.0 ppm, but other individuals tolerated 16 ppm without any such effect (Yokoyama 1972). A 10-min exposure at 4 to 5 ppm resulted in a 40% decrease in lung compliance 30 min after exposure ended (Abe 1967). Healthy subjects exposed at 2.5 and 7.5 ppm for 2 hr had increased airway resistance, but 1.0 ppm did not elicit any such effect (Beil and Ulmer 1976). Below 1.0 ppm, short-term exposures (2 hr or less) do not appear to cause adverse effects in healthy subjects, at least as indicated by traditional measurement of pulmonary function (Kagawa and Tsuru 1979; Kerr et al. 1979; Toyama et al. 1981; Hazucha et al. 1982; Bylin et al. 1985; Koenig et al. 1985, 1987, 1988; Kagawa 1986; Adams et al. 1987; Drechsler-Parks 1987; Mohsenin 1988; Samet and Utell 1990; Kim et al. 1991). Some investigators reported subtle effects, but those findings are rare and do not reveal any consistent pattern of response (Kulle 1982; Rehn et al. 1982; EPA 1993). Physiological changes in airway responsiveness to NO2 have been studied using a variety of stimuli to challenge the airways. With an acetylcholine challenge, a 2-hr exposure to NO2 at 7.5 ppm, but not at 5.0, 2.5, or 1.0 ppm, resulted in an increase in airway responsiveness to NO 2 (Beil and Ulmer 1976). However, Mohsenin (1988) reported increased airway reactivity to methacholine following a 1-hr exposure to NO 2 at 2.0 ppm. Table E-1D summarizes the data from clinical studies of human lung function following exposure to NO2 for 2 hr or less. Lung biochemical measures in BAL fluid — Markers of pulmonary effects. A number of studies examined the bronchoalveolar lavage (BAL) fluid from humans in an attempt to identify cellular and biochemical responses to NO 2 exposure. No significant changes occurred in the levels of total protein, albumin, or α-2-macroglobulin in BAL fluid taken from
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Assessment of Exposure-Response Functions for Rocket-Emission Toxicants healthy volunteers exposed for 3 hr at 0.05 ppm, including three 15-min peak exposures at 2.0 ppm, or exposed for 3 hr continuously at 0.6 or 1.5 ppm without peaks (Frampton et al. 1989; Utell et al. 1991). Individuals exposed to NO2 at 3 to 4 ppm for 3 hr had a decrease in activity of α-1-protease inhibitor. This inhibitor is important in protecting the lung from proteolytic damage. Mohsenin and Gee (1987) and Mohsenin (1991) suggested that such a reduction would be most significant in individuals with α-1-antitrypsin deficiency. Table E-1E summarizes the data on BAL-fluid markers of pulmonary effects in humans exposed to NO2 for 2 hr or less. Host defense mechanisms. The BAL fluid isolated from exercising individuals exposed to NO2 at 2.0 ppm for 240 min showed an increase in polymorphonuclear neutrophils (PMNs) and a decrease in the phagocytic activity of alveolar macrophages (Devlin et al. 1992). However, Sandstroem et al. (1990) exposed exercising individuals to NO2 at 4.0 ppm for 20 min on alternate days for 12 days and found enhanced phagocytic activity, a reduction in total cell count, and a decrease in number of mast cells, T and B lymphocytes, and natural killer cells in BAL fluid 24 hr post-exposure. A simple 20-min exposure at 2.25, 4.0, and 5.5 ppm resulted in a different response. The number of mast cells in BAL fluid increased at all exposure concentrations and the number of lymphocytes increased at 4.0 and 5.5 ppm 24 hr post-exposure (Sandstroem et al. 1989). Frampton et al. (1989) exposed humans to NO2 for 3 hr at 0.6 ppm and reported a reduced ability of macrophages to inactivate the influenza virus. Because of the effects observed on the alveolar macrophages, other studies have looked for possible consequences of those macrophage changes with other end points, such as increases in respiratory infections and decreases in pulmonary clearance. However, human data examining the effects of NO2 on normal pulmonary clearance are inconclusive. Although the clearance of soot particles was significantly slower following acute exposure at 5.0 ppm (Schlipköter and Brockhaus 1963), a later study by Rehn et al. (1982) failed to find any significant changes in clearance of radiolabeled Teflon aerosols following 1 hr exposures to NO2 at 0.3 or 1.0 ppm. Table E-1F summarizes the data on the effects of NO2 exposure for 3 hr or less on pulmonary defenses against infection in humans. Extrapulmonary effects. Extrapulmonary effects have been reported in humans following NO2 exposure. Chaney et al. (1981) observed increases in blood glutathione levels in exercising humans exposed at
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Assessment of Exposure-Response Functions for Rocket-Emission Toxicants TABLE E-1D Summary of NO2 Toxicity in Healthy Humans: Pulmonary Function Condition Exposure Duration Exposure Concentration ppm Effect Concentration, ppm End Points References Healthy 2 hr 5.0 5.0 Increased airway resistance; impaired oxygen exchange von Nieding and, Wagner 1977; vonNieding et al. 1979 Healthy 2 hr 1.0, 2.5, 7.5 ≥2.5 Increased airway resistance Beil and Ulmer 1976 Healthy 2 hr 1.0, 2.5, 5.0, 7.5 7.5 Increased airway responsiveness to acetylcholine Beil and Ulmer 1976 Healthy 75 min 4.0 — No change in airway resistance Linn et al. 1985b Healthy 2 hr 2.0 — No change in airway resistance Mohsenin 1988 Healthy 1 hr 2.0 2.0 Increased airway responsiveness to methacholine Mohsenin 1988 Healthy 10 min 0.7-2.0 0.7 Increased airway resistance; effect increased with dose Suzuki and Ishikawa 1965 Healthy 15 min 5.0 5.0 Decreased CO diffusion capacity von Nieding and Wagner 1977, von Nieding et al. 1979 Healthy 10-120 min 7.0, 16.0 7.0 7.0 Increased airway resistance in some subjects at 7.0 ppm, but some had no effect at 16.0 ppm Yokoyama 1972 Healthy 10 min 4-5 4-5 40% decrease in lung compliance and increase in airway resistance Abe 1967
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Assessment of Exposure-Response Functions for Rocket-Emission Toxicants Healthy ≤2hr <1 — No measured Adverse effects in Healthy subjects Kagawa and Tsuru 1979; Kerr et al. 1979; Toyama et al. 1981; Hazucha et al. 1982; Bylin et al. 1985, 1987, 1988; Kagawa 1986, Adams et al. 1987; Drechsler-Parks 1987; Mohsenin 1988; Samet and Utell 1990, Kim et al. 1991 TABLE E-1E Summary of NO2 Toxicity in Humans: Lung Biochemical Measures in BAL Fluid Condition Exposure Duration Exposure Concentration, ppm Effect Concentration, ppm End Points References Healthy 3 hr 0.05 with three 15-min peaks at 2.0 or at 0.6 or 1.5 ppm without peaks — No change in BAL fluid composition Utell et al. 1991 Frampton et al. 1989 Healthy 3 hr 3-4 3-4 Decrease in protease inhibitor Mohsenin and Gee 1987; Moshenin 1991 Abbreviations: BAL, bronchoalveolar lavage; MetHb, methemoglobin.
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Assessment of Exposure-Response Functions for Rocket-Emission Toxicants Experiments using the same exposure protocols on mice and rats as humans would be useful to identify the degree of difference in sensitivity to NO2 between laboratory animals and sensitive and healthy humans. To evaluate the potential for additive effects among the rocket-emission toxicants, exposure of healthy humans to various combinations of HCl, NO2, and HNO3 at concentrations expected to occur following a catastrophic abort might be useful. To be safe, the tests could be limited to exposure concentrations expected to produce mild effects only. Controlled human exposures at high NO2 exposure concentrations to determine the sensitivity of individuals with cardiopulmonary impairments and that of healthy individuals are not possible. Thus, to fill this data gap, an animal model that might be expected to react similarly to sensitive humans would be needed. The same animal model probably could be used to investigate this data gap for the other rocket-emission toxicants examined in this report. REFERENCES Abe, M. 1967. Effects of mixed NO2-SO2 gas on human pulmonary functions: Effects of air pollution on the human body. Bull. Tokyo Med. Dent. Univ. 14:415-433. Abraham, W.M., M. Welker, W. Oliver, Jr., M. Mingle, A.J. Januszkiewicz, A. Wanner, and M.A. Sackner. 1980. Cardiopulmonary effects of short-term nitrogen dioxide exposure in conscious sheep. Environ. Res. 22:61-72. ACGIH (American Conference of Governmental Industrial Hygienists). 1991. Documentation of the Threshold Limit Values and Biological Exposure Indices, 6th Ed. American Conference of Governmental Industrial Hygienists, Cincinnati, Ohio. Acton, J.D., and Q.N. Myrvik. 1972. Nitrogen dioxide effects on alveolar macrophages. Arch. Environ. Health 24:48-52.
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Assessment of Exposure-Response Functions for Rocket-Emission Toxicants Adams, W.C., K.A. Brookes, and E.S. Schelegle. 1987. Effects of NO2 alone and in combination with 03 on young men and women. J. Appl. Physiol. 62:1698-1704. Ahmed, T., R. Dougherty, and M.A. Sackner. 1983a. Effect of NO2 Exposure on Specific Bronchial Reactivity in Subjects with Allergic Bronchial Asthma. Final Report. Contract CR-83/07/BI. General Motors Research Laboratories, Warren, Mich. Ahmed, T., R. Dougherty, and M.A. Sackner. 1983b. Effect of 0.1 ppm NO2 on Pulmonary Functions and Non-specific Bronchial Reactivity of Normals and Asthmatics. Final Report. Contract CR-83/11/ BI. General Motors Research Laboratories, Warren, Mich. AIHA (American Industrial Hygiene Association). 1964. Emergency Exposure Limits. Am. Ind. Hyg. Assoc. J. 25:578-586. ATS (American Thoracic Society). 1996. Health effects of outdoor air pollution. Part 2. Am. J. Respir. Crit. Care Med. 153:477-498. Avol, E.L., W.S. Linn, R.C. Peng, G. Valencia, D. Little, and J.D. Hackney. 1988. Laboratory study of asthmatic volunteers exposed to nitrogen dioxide and to ambient air pollution. Am. Ind. Hyg. Assoc. J. 49:143-149. Bauer, M.A., M.J. Utell, P.E. Morrow, D.M. Speers, and F.R. Gibb. 1986. Inhalation of 0.30 ppm nitrogen dioxide potentiates exercise-induced bronchospasm in asthmatics. Am. Rev. Respir. Dis. 134:1203-1208. Beil, M., and W.T. Ulmer. 1976. Effect of NO2 in workroom concentrations on respiratory mechanics and bronchial susceptibility to acetylcholine in normal persons [in German]. Int. Arch. Occup. Environ. Health 38:31-44. Bondareva, E.N. 1963. Hygienic evaluation of low concentrations of nitrogen oxides present in acid. Pp. 98-101 in USSR Literature on Air Pollution and Related Occupational Diseases. A Survey, Vol. 8, B.S. Levine, ed. Publ. TT63-11570. U.S. Public Health Service, Washington, D.C. Book, S.A. 1982. Scaling toxicity from laboratory animals to people: An example with nitrogen dioxide. J. Toxicol. Environ. Health 9:719-725. Bylin, G., T. Lindvall, T. Rehn, and B. Sundin. 1985. Effects of short-term exposure to ambient nitrogen dioxide concentrations on human bronchial reactivity and lung function. Eur. J. Respir. Dis. 66:205-217. 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. Case, G.D., J.S. Dixon, and J.C. Schooley. 1979. Interactions of blood metalloproteins with nitrogen oxides and oxidant air pollutants. Environ. Res. 20:43-65. Chaney, S., W. Blomquist, P. DeWitt, and K. Muller. 1981. Biochemical changes in humans upon exposure to nitrogen dioxide while at rest. Arch. Environ. Health 36:53-58. Davis, J.K., M.K. Davidson, T.R. Schoeb, and J.R. Lindsey. 1992. Decreased
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Assessment of Exposure-Response Functions for Rocket-Emission Toxicants intrapulmonary killing of Mycoplasma pulmonis after short-term exposure to NO2 is associated with damaged alveolar macrophages. Am. Rev. Respir. Dis. 145(2 Part 1):406-411. Devlin, R. D. Horstman, S. Becker, T. Gerrity, M. Madden, and H. Koren. 1992. Inflammatory response in humans exposed to 2.0 ppm NO 2 [abstract]. Am. Rev. Respir. Dis. 145:A456. Dowell, A.R., K.H. Kilburn, and P.C. Pratt. 1971. Short-term exposure to nitrogen dioxide: Effects on pulmonary ultrastructure, compliance, and the surfactant system. Arch. Intern. Med. 128:74-80. Drechsler-Parks, D.M. 1987. Effect of Nitrogen Dioxide, Ozone, and Peroxyacetyl Nitrate on Metabolic and Pulmonary Function . Res. Rep. 6. Cambridge, Mass.: Health Effects Institute. Ehrlich, R. 1975. Interaction Between NO2 Exposure and Respiratory Infection. Scientific Seminar on Automotive Pollutants. EPA/600/9-75/003. U.S. Environmental Protection Agency, Office of Research and Development, Washington, D.C. Ehrlich, R. 1980. Interaction between environmental pollutants and respiratory infections. Environ. Health Perspect. 35:89-100. Elsayed, N.M., S. Smith, D. Ebel, N.V. Gorbounov, M.J. Topper, V.E. Eagon, and M.A. Mayorga. 1995. Pulmonary Alterations after Brief, Nose-Only Exposure of Rats to High Levels of Nitrogen Dioxide (Abstract 19-P-6). International Congress of Toxicology VII, July 2-6. EPA (U.S. Environmental Protection Agency). 1971. National primary and secondary ambient air quality standards. Fed. Regist. 36(April 30):8186-8201. EPA (U.S. Environmental Protection Agency). 1982. Air Quality Criteria for Oxides of Nitrogen. EPA/600/8-82-026. U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Research Triangle Park, N.C. Available from NTIS, Springfield, Va., Doc. No. PB83-131011. EPA (U.S. Environmental Protection Agency). 1987. Technical Guidance for Hazards Analysis: Emergency Planning for Extremely Hazardous Substances . Prepared in cooperation with the Federal Emergency Management Agency, Washington, D.C., and U.S. Department of Transportation, Washington, D.C. U.S. Environmental Protection Agency, Office of Solid Waste and Emergency Response, Washington, D.C. Available from NTIS, Springfield, Va., Doc. No. PB93-206910. EPA (U.S. Environmental Protection Agency). 1993. Air Quality Criteria for Oxides of Nitrogen, Vol. 3. EPA/600/8-91/049cF. U.S. Environmental Protection Agency, Office of Research and Development, Washington, D.C. Feldman, Y.G. 1974. The combined action on a human body of a mixture of the main components of motor vehicle exhaust gases (carbon monoxide, nitrogen dioxide, formaldehyde, and hexane) [in Russian]. Gig. Sanit. 10:7-10. Florey, C. du V., R.J.W. Melia, S. Chinn, B.D. Goldstein, A.G.F. Brooks, H.H.
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Representative terms from entire chapter: