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5
Graphite Smoke

Background Information

Military Applications

The Military uses graphite flakes to block electromagnetic waves that the enemy might detect and use to target troops in the field. Graphite flakes provide the military with protection beyond the visual and infrared spectrums (Driver 1993).

The military releases the graphite flakes into the environment from ground-based systems that mechanically disperse bulk powders into the atmosphere (Lundy and Eaton 1994). The powder is used directly or compressed into small pellets to improve handling and delivery to the air ejector of smoke generators. Because the aerodynamic sizes of air-dispersed flakes are small (<20 micrometers (µm)), there is little near-source surface deposition of particles. Near-source deposition can be substantial if the air ejector is oriented at the ground or nearly parallel to the ground. The long-range downwind patterns resulting from dispersion and deposition depend on local meteorological conditions.

Physical and Chemical Properties

Graphite is a soft, crystalline form of carbon that occurs naturally and is also synthesized for various uses (ACGIH 1991). Natural graphite usually is associated with such impurities as quartz, mica, iron oxide, and granite (Hanoa 1983; Taylor 1985). Synthetic graphite is produced by



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--> 5 Graphite Smoke Background Information Military Applications The Military uses graphite flakes to block electromagnetic waves that the enemy might detect and use to target troops in the field. Graphite flakes provide the military with protection beyond the visual and infrared spectrums (Driver 1993). The military releases the graphite flakes into the environment from ground-based systems that mechanically disperse bulk powders into the atmosphere (Lundy and Eaton 1994). The powder is used directly or compressed into small pellets to improve handling and delivery to the air ejector of smoke generators. Because the aerodynamic sizes of air-dispersed flakes are small (<20 micrometers (µm)), there is little near-source surface deposition of particles. Near-source deposition can be substantial if the air ejector is oriented at the ground or nearly parallel to the ground. The long-range downwind patterns resulting from dispersion and deposition depend on local meteorological conditions. Physical and Chemical Properties Graphite is a soft, crystalline form of carbon that occurs naturally and is also synthesized for various uses (ACGIH 1991). Natural graphite usually is associated with such impurities as quartz, mica, iron oxide, and granite (Hanoa 1983; Taylor 1985). Synthetic graphite is produced by

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--> heating a mixture of petroleum coke or coal, a binder (usually coal tar pitch), a petroleum-based oil to facilitate extrusion, and in some cases, anthracite coal (Watson et al. 1959; Zahorski 1960; Zahorski et al. 1975; Taylor 1985; Petsonk et al. 1988). The characteristics of the synthetic graphite depend on many factors, including the quality of the coke and binder, the degree of orientation of the particles during extrusion, and the temperature and time of processing (Taylor 1985). Only synthetic graphite is used as an obscurant by the U.S. military. When it was classified, it was called EA 5768. The military generates the graphite smokes from one of two synthetic graphite powders, Micro-260 (manufactured by Asbury Graphite Mills, Inc.) and KS-2 (manufactured by Dixon Ticonderoga Company). Those graphites are composed of platelets or flakes of various sizes. In a recent study of the particle size of graphite from an XM56 generator, the mass median diameters for Types 1 and 2 reprocessed infrared material were 3–5 µm and 47–106 µm, respectively (Guelta et al. 1993). The chemical composition of the bulk powders is predominantly carbon, with trace impurities totaling <1% of the total weight. The trace impurities include small quantities of silica, aluminum, iron, calcium, titanium, and magnesium (Lundy and Eaton 1994). Toxicokinetics No data on the toxicokinetics of graphite were found. It can be assumed, as discussed by Driver et al. (1993), that inhaled particles, deposited in the deep lung, can be removed through phagocytosis by macrophages or by direct movement of the particles into the blood or the lymphatic tissues. Toxicity Summary The term ''graphite'' is used throughout this chapter to refer to graphite in the form of platelets, flakes, or dusts. The different forms do not appear to be associated with different toxicities. A review of the potential environmental and health effects of graphite flakes is available (Driver et al. 1993).

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--> Effects in Humans Graphite pneumoconiosis is a well-recognized pulmonary lesion that is found in workers involved in the mining and processing of graphite. Lungs diseased by graphite inhalation manifest characteristic pathological features. In general, they are diffusely discolored, ranging in appearance from gray to black, and are described as resembling "sponges that have been soaked in ink" (Pendergrass et al. 1968). Microscopically, the lungs show a granulomatous reaction with areas of interstitial fibrosis, perifocal emphysema, necrosis, and severe vascular sclerosis (Jaffé 1951; Gaensler et al. 1966). Occasionally, widespread tissue necrosis results in the formation of large cavities that become filled by an oily black liquid (Dunner and Bagnall 1946). Nonasbestos bodies with a black graphite core, superficially resembling the characteristic iron-containing bodies seen after asbestos exposure, are dispersed in the lungs and, occasionally, are found in the sputum (Mazzucchelli et al. 1996). Hanoa (1983) analyzed over 600 cases of graphite pneumoconiosis published in the literature. The author concluded that graphite pneumoconiosis is probably a mixed-dust type of lung reaction in most cases. Although analytically pure graphite cannot be excluded as causing chronic lung lesions, most investigators (Hanoa 1983; Zahorski et al. 1975) believe that it is the silica contamination that contributes to the development of fibrosis. That view is also shared by earlier investigators (Gloyne et al. 1949; Harding and Oliver 1949), although some cases have been described in which pneumoconiosis developed following exposure to synthetic graphite without any substantial silica content (Lister and Wimborne 1972). Two surveys were conducted in 1972 and 1989 in the graphite industry in Sri Lanka (Ranasinha and Uragoda 1972; Uragoda 1989). In 1972, 22.7% of the examined workers had chest x-ray signs suggestive of pneumoconiosis; in 1989, only 3.4% of the workers had such signs. However, the surveys were conducted in two different mines, and the conclusion that improved control measures were solely responsible for the decrease in disease incidence is tentative. Effects in Animals Inhalation Exposures Acute inhalation of graphite elicited only a transient inflammatory reac-

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--> tion in the respiratory tract of experimental animals. Anderson et al. (1989) exposed male Fischer 344 (F344) rats for a single 4-hr period to synthetic graphite (Asbury Micro-266) at 1 to 500 milligrams per cubic meter (mg/m3). An increase in polymorphonuclear leukocytes in the bronchoalveolar lavage (BAL) fluid was observed 24 hr after exposure only in the animals exposed to a graphite concentration of 500 mg/m3. After 7 days, the signs of inflammation had disappeared. Concentrations of 100 mg/m3 or less failed to elicit any inflammatory response. Alveolar macrophages were activated only for 1 day following exposure and only at 500 mg/m3 (Anderson et al. 1989). The acute inhalation toxicity of graphite type 6353 and Microfyne graphite was determined in groups of five male and five female rats exposed for 1 hr at an airborne concentration of 23.7 milligrams per liter (mg/L) or 23,700 mg/m3 (particle diameter < 10 µm). The animals were observed for 2 weeks. Detailed histological or biochemical evaluations were not conducted; no gross signs of toxicity were seen (Manthei et al. 1980). Repeated exposures of experimental animals to graphite appear to produce minimal effects. Thomson et al. (1988) exposed male F344 rats in whole-body chambers to synthetic (Asbury Micro-260, > 1% silica) or natural graphite (Asbury Micro-650, 1.86% silica) at 100 mg/m3 for 4 days, 4 hr per day. Mass median aerodynamic diameters (MMAD) of the particles ranged from 2.2 to 2.4 µm (geometric standard deviation 2.53 to 2.60 µm). Pulmonary function tests conducted 24 hr after exposure revealed a transient decrease in pulmonary resistance in rats exposed to synthetic graphite, although that observation was not considered biologically significant. Analysis of BAL fluid from the lungs of exposed animals 24 hr after exposure showed increased protein content (not statistically significant) and increased activity of alkaline phosphatase and β-glucuronidase for both graphite materials and increased lactate dehydrogenase activity for natural graphite. After 2 weeks, all biochemical changes were reversed. Both graphite materials also produced an increased influx of polymorphonuclear leukocytes into BAL fluid (up to 145% of control values); that change was also reversed after 2 weeks. Pigment in alveolar macrophages and free pigment in the alveoli were found 24 hr after exposure; after 2 weeks, no free pigment was seen. Only minuscule foci of alveolar type II cell hyperplasia were found in the peripheral lung tissue of a few animals. The authors concluded that inhalation of both materials produced minimal adverse effects. Longer exposure durations were studied in another experiment

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--> (Thomson et al. 1987). Male and female F344 rats were exposed to Micro-260. Chamber concentrations were 1, 10, and 100 mg/m3, and exposures lasted for 2 hr per day, 5 days per week, for 2 weeks. MMADs followed by geometric standard deviations of the particles were 3.40 µm (1.90 µm), 2.90 µm (2.19 µm) and 1.78 µm (2.88 µm), respectively. Three days after exposure, increases in BAL-fluid protein and enzyme activity (lactate dehydrogenase, alkaline phosphatase, and ß-glucuronidase) were observed only in the highest-exposure group and were higher than those observed after a single exposure. All changes disappeared 3 months after exposure. Similarly, increased cell content was found in the BAL fluid, most pronounced and significant in the highest-exposure group, and changes diminished with time. There was no evidence that graphite could increase the pulmonary content of hydroxyproline, a biochemical indicator of fibrosis. Hyperplasia of type II alveolar cells, labeled adenomatous hyperplasia, and histiocytosis were seen only in the highest-exposure group. Graphite material persisted in alveolar macrophages for 3 months. Overall, changes induced by the highest graphite concentration (100 mg/m3) were considered mild and slowly reversible. An extensive inhalation study with pure graphite or mixtures of graphite and fog oil was carried out in rats (Aranyi et al. 1992). All exposures were administered for 4 hr per day, 4 days per week. In a 4-week study, the rats were exposed to either graphite alone at 200 mg/m 3, fog oil alone at 500 or 1,000 mg/m3, or a mixture of fog oil and graphite. Particle sizes were 1.82 µm for the graphite and 0.36 to 0.69 µm for the fog-oil. A depression in body weight was found only in animals exposed to the graphite or the graphite and fog-oil mixture. However, the authors did not consider the finding to be toxicologically relevant, mainly because no effects on body weight were seen in a longer study (Aranyi et al. 1992). In the longer study, rats were exposed for 13 weeks to mixtures of fog oil and graphite (Aranyi et al. 1992). The MMAD of the particles ranged from 0.40 to 0.69, µm. The lowest-concentration exposures were fog oil at 250 mg/m3 and graphite at 100 mg/m3 and the highest-concentration exposures were graphite at 200 mg/m3 and fog oil at 1,000 mg/m3. No overt signs of toxicity were observed during exposure; particularly, no differences in body weight were noted. Histopathological changes were found in the lungs of all animals exposed to the aerosol mixtures. The main finding was hyperplasia of the goblet cells in the nasal epithelium. Upon removal from the test chambers, the changes were reversible. The

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--> epithelia of the terminal bronchioles and of the alveoli showed some hyperplasia. The incidence of those changes was 100% in all exposure groups. In a recovery study, Aranyi et al. (1992) found that the changes did not disappear, presumably because of the continued presence of graphite particles in the lung. In addition, pulmonary and mediastinal lymph nodes and lymphoid tissues showed hyperplasia and graphite-containing granulomas. Oral Exposures Graphite type 6353 and Microfyne dissolved in corn oil were not acutely toxic in rats at oral exposures of 5 grams per kilogram (g/kg) of body weight (Manthei et al. 1980). Intratracheal Exposures A suspension containing 100 mg of graphite was instilled intratracheally into rats (Ray et al. 1951). Only a minimal pulmonary-tissue reaction was produced; most of the material disappeared from the lung and only a slight reticulosis occurred in the alveolar tissue. Intraperitoneal Injection Bovet (1952) injected aqueous suspensions of graphite (5 to 10 mg; particle size, 3 and 10 µm) into the peritoneal cavity of mice. After initial foreign-body inflammatory changes, fibrous nodules developed. Dermal Exposures Micro-260 (500 mg suspended in saline) was applied to the clipped skin of rabbits under a gauze pad covered with a polyethylene film (Manthei and Heitkamp 1988). After 24 hr the graphite was removed by gentle washing, and the skin was inspected for signs of irritation. No signs were observed. The test was repeated with graphite dissolved in a slurry of corn oil, and again no signs of skin irritation were observed. The negative findings were confirmed by histopathological examination of

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--> the tested skin areas. Negative results were also reported in a study that examined the skin irritation (24 hr) of graphite type 6353 and Microfyne (Manthei et al. 1980). No signs of toxicity in general and of skin irritation in particular were observed with applied doses of 2 g/kg. Ocular Exposures Micro-260 was instilled into the conjunctival sack of one eye in rabbits, the contralateral eye serving as control (Manthei and Heitkamp 1988). A volume of 0.1 milliliter (mL) was used, corresponding to 12 mg of the test material. The eyes appeared normal 1 hr later, but there were signs that the rabbits had removed the graphite with their forepaws. Four of six rabbits had mild redness of the nictitating membrane after 24 hr; the irritation disappeared after 72 hr. Fluorescein stain did not reveal abrasion or other lesions of the cornea. Graphite type 6353 and Microfyne were deposited in quantities of 100 mg into the conjunctival sac in rabbits (Manthei et al. 1980). The two materials were not found to be eye irritants. Carcinogenic Effects No data are available on the carcinogenicity of graphite. Reproductive and Developmental Effects No data are available on the reproductive and developmental effects of graphite exposure. In Vitro Tests Placke and Fisher (1987) evaluated Micro-260, KS-2, graphite fibers, and nickel-coated graphite fibers together with several other dusts in hamster tracheal-organ cultures. Explants were exposed to the dusts for 1 to 3 weeks. The tissues were examined under the light microscope and scored for metaplastic, dysplastic, and hyperplastic lesions in the mucosa. KS-2 elicited a tissue response thought to represent preneoplastic

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--> changes. The changes were somewhat more pronounced than those produced by the other forms of graphite, but were not as well-defined as those resulting from exposure to crocidolite asbestos or nickel-(Ni) coated graphite. Ni-coated graphite fibers together with brass dust were the most cytotoxic materials, whereas the toxicity of the other graphite materials was the same as the toxicity of carbon black or glass beads. The cytotoxicity of graphite was examined in alveolar macrophages harvested from rat lungs (Anderson et al. 1987). For graphite, the 4-hr lethal concentration for 50% of the test animals (LC50) was found to be 428/µg/mL higher than the LC50 for titanium dioxide, carbon, aluminum, or slate aluminum (from 115 to 285/µg/mL). Graphite type 6353 and Microfyne were evaluated in the Ames mutagenicity test, using five tester strains, with and without an activating system (Manthei et al. 1980). No mutagenic activity was observed. Summary of Toxicity Data Table 5-1 summarizes the studies of nonlethal effects of inhalation exposure to graphite particles of the type used by the military as an obscurant. The information on the noncarcinogenic effects are summarized here. In humans chronically exposed to graphite, graphite pneumoconiosis might develop. The condition is characterized by a granulomatous reaction, interstitial fibrosis, and vascular sclerosis. However, these changes are believed to be due to impurities, particularly silica, in the graphite dust that is mined (Gloyne et al. 1949; Harding and Oliver 1949; Hanoa 1983). Acute and subchronic exposure (up to 13 weeks) studies in animals involving inhalation exposure to graphite, with or without the concomitant presence of fog oil, showed only minimal inflammatory reactions in the respiratory tract. The inflammation was fully reversible most of the time. However, if graphite particles persist in the lung, epithelia of the terminal bronchioles and alveoli show signs of hyperplasia, and graphite-containing granulomas are found in lymphoid tissue. In vitro, graphite has minimal cytotoxicity and no mutagenic activity. Previous Recommended Exposure Limits The American Conference of Governmental Industrial Hygienists (ACGIH) has established a Threshold Limit Value time-weighted average

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--> TABLE 5-1 Summary of Nonlethal Effects of Exposure to Graphite Species Exposure Frequency and Duration NOAEL(mg/m3) LOAEL(mg/m3) End Point and Comments Reference Rat, Fischer 344 (Micro-266) 4 hr, 1 d 100 500 Measured number of pmn leukocytes in BAL fluid and alveolar macrophage activation, transient Anderson et al. 1989 Rat, Sprague-Dawley (type 6353 Microfyne) 1 hr, 1 d 23,700 — No signs of toxicity up to 2 wk after exposure Manthei et al.1980 Rat, Fischer 344 (Micro-260 and-650) 4 hr/d, 4 d — 100 Minimal adverse effects (transient biochemical changes in BAL fluid analysis) Thomson et al. 1988 Rat, Fischer 344 (Micro-260) 2hr/d, 5 d/wk, 2 wk — 100 Mild reversible changes in BAL fluid analysis Thomson et al.1990 Rat, Fischer 344 (graphite powder Al) 4 hr/d, 4 d/wk, 4 wk — 200 Decreased body weight Aranyi et al. 1992 Rat, Fischer 344 (graphite powder Al) 4 hr/d, 4 d/w, 13 wk — 100 250 (fog oil) Epithelial hyperplasia in terminal bronchioles and alveoli, not reversible Aranyi et al. 1992 Abbreviations: NOAEL, no-observed-adverse-effect level; LOAEL, lowest-observed-adverse-effect level; pmn, polymorphonuclear; BAL, bronchoalveolar lavage.

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--> (TLV-TWA) of 2 mg/m3 for graphite as a respirable dust (all forms except graphite fibers) (ACGIH 1991). The Occupational Safety and Health Administration (OSHA) established a permissible exposure limit (PEL)-TWA of 3.0 mg/m3 for natural graphite with the respirable fraction containing less than 1% quartz. The PEL-TWAs for synthetic graphite are 15 mg/m3 for total particulate material and 5 mg/m3 for the respirable fraction (U.S. Department of Labor 1997). The National Institute for Occupational Safety and Health (NIOSH) established a recommended exposure limit (REL)-TWA of 2.5 mg/m3 for respirable dust from natural graphite (NIOSH 1996). NIOSH has not established a REL-TWA for synthetic graphite. Subcommittee Evaluation and Recommendations Military Exposures Emergency Exposure Guidance Levels (EEGLs) No acute toxicity data are available that would indicate adverse health effects caused by graphite in humans. In acute inhalation studies with rats, no deaths occurred even at the highest concentrations used. A 4-hr exposure to synthetic graphite (Micro-260) at 100 mg/m 3 did not produce signs of acute inflammation (Anderson et al. 1989). The extensive inhalation data base for several other poorly soluble, low-toxicity particles (e.g., talc, titanium dioxide, carbon black; see Chapter 4 for a more detailed discussion) is also relevant to recommending emergency exposure limits for graphite. When doses of poorly soluble, low-toxicity particles are >1–2 mg/g of lung in the rat, extensive evidence shows that macrophage-mediated particle-clearance mechanisms are overloaded. That response results in an accumulation of particles in the lung (Morrow et al. 1991; Oberdorster 1994). Associated with the overload of particle clearance by low-toxicity particles in the rat is the development of pulmonary inflammation, fibrosis, and epithelial hyperplasia; inhalation exposures resulting in lung burdens below 1-2 mg/g of lung appear to be without adverse effect (Morrow et al. 1991; Oberdorster 1994). Analysis of the relation between lung-particle dose and particle-clearance overload indicates that clearance overload is more closely related to the particle volume than to the mass of particulate material in the lung

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--> (Morrow 1988; Morrow et al. 1991). In this respect, for graphite, with a density of 2.2 g/cm3, a lung mass burden of approximately >2 mg/g of lung would be expected to cause particle-clearance overload and adverse lung effects (Morrow et al. 1991). The approach the subcommittee used to recommend EEGLs for graphite was to estimate the maximal acute exposure concentration resulting in a lung-particle dose below that associated with impairment of alveolar clearance and adverse lung effects. Extrapolating from the data base on long-term inhalation studies using low-toxicity, poorly-soluble particles in rats, a lung dose of graphite at <2 mg/g of lung (incorporates a correction for the density of graphite) would not be expected to alter alveolar particle clearance and produce adverse effects in the rat lung. Because the lung dose associated with overload clearance is derived from long-term inhalation studies, the subcommittee considered the possibility that the response could be greater to a dose delivered by acute exposure (high-dose rate) than by chronic exposures. To address the potential for greater responses due to the high-dose rare in acute inhalation exposures, the subcommittee reduced the dose of 2 mg/g of lung by a factor of 10, and estimated the maximal 15-min, 1-hr, and 6-hr exposure concentrations that would result in a lung dose of <0.2 mg/g of lung. Making reasonable assumptions for minute volume (43 L/min, heavy work activity; Diem and Lentner 1970), deep-lung particle deposition (35% of respirable particles; Stahlhofen et al. 1989) and lung weight (1,000 g; Diem and Lentner 1970), the subcommittee calculated that a 15-min exposure to graphite at approximately 880 mg/m3 is the maximal concentration resulting in a deep-lung dose of <0.2 mg/g of lung that would not cause significant adverse effects.1 Support for that calculation can be found in the acute inhalation study in which exposure of rats to graphite at either 500 mg/m3 for 4 hr or 100 mg/m3 for 4 hr per day for 4 days resulted in only transient pulmonary inflammation (Anderson et al. 1989; Thomson et al. 1986). It is estimated that the deep-lung particle burden in the rat studies was approximately 2-2.5 mg/g of lung (assumes a rat minute volume of 200 mL/min and a particle deposition 1   Calculation of 15-min exposure concentration in humans resulting in a lung graphite dose of 0.2 mg/g of lung. Exposure concentration = [(0.2 mg/g of lung)(1,000 g/lung)]/ [(43 L/min)(15 min)(m3/1,000)(0.35)].

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--> of 10%), which is just at or above the dose associated with clearance overload in rats. Also supporting a 15-min EEGL of approximately 880 mg/m3 is the acute inhalation study of Manthei et al. (1980), who reported that a 1-hr exposure of rats to graphite at 23,700 mg/m 3 did not produce any gross signs of toxicity. Extrapolating from the 15-min EEGL, a 1-hr EEGL of 220 mg/m3 and a 6-hr EEGL of 40 mg/m 3 (rounded from 36.6 mg/m3) are recommended. Repeated Exposure Guidance Level (REGL) Because the graphite used by the Army is free of silica and has properties similar to other low-toxicity, poorly soluble particles (e.g., titanium dioxide, talc, and carbon black), the subcommittee believes it is reasonable to recommend a REGL by determining the maximal long-term exposure concentration that would not result in a lung burden that would overload particle-clearance mechanisms (after accounting for the density of graphite). The scientific rationale for this approach is discussed above in the context of recommending EEGLs. Making reasonable assumptions for minute ventilation (22 L/min, moderate work activity; Raabe 1979), the proportion of respirable particles depositing in the deep lung (35%; Stahlhofen et al. 1989), lung weight (1,000 g; Diem and Lentner 1970), and particle-clearance half-time (500 days; Bohning et al. 1982) for humans, the subcommittee estimated that chronic exposure to graphite at 1 mg/m3 would result in a lung burden of <2 mg/g of lung.2 The calculation takes into account sources of uncertainty in lung dosimetry between rodents and humans and, therefore, an additional uncertainty factor extrapolating from animals to humans was not applied. Additionally, the uncertainty factor was reduced to 1 because the rat is a more sensitive species than the human to the effects of poorly soluble particles in the lung. The subcommittee recommends a REGL for graphite of 1 mg/m3 for 8 hr per day, 5 days per week. 2   Calculation of exposure concentration (8 hr per day x 5 days per week) resulting in a lung dose of 2 mg/g of lung. Exposure concentration = [(2 mg/g lung)] ÷ {[(22 L/min)(60 min) (8 h/d)(5 d/7 d)(m3/1,000)(0.35) (lung/1,000 g)] ÷ [ln2/500 d]}

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--> Public Exposures Short-Term Public Emergency Guidance Levels (SPEGL) The general public may be assumed to have a greater range of individual susceptibilities compared with healthy military personnel. The subcommittee applied an uncertainty factor of 10 to take that into account. Accordingly, the 15-min SPEGL is 88 mg/m3, the 1-hr SPEGL is 22 mg/m3, and the 6-hr SPEGL is 4.0 mg/m3. Repeated Public Exposure Guidance Level (RPEGL) The subcommittee recommends that the RPEGL be derived by incorporating an uncertainty factor of 10 into the REGL to account for the potentially greater range of susceptibilities in the general public compared with healthy military personnel. Accordingly, the RPEGL for graphite is 0.1 mg/m3. Summary of Subcommittee Recommendations Table 5-2 summarizes the subcommittee's recommendations for the EEGLs and the REGL for military personnel, and Table 5-3 summarizes the recommendations for the SPEGLs and the RPEGL at the boundary of military facilities. Research Needs According to available data, graphite dusts behaves biologically like dusts with low biological activity both in vivo and in vitro. Those dusts do not produce signs of acute toxicity and might produce signs of chronic lung disease only under conditions of overload (see Chapter 4). The recommendations for EEGLs were derived by calculating exposure concentrations that would not yield sufficient deposited graphite to cause lung overload. The calculations were verified against biological data on rats for which the calculated graphite lung doses were such that conditions of lung overload were expected. In those cases, biological effects, notably inflammation, were observed. Because the biological data forming the basis for that verification are

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--> TABLE 5-2 EEGLs and REGL for Graphite Smoke for Military Personnel Exposure Guideline Exposure Duration Exposure Guidance Level (mg/m3) EEGL 15 min 880   1 hr 220   6 hr 40 REGL 8 hr/d, 5 d/wk 1 Abbreviations: EEGL, emergency exposure guidance level; REGL, repeated exposure guidance level. TABLE 5-3 SPEGLs and RPEGL for Graphite Smoke for the Boundaries at Military Training Facilities Exposure Guideline Exposure Duration Exposure Guidance Level (mg/m3) SPEGL 15 min 88   1 hr 22   6 hr 4 RPEGL 8 hr/d, 5 d/wk 0.1 Abbreviations: SPEGL, short-term public emergency guidance level; RPEGL, repeated public exposure guidance level. sparse, the subcommittee recommends that an acute inhalation study of graphite in rats be conducted, using multiple concentrations to describe fully the exposure dose-response relationship. Concentrations expected to yield lung burdens of graphite at or below the concentration expected to result in lung overload could be used. End points monitored should include lung burdens of graphite, histopathological, changes and markers of inflammation. References 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. Anderson, R.S., S.M. Thomson, and LL. Gutshall. 1989. Comparative effects

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--> of inhaled silica or synthetic graphite dusts on rat alveolar cells. Arch. Environ. Contam. Toxicol. 18:844–849. Anderson, R.S., L.L. Gutshall, and S.A. Thomson. 1987. Rat Pulmonary Alveolar Macrophages In Vitro Cytotoxicity to Six Metal Dusts. CRDEC-TR-88037. Chemical Research, Development and Engineering Center, U.S. Army Armament, Munitions and Chemical Command, Aberdeen Proving Ground, Edgewood, Md. Aranyi, C., N. Rajendran, and J. Bradof. 1992. Thirteen-week Inhalation Toxicity Study with Aerosol Mixtures of Fog Oil and Graphite Particles in F344/N Male Rats. DAMD17-89-C-9043. Prepared by IIT Research Institute, Chicago, for U.S. Army Medical Research and Development Command, Fort Detrick, Md. Bohning, D.E., H.L. Atkins, and S.H. Cohn. 1982. Long-term particle clearance in man: Normal and impaired. Ann. Occup. Hyg. 26:259–271. Bovet, P. 1952. Die wirkung von graphit und anderen kohlenstoffmo-difikationen im tierversuch; zugleich ein beitrag zur experimentellen silikoseforschung. Schweiz. Z. Allg. Pathol. Bakteriol. 15:548–565. Driver, C.J., M.W. Ligotke, W.G. Landis, J.L. Downs, B.L. Tiller, and E.B. Moore. 1993. Environmental and Health Effects Review for Obscurant Graphite Flakes. ERDEC-TR-056. Edgewood Research, Development and Engineering Center, U.S. Army Armament, Munitions and Chemical Command, Aberdeen Proving Ground, Edgewood, Md. Dunner, L., and J.T. Bagnall. 1946. Graphite pneumoconiosis complicated by cavitation due to necrosis. Br. J. Radiol. 19(220):165–168. Gaensler, E.A., J.B. Cadigan, A.A. Sasahara, E.O. Fox, and H.E. MacMahon. 1966. Graphite pneumoconiosis of electrotypers. Am. J. Med. 41:864–882. Gloyne, R.S., G. Marshall, and C. Hoyle. 1949. Pneumoconiosis due to graphite dust. Thorax 4:31–38. Diem, K., and C. Lentner, eds. 1970. Documenta Geigy: Scientific Tables, 7th Ed. Basle, Switzerland: Ciba-Geigy. Guelta, M.A., D.R. Banks, and R.S. Grieb. 1993. Particle Size Analysis of Graphite Obscurant Material from an XM56 Smoke Generator. ERDEC-TR-053. Edgewood Research, Development and Engineering Center, U.S. Army Armament, Munitions and Chemical Command, Aberdeen Proving Ground, Edgewood, Md. Hanoa, R. 1983. Graphite pneumoconiosis. A review of etiologic and epidemiologic aspects. Scand. J. Work Environ. Health 9:303–314. Harding H.E., and G.B. Oliver. 1949. Changes in the lungs produced by natural graphite. Br. J. Ind. Med. 6:91–99. Jaffé, F.A. 1951. Graphite pneumoconiosis. Am. J. Pathol. 17:909–923. Lister, W.B., and D. Wimborne. 1972. Carbon pneumoconiosis in a synthetic graphite worker. Br. J. Ind. Med. 29:108–110. Lundy, D., and J. Eaton. 1994. Occupational Health Hazards Posed by Inventory U.S. Army Smoke/Obscurant Munitions (Review Update). WRAIR/RT-

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