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3 Fog-Oil Smoke BACKGROUND INFORMATION Military Applications Fog-oil smoke is the term used to describe an oil smoke generated by injecting mineral oil into a heated manifold. The oil vaporizes upon heating and condenses when exposed to the atmosphere, producing respirable particles. Troops are exposed to fog-oil smoke when it is used as a visual obscurant during training or in combat. Graphite can be added to fog oil to provide screening in the infrared range of the electromagnetic spectrum. Fog oil used without graphite is evaluated in this chapter. Physical and Chemical Properties Composition: Variable; see description below Minimum flash point: 160°C Viscosity, kinematic, centistokes: 3.40 to 4.17 at 100°C Pour point: -40°C Boiling point: 300 to 600°C
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To meet military specifications (for pour point1 and cloud point2), fog oil historically has been produced from naphthenic oils. The composition varies from batch to batch from different sources and even from the same source. Samples taken from two sources of conventionally refined fog oil contained approximately 50% aromatic hydrocarbons, 1% acids, alcohols and esters, and nitrogen derivatives in the parts-per-million range (Katz et al. 1980). Only slight variation in chemical composition results from the smoke-generation process (Katz et al. 1980). The severely refined fog oil that is in use today should not contain detectable quantities of many aromatic hydrocarbons. Fog-oil smoke is a condensation aerosol (a mist) composed of liquid particles. Condensation aerosols are, in general, relatively small in aerodynamic size and respirable and are generated to obscure soldiers from view. A fraction of the oil (components with low boiling points) might remain in the vapor form. All measurements of fog-oil smoke reported or recommended in this chapter are referred to in milligrams of total particulates per cubic meter. The chemical and physical properties of fog oil are similar to those of lubricating and petroleum-based cutting oils. Substances added to cutting and lubricating oils to maintain their physical properties during use under extreme pressure and heat are responsible for the distinguishing characteristics of these oils. Although little information is available regarding the health effects of fog oil, inferences can be drawn to a large extent from the health effects of lubricating and mineral oils. However, only certain cutting oils would be appropriate in making such a comparison. Insoluble cutting oils composed of mineral oils with only small quantities of additives should have biological properties similar to fog oil. 1 The lowest temperature at which a liquid will flow when its container is inverted. 2 The temperature at which a waxy solid material appears as the liquid is cooled.
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Emulsified cutting oils have a greater complexity of additives than insoluble cutting oils, and synthetic cutting oils contain no mineral oil. Thus, those oils cannot be compared validly with fog oil. Droplets of cutting- and lubricating-oil mists found in occupational settings also are largely in the respirable range (Jones 1961). Increased incidences of skin cancer of the hands, arms, and scrotum have been observed in workers exposed to conventionally refined mineral oils in the jute, cotton-spinning, and metal-machining industries. Polycyclic aromatic hydrocarbons (PAHs) and related heterocyclic compounds are thought to be responsible for these effects (Bingham et al. 1965; Halder et al. 1984; IARC 1984; Kane et al. 1984). In this report, the subcommittee distinguishes between ''old" and "new" fog oils. Old fog oils (basically, naphthenic oils) are similar to conventionally refined mineral oils, which contain various carcinogenic or potentially carcinogenic substances, including PAHs and related heterocyclic compounds. The military specification for fog oil was changed after IARC (1984) concluded that untreated naphthenic oils were carcinogenic. The new military specification for fog oil excludes all carcinogenic or potentially carcinogenic constituents. Fog oil procured after the new specification was implemented in 1986 is referred to as new fog oil. Industry uses two processes to remove carcinogenic and potential carcinogenic constituents: (1) severe solvent refining or extraction removes undesirable compounds, and (2) hydro-treatment converts them to less toxic saturated compounds. Military Exposures Young et al. (1989) collected 1-hr personal3 and area air samples during training sessions at the U.S. Army Chemical School at 3 Personal air samples were taken by a device worn on the lapel and were used to measure ambient concentrations in the breathing zone of an individual.
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Fort McClellan. Students were learning operations and maintenance (O&M) for smoke generators and participating in field training exercises (FTX) in three courses: advanced individual training (54B10AIT), the basic noncommissioned officers' course (BNCOC), and the commissioned officers' basic course (COBC). Personal samples were taken for both cadre (O&M only) and students. Fog-oil-smoke exposure concentrations ranged from 0 to 680 mg/m3. The mean exposures were much higher for O&M training than for FTX (i.e., 69 ± 10 mg•hr/m3 versus 8.7 ± 1.3 mg•hr/m3). The O&M training took place for 4 hr each day for 2 days. Unlike FTX, students and cadre are required to stand near the smoke generators to make adjustments for the entire training session. The difference between students' and cadres' exposure concentrations was not statistically significant. Both students and cadre typically are exposed for a total of 8 hr in a 2-day course. However, the cadre teach many courses over a 3- to 4-year assignment at the Chemical School. Thus, the potential for chronic exposure is much greater for cadre than for students. Advanced individual training led to higher fog-oil-smoke exposures than the basic courses for both FTX and O&M. Area-sample-concentration measurements did not differ significantly from the personal-sample measurements taken simultaneously. The mass median aerodynamic diameter (MMAD) of the fog-oil-smoke particles ranged between 1 and 3 µm (Young et al. 1989). During one laboratory test, old-fog-oil smoke gave MMADs of 2.43 and 2.21 µm, with geometric standard deviations of 1.68 µm and 1.64 µm, respectively (Cataldo et al. 1989). In a study of smoke dispersion at Eglin Air Force Base, Florida, the mean diameter (presumably by count) of fog-oil-smoke particles ranged from 0.505 to 2.10 µm (Policastro and Dunn 1985). Because the count mean diameter should be less than the MMAD for a given distribution of particle sizes, that measurement is in rough agreement with the measurements of Young et al. (1989) and Cataldo et al. (1989). Thus, a large portion of the fog-oil-smoke particle mass is in the respirable-size range. Studies of fog-oil-smoke dispersion were conducted at Dugway
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Proving Ground in 1985 (Liljegren et al. 1988). Fog-oil-smoke plumes were produced using M3A3E3 smoke generators, and samples were taken from 25 to 800 m downwind to measure concentration, particle-size distribution, deposition on surfaces, and chemical composition. Concentration measurements, taken 25 m downwind of the source along the fog-oil plume centerline, were presented for only three experiments. The highest concentrations—120, 110, and 33 mg/m3—were observed at the sampling site nearest the generator. Two hundred meters from the source, two of the centerline concentrations were just above the detection limit (1 mg/m3) and one was below the detection limit. Farther than a few hundred meters downwind, the concentrations exhibited considerable spatial heterogeneity. Liljegren et al. (1988) found that particle size was distributed log-normally and that the MMAD was about 0.7 µm. The chemical compositions of the raw oil, the initial smoke particles, and the smoke particles at the farthest point from the generator were not detectably different, and deposition of smoke particles on vertical and horizontal surfaces was not statistically significant. TOXICOKINETICS No data are available to evaluate the toxicokinetics of fog-oil smoke or aerosols of similar oils in humans or in animals. TOXICITY SUMMARY Effects in Humans Dermal Exposures Noncancerous Skin Lesions Short exposures to lubricating oils can cause mild erythema. More prolonged exposure can cause inflammation, dermatitis, folliculitis,
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acne, eczema, and contact sensitivity (Cruickshank and Gourevitch 1952). Those effects have been reported for conventionally refined oils (i.e., those not having undergone severe solvent refining or hydro-treatment). The PAH content of those oils is thought to be responsible for those conditions. Support for that theory comes from skin-painting studies in animals, which show that highly refined mineral oils (similar to new fog oil) are not likely to cause serious chronic skin conditions (Bingham et al. 1965; Bingham and Horton 1966). Dermatitis, folliculitis, and warts have been reported in men exposed to poorly refined cutting and lubricating oils (Cruickshank and Squire 1950; Hodgson 1970). Cancer of the Skin and Scrotum There is ample evidence pointing to an association between exposure to conventionally refined mineral oils and skin and scrotal cancer (Bingham et al. 1980; IARC 1984). IARC (1984) concluded that evidence was sufficient to consider conventionally refined mineral oils to be carcinogenic to humans. Tumors of the skin of the scrotum, arms, and hands are a result of sprays from the machines and direct contact with oil-coated surfaces, particularly along the lower abdominal area (Cruikshank and Squire 1950; Cruikshank and Gourevitch 1952). Chronic inflammatory and cancerous lesions on the hands, forearms, and scrotum developed in 60% of workers exposed to liquid cutting lubricants for over 15 years at their jobs in the United Kingdom (Hodgson 1973). Case-control studies of Connecticut workers exposed to cutting oils demonstrated excess sinonasal and scrotal cancers (Roush et al. 1980, 1982). Benzo(a)pyrene and other PAHs in lubricating oils were identified in a region of France in which a high incidence of skin cancer was observed (Thony et al. 1975, 1976). In jute and cotton textile workers exposed to high concentrations of mineral oils, high rates of skin and scrotal cancer have been noted (Kinnear et al. 1954). Scrotal cancer is uncommon in men not exposed to mineral
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oil (Hodgson 1973). The incidence of scrotal and skin cancer in textile workers and machinists appears to have declined in recent years. That decrease has been attributed to the new refining processes that reduce the PAH content of oils (Falk et al. 1964; Bingham et al. 1980). Thus, exposure to new fog oil would not represent a major concern for skin and scrotal cancer. Multiple Routes of Exposure In addition to inhalation exposures in occupational settings, workers can be exposed to oil mists that settle on equipment, skin, and clothing, thereby causing dermal and oral exposures. The primary health effects associated with occupational exposures to oil mists include pulmonary effects and skin cancer. Pulmonary Effects Pulmonary effects, such as granulomas or pneumonias, can occur with exposure to highly refined mineral oils that lack PAHs. Over 400 cases of lipoid pneumonia resulting from ingestion, inhalation of oil-based nose drops, or intralaryngeal injection of medicinal oil were reported in the literature before 1978 (IARC 1984). Lipoid pneumonia can be of two types: (1) lipoid granuloma or paraffinoma, which is a local lesion within a single lobe of the lung, and (2) diffuse pneumonitis, which is characterized by oil droplets that are widely disseminated throughout one or more lobes of the lung. Fibrosis can result from lipoid pneumonia, leading to loss of lung function (Proudfit et al. 1950; Jampolis et al. 1953). Lipoid pneumonia, however, is rarely seen in the workplace even when concentrations of oil mists are over 50 mg/m3 (Liss-Suter et al. 1978). A survey conducted by the American Petroleum Institute of workers exposed to mineral-oil mists showed no instances
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in which lung abnormalities were associated with oil exposure. The threshold for discomfort seems to be 5 mg/m3 (Hendricks et al. 1962). In these studies, the average exposure was 15 mg/m3, with measurements ranging from 1 to 57 mg/m3. On the basis of these studies, Hendricks et al. (1962) recommended a maximum allowable exposure level of 5 mg/m3 to avoid nuisance and subjective complaints. In a study by Jones (1961), 19 workers from a steel-rolling mill were examined after having been exposed for 9 to 18 years to oil-mist concentrations as high as 9 mg/m3 for 2 hr per day, 5 days per week. The oil was a naphthenic spindle oil containing petroleum sulfonates, rosin soap, and cresylic acid. No respiratory diseases were noted, nor were any skin or gastric disorders observed; however, an increase in linear striations were discovered in the lungs of 12 men. Jones (1961) concluded that the importance of that finding was not known. Persistent minor respiratory-tract infections were evident in workers exposed to mineral-water emulsions resulting in oil-mist concentrations averaging 2 mg/m3. However, the symptoms could not be associated with occupational exposure to the mist (Hervin and Lucas 1972). Excess respiratory symptoms (cough and phlegm) were noted in nonsmoking and smoking machine-shop workers exposed to median oil-mist concentrations of 3.2 to 4.5 mg/m3 for at least 3 years (Jarvholm et al. 1982). The reported incidence of chronic cough and phlegm was higher for the more-exposed workers in grinding and hardening than for the less-exposed workers employed in the turning department; however, those symptoms might have been due to the additives in the oils (Jarvholm et al. 1982). Lung function (1-sec forced expiratory volume (FEV1), forced vital capacity (FVC), residual volume, closing volume, and diffusion capacity) was not impaired in the nonsmokers examined (lung function was not evaluated for smokers) (Jarvholm et al. 1982). Ely et al. (1970) found that oil-mist concentrations of about 1 mg/m 3 (median) to 5.2 mg/m3 (mean) did not result in any abnormalities in the incidence of cough, bronchitis, wheeze, and dyspnea
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or in FEV1 and FVC in machinists exposed for 8 hr per day, 5 days per week, for 1 to 38 years (mean 13 years). Individual measurements with air sampled for at least 1 hr ranged from 0.07 to 110 mg/m3. There have been case reports attributing occupational exposure to oil mists as the causative factor in respiratory illness. One subject with lipoid pneumonia, chronic cough, frequent colds, and substantial loss of pulmonary function was reported by Proudfit et al. (1950). Greaves et al. (1997a,b) examined a group of 1,882 automobile workers composed of machinists exposed to aerosols from metal-working fluids and unexposed assemblers at three plants. The metal-working fluids were either straight mineral oils, soluble-oil emulsions, or synthetic fluids. Average exposure of the three unexposed groups (assemblers) was 0.10 to 0.15 mg/m3, expressed as "thoracic" aerosol fraction, and average exposure of the three exposed groups (machinists) was 0.16 to 0.80 mg/m3. Individual exposures were 0.07 to 0.44 mg/m3 for the assemblers and 0.16 to 2.43 mg/m3 for the machinists. The machinists had all been exposed for at least 6 months, and a majority had been exposed for over 2 years. A respiratory questionnaire and lung spirometry were used to determine the effects of exposure. The straight oils, which would be most similar to fog oil, produced respiratory symptoms of phlegm and wheezing as well as chest tightness and breathlessness. Those effects were greater than those observed for the soluble-oil group and less than those observed for the synthetic-oil group (Greaves et al. 1997a,b). Lung spirometry demonstrated a greater effect on FEV1 than on FVC. The results were consistent with an obstructive ventilatory function and were evident at the highest exposure concentrations of straight and soluble oils (Greaves et al. 1997a,b). However, both the straight and soluble oils could have included up to 40% additives, which might have been responsible for the observed pulmonary effects. Drasche et al. (1974) evaluated respiratory questionnaires
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completed by German workers exposed to drilling- and cutting-oil mists at concentrations of 40 to 150 mg/m3 for long periods of time, and found no indications of respiratory irritation that could be attributed to the oil-mist exposures. However, Drasche et al. (1974) did not report how the air concentrations were measured or how the questionnaires were administered. Skyberg et al. (1986) found an increased prevalence of slight basal-cell lung fibrosis in workers exposed to oil mists and kerosene vapors compared with workers in the same company not exposed to those substances. Eight-hour time-weighted average (TWA) oil-mist concentrations measured by personal air samplers ranged from 0.15 to 0.3 mg/m3 among the exposed workers. However, most exposure would occur during short intervals when workers cleaned oil-containing pans (one to three daily) and cleaned large vessels from the inside (two to four times a month). A peak concentration of 2,000 to 4,000 mg/m3 was measured one time over a pan-cleaning operation (total number of area measurements not reported); no measurements were taken in the enclosed vessels entered by workers for cleaning. Calibration of the GF/A glass-fiber personal air monitors against Millipore HA membrane filters indicated that the personal air monitors underestimated ambient oil-mist concentrations by at least 20-fold. Thus, it is likely that those workers were exposed repeatedly to relatively high concentrations of oil mists for short periods of time and that actual 8-hr TWA exposures were higher than 5 mg/m3 for some workers. In considering all the data reporting respiratory effects of oil mists, isolated cases of adverse effects (dyspnea, bronchitis, wheeze, fibrosis, and impaired pulmonary function) resulted from occupational and nonoccupational exposures. The majority of studies, however, do not point to serious respiratory problems from concentrations commonly found in industrial settings, and the problems that have been reported could be due to the additives used to maintain the oils' physical characteristics under high pressure and temperature.
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Carcinogenic and Mutagenic Effects Excesses of lung cancer in oil-exposed workers have been observed in certain studies (Coggon et al. 1984; Vena et al. 1985), and other studies have been negative (Decoufle 1978; Jarvholm et al. 1981). In Kodak plants in New York State, exposures to oil mist in concentrations ranging from 0.07 to 110 mg/m3(median concentration, 1.5 mg/m3; mean concentration, 3.7 mg/m3) demonstrated no excess deaths from cancers at all sites combined or from respiratory tract cancer, Hodgkins disease, or leukemia (Ely et al. 1970). Waterhouse (1971) found a significant excess of primary cancers of the respiratory and upper digestive tracts in men with mineral-oil-related cancers of the scrotum. This study examined the records of primary cases of scrotal cancer in the Birmingham Regional Cancer Registry for 1950 to 1967. In a cohort study of men exposed to synthetic, emulsified, and insoluble cutting oils, an excess of gastrointestinal-tract cancer, but not respiratory-tract cancer, was found (Decoufle 1976, 1978). Due to the mixed exposures, the relevance of these results to mineral oils, including fog oil, can be questioned. Cancer mortality in a large number of workers in various Japanese industries demonstrated an association between gastric cancer and machine-oil exposure (Okubo and Tsuchiya 1974). Bell et al. (1987) determined that the risk for malignant melanoma was significantly increased in workers exposed to cutting oils but not in those exposed to mineral oils. They concluded that the risk for melanoma was probably due to nitrosamines in the cutting oils. Meaningful conclusions cannot be drawn from most of the studies linking cancers of other organs to mineral oil. Most of the studies provide no information regarding exposure concentrations or the chemical composition of the oils. Peripheral lymphocytes cultured from pressed-glass makers exposed to mineral-oil mists with relatively high concentrations of PAHs had a significantly higher frequency of aberrant cells and chromosome breaks per cell. The exposure concentration was less
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LC50 of 5,200 mg/m3 in rats exposed for 3.5 hr to old fog oil. Other reports of lethality from either oral (LD50 > 5 g/kg) or dermal (LD 50 > 2 g/kg) exposures also indicated that old fog oil is relatively nontoxic following short-term exposures. No acute toxicity information is available for humans. Existing guidelines for occupational exposures (e.g., those of ACGIH and the Michigan and Detroit Bureaus of Industrial Hygiene for 40-hr work weeks) have been set at 5 mg/m3 to avoid complaints by workers. Given the lack of data on health effects of short-term exposures of humans to mineral-oil mists, the subcommittee used the LOAEL for pulmonary effects in mice exposed for 2 hr at 4,500 mg/m3 (Shoshkes et al. 1950) as the point of departure for estimating EEGLs. The subcommittee divided the NOAEL by a factor of 10 to estimate effects in humans from data on animals and by another factor of 10 to estimate a NOAEL from a LOAEL. To estimate exposure guidance levels for exposure durations less than 2 hr, Haber's law was applied based on the similarity of fog-oil and diesel-fuel smokes (both petroleum based). Data for diesel-fuel smoke indicate that C•T is a good predictor of mortality (see Chapter 2). Applying Haber's law to the 2-hr exposure guidance level of 45 mg/m3 resulted in a 15-min EEGL of 360 mg/m3, a 1-hr EEGL of 90 mg/m3, and a 6-hr EEGL of 15 mg/m3. The Hendricks et al. (1962) study, which indicated that no adverse health effects in workers were associated with 8-hr exposures to an average of 15 mg/m3 mineral-oil mists, also supports a 6-hr EEGL of at least 15 mg/m3. The subcommittee believes that it is reasonable for the 15-min EEGL of 360 mg/m3 for fog-oil smoke to be higher than the 15-min EEGL of 300 mg/m3 for diesel-fuel smoke, because new fog oil contains essentially no aromatic hydrocarbons, whereas diesel fuel is approximately 15% aromatics, and because new fog oil is less irritating to the skin than is diesel fuel. The aromatic compounds are thought to contribute to the acute toxicity of these petroleum products. The fog-oil EEGL might be more conservative than necessary (i.e., it could be higher than 360 mg/m3) , and the subcommittee recommends that the U.S. Army conduct research to identify a more accurate value.
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Permissible Exposure Guidance Levels (PEGL)5 In the Hendricks et al. (1962) study in which a large number of individuals exposed to oil mists were investigated, the lack of illness related to inhalation of the mists was striking. Exposure concentrations ranged from 1 to 57 mg/m3, averaging 15 mg/m3. At concentrations less than 5 mg/m3, few or no complaints were noted. On the basis of these studies, the subcommittee developed an 8-hr, 5 days per week, PEGL of 5 mg/m3. Exposures during training exercises often exceed the recommended PEGL (Liljegren et al. 1988; Young et al. 1989). Thus, careful adherence to respiratory protection policy is recommended. Public Exposures to New-Fog-Oil Smoke The recommendations in this section are made with the assumption that the military is using new rather than old fog oil. Short-Term Public Emergency Guidance Level (SPEGL)6 Although the possibility is slight that a short-term public-health emergency would occur from new-fog-oil-smoke exposure, general discomfort might occur at concentrations above 5 mg/m3 (Hendricks et al. 1962). No serious effects have been reported in humans working in industrial atmospheres with concentrations averaging as high as 15 mg/m3; however, the subcommittee believes that a lower SPEGL would be appropriate to protect sensitive subpopulations that might be exposed. Therefore, the subcommittee 5 Guidance for repeated exposure of military personnel during training exercises. 6 Guidance for a rare, emergency situation potentially resulting in an exposure of the public to a military-training smoke.
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recommends dividing the EEGLs by an uncertainty factor of 10 to account for the potentially greater range in sensitivities of the general public compared with industrial workers. Thus, the 15-min SPEGL is 36 mg/m3, the 1-hr SPEGL is 9.0 mg/m3, and the 6-hr SPEGL is 1.5 mg/m3. Permissible Public Exposure Guidance Level (PPEGL)7 There is a dearth of information on the effects of exposure to old or new fog oil on reproduction and development as well as on sensitive populations. Thus, the subcommittee recommends that a safety factor of 10 be applied to the PEGL to estimate the PPEGL. The resultant PPEGL is 0.5 mg/m3. Summary of Subcommittee Recommendations Table 3-3 summarizes the subcommittee's recommended exposure guidance levels for exposure of military personnel to new-fog-oil smoke. Table 3-4 summarizes the subcommittee's recommended exposure guidance levels for new-fog-oil smoke for the boundaries of military-training facilities to ensure that public communities near the training facilities are not at risk of adverse effects. RESEARCH NEEDS There is no information regarding the health effects of short-term (i.e., from a few minutes to a few hours) exposure of humans to fog-oil or severely refined mineral-oil aerosols at concentrations above 15 to 60 mg/m3. Moreover, there are no human or animal 7 Guidance for repeated exposures of public communities near military-training facilities.
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TABLE 3-3 EEGLs and PEGL for New-Fog-Oil Smoke for Military Personnel Exposure Guideline Exposure Duration Guidance Level (mg/m3) EEGL 15 min 360 1 hr 90 6 hr 15 PEGL 8 hr/d, 5 d/wk 5 TABLE 3-4 SPEGLs and PPEGL for New-Fog-Oil Smoke at the Boundaries of Military Training Facilities Exposure Guideline Exposure Duration Guidance Level (mg/m3) SPEGL 15 min 36 1 hr 9.0 6 hr 1.5 PPEGL 8 hr/d, 5 d/wk 0.5 data that can be used to evaluate the extent to which Haber's law applies to health effects of these oils. The development of dangerously low visibility and slippery surfaces might occur at concentrations less than those that could impair human performance as a result of toxic effects or physical impairment of pulmonary function; however, no data are available to evaluate that possibility. Thus, studies on the health effects of short-term exposures that also evaluate the applicability of Haber's law are needed to provide more sound guidance for emergency exposures. The information available from studies of occupational exposure of humans is insufficient to rule out the possibility of long-term health effects. Moreover, few animal studies are available to evaluate the long-term health effects of repeated exposures to new-fog-oil smoke at concentrations of 5 to 60 mg/m3. Thus, long-term,
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repeated-exposure studies should be conducted by using appropriate small mammal species and exposure levels likely to be experienced by military personnel in the field. Information is not available on reproductive and developmental toxicity in mammals. Increasing numbers of females are recruited into the military. Thus, studies should also be conducted to ascertain reproductive developmental toxicity in mammals. These studies should use the inhalation route if possible. To ensure protection of the public, some effort is warranted to determine whether some human subpopulations might be more sensitive than others. Short-term exposure of individuals with and without asthma at the SPEGL, followed by pulmonary-function tests (spirometry and diffusing capacity as a minimum requirement), could be useful both in determining whether those with asthma are more sensitive and whether the SPEGL is adequate or overprotective. Finally, the subcommittee notes that Army personnel who work with this smoke, trainers in particular, are potentially a rich source of information on the health effects of the smoke. The subcommittee recommends that the Army conduct a prospective study with appropriate controls in which pulmonary-function tests and routine chemistry tests (panel 20 plus Mg and thyroid tests as a minimum requirement) are performed on personnel who are exposed repeatedly to the smoke. 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. ACGIH (American Conference of Governmental Industrial Hygienists). 1995. 1995-1996 Threshold Limit Values and Biological Exposure Indices. American Conference of Governmental Industrial Hygienists, Cincinnati, Ohio.
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Beck, L.S., D.I. Hepler, and K.L. Hansen. 1982. The acute toxicology of selected petroleum hydrocarbons. Pp. 1-12 in Proceedings of the Symposium: The Toxicology of Petroleum Hydrocarbons, N.H. MacFarland, C.E. Holdsworth, J.A. MacGregor, R.W. Call, and M.L. Kane, eds. Washington, D.C.: American Petroleum Institute. Bell, C.M.J., C.M. Jenkinson, T.J. Murrells, R.G. Skeet, and J.D. Everall. 1987. Aetiological factors in cutaneous malignant melanomas seen at a UK skin clinic. J. Epidemiol. Community Health 41:306-311. Bingham, E., and A.W. Horton. 1966. Environmental carcinogenesis: Experimental observations related to occupational cancer. Adv. Biol. Skin 7:183-193. Bingham, E., A.W. Horton, and R. Tye. 1965. The carcinogenic potency of certain oils . Arch. Environ. Health 10:449-451. Bingham, E., R.P. Trosset, and D. Warshawsky. 1980. Carcinogenic potential of petroleum hydrocarbons. A critical review of the literature. J. Environ. Pathol. Toxicol. 3:483-563. Blackburn, G.R., R.A. Deitch, C.A. Schreiner, and C.R. Mackerer. 1986. Predicting carcinogenicity of petroleum distillation fractions using a Salmonella mutagenicity assay. Cell Biol. Toxicol. 2:63-84. Cataldo, D.A., P. Van Voris, M.W. Ligotke, R.J. Fellow, B.D. McVeety, S.-m.W. Li, H. Bolton, Jr., and J.K. Frederickson. 1989. Evaluate and Characterize Mechanisms Controlling Transport, Fate and Effects of Army Smokes in an Aerosol Wind Tunnel: Transport, Transformations, Fate and Terrestrial Ecological Effects of Fog Oil Obscurant Smokes. AD-A20414. Pacific Northwest Laboratory, Richland, Wash. Coggon, D., B. Pannett, and E.D. Acheson. 1984. Use of job-exposure matrix in an occupational analysis of lung and bladder cancers on the basis of death certificates. J. Natl. Cancer Inst. 72:61-65. Conaway, C.C., C.A. Schreiner, and S.T. Cragg. 1984. Mutagenicity evaluation of petroleum hydrocarbons. Pp. 89-107 in Advances in Modern Environmental Toxicology, Vol. 6. Applied Toxicology of Petroleum Hydrocarbons, M.A. Mehlman, ed. Princeton, N.J.: Princeton Scientific Publishers. Costa, D.L., and M.O. Amdur. 1979. Respiratory response of guinea pigs to oil mists. Am. Ind. Hyg. Assoc. J. 40:673-679. Cragg, S.T., C.C. Conaway, and J.A. MacGregor. 1985. Lack of concordance of the Salmonella/microsome assay with the mouse dermal
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Representative terms from entire chapter: