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Toxicity of Military Smokes and Obscurants: Volume 1 (1997)

Chapter: 3 - Fog-Oil Smoke

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Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
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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

Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
×

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.

Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
×

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.

Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
×

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

Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
×

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,

Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
×

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

Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
×

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

Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
×

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

Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
×

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

Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
×

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.

Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
×
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

Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
×

than 5 mg/m3, and the exposure duration was not reported (Sram et al. 1985).

Effects in Animals

Dermal Exposures
Lethality

Lethality of old fog oil in rabbits by single dermal application was more than 2 g/kg (Mayhew et al. 1985), indicating low potential for acute toxicity from dermal exposures.

Skin Irritation

Slight-to-moderate irritation was produced by a single application of mineral oils to the skin of rabbits (Beck et al. 1982; Mayhew et al. 1985). Repeated application, however, can cause more damage. Marked epidermal hypertrophy, hyperplasia, hyperkeratosis, and depilation were produced when conventionally refined light mineral oil was applied every other day for 1 week to the skin of guinea pigs. Those effects were produced by nonaromatic as well as aromatic compounds. Hydrocarbons with carbon numbers from C14 to C19 caused greater damage than those with higher carbon numbers (C21 to C23) (Hoekstra and Phillips 1963).

Cancer

Several skin-painting studies have shown that conventionally refined mineral oils are carcinogenic via dermal exposures (Bingham et al. 1965; Jepsen et al. 1977). Severe solvent extraction or hydro-treatment reduces or eliminates the tumorigenicity of mineral

Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
×

oils (Bingham and Horton 1966; Kane et al. 1984). The PAH content of the oils is thought to be responsible for the tumorigenicity (Bingham et al. 1965). Used oils, which are likely to have more PAHs due to the formation of pyrolysis products, tend to be more tumorigenic (Jepsen et al. 1977), although that is not always the case (Stemmer and King 1979).

Cragg et al. (1985) found that the Salmonella/microsome assay did not predict the dermal carcinogenic activity of complex petroleum mixtures; the mixtures were not mutagenic in the bacterial bioassay but were slightly to highly carcinogenic in mouse skin. McKee et al. (1989) found that repeated dermal application of diesel fuel, which contains low levels of biologically active PAHs, caused tumors in mouse skin. They suggested that the chronic irritation and hyperplasia produced by the diesel fuel act as tumor promoters. Similar considerations might apply to the tumorigenicity of mineral oils, although they are less irritating than diesel fuel. Mineral oils have been found to contain co-carcinogens, tumor promoters, and tumor antagonists, which more than likely account for the lack of direct correlation between PAH content and tumorigenicity (Roe et al. 1967; Bingham et al. 1980).

A histological examination of mouse skin removed from mice after exposure to oil for 3 days showed enlargement of nuclei. The enlargement correlated well with the carcinogenicity of the oils as demonstrated by mouse-skin-painting studies (Ingram and Grasso 1987).

Oral Exposures
One-Time Exposures

Lethality of old fog oil and paraffinic and naphthenic lubricating oils in rats by single oral intubation was more than 5 g/kg (Beck et al. 1982), indicating little potential for acute lethality with oral administration.

Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
×
Repeated Exposures

In one study using dietary administration of 2% liquid paraffin (comparable to medicinal-grade mineral oil) for 500 days and in another study using three grades of 5% petrolatum for 2 years, no oil-related tumors were found (Schmal and Reiter 1953; Oser et al. 1965).

Inhalation Exposures
One-Time Exposures

Lethality. A steep dose-response curve was found for single exposures to old fog oil when inhaled by rats. After 3.5 hr of exposure at a concentration of 1,000 mg/m3, no animals died, but after 6 hr of exposure at the same concentration, 20% of the exposed animals died. The concentration estimated to kill 50% of test organisms (LC50) after a 3.5-hr exposure was 5,200 mg/m3. After the same exposure duration, less than 15% of the animals died at 4,000 mg/m3 and over 80% died at 6,000 mg/m3(Grose et al. 1986; Selgrade et al. 1987) (see Table 3-1).

Pulmonary Effects. Submicron mists of medicinal-grade mineral oil, laboratory-grade paraffin oil, grade S-75 light lubricating oil, and SAE 10W-30 motor oil were tested on guinea pigs. Single 1-hr exposures at concentrations of 10 and 40 mg/m3 produced alterations in pulmonary function (Costa and Amdur 1979). Light lubricating oil at a concentration of 200 mg/m3, however, caused a decrease in pulmonary compliance (Costa and Amdur 1979). Shoshkes et al. (1950) found that 2-hr exposures of mice to animal, vegetable, mineral, and SAE No. 10 motor oil at atmospheric concentrations of 4,500 mg/m3 caused only the appearance of scattered macrophages in lung tissue.

Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
×

TABLE 3-1 Acute Lethality of Old-Fog-Oil Smoke via Inhalation Exposure

Species

Exposure Duration

Exposure Concentration (mg/m3 )

End Point and Comments

Reference

Rat

6 hr

1,000

20% died

Grose et al. 1986

Rat

3.5 hr

1,000

No mortality

Selgrade et al. 1987

 

4,000

<15% died

 

5,200

LC50

 

6,000

> 80% died

Repeated Exposures

Lethality. Two of six monkeys exposed to mists of SAE No. 10 automobile lubricating oil at a concentration of 132 mg/m3 (30 min per hr, 24 hr per day, for up to 100 days) died within 100 days (Lushbaugh et al. 1950). However, six of seven monkeys exposed to mists of SGF No. 1 diesel lubricating oil at 63 mg/m3 (for up to 1 year) died, indicating a higher toxicity of SGF No. 1 compared with SAE No. 10 oils (Lushbaugh et al. 1950).

Pulmonary Effects. Four-week exposures of mice to mineral-oil aerosols at a concentration of 4,500 mg/m3 caused localized foreign-body reactions and lipoid pneumonia (Shoshkes et al. 1950). Edible oils had no effects.

Monkeys and CF1 mice were exposed to mists of SAE No. 10 automobile lubricating oil at concentrations of 132 mg/m3 for 30 min per hr, 24 hr per day, for up to 100 days. Rats, rabbits, monkeys, and strain-A mice were exposed to SGF No. 1 diesel-engine lubricating oil at concentrations of 63 mg/m3 for up to 1 year, presumably for 30 min per hr, 24 hr per day, 7 days per week. Small amounts of oil were retained in the lungs of mice, rats, and rabbits, and macrophages with dispersed small oil droplets were seen.

Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
×

Increases in macrophages were seen initially, but remained constant from week 5 to the end of the study (Lushbaugh et al. 1950).

The effects were more severe in monkeys, which retained a larger amount of the oils in their lungs. As indicated above, SGF No. 1 oil was more toxic (killing six of seven animals tested) than SAE No. 10 (killing two of six within 100 days). Infectious pneumonitis, pulmonary lipophages, and severe hyperplastic gastritis were observed in animals exposed to both oils. Increases in the number of alveolar macrophages, diffuse pneumonitis, and acute pneumonia with edema were among the other effects observed. Longer exposures resulted in diffuse acute bronchopneumonia with edema and hemorrhage, lobular pneumonia, diffuse pneumonitis, and fibroplasia. Notwithstanding the respiratory effects, the cause of death for most monkeys was severe hyperplastic gastritis.

Grose et al. (1986) exposed rats to old fog oil at 500 and 1,500 mg/m3 for 70 min or 3.5 hr per day for 2 or 4 days per week for 4 weeks. Dose-related accumulation of alveolar macrophages and wet and dry lung weights were elevated in animals exposed at 1,500 mg/m3 for 70 min or 3.5 hr for both 2 and 4 days. In all groups of animals exposed at 1,500 mg/m3, total lung protein, total cell count, and polymorphonuclear leukocytes were elevated in bronchoalveolar lavage fluid. The animals also exhibited mild inflammatory pulmonary edema. End-expiratory volume was elevated 21% in high-dose animals, and no significant changes occurred in low-dose animals.

Rats exposed to old fog oil at 500 and 1,500 mg/m3 for 4 hr per day, 4 days per week, for 13 weeks demonstrated concentration-dependent accumulation of macrophages in alveoli and peribronchial lymph nodes. The effects persisted after a 4-week recovery period. Male rats exposed to 1,500 mg/m3 showed focal hemorrhage and multifocal granulomatous pneumonia. The appearance of the granulomas 4 weeks after exposure suggests development of a progressive lesion (Grose et al. 1986).

In a final study, Grose et al. (1986) exposed rats to old fog oil at 200 and 500 mg/m3 for 3.5 hr per day, 4 days per week, for 13 weeks. The increase in alveolar macrophages was slight to moderate

Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
×

at 500 mg/m3 and minimal to slight at 200 mg/m3. Increases in dry and wet lung weight were not significant at 200 mg/m3 but were significant at 500 mg/m3. Bronchial alveolar lavage protein and liver aryl hydrocarbon hydroxylase (AHH) activity increased, but a decrease was observed in zoxazolamine-induced paralysis time. It was thought that the AHH increase was due to the PAH in the fog oil (Grose et al. 1986).

The series of studies by Grose et al. (1986) demonstrated adverse effects down to 200 mg/m3 after 13 weeks of exposure. Thus, a no-observed-adverse-effect level (NOAEL) was not determined. Four- and 13-week exposures of male and female rats to old-fog-oil aerosols caused inflammatory edema, but pulmonary function and gas exchange were not significantly affected. Granulomas in rats exposed to 500 and 1,500 mg/m3 persisted through the 4-week recovery period, suggesting a progressive lesion in the lung after subchronic exposure.

Wagner et al. (1964) exposed five species—the rat, rabbit, dog, hamster, and mouse—to white mineral-oil mists at 5 or 100 mg/m3 for varying periods of 6 months to 2 years. Mice were exposed daily for 6 hr at 5 mg/m3 for 12 months or at 100 mg/m3 for 16 months. For dogs, 6, 12, or 26 months of daily 6-hr exposures were conducted for the 5- and 100-mg/m3 concentrations. Rabbits were exposed at 5 mg/m3 daily for 6 or 12 months or at 100 mg/m3 daily for 6, 12, or 18 months. Rats and hamsters were exposed similarly to rabbits, the exception being that the rat and hamster 100-mg/m3 groups were sacrificed at 16 and 15 months, respectively.

The white mineral oil is comparable to new fog oil. Rats and dogs were most affected by the oil. Exposures at 100 mg/m3 caused pulmonary lipoid granulomas in the dog and pneumonitis in the rat. No pathological effects were found at 5 mg/m3. Based on the study by Wagner et al. (1964), the 5-mg/m3 concentration could represent a NOAEL. Because serum alkaline phosphatase levels correlated well with histopathological findings in the dog, rat, and rabbit, Wagner et al. (1964) concluded that alkaline phosphatase

Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
×

could be used as an indicator of early injury from pulmonary irritants.

Gastrointestinal Effects. In the Lushbaugh et al. (1950) experiments with monkeys exposed to mists of SAE No. 10 automobile lubricating oil and SGF No. 1 diesel lubricating oil (described above), the cause of death of most monkeys was severe hyperplastic gastritis.

Carcinogenic Effects. Exposure for 1 year to SGF No. 1 diesel-engine lubricating oil at 63 mg/m3 did not cause tumors in strain-A mice (Lushbaugh et al. 1950); neither did exposure of CAF1/Jax mice to mineral oil (comparable to new fog oil) at 5 and 100 mg/m3 for 13 months (Wagner et al. 1964). Both strains are highly susceptible to the development of lung tumors.

Reproductive and Developmental Toxicity

No data are available on the reproductive and developmental toxicity of fog oil in mammals by any exposure route.

Screening Tests for Carcinogenicity and Mutagenicity

A naphthenic-based lubricating oil stock similar in viscosity to fog oil was negative in the L5178-Y-mouse-lymphoma assay and did not cause chromosomal aberrations in the rat bone-marrow cytogenetics assay (Conaway et al. 1984).

Using a modification of the Ames assay, Blackburn et al. (1986) determined that the mutagenicity of 18 oil samples correlated well with their tumorigenic potency in mouse-skin-painting studies. Skisak et al. (1987) used this modified assay to test 26 distillation fractions and found a high correlation between mutagenic activity and the tumorigenic potency demonstrated in

Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
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mouse-skin-painting assays. Severe hydrogenation decreases the mutagenicity of lubricating-oil base stocks (Venier et al. 1987). Solvent refining also decreases the mutagenicity of these stocks (Hermann et al. 1980a, b). New fog oil was negative in the Salmonella Ames assay (Lee et al. 1989).

Summary of Toxicity Data

Table 3-1 (above) summarized the acute lethality of inhalation exposure of rats to old-fog-oil aerosols. Table 3-2 summarizes the available exposure-response data for nonlethal effects in humans and animals of exposures to aerosols of fog oil and similar mineral oils. The type of oil aerosol to which the humans or animals were exposed is indicated in the first column of the table.

Noncancer Toxicity

Dermal exposures to oils that are similar to old fog oils can produce adverse effects, including skin inflammation, dermatitis, and folliculitis, but short-term dermal exposures to the oils that are similar to new fog oil are unlikely to produce more than temporary irritation.

The acute lethality of exposure to old fog oil is low. One report from Grose et al. (1986) indicates an inhalation LC50 of 5,200 mg/m3 in rats exposed for 3.5 hr to old fog oil. Similarly, reports of lethality from either oral (lethal dose to 50% of the test animals, or LD50 > 5,000 mg/kg) or dermal (LD50 > 2,000 mg/kg) exposures of animals indicate that old fog oil is relatively nontoxic following short-term exposures.

The respiratory tract is a primary target organ for exposure to fog-oil aerosols. A single 2-hr exposure of mice to conventionally refined mineral oil at 4,500 mg/m3 produced scattered macrophages in lung tissue, but no other pulmonary effects (Shoshkes et

Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
×

TABLE 3-2 Summary of Exposure-Response Data for Nonlethal Effects of Exposure to Aerosols of Fog Oil and Similar Oils

Receptor; Type of Oil

Exposure Frequency and Duration

NOAEL (mg/m3)

LOAEL (mg/m3)

End Point and Comments

Reference

Effects in Humans

Repeated Exposures

 

 

 

 

 

Pulmonary Effects

 

 

 

 

 

Workers; mineral oil

Not reported

2 (mean)

No adverse pulmonary effects

Hervin and Lucas 1972

Workers; mineral oil

Not reported

≤ 5

Threshold for ''discomfort"

Hendricks et al. 1962

Workers; mineral oil

Not reported

15 (mean)

No adverse pulmonary effects

Hendricks et al. 1962

Workers; napthenic spindle oil

2 hr/d, 5 d/wk, 9 to 18 yr

up to 9 (mean)

Increased striations in lungs of 12/19 men; significance unknown

Jones 1961

Nonsmoking machinists; various oils

8 hr/d, 5 d/wk, 1 to 38 yr (mean 13 yr)

1.0 to 5.2a

No respiratory effects

Ely et al. 1970

Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
×

Receptor; Type of Oil

Exposure Frequency and Duration

NOAEL (mg/m3)

LOAEL (mg/m3)

End Point and Comments

Reference

Machinists (smoking and nonsmoking); various

8 hr/d, 5 d/wk, at least

2.0b (median)

3.2b (median)

Increasing chronic cough and phlegm

Jarvholm et al. 1982

mineral oils

3 yr

 

 

 

 

Machinists (smoking and nonsmoking); various mineral oils

8 hr/d, 5 d/wk, at least 3 yr

4.5 (median)

No effects on measures of pulmonary function

Jarvholm et al. 1982

Machinists; straight mineral oils, with from 0% to 40% additives

8 hr/d, 5 d/wk, D 6 mo

0.16 to 2.43c

Phlegm, wheezing, chest tightness, breathlessness, obstructive ventilatory function

Greaves et al. 1997a,b

Workers; drilling and cutting oils

Not reported

40 to 150

No respiratory effects; methods not reported

Drasche et al. 1974

Carcinogenic Effects

Workers in various industrial settings (exposures not quantified) experienced elevated skin and scrotum cancer associated with exposures to conventionally refined mineral oils (like old fog oil)

Kodak plant workers; various oils

8 hr/d, 5 d/wk, > 5 yr

3.7 (mean)

No excess deaths from cancer at any site

Ely et al. 1970

Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
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Effects in Animals

One-Time Exposures

 

 

 

 

 

Pulmonary Effects

 

 

 

 

 

Guinea pig; various oils

1 hr

10

Altered pulmonary function

Costa and Amdur 1979

Guinea pig; various oils

1 hr

200

Decreased pulmonary compliance

Costa and Amdur 1979

Mouse; mineral oil

2 hr

4,500

Scattered macrophages in lung tissue

Shoshkes et al. 1950

Repeated Exposures

 

 

 

 

 

Lethality

 

 

 

 

 

Monkey; SGF No. 1 oil

30 min/hr, 24 hr/d, 100 d

132

6/7 animals died

Lushbaugh et al. 1950

Monkey; SAE No. 10 oil

30 min/hr, 24 hr/d, 100 d

132

2/6 died within 100 d

Lushbaugh et al. 1950

Pulmonary Effects

 

 

 

 

 

Mouse; mineral oil

4 wk

4,500

Lipoid pneumonia

Shoshkes et al. 1950

Monkey; SGF No. 1 and SAE No. 10 oils

30 min/hr, 24 hr/d, up to 100 d

132

Infections pneumonitis, pulmonary lipophages, edema, other pulmonary effects

Lushbaugh et al. 1950

Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
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Receptor; Type of Oil

Exposure Frequency and Duration

NOAEL (mg/m3)

LOAEL (mg/m3)

End Point and Comments

Reference

Rat; old fog oil

70 or 210 min/d, 2 or 4 d/wk, 4 wk

500

1,500

Elevated total lung protein, cell count, and pmn leukocytes in lavage fluid; mild inflammatory edema

Grose et al. 1986

Rat; old fog oil

4 hr/d, 4 d/wk, 13 wk

500

Accumulation of macrophages in alveoli and peribronchial lymph nodes

Grose et al. 1986

Male rat; old fog oil

4 hr/d, 4 d/wk, 13 wk

500

1,500

Granulomatous pneumonia after 4 wk exposure

Grose et al. 1986

Rat; old fog oil

3.5 hr/d, 4 d/wk, 13 wk

200

500

Increase in alveolar macrophages; changes in lung weight

Grose et al. 1986

Mouse; white mineral oil

6 hr/d, 7 d/wk, 16 mo

100

No adverse effects

Wagner et al. 1964

Rat; white mineral oil

6 hr/d, 7 d/wk, 6 to 16 mo

5

100

Pneumonitis

Wagner et al. 1964

Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
×

Dog; white mineral oil

6 hr/d, 7 d/wk, 6 to 24 mo

5

100

Pulmonary lipoid granulomas

Wagner et al. 1964

Rabbit; white mineral oil

6 hr/d, 7 d/wk, 18 mo

100

No adverse effects

Wagner et al. 1964

Hamster; white mineral oil

6 hr/d, 7 d/ wk, 6 to 15 mo

5

100

Increase in basic alkaline phosphatase and magnesium-activated alkaline phosphatase

Wagner et al. 1964

Gastrointestinal Effects

 

 

 

 

 

Monkey; SGF No. 1 and SAE No. 10 oils

30 min/hr, 24 hr/d, up to 100 d

63

Hyperplastic gastritis

Lushbaugh et al. 1950

Carcinogenic Effects

 

 

 

 

 

Strain A mouse; SGF No. 1 oil

30 min/hr, 24 hr/d, 1 yr

63

No tumors

Lushbaugh et al. 1950

CAF1-Jax mouse; white mineral oil

6 hr/d, 7 d/wk, 13 mo

100

No tumors

Wagner et al. 1964

Abbreviations: hr, hour(s); min, minute(s); d, day(s); wk, week(s); mo, month(s); yr, year(s); NOAEL, no-observed-adverse-effect level; LOAEL, lowest-observed-adverse-effect level; pmn, polymorphonuclear.

a The time-weighted average exposure was likely to be somewhere between the median (1.0 mg/m3) and mean (5.2 mg/m3) exposure concentrations recorded.

b The authors believed that the increased cough and phlegm could be due to the additives in the oil.

c The observed effects could have resulted from the additives in the oils.

Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
×

al. 1950). Studies of dogs, rabbits, rats, hamsters, and mice exposed to white mineral oils for 1 to 2 years identified a NOAEL for repeated exposures of 5 mg/m3 and a lowest-observed-adverse-effect level (LOAEL) of 100 mg/m3 for pulmonary effects (Wagner et al. 1964). Repeated-exposure concentrations higher than that can result in a variety of adverse pulmonary effects in animals.

Adequate human data are not available to establish NOAEL values for adverse health effects resulting from short-term exposures. For long-term exposures, Hendricks et al. (1962) found no illnesses related to inhalation of oil aerosols in a considerable population of individuals occupationally exposed for long periods. Long-term average exposure concentrations were 15 mg/m3. Concentrations in individual air samples ranged from 1 to 57 mg/m3; at concentrations less than 5 mg/m3, few complaints were noted.

Carcinogenicity

Conventionally refined mineral oils, which are chemically similar to old fog oil, have been shown to cause cancer of the skin of the arms, hands, and scrotum of humans. IARC (1984) recognizes eight classes of mineral oils based on increasing severity of processing or refinement. New fog oil might correspond roughly to the more severely refined oils included in IARC class 4, which are hydro-treated oils, or to the less severely refined oils in class 5, such as analytic-grade white mineral oils. IARC (1984) stated that there is sufficient evidence that mildly hydro-treated mineral oils in class 4 are carcinogenic to experimental animals, but the available data on severely hydro-treated oils in class 4 are inadequate to permit an evaluation of their carcinogenicity to experimental animals. IARC (1984) stated further that the combination of hydro-treatment and solvent extraction appears to reduce or eliminate skin tumorigenicity of mineral oils. Moreover, there is no evidence of tumorogenicity of analytic-grade white mineral oils (class 5) by any route of administration except by intraperitoneal injection; the relevance of that route of exposure is unclear. Thus, fog

Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
×

oil that has undergone hydro-treatment and solvent extraction is unlikely to be carcinogenic via inhalation or dermal exposures.

EXISTING RECOMMENDED EXPOSURE LIMITS

The U.S. Occupational Safety and Health Administration (OSHA) and the American Conference of Governmental Industrial Hygienists (ACGIH) established a Threshold Limit Value (TLV) TWA of 5 mg/m3 for exposures to severely refined mineral-oil mists of 8 hr per day, 5 days per week, based on the studies by Hendricks et al. (1962) and Wagner et al. (1964) (ACGIH 1991). ACGIH (1995) recently proposed further that the sum total of PAHs listed as carcinogenic by the National Toxicology Program (NTP) should not exceed 5 µg/m3. Palmer (1990) reviewed the effects of exposure to fog-oil smoke in humans and animals and recommended that the U.S. Army adopt the ACGIH TLV-TWA of 5 mg/m3 for new fog oil.

SUBCOMMITTEE EVALUATION AND RECOMMENDATIONS

The subcommittee endorses the recommendations of Palmer (1990) to ensure that carcinogenic compounds are not in the fog oil used by the military and also recommends that representative batches of the oil be analyzed for the 15 PAHs listed as carcinogens by the NTP. The subcommittee also recommends exposure guidance levels for new fog oil, as described below.

Type of Fog Oil

Conventionally refined mineral oils, which are similar to old fog oil, have been shown to cause cancer of the skin of the arms, hands, and scrotum of humans, whereas mineral oils are thought unlikely to be carcinogenic after undergoing severe solvent refining or hydro-treatment. To protect military personnel from cancer

Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
×

risks associated with old fog oil, the exposure limits would be so low that it would require continuous masking in the vicinity of fog oil. Prohibiting the use of old fog oil might be more feasible than recommending an exposure limit for it. Given the impracticality of donning appropriate protective apparel in most situations in which fog oil would be used and given the fact that the oil can penetrate ordinary military uniforms, the subcommittee endorses prohibiting the use of old fog oil for production of smokes to which military personnel would be exposed.

In some cases, severe solvent refining or hydro-treatment does not remove all carcinogens. Thus, the subcommittee also endorses a military specification for fog oil that requires manufacturer testing of the oil to ensure the absence of carcinogenic constituents. The subcommittee recommends that manufacturers use the modified Ames test of Blackburn et al. (1986) and the Food and Drug Administration (FDA 1979) test for white-oil purity.

Finally, the subcommittee endorses testing the current inventory of fog oil purchased after the specifications were revised by using the FDA test for white-oil purity (FDA 1979) and the modified Ames test of Blackburn et al. (1986) to ensure that all batches are not carcinogenic.

Military Exposures

The recommendations in this section are made with the assumption that exposures of military personnel are to smokes generated from new rather than old fog oil.

Emergency Exposure Guidance Level (EEGL)4

The potential for death of animals from a one-time exposure to fog oil is low. One report from Grose et al. (1986) indicated an

4  

Guidance for a rare, emergency situation resulting in an exposure of military personnel.

Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
×

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.

Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
×
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.

Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
×

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.

Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
×

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,

Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
×

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.

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Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
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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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Suggested Citation:"3 - Fog-Oil Smoke." National Research Council. 1997. Toxicity of Military Smokes and Obscurants: Volume 1. Washington, DC: The National Academies Press. doi: 10.17226/5582.
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