Cover Image

PAPERBACK
$54.75



View/Hide Left Panel

2
Diesel-Fuel Smoke

BACKGROUND INFORMATION

Military Applications

Diesel-fuel smoke is one of the visual obscurants used by the armed forces to conceal personnel and equipment. Diesel-fuel smoke is formed by injecting diesel fuel into the exhaust manifold of a tactical vehicle where the fuel is vaporized and expelled with the vehicle's exhaust. Upon dilution and cooling to the ambient temperature, the fuel condenses into a dense white smoke. Because military personnel might be exposed to this aerosol in routine training situations and in actual combat, its effects on their performance and health are of interest.

Physical and Chemical Properties

Diesel fuel is a mixture of aliphatic, olefinic, and aromatic hydrocarbons obtained from the distillation of petroleum. The composition of the fuel purchased by the U.S. Army to generate smoke is controlled only by specifications on boiling point, cetane



The National Academies | 500 Fifth St. N.W. | Washington, D.C. 20001
Copyright © National Academy of Sciences. All rights reserved.
Terms of Use and Privacy Statement



Below are the first 10 and last 10 pages of uncorrected machine-read text (when available) of this chapter, followed by the top 30 algorithmically extracted key phrases from the chapter as a whole.
Intended to provide our own search engines and external engines with highly rich, chapter-representative searchable text on the opening pages of each chapter. Because it is UNCORRECTED material, please consider the following text as a useful but insufficient proxy for the authoritative book pages.

Do not use for reproduction, copying, pasting, or reading; exclusively for search engines.

OCR for page 26
2 Diesel-Fuel Smoke BACKGROUND INFORMATION Military Applications Diesel-fuel smoke is one of the visual obscurants used by the armed forces to conceal personnel and equipment. Diesel-fuel smoke is formed by injecting diesel fuel into the exhaust manifold of a tactical vehicle where the fuel is vaporized and expelled with the vehicle's exhaust. Upon dilution and cooling to the ambient temperature, the fuel condenses into a dense white smoke. Because military personnel might be exposed to this aerosol in routine training situations and in actual combat, its effects on their performance and health are of interest. Physical and Chemical Properties Diesel fuel is a mixture of aliphatic, olefinic, and aromatic hydrocarbons obtained from the distillation of petroleum. The composition of the fuel purchased by the U.S. Army to generate smoke is controlled only by specifications on boiling point, cetane

OCR for page 26
number (a measurement of ignition quality), viscosity, and flash point. Additives might also be present in small quantities to improve combustibility (alkyl nitrates), reduce corrosion of storage vessels (surfactant), or reduce gum formation (antioxidants such as aromatic amides or phenols). Diesel fuels are categorized as the middle distillates from crude oil and are more dense than gasoline. As defined in the U.S. Chemical Substances Inventory under the Toxic Substances Control Act, diesel fuels consist of hydrocarbons with carbon numbers predominantly in the range of C9 to C20 and boils in the range of 163 to 357°C (IARC 1989). That definition encompasses both diesel fuels No. 1 (DF1) and No. 2 (DF2). DF1 is essentially kerosene and consists of hydrocarbons with numbers predominantly in the range of C9 to C16 and boiling in the range of 150 to 300°C. DF1 contains little benzene (e.g., less than 0.02%) or polycyclic aromatic hydrocarbons (Millner et al. 1991). DF2 is essentially equivalent to fuel oil No. 2 used for automobiles and boils between 160 and 360°C (IARC 1989). DF2 is more viscous than DF1 and spans a carbon number range of C11 to C20 (IARC 1989). DF2 also contains a greater variety of compounds and includes olefins and mixed aromatic olefin-type compounds, such as styrenes. More information on the composition of diesel fuels can be found in IARC (1989) and Millner et al. (1992). The characteristics of DF2 (Jenkins et al. 1983a) are the following: Composition     Saturated hydrocarbons 70.0%   Substituted benzenes 16.0%   2-Ring aromatics 12.0%   3-Ring aromatics 2.0%   Polar aromatics 0.2% Refractive index 1.477 Density at 25°C (grams per milliliter) 0.844 Viscosity at 25°C (centistokes) 3.35

OCR for page 26
Flash point (°C minimum) Distillation range 74.0   10% Point, °C 186.0   50% Point, °C 271.0   90% Point, °C 298.0 Diesel-fuel smoke—technically, a fog—is a condensation aerosol, consisting of a suspension of 0.5 to 1.0 micrometer (µm) fuel droplets in air. The droplets are individually translucent but opaque en mass. Particles in this range are respirable. The generation of the condensation aerosol is for the purpose of obscuring the soldiers from view; if conditions were such that a major portion of the fuel remained in the vapor form, the system would not achieve its purpose. However, a fraction of the fuel (components with low boiling points) might remain in the vapor form. Combusted fuel might also contribute to the total mass of the smoke, but Callahan et al. (1983) found that vehicle exhaust contributed only 1% to 2% of the total hydrocarbon concentration of the smoke. All measurements of and recommendations for diesel-fuel-smoke concentrations are reported as milligrams of total particulates per cubic meter. TOXICOKINETICS Although no toxicokinetic studies have been conducted with diesel-fuel smoke, some evidence of the deposition and clearance pattern of the smoke is available from studies of Dalbey et al. (1982, 1987) and Lock et al. (1984). In these studies (described in detail in the Toxicity Summary below), the lung was the primary target organ, with several indicators of an inflammatory response. The material appears to deposit and accumulate in the lung, remaining there long enough to induce an inflammatory response. Within a 2-week period, neutrophil levels are back to control levels,

OCR for page 26
suggesting that most of the particles are cleared. However, the macrophage levels are still elevated after that time period, indicating that some inhaled particles might still be in the lung. Dalbey et al. (1982, 1987) and Dalbey and Lock (1982) made use of dodecachlorobiphenyl as a dosimetric tracer for aerosols of diesel-fuel (Jenkins et al. 1983b). The fraction of inhaled diesel-fuel aerosol retained by the rats at the end of exposure was 4% to 8%. The largest internal amounts of the tracer were found in the lungs. Animals exposed to CT products at 8,000 milligrams per cubic meter multiplied by hour (mg•hr/m3) had between 2 and 4 mg of the aerosol particles in their lungs, and animals exposed to CT products at 12,000 mg•hr/m3 had between 3 and 6 mg of particles in their lungs. Tracer found in the upper respiratory tract accounted for less than 1.5% of the total internal dose, and that found in the digestive system accounted for approximately 30% of the total internal dose. TOXICITY SUMMARY Effects in Humans Although extensive data are available on the health effects of combusted diesel-fuel exhaust, little information is available on the health effects of uncombusted diesel-fuel smoke in humans. Volunteers who were exposed to concentrations of 170 and 330 mg/m3 for 10 min reported no irritant effects (Dautrebande and Capps 1950). No other studies involving inhalation exposure of humans have been reported. Repeated exposure to diesel fuel was reported to cause contact dermatitis in sensitive individuals (Il'in et al. 1969), but inadequate personal hygiene was indicated as a contributing factor. The literature regarding gastritis from ingested diesel fuel and pneumonia from aspiration of diesel fuel has been reviewed (Liss-Suter et al. 1978).

OCR for page 26
Effects in Animals Dermal and Ocular Exposures Lethality Repeated application of commercial diesel fuel to the shaved skin of rabbits at 4 and 8 milliliters per kilogram (mL/kg) of body weight produced 0 and 67% mortality, respectively (Beck et al. 1982). Toxic signs included weight loss, anorexia, and severe dermal irritation. Necropsy revealed congested kidneys and livers. Eye and Skin Irritation Commercial diesel fuel did not induce eye irritation in rabbits during a 30-sec application or skin sensitization in guinea pigs (Beck et al. 1982). The fuel was, however, extremely irritating to the skin when applied for 24 hr. Carcinogenic Effects DF2 was positive when tested as a tumor promoter in the SENCAR mouse-skin tumorigenesis bioassay but was negative as a complete carcinogen in the same assay (Slaga et al. 1983). Although no chronic in vivo bioassays have been conducted with diesel fuel per se, mouse skin-painting studies have found some middle distillate fractions of crude oil to be tumorigenic when applied to the skin (clipped free of fur) twice weekly for a lifetime (Blackburn et al. 1984, Lewis et al. 1984). However, Ingram and Grasso (1991) noted that the distillate fractions acted as irritants and, under the conditions of the chronic applications, caused overt skin damage, giving rise to epidermal hyperplasia, which might have enhanced the development of the tumors.

OCR for page 26
Inhalation Exposures Two major sets of animal studies on the toxicity of inhaled diesel-fuel smokes have been produced; one was conducted at Aberdeen Proving Ground (Callahan et al. 1983, 1986) and one at Oak Ridge National Laboratory (Dalbey and Lock 1982; Dalbey et al. 1982, 1987; Lock et al. 1984). These studies cover both one-time and repeated exposures for up to 13 weeks. For one-time exposures, the product of exposure concentration and time is provided. One-Time Exposures Lethality. In a single-exposure study (Callahan et al. 1983), rats (Sprague-Dawley and Fischer 344), mice (B6C3F1), and guinea pigs (Hartley) were exposed to high concentrations of DF1 or DF2 smoke and exhaust for 15, 60, 120, or 300 min under static airflow conditions. The goal was to expose the animals to 10,000 to 12,000 mg/m3 of smoke, as the theoretical average smoke concentration predicted for exposure of military personnel standing within 10 m downwind from the tank, operating at maximal smoke-generating efficiency under strong inversion and low-wind-speed atmospheric conditions. Generation and dissemination of the diesel-fuel smokes were accomplished by accelerating the 750-hp Chrysler engine of the tanks up to 1,700 revolutions per minute (rpm) for approximately 5 min. When the engine manifold temperature reached 1,180°F, the fuel was expelled into the manifold through an orifice and the generated smoke was drawn through a stainless steel tube into a wind tunnel. After a generation period of 5 min, the smoke was shunted into a 20,000-liter cylindrical exposure chamber. Caged animals were placed in the chamber before the introduction of the smoke. For exposures exceeding 60 min, the generation procedure was repeated every 60 min because the hydrocarbon concentrations

OCR for page 26
in the air of the exposure chamber decreased by 65% in 60 min. The average concentration of the DF2 smoke for the 15- and 60-min exposures was 35,000 mg/m3 . The average concentration for the DF1 smoke was 15,000 mg/m3 for exposures from 15 to 300 min. Because dissemination of smoke generated from the M60A1 tank also involves normal exhaust emission from internal engine combustion, the concentration of the exhaust component was monitored. The hydrocarbon concentration from the exhaust of the engine was only 1% to 2% of the total smoke plus exhaust hydrocarbon concentration. The mass median aerodynamic diameter of the smoke particles was 0.23 µm or less (measured by cascade impaction at concentrations of 15,000 to 18,000 mg/m3). Gases were also monitored in the exposure chambers and were reported as not exceeding the following values: NO2, 40 parts per million (ppm); SO2, 20 ppm; CO, 130 ppm; and CO2, 11,000 ppm. Oxygen never dropped below 18.9%. Animals could not be observed during the exposures because of the density of the smoke. At the end of the 15-min exposures to DF2 smoke and exhaust, all animals but the mice appeared lethargic. The 1-hr exposures resulted in lacrimation, oral and nasal frothiness, nasal hemorrhage, and tremors in the guinea pigs. Sprague-Dawley rats manifested cyanosis, and mice showed piloerection. One of 10 F344 rats and 4 of 10 guinea pigs died from the 60-min exposure. Mortality of animals exposed to DF1 smoke increased with increasing length of exposure; after 300 min of exposure, all but 4 mice (out of 10 mice per strain) died. Dalbey and Lock (1982) conducted experiments to establish the maximum tolerated concentration for a given exposure duration in male and female Sprague-Dawley rats. The generation of the aerosol, which was designed to model the vehicle exhaust system used by the military to produce smoke from diesel fuel, consisted of a 1-in. O.D. stainless steel tube about 1 m long, with a Vycor heater fitted into one end. The heater was maintained at 600°C. The distal end of the generator was heated to 350°C by

OCR for page 26
heating tape. Nitrogen entered the tube near the Vycor heater and exited at the opposite end. Diesel fuel was metered onto the tip of the Vycor heater, where it was flash evaporated and carried by the hot nitrogen out of the generator into the cool supply air entering the exposure chamber. Aerosol concentration in the chamber was monitored continuously by infrared backscatter probes at the top and bottom of the chamber. Particle size was determined by cascade impaction at random intervals during the study. The mass median aerodynamic diameter of the particles ranged from 0.43 to 0.75 µm with a geometric standard deviation of 1.4 to 1.5. Air flow through the chamber was maintained at 425 L/m, and aerosol distribution within the chamber was uniform. Exposures were for 2, 4, or 6 hr at concentrations ranging from 670 to 16,000 mg/m3. Exposure groups consisted of five males and five females. Mortality was observed for 2 weeks after the exposures. Mortality was the same in both sexes, and the data were combined. Mortality was found to be highly correlated with C·T, the CT product explaining 83% of the variation in mortality. A probit analysis was used to relate mortality to the log of the CT product so that the CT product that induces 1% mortality could be estimated. That estimate was 12,200 mg·hr/m3, and the 97.5% lower confidence bound of that value was calculated to be 8,200 mg·hr/m3. Pulmonary Effects. The histopathology studies conducted by Callahan et al. (1983, 1986) indicated that the major lesions in the exposed animals were in the respiratory tract. Lesions were found in the nasal turbinates and lungs, and included congestion in the nasal turbinate, bronchopneumonia, bronchitis, peribronchiolitis, peribronchiolar lymphocytosis, pulmonary histiocytosis, and pulmonary congestion with edema and hemorrhage. Dalbey and Lock (1982) found upon necropsy of the rats in their experiments that the only significant gross abnormality was edema in the lungs and occasionally in the trachea.

OCR for page 26
Repeated 15- or 60-Minute Exposures Callahan et al. (1986) exposed B6C3F1 mice and F344 rats to an average of 2,300 mg/m3 of M60A1 tank-generated exhaust and DF2 smoke for 15 or 60 min daily (5 days per week) for up to 13 weeks. Analysis of gas concentrations indicated an average of 4.4 ppm for NO2, 7.5 ppm for SO2, and 16 ppm for CO. CO2 did not exceed 1,000 ppm, and O2 did not go below 20%. The exposures were performed under static airflow conditions as described for the acute toxicity studies (Callahan et al. 1983). Toxicological, physiological, hematological, blood chemical, behavioral, reproductive, mutagenic, teratogenic, and pathological effects were evaluated. The only clinical sign of toxicity observed in the exposed rodents was hypoactivity following the 32 or more consecutive daily exposures. After the daily exposure ended, hypoactivity diminished within 24 hr. Carboxyhemoglobin levels in the exposed rodents did not exceed 11%. No gross pathological change was observed in exposed animals, but the incidence of mild-to-moderate pulmonary congestion increased as compared with controls. Exposed rats also had increased incidences of inflammatory and vascular lesions in nasal turbinates and tracheas. The respiratory-tract changes were of low severity and were not related to the duration of exposure. Therefore, the investigators did not consider the findings likely to be exposure-related. Repeated 4-Hour Exposures Lock et al. (1984) conducted a 13-week study to determine if there were cumulative toxic effects from repeated exposures to low concentrations of diesel-fuel smoke. Male and female Sprague-Dawley rats were exposed for 4 hr, twice a week for 13 weeks (26 exposures). The exposure pattern was meant to mimic what humans might experience in the field. Animals were observed either

OCR for page 26
5 days after the last exposure or after a recovery period of 2 months. Actual exposure concentrations of the smoke were 170, 870, and 1,600 mg/m3, as measured by infrared backscatter probes and averaged over the entire 4-hr exposure period. Observations made during the study included body weight, food consumption, breathing frequency, and startle reflex. After the last exposure, measurements and observations were made of the number of alveolar cells removed by lavage, clinical chemistry, pulmonary function, organ weights, and histopathology. An analysis of variance was conducted, and statistical significance was based on a significance level of 0.05. Body Weight. No deaths occurred during this study, nor were there any overt clinical signs of toxicity. Sham-exposed animals had an initial weight loss during the exposure and then returned to normal weight. The exposed animals also had an initial weight loss upon exposure, but continued to lose weight until the beginning of the fourth week of exposure. After the fourth week, the animals started to gain weight. The males exposed to the lowest concentration gained weight more rapidly than those in the two higher concentrations; females gained little weight throughout the exposure period. During the 2-month recovery period, females in all exposed groups grew more rapidly than males, so the end weights of the females were not different from those of the sham-exposed animals. On the other hand, males gained weight slowly, so only the lowest exposure group had body weights equal to those of the sham-exposed animals. Food consumption in rats of both sexes exposed to the lowest exposure concentration did not differ significantly from that in the sham-exposed group. In the two highest exposure groups, food consumption was less than that in the sham controls. Thus, in terms of weight loss, the aerosol concentrations used were above the no-observed-effect level. Neurological Effects. A startle-reflex assay was used to test the time to reaction and the force of response to a sharp auditory

OCR for page 26
stimulus. Rats were placed in a wire box within a larger sound-insulated box. A constant white noise at 85 decibels (dB) within the larger box helped eliminate outside noises. After an acclimation period of 10 min, rats received five 10-msec pulses of noise at 13,000 Hz and 110 dB separated by 25 sec. Their responses, or startle reflexes, were monitored by a Gould load cell under the wire box. The number of responses made by exposed versus sham-exposed animals was not significantly different in any case. Reaction time (time from start of acoustic stimulus to start of response) was slightly longer in males examined 5 days after 13 weeks of exposure at the highest test concentration (1,600 mg/m3). Female rats exposed at the middle test concentration (870 mg/m3) also had increased reaction times. In both instances, the authors suggested that those differences, although statistically significant, were of doubtful biological importance because the changes were so small (less than 2 msec). The maximum amplitude of the response was statistically significantly higher in the sham-exposed controls than in other groups of males; recovery was complete 1 month after exposure. A similar effect was not observed in females. Statistically significant increases in peak time (time from acoustic stimulus to peak response) occurred in males, particularly in the group exposed at the highest concentration, for which every value measured at every time point through 2 months of recovery was higher than that in the sham-exposed controls. Males exposed at the two lowest concentrations also showed some statistically significant increases in peak time through 1 month of recovery. The differences varied up to 5 msec in females and 3 msec in males; the authors interpreted those values as a significant decrement in performance. In females, the increases in peak time were observed only in the two highest exposure groups, and the differences were no longer seen after 2 months of recovery. The increases in time to peak response in these assays, in the absence of changes in reaction time and in the force exerted, represent a lengthening of the duration of the response. These changes are difficult to interpret. Most of the changes were approximately

OCR for page 26
Rat, DF2 60 min/d, 5 d/wk, 13 wk NOAEL 2,300 Subchronic study: No observed adverse effects on testes weight or histopathology of reproductive organs Callahan et al. 1986 Abbreviations: hr, hour(s); d, day(s); wk, week(s); min, minute(s); FP, focal pneumonitis; GD, gestation day; ♂ male;, male; ♀ female;, female; DF2, diesel-fuel grade 2; DF1, diesel-fuel grade 1; NOAEL, no-observed-adverse-effects level.

OCR for page 26
and Lock (1982) and Callahan et al. (1983) indicated that the major target-organ system for diesel smoke via inhalation exposure is the respiratory tract. They found mortality from the smoke to be dependent on the product of exposure concentration and time (CT). Dalbey et al. (1982, 1987) found that the frequency of exposure also influences the toxicity of diesel-fuel smoke. Once-a-week exposures for 6 hr were much less toxic than 2-hr exposures, three times a week, to the same concentration of smoke. The study of Lock et al. (1984) was designed to determine if repeated exposures to low concentrations of diesel-fuel smoke would cause cumulative toxicity. Rats were exposed for 4 hr, twice a week, for 13 weeks, and observations were made 5 days and 2 months after the end of the exposures. The results indicated little toxicity at exposure concentrations of up to 1,600 mg/m3, except for weight losses at all exposure concentrations, minimal pulmonary-function changes at the highest exposure concentration, and small reversible changes in time to peak startle response. Carcinogenicity Several tests for potential mutagenic activity of diesel fuels were negative (Conaway et al. 1982; Callahan et al. 1986). DF2 tested positive as a tumor promoter, but not as a complete carcinogen, in a mouse skin bioassay (Slaga et al. 1983). No long-term in vivo cancer bioassays have been done for diesel fuel per se. The appearance of tumors in mice exposed to some crude-oil-distillate fractions might be the result of the skin damage produced by repeated applications of the liquids to their shaved skin. Finally, IARC (1989) has concluded that there is inadequate evidence for the carcinogenicity of diesel fuels in humans, but limited evidence for the carcinogenicity of diesel fuel No. 4 (DF4) (also called marine diesel fuel), but not DF1 or DF2, in experimental animals. Diesel exhaust (combusted diesel fuel) might account for 1% to 2% of diesel-fuel smoke if the smoke is generated by a diesel-powered vehicle. IARC has designated diesel exhaust as a 2B carcinogen

OCR for page 26
(i.e., a possible human carcinogen with inadequate evidence in humans and adequate evidence in animals). However, the charge of the subcommittee was to review the toxicity of diesel-fuel smokes per se. The risk assessments for the diesel-fuel smoke were based on the concentration of particles of condensed fuel in the smoke, which, under obscuring conditions, are present at extremely high concentrations compared with soot from the diesel engines that are running the tanks. EXISTING RECOMMENDED EXPOSURE LIMITS Exposure limits have not been recommended for diesel-fuel smoke or its components. The ACGIH TLV-TWA value for diesel fuel of 350 mg/m3 refers to total hydrocarbons as vapor, not as an aerosol of the total fuel (ACGIH 1995). SUBCOMMITTEE EVALUATION AND RECOMMENDATIONS On the basis of the toxicity information described above, the subcommittee has developed exposure guidance levels for military personnel exposed during an emergency release or during regular training exercises and for communities nearby training facilities to protect them from emergency or repeated releases of diesel-fuel smoke. Inhalation studies indicate that the respiratory tract is the primary target organ system following exposure to diesel-fuel smoke and that mortality from a one-time exposure is dependent on C•T. Repeated-exposure studies indicate that pulmonary toxicity also depends on the frequency of exposure. One 6-hr exposure per week at the same concentration (4,000 mg/m3) of smoke was less toxic to the lung than three 2-hr exposures a week (Dalbey et al. 1982, 1987). That finding indicates that for a given CT product, toxicity increases with the frequency of exposure. Therefore,

OCR for page 26
the subcommittee recommends that training exercises without masking be conducted no more frequently than twice a week. Military Exposures Emergency Exposure Guidance Level (EEGL)1 For the EEGLs, the subcommittee considered the acute toxicity studies of Dalbey and Lock (1982) and Callahan et al. (1983). Dalbey and Lock (1982) used a probit analysis to estimate the CT product that induced 1% mortality. The 97.5% lower confidence bound of this value was 8,200 mg•hr/m3. Considering the severity of the end point (death), the subcommittee divided that value by an uncertainty factor of 10 to predict a nonpermanent health impairment and by another uncertainty factor of 10 to account for interspecies sensitivity to arrive at an EEGL of 80 mg•hr/m3. That CT product results in a 15-min EEGL of 320 mg/m3, rounded to 300 mg/m3, a 1-hr EEGL of 80 mg/m3, and a 6-hr EEGL of 15 mg/m3. Support for the assumption that permanent health effects would not occur from exposure at these concentrations comes from the repeated exposure studies of Dalbey et al. (1987), in which rats exposed once a week for 9 weeks to a weekly CT product of 8,000 mg•hr/m3 exhibited only equivocal pulmonary inflammation, which remained equivocal after a 2-week recovery period. In addition, human volunteers exposed to diesel-fuel smoke at 330 mg/m3 for 10 min reported no irritant effects. Permissible Exposure Guidance Level (PEGL)2 The most relevant toxicity study for recommending PEGLs 1   Guidance for a rare, emergency situation resulting in an exposure of military personnel. 2   Guidance for repeated exposure of military personnel during training exercises.

OCR for page 26
involved repeated exposures of rats twice a week for 13 weeks (Lock et al. 1984). Exposure of rats for 4 hr, twice a week, to diesel-fuel smoke at concentrations as high as 1,600 mg/m3 caused no lesions in the respiratory tract. The exposures did cause weight losses and reduced weight gains that resulted in weight deficits of greater than 10% for males, as compared with sham-exposed rats at the two highest exposure concentrations and with females even at the lowest exposure concentration. At the lowest exposure concentration, the weight deficit did not increase beyond 10% until after 10 weeks of exposure. Two months after the exposure, male body weights only returned to those of sham-exposed controls. Female weights in all exposure groups returned to control concentrations. If one considers the lower exposure concentration of 170 mg/m3 for 4 hr, twice a week for at least 10 weeks, to be a no-observed-adverse-effect level (NOAEL, i.e., 1,360 mg•hr/m3 per week), then the PEGL would be calculated as one-tenth that value (140 mg•hr/m3 per week) to account for species differences. The subcommittee also considered the studies of Dalbey et al. (1982, 1987). In those studies, rats exposed to 4,000 mg/m3 of smoke for 2 hr, once a week for 9 weeks had equivocal signs of focal pneumonitis, and the equivocal lesion had not recovered 2 weeks later (Table 2-1). That regimen amounted to a weekly exposure of 8,000 mg•hr/m3 and is considered a lowest-observed-adverse-effect level (LOAEL). Dividing by 100 to convert from the LOAEL to an expected NOAEL and to account for species differences, the PEGL is 80 mg•hr/m3 within 1 week, with no more than two exposures per week. The subcommittee chose 80 mg•hr/m3 per week as the PEGL because it was the lower value of the two alternatives. The subcommittee assumed that an exposure event occurred over an extended period, such as 8 hr. Thus, the PEGL for a single exposure in 1 week would equal 10 mg/m3 for an 8-hr exposure, and the PEGL for two exposures in 1 week would equal 5 mg/m3 for each of two 8-hr exposures. The subcommittee recommends those PEGLs as ceiling values; in other words, those PEGLs apply even if the exposure events are less than 8 hr in a given day. The CT

OCR for page 26
product for the PEGLs is the same as the CT product for the EEGLs; however, the maximum exposure concentration and rate of exposure are less for the PEGLs than for the EEGLs. The subcommittee also recommends that protective equipment be worn if exposures to diesel-fuel smoke during training appears to produce chronic dermatitis in any individuals. Public Exposures Short-Term Public Emergency Guidance Level (SPEGL)3 The SPEGL should accommodate the wide range of sensitivity possible in the general population compared with military personnel; therefore, a value equal to one tenth the EEGL is recommended (NRC 1986). It should be emphasized that the EEGL and SPEGL values are for emergency situations only. The SPEGL is 8 mg•hr/m3 for a maximum of 6 hr for an emergency exposure. Permissible Public Exposure Guidance Level (PPEGL)4 This value is equal to the PEGL divided by 10 to protect sensitive members of the public (NRC 1986). Thus, the subcommittee chose 8 mg•hr/m3 per week as the PPEGL, with no more than two exposures per week. As for the PEGL, the subcommittee assumed that an exposure event occurs over an extended period, such as 8 hr. Thus, the PPEGL for a single exposure in 1 week would equal 1 mg/m3 for an 8-hr exposure, and the PPEGL for two exposures in 1 week would equal 0.5 mg/m3 for each of two 8-hr 3   Guidance for a rare, emergency situation potentially resulting in an exposure of the public to a military-training smoke. 4   Guidance for repeated exposures of public communities near military-training facilities.

OCR for page 26
exposures. The PPEGLs represent ceiling values; in other words, those PPEGLs apply even if the exposure events are less than 8 hr in a given day. The CT product for the PPEGLs is the same as the CT product for the SPEGLs; however, the maximum exposure concentration and rate of exposure are less for the PPEGLs than for the SPEGLs. Summary of Subcommittee Recommendations The exposure guidance levels for diesel-fuel smoke for military personnel are summarized in Table 2-3. The exposure guidance levels for diesel-fuel smoke to protect the public in the vicinity of training facilities are summarized in Table 2-4. TABLE 2-3 EEGLs and PEGLs for Diesel-Fuel Smoke for Military Personnel Exposure Guideline Exposure Duration Guidance Level (mg/m3) EEGL 15 min 300   1 hr 80   6 hr 15 PEGL 8 hr/d, 1 d/wk 10   8 hr/d, 2 d/wk 5 TABLE 2-4 SPEGLs and PPEGLs for Diesel-Fuel Smoke at the Boundaries of Military Training Facilities Exposure Guideline Exposure Duration Guidance Level (mg/m3) SPEGL 15 min 30   1 hr 8.0   6 hr 1.5 PPEGL 8 hr/d, 1 d/wk 1   8 hr/d, 2 d/wk 0.5

OCR for page 26
RESEARCH NEEDS Recommendations for diesel-fuel smoke were based on studies conducted in laboratory animals over relatively short durations, all less than 3 months. It is not known if the modest adverse effects noted at the end of these exposures would have increased in severity had the exposures continued for longer durations. Some military personnel are exposed to smoke during training exercises over several years. Toxicity studies conducted over exposure durations longer than 10 weeks, perhaps up to 1 or 2 years, would provide the information necessary to evaluate human health risks due to years of exposure to diesel-fuel smoke during training exercises. Army personnel who work with this smoke, trainers in particular, represent a rich source of potential information on the health effects of the smoke. The subcommittee recommends that the U.S. Army conduct a prospective study with appropriate controls in which pulmonary-function tests (spirometry and diffusing capacity at a minimum) and routine chemistry tests (panel 20 plus Mg and thyroid tests as a minimum) are conducted on personnel who are exposed repeatedly to the smoke. Additional studies are recommended to explore fully the potential for reproductive and developmental effects of exposure to diesel-fuel smokes. To evaluate male and female reproductive toxicity, a two-generation study, including a detailed evaluation of reproductive effects, is recommended. Developmental effects have been evaluated only in Sprague-Dawley rats; conclusions would be more robust if similar findings were observed in a second species of mammal. REFERENCES 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. Blackburn, G.R., R.A. Deitch, C.A. Schreiner, M.A. Mehlman, and

OCR for page 26
C.R. Mackerer. 1984. Estimation of the dermal carcinogenic activity of petroleum fractions using a modified Ames assay. Cell Biol. Toxicol. 1:67-80. 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. Callahan, J.F., C.L. Crouse, G.E. Affleck, R.L. Farrand, R.W. Dorsey, M.S. Ghumman, R.J. Pellerin, D.H. Heitkamp, C. Lilly, J.J. Feeney and J.T. Weimer. 1983. The Acute Inhalation Toxicity of Diesel Fuels (DF2 and DF1) Used in Vehicle Engine Exhaust Smoke Systems (VEESS). Tech. Rep. ARCSL-TR-82064. Chemical Systems Laboratory, U.S. Army Armament, Munitions and Chemical Command, Aberdeen Proving Ground, Edgewood, Md. Callahan, J.F., C.L. Crouse, G.E. Affleck, E.G. Cummings, R.L. Farrand, R.W. Dorsey, M.S. Ghumman, R.D. Armstrong, W.C. Starke, R.J. Pellerin, D.C. Burnett, D.H. Heitkamp, C. Lilly, J.J. Feeney, M. Rausa, E.H. Kandel, J.D. Bergmann, and J.T. Weimer. 1986. The Subchronic Inhalation Toxicity of DF2 (Diesel Fuel) Used in Vehicle Engine Exhaust Smoke Systems (VEESS). Tech. Rep. CRDCTR-85009. Chemical Research and Development Center, U.S. Army Armament, Munitions and Chemical Command, Aberdeen Proving Ground , Edgewood, Md. Conaway, C.C., C.A. Schreiner, and S.T. Cragg. 1982. Mutagenicity evaluation of petroleum hydrocarbons. Pp. 128-138 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. Dalbey, W., and S. Lock. 1982. Chemical Characterization and Toxicological Evaluation of Airborne Mixtures. Inhalation Toxicology of Diesel Fuel Obscurant Aerosol in Sprague-Dawley Rats, Final Report, Phase 1, Acute Exposures. ORNL/TM-8867. AD-A132 650. Oak Ridge National Laboratory, Oak Ridge, Tenn. Dalbey, W., S. Lock, and R. Schmoyer. 1982. Chemical Characterization and Toxicological Evaluation of Airborne Mixtures. Inhalation Toxicology of Diesel Fuel Obscurant Aerosol in Sprague-Dawley Rats, Final Report, Phase 2, Repeated Exposures. ORNL/TM-9169.

OCR for page 26
AD-A142 540. Oak Ridge National Laboratory, Oak Ridge, Tenn. Dalbey W., M. Henry, R. Holmberg, J. Moneyhun, R. Schmoyer, and S. Lock. 1987. Role of exposure parameters in toxicity of aerosolized diesel fuel in the rat. J. Appl. Toxicol. 7:265-275. Dautrebande, L., and R. Capps. 1950. Studies on aerosols. IX. Enhancement of irritating effects of various substances on the eye, nose, and throat by particulate matter and liquid aerosols in connection with pollution of the atmosphere. Arch. Int. Pharmacodynam. Ther. 82:505-528. IARC (International Agency for Research on Cancer). 1989. Diesel fuels. Pp. 219-237 in IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Occupational Exposures in Petroleum Refining; Crude Oil and Major Petroleum Fuels, Vol. 45. Lyon, France: International Agency for Research on Cancer. Il'in, B.I., L.I. Kogan, and N.V. Buzulutskii. 1969. Suppurative diseases in persons working with fuels and lubricants [in Russian]. Voen. Med. Zh. 9:69. Ingram, A.J., and P. Grasso. 1991. Evidence for and possible mechanisms of non-genotoxic carcinogenesis in mouse skin. Mutat. Res. 248:333-340. Jenkins, R.A., R.W. Holmberg, J.S. Wike, J.H. Moneyhan, and R.S. Brazell. 1983a. Chemical Characterizations and Toxicologic Evaluation of Airborne Mixtures. ORNL/TM-9196. AD-A142 718. Oak Ridge National Laboratory, Oak Ridge, Tenn. Jenkins, R.A., D.L. Manning, M.P. Maskatinec, J.H. Moneyhun, and W. Dalbey. 1983b. Chemical Characterization and Toxicologic Evaluation of Airborne Mixtures. Diesel Fuel Smoke Particulate Dosimetry in Sprague-Dawley Rats. ORNL/TM-9195. AD-A142 914. Oak Ridge National Laboratory, Oak Ridge, Tenn. Lewis, S.C., R.W. King, S.T. Cragg, and D.W. Hillman. 1984. Skin carcinogenic potential of petroleum hydrocarbons: Crude oil, distillate fractions and chemical class subfractions. Pp. 139-150 in Advances in Modern Environmental Toxicology: Applied Toxicology of Petroleum Hydrocarbons, Vol. 6, N.H. MacFarland, C.E. Holdsworth, J.A. MacGregor, R.W. Call, and M.L. Kane, eds. Princeton, N.J.: Princeton Scientific Publishers. Liss-Suter, D., R. Mason, and P.N. Craig. 1978. A Literature Review—Problem Definition Studies on Selected Toxic Chemicals: Occupational Health and Safety Aspects of Diesel Fuel and White Smoke

OCR for page 26
Generated From It, Vol. 1. DAMD17-77-C-7020. AD-A056 018. Science Information Services Department, Franklin Institute Research Laboratories, Rockville, Md. Lock, S., W. Dalbey, R. Schmoyer, and R. Griesemer. 1984. Chemical Characterization and Toxicological Evaluation of Airborne Mixtures. Inhalation Toxicology of Diesel Fuel Obscurant Aerosol in Sprague-Dawley Rats, Final Report, Phase 3, Subchronic Exposures. ORNL/TM-9403. AD-A150 100. Oak Ridge National Laboratory, Oak Ridge, Tenn. NRC (National Research Council). 1986. Criteria and Methods for Preparing Emergency Exposure Guidance Level (EEGL), Short-term Public Emergency Guidance Level (SPEGL), and Continuous Exposure Guidance Level (CEGL) Documents. Washington, D.C.: National Academy Press. Slaga, T.J., L.L. Triplett, and R.J.M. Fry. 1983. Chemical Characterization and Toxicological Evaluation of Airborne Mixtures. Tumorigenicity Studies of Diesel Fuel-2, Red Smoke Dye, and Violet Smoke Dyes in the SENCAR Mouse Skin Tumorigenesis Bioassay System. ORNL/TM-9752. AD-A159 728. Oak Ridge National Laboratory, Oak Ridge, Tenn. Starke, W.C., R.J. Pellerin, D.C. Burnett, J.H. Manthei, and D.H. Heitkamp. 1987. Teratogenicity, Mutagenicity, and Effects of Grade 2 Diesel Fuel on Reproduction in a Single Generation of Rats. Tech. Rep. CRDEC-TR-87083. Chemical Research, Development and Engineering Center, U.S. Army Armament, Munitions and Chemical Command, Aberdeen Proving Ground, Edgewood, Md.