White Phosphorus Smoke

National Research Council (US) Subcommittee on Military Smokes and Obscurants

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National Research Council (US) Subcommittee on Military Smokes and Obscurants. Toxicity of Military Smokes and Obscurants: Volume 2. Washington (DC): National Academies Press (US); 1999.

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Toxicity of Military Smokes and Obscurants: Volume 2.

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2White Phosphorus Smoke

Background Information

Obscurants, such as phosphorus smokes, are effective in blocking the transmission of a particular part of the electromagnetic spectrum, such as visible light, infrared light, or microwaves. Military application of phosphorus smokes for screening during a military operation can make use of either white phosphorus (WP) or red phosphorus (RP). WP is the most effective smoke agent to defeat thermal imagery systems. It can be absorbed by the inhalation, ingestion, or dermal routes; however, the primary route is inhalation. This chapter provides an evaluation of the health effects of elemental WP and WP smoke. Volume 1 of this series reviewed the toxicity associated with the inhalation of red phosphorus smoke (NRC 1997).

Military Applications

The military uses smokes, such as WP, to protect friendly forces, support deception operations, identify enemy targets and tactical locations, and obscure certain reconnaissance activities, surveillance, and targets from enemy forces. WP is used in mortar and artillery shells and in grenades. WP used as a military obscurant is impregnated in a felt matrix and is referred to as white phosphorus-felt. Unprotected troops in training exercise or combat are likely to inhale the smoke from a detonated grenade. The U.S. Environmental Protection Agency (EPA) estimated that an exposure concentration of WP could reach 146 milligrams per cubic meter (mg/m³) as phosphorus pentoxide (P_{2 O5}) (202 mg/m³ as orthophosphoric acid (H₃PO₄)) 100 m downwind from deployment and about 1.0 mg/m³ as P₂O₅ (1.4 mg/m³ as H₃PO₄) 5,000 m downwind (EPA 1990). EPA does not expect community exposures to be severe at a distance of greater than 300 m; however, particularly susceptible individuals might experience respiratory irritation even at a distance of 5,000 m (EPA 1990).

PHYSICAL AND CHEMICAL PROPERTIES

CAS no.:	12185-10-3
Synonyms:	yellow phosphorus, phosphorus
Chemical formula:	tetramer
Chemical weight:	P₄
Physical state:	123.9
Density at 20°C:	waxy solid 1.82 g/cm³
Melting point:	44.1°C
Boiling point:	280°C
Vapor pressure (20°C):	0.025 mm Hg
Flash point:	spontaneous in air
Solubility in water:	3 mg/L
Conversion factor:	1 ppm = 5.150 mg/m³ at 20°C

Elemental phosphorus exists in a number of allotropic forms. WP is an inorganic chemical that has a slight yellow color caused by traces of red phosphorus impurities and is often referred to as yellow phosphorus. WP is poorly soluble in water but is soluble in nonpolar organic solvents, such as benzene. WP can react with water to form a gaseous compound, phosphine (PH₃), which is toxic to the central nervous system and the liver. PH₃ will rapidly volatilize from water into air because of its low water solubility and high vapor pressure. In the air, PH₃ is converted to less harmful chemicals.

Occurrence and Use

WP is a form of phosphorus that does not occur naturally. It is manufactured from naturally occurring phosphate rocks (ATSDR 1997). WP has been used in producing phosphoric acid, fertilizers, additives in food and beverages, cleaning compounds, fireworks, and smoke bombs. WP can enter the environment in areas of elemental phosphorus production sites and hazardous dump sites, near industries that use it, from accidental spills, and during military use in training and warfare. Because of the high reactivity of WP, it usually is not found far from the source of contamination.

Combustion Products

When munitions containing WP are fired, they burn and produce smoke. The combustion of WP will produce smoke made up of various oxides of phosphorus, including P₂O₅ and phosphorus trioxide (P₄O₆). These oxides react rapidly with moisture to form a number of transformation products, such as H₃PO₄ and pyrophosphoric acid (H₄P₂O₇) (Table 2-1; Brazell et al. 1984) and about 10% unburned phosphorus (Spanggord et al. 1985; ATSDR 1997). Organic compounds (concentrations in parts per billion) and some inorganic gases might be present, but only at trace levels. Because WP is not likely to persist long in air, a majority of phosphorus compounds released and dispersed in air during military use of smokes are likely to be deposited as phosphoric acid or phosphates on land and water (EPA 1990). The smoke particle diameter is about 1 micrometer (µm) by count, 98% of the particles are below 2µm in diameter (Katz et al. 1981).

TABLE 2-1

Composition of Phosphoric Acids in White Phosphorus Smokes Produced from Static Burn.

The chemical characteristics of WP and red-phosphorus-butyl-rubber (RP-BR) smokes are similar; both are primarily phosphoric acids, present as a complex mixture of polymeric forms. WP reacts more rapidly in air (t_1/2= 5 min), and RP-BR is more persistent in air (t_1/2= 1.8 years) (Spanggord et al. 1985; EPA 1990). However, if the particulate phosphorus is coated with a protective layer of oxide, further oxidation might not occur, increasing the lifetime of the elemental phosphorus in the air and on the ground after deposition (ATSDR 1997).

Measurement

Different methods have been used to measure or estimate the concentration of WP smoke in the air. In the toxicological literature, some authors have reported concentrations in terms of P₂O₅ (molecular weight (mol wt) 141.94; which exists as P₄O₁₀; mol wt 283.89) equivalents (White and Armstrong 1935) and others in terms of H₃PO₄ (mol wt 98.00) equivalents (Brown et al. 1980, 1981; Starke et al. 1982). Concentrations in the air can also be estimated by subtracting the residue remaining from the mass of a quantity burned in an enclosed area of known volume.

To estimate P₂O₅, Armstrong and White (1935) captured the phosphorus smoke on dry asbestos filters and brought the residue into solution by rinsing with water and then boiling the solution for 30 min. They found that boiling for 30 min yields practically complete hydration of P₂O₅ to H₃PO₄, which then can be measured by titration with a phenolphthalein indicator. Brown et al. (1980, 1981), Weimer et al. (1977), and presumably Starke et al. (1982) boiled the solution for 10 min to convert the phosphorus acids to H₃PO₄ and, using a pH meter as an indicator, titrated the solution to a pH of 9.6 with sodium hydroxide. The molecular weight of H₃PO₄ is 98.00, or 32.66 mg/mole of hydrogen atoms. Brown et al. (1981) stated that they multiplied the normality of the acid by 32.66 mg. That calculation assumes that all three hydrogens on the acid are ionized at pH 9.6; that is not the case. The dissociation constants, pK, for H₃PO₄, steps 1, 2, and 3, are 2.12 (at 25°C), 7.21 (at 25°C), and 12.67 (at18°C), respectively (Lide 1991). Thus, at pH 9.6, only two of the hydrogen ions are dissociated. Hence, the subcommittee multiplied the H₃PO₄ equivalents estimated by Brown et al. (1980, 1981) and Starke et al. (1982) by 3/2 to correct for the undissociated HPO₄ ^-2 not accounted for in the original estimates. For example, if Brown et al. (1981) reported that an average exposure concentration of H₃PO₄ equivalents was 589 mg/m³, that concentration was multiplied by 3/2 to yield H₃PO₄ equivalents at 884 mg/m³.

For the sake of consistency in this report, toxicity data for WP smoke are reported as H₃PO₄ equivalents when possible. Exposure to H₃PO₄ would occur because it is a combustion endproduct. To convert P₂O₅ equivalents to H₃PO₄ equivalents, the concentration of the former is multiplied by a factor of 195.99/141.94 or 1.381. Each P₂O₅ molecule (mol wt 141.94) produces two H₃PO₄ molecules (mol wt 98.00) when hydrated. Thus, 141.94 grams (g) of P₂O₅ is equivalent to 195.99 g of H₃PO₄.

Toxicokinetics

The toxicokinetics and ultimate fate of inhaled WP in the body are unknown. No studies have been conducted on the absorption, distribution, metabolism or excretion of WP following inhalation of WP smoke by either humans or animals. Although it is not known whether inhaled WP enters the blood, the oxides and acids of WP that occur in the smoke might be absorbed, but to an unknown extent, and possibly distributed systemically.

Toxicity Summary: White Phosphorus And White Phosphorus Smoke

White Phosphorus: Human and Animal Studies

Generally, WP is highly toxic when individuals accidentally or intentionally ingest a single dose, in contrast to RP, which is insoluble and not absorbed when ingested (Simon and Pickering 1976; Wasti et al. 1978). Oral ingestion of WP in humans can be lethal at concentrations of 1 mg/kilogram (kg) of body weight (H₃PO₄ at 3.2 mg/kg). Amounts as low as 0.2 mg/kg (H₃PO₄ at 0.63 mg/kg) can cause severe effects (Wasti et al. 1978; Yon et al. 1983). Fatal or near-fatal human exposures have occurred as a consequence of oral ingestion during a suicide attempt or as a consequence of dermal burns during munitions explosions. Systemic effects following oral ingestion in humans and animals usually begin with severe gastrointestinal distress resulting from irritation of the gastrointestinal lining. That can be followed (during the next 3 weeks) by potentially life-threatening organ impairments such as cardiac arrest, fatty infiltration of the liver and kidneys, and hepatomegaly. Hematological and neurological effects have also been observed.

No studies have investigated the lethal effects of inhalation of WP by humans nor have they reported possible effects from short-term exposures; such effects might include respiratory, cardiovascular, gastrointestinal, hematological, hepatic, renal, dermal and ocular, immunological, neurological, reproductive, developmental, genotoxic, and carcinogenic effects.

However, long-term occupational exposure to airborne phosphorus vapors present in the atmosphere of a factory has been found to produce a degenerative condition resulting in necrosis of the jaw, known as phossy jaw, in some workers. The effects can be extreme, involving severe necrosis of the entire oral cavity, including the soft tissue, teeth, and bones (Heimann 1946 and Hughes et al. 1962, as cited in ATSDR 1997). Massive life-threatening infections can follow. The effect is thought to be a result of direct contact of the inhaled white phosphorus particles with the tissues in the mouth.

No laboratory animal studies have investigated the gastrointestinal, musculoskeletal, dermal and ocular, immunological, developmental, reproductive, neurological, genotoxic, or carcinogenic effects of inhaled WP. One study found the lowest published lethal concentration of WP for mice to be 500 mg/m³ (H₃PO₄ at 1,600 mg/m³) for 10 min (Lee et al. 1975). In another study, rabbits exposed for 30 min to WP at concentrations of 150–160 mg/m³ (H₃PO₄ at 470–500 mg/m³) for 60 days exhibited a decrease in hemoglobin and erythrocyte counts (Maruo 1955). A study that placed rats for an intermediate duration in a phosphorus factory that was reported to contain WP and certain inorganic compounds described degeneration of the tongue and oral mucous of the cheek, gum, and hard palate (Ruzuddinov and Rys-Uly 1986, as cited in ATSDR 1997). The exposure duration and concentrations were not reported.

WP has been tested for mutagenicity in the Ames test. WP in water at a concentration of 100 microliters (µL) per plate produced no mutagenic activity in Salmonella strains TA100, TA1535, TA98, TA1537, and TA1538 in either the presence or the absence of metabolic activation (Ellis et al. 1978, as cited in EPA 1990).

White Phosphorus Smoke: Effects In Humans

Relatively little information has been reported on human responses to inhalation of WP smoke. Exposure of 108 men to WP smoke at 87–1,770 mg/m³ resulted in coughing and irritation of the throat (Cullumbine 1944, as cited in Wasti et al. 1978). The method used to measure the smoke concentration and the length of exposure were not reported. From those data, Cullumbine (1944, as cited in Wasti et al. 1978) estimated that the minimal exposure concentration causing coughing and throat irritation is about 700 mg/m³ for working individuals and 1,000 mg/m³ for individuals at rest.

A number of studies were conducted by White and Armstrong in 1935 with human volunteers. In most of those studies, the individuals were placed in a chamber, and then WP smoke was introduced. Male subjects were exposed to WP smoke with average concentrations of P₂O₅ at 188–514 mg/m³ for 2 to 15 min (White and Armstrong 1935). At the lowest concentration (P₂O₅ at 188 mg/m³ or H₃PO₄ at 259 mg/m ³), a 5-min exposure resulted in 50% of the individuals reporting respiratory distress, coughing, congestion, and throat irritation. At the highest concentration (P₂O₅ at 514 mg/m³ or H₃PO₄ at 710 mg/m ³), a 15-min exposure resulted in all subjects reporting tightness in the chest, coughing, nose irritation, and difficulty in speaking. The authors stated that exposure at an average concentration of P ₂O₅ at 514 mg/m³ (H₃PO₄ at 710 mg/m³) approaches the maximum concentration that can be tolerated for 15 min without serious effects. White and Armstrong (1935) stated that the concentration reported for the studies did not represent the maximum concentration to which the subjects were exposed, but instead represented an average of the concentration measurements taken throughout the exposure period. Thus, the maximum concentration in the chamber must have been considerably higher than the average concentration reported. For that reason, the White and Armstrong studies were not used in recommending guidance levels.

White and Armstrong (1935) conducted two additional studies in which the volunteers entered the chamber after the WP smoke concentration reached the desired level. In one study, a 2-min exposure of P₂O₅ at 588 mg/m³ (H₃PO₄ at 812 mg/m³) resulted in coughing, tightness in the throat, and headaches. One individual developed acute bronchitis. In the second study, six volunteers were exposed for 3.5 min at a concentration of P₂O₅ at 592 mg/m³ (H₃PO₄ at 818 mg/m³). The effects reported were similar to those reported for the 2-min exposure. All effects were reversible.

An accidental exposure of four females to WP smoke in a closed room for 15–20 min (concentration not reported) resulted in numerous respiratory symptoms (i.e., nose and throat irritation), edema of larynx and vocal cords, and coughing. Injury apparently extended into the bronchi. Chest X-rays revealed patchy areas of infiltration that later cleared; however, laryngitis persisted for several months (Walker et al. 1947).

Five males were exposed to WP smoke composed of phosphorus at 35 mg/m³ and P₂O₅ at 22 mg/m³ for 2 to 6 hr at 7-hr intervals, equivalent to H₃PO₄ at 140 mg/m³ (total exposure time not given). Within 6 to 20 hr, all developed symptoms of weakness, dry cough, headaches, tracheobronchitis, rales, tender and enlarged liver, and evidence of leukocytosis with relative lymphocytopenia (Aizenshtadt et al. 1971, as cited in Wasti et al. 1978). Erythrocyte acetylcholinesterase was reduced by 17%, and plasma acetylcholinesterase was reduced by 35%.

No deaths were reported in humans exposed to WP smoke with H₃PO₄ at concentrations as high as 817 mg/m³ (P₂O₅, at 592 mg/m³) for 3 to 5 min or with H₃PO₄ at 709 mg/m³ (P₂O₅ at 514 mg/m³) for 15 min White and Armstrong 1935).

There are no data on gastrointestinal, cardiovascular, musculoskeletal, hepatic, renal, dermal and ocular, immunological, neurological, reproductive, developmental, genotoxic, or carcinogenic effects from inhalation of WP smoke by humans.

White Phosphorus Smoke: Effects in Animals

Lethality

Lethality studies have been conducted on mice, rats, guinea pigs and goats following the inhalation of WP smoke. In mice, exposure for 1 hr resulted in mortality ranging from 5% with P₂O₅ at 110 mg/m ³ (H₃PO₄ at 150 mg/m³) to 95% with P₂O₅ at 1,690 mg/m³ (H₃PO₄ at 2,330 mg/m³) (White and Armstrong 1935). The authors stated that the mice appeared to have died of mechanical obstruction to respiration, and the data probably have little or no relevance to the true toxicity of WP smoke to mice. Rats and goats appeared to be more tolerant; mortality following a 1-hr exposure ranged from 0% with P₂O₅ at 380 mg/m³ (H₃PO₄ at 525 mg/m³) to 100% with P₂O₅ at 4,810 mg/m³ (H₃PO₄ at 6,200 mg/m³) for rats and 0% with P₂O₅ at 4,810 mg/m³ (H₃PO₄ at 6,640 mg/m³) to 100% with P₂O₅ at 8,010 mg/m³ (H₃PO₄ at 11,100 mg/m³) for goats (White and Armstrong 1935). Shinn et al. (1985) estimated that the lethal concentration for 50% of the test animals (LC₅₀ for rats exposed to WP smoke for 1 hr was 2,500 mg/m³ (chemical form not reported). Shinn et al. (1985) noted that the LC₅₀ values from four inhalation toxicity studies of rats exposed to WP smoke ranged from 1,300 to 4,800 mg/m³ (method of measuring WP-smoke concentration not reported). The acute signs of toxicity reported were pulmonary congestion, hemorrhage, inflammation of the trachea, pneumonia, and cloudy swelling of the liver, heart, and kidney.

Rats were exposed for 60–90 min to concentrations of WP smoke with H₃PO₄ ranging from 758 to 3,030 mg/m³. The C x T values for H₃PO₄ ranged from 45,400 to 272,000 mg•min/m³ (Brown et al. 1980). With a 90-min exposure, the mortality of rats ranged from 0% at H₃PO₄ concentrations up to 1,200 mg/m³ to 90% at H₃PO₄ concentrations of 3,030 mg/m³ (Brown et al. 1980; EPA 1990). The lethal concentration for 50% of the test animals multiplied by exposure time (LCt₅₀) for H₃PO₄ was determined to be 141,000 mg•min/m³ (Brown et al. 1980). In those studies, the signs of toxicity from H₃PO₄ were gasping and ataxia at 1,200 mg/m³ (108,000 mg•min/m³), but all animals exposed at that concentration recovered. Histopathological examination from the highest exposure group showed fibrin thrombi in heart and lungs, acute diffuse congestion, focal perivascular edema, and hemorrhage in the lungs.

With subchronic exposures (15 min per day, 5 days per week for 13 weeks) to WP smoke with H₃PO₄ at 1,740 mg/m³, 23 of 72 rats died within 6 weeks, and a total of 29 died by the end of the 13-week study (Brown et al. 1981). There were no deaths at concentrations of H₃PO₄ of <884 mg/m³.

Death occurred in all guinea pigs exposed for 30 min to WP smoke with H₃PO₄ at 716 mg/m³ or for 60 min with H₃PO₄ at 1,200 mg/m³ (C x T = 21,500 and 72,100 mg•min/m³, respectively) (Brown et al. 1980). The LCt₅₀ estimate for H₃PO₄ was 7,980 mg•min/m³, with a 95% confidence limit for H₃PO₄ of 7,124 to 8,943 mg•min/m³ (Brown et al. 1980). Respiratory distress was evident in animals exposed to WP smoke with H₃PO₄ at a C × T > 8,120 mg•min/m³. Studies that measured pulmonary resistance in guinea pigs exposed at 5,760 and 7,920 mg•min/m³ did not reveal any difference from controls (Brown et al. 1980).

Respiratory Effects

Signs of respiratory-tract irritation (slight-to-intense congestion, edema, and hemorrhage) were observed in the lungs of mice, rats, and goats following inhalation exposure to WP smoke (White and Armstrong 1935; Brown et al. 1980). A 60-min exposure of mice, rats, and goats produced clear signs of irritation to H₃PO₄ at concentrations of 152, 525, 745 mg/m³, respectively (White and Armstrong 1935). Longer-term exposures (15 min per day, 5 days per week for 6 or 13 weeks) of rats with H₃PO₄ at 884 mg/m³ resulted in slight laryngitis and tracheitis (Brown et al. 1981). A similar exposure, but at higher concentrations (H₃PO₄ at 1,742 mg/m³), resulted in wheezing, dyspnea, moderate-to-severe laryngitis and tracheitis, and interstitial pneumonia (White and Armstrong 1935; Brown et al. 1981).

Hepatic Effects

A slight clouding and swelling was observed in the livers of rats exposed for 1 hr to WP smoke with H₃PO₄ at >1,615 mg/m³ (White and Armstrong 1935) or at 3,027 mg/m³ for 90 min (Brown et al. 1980). Those effects were also seen in mice and goats exposed for 1 hr at H₃PO₄ concentrations of 649 and 10,104 mg/m³, respectively (White and Armstrong 1935). No such hepatic effects were reported in 6 of 10 guinea pigs that died from exposure for as long as 10 min to H ₃PO₄ at 984 mg/m³ (Brown et al. 1980).

Renal Effects

A slight clouding and swelling in the kidneys of rats, mice, and goats were reported following a 1-hr exposure to WP smoke with H₃PO ₄ at >1,615, 649, or 10,104 mg/m³, respectively (White and Armstrong 1935). No renal effects were observed in rats exposed for 90 min to WP smoke with H₃PO₄ at 3,030 mg/m³ or guinea pigs exposed for 10 min at 984 mg/m³, respectively (Brown et al. 1980). Longer-term exposures (15 min per day, 5 day per week for 13 weeks) to WP smoke with H₃PO₄ at concentrations as high as 1,742 mg/m³ failed to produce any significant gross or histological changes in the kidneys (Brown et al. 1981).

Reproductive and Developmental Effects

In a teratology study, pregnant female rats were exposed by inhalation to WP smoke with H₃PO₄ at concentrations of 884 and 1,742 mg/m³ for 15 min per day for 10 days on gestation days 6–15, and fetuses were collected and observed on gestation day 20 (Starke et al. 1982). No significant maternal or developmental effects were observed in any of the exposure groups, except for an increase in certain types of visceral anomalies. In particular, the incidence of ectopic testes increased in the high-dose group compared with the control group (three in the high-dose group versus zero in the control group). Nine cases of reversed ductus arteriosus also occurred in the high-dose group compared with none in the control group. Although the authors discounted reversed ductus arteriosus as being a minor effect, the condition is suggestive of reversal of the great vessels of the heart, which is a serious cardiovascular defect.

In a dominant lethal mutation study, male rats were exposed by inhalation to WP smoke H₃PO₄ at concentrations of 884 and 1,742 mg/m³ for 15 min per day, 5 days per week for 10 weeks (Starke et al. 1982). Four out of 18 exposed at a concentration of 1,742 mg/m³ died during the exposure period; none out of 18 exposed at a concentration of 884 mg/m³ died during the exposure period. After exposure, the males were mated to unexposed females. Females mated to males exposed at a concentration of 884 mg/m³ had significantly more resorptions, but that was not a dose-related effect. No other significant effects were seen in this study. A limitation in the interpretation of this study is that the data were analyzed using the number of offspring as the experimental group size instead of using the number of males exposed to WP smoke.

In a single-generation study, F₀-generation male and female rats were exposed by inhalation to WP smoke with H₃PO₄ at concentrations of 884 and 1,742 mg/m³ for 15 min per day, 5 days per week for 10 weeks (males) or 3 weeks (females) before mating (Starke et al. 1982). Females continued to be exposed through gestation and lactation (until day 21). F₁-generation offspring were weighed 1, 4, 7, 14, and 21 days after birth, then sacrificed and examined for gross external and visceral abnormalities on postnatal day 21. The number of pups per litter was not significantly affected, and no abnormalities were seen in a subset of pups examined. However, offspring weights were significantly less in rats exposed at 1,742 mg/m³ than in rats exposed at 884 mg/m³ and in the controls. Additionally, survivability, viability, and lactation indices were also significantly affected in the high-dose group. The effects were severe and were likely due to exposure to WP smoke. A limitation of the study is that the data appear to have been analyzed using the number of pups examined; the effect of variability between mated males or litters was not taken into account.

Other End Points

No significant changes in erythrocyte, hematocrit, hemoglobin, or total and differential leukocyte levels were observed in rats exposed for 90 min to WP smoke with H₃PO₄ at 3,027 mg/m³ or in guinea pigs exposed for 10 min with H₃PO₄ at 984 mg/m³. No hematological effects were reported in rats exposed for 13 weeks with H₃PO₄ at 1,742 mg/m ³ (Brown et al. 1981).

Rats exposed for 13 weeks (15 min per day, 5 days per week) to WP smoke with H₃PO₄ as high as 1,742 mg/m³ showed no effects on the skin or eye or any histological alterations in the brain, heart, or gastrointestinal tract (Brown et al. 1981). No studies were identified regarding immunological, muscular-skeletal, genotoxic, or carcinogenic effects associated with the inhalation of WP smoke.

Summary of Toxicity Data

Tables 2-2 and 2-3 summarize the toxicological effects in animals and humans associated with exposure to WP-smoke inhalation.

TABLE 2-2

Acute Lethality of White Phosphorus Smoke (Expressed as H₃PO₄) via Inhalation Exposure.

TABLE 2-3

Nonlethal Effects of White Phosphorus Smoke (Expressed as H₃PO₄) via Inhalation Exposure.

Previous Recommended Exposure Limits

Although no exposure limits have been established for WP smoke, limits have been recommended for white (yellow) phosphorus particles. WP concentrations in workplace air are regulated by the Occupational Safety and Health Administration (OSHA), and recommendations for safe levels have been made by the National Institute of Occupational Safety and Health (NIOSH) and the American Conference of Governmental Industrial Hygienists (ACGIH) (Table 2-4).

TABLE 2-4

Existing Exposure Limits for White (Yellow) Phosphorus Particles.

EPA (1998) has listed WP as a hazardous air pollutant and has classified it as a Group D carcinogen (inadequate evidence of carcinogenicity). Various states also have established acceptable ambient concentration guidelines or standards for different exposure durations (see examples in Table 2-5).

TABLE 2-5

Selected State Guidelines for White Phosphorus (Expressed as Elemental Phosphorus).

Subcommittee Evaluation and Recommendations

On the basis of the available toxicity information, the subcommittee recommended exposure guidance levels for military personnel exposed during an emergency release and during regular training exercises and for consideration at training-facility boundaries to protect nearby communities from an acute exposure or repeated releases of WP smoke.

Military Exposures

Emergency Exposure Guidance Levels (EEGLs)

In recommending the EEGLs for WP smoke, the most sensitive response to short-term exposure is respiratory irritation and distress. Animal studies indicate that such an effect becomes evident in goats and rats following a 1-hr exposure to WP smoke with H₃PO₄ at 745 and 525 mg/m³, respectively (P₂O₅ at 540 and 380 mg/m³, respectively). Human volunteers exposed for 3.5 min to WP smoke with H₃PO₄ at 818 mg/m³ (P₂O₅ at 592 mg/m³) reported respiratory irritation, tightness of chest, cough, and difficulty in breathing (White and Armstrong 1935). In those cases, the subjects refused to be exposed to higher concentrations and thought it would be impossible, without more serious effects, to perform any physical exercise or labor at that concentration.

The subcommittee considered both human and animal data in recommending the EEGLs. Several EEGLs were estimated on the basis of data from humans and animals, as shown in Table 2-6. The lowest-observed-adverse-effect level (LOAEL) identified in mice of 152 mg/m³ was not included in the subcommittee's evaluation because the mice apparently were sensitive to mechanical obstruction to respiration and the data probably had little or no relevance to the true toxicity of WP smoke to mice (White and Armstrong 1935). Therefore, using the animal LOAEL identified in rats of 525 mg/m³ (White and Armstrong 1935), an uncertainty factor of 10 was used to extrapolate from a LOAEL to a no-observed-adverse-effect level (NOAEL), and an additional factor of 10 was used to extrapolate from animal to human. Assuming that Haber's rule (that is, the product of exposure concentration and time is a constant, C × T = k) applied, the estimated EEGLs were calculated to be 21, 5, and 1 mg/m³ for WP smoke expressed as H₃PO₄ for 15 min, 1 hr, and 6 hr, respectively. The estimated EEGLs derived from human data were calculated to be 19, 5, and 0.8 mg/m³ for WP smoke expressed as H₃PO₄ for 15 min, 1 hr, and 6 hr, respectively. The subcommittee's decision to use the data from the White and Armstrong (1935) study to recommend EEGLs is supported by a more recent inhalation toxicity study (Brown et al. 1980). In that more recent study, rats were exposed for 90 minutes at 707 mg/m³ and showed signs of gasping and became ataxic, but recovered. Because human data are available and the animal data are consistent with the human data, the subcommittee recommends using EEGLs derived from human data.

TABLE 2-6

Estimated EEGLs from Human and Animal Data for White Phosphorus Smoke (Expressed as H₃PO₄).

The subcommittee recognizes that these EEGLs are lower than those recommended by this subcommittee for RP-BR (NRC 1997), even though the final combustion products for both smokes are expected to be phosphoric acid. However, the human and animal data indicate that WP smoke appears to produce respiratory irritation at lower concentrations than does RP-BR smoke. For example, the rats exposed for 1 hr to RP-BR showed signs of respiratory irritation with H₃PO₄ at 1,692 mg/m³, but none died (Weimer et al. 1977). Rats exposed to WP smoke, with H₃PO₄ at 1,794 mg/m³, a concentration similar to that of RP-BR, had a 20% mortality during the 1-hr exposure (Brown et al. 1980). The difference might result from the presence of some uncombusted WP in the WP smoke. That would contribute to the smoke's toxicity.

A similar difference in sensitivity to the two phosphorus smokes can be observed when comparing the human data on WP and RP-BR smokes. For example, Mitchell and Burrows (1990) stated that acute exposure to RP-BR smoke at 1,000 mg/m³ (chemical form not reported) would be intolerable and that 700 mg/m³ (chemical form not reported) is the highest tolerable concentration. In contrast, White and Armstrong (1935) stated that human volunteers exposed to WP smoke with P₂O₅ at 592 mg/m³ (H₃PO₄ at 818 mg/m³) said that was the limit of their tolerance.

Repeated Exposure Guidance Level (REGL)

Although there is an existing ACGIH Threshold Limit Value-time-weighted average (TLV-TWA) for WP particles (0.1 mg/m³), that value does not seem appropriate for WP smoke. The short-term exposure data for WP smoke suggest that the REGL (8 hr per day, 5 days per week) could be higher than the TLV-TWA of 0.1 mg/m³ for WP alone but should be lower than the TLV-TWA of 1 mg/m³ for phosphoric acid. Rats exposed for 15 min per day, 5 days per week for 13 weeks showed moderate laryngitis and tracheitis with H₃PO₄ at 1,400 mg/m³ and slight laryngitis and tracheitis with H₃PO₄ at 690 mg/m³, and no such effects were reported with H₃PO₄ at 280 mg/m³. Because that result identifies a no-effect exposure concentration, the subcommittee recommends that it be used to establish a REGL. An uncertainty factor of 10 is used to extrapolate the animal data to humans. Dividing 28 mg/m³ by 32 to estimate a value for 8 hr from a 15-min exposure using Haber's rule yields a value of 0.9 mg/m³. Applying an uncertainty factor of 10 to extrapolate from subchronic to chronic exposure yields a value of 0.09 mg/m³. Therefore, the subcommittee recommends the REGL for WP (expressed as H₃PO₄) to be 0.09 mg/m³ for 8 hr per day, 5 days per week.

Public Exposures

Short-Term Public Emergency Guidance Levels (SPEGLs)

Assuming that the general population includes a variety of susceptible individuals, an additional uncertainty factor of 10 is appropriate to extrapolate from an EEGL for military personnel to a level protective of the general public. Thus, the SPEGLs for a single emergency exposure to WP smoke expressed as H₃PO₄ are 1.9, 0.5, and 0.08 mg/m³ for exposures of 15 min, 1 hr, and 6 hr, respectively.

Summary of Subcommittee Recommendations

The subcommittee's recommendations for exposure to WP smoke for military personnel and for the public (i.e., the boundaries of military-training facilities) are summarized in Tables 2-7 and 2-8.

TABLE 2-7

EEGLs and REGL for White Phosphorus Smoke (Expressed as H₃PO₄) for Military Personnel.

TABLE 2-8

SPEGLs and RPEGL for White Phosphorus Smoke (Expressed as H₃PO₄) at the Boundaries of Military-Training Facilities.

Research Needs

The subcommittee recognizes the need for further research to better understand the potential toxicity associated with inhaling WP smoke. Research in the following areas would provide better insight into possible health effects of exposure to WP smoke and help to determine, with greater confidence, a guidance level that is not overly conservative but is scientifically defensible in ensuring minimal risk to the exposed population. The subcommittee recommends that the following studies be conducted:

Studies designed to measure the absorption, distribution, and metabolism of WP smoke would be of help in assessing human risk.
Only a limited number of biological and biochemical end points have been studied in relation to inhalation of WP smoke. Inhalation studies are needed to evaluate possible neurobehavioral, immunological, reproductive and developmental, and carcinogenic effects of WP smoke.
All studies should include improved characterization of the composition and particle properties of the WP smoke used and actual exposure concentrations.
Long-term chronic inhalation studies would be of value to identify target organs of toxicity and possible long-term health effects.

References

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