10
Phosphine and Eight Metal Phosphides1,2
Acute Exposure Guideline Levels

PREFACE

Under the authority of the Federal Advisory Committee Act (P.L. 92-463) of 1972, the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances has been established to identify, review, and interpret relevant toxicologic and other scientific data and develop Acute Exposure Guideline Levels (AEGLs) for high-priority, acutely toxic chemicals.

AEGLs represent threshold exposure limits for the general public and are applicable to emergency exposure periods ranging from 10 min to 8 h. AEGL-2 and AEGL-3, and AEGL-1 levels as appropriate, will be developed for each of five exposure periods (10 min, 30 min, 1 h, 4 h, and 8 h) and will be distinguished by varying degrees of severity of toxic effects. It is believed that the recommended exposure levels are applicable to the general population, including infants and children and other individuals who may be susceptible. The three AEGLs have been defined as follows:

1

This document was prepared by AEGL Development Team member Cheryl Bast of Oak Ridge National Laboratory and Ernest Falke (Chemical Manager) of the National Advisory Committee on Acute Exposure Guideline Levels for Hazardous Substances (NAC). The NAC reviewed and revised the document, which was then reviewed by the National Research Council (NRC) Committee on Acute Exposure Guideline Levels. The NRC Committee concludes that the AEGLs developed in this document are scientifically valid conclusions based on data reviewed by the NRC and are consistent with the NRC guideline reports (NRC 1993, 2001).

2

After an earlier version of this document was released in 2007, the committee evaluated AEGLs that were developed for eight metal phosphides: aluminum phosphide, potassium phosphide, sodium phosphide, zinc phosphide, calcium phosphide, magnesium phosphide, strontium phosphide, and magnesium aluminum phosphide. Because their acute toxicity results from the phosphine generated from hydrolysis of the metal phosphides, their AEGL values are likewise based upon phosphine AEGLs. AEGL values for the eight metal phosphides have been added as Appendix D of this document, Appendix 10.



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10 Phosphine and Eight Metal Phosphides1,2 Acute Exposure Guideline Levels PREFACE Under the authority of the Federal Advisory Committee Act (P.L. 92-463) of 1972, the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances has been established to identify, review, and interpret relevant toxicologic and other scientific data and develop Acute Exposure Guideline Levels (AEGLs) for high-priority, acutely toxic chemicals. AEGLs represent threshold exposure limits for the general public and are applicable to emergency exposure periods ranging from 10 min to 8 h. AEGL-2 and AEGL-3, and AEGL-1 levels as appropriate, will be developed for each of five exposure periods (10 min, 30 min, 1 h, 4 h, and 8 h) and will be distin- guished by varying degrees of severity of toxic effects. It is believed that the recommended exposure levels are applicable to the general population, includ- ing infants and children and other individuals who may be susceptible. The three AEGLs have been defined as follows: 1 This document was prepared by AEGL Development Team member Cheryl Bast of Oak Ridge National Laboratory and Ernest Falke (Chemical Manager) of the National Advisory Committee on Acute Exposure Guideline Levels for Hazardous Substances (NAC). The NAC reviewed and revised the document, which was then reviewed by the National Research Council (NRC) Committee on Acute Exposure Guideline Levels. The NRC Committee concludes that the AEGLs developed in this document are scientifically valid conclusions based on data reviewed by the NRC and are consistent with the NRC guideline reports (NRC 1993, 2001). 2 After an earlier version of this document was released in 2007, the committee evalu- ated AEGLs that were developed for eight metal phosphides: aluminum phosphide, po- tassium phosphide, sodium phosphide, zinc phosphide, calcium phosphide, magnesium phosphide, strontium phosphide, and magnesium aluminum phosphide. Because their acute toxicity results from the phosphine generated from hydrolysis of the metal phosphides, their AEGL values are likewise based upon phosphine AEGLs. AEGL val- ues for the eight metal phosphides have been added as Appendix D of this document, Appendix 10. 260

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261 Phosphine and Eight Metal Phosphides AEGL-1 is the airborne concentration [expressed as parts per million (ppm) or milligrams per cubic meter (mg/m3)] of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic nonsensory effects. However, the effects are not disabling and are transient and reversible upon cessation of exposure. AEGL-2 is the airborne concentration (expressed as ppm or mg/m3) of a substance above which it is predicted that the general population, including sus- ceptible individuals, could experience irreversible or other serious, long-lasting adverse health effects or an impaired ability to escape. AEGL-3 is the airborne concentration (expressed as ppm or mg/m3) of a substance above which it is predicted that the general population, including sus- ceptible individuals, could experience life-threatening health effects or death. Airborne concentrations below the AEGL-1 represent exposure levels that could produce mild and progressively increasing but transient and nondisabling odor, taste, and sensory irritation or certain asymptomatic nonsensory effects. With increasing airborne concentrations above each AEGL, there is a progres- sive increase in the likelihood of occurrence and the severity of effects described for each corresponding AEGL. Although the AEGL values represent threshold levels for the general public, including susceptible subpopulations, such as in- fants, children, the elderly, persons with asthma, and those with other illnesses, it is recognized that individuals, subject to unique or idiosyncratic responses, could experience the effects described at concentrations below the correspond- ing AEGL. SUMMARY Phosphine is a colorless gas used as a fumigant against insects and rodents in stored grain. The pesticide is usually applied as a metal phosphide and reacts with moisture to liberate phosphine gas. Phosphine is also used in the semicon- ductor industry. Information concerning human exposure to phosphine is of lim- ited use in the derivation of AEGL values since exposure durations and concen- trations are not precisely reported. Appropriate animal data are more abundant; however, data consistent with the definition of AEGL-1 values are not available. Therefore, due to insufficient data, AEGL-1 values were not derived. The AEGL-2 was based on red mucoid nasal discharge in Fischer 344 rats exposed to 10 ppm phosphine for 6 h (Newton et al. 1993). An uncertainty fac- tor (UF) of 3 was applied to account for interspecies variability since time-to- death lethality data from 45 min to 30 h for rats, mice, rabbits, and guinea pigs suggest little species variability (see Figure 10-2). A UF of 10 was applied to account for intraspecies variability since the human data suggest that children may be more sensitive than adults when exposed to presumably similar phosphine concentrations (total UF = 30). The concentration-exposure time rela-

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262 Acute Exposure Guideline Levels tionship for many irritant and systemically acting vapors and gases may be de- scribed by Cn × t = k, where the exponent n ranges from 0.8 to 3.5 (ten Berge et al. 1986). For scaling the AEGL values for phosphine for the 30-min, 1-, 4-, and 8-h time points, the empirically derived value of 1 was used as the exponent n. The exponent n was derived from rat lethality data ranging from 1 to 6 h. The 30-min AEGL-2 was also adopted as the 10-min value due to the added uncer- tainty of extrapolating from a 6-h time point to 10 min. The AEGL-3 was based on a concentration causing no deaths (18 ppm) in Sprague Dawley rats exposed to phosphine for 6 h. An uncertainty factor of 3 was applied to account for interspecies variability since lethality data from rats, mice, rabbits, and guinea pigs suggest little species variability. An uncertainty factor of 10 was applied to account for intraspecies variability since human data suggest that children may be more sensitive than adults when exposed to pre- sumably similar phosphine concentrations (total UF = 30). The concentration- exposure time relationship for many irritant and systemically acting vapors and gases may be described by Cn × t = k, where the exponent n ranges from 0.8 to 3.5 (ten Berge et al. 1986). For scaling the AEGL values for phosphine for the 30-min, 1-, 4-, and 8-h time points, the empirically derived value of 1 was used as the exponent n. The exponent n was derived from rat lethality data ranging from 1 to 6 h. The 30-min AEGL-3 was also adopted as the 10-min value due to the added uncertainty of extrapolating from a 6-h time point to 10-min. The cal- culated values are listed in the Table 10-1. AEGL values for the eight metal phosphides are presented in Appendix D. 1. INTRODUCTION Phosphine is a colorless gas used as a fumigant against insects and rodents in stored grain. Paper sachets containing aluminum phosphide are added to grain and the grain is then sealed. The aluminum phosphide reacts with moisture in the grain to produce the phosphine gas. Phosphine is also used as a doping agent to treat silicon crystals in the semiconductor industry and is a byproduct of met- allurgical reactions (Hryhorczuk et al. 1992). Pure phosphine is odorless at con- centrations up to 200 ppm (IPCS 1988); however, technical-grade phosphine contains impurities (up to 5% higher phosphines and substituted phosphines) that may be responsible for a garlic-like odor that can be detected at 1.5-3 ppm (Hryhorczuk et al. 1992). A concentration of 7.58 ppm has been reported as “ir- ritating” to humans; however, no data to support this claim were provided (Ruth 1986). Naturally occurring phosphine is rare. It may occur transiently in marsh gas and other areas of anaerobic degradation of materials containing phospho- rus. Phosphine is produced by the hydrolysis of aluminum phosphide or the electrolysis of phosphorus in the presence of hydrogen. The physicochemical data for phosphine are given in Table 10-2.

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263 Phosphine and Eight Metal Phosphides TABLE 10-1 Summary of AEGL Values for Phosphine End Point Classification 10 min 30 min 1h 4h 8h (Reference) AEGL-1 NR NR NR NR NR Appropriate data (Nondisabling) not available AEGL-2 4.0 ppm 4.0 ppm 2.0 ppm 0.50 0.25 Red mucoid nasal (Disabling) (5.6 (5.6 (2.8 ppm ppm discharge in rats mg/m3) mg/m3) mg/m3) (0.71 (0.35 exposed to 10 mg/m3) mg/m3) ppm of phosphine for 6 h (Newton et al. 1993) AEGL-3 7.2 ppm 7.2 ppm 3.6 ppm 0.90 0.45 Concentration (Lethality) (10 (10 (5.1 ppm ppm causing no death mg/m3) mg/m3) mg/m3) (1.3 (0.63 in rats exposed to mg/m3) mg/m3) 18 ppm of phosphine for 6 h (Newton 1991) Note: The AEGL-2 and AEGL-3 values for phosphine are only 1.8-fold different from one another. This closeness of AEGL tiers is reflective of the very steep concentration- response curve observed for phosphine toxicity. NR: not recommended. Absence of an AEGL-1 does not imply that exposure below the AEGL-2 is without adverse effects. TABLE 10-2 Physical and Chemical Data Property Descriptor or Value Reference Synonyms Hydrogen phosphide, phosphorus trihydride, phosphoretted hydrogen, phosphane CAS Registry No. 7803-51-2 IPCS 1989 Chemical formula PH3 IPCS 1989 Molecular weight 34.00 Budavari et al. 1989 Physical state Gas IPCS 1988 Vapor pressure Braker and 41.3 atm at 20°C Mossman 1980 Vapor density 1.17 IPCS 1988 −133.5°C/−87.4°C Melting/boiling point IPCS 1988 Solubility in water IPCS 1989 2.5% v/v at 20°C 3 Conversion factors 1 mg/m = 0.71 ppm IPCS 1989 1 ppm = 1.41 mg/m3 in air

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264 Acute Exposure Guideline Levels 2. HUMAN TOXICITY DATA 2.1. Acute Lethality 2.1.1. Case Reports Numerous case reports concerning human lethality from phosphine expo- sure were located; however, exposure time and concentrations were not speci- fied in most of the reports. Two siblings, 2 and 4 year old, weighing 11 and 17 kg, respectively, died within 18 h of playing on fumigated wheat for 1 h (Heyn- drickx et al. 1976). The wheat had been treated with pyrethrum and malathion (120 kg/2,000 tons of grain) and aluminum phosphide tablets (1 kg/2,000 tons of grain). Analysis of wheat samples taken the morning after the children were exposed yielded 0.95 mg/100 g to 1.6 mg/100 g malathion (1.3 mg/100 g aver- age) and 0.02-0.5 ppm phosphine (0.2 ppm average). Two days after the chil- dren played on the wheat 1 ppm of phosphine was detected in several places just above the grain. Postmortem examinations suggested that the deaths were due to acute intoxication, most likely from phosphine, although malathion exposure may have been a contributing factor. The lungs of both children were congested and had atelectatical areas. Ethanol, commonly formed postmortem in both blood and tissues, also was detected in both children. In another report, two deaths were reported in fumigated boxcars (MMWR 1994). Four males—12, 35, 39, and 52 years old—were discovered in a boxcar containing loose bulk lima beans that had been fumigated with aluminum phosphide. The men had been in the car for approximately 16 h and had periodi- cally opened the hatch for fresh air as needed. When discovered, the 12-year-old was dead and the three men were ill, suggesting that children may be more sus- ceptible than adults. The three survivors reported nausea, vomiting, headache, and abdominal discomfort. In another incident the body of a 23-year-old man was discovered in a rice-filled boxcar during unloading. The rice had been fu- migated with aluminum phosphide 12 days prior to unloading, and autopsy re- sults showed phosphine in tissue samples. No phosphine concentrations were reported in either incident. Aluminum phosphide fumigation aboard a grain freighter on September 24, 1978, resulted in acute illness in two female children and 29 of 31 crew members (Wilson et al. 1980). Phosphine gas escaped from the holds of the ship through a cable housing located near the ship’s ventilation intake and around hatch covers on the forward deck; illness was associated with living or working on the forward deck. Phosphine concentrations were measured on September 30, 1978, 1-4 days after the onset of illness. The highest concentration of 20-30 ppm was detected in a void space of the main deck adjacent to the air ventilation in- take. Concentrations between 7.5 and 10 ppm were measured around a hatch on the forward deck, while 0.5 ppm of phosphine was measured in some living quarters. Concentrations were measured with a Drager tube and are estimates of phosphine levels at that time. Wilson et al. stated that phosphine levels reach

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265 Phosphine and Eight Metal Phosphides peak concentrations in 4-5 days. They note that there was an association be- tween severity of illness and living or working amid ships on the forward deck (phosphine was not detected in the rear crew cabins). Measurements were made shortly after peak exposures are likely to have occurred. Phosphine levels and exposure durations to those peak levels cannot be estimated from the data pro- vided. Exposures were probably continuous for a period of days to levels above a range of 0.5-20 or 30 ppm. One of the two exposed children died (age 2), and postmortem examination revealed congestive heart failure, focal myocardial necrosis with mononuclear infiltrates and fragmented fibers, inflamed mitral and aortic valves, pulmonary edema, pleural effusion, desquamated respiratory epi- thelium with alveoli thickened by hemolyzed red cells, congested capillaries, an enlarged spleen, and aspirated gastrointestinal contents. The surviving child (age 4 years, 9 months) exhibited nausea, vomiting, dizziness, epigastric pain, and fatigue. An electrocardiogram (ECG) revealed tachycardia with ST depression, and an echocardiogram 24 h later showed dilation and poor function of the left ventricle. A transient increase in the myocardial band (MB) fraction of creatinine phosphokinase (CPK) was also observed. Clinical signs and symp- toms resolved within 18 h, and ECG, echo, and CPK abnormalities resolved within 72 h. Crew members exhibited shortness of breath, cough, sputum pro- duction, nasal drainage, nausea, jaundice, vomiting, diarrhea, fatigue, headache, drowsiness, paresthesias, tremor, and weakness. Abnormal urinalyses and in- creased liver enzyme activities were observed in approximately 10% of exposed crew members compared to normal human values. A 16-year-old male who was employed as an acetylene generator operator for approximately 1 month died from apparent phosphine poisoning (Harger and Spolyar 1958). The subject had experienced periods of dizziness while filling generator hoppers with calcium carbide and became unconscious on two occa- sions. On a third occasion he was found with his face near an open hopper, where the measured phosphine concentration was 75-95 ppm. On this occasion he could not be aroused and later died. Autopsy revealed lividity of the head and shoulder, bloody exudate from the nose and mouth, edematous lungs, and frothy exudate in the bronchioles and bronchi. Samples of air over the generators con- tained concentrations of phosphine between 1 and 14 ppm and <3 ppm arsine. The cause of death was reported to be acute pulmonary edema from inhalation of phosphine gas. Garry et al. (1993) reported the accidental death of a 24-year-old woman who was 7 months pregnant. The victim’s home was located approximately 30 yards from a large bunker-type grain storage facility. The storage facility was topographically more than 5 feet higher than the home and was routinely fumi- gated with 49,000-82,950 aluminum phosphide pellets. Residents in the area complained of odor and dust coming from the grain, particularly in the evenings. On the afternoon of the fatal exposure there was a rain shower, followed by clear skies and wind of 5 mph in the direction of the patient’s home. She went outside between 8 and 9 p.m. and commented that the odor was “real strong.” At approximately 10:30 p.m. she was tachycardiac and vomiting, and clear frothy

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266 Acute Exposure Guideline Levels sputum was coming from her nose and mouth. She suffered cardiac arrest shortly after midnight and died. The autopsy revealed pulmonary edema and aluminum concentrations of 713 ng/mL in the blood and >200 ppm in alveolar macrophages. The tachycardia and pulmonary edema noted are consistent with phosphine poisoning. The authors stated that because the phosphine generated from the metal phosphide is highly reactive and unstable, quantitative analysis of aluminum in blood and tissues was used as a marker of exposure to test for possible fumigant intoxication. Shadnia et al. (2008) reported the accidental poisoning of a woman (age 35 years), her daughter (age 18 years), and son (age 6 years) from phosphine inhalation. The phosphine was released from 20 aluminum phosphide tablets stored in 15 bags of rice. The boy died 2-days postexposure; he had received no medical attention. The other two victims were admitted to the hospital 48 h postexposure and presented with metabolic acidosis, electrocardiogram abnor- malities, and hypotension. The patients were discharged after 3 days. Poisoning from ingestion of aluminum phosphide tablets for attempted suicides has also been reported (Misra et al. 1988a). Eight people (three females, five males; ages 14-25 years) ingested 0.5-20 aluminum phosphide tablets each. Gastritis, drowsiness/dizziness/coma, and peripheral vascular failure were ob- served in all patients, while cardiac arrhythmia was seen in three cases, and jaundice and kidney failure were observed in one case each. Six of the patients died, and autopsies of two revealed pulmonary edema, gastrointestinal mucosal congestion, petechial hemorrhage on liver and brain surfaces, desquamation of bronchiole epithelium, vacuolar degeneration of hepatocytes, and dilation and engorgement of hepatic central veins and sinusoids. 2.2. Nonlethal Toxicity 2.2.1. Case Reports Case reports concerning human phosphine exposure were available; how- ever, exposure times and concentrations were not specified in most of the re- ports. Sixty-seven male grain fumigators in New South Wales were occupation- ally exposed to phosphine concentrations ranging from 0.4 to 35 ppm (measured in the breathing zone; Jones et al. 1964). Exposure durations were described as “intermittent.” Symptoms occurred immediately in some workers, while the onset of symptoms were delayed from several hours to 2 days in others. Symp- toms included diarrhea (82%), nausea (73%), epigastric pain (65%), vomiting (29%), chest tightness (52%), breathlessness (34%), chest pain (29%), palpita- tions (27%), severe retrosternal pain (6%), headache (83%), dizziness (35%), and staggering gait (12%). There was no evidence of cumulative effects and no tendency to develop immunity.

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267 Phosphine and Eight Metal Phosphides Zaebst et al. (1988) reported odor but no adverse effects in grain fumigant workers exposed to >50 ppm phosphine for 2-5 min. Verma et al. (2007) reported acute pancreatitis and myocarditis in a man after ingestion of aluminum phosphide pellets. Twenty-two fumigation workers 24 to 60 years old (mean age 48) were evaluated for possible phosphine-related toxicity (Misra et al. 1988b). The mean duration of employment using aluminum phosphide was 11.1 years (range 0.5- 29 years) and phosphine concentrations ranged from 0.17 to 2.11 ppm. The workers had also been exposed to malathion, hexachlorocyclohexane, and ethyl- ene dibromide; however, during the study and for 4 weeks preceding the study, the workers were exposed only to phosphine. The following effects were re- ported: cough (18.2%); dyspnea (31.8%); chest tightness (27.3%); headache (31.8%); giddiness, numbness, lethargy (13.6% each); irritability (9.1%); ano- rexia and epigastric pain (18.2%); nausea (9.1%); and dry mouth (13.6%). Sen- sory and motor nerve conduction velocities were normal. In another case, a 53-year-old man used a pesticide powder containing 28% calcium phosphide to poison moles in his garden (Schoonbroodt et al. 1992). He worked for approximately 2 h in rainy weather, and 18 h later experi- enced fever (40○C), dry cough, weakness, myalgia, headache, dizziness and nau- sea. Upon hospital admission he was anxious and cyanotic and complained of severe nasal obstruction. He had interstitial infiltrates of the left upper and right lower lobes of the lungs, sinus tachycardia, left anterior fascicular block, leuco- cyturia, and necrosis of the nasal mucosa. Despite antibiotic treatment, symp- toms progressed and the patient developed pulmonary edema, left pleural effu- sion, and pericardial effusion. He was placed on a ventilator for 18 days and was discharged on day 32; one month after discharge his clinical profile was unre- markable. Five workers were reportedly exposed to 0.01-0.001 ppm of phosphine during corn fumigation (Modrzejewski and Myslak 1967). However, no valida- tion of analytical methods and no exposure times were reported, and there was no mention of probable occupational exposure to other pesticides. Vertigo, headache, nausea, and vomiting were observed in all subjects. Four workers exhibited dyspnea and bronchial inflammation; three had fever; and one had an enlarged liver, bilirubinemia, and jaundice. In another occupational exposure, three grain inspectors were instantaneously exposed to approximately 159-2,029 ppm of phosphine (no analytical validation provided) while inspecting railroad cars (Feldstein et al. 1991). Immediately after the exposures they experienced facial numbness and tingling, dizziness, nausea, shortness of breath, headache, disorientation, diaphoresis, despondency, and a “sense of doom.” 2.2.2. Epidemiologic Studies Epidemiologic studies regarding human exposure to phosphine were not available.

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268 Acute Exposure Guideline Levels 2.3. Developmental/Reproductive Toxicity No developmental/reproductive toxicity data concerning phosphine were identified in the available literature. 2.4. Genetic Toxicology Barbosa and Bonin (1994) observed no increase in clastogenicity or ane- uploidy in lymphocytes of 31 long-term phosphine fumigators compared to a group of 21 matched controls. Sporadic phosphine exposure ranged from 0.1 to 2 ppm for an average of 11.6 years. Specific chromosome aberrations associated with occupational pesticide exposure are discussed in Section 2.5. 2.5. Carcinogenicity Epidemiologic data suggest that farm and grain industry workers have an increased incidence of non-Hodgkin’s lymphoma; however, because these workers are generally exposed to myriad pesticides and solvents throughout their working lives, it is difficult to use the data to determine whether there is an association between increased cancer incidence and exposure to a particular pes- ticide (Garry et al. 1992). Several studies of chromosomal analysis of male pesticide applicators suggest that occupational exposure to phosphine or mixed exposure to phosphine and other pesticides may contribute to an increased incidence of aber- rations (Garry et al. 1989, 1990, 1992). Although dose-related stable (transloca- tions) and unstable (gaps and chromatid deletions) aberrations have been identi- fied in the lymphocytes of phosphine applicators (Garry et al. 1989, 1990), the most convincing link between phosphine exposure and non-Hodgkin’s lym- phoma is observed in molecular analyses of the stable aberrations (Garry et al. 1992). A group of 18 pesticide appliers exposed to phosphine or to phosphine and a mixture of other chemicals had an increased incidence of stable aberra- tions (1.3% of cells with aberrations) compared to five appliers who had ceased phosphine application for 8 months or 26 control subjects (0.2% cells with aber- rations). There were four bands with an excess of breaks (over what would be expected on band length alone) in the exposed group and no breaks in the con- trol group. These breaks were also not observed in the group that had ceased phosphine application. Each of these breaks is in a protooncogene region associ- ated with non-Hodgkin’s lymphoma as follows: 1p13 (NRAS), 2p23 (NMYC), 14q32 (ELK2), and 21q22 (ETS-2). More breaks than expected were also ob- served in 1q32, 3p14, 7p15, and 14q11; however, these breaks are likely not due to pesticide exposure since increases were observed in both exposed and control subjects.

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269 Phosphine and Eight Metal Phosphides 2.6. Summary Reports of occupational exposures and attempted suicides are numerous; however, data on exposure durations and concentrations are limited. Common clinical signs are headache, nausea, vomiting, coughing, shortness of breath, paresthesia, weakness, tremors, and jaundice. Pulmonary congestion, pleural effusion, and congestive heart failure may be observed upon postmortem exami- nation. Fumigation workers exposed long term to phosphine have a higher inci- dence of both stable and less stable chromosomal aberrations. Molecular analy- sis of these lesions suggests that the breakpoints are near protooncogenes involved in non-Hodgkin’s lymphoma, possibly contributing to the increased incidence of lymphomas in pesticide workers. No reproductive or developmental data were available. 3. ANIMAL TOXICITY DATA 3.1. Acute Lethality 3.1.1. Rats A 4-h LC50 of 11 ppm (15.5 mg/m3) phosphine was reported for male Charles River-CD rats (Waritz and Brown 1975). The phosphine was analyzed by scrubbing samples of the chamber atmosphere through H2SO4 and analyzing the resulting solution for phosphorus. One sample was taken during each expo- sure. Signs of respiratory irritation, including salivation, lacrimation, face paw- ing, and dyspnea, were observed. Hyperemia of the ears also was observed. No effects attributable to phosphine exposure were observed at necropsy. Newton (1991) reported a combined 6-h LC50 of 28 ppm (39.5 mg/m3) for male and female Sprague-Dawley rats. No deaths occurred in rats exposed to 18 ppm of phosphine for 6 h, suggesting a steep concentration-response curve. This study is discussed in further detail in Section 3.2.1. Muthu et al. (1980) exposed groups of six adult female albino rats to vary- ing concentrations of phosphine for 1, 4, 6, or 8 h and observed the animals for up to 4 weeks. The gas was generated by dropping aluminum phosphide pellets into distilled water in a beaker in the middle of the exposure chamber. By vary- ing the number of aluminum phosphide pellets and the exposure times, different concentration-time products were obtained. Rats were exposed in a wire mesh cage that was placed in an “insulated aluminum paneled gas-tight atmospheric vault” with a volume of 5,943 L. Phosphine concentrations were measured every hour during the exposure periods with a “phosphine detector tube” developed by the study authors. No other study details were reported. A 1-h LC50 of 134 ppm and a 5.2-h LC50 of 28 ppm were calculated. LC95 values of 45 ppm and 33.3 ppm were calculated for 6.2-h and 8.8 h, respectively.

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270 Acute Exposure Guideline Levels Groups of four male F344 rats were exposed to 0, 1, 5, or 10 ppm of phosphine for 6 h/day for up to 4 days. All rats died by the end of the third ex- posure to 10 ppm (Morgan et al. 1995). Deaths were not observed in rats ex- posed to 1 or 5 ppm, suggesting a steep concentration-response curve. Neubert and Hoffmeister (1960) exposed groups of eight rats constantly to phosphine concentrations ranging from 71 to 3,294 ppm. Survival times ranged from 16 through 600 min. No further data were provided. 3.1.2. Mice Omae et al. (1996) exposed groups of 10 male ICR mice to 17.2, 25.1, 31.7, 41.6, or 59.2 ppm of phosphine for 1-h or to 22.5, 26.5, 33.4, 45.5, or 66.9 ppm for 4 h. The source gas was 99.995% pure phosphine (used in semiconduc- tor manufacturing) diluted with purified nitrogen. It was supplied at a constant rate, mixed with filtered room air, and introduced into the whole-body 550-L exposure chamber. Phosphine concentrations were measured via gas chromatog- raphy every 12 min during exposure. The oxygen concentration in the chamber was measured simultaneously with a digital oximeter. The 1-h LC50 was >59.2 ppm, whereas the 4-h LC50 was between 26.5 and 33.4 ppm. In all of the 1-h exposed animals, the mice exhibited face-washing movements and were very active in the initial exposure period. No adverse signs were noted during the 3- day observation period after exposure. In the 4-h exposed mice, the initial ob- servations were similar to those of the 1-h group. However, 3 h after the start of exposure at 33.4 ppm and above, the mice became slower in response to tapping on the chamber glass and supine posture was observed. After the completion of exposure at 22.5 ppm and above, slight tremor and piloerection were observed. At 33.4 ppm and above, mild loss of spontaneous motor activity and piloerection were observed, and at 45.4 ppm and above, complete loss of motor activity, ocu- lar cloudiness, and moribundity were noted. A 2-h LCL0 of 270 ppm (380 mg/m3) phosphine was reported for an un- specified strain of mice (NIOSH 1994, 2005). No further experimental details were provided. 3.1.3. Guinea Pigs A 4-h LCL0 of 100 ppm (141 mg/m3) phosphine was reported for an un- specified strain of guinea pigs (NIOSH 1994, 2005). No further experimental details were provided. 3.1.4. Cats A 2-h LCL0 of 50 ppm (70.5 mg/m3) of phosphine was reported for an un- specified strain of cat (NIOSH 1994, 2005). In another report an unspecified

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294 Acute Exposure Guideline Levels APPENDIX D AEGL Values for Selected Metal Phosphides Aluminum Phosphide (AlP) Potassium Phosphide (K3P) Sodium Phosphide (Na3P) Zinc Phosphide (Zn3P2) Calcium Phosphide (Ca3P2) Magnesium Phosphide (Mg3P2) Strontium Phosphide (Sr3P2) Magnesium Aluminum Phosphide (Mg3AlP3) SUMMARY Metal phosphides are solids and are typically used as fumigants against in- sects and rodents in stored grain. The metal phosphides react rapidly with water and moisture in the air or stored grain to produce phosphine gas. It is the phosphine gas that is responsible for acute toxicity, and the rate of phosphine generation is dependent on ambient temperature and humidity and the chemical structure of the phosphide (Anger et al. 2000). In the absence of appropriate chemical-specific data for the metal phosphides considered in this appendix, the AEGL-2 and AEGL-3 values for phosphine were used to obtain AEGL-2 and AEGL-3 values, respectively, for the metal phosphides. The use of phosphine as a surrogate for the metal phosphides is deemed appropriate because qualitative (clinical signs) and quan- titative (phosphine blood level) data suggest that the phosphine hydrolysis prod- uct is responsible for acute toxicity from metal phosphides. The phosphine AEGL-2 and AEGL-3 values were used as target values for calculating the con- centrations of metal phosphide needed to generate the phosphine AEGL values. Because AEGL-1 values for phosphine are not recommended (due to in- sufficient data), AEGL-1 values for the metal phosphides considered in this ap- pendix are also not recommended. The calculated values are listed in Table D-1 below. D.I. INTRODUCTION Metal phosphides are solids and are typically used as fumigants against in- sects and rodents in stored grain. The metal phosphides react rapidly with water and moisture in the air or stored grain to produce phosphine gas. It is the phosphine gas which is responsible for acute toxicity, and the rate of phosphine generation is dependent on ambient temperature and humidity and the chemical structure of the phosphide (Anger et al. 2000).

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295 Phosphine and Eight Metal Phosphides TABLE D-1 AEGL Values for Metal Phosphidesa Compound Classification 10-min 30-min 1-hr 4-hr 8-hr Aluminum AEGL-1 NR NR NR NR NR Phosphide 9.5 mg/m3 9.5 mg/m3 4.7 mg/m3 1.2 mg/m3 0.59 mg/m3 AEGL-2 17 mg/m3 17 mg/m3 8.5 mg/m3 2.1 mg/m3 1.1 mg/m3 AEGL-3 Potassium AEGL-1 NR NR NR NR NR Phosphide 24 mg/m3 24 mg/m3 12 mg/m3 3.0 mg/m3 1.5 mg/m3 AEGL-2 44 mg/m3 44 mg/m3 22 mg/m3 5.5 mg/m3 2.7 mg/m3 AEGL-3 Sodium AEGL-1 NR NR NR NR NR Phosphide 16 mg/m3 16 mg/m3 8.2 mg/m3 2.0 mg/m3 1.0 mg/m3 AEGL-2 29 mg/m3 29 mg/m3 15 mg/m3 3.7 mg/m3 1.8 mg/m3 AEGL-3 Zinc Phosphide AEGL-1 NR NR NR NR NR 21 mg/m3 21 mg/m3 11 mg/m3 2.6 mg/m3 1.3 mg/m3 AEGL-2 38 mg/m3 38 mg/m3 19 mg/m3 4.8 mg/m3 2.4 mg/m3 AEGL-3 Calcium AEGL-1 NR NR NR NR NR Phosphide 15 mg/m3 15 mg/m3 7.5 mg/m3 1.9 mg/m3 0.93 mg/m3 AEGL-2 27 mg/m3 27 mg/m3 13 mg/m3 3.4 mg/m3 1.7 mg/m3 AEGL-3 Magnesium AEGL-1 NR NR NR NR NR Phosphide 11 mg/m3 11 mg/m3 5.5 mg/m3 1.4 mg/m3 0.69 mg/m3 AEGL-2 20 mg/m3 20 mg/m3 9.9 mg/m3 2.5 mg/m3 1.2 mg/m3 AEGL-3 Strontium AEGL-1 NR NR NR NR NR Phosphide 27 mg/m3 27 mg/m3 13 mg/m3 3.3 mg/m3 1.7 mg/m3 AEGL-2 48 mg/m3 48 mg/m3 24 mg/m3 6.0 mg/m3 3.0 mg/m3 AEGL-3 Magnesium AEGL-1 NR NR NR NR NR Aluminum 11 mg/m3 11 mg/m3 5.3 mg/m3 1.3 mg/m3 0.66 mg/m3 AEGL-2 Phosphide 19 mg/m3 19 mg/m3 9.5 mg/m3 2.4 mg/m3 1.2 mg/m3 AEGL-3 a These airborne concentrations will produce the equivalent AEGL values for phosphine. Note: Absence of an AEGL-1 does not imply that exposure below the AEGL-2 is without adverse effects. NR, not recommended. Aluminum Phosphide (CAS No. 20859-73-8), Potassium Phosphide (CAS No. 20770-41-6), and Sodium Phosphide (CAS No. 12058-85-4): One mole of aluminum phosphide, potassium phosphide, or sodium phosphide will react rapidly with water or moisture to produce a maximum of 1 mole of phosphine gas as follows: AlP + 3H2O PH3 + Al(OH)3 K3P + 3H2O PH3 + 3KOH Na3P + 3H2O PH3 + 3NaOH

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296 Acute Exposure Guideline Levels Zinc Phosphide (CAS No. 1314-84-7), Calcium Phosphide (CAS No. 1305-99-3), Magnesium Phosphide (CAS No. 10257-74-8), and Strontium Phosphide (CAS No. 12504-13-1): One mole of zinc phosphide, calcium phosphide, magnesium phosphide or strontium phosphide will react rapidly with water or moisture to produce a maximum of 2 moles of phosphine gas as fol- lows: Zn3P2 + 6H2O 2PH3 + 3Zn(OH)2 Ca3P2 + 6H2O 2PH3 + 3Ca(OH)2 Mg3P2 + 6H2O 2PH3 + 3Mg(OH)2 Sr3P2 + 6H2O 2PH3 + 3Sr(OH)2 Magnesium Aluminum Phosphide (CAS No. None): One mole of mag- nesium aluminum phosphide will react rapidly with water or moisture to pro- duce a maximum of 3 moles of phosphine gas as follows: Mg3AlP3 + 9H2O 3PH3 + Al(OH)3 + 3Mg(OH)2 Aluminum phosphide is a gray or yellow crystalline solid prepared from red phosphorus and aluminum powder (O’Neil et al. 2001). Commercial alumi- num phosphide sachets contain 70% aluminum phosphide and 30% aluminum carbonate (Bajaj et al. 1988). Calcium phosphide is a red-brown or gray solid prepared by heating calcium phosphate with aluminum or carbon by passing phosphorus vapors over metallic calcium. In addition to its use as a rodenticide, calcium phosphide is also used in signal fires and pyrotechnics and in the purifi- cation of copper and copper alloys (HSDB 2007a). Zinc phosphide is a gray solid and may be produced by passing phosphine through a solution of zinc sul- fate (HSDB 2007b). Manufacturing information on the other metal phosphides considered in this appendix was not located. Available physico-chemical data for the metal phosphides are shown in Tables D-2 through D-9. TABLE D-2 Physicochemical Data for Aluminum Phosphide Parameter Description/Value Reference Synonyms (commercial Celphos, Phostoxin, Quickphos O’Neil et al. 2001 product) CAS Registry No. 20859-73-8 O’Neil et al. 2001 Chemical formula AlP O’Neil et al. 2001 Molecular weight 57.96 O’Neil et al. 2001 Physical state Solid, gray of yellow crystals O’Neil et al. 2001 (Continued)

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297 Phosphine and Eight Metal Phosphides TABLE D-2 Continued Parameter Description/Value Reference Relative density (water = 1) 2.9 IPCS 1989 Melting point >1350°C IPCS 1989 Solubility in water Reactive produces phosphine gas IPCS 1989 TABLE D-3 Physicochemical Data for Potassium Phosphide Parameter Description/Value Reference CAS Registry No. 20770-41-6 ChemIDPlus 2005a Chemical formula K3P ChemIDPlus 2005a Molecular weight 148.3 ChemIDPlus 2005a TABLE D-4 Physicochemical Data for Sodium Phosphide Parameter Description/Value Reference Synonyms Trisodium phosphide ChemIDPlus 2005b CAS Registry No. 12058-85-4 ChemIDPlus 2005b Chemical formula Na3P ChemIDPlus 2005b Molecular weight 99.94 Lewis 1996a Physical state Solid, red crystals Lewis 1996a Melting point Decomposes Lewis 1996a Solubility in water Reacts violently Lewis 1996a TABLE D-5 Physicochemical Data for Zinc Phosphide Parameter Description/Value Reference Synonym Trizinc diphosphide IPCS 1989 CAS Registry No. 1314-84-7 IPCS 1989 Chemical formula Zn3P2 IPCS 1989 Molecular weight 258.1 IPCS 1989 Physical state Solid, gray powder or crystals O’Neil et al. 2001 Relative density (water = 1) 4.55 O’Neil et al.2001 Melting point Sublimes IPCS 1989 Solubility in water Insoluble, reacts IPCS 1989 TABLE D-6 Physicochemical Data for Calcium Phosphide Parameter Description/Value Reference Synonyms (commercial Calcium photophor, O’Neil et al. 2001 product) photophor CAS Registry No. 1305-99-3 O’Neil et al. 2001 Chemical formula Ca3P2 O’Neil et al. 2001 (Continued)

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298 Acute Exposure Guideline Levels TABLE D-6 Continued Parameter Description/Value Reference Molecular weight 182.18 O’Neil et al. 2001 Physical state Solid, red-brown crystals or O’Neil et al. 2001 gray lumps Relative density (water = 1) 2.51 O’Neil et al. 2001 Melting point 1600°C O’Neil et al. 2001 Solubility in water Decomposes O’Neil et al. 2001 TABLE D-7 Physicochemical Data for Magnesium Phosphide Parameter Description/Value Reference Synonyms Trimagnesium diphosphide IPCS 1989 CAS Registry No. 12057-74-8 IPCS 1989 Chemical formula Mg3P2 IPCS 1989 Molecular weight 134.87 IPCS 1989 Physical state Solid, gray or bright yellow IPCS 1989 crystals Relative density (water = 1) 2.1 IPCS 1989 Melting point >750°C IPCS 1989 Solubility in water Moisture sensitive, reacts IPCS 1989 TABLE D-8 Physicochemical Data for Strontium Phosphide Parameter Description/Value Reference CAS Registry No. 12504-13-1 Lewis 1996b Chemical formula Sr3P2 Lewis 1996b Molecular weight 324.9 Lewis 1996b Physical state Solid Lewis 1996b TABLE D-9 Physicochemical Data for Magnesium Aluminum Phosphide Parameter Description/Value Reference CAS Registry No. None ChemIDPlus 2005c Chemical formula Mg3AlP3 ChemIDPlus 2005c Molecular weight 192.8 — Physical state Solid ChemIDPlus 2005c D.II. SPECIAL CONSIDERATIONS Metabolism and Disposition Solid metal phosphides deposited on moist respiratory tract surfaces may hydrolyze and release absorbable phosphine. However, a more likely scenario would involve atmospheric hydrolysis of metal phosphides to phosphine gas.

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299 Phosphine and Eight Metal Phosphides Chan et al. (1983) detected phosphine in postmortem stomach, blood, and liver specimens from a 27-year-old man who had ingested aluminum phosphide tablets. The phosphine was released from the samples after acid treatment. Simi- larly, Anger et al. (2000) identified phosphine in postmortem brain, liver, and kidneys of a 39-year-old man who had committed suicide by ingestion of alumi- num phosphide tablets. Chugh et al. (1996) measured blood phosphine levels in patients with se- vere (n = 30), mild (n = 10), or minimal (n = 5) toxicity due to aluminum phosphide ingestion. Patients with severe toxicity had ingested “fresh” alumi- num phosphide compound and were in a state of shock. Those with mild toxicity had ingested “old” aluminum phosphide compound and presented with hypoten- sion and gastrointestinal symptoms. Patients with minimal toxicity ingested some powder from the aluminum phosphide tablets and presented with only nausea and occasional vomiting. Blood phosphine levels were positively corre- lated with severity of clinical signs and to dose of pesticide. At admission, blood phosphine levels were 71% higher (p < 0.001) in patients in the severe toxicity group than in the mild toxicity group of patients; blood phosphine was not de- tected in the minimal toxicity group of patients. Blood phosphine levels were also correlated to mortality; patients having blood phosphine levels ≤ 1.067 ± 0.16 mg% survived, whereas those with blood phosphine above this apparent threshold died (6 of 30 in the severe toxicity group). Garry et al. (1993) described a fatality from inhalation of aluminum phos- phide aerosol In this case report, blood aluminum concentration was used as a marker of exposure (see Section 2.1.1). Mechanism of Toxicity Metal phosphides react rapidly with moisture in air to produce phosphine gas. It is the phosphine gas that is responsible for acute inhalation toxicity from metal phosphide exposure. The rate of phosphine generation is dependent on ambient temperature and humidity (Anger et al. 2000) in addition to the chemi- cal structure of the metal phosphide. The hydrolysis reactions and phosphine evolution rates (OECD 2001) of the metal phosphides considered in this appen- dix are summarized in Table D-10. D.III. RATIONALE AND AEGL-1 Summary of Human Data Relevant to AEGL-1 No human data are available for the derivation of AEGL-1 for the metal phosphides considered in this appendix.

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300 Acute Exposure Guideline Levels TABLE D-10 Hydrolysis of Metal Phosphides Maximum Number of Phosphine moles of phosphine evolution rate at produced per mole of 20°C and 1 atm Hydrolysis metal phosphide Metal Phosphide Reaction hydrolyzed (mL/kg• min) Aluminum AlP + 3H2O 1 2069.7 Phosphide PH3 + Al(OH)3 Potassium K3P + 3H2O 1 807.6 Phosphide PH3 + 3KOH Sodium Na3P + 3H2O 1 997.8 Phosphide PH3 + 3NaOH Zinc Zn3P2 + 6H2O 2 929.9 Phosphide 2PH3 + 3Zn(OH)2 Calcium Ca3P2 + 6H2O 2 1274.6 Phosphide 2PH3 + 3Ca(OH)2 Magnesium Mg3P2 + 6H2O 2 1781.4 Phosphide 2PH3 + 3Mg(OH)2 Strontium Sr3P2 + 6H2O 2 737.1 Phosphide 2PH3 + 3Sr(OH)2 Magnesium Mg3AlP3 + 9H2O 3 1865.2 Aluminum 3PH3 + Al(OH)3 + Phosphide 3Mg(OH)2 Summary of Animal Data Relevant to AEGL-1 No animal data are available for the derivation of AEGL-1 for the metal phosphides considered in this appendix. Derivation of AEGL-1 No human or animal data are consistent with the effects defined by AEGL-1. Data were also insufficient for derivation of AEGL-1 values for phosphine; thus phosphine cannot be used as a surrogate. Therefore, AEGL-1 values for the metal phosphides considered in this appendix are not recom- mended (Table D-11). D.IV. RATIONALE AND AEGL-2 Summary of Human Data Relevant to AEGL-2 No human data are available for the derivation of AEGL-2 for the metal phosphides considered in this appendix.

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301 Phosphine and Eight Metal Phosphides TABLE D-11 AEGL-1 Values for Metal Phosphides Compound 10 min 30 min 1h 4h 8h Aluminum Phosphide NR NR NR NR NR Potassium Phosphide NR NR NR NR NR Sodium Phosphide NR NR NR NR NR Zinc Phosphide NR NR NR NR NR Calcium Phosphide NR NR NR NR NR Magnesium Phosphide NR NR NR NR NR Strontium Phosphide NR NR NR NR NR Magnesium Aluminum Phosphide NR NR NR NR NR NR: not recommended. Absence of an AEGL-1 does not imply that exposure below the AEGL-2 is without adverse effects. Summary of Animal Data Relevant to AEGL-2 No animal data are available for the derivation of AEGL-2 for the metal phosphides considered in this appendix. Derivation of AEGL-2 In the absence of appropriate chemical-specific data for the metal phosphides considered in this appendix, the AEGL-2 values for phosphine will be used to obtain AEGL-2 values for the metal phosphides. The use of phosphine as a surrogate for the metal phosphides is deemed appropriate be- cause qualitative (clinical signs) and quantitative (phosphine blood level) data suggest that the phosphine hydrolysis product is responsible for acute toxicity from metal phosphides. The phosphine AEGL-2 values will be used as target values for calculating the concentrations of metal phosphide needed to generate the phosphine AEGL values. Calculations were done using the methodology in NRC (2001) and are for 25 degrees C and 760 mm Hg. The metal phosphide values for AEGL-2 are given in Table D-12. D.V. RATIONALE AND AEGL-3 Summary of Human Data Relevant to AEGL-3 No human data are available for the derivation of AEGL-3 for the metal phosphides considered in this appendix. Summary of Animal Data Relevant to AEGL-3 No animal data are available for the derivation of AEGL-3 for the metal phosphides considered in this appendix.

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302 Acute Exposure Guideline Levels TABLE D-12 AEGL-2 Values For Metal Phosphidesa Compound 10-min 30-min 1-hr 4-hr 8-hr 9.5 mg/m3 9.5 mg/m3 4.7 mg/m3 1.2 mg/m3 0.59 mg/m3 Aluminum Phosphide 24 mg/m3 24 mg/m3 12 mg/m3 3.0 mg/m3 1.5 mg/m3 Potassium Phosphide 16 mg/m3 16 mg/m3 8.2 mg/m3 2.0 mg/m3 1.0 mg/m3 Sodium Phosphide 21 mg/m3 21 mg/m3 11 mg/m3 2.6 mg/m3 1.3 mg/m3 Zinc Phosphide 15 mg/m3 15 mg/m3 7.4 mg/m3 1.9 mg/m3 0.93 mg/m3 Calcium Phosphide 11 mg/m3 11 mg/m3 5.5 mg/m3 1.4 mg/m3 0.69 mg/m3 Magnesium Phosphide 27 mg/m3 27 mg/m3 13 mg/m3 3.3 mg/m3 1.7 mg/m3 Strontium Phosphide 11 mg/m3 11 mg/m3 5.3 mg/m3 1.3 mg/m3 0.66 mg/m3 Magnesium Aluminum Phosphide a These airborne concentrations will produce the equivalent AEGL values for phosphine. Derivation of AEGL-3 In the absence of appropriate chemical-specific data for the metal phosphides considered in this appendix, the AEGL-3 values for phosphine will be used to obtain AEGL-3 values for the metal phosphides. The use of phosphine as a surrogate for the metal phosphides is deemed appropriate be- cause qualitative (clinical signs) and quantitative (phosphine blood level) data suggest that the phosphine hydrolysis product is responsible for acute toxicity from metal phosphides. The phosphine AEGL-3 values will be used as target values for calculating the concentrations of metal phosphide needed to generate the phosphine AEGL values. Calculations were done using the methodology in NRC (2001) and are for 25 degrees C and 760 mm Hg. The metal phosphide values for AEGL-3 are given in Table D-13. D.VI. Comparison with Other Standards and Criteria No other exposure criteria or guidelines were located for the metal phos- phides.

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303 Phosphine and Eight Metal Phosphides TABLE D-13 AEGL-3 Values for Metal Phosphidesa Compound 10-min 30-min 1-hr 4-hr 8-hr 17 mg/m3 17 mg/m3 8.5 mg/m3 2.1 mg/m3 1.1 mg/m3 Aluminum Phosphide 44 mg/m3 44 mg/m3 22 mg/m3 5.5 mg/m3 2.7 mg/m3 Potassium Phosphide 29 mg/m3 29 mg/m3 15 mg/m3 3.7 mg/m3 1.8 mg/m3 Sodium Phosphide 38 mg/m3 38 mg/m3 19 mg/m3 4.8 mg/m3 2.4 mg/m3 Zinc Phosphide 27 mg/m3 27 mg/m3 13 mg/m3 3.4 mg/m3 1.7 mg/m3 Calcium Phosphide 20 mg/m3 20 mg/m3 9.9 mg/m3 2.5 mg/m3 1.2 mg/m3 Magnesium Phosphide 48 mg/m3 48 mg/m3 24 mg/m3 6.0 mg/m3 3.0 mg/m3 Strontium Phosphide 19 mg/m3 19 mg/m3 9.5 mg/m3 2.4 mg/m3 1.2 mg/m3 Magnesium Aluminum Phosphide a These airborne concentrations will produce the equivalent AEGL values for phosphine.

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