인화 알루미늄

Wear self-contained breathing apparatus when fighting fires involving this material. If contact with the material is anticipated, wear full protective clothing.

Use dry powder, dry sand, carbon dioxide. NO water.

Fresh air, rest. Half-upright position. Artificial respiration may be needed. No mouth-to-mouth artificial respiration. Refer immediately for medical attention.

Remove contaminated clothes. Rinse and then wash skin with water and soap. Wear protective gloves when administering first aid.

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

Rinse mouth. Do NOT induce vomiting. Refer immediately for medical attention.

· CALL 911. Then call emergency response telephone number on shipping paper. If shipping paper not available or no answer, refer to appropriate telephone number listed on the inside back cover.

· ELIMINATE all ignition sources (no smoking, flares, sparks or flames) from immediate area.

Warning: Effects may be delayed for several hours. Caution is advised.

General First Aid:

· Wear positive pressure self-contained breathing apparatus (SCBA).

TIH (Toxic Inhalation Hazard) - Term used to describe gases and volatile liquids that are toxic when inhaled. Some are TIH materials themselves, e.g., chlorine, and some release TIH gases when spilled in water, e.g., chlorosilanes. [ERG 2016].

If material on fire or involved in fire: Do not use water. Use dry chemical or carbon dioxide.

/Use/ carbon dioxide, dry chemical extinguisher. Do not use water.

Smother with dry sand, dry clay, dry ground limestone, or use approved Class D extinguishers. DO NOT use water. Violent reaction may result. Where access to the area is strictly controlled, it may be best to allow the release to burn.

Stop flow of liquid before extinguishing fire. Use dry chemical or carbon dioxide. DO NOT use water as straight stream directly on spilled material. Water fog can be used to control fire. DO NOT use halogenated extinguishing agents on spilled material. Violent reaction may result. Use water spray to keep fire-exposed containers cool. Fight fire from protected location or maximum possible distance. /Aluminum Alkyls/

Do not use water or water-based foam, as phosphine gas is formed. Small fires can be extinguished with dry chemical, soda ash, clay, or ground limestone, or use an approved Class D extinguisher. Large fires: Withdraw from area and let fire burn. Move container from fire only if you can do it without risk. ... The only respirators recommended for firefighting are self-contained breathing apparatuses that have full face-pieces and are operated in a pressure-demand or other positive-pressure mode. Wear self-contained breathing apparatus when fighting fires involving this material. If contact with the material is anticipated, wear full protective clothing.

Always keep container closed, dry. Store in a noncombustible, nonsprinklered building away from all combustible material. Isolate from strong acids.

Extremely reactive with air, moisture and compounds containing active hydrogen and therefore must be kept under a blanket of inert gas. /Aluminum alkyls/

Wear special protective clothing and positive pressure self-contained breathing apparatus. ... Blanket release with dry sand, clay, or ground limestone. Shovel into suitable dry container.

Shut off ignition; no flares, smoking, or flames in hazard area. Do not touch spilled material. Do not get water on spilled material or inside container. Dike spill for later disposal. Blanket release with dry sand, clay, or ground limestone. Shovel small spill into clean, dry container, and cover. Move containers from spill area. Avoid breathing dust. Wear appropriate protective clothing and use appropriate respiratory protection. Cover large powder spill with plastic sheet or tarp to minimize spreading. Clean up only under supervision of an expert. DOT warns that this chemical is spilled in water: Dangerous from 0.5 to 10 km (0.3-6.0 miles) downwind. Small spills (from a small package or a small leak from a large package) when spilled in water: First: Isolate in all directions (feet/meters) 300/100. Then: Protect persons downwind (miles/kilometers) Day 0.3/0.5, Night 1.2/1.9. Large spills (from a large package or from many small packages): First: Isolate in all directions (feet meters) 2000/600. Then: Protect persons downwind (miles/kilometers) Day 3.6/5.8, Night 7.0+/11.0+.

Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number P006, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.

SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.

Consult with environmental regulatory agencies for guidance on acceptable disposal practices. ... Allow to react slowly with moisture in the open, being sure that phosphine gas evolved is dissipated. Alternatively, mix with dry diluent and incinerate at temperature above 1000 °C with effluent gas scrubbing. In accordance with 40CFR165, follow recommendations for the disposal of pesticides and pesticide containers. Must be disposed of properly by following package label directions or by contacting your local or federal environmental control agency or by contacting your regional EPA office.

A poor candidate for incineration.

The present study was designed for determining the exact mechanism of cytotoxic action of aluminum phosphide (AlP) in the presence of iron sucrose as the proposed antidote. Rats received AlP (12 mg/kg) and iron sucrose (5-30 mg/kg) in various sets and were connected to cardiovascular monitoring device. After identification of optimum doses of AlP and iron sucrose, rats taken in 18 groups received AlP (6 mg/kg) and iron sucrose (10 mg/kg), treated at six different time points, and then their hearts were surgically removed and used for evaluating a series of mitochondrial parameters, including cell lipid peroxidation, antioxidant power, mitochondrial complex activity, ADP/ATP ratio and process of apoptosis. ECG changes of AlP poisoning, including QRS, QT, P-R, ST, BP and HR were ameliorated by iron sucrose (10 mg/kg) treatment. AlP initiated its toxicity in the heart mitochondria through reducing mitochondrial complexes (II, IV and V), which was followed by increasing lipid peroxidation and the ADP/ATP ratio and declining mitochondrial membrane integrity that ultimately resulted in cell death. AlP in acute exposure (6 mg/kg) resulted in an increase in hydroxyl radicals and lipid peroxidation in a time-dependent fashion, suggesting an interaction of delivering electrons of phosphine with mitochondrial respiratory chain and oxidative stress. Iron sucrose, as an electron receiver, can compete with mitochondrial respiratory chain complexes and divert electrons to another pathway. The present findings supported the idea that iron sucrose could normalize the activity of mitochondrial electron transfer chain and cellular ATP level as vital factors for cell escaping from AlP poisoning.

Aluminum phosphide (ALP), as an effective pesticide and a substance used for protecting rice during storage, has become one of the commonest causes of poisoning and even suicide in developing countries including Iran and India. The authors aimed to study the efficacy of sweet almond oil as an antidote in ALP toxicity. The present experimental study was conducted over 35 rats. The animals were divided into four groups: one group as the control group and three other groups which received ALP alone or ALP and sweet almond oil with different time intervals. In addition to estimating the survival rate of the animals, plasma cholinesterase activity as a possible factor affected in ALP poisoning was evaluated. Treatment by intragastric irrigation of sweet almond oil resulted in significant reduction of mortality. Moreover, mean plasma cholinesterase levels were inhibited in groups receiving ALP. Oral sweet almond oil, if especially used immediately after poisoning with ALP, improves the survival rate.

Aluminum phosphide (AlP), one of the most commonly used pesticides worldwide, has been the leading cause of self-poisoning mortalities among many Asian countries. The heart is the main organ affected in AlP poisoning. Melatonin has been previously shown to be beneficial in reversing toxic changes in the heart. The present study reveals evidence on the probable protective effects of melatonin on AlP-induced cardiotoxicity in rats. The study groups included a control (almond oil only), ethanol 5% (solvent), sole melatonin (50 mg/kg), AlP (16.7 mg/kg), and 4 AlP + melatonin groups which received 20, 30, 40 and 50 mg/kg of melatonin by intraperitoneal injections following AlP treatment. An electronic cardiovascular monitoring device was used to record the electrocardiographic (ECG) parameters. Heart tissues were studied in terms of oxidative stress biomarkers, mitochondrial complexes activities, ADP/ATP ratio and apoptosis. Abnormal ECG records as well as declined heart rate and blood pressure were found to be related to AlP administration. Based on the results, melatonin was highly effective in controlling AlP-induced changes in the study groups. Significant improvements were observed in the activities of mitochondrial complexes, oxidative stress biomarkers, the activities of caspases 3 and 9, and ADP/ATP ratio following treatment with melatonin at doses of 40 and 50 mg/kg. Our results indicate that melatonin can counteract the AlP-induced oxidative damage in the heart. This is mainly done by maintaining the normal balance of intracellular ATP as well as the prevention of oxidative damage. Further research is warranted to evaluate the possibility of using melatonin as an antidote in AlP poisoning.

Aluminum phosphide is used as a fumigant. It produces phosphine gas (PH3). PH3 is a mitochondrial poison which inhibits cytochrome c oxidase, it leads to generation of reactive oxygen species; so one of the most important suggested mechanisms for its toxicity is induction of oxidative stress. In this regard, it could be proposed that a drug like N-acetylcysteine (NAC) as an antioxidant would improve the tolerance of aluminum phosphide-intoxicated cases. The objective of this study was to evaluate the protective effects of NAC on acute aluminum phosphide poisoning. This was a prospective, randomized, controlled open-label trial. All patients received the same supportive treatments. NAC treatment group also received NAC. The blood thiobarbituric acid reactive substances as a marker of lipid peroxidation and total antioxidant capacity of plasma were analyzed. Mean ingested dose of aluminum phosphide in NAC treatment and control groups was 4.8 +/- 0.9 g vs. 5.4 +/- 3.3 g, respectively (p = 0.41). Significant increase in plasma malonyldialdehyde level in control group was observed (139 +/- 28.2 vs. 149.6 +/- 35.2 umol/L, p = 0.02). NAC infusion in NAC treatment group significantly decreased malondialdehyde level (195.7 +/- 67.4 vs. 174.6 +/- 48.9 umol/L, p = 0.03), duration of hospitalization (2.7 +/- 1.8 days vs. 8.5 +/- 8.2 days, p = 0.02), rate of intubation and ventilation (45.4% vs. 73.3%, p = 0.04). Mortality rate in NAC treatment and control groups were 36% and 60%, respectively with odds ratio 2.6 (0.7-10.1, 95% CI). NAC may have a therapeutic effect in acute aluminum phosphide poisoning.

The aim of the present study was to investigate the efficacy of acetyl-L-carnitine (ALCAR) on pathologic changes of mitochondrial respiratory chain activity, ATP production, oxidative stress, and cellular apoptosis/necrosis induced by aluminum phosphide (AlP) poisoning. The study groups included: the Sham that received almond oil only; the AlP that received oral LD50 dose of aluminum; the AC-100, AC-200, and AC-300 which received concurrent oral LD50 dose of AlP and single 100, 200, and 300 mg/kg of ALCAR by intraperitoneal injection. After 24 hr, the rats were sacrificed; the heart and blood sample were taken for measurement of biochemical and mitochondrial factors. The results specified that ALCAR significantly attenuated the oxidative stress (elevated ROS and plasma iron levels) caused by AlP poisoning. ALCAR also increased the activity of cytochrome oxidase, which in turn amplified ATP production. Furthermore, flow cytometric assays and caspase activity indicated that ALCAR prohibited AlP-induced apoptosis in cardiomyocytes.

Aluminum targets the nervous system and causes decreased nervous system performance and is associated with altered function of the blood-brain barrier. The accumulation of aluminum in the body may cause bone or brain diseases. High levels of aluminum have been linked to Alzheimer's disease. A small percentage of people are allergic to aluminium and experience contact dermatitis, digestive disorders, vomiting or other symptoms upon contact or ingestion of products containing aluminium. Inhalation of phosphine may cause severe pulmonary irritation leading to acute pulmonary oedema, cardiovascular dysfunction, CNS excitation, coma and death. Gastrointestinal disorders, renal damage and leukopenia may also occur. Chronic exposure to phosphine can result in anemia, bronchitis, gastrointestinal effects, and visual, speech and motor problems. (L980, L982, L739, L740)

Phosphine residues present after fumigation of packaged fruits and vegetables decreased to 0.18-0.3 ppb after 1 day of storage.

At a dose of 3 aluminum phosphate tablets/ton free phosphine residue in coffee beans is just half of that found in the round pea berry. Coffee beans (0.097 ppm) are free of free phosphine residue at 20 days compared to that in the peaberry (0.176 ppm) which takes 33 days. Decrease of computed residues from coffee beans is faster (14 days) than that from the peaberry (26 days). Coffee beans have higher free phosphine holding capacity than the peaberry variety. In its initial pattern of free phosphine desorption, coffee resembles wheat. Coffee beans and peaberry dosed at aluminum phosphate tablets/ton had desorbed large amounts of free phosphine than those dosed at 3 tablets/ton. Even at this higher dose, both coffee beans and the peaberry varieties are free of free phosphine residue within 34 days. Absorption spectra of these fumigated coffee varieties reveal the absence of any bound residues of free phosphine. Air oxidation of free phosphine to phosphorus compounds is predominant in coffee beans. Coffee beans can safely be fumigated at 3 aluminum phosphate tablets/ton without having traces of either free or bound residues of free phosphine. /Aluminum phosphate/

The substance can be absorbed into the body by inhalation of its aerosol and by ingestion.

Oral (L739) ; Inhalation (L739)

IDENTIFICATION AND USE: Aluminum phosphide forms green or yellow cubic crystals with a garlic odor. It is used as fumigant, rodenticide, and insecticide for stored cereal grains; fumigant for control of burrowing rodents. HUMAN STUDIES: 195 patients with aluminum phosphide ingestion were admitted to hospital. Of 195 patients, 115 died. The nonsurvivors had more severe hypotension and metabolic acidosis than the survivors who had more severe vomiting. Autopsies conducted in 115 subjects revealed congestion of liver, spleen, kidneys, adrenals, gastrointestinal tract and brain that correlated with the severity of hypotension. Aluminum phosphide when ingested is highly toxic with fatal dose as low as 1.5 g. The dominant clinical feature is severe hypotension refractory to dopamine. There was a significantly greater rise in serum magnesium in patients with severe toxicity compared to patients with mild to moderate toxicity. Aluminum phosphide induced genotoxic effects such as sister chromatid exchange (SCE) and chromosome aberration (CA) in cultured human blood cells in the presence of a metabolic activator. ANIMAL STUDIES: Aluminum phosphide, a widely used fumigant and rodenticide leads to high mortality if ingested. Its toxicity is due to phosphine liberated when it comes in contact with moisture. Toxicity in rats appears to result as a consequence of both-energy insufficiency and oxidative stress, with a possible and preferential interaction with the tissue cytochromes. In rats, the deleterious effect of aluminum phosphide on heart is mediated by both declined cellular metabolism of the myocardium as well as by necrosis of the cardiac tissue resulting in the release of reactive oxygen intermediates. In a two-year rat feeding study no evidence of carcinogenicity was seen. Aluminum phosphide induced genetic and oxidative damages in rats. Chromosomal aberrations (CAs) and micronucleus (MN) assay were used for monitoring genotoxic damage. Aluminium phosphide caused increase in CA and MN assay rates. ECOTOXICITY STUDIES: One use pattern of aluminum and magnesium phosphide, as a burrow fumigant, poses a risk to threatened and endangered species of mammals and reptiles. The risks posed to these species occur if they are found in a burrow that is fumigated. Because of the high degree of toxicity of phosphine gas, all animals in a treated burrow will be killed. In 1981, the United States Fish and Wildlife Service determined that use of aluminum and magnesium phosphide as a burrow fumigant may jeopardize the black-footed ferret, the Utah prairie dog, the San Joaquin kit fox, the blunt-nosed leopard lizard, the eastern indigo snake, and the desert tortoise.

The main target organs of aluminum are the central nervous system and bone. Aluminum binds with dietary phosphorus and impairs gastrointestinal absorption of phosphorus. The decreased phosphate body burden results in osteomalacia (softening of the bones due to defective bone mineralization) and rickets. Aluminum's neurotoxicity is believed to involve several mechanisms. Changes in cytoskeletal protein functions as a results of altered phosphorylation, proteolysis, transport, and synthesis are believed to be one cause. Aluminum may induce neurobehavioral effects by affecting permeability of the blood-brain barrier, cholinergic activity, signal transduction pathways, lipid peroxidation, and impair neuronal glutamate nitric oxide-cyclic GMP pathway, as well as interfere with metabolism of essential trace elements because of similar coordination chemistries and consequent competitive interactions. It has been suggested that aluminum's interaction with estrogen receptors increases the expression of estrogen-related genes and thereby contributes to the progression of breast cancer (A235), but studies have not been able to establish a clear link between aluminum and increased risk of breast cancer (A15468). Certain aluminum salts induce immune responses by activating inflammasomes. Phosphine inhibits cytochrome c oxidase, preventing mitochondrial oxidative phosphorylation. This non-competitive inhibition prevents cellular respiration and leads to multi-organ dysfunction. Phosphine can also react with hydrogen peroxide to form the highly reactive hydroxyl radical, which can cause lipid peroxidation. (A291, A292, L739, A235, A236)

/BIRDS and MAMMALS/ One use pattern of aluminum and magnesium phosphide, as a burrow fumigant, poses a risk to threatened and endangered species of mammals and reptiles. The risks posed to these species occur if they are found in a burrow that is fumigated. Because of the high degree of toxicity of phosphine gas, all animals in a treated burrow will be killed. In 1981, the United States Fish and Wildlife Service (USFWS) determined that use of aluminum and magnesium phosphide as a burrow fumigant may jeopardize the black-footed ferret, the Utah prairie dog, the San Joaquin kit fox, the blunt-nosed leopard lizard, the eastern indigo snake, and the desert tortoise.

Sore throat. Cough. Shortness of breath. Headache. Dizziness. Nausea. Vomiting. Diarrhoea.

Redness. Burning sensation.

Redness. Pain.

Nausea. Vomiting. Diarrhoea. Abdominal pain. Headache. Convulsions. Shock or collapse. Unconsciousness.

Inhalating aluminum dust causes coughing and abnormal chest X-rays. A small percentage of people are allergic to aluminium and experience contact dermatitis, digestive disorders, vomiting or other symptoms upon contact or ingestion of products containing aluminium. Early symptoms of acute phosphine intoxication include pain in the diaphragm, nausea, vomiting, excitement, and a phosphorus smell on the breath. Higher levels can cause weakness, bronchitis, pulmonary edema, shortness of breath, convulsions, and death. Some effects, such as pulmonary edema, convulsions, and liver injury, may appear or continue to be present days after an exposure. Ingestion of metal phosphides results in release of phosphine in your stomach which can cause nausea, vomiting, abdominal pain, and diarrhea. (L980, L739, L740)

Aluminum phosphide

4 x 10 ^-4 mg/kg-day

/SIGNS AND SYMPTOMS/ Symptoms of overexposure are headache, dizziness, nausea, difficulty in breathing, vomiting, and diarrhea.

/SIGNS AND SYMPTOMS/ Coincidental systemic and coincidental eye categories were associated with the majority of the exposures reported in California. Such coincidental cases typically occur when bystanders are accidently exposed. Out of a total of 22 systemic coincidental exposures, 16 workers became ill after their almond sorting building was fumigated the previous day. Symptoms included headache, nausea, vomiting, chills, abdominal cramps, weakness, dizziness, and difficulty breathing. Out of the 25 coincidental eye exposures, 14 workers experienced eye irritation after their storage building was fumigated the previous weekend. Symptoms included red and watery eyes, and nasal secretions. The other 11 workers out of the 25 coincidental eye exposures had re-occurring eye irritations while working in an almond/pistachio processing plant.

/SIGNS AND SYMPTOMS/ ... Between March 1989 and March 1994, 195 patients with aluminum phosphide ingestion were admitted to Nehru Hospital of the Postgraduate Institute of Medical Education and Research, Chandigarh in Northwest India. The information regarding demography, time elapsed between ingestion and arrival in the hospital, nature of ingestion, dose ingested, symptoms and signs at admission and course during hospital stay was recorded on a proforma. Of 195 patients, 115 died. The deaths could be related to the dose ingested but not to the time elapsed between ingestion and arrival at the hospital. The nonsurvivors had more severe hypotension and metabolic acidosis than the survivors who had more severe vomiting. Autopsies conducted in 115 subjects revealed congestion of liver, spleen, kidneys, adrenals, gastrointestinal tract and brain that correlated with the severity of hypotension. Histopathology did not reveal any specific changes beyond visceral congestion and patchy necrosis of the liver. Aluminum phosphide when ingested is highly toxic with fatal dose as low as 1.5 g. The dominant clinical feature is severe hypotension refractory to dopamine.

/SIGNS AND SYMPTOMS/ ... The present study includes 121 patients of proven aluminium phosphide (ALP) poisoning. The age varied between 20 and 45 years, and the majority (95) were females. Clinical manifestations were nausea and vomiting in all the patients, dyspnea and palpitation (78 each), cyanosis (65), hypotension (43) and shock (57). Cardiac arrhythmias were present in 96 cases and hypermagnesaemia in 51 patients. The mean serum total magnesium level (1.94 +/- 0.29 mEq/l) was significantly (p less than 0.01) elevated compared to the mean total magnesium level in control subjects (1.62 +/- 0.26 mEq/l). There was a significantly greater rise in serum magnesium in patients with severe toxicity compared to patients with mild to moderate toxicity. Out of 121 cases studied, 86 died; 76 died within 24 h of ALP ingestion. Mortality was commoner (45 out of 57) in patients with severe toxicity.

P006; As stipulated in 40 CFR 261.33, when aluminum phosphide, as a commercial chemical product or manufacturing chemical intermediate or an off-specification commercial chemical product or a manufacturing chemical intermediate, becomes a waste, it must be managed according to federal and/or state hazardous waste regulations. Also defined as a hazardous waste is any container or inner liner used to hold this waste or any residue, contaminated soil, water, or other debris resulting from the cleanup of a spill, into water or on dry land, of this waste. Generators of small quantities of this waste may qualify for partial exclusion from hazardous waste regulations (40 CFR 261.5(e)).

Classified for restricted use and limited to use by or under the direct supervision of a certified applicator. Active Ingredient: Aluminum phosphide; Formulation: As sole ingredient. No mixtures registered; Use Pattern: Agricultural crop uses; Classification: Under further evaluation; Criteria Influencing Restriction: Inhalation hazard to humans.

Based on the reviews of the generic data for the active ingredients aluminum phosphide and magnesium phosphide, the Agency has sufficient information on the human health effects of aluminum phosphide and magnesium phosphide and on their potential for causing adverse effects in fish and wildlife and the environment. The Agency has determined that all uses of aluminum phosphide and magnesium phosphide as specified in this document require mitigation of the risks associated with the exposure to these pesticides. The Agency will conduct a public process to identify the best ways to reduce the risks associated with aluminum and magnesium phosphide exposure. This process will include a public comment period and a stakeholder meeting. Following the conclusion of this process, the Agency will make a final determination on the mitigation measures that must be adopted in order for products containing aluminum and magnesium phosphide to be eligible for reregistration.

As the federal pesticide law FIFRA directs, EPA is conducting a comprehensive review of older pesticides to consider their health and environmental effects and make decisions about their continued use. Under this pesticide reregistration program, EPA examines newer health and safety data for pesticide active ingredients initially registered before November 1, 1984, and determines whether the use of the pesticide does not pose unreasonable risk in accordance to newer safety standards, such as those described in the Food Quality Protection Act of 1996. Aluminum phosphide is found on List A, which contains most pesticides that are used on foods and, hence, have a high potential for human exposure. List A consists of the 194 chemical cases (or 350 individual active ingredients) for which EPA issued registration standards prior to FIFRA '88. Case No: 0025; Pesticide type: insecticide; Registration Standard Date: 10/08/1986 PB87-117172; Case Status: OPP is reviewing data from the pesticide's producers regarding its human health and/or environmental effects, or OPP is determining the pesticide's eligibility for reregistration and developing the RED document.; Active ingredient (AI): aluminum phosphide; Data Call-in (DCI) Date(s): 08/06/1990, 04/06/1993; AI Status: The producers of the pesticide have made commitments to conduct the studies and pay the fees required for reregistration, and are meeting those commitments in a timely manner.

Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount equal to or greater than its reportable quantity of 100 lb or 45.4 kg. The toll free number of the NRC is (800) 424-8802. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV. D.3.b).

Releases of CERCLA hazardous substances are subject to the release reporting requirement of CERCLA section 103, codified at 40 CFR part 302, in addition to the requirements of 40 CFR part 355. Aluminum phosphide is an extremely hazardous substance (EHS) subject to reporting requirements when stored in amounts in excess of its threshold planning quantity (TPQ) of 500 lbs. Note: This material is a reactive solid. The TPQ does not default to 10,000 pounds for non-powder, non-molten, non-solution form.

Aluminum phosphide

A Commercial Grade

A Placarded Amount

Chemical or material that can be mixed with readily available materials.

(AZ) ARIZONA 73 ug/L /Aluminum/

(CA) CALIFORNIA 200 ug/L /Aluminum/

(ME) MAINE 1430 ug/L /Aluminum/