Monosodium phosphate

119.97700

119.95900

618-243-1

KH7I04HPUU

DTXSID7035222

Colorless, monoclinic crystals|White crystalline powder

2835220000

90.40000

-0.49040

DryPowder; DryPowder, PelletsLargeCrystals; Liquid; PelletsLargeCrystals

1.40 g/mL at 20ºC

60 °C

158ºC at 760 mmHg

In water, 85 g/100 mL

Store at RT.

LD50 orally in Rabbit: 8290 mg/kg LD50 dermal Rabbit > 7940 mg/kg

Odorless

Between 4,1 and 5,0 (1 % solution)

The pKa of monosodium phosphate is 6.8-7.2 (depending on the physicochemical characteristics during pKa determination)

SOLN PRODUCES EFFERVESCENCE WITH SODIUM CARBONATE; NEUTRAL, OR PRACTICALLY NEUTRAL, TO METHYL ORANGE TEST SOLN /SODIUM DIHYDROGEN PHOSPHATE MONOHYDRATE/|Slightly hygroscopic ... Has acid reaction; forms sodium acid pyrophosphate at 225-250 °C and sodium metaphosphate at 350-400 °C|Colorless, orthorhombic crystals; MP: 60 °C (decomposes); density: 1.91 g/cu cm; 94.9 g/100 g water at 25 °C. Insoluble in ethanol /Sodium dihydrogen phosphate dihydrate/|Orthorhombic bisphenoidal colorless crystals, mp 60 °C, specific gravity 1.915. At room temp crystallizes with 2H2O. /Sodium dihydrogen phosphate dihydrate/|White, odorless, slightly deliquescent crystals or granules. At 100 °C loses all its water; when ignited it converts into metaphosphate. Freely soluble in water; practically insoluble in alcohol. The aqueous soln is acid. pH of 0.1 molar aq soln at 25 °C: 4.5. /Sodium dihydrogen phosphate monohydrate/|Reacts slowly on exposure to water (moisture) with (some) metals. On burning: release of toxic and corrosive gases/vapours (phosphorus oxides). Reacts violently with (some) acids/bases.

1

R36/37/38

S26-S36

WA1900000

Xi

Stable. Incompatible with heavy metals, strong acids.

P264, P280, P302+P352, P321, P332+P313, P362

H315

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal and plant life; and conformance with environmental and public health regulations.|Waste treatment methods. Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contaminated packaging: Dispose of as unused product.

Incompatible materials: Strong oxidizing agents.|Incompatibilities: Since sodium biphosphate is an acid salt, it is incompatible with carbonates & alkalies in general. In solution with methenamine it causes slow evolution of formaldehyde. /Sodium dihydrogen phosphate monohydrate/

Monosodium orthophosphate is a food additive permitted for direct addition to food for human consumption, as long as 1) the quantity of the substance added to food does not exceed the amount reasonably required to accomplish its intended physical, nutritive, or other technical effect in food, and 2) any substance intended for use in or on food is of appropriate food grade and is prepared and handled as a food ingredient.|Sodium phosphate (mono-, di-, & tribasic) used as a multiple purpose food substance in food for human consumption is generally recognized as safe when used in accordance with good manufacturing practice. /Sodium phosphate (mono-, di-, & tribasic)/|Sodium acid phosphate used as a sequestrant in food for human consumption is generally recognized as safe when used in accordance with good manufacturing practice.|Sodium phosphate (mono-, di-, & tribasic) used as a sequesterant in food for human consumption is generally recognized as safe when used in accordance with good manufacturing practice. /Sodium phosphate (mono-, di-, & tribasic)/|For more FDA Requirements (Complete) data for SODIUM DIHYDROGEN PHOSPHATE (9 total), please visit the HSDB record page.

WHO; Diseases Caused by Phosphorus and Its Toxic Compounds; Early Detection of Occupational Diseases pg 53-62 (1986). Review of diseases and health related effects resulting from exposure to phosphorus or phosphorus cmpd.|European Commission, ESIS; IUCLID Dataset, Sodium dihydrogenorthophosphate (7558-80-7) (2000 CD-ROM edition).[Available from, as of March, 6 2009: http://esis.jrc.ec.europa.eu/]

Not Classified| |Warning|H315 (100%): Causes skin irritation [Warning Skin corrosion/irritation]|P264, P280, P302+P352, P321, P332+P313, and P362|Aggregated GHS information provided by 172 companies from 2 notifications to the ECHA C&L Inventory.

Eye/face protection: Safety glasses with side-shields conforming to EN166. Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU).|Skin protection: Handle with gloves.|Body Protection: Impervious clothing, The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace.|Respiratory protection: For nuisance exposures use type P95 (US) or type P1 (EU EN 143) particle respirator. For higher level protection use type OV/AG/P99 (US) or type ABEK-P2 (EU EN 143) respirator cartridges. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU).|Local exhaust ventilation is required where solids are handled as powders or crystals; even when particulates are relatively large, a certain proportion will be powdered by mutual friction. If in spite of local exhaust an adverse concentration of the substance in air could occur, respiratory protection should be considered.

Nonflammable

Suitable extinguishing media: Use extinguishing measures that are appropriate to local circumstances and the surrounding environment.|Advice for firefighters: Wear self contained breathing apparatus for fire fighting if necessary.|The product itself does not burn.

Behavior in fire: May melt with loss of steam. /Sodium Phosphates/

Accidental Release Measures. Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Avoid breathing dust. Environmental precautions: Do not let product enter drains. Methods and materials for containment and cleaning up: Pick up and arrange disposal without creating dust. Sweep up and shovel. Keep in suitable, closed containers for disposal.

Precautions for safe handling: Avoid contact with skin and eyes. Avoid formation of dust and aerosols. Provide appropriate exhaust ventilation at places where dust is formed.|Appropriate engineering controls: Handle in accordance with good industrial hygiene and safety practice. Wash hands before breaks and at the end of workday.|Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.|SRP: Local exhaust ventilation should be applied wherever there is an incidence of point source emissions or dispersion of regulated contaminants in the work area. Ventilation control of the contaminant as close to its point of generation is both the most economical and safest method to minimize personnel exposure to airborne contaminants. Ensure that the local ventilation moves the contaminant away from the worker.

Intamuscular LD50 of 250mg/kg and oral LD50 of 8290 mg/kg reported in rats. Phosphate toxicity is likely due to the disturbance of other electrolytes when phosphate levels are high, producing symptoms including tetany, dehydration, hypotension, tachycardia, hyperpyrexia, cardiac arrest and coma. Risk of raising phosphate levels through use of sodium phosphate appears to be higher in smaller patients.|IDENTIFICATION AND USE: Sodium dihydrogen phosphate is a white crystalline powder. It is used as a pH buffer, in baking powders; in boiler water treatment; and as a dry acidulant and sequestrant for foods. In addition, it is a buffering agent (electroplating baths); acidulant (processed meats, egg products, powdered drinks); builder (industrial cleaning formulations); metal phosphatizing reagent; mineral supplement; softening/conditioning agent (boiler water treatment); textile dyeing/printing auxiliary. In medicine, it is used as an enema solution. HUMAN EXPOSURE AND TOXICITY: Purposeful or accidental ingestion of more than the recommended dosage of tablets might be expected to lead to severe electrolyte disturbances, including hyperphosphatemia, hypocalcemia, hypernatremia, or hypokalemia, as well as dehydration and hypovolemia, with attendant signs and symptoms of these disturbances. Certain severe electrolyte disturbances may lead to cardiac arrhythmias, seizure, renal failure, and death. Prolongation of the QT interval has been observed in some patients who were dosed with Visicol tablets (sodium phosphate, monobasic, monohydrate and sodium phosphate, dibasic anhydrous). QT prolongation with Visicol tablets has been associated with electrolyte imbalances, such as hypokalemia and hypocalcemia. The estimated fatal dose of sodium phosphates is 50 g. Orally administered sodium phosphate-associated colonic mucosal abnormalities are infrequent but can mimic non-steroidal anti-inflammatory drug-induced injury or inflammatory bowel disease, and in particular must be differentiated from Crohn's disease. ANIMAL STUDIES: Doses of 250 g/kg by mouth produced diarrhea in rats, guinea pigs and rabbits. Six days of sodium dihydrogen phosphate treatment in rats consistently produced calcification of basement membranes of proximal tubules in the mid-cortex, followed by calcification of casts and basement membranes in the outer medulla and papilla after 10 days. Injection of 10.0 mg/chicken egg in air cell & yolk caused celosomia, exencephaly, microcephaly, brachygnathia, hyperplasia of heart, ablepharia, torticollis, microphthalmia, anophthalmia, coloma, ectromelia, phocomelia, buphthalmia, and cleft palate anomalies. In vitro mammalian chromosome aberration test in Chinese hamster lung fibroblasts without metabolic activation was negative. Study of the genotoxic potential of with the SOS chromatest in E. coli PQ37, PQ35 with and without metabolic activation was negative.

Sodium dihydrogen phosphate and sodium glycerophosphate inhibited intestinal calcium absorption in rats when administered simultaneously with 5-50 mmoles calcium chloride solution by gavage or in situ in ligatured jejunal loops.|The effects of sodium phosphate dibasic disodium phosphate buffer on in vivo release and on ocular and systemic absorption of timolol administered in matrices of monoisopropyl ester of polymethylvinyl ether/maleic anhydride ocularly to rabbits was studied; the vasoconstrictor phenylephrine methaoxedrine was added to some matrices to reduce the systemic absorption of timolol. The unbuffered matrix yielded a lower peak concentration of timolol in tear fluid and a lower steady-state concentration in plasma 3 hr later than the buffered one. Thus, sodium phosphate dibasic increases the rate of timolol release from the inserts several fold in tear fluid. Coadministration of phenylephrine in buffered matrices decreased the peak timolol concentration in plasma about 3 times and increased that in tear fluid about 2 fold. In iris-ciliary body, administration of buffered matrices resulted in timolol concentrations that were comparable with the levels after eye drop instillation. Compared to the unbuffered matrices, sodium phosphate dibasic, with or without phenylephrine, at least doubled the concentration ratio of iris-ciliary body to plasma.|The effect of aluminum on the renal handling of phosphate was studied in rats. Male Sprague Dawley rats were divided into 3 groups. The first group consisted of intact animals. The second consisted of rats that had been thyroparathyroidectomized. The third group consisted of thyroparathyroidectomized rats that were infused with 18.0 millimolar phosphate solution (disodium-phosphate monosodium-phosphate) ratio 4 to 1). Each group was subdivided into animals that were infused with 2.8 micrograms per milliliter aluminum for 3 hours or saline (controls). Glomerular filtration rate, urine flow rate, fractional excretion of phosphate, plasma calcium, sodium, and phosphate, blood pH, and urinary cyclic-adenosine-3',5'-monophosphate were measured at selected intervals. Liver, kidney, and brain aluminum concentrations were measured at selected times. In intact animals, fractional excretion of phosphate increased significantly after 3 hours of aluminum infusion. Plasma calcium and phosphate decreased. In the thyroparathyroidectomized animals, fractional excretion of phosphate increased after 3 hours of aluminum infusion and after 2 and 3 hours in animals that also received phosphates. Urinary cyclic-adenosine-3',5'- monophosphate concentrations were not significantly affected in thyroparathyroidectomized rats infused with phosphates. Glomerular filtration rate, urine flow rate, and plasma sodium were also not significantly affected. Blood pH was not significantly different between saline and aluminum infused rats in any group. Brain and kidney aluminum concentrations were not significantly affected by aluminum infusion. Liver aluminum concentrations were not significantly higher in all aluminum infused animals. The authors conclude that aluminum infusion inhibits renal phosphate reabsorption by a mechanism that does not involve parathyroid hormone, blood pH, or 3',5'-monophosphate.|Oral administration is safer, but careful monitoring of serum electrolyte levels and renal function is necessary. Nausea, vomiting, and diarrhea may occur and may be dose dependent. Concomitant use of antacids containing aluminum and/or magnesium should be avoided, because they may bind phosphate and prevent it absorption (calcium antacids also may bind phosphate, and it is assumed that these agents are not given to hypercalcemic patients). /Monobasic or dibasic sodium or potassium phosphate/

The estimated fatal dose of sodium phosphates is 50 g.

LD50 Rat intramuscular 250 mg/kg|LD50 Rat oral 8290 mg/kg|LD50 Mouse oral /greater than/ 2000 mg/kg bw.|LD50 Rabbit dermal /greater than/ 7940 mg/kg bw.

Phosphate should not be given to patients with impaired renal function or hyperphosphatemia. They should not be given to patients with alkaline urine due to urinary tract infections because increased calcium and phosphate concentrations in the alkaline urine increase the risk of calcium phosphate stones. /Monobasic or dibasic sodium or potassium phosphate/|An elderly woman developed severe hyperphosphatemia, hypocalcemia, and cardiac arrest after oral administration of sodium phosphate in preparation for colonoscopy. This is an unusual complication and is attributed to decreased phosphate excretion by the kidneys. At increased risk are patients with impaired renal function, age more than 65 years, and presenting with intestinal obstruction or decreased intestinal motility, increased intestinal permeability, liver cirrhosis, or congestive heart failure...|A case of hypocalcemia is reported in a 58-yr-old man with polycystic kidney disease given rectal Fleet enema (sodium phosphate monobasic (sodium biphosphate), combination, sodium phosphate dibasic) for the treatment of constipation. Two ampuls of calcium chloride were administered IV followed by an infusion. The patient responded rapidly to therapy. Since constipation is often a problem in patients with renal insufficiency, physicians should be aware in specifying mineral oil enema on prescriptions instead of simply Fleet enema. /Sodium phosphate monobasic (sodium biphosphate), combination, sodium phosphate dibasic/|... It was recommended that phosphate enemas not be used in children under 3 yr of age, and that they should be used only with caution at reduced doses in older children. /Sodium phosphate dibasic and sodium phosphate monobasic/|For more Populations at Special Risk (Complete) data for SODIUM DIHYDROGEN PHOSPHATE (11 total), please visit the HSDB record page.

According to the 2012 TSCA Inventory Update Reporting data, the number of persons reasonably likely to be exposed in the industrial manufacturing, processing, and use of sodium dihydrogen phosphate is 1000 or greater; the data may be greatly underestimated(1).|NIOSH (NOES Survey 1981-1983) has statistically estimated that 289,281 workers (145,939 of these are female) are potentially exposed to sodium dihydrogen phosphate in the US(1).

Used to treat constipation or to clean the bowel before a colonoscopy.|FDA Label

Visicol Tablets are indicated for cleansing of the colon as a preparation for colonoscopy in adults 18 years of age or older. /Included in US product label; sodium phosphate, monobasic, monohydrate and sodium phosphate, dibasic anhydrous/|To determine whether phosphate supplementation, started soon after birth in adequate quantity, would prevent rickets in very low birth weight infants with prenatal deficiency of phosphate, 40 neonates were given an initial dose of 50 mg/day of phosphate administered as a mixture of 189 g of sodium phosphate dibasic (disodium hydrogen phosphate) and 82 g of sodium phosphate monobasic (sodium dihydrogen phosphate) made up to 2 liters with single strength chloroform water or placebo (single strength chloroform water). Supplementation was increased to 37.5 mg every 12 hr if the plasma phosphate concentration remained less than 1.5 mmol/L after one wk. Results showed that no infant receiving phosphate supplements had radiological evidence of rickets whereas bone changes were apparent in 42% of the control group. It was concluded that prenatal deficiency of phosphate, due to placental insufficiency, can be corrected by phosphate supplementation, thereby preventing rickets of prematurity.|The objective of this study was to determine the safety and efficacy of 0.15 mmol/kg phosphorus (PHOS), administered intravenously as sodium or potassium phosphate over 120 minutes, in the treatment of adults suffering from severe hypophosphatemia. Severe hypophosphatemia was defined as a serum PHOS concentration of /LE/ 1.5 mg/dL. Exclusion criteria were renal impairment and hypercalcemia. Patient assessments included mental status, heart rate, and blood pressure. The timing of post-infusion serum PHOS sampling was at physician discretion. Six men and four women were enrolled in the study. During the study period, the only parenteral PHOS administered was the study dose. There were no patient adverse events associated with PHOS administration. One patient who received potassium phosphates had an elevated post-infusion serum potassium (5.2 mEq). Serum PHOS increased above the study criteria for severe hypophosphatemia in all ten patients, although nine patients received concomitant oral PHOS supplements. The dosing of intravenous sodium or potassium phosphate in the treatment of patients with severe hypophosphatemia is empiric. Historical evidence of toxicity has caused dosing recommendations to be low and slow. These data demonstrate the safety of a moderate PHOS dose when administered over two hours to adults, as measured by patient mental status, vital signs, and blood chemistry analysis.|Sixty patients were randomly divided into three groups of 20 each. Each group was submitted to a bowel preparation with one of the following solutions: 10% manitol, sodium picosulfate or sodium phosphate. The parameters evaluated were: taste, tolerance, associated side effects and quality of cleansing. Postural blood pressure and pulse rate as well as serum sodium, potassium, calcium and phosphate were compared. ... Sodium phosphate and 10% manitol solutions provided superior results in terms of colon cleansing compared to sodium picosulfate solution...|For more Therapeutic Uses (Complete) data for SODIUM DIHYDROGEN PHOSPHATE (9 total), please visit the HSDB record page.

/BOXED WARNING/ There have been rare, but serious reports of acute phosphate nephropathy in patients who received oral sodium phosphate products for colon cleansing prior to colonoscopy. Some cases have resulted in permanent impairment of renal function and some patients required long-term dialysis. While some cases have occurred in patients without identifiable risk factors, patients at increased risk of acute phosphate nephropathy may include those with increased age, hypovolemia, increased bowel transit time (such as bowel obstruction), active colitis, or baseline kidney disease, and those using medicines that affect renal perfusion or function (such as diuretics, angiotensin converting enzyme [ACE] inhibitors, angiotensin receptor blockers [ARBs], and possibly nonsteroidal anti-inflammatory drugs [NSAIDs]).|FDA has become aware of reports of acute phosphate nephropathy, a type of acute kidney injury, associated with the use of oral sodium phosphate products (OSP) for bowel cleansing prior to colonoscopy or other procedures. These products include the prescription products, Visicol and OsmoPrep, and OSPs available over-the-counter without a prescription as laxatives (e.g., Fleet Phospho-soda). In some cases when used for bowel cleansing, these serious adverse events have occurred in patients without identifiable factors that would put them at risk for developing acute kidney injury. We cannot rule out, however, that some of these patients were dehydrated prior to ingestion of OSPs or they did not drink sufficient fluids after ingesting OSP. Acute phosphate nephropathy is a form of acute kidney injury that is associated with deposits of calcium-phosphate crystals in the renal tubules that may result in permanent renal function impairment. Acute phosphate nephropathy is a rare, serious adverse event that has been associated with the use of OSPs. The occurrence of these events was previously described in an Information for Healthcare Professionals sheet and an FDA Science Paper issued in May 2006. Additional cases of acute phosphate nephropathy have been reported to FDA and described in the literature since these were issued. Individuals who appear to have an increased risk of acute phosphate nephropathy following the use of OSPs include persons: who are over age 55; who are hypovolemic or have decreased intravascular volume; who have baseline kidney disease, bowel obstruction, or active colitis; and who are using medications that affect renal perfusion or function (such as diuretics, angiotensin converting enzyme [ACE] inhibitors, angiotensin receptor blockers [ARBs], and possibly nonsteroidal anti-inflammatory drugs [NSAIDs]). As a result of new safety information received, FDA is requiring the manufacturer of Visicol and OsmoPrep, the two OSPs available by prescription only, to add a Boxed Warning to the labeling for these products. FDA is also requiring that the manufacturer develop and implement a risk evaluation and mitigation strategy (REMS), which will include a Medication Guide, to ensure that the benefits of these products outweigh the risk of acute phosphate nephropathy, and to conduct a postmarketing clinical trial to further assess the risk of acute kidney injury with use of these products. /Sodium phosphate, monobasic, monohydrate and sodium phosphate, dibasic anhydrous/|Sodium phosphate and 10% mannitol solutions provided superior results in terms of colon cleansing compared to sodium picosulfate solution. All serum electrolytes evaluated were significantly altered in the three groups, without important clinical signs. High levels of serum phosphate were the most striking alteration in patients prepared with sodium phosphate solution, again with no clinical signs. Variations related to blood pressure and pulse rate suggested contraction of intravascular volume, with no clinical effects.|Fifteen male subjects received 50 mL of commerical laxative containing 24 g of sodium biphosphate (sodium phosphate monobasic) and 6 g of sodium phosphate (sodium phosphate dibasic; I) (7 g of elemental phosphorus) administered with 500 mL of water and 11 patients received 300 mL of magnesium citrate (II) containing 3.2 g of elemental magnesium. Patients ranged in age from 26 to 86 yr. Serum magnesium, calcium, phosphorus, total protein, and albumin were determined before and at various intervals up to 16 hr after administration of the laxative and prior to radiological study. The administration of I in conventional doses to normal subjects prior to barium enema resulted in a striking increase in serum phosphorus levels followed by a decline in serum calcium levels in all subjects. Changes were highly significant when compared with control subjects who were prepared for the same procedure with II. Levels of serum potassium also decreased significantly but not serum sodium, chloride, bicarbonate, or magnesium. It would seem wise to caution against the use of phosphate containing laxatives in the presence of severe renal insufficiency, hypocalcemia, or convulsive disorders. In patients who are receiving frequent, repetitive dosages because of difficulty in cleansing the bowel for radiological procedures, serum calcium should be closely monitored. /Sodium phosphate, monobasic, monohydrate and sodium phosphate, dibasic anhydrous/|For more Drug Warnings (Complete) data for SODIUM DIHYDROGEN PHOSPHATE (39 total), please visit the HSDB record page.

The estimated fatal dose of sodium phosphates is 50 g.

Sodium phosphate inceases fecal water content to increase mobility through the large intestine.

Tmax for phosphate absorption with orally administered liquid sodium phosphate is 1-3h.|... Phosphates are slowly and incompletely absorbed ... . /Dibasic and monobasic sodium phosphate/|Intravenously infused phosphorus not taken up by the tissues is excreted almost entirely in the urine. Plasma phosphorus is believed to be filterable by the renal glomeruli, and the major portion of filtered phosphorus (greater than 80%) is actively reabsorbed by the tubules. Many modifying influences tend to alter the amount excreted in the urine.|An open-label pharmacokinetic study of Visicol in healthy volunteers was performed to determine the concentration-time profile of serum inorganic phosphorus levels after Visicol administration. All subjects received a total of 60 grams of sodium phosphate with a total liquid volume of 3.6 quarts. Subjects received a 30 gram dose (20 tablets given as 3 tablets every 15 minutes with 8 ounces of clear liquids) beginning at 6 PM and then received a second 30 gram dose (20 tablets given as 3 tablets every 15 minutes with 8 ounces of clear liquids) the following morning beginning at 6 AM. Twenty-three healthy subjects (mean age 57 years old; 57% male and 43% female; and 65% Hispanic, 30% Caucasian, and 4% African-American) participated in this pharmacokinetic study. The serum phosphorus level rose from a mean (+/- standard deviation) baseline of 4.0 (+/- 0.7) mg/dL to 7.7 (+/- 1.6 mg/dL), at a median of 3 hours after the administration of the first 30 gram dose of Visicol tablets The serum phosphorus level rose to a mean of 8.4 (+/- 1.9) mg/dL, at a median of 4 hours after the administration of the second 30 gram dose of Visicol tablets. The serum phosphorus level remained above baseline for a median of 24 hours after the administration of the initial dose of Visicol tablets (range 16 to 48 hours).

Sodium phosphate is thought to work by increasing the amount of solute present in the intestinal lumen thereby creating an osmotic gradient which draws water into the lumen.|... /Promotes/ defecation by retaining water in the intestinal lumen through osmotic forces. ... May also act by stimulating release of cholecystokinin. /Sodium phosphate & sodium biphosphate (Fleet's enema & Fleet's Phospho-soda)/|Phosphorus in the form of organic and inorganic phosphate has a variety of important biochemical functions in the body and is involved in many significant metabolic and enzyme reactions in almost all organs and tissues. It exerts a modifying influence on the steady state of calcium levels, a buffering effect on acid-base equilibrium and a primary role in the renal excretion of hydrogen ion.

Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand-valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR as necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Inorganic acids and related compounds/|Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist respirations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. Activated charcoal is not effective. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Do not attempt to neutralize because of exothermic reaction. Cover skin burns with dry, sterile dressings after decontamination ... . /Inorganic acids and related compounds/|Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Early intubation, at the first sign of upper airway obstruction, may be necessary. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's(LR) if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Consider vasopressors if patient is hypotensive with a normal fluid volume. Watch for signs of fluid overload ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Inorganic acids and related compounds/|After major surgery, seven infants aged 4 to 29 weeks, under parenteral nutrition, received monosodium phosphate (4.2 to 14.3 mEq/kg body weight) instead of prescribed calcium gluconate. The wrong solution was perfused during 16 hours. At the 15th hour, blood samples showed hyperphosphatemia in all (8.0 to 14.4 mg/100 mL) and hypocalcemia in four infants (6.1 to 8.9 mg/100 mL), but all were asymptomatic. Under a perfusion of glucose in water, calcemia and phosphatemia returned to normal within 24 hours. In a review of the pediatric literature, ... 11 subjects /were found/ with symptomatic acute phosphate intoxication, who also presented with hypocalcemia and hyperphosphatemia. The differences were that they received high bolus doses of phosphate orally or rectally and showed symptomatic features. Normalization of the calcemia occurred only when hyperphosphatemia was corrected throughout intravenous hydration.|For more Antidote and Emergency Treatment (Complete) data for SODIUM DIHYDROGEN PHOSPHATE (10 total), please visit the HSDB record page.

/HUMAN EXPOSURE STUDIES/ Within a 16-month period, 730 of patients referred for elective colonoscopy entered the study. Patients with known inflammatory bowel disease and those taking non-steroidal anti-inflammatory drugs were excluded. A sodium phosphate solution was ingested orally 14 and 8 hours before endoscopy. After standard colonoscopy, a 3-year clinical follow-up program was conducted. Endoscopically, mucosal lesions, possibly associated with sodium phosphate ingestion, were visible in 24 patients (3.3%). Erosions were found in 3 patients, aphthoid lesions in 21 patients, and an ulcer in one patient. Lesions often were multiple. Histopathologically, findings included focal active inflammation in 14 of 24 patients, mucosal disruption and erosion (7/24), edema of the lamina propria (5/24), mucosal hyperemia or focal hemorrhage (5/24), lymphoid nodules (5/24), and ulceration (1/24). Orally administered sodium phosphate-associated colonic mucosal abnormalities are infrequent but can mimic an non-steroidal anti-inflammatory drug-induced injury or inflammatory bowel disease, and in particular must be differentiated from Crohn's disease. /Sodium phosphate solution/|/SIGNS AND SYMPTOMS/ The estimated fatal dose of sodium phosphates is 50 g. The corrosive effect is strong irritation & erythema, blistering. /Alkalies & phosphates; from table/|/SIGNS AND SYMPTOMS/ Purposeful or accidental ingestion of more than the recommended dosage of Visicol tablets might be expected to lead to severe electrolyte disturbances, including hyperphosphatemia, hypocalcemia, hypernatremia, or hypokalemia, as well as dehydration and hypovolemia, with attendant signs and symptoms of these disturbances. Certain severe electrolyte disturbances may lead to cardiac arrhythmias, seizure, renal failure, and death. /Sodium phosphate, monobasic, monohydrate and sodium phosphate, dibasic anhydrous/|/SIGNS AND SYMPTOMS/ Acute phosphate nephropathy (APN) is a clinicopathological entity causing renal failure, after ingestion of oral sodium phosphate solution (OSPS). Approximately 25 cases have been described, but OSPS is still widely used. This study reports a further 5 cases and discusses the ever-growing significance of APN. Five cases of APN were included, 3 retrospectively whereas 2 were diagnosed prospectively. In all, use of OSPS was established, and other causes of nephrocalcinosis were excluded. Average age was 67.4 +/- 7.0 years, with a female preponderance (4:1). All patients had hypertension. Baseline serum creatinine: 0.7 to 1.2 mg/dL (creatinine clearance: 52 to 77 mL/min). Time from colonoscopy to presentation was 56 +/- 36 days. Serum creatinine levels at presentation: 1.4 to 3.6 mg/dL. Time from colonoscopy to renal biopsy was 123 +/- 88 days. Urinalysis showed minimal proteinuria, leucocyturia, and hematuria. One patient had renal glucosuria. All patients were anemic (hemoglobin 8.8-11.4 gr/dL). Serum calcium and phosphate were normal. One required hemodialysis. Mean follow-up was 36 +/- 17 months. Serum creatinine levels at end of follow-up were 1.3 to 3.1 mg/dL. Renal function did not recover completely in any patient. Four required long-term erythropoietin treatment. The prominent histopathological findings were calcium-phosphate tubular depositions (100%), interstitial fibrosis (80%), hypertensive changes (80%), and acute tubular degenerative and regenerative changes (60%). /Sodium phosphate solution/|For more Human Toxicity Excerpts (Complete) data for SODIUM DIHYDROGEN PHOSPHATE (27 total), please visit the HSDB record page.

dibasic sodium phosphate, anhydrous

44% AS AN ADDITIVE FOR ANIMAL FEEDS; 35-41% AS AN INDUSTRIAL & INSTITUTIONAL DETERGENT BUILDER, AND IN WATER TREATMENT; 12-15% IN TEXTILE PROCESSING; 1-2% IN THE CURING OF RED MEATS; 1-2% AS AN EMULSIFIER IN PROCESSED CHEESE; 3-6% AS A FOOD ADDITIVE IN OTHER APPLICATIONS; 3-6% IN MISC APPLICATIONS, INCL TO ADJUST PH IN ELECTROPLATING SOLUTIONS, & FOR EXPORT (1973)

Visicol: sodium phosphate, monobasic, monohydrate and sodium phosphate, dibasic anhydrous|Fleet's enema: soln (sodium phosphate 6 g & sodium biphosphate 16 g). Fleet's phospho-soda: ... (sodium phosphate 18 g & sodium biphosphate 48 g). /Sodium phosphate & sodium biphosphate- from table/|Sodium Phosphates Injection, USP, 3 mM P/mL (millimoles/mL)... Each mL contains 276 mg of monobasic sodium phosphate, monohydrate and 142 mg of dibasic sodium phosphate, anhydrous (equivalent to 268 mg of dibasic sodium phosphate, heptahydrate). ... It contains no bacteriostat, antimicrobial agent or added buffer.|Purity: It is about 99% pure.|For more Formulations/Preparations (Complete) data for SODIUM DIHYDROGEN PHOSPHATE (7 total), please visit the HSDB record page.

Adhesive manufacturing|Phosphoric acid, sodium salt (1:1): ACTIVE|Biological denitrification of wastewater for human waste treatment|Sodium dihydrogen phosphate was added to waste solution from regeneration of ammonia-adsorbed zeolite, to remove ammonia from resulting precipitate.|Sodium dihydrogen phosphate enhanced dentifrice composition|Various phosphoric acids and phosphates were examined and effects of concentration, temperature, and metal ions on stability of ascorbic acid were investigated to develop a good stabilizer for ascorbic acid. A considerable stabilizing effect was observed for sodium dihydrogen phosphate.

Method: NIOSH 7300, Issue 3; Procedure: inductively coupled argon plasma, atomic emission spectroscopy (nitric/perchloric acid ashing); Analyte: phosphorus; Matrix: air; Detection Limit: 3.7 ng/mL. /Phosphorus/|Method: NIOSH 7301, Issue 1; Procedure: inductively coupled argon plasma, atomic emission spectroscopy (aqua regia ashing); Analyte: phosphorus; Matrix: air; Detection Limit: 3.7 ng/mL. /Phosphorus/|Method: NIOSH 7303, Issue 2; Procedure: inductively coupled argon plasma, atomic emission spectroscopy (hot block/HCl/HNo3 digestiion; Analyte: phosphorus; Matrix: air; Detection Limit: 0.3 ug/mL. /Phosphorus/|Method: NIOSH 7905, Issue 2; Procedure: gas chromatography, flame photometric detector (phosphorus mode); Analyte: phosphorus; Matrix: air; Detection Limit: 0.005 ug/sample. /Phosphorus/|Method: NIOSH 9102, Issue 1; Procedure: inductively coupled argon plasma, atomic emission spectroscopy; Analyte: phosphorus; Matrix: air; Detection Limit: 0.043 ug/wipe. /Phosphorus/

Food additives|Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients|Cosmetics -> Buffering

Food Additives -> ACIDITY_REGULATOR; SEQUESTRANT;