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Wednesday, 03 August 2011 06:30

Phosphates, Inorganic and Organic

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Occurrence and Uses

Phosphorus does not occur in a free state in nature, but it is found in combination in many plant and animal compounds. In addition, it is found in phosphate rock formations such as apatite (a form of calcium phosphate). Large deposits of phosphate rocks are located in the United States (Tennessee and Florida), in parts of North Africa, and on some Pacific Islands.

Inorganic and organic phosphates are widely used in industry as lubricant additives, fire retardants, plasticizers and chemical intermediates. They are found in the rubber, plastics, paper, varnish and metal industries, and as ingredients in pesticides and cleaning compounds.

Dibutyl phenyl phosphate and tributyl phosphate are components of hydraulic fluid in aircraft engines, and hexamethylphosphoramide is a de-icing additive for jet fuels. Dibutyl phosphate is used in metal separation and extraction, and as a catalyst in the manufacture of phenol and urea resins. Trimethyl phosphate is found in the automobile industry as an antifoulant for spark plugs and as a gasoline additive for the control of surface ignition and rumbling.

Phosphoric acid is found in dental cement, rubber latex, fire-control agents and drilling muds for oil-well operations. It is used for flavouring non-alcoholic beverages, dyeing cotton, water treatment, refractory bricks, in the manufacture of superphosphate fertilizer, cleaning of metals before painting, and as an additive in gasoline and a binder in ceramics.

Tricresyl phosphate (TCP) is used as a solvent for nitrocellulose esters and numerous natural resins. It is a plasticizer for chlorinated rubber, vinyl plastics, polystyrene and polyacrylic and polymethacrylic esters. Tricresyl phosphate also acts as a binder for resins and nitrocellulose to improve toughness, elasticity and polishing properties of coatings. Alone or associated with hydrocarbons, it is used as an antiwear and antifriction additive in numerous synthetic lubricants, incorrectly termed “oils” by reason of their appearance. It is also employed as a hydraulic fluid. When incorporated in gasoline, tricresyl phosphate counteracts the harmful effects of lead deposits. In addition, it is an excellent fire retardant in many industries.

Tetrasodium pyrophosphate has a wide range of applications in the paper, food, textile and rubber industries. It is also used in oil-well drilling, water treatment, cheese emulsification, laundry detergents, and in the electrodeposition of metals. Tetrasodium pyrophosphate is useful for textile dyeing, scouring of wool, and clay and paper processing. Tributyl phosphate functions as a plasticizer for cellulose esters, lacquers, plastics and vinyl resins. It is also a complexing agent in the extraction of heavy metals and an antifoam agent in ore separation processes. Triphenyl phosphate is a flame-retardant plasticizer for cellulosics and a plasticizer for hot-melt adhesives. It is useful in the upholstery and roofing paper industries.

Several of the organic phosphates are used for the production of pyrotechnics, explosives and pesticides. Calcium phosphide is used for signal fires, torpedoes, pyrotechnics, and as a rodenticide. Phosphorus sulphide finds use in the manufacture of safety matches, ignition compounds, lube oil additives and pesticides. Phosphine is used for rodent control and as an insecticide applied for the fumigation of animal feed, leaf-stored tobacco and box cars.

White phosphorus is utilized for the manufacture of rat poisons; red phosphorus is used in pyrotechnics, safety matches, chemical synthesis, pesticides, incendiary shells, tracer bullets and smoke bombs. Tetraphosphorus trisulphide is used for making match heads and friction strips for boxes of “safety” matches.

Phosphorus pentoxide is added to asphalt in the air blowing process to increase the melting point and is used in the development of specialty glasses for vacuum tubes. Phosphorus trichloride is a component of textile finishing agents and an intermediate or reagent in the manufacture of many industrial chemicals, including insecticides, synthetic surfactants and ingredients for silver polish. Phosphorus oxychloride and phosphorus pentachloride serve as chlorinating agents for organic compounds.


Phosphorus (P) exists in three allotropic forms: white (or yellow), red and black, the last being of no industrial importance. White phosphorus is a colourless or waxlike solid that darkens when exposed to light and glows in the dark (phosphoresces). It ignites spontaneously in the presence of air and burns with a blue flame, producing a characteristically disagreeable odour that is somewhat reminiscent of garlic. The red form is more stable.

Historical importance

Elemental phosphorus was first extracted from animal matter, especially from bone, in the early part of the nineteenth century. Its usefulness in “strike-anywhere” matches was quickly seen and much demand for this element developed as a result. Shortly thereafter, a serious disease appeared in people handling it; the first cases were recognized in 1845, when jaw-bone necrosis occurred in phosphorus-processing workers. This severe and face-disfiguring malady, which terminated fatally in about 20% of the cases during the nineteenth century, was soon recognized and measures sought for its alleviation. This became possible with the development of effective substitutes in the form of red phosphorus and the relatively safe phosphorus sesquisulphide. The European countries also entered into an agreement (the Berne Convention of 1906) in which it was stipulated that the signatories would not manufacture or import matches that were made with white phosphorus.

A major phosphorus hazard in some countries, however, continued to exist from the use of white phosphorus in the pyrotechnics industry until agreement for its exclusion was reached with these manufacturers. At the present, health hazards from white phosphorus still endanger people who are involved with the various stages of production and in the manufacture of its compounds.

The mechanism involved in this jaw-bone damage has not been fully explained. It is believed by some that the action is due to the local effect of the phosphorus in the oral cavity, and that the infection occurs in the constant presence of infective organisms in the mouth and about the teeth. In fact, it is found that exposed persons with carious teeth are more likely to be affected by the condition, although it is difficult to explain the disease in workers with no teeth at all.

A second, possibly more plausible, explanation is that phosphorus necrosis of the jaw is a manifestation of a systemic disease, one that involves many organs and tissues and, principally, the bones. Supporting this concept are the following significant facts:

  • As mentioned previously, edentulous individuals have been known to develop jaw necrosis when exposed to phosphorus in their work, even though their “dental hygiene” may be said to be good.
  • Young, growing, experimental animals, given appropriate doses of white phosphorus, develop bone changes in the “growing” areas of their bones, the metaphyses.
  • On occasion, injured bones in adults exposed to phosphorus have been found to heal exceedingly slowly.



Health hazards. Acute exposure to yellow phosphorus vapour released by spontaneous combustion causes severe irritation of the eye, with photophobia, lacrimation and blepharospasm; severe respiratory tract irritation; and deep, penetrating burns of the skin. Direct skin contact with phosphorus, which occurs both in production and during wartime, leads to deeply penetrating second- and third-degree burns, similar to hydrogen fluoride burns. Massive haemolysis with subsequent haematuria, oliguria and renal failure have been described, although this constellation of events is most likely due to previously advocated treatment with copper sulphate.

Upon ingestion, phosphorus induces burns of the mouth and gastrointestinal (GI) tract, with oral sensations of burning, vomiting, diarrhoea and severe abdominal pain. Burns progress to second and third degree. Oliguria may occur secondary to fluid loss and poor perfusion of the kidney; in less severe cases, the proximal renal tubule is transiently damaged. Absence of sugar in otherwise normal cerebrospinal fluid (CSF) is reportedly pathognomonic.

Following absorption from the GI tract, yellow phosphorus has direct effects on the myocardium, circulatory system in the limbs (peripheral vasculature), liver, kidneys and brain. Hypotension and dilated cardiomyopathy have been reported; interstitial myocardial oedema without cellular infiltration has been observed on autopsy. Intracellular protein synthesis appears to be depressed in heart and liver.

Three clinical stages have been described following ingestion. In Stage I, immediately after ingestion, there is nausea and vomiting, abdominal pain, jaundice and garlic odour of the breath. Phosphorescent vomitus may be hazardous to attending medical staff. Stage II is characterized by a 2- to 3-day latent period where the patient is asymptomatic. During this time, cardiac dilatation as well as fatty infiltration of the liver and kidney may occur. Severe, bloody vomiting, bleeding into many tissues, uremia and marked anaemia precede death, defined as Stage III.

Prolonged intake (10 months to 18 years) may cause necrosis of the mandible and maxilla with sequestration of bone; release of sequestra leads to facial deformity (“phossy jaw”). Toothache and excessive salivation may be the first symptoms. Additionally, anaemia, cachexia and liver toxicity may occur. With chronic exposure, necrosis of the mandible with facial deformity was frequently described in the literature until the early 1900s. There are rare reports of this phenomenon among production workers and rodenticide manufacturers.

Reproductive and carcinogenic effects have not been reported.

Phosphine (PH3) gas is generated by the reaction of phosphoric acid heated with metals which are being treated for cleaning (similar to phosgene), from heating of phosphorus trichloride, from wetting of aluminium phosphate, from flare manufacture using calcium phosphide, and from acetylene gas production. Inhalation causes severe mucous membrane irritation, leading to coughing, shortness of breath, and pulmonary oedema up to 3 days following exposure. The pathophysiologic effect involves inhibition of mitochondrial respiration as well as direct cytotoxicity.

Phosphine is also liberated from accidentally or intentionally ingested aluminium phosphide by chemical interaction with hydrochloric acid in the stomach. There is a large body of literature from India describing cases of suicidal ingestion of this rodenticide. Phosphine is also used as a fumigant, and there are many case reports which describe accidental death from inhalation when in proximity to grain fumigated during storage. Toxic systemic effects which have been described include nausea, vomiting, abdominal pain, central nervous system excitation (restlessness), pulmonary oedema, cardiogenic shock, acute pericarditis, atrial infarction, renal damage, hepatic failure and hypoglycemia. A silver nitrate test was positive in gastric aspirate and in the breath (the latter with a lower sensitivity). Measurement of blood aluminium may serve as a surrogate for toxin identification. Treatment includes gastric lavage, vasopressive agents, respiratory support, administration of anti-arrhythmics, and high-dose magnesium sulphate infusion.

Zinc phosphide, a commonly used rodenticide, has been associated with severe intoxication of animals that ingest treated bait or the carcasses of poisoned animals. Phosphine gas is liberated in the stomach by stomach acid.

Organophosphorus Compounds

The tricresyl phosphates (TCPs) are part of a series of organophosphorus compounds which have been shown to cause delayed neurotoxicity. The 1930 outbreak of “ginger jake” paralysis was caused by the contamination of ginger extract by cresyl phosphates, used in the processing of the spice. Since that time, there have been several incidents reported of accidental poisoning of food by tri-o-cresyl phosphate (TOCP). There are few case series reports of occupational exposure in the literature. Acute occupational exposures have been described as causing gastrointestinal symptoms followed by a latent period of days to 4 weeks, after which extremity pain and tingling progress to motor paralysis of the lower extremities up to the thighs, and of the upper extremities to the elbow. There is rarely sensory loss. Partial to total recovery may take years. Fatalities have occurred in high-dose ingestion. The anterior horn cells and pyramidal tracts are affected, with autopsy finding of demyelination and anterior horn cell damage. In humans the oral lethal dose is 1.0 g/kg; 6 to 7 mg/kg produces severe paralysis. There is no reported skin or eye irritation, though TOCP is absorbed through the skin. Inhibition of cholinesterase activities does not appear to correlate with symptoms or quantity of exposure. Exposed cats and hens developed damage in the spinal cord and sciatic nerves, with damage to the Schwann cells and myelin sheath resulting from dying back of the longer axons. There was no evidence of teratogenicity in rats dosed up to 350 mg/kg/day.

Three molecules of o-, m- or p-cresol esterify one molecule of phosphoric acid, and, since commercial cresol is normally a mixture of the three isomers with an ortho isomer content varying between 25 and 40% according to the source, the resultant TCP is a mixture of the three symmetrical isomers, which are very difficult to separate. However, since the toxicity of commercial TCP derives from the presence of the ortho isomer, many countries stipulate that the esterified phenolic fraction should contain no more than 3% o-cresol. Consequently, the difficulty lies in the selection of a cresol free of the ortho isomer. A TCP prepared from m- or p-cresol has the same properties as the technical product, but the cost of separating and purifying these isomers is prohibitive.

Two related phosphate-containing esters, cresyldiphenyl phosphate and o-isopropylphenyldiphenyl phosphate, are also neurotoxic to several species, including humans, chickens and cats. Adult animals are generally more susceptible than the young. After a single, large exposure to these neurotoxic organophosphorus compounds, axonal damage becomes apparent after 8 to 10 days. Chronic low-level exposures can also lead to neurotoxicity. Axons of the peripheral nerves and the ascending and descending tracts of the spinal cord are affected through a mechanism other than cholinesterase inhibition. While a few of the organophosphate anticholinesterase insecticides cause this effect (diisopropyl fluorophosphate, leptofos and mipafox), the delayed neuropathy apparently occurs through a mechanism other than cholinesterase inhibition. There is a poor correlation between the inhibition of pseudo- or true cholinesterase and the neurotoxic effect.

Triphenyl phosphate may cause a slight reduction in cholinesterase activity, but is otherwise of low toxicity in humans. This compound sometimes occurs in combination with tri-o-cresyl phosphate (TOCP). No teratogenicity was found in rats fed up to 1% in their diet. Intraperitoneal injection of 0.1 to 0.5 g/kg in cats caused paralysis after 16 to 18 days. Skin irritation has not been demonstrated, and eye effects have not been reported.

Triphenyl phosphite (TPP) has been shown to cause neurotoxicity in laboratory animals which is similar to that described for TOCP. Studies of rats showed early hyperexcitability and tremors followed by flaccid paralysis, with the lower extremities more affected than the upper extremities. The pathologic lesion showed spinal cord damage with mild cholinesterase inhibition. A study of cats receiving injections showed virtually the same clinical findings. TPP has also been demonstrated to be a skin irritant and sensitizer.

Tributyl phosphate causes eye, skin and mucous membrane irritation, as well as pulmonary oedema in laboratory animals. Rats exposed to a commercial formulation (bapros) of 123 ppm for 6 hours developed respiratory irritation. When ingested, the LD50 was 3 g/kg, with weakness, dyspnea, pulmonary oedema and muscle twitching observed. It weakly inhibits plasma and red blood cell cholinesterase.

Hexamethyl phosphoramide has been shown to cause cancer of the nasal cavity when administered to rats at levels between 50 and 4,000 ppb over 6 to 24 months. Squamous metaplasia was seen in the nasal cavity and trachea, the latter at the highest dose. Other findings included dose-dependent increases in tracheal inflammation and desquamation, bone marrow erythropoietic hyperplasia, testicular atrophy, and degeneration of the convoluted tubules of the kidney.

Other Inorganic Phosphorus Compounds

Phosphorus pentoxide (phosphorus anhydride), phosphorus pentachloride, phosphorus oxychloride, and phosphorus trichloride have irritant properties, causing a spectrum of mild effects such as eye corrosion, skin and mucous membrane burns, and pulmonary oedema. Chronic or systemic exposure generally is not as important because of the low tolerance to direct contact with these chemicals.

The mist of phosphoric acid is mildly irritating to the skin, the eyes, and the upper respiratory tract. In groups of workers, phosphorus pentoxide (the anhydride of phosphoric acid) fumes were shown to be perceptible but not uncomfortable at concentrations of 0.8 to 5.4 mg/m3, to produce cough at concentrations between 3.6 and 11.3 mg/m3, and to be intolerable to unacclimated workers at a concentration of 100 mg/m3. There is a small risk of pulmonary oedema with inhalation of the mist. Skin contact with the mist leads to mild irritation, but no systemic toxicity. A 75% solution of phosphoric acid dropped on the skin causes severe burns. A study of a cohort of phosphate workers who were occupationally exposed to phosphoric acid showed no increase in cause-specific mortality.

The median lethal concentration for phosphorus oxychloride and its ammonia neutralization products were found to be 48.4 and 44.4 micromoles per mole of air for rats, and 52.5 and 41.3 for guinea-pigs. Fifteen per cent of phosphorus oxychloride was hydrolyzed. Most case series reports of health effects from phosphorus oxychloride also include exposure to other phosphorus-containing compounds. Alone, it is described as causing stomach necrosis when ingested, necrosis of the respiratory tract on inhalation, skin ulceration from direct application, and eye ulceration with loss of vision in rabbits. Chronic exposure of animals showed abnormalities in mineral metabolism, and osteoporosis with elimination of excessive amounts of inorganic phosphorus, calcium salts and chlorides from the body. In combination with other phosphorus compounds, phosphorus oxychloride has been shown to cause asthma and bronchitis in case series reports.

Phosphorus pentasulphide is hydrolyzed to hydrogen sulphide gas and phosphoric acid, exerting effects of these substances on contact with mucus membranes (see phosphoric acid, above, and also hydrogen sulphide elsewhere in this Encyclopaedia). The oral LD50 was 389 mg/kg in rats. Twenty milligrams instilled in rabbit eyes was severely irritating after 24 hours. After 24 hours, 500 mg applied to rabbit skin was found to be moderately irritating.

The vapour of phosphorus trichloride is a severe irritant of the mucous membranes, eyes and skin. Similar to phosphorus pentasulphide, hydrolysis to hydrochloric acid and phosphoric acid on contact with mucous membranes accounts for much of this effect. Inhalation of the vapour can cause throat irritation, bronchospasm and/or pulmonary oedema for up to 24 hours after exposure, depending on the dose. Reactive airways disease syndrome (RADS), with prolonged symptoms of wheezing and cough, can occur from acute or repeated exposure to the vapour. On contact, phosphorus trichloride causes severe burns of the eyes, skin and mucous membranes. Ingestion, inadvertent or suicidal, causes burns of the gastrointestinal tract. Seventeen people who were exposed to phosphorus trichloride and its hydrolysis products following a tanker accident were medically evaluated. Dyspnea, cough, nausea, vomiting, eye burning and lacrimation were experienced by those closest to the spill. Lactate dehydrogenase was transiently elevated in six. While chest radiographs were normal, pulmonary function tests showed a significant drop in forced vital capacity and FEV1. Improvement in these parameters was seen in the 17 patients re-tested after 1 month. The LC50 was 104 ppm for 4 hours in rats. Nephrosis was the chief finding at autopsy, with negligible pulmonary damage.

Phosphorus pentachloride fume inhalation causes severe irritation of the respiratory tract, leading to documented bronchitis. Delayed onset of pulmonary oedema could occur, although it has not been reported. Exposure of the eyes to fumes also leads to severe irritation, and skin contact would be expected to cause contact dermatitis. The LC50 for 4 hours of inhalation is 205 mg/m3..

Phosphates and superphosphates. The principal problem with phosphates in the environment is the causation of eutrophication of lakes and ponds. Phosphates enter bodies of water from run-off of agriculture (sources include phosphorus-containing compounds used as fertilizer and pesticides, and plant and animal decay) and from detergents used in homes and industry. Excessive growth of blue-green algae occurs because phosphorus is generally the limiting nutrient essential for growth. Rapid algae growth affects use of lakes for fishing and recreational activities. It also complicates purification of drinking water.

Toxicity of Phosphates

Phosphate mining has been associated with physical trauma. Pneumoconiosis is not of concern in this setting because of the small amount of dust that is generated. Phosphate dust is created in the drying process, and is of concern in causation of pneumoconiosis in the handling and transport of the material. Fluorides may be present in the dust and lead to toxicity.

In addition, phosphate dust is created in the creation of superphosphates, which are used for fertilization. A study of women employed in the manufacture of superphosphates found abnormalities of menstrual function. Severe eye damage and blindness have been described in humans and animals from direct contact with superphosphates.

Safety and Health Measures

Fire hazard. Phosphorus can ignite spontaneously when exposed to air and start fires and cause explosions. Severe burns can be caused when chips and bits of white phosphorus contact the skin and ignite after drying.

Owing to its flammability in air, white phosphorus should be kept covered with water at all times. In addition, scattered pieces should be doused with water, even before they dry and begin to burn; phosphorus fires may be controlled with water (fog or spray), by covering with sand or earth, or with carbon dioxide extinguishers. The substance should be stored in a cool, ventilated, isolated area and away from powerful oxidizing agents, acute fire hazards, and the direct rays of the sun.

In case of skin contact by burning phosphorus slivers, dousing them with a 1 to 5% solution of aqueous copper sulphate will put out the fire and at the same time form a non-flammable compound on the surface of the phosphorus. Following this treatment, the slivers may be removed with more large quantities of water. A soft-soap solution containing a similar concentration of copper sulphate may be more effective than the simple aqueous solution.

Inorganic and organic phosphates tables

Table 1 - Chemical information.

Table 2 - Health hazards.

Table 3 - Physical and chemical hazards.

Table 4 - Physical and chemical properties.



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