Phosphorus

PHOSPHORUS, chemical element (symbol P) with atomic weight 31.02, belonging to Group V and the 3rd row of Mendeleev's periodic system (atomic number 15). Phosphorus is widely distributed in nature, but only in the form of oxygen compounds: soil contains it in the form of phosphoric acid salts from 1% to 10%. Phosphorus is part of many minerals: apatites [CaX₂-3Ca(PO₄)₂, where X=Cl or F], vivianite (hydrated ferrous phosphate), taggite (hydrated copper phosphate + copper hydrate), turquoise (hydrated aluminum phosphate), etc. Of these minerals, apatites have the greatest importance, especially in the USSR, where their extensive deposits in the Murmansk region (Kirovsk) are developed on a large scale mainly to obtain superphosphates necessary for agricultural industry as fertilizer. Phosphorites, similar in chemical composition to apatites and representing products of accumulation of bone remains and vital activity of fossil animals, are also used as fertilizer. Deposits of phosphorites are exploited in the Urals, Kazakhstan, the North Caucasus, the Moscow region, and other regions of the USSR. Phosphorus is obtained from phosphates or apatites or from calcined bones. According to the most common method of Wohler, a mixture of raw material with coal and sand is subjected to the action of bright red heat, during which the reduction of phosphates occurs with the release of phosphorus in the form of vapors; the latter, condensing under the water of the condenser, form a liquid mass, which is poured under water into molds. Phosphorus forms several allotropic modifications, of which the most well-known are white, sometimes incorrectly called yellow, and red phosphorus. Red phosphorus is formed from white during various reactions, for example, during electrical discharges in the vapors of white phosphorus, under the action of light; partially during the process of combination of white phosphorus with oxygen, chlorine, bromine. Vapors of red phosphorus, when rapidly cooled, form white phosphorus. White phosphorus is a translucent, waxy colorless or yellowish substance with specific gravity 1.84 (modification «?»-1.88), melts at 44.5°, boils at 280.5°, is almost insoluble in water, difficult to dissolve in alcohol (1:350), easier in ether (1:100) and fatty oils (1:80), easily soluble in essential oils and chloroform (1:25), very easily in carbon disulfide (1:0.5); on air it smokes, emitting an unpleasant garlic odor, and, oxidizing, glows in the dark; it easily ignites spontaneously and even more easily ignites from friction; it takes oxygen from many substances and easily combines with various metals, sulfur, chlorine, and other elements. It should be kept under water in a well-sealed bottle. Red phosphorus (incorrectly called amorphous) is a powdery opaque substance of reddish-brown color with specific gravity 2.05 to 2.3, melts at 589.5-592.5°, does not oxidize in air, and therefore does not glow, does not ignite from friction, is insoluble in carbon disulfide and fatty oils, reacts not only with oxygen but also with other elements, not so energetically as white phosphorus. In medicine, only white phosphorus is used. Phosphorus is a necessary element that is part of all living organisms; in particular, it is part of cellular nucleoproteins (see Phosphoric acid). Plants absorb phosphorus from the soil, and they can utilize it only in the form of phosphoric acid, while other compounds of phosphorus are harmful to plants. With food, most of the phosphorus enters in the form of phosphoric acid salts and is absorbed mainly in the upper part of the small intestine, where the absorption of elementary phosphorus and its other compounds also occurs. Glycerophosphates and generally organic compounds of phosphorus are almost completely hydrolyzed in the digestive tract, forming inorganic phosphates (Plimmer, Oeri). The amount of absorbed phosphorus compounds depends, on one hand, on the duration of their stay in the intestine, and on the other, on the amount of calcium contained there, which, by converting phosphorus into insoluble phosphates, reduces its absorption. If insoluble salts of phosphoric acid are introduced as such per os, they are partially dissolved by gastric juice and absorbed. Salts of phosphorous acid enter the blood unchanged. Phorus in vapor form is absorbed mainly through the lungs; when phosphorus enters the body in solid form, both per os and subcutaneously, its absorption is very slow, but it is accelerated when introduced in finely ground form, as well as in the presence of fatty oils and fats. Phosphorus compounds are excreted from the body, with the exception of salts of phosphorous acid, in the form of phosphates with urine and feces. With food rich in calcium, the amount of phosphates excreted through the intestine increases, with food poor in calcium-through the kidneys. In the first case, the amount of phosphates in the urine decreases, which can lead to a decrease in its acidity. With urine, a very small amount of phosphorus can be excreted in the form of organic compounds, such as glycerophosphoric and phospholactic acids; the amount of such compounds in the urine increases under the influence of fasting, chloroform anesthesia, morphine poisoning, and certain diseases. Salts of phosphorous acid are excreted with urine unchanged. When introduced in pure form, phosphorus, circulating in the blood and tissues as such, before excretion is oxidized to salts of phosphorous acid, which are excreted through the kidneys, and only in negligible amounts (traces) it is excreted through the lungs in vapor form. The body of an adult person normally excretes from 1.5 g to 1.75 g of phosphorus per day, and this loss is compensated by its daily intake with food (with a normal diet, an average of 1.6 g of phosphorus). When introduced in excess of the amount lost, its excretion increases, while part of it is retained in the body, especially during the period of growth or after exhausting disease. The amount of phosphorus retained by the body decreases with a deficiency of calcium or excess of magnesium in food. Bone tissue is the main place of phosphorus reserves, which decrease under the influence of inorganic acids, ions that precipitate calcium, high potassium content or low sodium content in food. Phosphorus has a relatively weak local action: it can cause irritation and later necrosis of tissues, but not rapid cauterization. Its resorptive action is manifested on various organs in acute and chronic poisoning (see below), while the effect of therapeutic doses is most noticeably manifested in the condition of bones. For a long time, various authors have noted that prolonged use of phosphorus in very small doses in rickets in children (for example, 0.5-1.0 mg per day) has a beneficial effect not only on the condition of bones but also on other accompanying rickets disease symptoms, however, these cumulative observations were not confirmed either by strictly conducted clinical studies or by experimental evidence, which were obtained only in relation to the effect of phosphorus on bones (Kassowitz, Hagenbach). Thus, in young animals receiving therapeutic doses of phosphorus, an enhanced formation of compact bone tissue in the growing layer of epiphyses was observed, simultaneously with which the resorption of spongy substance proceeded. The bone formed at this time does not differ in chemical composition from normal, but it is denser and Haversian channels in it are poorly developed. The data of these experiments contributed to the widespread use of phosphorus in rickets, osteomalacia and delayed fracture healing, but the results were contradictory. The latter circumstance finds its explanation in the fact that the cause of rickets is most often a deficiency of vitamin D in the body, and osteomalacia is mainly a violation of the function of the sex glands, and possibly other endocrine glands; in these cases, it is hardly possible to expect favorable results only from the introduction of phosphorus into the body. At present, its use in rickets is almost completely abandoned, because a much more effective means is cod liver oil rich in vitamin D, which also does not have toxic properties, while phosphorus can, even when using therapeutic doses, cause symptoms of poisoning (Nebelthau). In view of the fact that in the treatment of rickets phosphorus was usually prescribed together with cod liver oil, the opinion was repeatedly expressed that in these cases the successful treatment of rickets is due to the action not of phosphorus, but of vitamin D. However, there are experimental data showing that with the simultaneous administration of phosphorus and cod liver oil, the amount of calcium deposited in the bones is greater than with the administration of cod liver oil alone (Shabad). The use of phosphorus to accelerate the healing of bone fractures in many cases gave a favorable result. In therapeutic doses, phosphorus can affect the blood, increasing the number of erythrocytes and not changing hemoglobin. Of the compounds of phosphorus, its organic derivatives-glycerophosphates, phosphatides (for example, lecithin) and nucleoalbumins-have had the greatest application and have not been abandoned even now in various diseases, especially those associated with lesions of the central and peripheral nervous system (tabes, neuritis, neurasthenia, etc.).

The reason for this was the a priori assumption that in such compounds P. could be better utilized by the organism for nutrition and tissue restoration, especially nervous tissue. This assumption, however, is erroneous, because glycerophosphates and other organic compounds of P. are almost completely broken down in the intestine, forming inorganic phosphates; moreover, with a normal diet, the organism receives a fully sufficient amount of organic compounds of P:, and there is no reason to assume that a small addition of organic P. in the form of a pharmaceutical preparation can have any pharmacological effect different from that of inorganic phosphates; if it is observed in individual cases, the obtained effect must be attributed, according to a number of outstanding pharmacologists (Cushny, Soll-mann), exclusively to suggestive influence, with which some clinicians also agree (Penzoldt). Nucleic acid, when administered subcutaneously, after an initial leukopenia, causes a sharp increase in the number of leukocytes after 24 hours, which is why it was tried to be used in tbc and other infectious diseases to enhance phagocytosis, but with very doubtful success, all the more so that the leukocytosis is transient in such cases. White P. has strong toxicity and, having cumulative properties, can cause symptoms of chronic poisoning with prolonged entry into the body even of very small doses. Red P. is little toxic because it is very poorly absorbed, but when introduced into the bloodstream it is no less toxic than white P. The lethal dose of the latter varies widely, averaging about 0.1 for an adult (Richaud).-In acute poisoning per os, the first symptoms appear after several hours in the form of stomach pain, nausea, belching with a garlic odor, and then vomiting; the vomit glows in the dark. Later, bile is discharged during vomiting and sometimes diarrhea occurs. Nausea and vomiting may continue for several days, but more often they cease, and the patient feels on the road to recovery; however, after 2-3 days the same symptoms reappear, usually accompanied by not strongly expressed jaundice; pain is felt not only in the stomach area but also in the liver, which is sharply enlarged, and the intestine. The vomit is already free of P., but contains blood; the pulse is weak, urination is decreased, and the urine undergoes characteristic changes (see below); there are nosebleeds, intestinal bleeding, uterine bleeding, and subcutaneous hemorrhages, collapse, a comatose state develops and death occurs.-Patho-anatomical data show that acute poisoning with P. causes fatty degeneration of the liver, kidneys, glands of the digestive tract and its mucous membrane, heart, small arteries and sometimes skeletal muscles. The symptoms of the first period of poisoning are probably due to the beginning of this pathological process in the stomach, and perhaps also to the local irritating effect of phosphorus, while in the second period the entire symptom complex is associated with the already developed degeneration of the organs. The dispute as to whether the latter is the result of fat formation from the protoplasm of affected cells (degeneration) or whether fat is brought by the blood and deposited in them (infiltration) is decided in favor of the latter opinion by experiments in which, in a dog that had received mutton fat after fasting and then was poisoned with P., fat of non-autogenous origin was found in the cells of affected organs, identical with mutton fat (Rosenberg, Foulerton). In addition, experiments showed that in P. poisoning the amount of fat in the body does not increase (Pfluger). There are two opinions on the pathogenesis of this main organ damage in P. poisoning. According to the first, the existing autolytic processes in the affected organs, which are also present in normal conditions, are intensified and the oxidative processes are inhibited, as a result of which intermediate metabolic products accumulate in the tissues and are excreted in the urine: leucine, tyrosine, other amino acids, peptone-like substances, sulfates, phosphates, lactic acid and especially ammonium salts. The fatty infiltration is a secondary result of this enhanced autolysis: the cells in larger quantities take up fat from the blood, in which the loss is compensated from its local reserves, but the cells have already largely lost the ability to break down fat, which is therefore deposited in them in the form of droplets. According to another (later) opinion, the process is related to a violation of carbohydrate metabolism (Frank and Isaak): under the influence of P., liver glycogen turns into lactic acid, which is neutralized by ammonia from proteins that break down intensely with the release of energy in connection with the expenditure of glycogen; during this, the fat reserves are mobilized, which is then brought by the blood to the liver, in whose cells it is deposited, as they are no longer able to break it down. The same happens in other organs, but not as intensely as in the liver. The second opinion, however, is not confirmed by sufficient experimental evidence, and in addition it does not agree with the results of carefully conducted experiments, which showed that in phosphorus poisoning proteins break down in larger quantities than during complete starvation. Although the main cause of organ damage is the infiltration of their cells with fat brought by the blood, there are still reasons to admit that along with this a certain amount of fat is formed from the protoplasm of the cells, especially in the kidneys (Rubow, Mansfeld). In acute poisoning, the blood coagulability is sharply decreased due to the destruction of fibrinogen. This is partly due to this, and mainly to the damage to the muscular layer of small arteries, that the hemorrhages in P. poisoning are explained. Skeletal 8» muscles are affected less than other organs, while the central and peripheral nervous system undergo only late degenerative changes. In addition to fatty infiltration, in P. poisoning, especially with repeated administration of smaller doses, proliferation of interstitial connective tissue in the stomach, liver and kidneys is observed, which leads to the typical cirrhosis of these organs. First aid measures in acute poisoning see Poisoning. Preparations of P. Phosphorus, P. (P VII)-properties see above; orally 0.0005- 0.001, for children-0.0002-0.0005 per day in cod liver oil for rickets, osteomalacia, leukemia. Glycerophosphates (see). Phytin (see). Lecithin (see). Sanatogen - a compound of casein with sodium glycerophosphate. Natrium nucleinicum, sodium nucleinate, grayish or yellowish-white powder, easily soluble in water; orally 0.1 several times a day for rickets, phosphaturia, anemia, diabetes, etc.; was used to enhance phagocytosis in tbc and other infectious diseases subcutaneously 0.05. Casein and its preparations (larosan, calcium caseinate, etc.) are used to enhance nutrition; calcium caseinate, provided its solutions are of high dispersion-is also used for feeding infants.

M. Likhachev. Phosphorus as an industrial poison. Of the modifications of P. used in industry, red P. is applied. White, or yellow P., belongs to industrial poisons, which to a large extent represent historical interest. Before its use in match production was prohibited (in different countries in different years of the late 19th and early 20th centuries), it caused a colossal number of very severe poisonings. By 1905, Geltshe had collected data for a number of European countries on 947 cases, in Austria for the years 1896-1905 up to 400 cases were found, etc., and it should be borne in mind that the actual number of cases is much greater than the number published. At present, white P. is used to obtain red P., certain synthetic dyes, phosphor bronze, fireworks, some medicinal substances; it is contained in ferrosilicon, and no less poisonous phosphine-in technical acetylene. Red P. is used to obtain various compounds-ganoid, sulfur, and others-for the production of fireworks, incendiary bombs, in metallurgy. Reports of poisonings in individual industries still appear from time to time: in England for the years 1915-19, 21 cases were registered, of which 12 occurred in the production of P.; in the USA in 1928 a report appeared of 14 cases of necrosis of the jaw in workers in the fireworks industry; in the USSR from 1931 there were 7 cases of poisoning at a plant where P. was extracted from natural phosphates. Vapors of P. penetrate through the lungs into the blood, where their slow oxidation occurs; the end product of oxidation-phosphoric acid-is not poisonous. Acute poisonings with white P. in industrial conditions have almost never been encountered, they are mainly the result of accidents (introduction per os by mistake or intentionally). On the basis of degeneration and necrosis of tissues, mainly of parenchymal organs, severe disorders develop, very often with a fatal outcome. Chronic poisonings in the initial stage are expressed by dyspeptic phenomena, lack of appetite, irritation of the nasal, ocular, laryngeal mucosa, progressive anemia, pains, etc. Subsequently, degenerative changes develop in various organs, first of all in the liver and kidneys, the body's resistance to tuberculous infection sharply decreases. From the side of the skeletal system, changes in the periosteum develop, which leads to a disturbance in the nutrition of the bones; at the same time, the mineral composition of the bones is disturbed (decalcification). The resistance of bone tissue to the action of infection is reduced and when pyogenic microbes penetrate there, for which the most favorable conditions exist in the oral cavity, a very characteristic disease of phosphorus poisoning develops-necrosis of the upper or lower jaw. This process proceeds for a very long time, is accompanied by the formation of fistulas, sequestra, loss of teeth (see Teeth), very often general cachexia develops; the outcome of the process is severe disfigurement, and sometimes, death due to general exhaustion or as a result of the infection spreading to the meninges. Necrotic processes usually occurred in workers as a result of long-term work with P.; they may manifest themselves after a long time, even after leaving production. Besides jaw necrosis in workers of match factories, bone fractures were very often observed. Red phosphorus when inhaling large amounts of its dust or vapors can also cause pathological changes: anemia, degenerative changes in the liver or kidneys, tendency to bleeding, etc. In industrial conditions, poisonings in workers were rarely observed. Of the compounds of P., toxic properties are possessed by: phosphine, PH₃,-a gas formed in cases where in the presence of P. reduction processes occur with the formation of free hydrogen. Such cases occurred during the decomposition of ferrosilicon and some fertilizers under conditions of high humidity, during the extraction of P. from bones, during the production of acetylene from carbide, etc. This substance has strong toxicity-concentrations of 0.6-0.1 mg/l kill rabbits and cats with hourly exposure; the same concentration is also fatal for humans; in humans acute poisoning causes fatty degeneration of the liver and heart and severe phenomena from the nervous system, up to coma and death. Phosphorus trichloride, PCl₃,-vapors; are released during chemical work; cause disorders from the respiratory tract. Some importance is attached to phosphorus pentachloride, P₂Cl₆, and phosphorus oxychloride, POCl₃. Prevention. Complete elimination of white P. where it can be replaced by red P. or other substances, as has already been done in match production and almost completely carried out in the production of fireworks. In phosphorus plants and in other work with P.-hermetization of equipment and powerful exhaust; frequent change of workers dealing directly with P.; care of the oral cavity (teeth).-Treatment in acute poisonings-see Poisoning. In chronic poisonings-general strengthening treatment, abundant nutrition, administration of insulin, calcium, in necroses-removal of sequestra.

n. Rozenbaum. Discovery of white (yellow) phosphorus in forensic and other cases and in professional poisonings. Objects (internal organs, etc.) after acidification are distilled with steam water vapor (see Poisons, isolation). During this distillation, yellow phosphorus and the first product of its oxidation-phosphorous-molybdic acid are distilled over. If white phosphorus was present in the object, then, performing the distillation in the dark, one can notice the glow of the vapors and distillate (Mitcherlich). Part of the distillate is mixed with fuming nitric acid or bromine water and evaporated to dryness on a water bath. The residue is dissolved in a few drops of water. The solution is heated with a solution of ammonium molybdate in nitric acid and the aforementioned test solution is added drop by drop. If phosphoric acid, the oxidation product of white phosphorus, and phosphorous acid are present, a yellow precipitate is obtained. If to the test solution (heated) add Dencke's reagent (sulfuric acid solution of molybdic acid), then when the mixture is reduced with metallic copper or stannous chloride, a blue coloration appears. Many substances (e.g. alcohol, hydrogen sulfide) interfere with the above-mentioned glow of the distillate. In these cases, the distillate is shaken with lead carbonate and distilled again (removal of hydrogen sulfide). The distillate is then extracted with several cubic centimeters of freshly distilled carbon disulfide. The solution is evaporated on a watch glass in a dark room and it is observed whether a glow appears when the residue is rubbed with a glass rod. As a preliminary test, which can only prove the absence of P., serves as the absence of blackening of a paper moistened with silver nitrate when acted upon by the vapors developing from acidified internal organs when heated in a flask on a water bath. Blackening of the silver paper may also be caused by other substances (first of all hydrogen sulfide). To detect P. in the air along with phosphine, the air is passed through an absorber with a solution; bromine in the presence of potassium bromide. Bromine is removed from the liquid by heating on a water bath. Denige's reagent is added and heated: blue coloration.