Carbolic Acid

CARBOLIC ACID, or phenol (Acidum carbolicum, s. Phenolum), C₆H₅OH, the first member of the series of monohydric phenols, i.e., aromatic hydrocarbons in which one hydrogen atom is replaced by a hydroxyl residue. Carbolic acid is contained in significant quantities along with higher phenols (cresol, xylenol, etc.) in the fractions of coal tar boiling at temperatures from 150° to 180° and from 210° to 240°, from which it is extracted by converting the phenols into sodium phenolates through the action of caustic soda, isolating carbolic acid from them, and subjecting the resulting crude product to purification by distillation and recrystallization. Synthetically, carbolic acid is obtained by the sulfonation of benzene, fusing the resulting sulfonic acids with caustic potash, and isolating the carbolic acid from the resulting phenolate by the action of sulfuric acid. Pure carbolic acid at room temperature appears as colorless rhombic crystals with a characteristic odor and burning taste, easily turning reddish upon exposure to light in the presence of air and some organic and inorganic substances. It melts at 42°, boils at 182°–183°, dissolves in 20 parts of water, easily in chloroform and fatty oils, and in almost all proportions in alcohol and ether; when 100 parts of molten carbolic acid are mixed with 10 parts of water, liquid carbolic acid (Acidum carbolicum liquefactum) is obtained, which dissolves in 14 parts of water. Carbolic acid has a weakly acidic reaction; its solutions color litmus paper pink. With solutions of caustic alkalis, it forms easily soluble phenolates; it is less soluble in ammonia solution and almost insoluble in soda solution. Due to its ability to dissolve in lipoids, carbolic acid easily penetrates living cells, denaturing the proteins of the protoplasm, which explains its disinfecting action. In doing so, carbolic acid does not cause the formation of an insoluble precipitate on the cell surface that would prevent the substance from penetrating inside the cells, as occurs with the action of substances forming insoluble albuminates, e.g., sublimate. The disinfecting property of carbolic acid became known in 1859, when Le Boeuf and later Lemaire pointed out its antiputrefactive action; but its practical application began from the time Lister proposed his antiseptic method (see Antiseptics and Asepsis). The bactericidal action of carbolic acid, like other disinfectants, is subject to variations depending on various conditions. Not all microbes are equally sensitive to carbolic acid; thus, cholera vibrios placed as a suspension in a 1% carbolic acid solution die after 4 minutes, typhoid bacilli after 20 minutes, staphylococci after 45 minutes (Moldovan); reproduction of microbes after an hour of exposure to a carbolic acid solution in experiments using the Rideal-Walker method ceases in Bacterium proteus, dysenteriae Shiga, typhi abdominis, Sarcina rosea at 0.5%, and in Bacterium prodigiosus, xerosis, diphtheriae only at 1% (M. Likhachev and S. Romanov). Carbolic acid has a very weak effect on bacterial spores: according to Robert Koch's experiments, anthrax spores do not die in a 2% carbolic acid solution within 5 days, while 4% and 5% solutions kill them only after nearly 4 days. The bactericidal action of carbolic acid increases with an increase in the temperature of its solution, e.g., for the paratyphoid bacillus by 3.8 times when the temperature is raised from 11° to 21°, by 4.8 times from 15° to 25°, by 8.3 times from 25° to 35°; a carbolic acid solution that did not act on anthrax spores killed them within 4 hours if heated to 40°, after 2 hours at 55°, and in 3 minutes at 75°. The intensification of the disinfecting action of carbolic acid is promoted by the addition of alkali metal salts to its solution, with the salts arranged in the following order of activity of their anions and cations: SO₄ > Cl > Br > NO₃ and Na > K > Li > NH₄. The reason for such an influence of salts is considered to be that the distribution of carbolic acid between the two phases—water and bacterial bodies—shifts toward the second phase upon the addition of salts that reduce the solubility of carbolic acid in water; conversely, substances incapable of salting out carbolic acid from solution do not enhance its action (urea, glycerin, sodium benzoate). The addition of acids also enhances the disinfecting action of carbolic acid, with sulfuric, oxalic, acetic, tartaric, citric, and boric acids following in descending order of such influence. The presence of proteins in the carbolic acid solution, in particular blood serum, lowers the action of these solutions; oils and alcohol exert a similar influence: according to Koch's experiments, a 5% solution of carbolic acid in oil has no effect at all on the anthrax bacillus, and a solution of the same strength prepared with the addition of ethyl alcohol is less active the higher its alcohol content. Carbolic acid has a relatively weak depressing effect on enzymatic processes; thus, a mixture of starch paste and saliva gives no iodine reaction upon the addition of an equal volume of a 10% carbolic acid solution; protein digestion by pepsin is also delayed by it, but it has no effect on some enzymes, such as emulsin and myrosin. In the animal organism, the poisonous action of carbolic acid manifests itself already upon its local application not only on mucous membranes, but also on the skin, through which it is very easily absorbed as a substance well soluble in lipoids. Liquid carbolic acid causes the formation of a white eschar on the skin, which then turns brown, later becomes white, and is surrounded by a red border that disappears in a few days, with the eschar becoming mummified and shedding. Weaker solutions, e.g., 5%, upon sufficiently prolonged exposure to the skin cause first a sensation of burning and pain, and then a loss of sensitivity at that spot, because carbolic acid first excites and then paralyzes the endings of sensory nerves, like other anaesthetica dolorosa. With prolonged use of even a 2% solution, for example in the form of antiseptic wet bandages, cases of gangrene of the fingers and toes (carbolic gangrene) have been repeatedly observed, which is explained on the one hand by the fact that carbolic acid penetrates into the deeper layers of the skin, necrosing their cells, and on the other hand by vasoconstriction, stases, and thromboses. Analogously to the skin, but more strongly, carbolic acid acts on mucous membranes, causing their inflammation and necrosis. If it is administered per os in a high concentration solution, the consequence of local damage to the digestive tract mucosa can be death from shock and collapse as a result of a strong reflex action on the central nervous system and heart, as also happens with poisonings by other caustic substances. The resorptive poisonous action of carbolic acid with the symptoms described below can manifest itself upon the careless application of its solutions on mucous membranes and wound surfaces, for example during uterine washings or, as was frequently observed formerly, after operations using Listerian antisepsis ("carbolism"). Carbolic acid administered per os is absorbed mainly in the stomach, and only part of it passes into the intestine, with absorption initially proceeding rapidly and then slowing down due to vasoconstriction. Having entered the blood by one route or another, carbolic acid exerts an effect on various organs, of which the central nervous system is the most sensitive to it, where the concentration of carbolic acid can be, as animal poisoning experiments showed, 2–3 times greater than in other organs. In animals, carbolic acid first excites and then paralyzes the motor regions of the spinal cord and cerebral cortex, causing contractures of individual muscles, tremor, and clonic convulsions, after which paralysis phenomena develop. In humans, convulsions are rarely observed in carbolic acid poisonings, but there are no well-founded explanations for such a difference in the action of carbolic acid on animals and humans. It acts on the respiratory center in an analogous manner, causing first accelerated dyspneic respiration, followed by its weakening and paralysis. The heart is more resistant to carbolic acid, but with large doses, there is an acceleration of cardiac contractions followed by a weakening of its work, apparently as a result of the direct action of carbolic acid on the heart muscle, which, together with its depressing effect on the vasomotor center, leads to a drop in blood pressure and collapse. Most authors associate the antipyretic effect of carbolic acid with collapse phenomena, admitting only as a secondary cause the depressing action of carbolic acid on the heat-regulating center. The increased secretion of saliva and sweat observed in carbolic acid poisonings is, as animal experiments have shown, of central origin, although it is probably also related to nausea and vomiting, which are always accompanied by an increase in the secretion of these glands. Preparations: Acidum carbolicum crystallisatum, Phenolum purum, crystalline carbolic acid; Acid. carbolic. liquefactum, Phenolum purum liquefactum—a liquid containing about 88% pure carbolic acid and about 12% water; Aqua carbolisata—a 2% aqueous solution of carbolic acid; Acidum carbolic. crudum (Phenolum crudum), crude phenol (cresol), does not belong to carbolic acid preparations because it consists mainly of cresols and xylenols.—Application of carbolic acid.

In pure form, carbolic acid (crystalline or lique-factum) is used as a caustic agent for the destruction of small diphtheritic membranes at the beginning of the disease, in malignant pustule, soft chancre, cadaveric poison infection, etc.; in dental practice, as a caustic and analgesic agent (in a mixture with novocaine) and in the form of a paste with arsenic trioxide for the destruction of the pulp of a carious tooth; in the form of a 1-3% solution in surgical practice for washing wounds, disinfecting hands, instruments, storing ligatures, etc., for the preparation of antiseptic dressing materials: cotton wool (5 and 10% carbolic acid) and gauze (10%); for skin diseases—scabies, chronic eczema, pityriasis, impetigo, prurigo—a 4% solution for washing 1-3 times a day; for burns in a mixture with lime liniment (1:30) and for frostbite in a mixture with fat (1:60); for diphtheria, putrid bronchitis, gangrene of the lungs—a 0.5-1.5% solution for inhalations; for washing the urinary bladder in cystitis—a 0.05-0.1% solution, the urethra in gonorrhea—0.1-0.5%, the vagina and uterus—0.05%, the nasal cavity in ozaena—0.25-1%; in otitis media for instillation into the ear as drops—a 10% solution in anhydrous glycerin. Internally (rarely) 0.01-0.05-0.1 (!) pro dosi, 0.3 (!) pro die in pills for typhoid fever, cholera, flatulence, gastrointestinal catarrh. Subcutaneously—a 2% solution: in phlegmons 1-2 cm³ once a day repeatedly in the area bordering the phlegmon, in neuralgias, articular and muscular rheumatism 1-2 cm³ into the area of the pain focus. Carbolic acid is used for the disinfection of infected places and materials: living quarters, cesspools, hospital material, excreta of patients, etc. (see Disinfectants).

M. Likhachyov. Carbolic acid poisoning is encountered in forensic medical practice most often as accidental or intentional—in suicide. In particular, cases of poisoning have occurred, for example, after the application of carbolic ointment, etc. There are also indications that carbolic acid was sometimes used for the purpose of murder and infanticide. In one woman, after taking 120 g of crude carbolic acid, abortion occurred, and the next day—death. It is noted that with external use of carbolic acid, the danger of poisoning is proportional not so much to the concentration of the solution as to the duration of its contact with the wound surface. After the administration per os of a sufficient quantity of a strong solution of carbolic acid, burning along the digestive tract is felt initially, then anesthesia sets on, and gastric phenomena very often do not manifest at all; due to rapid absorption, dizziness appears, the poisoned person falls unconscious with a loss of reflexes; the face is pale, the pupils are initially constricted, breathing becomes slowed, hoarse, the pulse weakens and quickens (collapse), sometimes convulsions are observed, body temperature drops to 33° and even lower; death can occur within a few minutes (sometimes 10-12 minutes after taking carbolic acid). More often, however, under more favorable conditions, along with the named symptoms, consciousness is partly preserved, and vomiting of whitish bloody masses appears, followed by diarrhea. Consequently, symptoms of toxic gastroenteritis take place. In some cases, erythrocytes or blood coloring substances are contained in the urine. Death occurs in 1-2 days; if the disease drags on, pneumonia and nephritis may develop. Upon recovery, an irregular-type "carbolic fever" is observed with an increase in temperature to 39° and higher. Regarding carbolic acid, cases of idiosyncrasy are also noted; in some, dangerous phenomena occur from insignificant doses. Children and partly women are very sensitive to carbolic acid. Sometimes persons who frequently handle carbolic acid suffer from eczema of the hands, nephrosis, so that they are forced to abandon their profession. Regarding the lethal dose of carbolic acid, there are large disagreements. According to Kobert, it is calculated at 10 g. In fatal cases, slow decomposition of the corpse, intense and prolonged rigor mortis are noted. In addition, upon examination, a characteristic smell of carbolic acid is found during the inspection of the mouth and autopsy of cavities; dirty-yellowish spots are noticeable on the skin around the mouth, sometimes with signs of reactive inflammation. On the mucous membrane of the oral cavity, esophagus, depending on the concentration of the carbolic acid solution, white, almost milk-white eschars are noticeable, somewhat dense to the touch. The changed mucous membrane of the stomach has the same color, since carbolic acid does not possess the ability to convert blood hemoglobin into hematin and impregnate the eschar with it. Usually, changes in the stomach are more sharply expressed, its mucous membrane is turned into a white, dense, and brittle eschar and when bent gives small cracks like old rubber plates; hemorrhages and reactive redness of varying degrees are also frequent. In some cases, necrotic changes are expressed only on the folds of the gastric mucosa. When using crude carbolic acid, the eschars may be colored in a more or less brownish color. In some cases, the stomach contents and the surface of the mucosa take on a pink color, which depends mainly on the change in the color of the carbolic acid itself. On the mucous membrane of the intestines, either only inflammatory phenomena are observed, or in the upper section there are signs of the caustic action of carbolic acid. Regarding the effect of carbolic acid on the blood, the opinions of authors diverge, although Kosorotov believes that one can hardly doubt that during poisoning, erythrocytes are also partially destroyed. It is noted that the blood in the corpse is poorly coagulated and for the most part dark, while sometimes, conversely, it is bright red. The larger vessels contain thrombi. In internal organs here and there are small hemorrhages. Parenchymatous organs undergo first protein degeneration, then degenerative fatty degeneration; jaundice is sometimes observed. Extravasations are often noted in the lungs, and in prolonged cases—foci of lobular pneumonia. In cases of poisoning, parts of the corpse are sent for chemical examination. With chronic carbolic acid poisoning, phenomena of so-called ochronosis may occur.

V. Vladimirsky. Measures for assistance in cases of poisoning with Carbolic Acid per os consist of washing out the stomach as quickly as possible, first with a 10% alcohol solution (in which Carbolic Acid is more soluble than in water), and then with water to completely remove the alcohol, so that the absorption of the remaining Carbolic Acid is not increased; demulcents are given internally in abundant quantities, and upon the onset of a comatose state and collapse, stimulants (camphor, strychnine) are administered. The administration of magnesium sulfate, recommended by some authors for the formation of more harmless compounds of Carbolic Acid with sulfuric acid, hardly achieves the goal, since in the organism Carbolic Acid does not combine directly with sulfates, but with organic sulfur derivatives, which then undergo oxidation. Detection in forensic medical cases and in occupational poisonings. Objects of investigation (viscera, vomitus, etc.), after acidification with tartaric acid, are subjected to steam distillation (see Poisons, Isolation). The resulting distillate is alkalized with soda (to bind carboxylic acids) and extracted with ether. The extract is evaporated at room temperature, the residue (with the odor of Carbolic Acid) is dissolved in the smallest possible amount of water, and the following reactions are performed: 1) with ferric chloride, a blue or blue-violet coloration is obtained, which disappears upon the addition of ethyl alcohol; 2) with bromine water, a white precipitate or turbidity of tribromophenol. Other reactions for phenol, such as Millon's reagent, the formation of indophenol, being very sensitive, can lead to the detection of such quantities of phenol (and cresol) that are formed as a result of the putrefaction of proteins (tyrosine).-- Quantitative determination of phenol is based on the formation of tribromophenol from it. A specific volume (in excess) of bromine water (about 1/10 N, its titer is simultaneously determined) is added to the phenol solution. After 15 minutes, a 10% solution of potassium iodide is added, and the liberated iodine, corresponding to the bromine that did not enter into the reaction with phenol, is titrated with a 1/100 solution of hyposulfite. Instead of bromine water, it is convenient to use a bromide-bromate solution (5KBr + KBrO3), which releases bromine upon acidification (5KBr + KBrO3 + 6H2SO4 = 6Br + 3H2O + 6KHSO4). To detect free phenol in urine, the latter is slightly acidified with acetic acid and the phenol is distilled off, proceeding as described above. The urine of those poisoned with Carbolic Acid often has a dark green or brown color in an alkaline reaction, which is caused by the presence of quinhydrone (a molecular compound of hydroquinone and its oxidation product, quinone - C6H4O2.C6H4(OH)2). Hydroquinone itself, para-dihydroxybenzene (C6H4(OH)2), along with pyrocatechin, ortho-dihydroxybenzene, is a product of the oxidation of Carbolic Acid. The latter is excreted in significant part in the form of the potassium salt of phenylsulfuric acid (a salt of an ester of sulfuric acid - C6H5.SO4K), which entails a decrease and even the disappearance of the "sulfates" of urine (precipitating them with barium chloride after acidifying the urine with acetic acid) and an extreme increase in "ethereal sulfuric acids" (precipitating sulfuric acid with barium chloride after boiling the urine with HCl) in comparison with "ordinary" urine (in which phenols, formed as a result of putrefaction in the intestines, are excreted in the form of ethereal sulfuric acids). In protection against occupational poisonings (still little accounted for, despite the wide technical use of phenols, e.g., in the manufacture of artificial resins and other masses), examination of urine and examination of air are required. When examining urine, essential is the decrease in the ratio of sulfate-sulfuric acid to ethereal-sulfuric acid, which is independent of the processes of putrefaction in the intestines, and an increase in the amount of phenols in the form of esters of sulfuric acid. To determine the latter, the urine is strongly acidified with sulfuric acid and distilled (until the reaction for phenol with bromine water ceases). The distillate is alkalized with soda and repeatedly extracted with ether until the residue after evaporation of the ether no longer gives reactions for phenols. The ether is evaporated, and in the residue, Carbolic Acid is determined bromometrically, as described above, or colorimetrically, by converting the phenol into indophenol with the help of aniline and hypochlorite in the presence of ammonia. To determine phenol in the air, the latter is drawn through flasks with a solution of sodium hydroxide using an aspirator (see Poisons, Isolation). Then the contents of the flasks are combined, the liquid is acidified, again alkalized with soda, repeatedly extracted with ether, and after evaporation of the ether, the Carbolic Acid is quantitatively determined as described above.

A. Stepanov. Carbolic Acid is used in microscopic technique for the disinfection of various solutions, e.g., certain dyes, infectious masses, gelatin mixtures, etc. In view of its high refractive index (n=1.54), Carbolic Acid is also used for the clearing of macro- and microscopic preparations. Carbolic Acid is easily miscible in any proportions with benzene, xylene, and essential oils, and at the same time reduces the sensitivity of the latter to traces of water. Therefore, the mentioned mixtures are used for transferring celloidin sections from 90% alcohol into pure xylene (see Carbol-xylene, Xylene). For the latter purpose, a mixture of 2 parts Carbolic Acid and 3 parts turpentine, or 1 part Carbolic Acid, 1 part creosote, and 8 parts toluene, or 1 part Carbolic Acid, 1 part bergamot oil, and 1 part cedar oil is also used. Carbolic Acid is added to solutions of basic dyes to obtain more intense staining. Such carbolic dye solutions are used especially widely in bacterioscopic technique (for example, carbol-fuchsin, carbol-gentian violet, etc.).-- Method of preparing carbolic dye solutions: 1.0 of dye is triturated in a mortar with 1.0 of crystalline Carbolic Acid, dissolved in 10 cm3 of 96% alcohol, and 90 cm3 of distilled water is added.-- For histological fixation, the filtrate of a mixture of Carbolic Acid with a concentrated solution of mercuric chloride (Pappenheim) or a mixture of 30 parts of a concentrated aqueous solution of Carbolic Acid, 8 parts of formol, and 3 parts of 20% trichloroacetic acid (Champy) is recommended.