Aniline

ANILINE (aminobenzol, aminobenzol, phenylamine), C₆H₆NH₂, is a strongly light-refracting, almost colorless oily liquid; when standing, it gradually changes color from yellow to brown through oxidation. Sp. gr. of A. 1,036; freezing point -8°, boiling point +184°. A. is produced in aniline factories from nitrobenzene by reducing the latter with hydrogen. Iron filings and dilute HCl are used as reducing agents; as a result of reduction, an amide compound is obtained: C₆H₆N0₂+3H₂=2H₂0 + C₆H₅NH₂. Like many other derivatives of benzene, A. is a serious industrial poison. As a volatile substance, A. penetrates the body in the form of vapors through the lungs; in addition, A. is also absorbed through intact skin, dissolving the skin's fatty tissue and penetrating to the layers containing blood vessels, where the blood draws and captures particles of the poison (Levin). Through damaged skin and mucous membranes, absorption of the poison occurs more quickly. The penetration of A. into the body through external coverings plays a very important role under industrial conditions: on chemical plants, workers who do not observe sufficient cleanliness mainly become ill; washing the hands with a solution of bleaching lime, which causes increased sweating, increases the danger of poisoning.- Teenagers and young people (18-22 years), as well as the elderly (over 50 years), become ill more quickly than people aged 30-40 years; the danger of poisoning is also increased in women, especially during puberty, menstruation, pregnancy, and lactation, as well as in persons with various organic diseases (especially of the circulatory and excretory organs) and metabolic diseases. Furthermore, according to Kurschmann (Curschmann) and others, poor ventilation of workrooms and warm, humid air are favorable moments for poisoning; on enterprises, the majority of poisonings (up to 3/4) are observed in summer. Consumption of alcohol is particularly important as a predisposing factor for poisoning. It has been repeatedly observed that workers who left work in perfectly good health developed symptoms of poisoning immediately after consuming alcohol with lunch. These practical observations are confirmed by experimental research; thus, Günther (Günther) and Liepschutz when studying the effect of various aromatic compounds on frog sperm found that weak solutions of them had almost no effect, but when alcohol (as well as nicotine and chloral hydrate) was added, much weaker solutions of the poison caused almost complete cessation of sperm movement.- In humans, Lehmann and his students established that inhaling air containing 0.3-0.6 mg of A. per liter for half an hour is tolerated without special consequences (without the appearance of bluish discoloration). It is difficult to determine the exact toxic dose for humans. Acute poisoning. The main symptoms of acute poisoning in humans should be considered cyanosis and nervous phenomena. Symptoms of mild poisoning: indefinite complaints of malaise, fatigue, headache, heaviness in the head, slight cyanotic discoloration; further-unsteady gait, sometimes vomiting and diarrhea. With an increase in the dose of poison, marked pallor and cyanosis develop. In severe cases, the latter reaches a dark blue tint, the blood is colored brown, clots easily and contains methemoglobin. Other symptoms: vomiting, severe dizziness, stupor, marked weakness, shortness of breath, increased heartbeat, characteristic twitching in the muscles. Some poisoned persons become apathetic, others-manically excited. Sometimes disturbances of vision (diplopia, scotoma), increased urge to urinate, and bloody urine are also observed. In very severe cases, patients lose consciousness, breathing stops, convulsions appear, reflexes disappear, the skin becomes moist and cold, temperature drops, pupils become immobile, sensitivity disappears. With continuously increasing symptoms, death may occur (as a result of deep collapse), sometimes during convulsions; the causes of death are progressive changes in the blood and paralysis of the central nervous system. Poisoning develops immediately after the poison enters the body, although sometimes a latent period of several hours is observed. Acute poisoning is usually the result of an accident (damage to equipment, pipe rupture, careless handling of vessels containing aniline oil-clothing gets soaked with A., etc.).- Much more common are cases of subacute and chronic poisoning. As a result of experimental research on animals, Kurschmann became convinced that minimal doses of A., administered daily for a long time, eventually cause the development of pathological phenomena. Poisoning occurs mainly through the skin, with subcutaneous fatty tissue serving as a kind of storage place; when a sufficient amount of poison accumulates in it, poisoning develops. Chronic forms of anilism have a fairly typical course. The first symptom to develop is a marked decrease in the amount of Hb. A worker whose blood Hb content has decreased by more than 20%, in Kurschmann's opinion, is in danger of poisoning; when the Hb content drops to 70%, Kurschmann found weak traces of methemoglobin in the blood in the absence of subjective complaints. With mild subjective symptoms, cyanosis quickly appears. With further progression of the disease, changes in the blood increase: methemoglobin appears, the number of red blood cells decreases, various pathological forms of red blood cells appear: anisocytosis, poikilocytosis, polychromatophilia, nucleated red blood cells, etc. From the subjective symptoms of chronic A. poisoning, one should note weakness, muscle pain, headaches, insomnia, loss of appetite, constipation.- A. is excreted from the body through the respiratory tract, partly through the skin, but mainly with urine. Unchanged A. is not found in it, however; it is excreted in the form of para-aminophenol in combination with sulfuric acid, forming conjugated compounds with it (Schmiedeberg). - In autopsies of people who died from aniline poisoning, brown discoloration of the blood, engorgement of veins with blood, many small hemorrhages on serous and mucous membranes, fatty degeneration of the liver, kidneys, etc., are found. In evaluating the action of amide compounds, Kurschmann comes to the conclusion that A. (and its derivatives) is a blood poison; it converts Hb inside red blood cells into methemoglobin. Further, the red blood cells disintegrate, and regenerative phenomena develop in the bone marrow. Oxygen-poor blood irritates the central nervous system, mainly the medulla oblongata; the change in blood should explain the development of cyanosis. If in severe cases cerebral phenomena predominate, this, in Kurschmann's opinion, does not contradict the theory of action on blood; changes in the latter are also observed here, while cerebral phenomena develop secondarily. However, recent research has shown that Kurschmann's theory does not fully explain the phenomena observed in A. poisoning. The development of cyanosis is explained partly by the formation of methemoglobin, but here, probably, the deposition of a black coloring substance (black A.) also occurs in the skin, because when pressure is applied with a finger to the skin, the cyanotic discoloration does not disappear. There can be no question of cyanosis in the true sense here, since cyanotic discoloration appears even when there are no cardiovascular disorders. Some authors also dispute the theory of one-sided action of A. on blood; according to Falkenheim, and especially Heubner, along with changes in blood, there is also a direct effect of the poison on the nervous system; for example, in rabbits, phenomena of central paralysis were observed, with phenomena from the side of oxyhemoglobin being barely noticeable. Heubner believes that derivatives of benzene (including A.) have an effect on the nervous system similar to phenol. At the same time, however, in the blood A. acts directly on the molecule containing iron, which is the oxygen carrier, and on the basis of oxygen starvation, secondary phenomena develop, among other things, from the side of the central nervous system, which is thus subjected to a double action-direct and indirect. As for the nature of A.'s action on blood, this problem has been the subject of careful study by numerous authors. In the recently published brief summary, Heubner and Meyer believe that from A., as from nitrobenzene, phenylhydroxylamine CH₃N0₂ . NH. OH is probably formed, which promotes the formation of methemoglobin. This action is quite complex, since phenylhydroxylamine is not an oxidizing but a reducing substance, while the transformation of oxyhemoglobin into methemoglobin is an oxidative process.

According to Meyer and Geibner, this process occurs as follows: oxyhemoglobin catalytically causes the oxidation of phenylhydroxylamine, during which oxygen is activated and, in turn, oxidizes the blood's coloring substance, forming methemoglobin. The latter is fairly quickly subject to reverse development - in acute poisoning, all methemoglobin within 1-2 days reverts back to oxyhemoglobin, leaving no consequences. Furthermore, one should note an extremely severe professional disease - this is the formation of new growths of the bladder, developing in persons working with aromatic compounds, among other things, with A. Such new growths, predominantly malignant (cancer), in workers of the chemical industry have been described in Germany to date in 177 cases. These new growths develop after prolonged work with aromatic compounds (the incubation period lasts, on average, about 18 years). To explain the origin of this extremely dangerous lesion, many theories have been proposed, of which the most ingenious is the theory of Leuenberger, which assumes the effect on the bladder tissues of hydroxylated aromatic compounds contained in urine; the latter cause irritation of the urinary tract, leading to proliferation of tissues and atypical growth of the mucous membrane with the formation of tumors. Aniline production. The danger of poisoning A. for a large number of workers exists in the chemical industry (aniline plants), textile (dyeing and printing), pharmaceutical (production of neo-salvarsan) and rubber (use of aniline as a solvent). In well-equipped aniline plants, the entire process of obtaining A. from beginning to end is mechanized, the apparatus is hermetically sealed, and workers do not have to come into contact with raw materials, semi-finished products and finished products, nor inhale vapors. Even here, cases (and in fact do occur) - such as (rupture of pipes, damage to equipment, etc.), in which acute poisoning of workers can occur. In poorly equipped plants, favorable conditions exist for both acute and chronic poisoning of workers. A. has much greater significance as an industrial poison in the USSR in the textile industry, where it is widely used for black-aniline dyeing of cotton and silk fabrics. In view of the fact that in black-aniline dyeing and printing very beautiful and at the same time durable fabric colors are obtained, this method of dyeing and printing finds wide application, and a significant number of workers are employed in it. To obtain a black color on the fabric, it is necessary that the following three main components be included in the dye: aniline salt (hydrochloric acid), oxidizer and catalyst. As an oxidizer, NaCl is usually used, as a catalyst - yellow prussiate of iron. Sometimes other substances are also used. Solid black dyeing with aniline is done in two ways: 1. Oxidative black; this method is used for dyeing heavy paper fabrics (clothing goods). The fabric is impregnated with a dye solution in a padding mangle; the latter represents a box with rollers, along which the goods being soaked in the box pass, and two or three rollers that squeeze out the excess absorbed solution from the goods. Then the goods go to special dryers, so-called Matter-Platt apparatuses (the temperature inside the chamber reaches 50-60°), where oxidation into 'black aniline' occurs. Oxidation ends with chroming - the goods pass through the padding mangle, where it is impregnated with a solution of chrome alum. 2. Steaming black; according to this method, light paper goods are dyed. The goods pass through the padding mangle with a dye solution, then through a dryer where it is exposed to a temperature of 60-70°; after this, it is passed through an oxidation apparatus (Matter-Platt ripener), where, at a temperature of 100-105°, in an atmosphere saturated with water vapor, it remains for 1-2 minutes; here the final oxidation occurs. Chroming is not necessary with this method. In almost all compositions used for the steaming black method, there is a significant amount of free aniline, not bound with HCl. Black A. in printing. To apply patterns to the goods on printing machines, a thickened mass is used, which also contains free A. The main production processes in which workers have to deal with black aniline are: 1) preparation of aniline salt; 2) preparation of the black-aniline padding (addition of oxidizer and catalyst), preparation of the printing ink (the same + mixing with the thickener); 3) dyeing in padding mangles; 4) printing with black-aniline ink or on black aniline; 5) drying; 6) ripening in the Preibisch ripener (for oxidative black) or Matter-Platt (for steaming black, as well as for printing); 7) washing with a soda solution (or chroming). In all the listed processes, vapors of A. are released into the air; moreover, in some of them, workers come into direct contact with solutions, or the latter contaminate their clothing. It should also be taken into account that in most of the premises where these works are carried out, the temperature, and in some places also the humidity, is significantly increased (temperature at dryers in places where female workers are, as well as near ripeners, in summer reaches 40-42°; in the steeping department, where the dyed goods are washed with alkali, at a temperature of 28-30°, the relative humidity reaches 70-75%, etc.). In factories, work with aniline is not carried out in isolated premises. Thanks to this, aniline vapors have to be inhaled by a large number of workers who do not work with aniline. For example, the etching of aniline salt and the preparation of the padding, which is usually done by 3-4 people, is carried out in the general paint-boiling room, and in the absence of proper ventilation equipment (which is observed in many factories), aniline vapors spread throughout the paint-boiling room. Padding mangles, on which black-aniline dyeing is carried out, are usually placed between printing machines, and therefore A. vapors contaminate the air of the entire printing department. Printing with black A. and on black A. is also carried out in a general room. Dryers, through which goods dyed with black A. (or on which black A. was printed) pass, are also not isolated - they are located next to dryers of other printing machines; similarly, ripeners may not be isolated. Tubs, in which the goods pass through a soda solution, are placed in a general washing department. Thus, on dyeing and printing factories, a very large number of workers are exposed to A. Observations by sanitary inspection show that on our dyeing factories and departments, cases of acute poisoning with A. occur quite often; especially many reports have been received after the introduction of mandatory registration of cases of professional poisoning (these cases are mostly mild). Furthermore, research has shown that many workers in the above-mentioned departments undoubtedly suffer from chronic aniline poisoning. The danger of poisoning with A. also exists in the production of neo-salvarsan, namely in the first stage of production, when preparing arsanilic acid. The latter is obtained by fusing arsenic acid with A.; to the resulting arsenic salt of A., a solution of caustic soda is added and then precipitated with hydrochloric acid - free arsanilic acid precipitates. The excess A. is drained and distilled in a still for purification from impurities, after which it is used again. In these works, a significant amount of A. vapors is released; despite the fact that the first processes are carried out under a hood, and the still for distillation represents closed equipment, it turns out to be impossible to avoid the release of A. vapors into the air. - Poisoning with A. is also possible in rubber production, where A. is sometimes used as a solvent - such cases (chronic poisonings) have been described in the U.S.A. A number of cases of acute poisoning with A. have occurred in Moscow warehouses among loaders working on transferring aniline oil. Preventive measures. 1. Aniline plants; the most radical measure of control is the complete mechanization of the process with absolute sealing of the apparatus (in the presence of good supply and exhaust ventilation). 2. Dyeing-finishing and printing productions; to reduce the danger of poisoning with A., it is necessary: a) to isolate premises where the padding is prepared; b) aniline salt should be prepared not in textile factories, but in aniline plants where appropriate equipment is available; c) padding mangles on which black-aniline dyeing is carried out, dryers for pre-drying goods dyed by this method, and printing machines on which printing is done on reserve, should be isolated in special premises; d) in all premises where work is carried out on black-aniline dyeing and printing, powerful supply and exhaust ventilation must be installed. - Reducing the content of A. in the padding and printing ink is of very great importance; it is especially important to eliminate excess free A. In this direction, research has been carried out by engineer N.N.

by Voznesensky, who proposed for printing inks a significantly reduced amount of aniline compared to the previous practice, where the excess aniline was completely removed. At present, a number of factories operate according to the formula proposed by Voznesensky. Chemical analyses of the air at the Tregornaya Manufactory showed that when working with new formulas (according to Voznesensky), the content of aniline vapor in the air of the printing department, drying rooms, and other departments is reduced by two to three times compared to the previous amount. In other industries (arsanilic acid, rubber, etc.), it is necessary to seal the equipment and install powerful supply and exhaust ventilation.

H. Rosenbaum.

Aniline Dyes. In the strict sense of the term, aniline dyes are one of the groups of artificial dyes of the aromatic series or coal-tar dyes, namely, derivatives of triphenyl- and diphenylmethane, but often this term is used to refer to all artificial dyes. - From the 50-60s of the XIX century, aniline dyes began to be used for coloring wines and other beverages and food products: fuchsine was first discovered in the production of red wines. Soon descriptions of poisonings caused by colored wines and food products appeared. As a result, in many countries (also in ours) the use of aniline dyes for coloring beverages and food products was prohibited. Despite the prohibition, aniline dyes are still often used in the food industry, especially in confectionery, and for coloring beverages. - The production of aniline dyes causes in workers various types of diffuse skin diseases (eczemas, erythemas, dermatitis) and abnormally increased sweating of the hands - hyperhidrosis manuum. The dyes that are harmful to the skin of workers are the following: aurantia (Gnem), chrysoidin (Blazhko), malachite green (Blazhko), Bismarck brown (Blazhko), oil yellow (Veil); nitro-zodimethyl-aniline (Elssesser), flavaniline (Laubenheimer), the vapors and gases that develop during the preparation of aniline yellow (Elssesser), alcohol and water blue (Levin), Marches yellow (Kober), urzol D (Khlopin). In addition, in this respect, the following are also suspicious: fast blue, fast yellow, ruby, and acid yellow (Blazhko). The listed aniline dyes belong to professional skin poisons. Among the workers of aniline factories, another disease is relatively often observed - cancer of the scrotum, apparently due to repeated irritation by coal tar and the intermediate products of dye manufacturing. - The action of aniline dyes on animals and humans per os has been studied by several authors, and it was established that many of the studied aniline dyes are harmful, and some of them are poisonous. Thus, in a review of the literature on aniline dyes up to 1903 by Khlopin, 60 studied dyes and among them 22 dyes, i.e. 37.6%, were recognized by the authors as poisonous or harmful. In 1903, Khlopin studied 50 aniline dyes on animals and among them found 15, i.e. 30%, poisonous and 20 dyes, i.e. 40%, suspicious. The latter, without causing death, caused in experimental animals disturbances of digestion, kidney function, or general condition. It was found that between the chemical composition and the toxicity of dyes, it is not possible to establish a constant dependence: with the exception of the group of nitro dyes, which are all poisonous, in other groups one can find both harmless and harmful ones. Poisonous and harmful dyes have been found among azo dyes, auramines, triphenylmethane, pyronins, acridines, thiophenins, and oxazines, in the quinoline group and among sulfur or Vidal dyes, i.e. in 12 out of 18 groups. List of poisonous and harmful dyes based on experiments on animals per os. (Kazenev, Veil, Lepin, Santori, Khlopin). Groups I. Nitro dyes .... picric, saffron surrogate, Marches yellow, aurantia, or royal yellow. V. Azo dyes . . . Echtgelb R, mandarin, naphol-schwarz, methanilgelb, methylorange, oil yellow, anilineorange G, pyrotin RR, ponso RR, benzopurpurin, erica and citrongelb. VI. Auramines . . . auramine O. VII. Triphenylmethane . . . wasserblau, victoriablau, gencyanblau, corallin, brilliant green, aurin, seris J0, acid green, Metternich green, Bavarian blue DBF and DSF. VIII. Pyronines . . . cerulean (when injected into a vein), eosin, rhodamines B and G. X. Acridines . . . chrysaniline, benzoflavin II. XI. Oxiketones and other related dyes alizarin S. VIII. Oxazines and thiazines . . . neublaue, gallocyanine, methylene blue, ethylene blue, echtblau (crystalline for cotton), methylenegrün. XIV. Azines .... safranin, indulines. XV. Thiazoles . . . primulin. XVI. Quinoline . . . quinoline yellow. XVIII. Of unknown exact chemical constitution . . . urzol D, thiocatechins: M?Ж 1, 2, 8 and B, Vidal black, Noir autogenique. Among these dyes, urzol B (paraphenylenediamine), which is used to dye furs and hair black, deserves special attention; it is poisonous, when taken per os it causes characteristic eczemas on the skin and attacks of bronchial asthma when its dust is inhaled. With further research and observations regarding the action of aniline dyes on the animal organism, it is to be expected that among them other poisonous dyes, no less important from the point of view of labor protection, will be discovered. - As for the more intimate pharmacological action of aniline dyes, in this respect they have been studied very insufficiently. Some of the starting and intermediate compounds from which aniline dyes are synthesized have been studied much more completely, e.g., aniline (aniline oil), benzene, nitrated benzene and its homologs (nitrobenzene, nitrotoluene, etc.) and amino derivatives of benzene (paraphenylenediamine = urzol B) and others. Depending on the dye and dosage, poisoning by aniline dyes is manifested in vomiting, diarrhea, and the appearance of protein in the urine. Vidal sulfur dyes cause per os rapid, almost instantaneous stupor in animals: dogs with convulsions fall to the floor; protrusion of the tongue from the mouth and profuse salivation are observed; then vomiting begins, the dog gradually revives and returns to normal after a few hours. These poisoning phenomena resemble the so-called "apoplectic form" of poisoning by hydrogen sulfide gas, studied in animals by K. Lehmann. Some dyes, e.g., mandarin, cause in people general malaise, weakness, and a tendency to fainting. Death occurs from paralysis of the heart. A dog that received per os the dye methylorange dies from symptoms of spinal cord paralysis. The action of small doses of aniline dyes on animals has not yet been studied. It has been established that some aniline dyes inhibit pepsin digestion in vitro until its complete stop (Vinogradov), delay sugar fermentation (Merezhkovsky), and also give precipitates with pure gastric juice (Khlopin). The latter observations indicate that an admixture of coal-tar dyes should have an unfavorable effect on the digestion and assimilation of food prepared from products colored by them. Some aniline dyes also have a harmful effect on the fish fauna of rivers, and therefore, in order to avoid harming fishing, the content of aniline dyes in wastewater discharged into public water bodies must also be regulated. It has been proven (Haempel) that for lower aquatic animals and fish, very weak solutions (1:100,000 and 1:1,000,000) of aniline dyes 1) auramine and canarigelb-are already weakly poisonous; 2) methyl violet-are even more poisonous and 3) victoriablau B extra, crystalline brilliant green and benzolgrün EO-are very poisonous. - It has long been known that some aniline dyes possess bacteriostatic and bactericidal properties and are used for this purpose in bacteriology (e.g., crystal violet) and in therapy. The relationship of aniline dyes to the protoplasm of living cells has been studied insufficiently. Aniline dyes neutralize the tetanus toxin, which is very similar to enzymes (Gabričevsky). In the USSR, the use of aniline dyes for coloring wines and food products is prohibited by law (decree of the People's Commissariat of Health of 10/X 1922). In Germany and France, only some of the aniline dyes recognized as poisonous and harmful are prohibited for this purpose; others, so-called harmless ones, are permitted.