OXIDES

OXIDES, compounds of elements with oxygen. Oxygen combines with all elements except the noble gases. The recently discovered oxide of fluorine fills the gap that existed regarding fluorine. Depending on the degree of oxidation and valence of the element, O. contain varying numbers of oxygen atoms per atom of the element. The higher salt-forming O. were among the foundations for the construction of Mendeleev's periodic system. The number of oxygen atoms in them indicates the belonging of the element to the corresponding group.

I II III IV V VI VII VIII R₂O₀R₂O R₂O₂ R₂O₃ R₂O₄ R₂O₅ R₂O_e R_aO, R₂O₈ Some elements form a whole ladder of oxides of decreasing degrees of oxidation, for example N₂O₅-nitric anhydride, N₂O₄-nitrogen tetroxide, N₂O₃-nitrous anhydride, N₂O₂-nitric oxide, N₂O-nitrous oxide; others- only individual steps of such a series. The nomenclature is such that the lower degree of oxidation is called suboxide, the higher-oxide, e.g. suboxides: FeO, Hg₂O, Cu₂O, Ti₂O, oxides: Fe₂O₃, HgO, CuO, Ti₂O₃. O. of trivalent elements are sometimes called sesquioxides: R₂O₃ or* "RO_1.5" (obsolete). According to chemical properties, salt-forming O. are divided into basic and acidic. Basic ones give bases with water (they are formed mainly by metals), acidic ones-acids (they are formed mainly by metalloids). Interacting with each other, O. give salts. There is a whole series of transitions in these properties. The extreme members of the series are typical basic or acidic O.; in between this characteristic gradually decreases, so that their hydrates become amphoteric, i.e. capable of decomposing in aqueous solutions, giving H+, which is characteristic of acids, and OH-, which is characteristic of bases. Such a complete series we have for example in the 3rd period, Na₂O, MgO, Al₂O₃, SiO₂, P₂O₅, SO₃, Cl₂O₇, starting with the typical basic oxide Na₂O and ending with the typical acidic oxide Cl₂O₇; Al₂O₃ possesses both properties to a lesser degree. The atomic-theoretical explanation is as follows (Kossel). The force of attraction between two ions follows Coulomb's law f=- ¹/^r2; the larger their size r, the weaker the attraction, the larger their charges e, the stronger it is. The minus sign stands because oppositely charged ions attract. Let us consider the compounds of O. with water: NaOH, Mg(OH)₂, Al(OH)₃, Si(OH)₄, H₃PO₄, H₂SO₄, HClO₄. The sizes of the ions Na+, Mg++, etc. are almost the same, as they have the same number of electrons. In the series their charges increase, which is due to the increase in the charge of their nucleus. Schematically these molecules look like: O^--Na⁺ O^--Mg⁺⁺ O^--Al⁺⁺⁺ O^--Si⁺⁺⁺⁺ O^--P⁺⁺⁺⁺⁺ O^--S⁺⁺⁺⁺⁺⁺ O^--Cl^+++++++ The O^- ion in the first of them should attract H⁺ much more strongly than Na⁺, since the charges of the latter are equal, and the distance to the center of the positive ion is much smaller for H⁺ than for Na⁺. Consequently NaOH, dissociating into ions, should give Na⁺ and OH^-. In Mg(OH)₂ the relations are the same, but here the influence of the second factor begins-the charge of the central ion (Mg⁺⁺); since there are two charges here, the attraction of O^- by magnesium is stronger than in the case of sodium, which had only 1 charge; therefore Mg(OH)₂ will already be more difficult to dissociate into ions Mg⁺⁺ and OH^-, i.e. the base is weaker. The attraction between the three-charged Al⁺⁺⁺ and O^- will be even stronger, so here the tendencies to dissociate into ions Al⁺⁺⁺ and OH^- and into AlO₃^- and H⁺ already compete. In the further representatives of the series the latter tendency predominates and the stronger the larger the charge of the central ion. Thus we have a continuous transition from the strong base NaOH to the strong acid HClO₄. If we consider the series vertically in Mendeleev's system, i.e. take a series of elements located in one group, for example H₃PO₄, H₃AsO₃, H₃SbO₃, H₃BiO₃, then the strength of the acid will decrease in the direction of increasing atomic weight, which is again connected with the fact that although the central ions P, As, Sb and have the same charges, their sizes increase and the strength of their attraction to the O^- ion decreases. Bi(OH)₃ already clearly shows basic properties. Thus the more to the right an element is in the periodic system, the more basic character its O. has; similarly the lower it is in the vertical series, the more basic properties it shows. These two tendencies can overlap each other due to the incomplete coincidence of the groups of small and large periods and thus there are exceptions to this rule. Furthermore, O. of lower degrees of oxidation are more basic, of higher degrees-more acidic, e.g. MnO and Mn₂O₇. This also fits into the scheme presented, since the increase in the charge of the central ion corresponds to the transition from Mg⁺⁺ to Cl⁷⁺, discussed above. Combining with each other, oxides of different degrees of oxidation can give salts, for example MnO + MnO₂ = Mn₃O₄, etc. A special group among oxides is the group of peroxides (see).

A. Balandin. OXIDE OF CARBON (CO), gas with specific weight 0.697, colorless, odorless, slightly soluble in water, burns with a blue flame, is formed by incomplete combustion of carbonaceous substances under conditions of excess carbon; the CO₂ formed during combustion is reduced by carbon to CO in this case; CO₂ + C = 2CO (the reaction is reversible). Thus CO is a secondary product of combustion, the primary one is always CO₂. Carbon monoxide is formed by passing CO₂ through heated iron and zinc dust (CO₂ + Zn = ZnO + CO), by the action of H₂ on CO₂ (CO₂ + H₂ = H₂O + CO; excess CO₂ can be absorbed by alkali). CO is also obtained from formic acid upon decomposition by sulfuric acid (HCOOH = H₂O + CO), from salts of formic acid upon heating with H₂SO₄, upon heating citric acid with H₂SO₄. A mixture of CO with oxygen explodes upon ignition. CO is a reducing agent although weak: reduces salts of Cu, Ag, but does not reduce salts of Zn, Fe. By passing CO into heated NaOH or by interaction with soda lime at 200°, formic acid is obtained technically. Passing CO into heated alcoholates leads to esters of formic acid: C₂H₅OH + CO = C₂H₅O·CO·H. Catalytic reduction of CO with hydrogen gives methyl alcohol; this reaction is applied technically. The presence of even very small traces of CO in the air can be detected by the change in the absorption spectrum of blood (see below). Linseed oil and oil paints upon drying (absorption of oxygen) can give CO, whereby they can serve as a source of CO poisoning. In the gases formed when firing from guns charged with smokeless powder, there is CO, which can cause poisoning.

and of the Ovaries. Being a product of incomplete combustion of carbon-containing substances, carbon monoxide is found almost everywhere where combustion takes place with insufficient access of oxygen: in blast furnaces (flue gases), generator, shaft, tunnel, exhaust gases, in street air with more or less intense movement of automobiles, buses, etc. Coal gas, formed during the dry distillation of coal, contains about 10% CO; water gas (formed by passing steam through red-hot coke) - 30-40%, generator gas - 20-25%, exhaust gases - 1-7%. Carbon monoxide, as recent research has shown, is an almost constant component of mine air, in which the concentration of CO in mine workings sometimes reaches 0.3-0.4 mg per liter. The development of the chemical industry has led to the use of carbon monoxide as a raw material for obtaining a whole series of chemical compounds (phosgene, methyl alcohol, formaldehyde, etc.). Thus, carbon monoxide is an extremely widely distributed professional poison, the danger of poisoning from which exists in a huge number of industrial enterprises. In the USSR, carbon monoxide occupies first place among poisons causing professional poisonings. According to data from the NKT USSR for the five-year period 1924/25-1928/29, the following number of acute professional poisonings from carbon monoxide occurred: 1924/25 - 146; 1925/26 - 1056; 1926/27 - 1,682; 1927/28 - 3,246; 1928/29 - 3,488; a total of 9,612 cases, which constitutes 60% of all poisonings that occurred during this period. Over 70% of these poisonings occur in Ukraine, where heavy industry (metallurgy) is most developed, representing the main source of carbon monoxide poisonings. Toxicology of CO. According to the opinion of Henderson and Haggard, which is almost dominant, carbon monoxide should be considered a gas that does not have a direct toxic effect, so that its harmful effect on the organism is expressed only in subsequent anoxemia. Having an extremely pronounced affinity for hemoglobin, 235 times greater than the affinity of oxygen, carbon monoxide displaces oxygen from Hb when inhaled, converting it into carboxyhemoglobin and thus deprives the red blood cells of the blood of the ability to perform oxidative functions, as a result of which asphyxia of tissues occurs with all the ensuing serious consequences; a reflection of this is the so diverse clinic of acute carbon monoxide poisonings. Thus, according to the supporters of the anoxemic theory, the main phenomena of both morphological and functional character, observed in the tissues and organs in carbon monoxide poisoning, are explained exclusively by oxygen starvation and the associated accumulation in the organs and tissues of products of intermediate metabolism. The amount of carboxyhemoglobin formed when inhaling CO depends on a whole series of factors, among which the ratio of carbon monoxide to oxygen in the inhaled air (partial pressures of these gases) is in the first place. In the reaction of the human organism to the inhalation of air containing CO, individual differences, as well as the circumstances in which carbon monoxide poisoning occurs, in particular temperature conditions, are of extremely great importance. It is also very important to emphasize that the so-called anoxemic theory of the action of CO on the organism is by no means currently finally accepted: a number of researchers believe that oxygen starvation alone, which also occurs in suffocation as a result of poisoning by nitrogen, carbon dioxide, etc., can in no way explain a whole series of patho-anatomical phenomena (parenchymatous degeneration of the kidneys, liver, glands, stomach, etc.), which are observed in acute carbon monoxide poisoning and which are not encountered in poisoning by nitrogen, carbon dioxide and other suffocating gases. The anoxemic theory also does not explain cases of the lightning-fast action of carbon monoxide, in which no disturbances in nutrition could yet have occurred, as well as the chronic action of CO, which is denied by many supporters of the anoxemic theory (e.g. Lewin). In professional pathology, however, the possibility of the chronic action of small doses of CO, causing a certain complex symptom complex, which includes phenomena from the blood and circulatory system, and from the digestive tract, and especially from the nervous system, is considered undoubtedly established. Whether these chronic effects are due only to the accumulation of numerous, though individually insignificant, moments of disturbance of tissue nutrition and, above all, of the nervous system, or to the direct action of CO on the cells of one or another organ, it is difficult to say with certainty at the present time. Most likely, both are present here, i.e., both the so-called functional cumulation and the direct action on the cellular elements of the organism. As for the doses that can create a danger of acute poisonings, the experimental data of different authors give more or less similar data. 1. When inhaling air containing 0.4-0.5% (by volume) CO for 20-30 minutes, 70% of Hb in the blood is saturated with CO, and the danger of a fatal outcome is very great. 2. When inhaling air containing 0.21% CO for one hour, 50% of Hb is saturated with CO, and a danger to life arises. 3. When inhaling air containing 0.05% CO (which corresponds to approximately 0.6 mg per 1 liter of air), 30% of Hb is saturated with CO, and at this time clear signs of poisoning appear. The effect produced in the body by different degrees of saturation of the blood with carboxyhemoglobin is visible from the following table, borrowed from Henderson and Haggard. -Table 1. Carboxyhemoglobin in % Physiological effect 20 30 40-50 60-70 80 Over 80 No perceptible effect except shortness of breath with strong muscular work Shortness of breath with moderate work, sometimes headache Noticeable headache, irritability, slight fatigue Headache, confusion, fainting during work Unconscious state, weakness of breathing and death Rapid death Instant death Similar data were obtained by Nicloux: Table 2. i Content of CO in Carboxy- air in hemoglo- mg per 1 bin in % Physiol. effect liter 0.06 5.0 No symptoms 0.12 9.5 No symptoms 0.24 17.5 First signs, headache, redness of skin 0.48 29.6 Severe headache 0.6 34.4 Weakness, dizziness, vomiting, signs of collapse 1.2 52.0 Severe headache, weakness, shortness of breath, rapid pulse 2.4 66.0 Suffocation¹, weak breathing, coma 4.0 76.0 Coma, danger of death 6.0 83.5 Death Thus, if more than 60% of Hb in the blood is saturated with CO, the danger of death occurs. The first clearly expressed signs of the beginning toxic action of CO appear when about 17% carboxyhemoglobin is formed in the blood. The picture of acute carbon monoxide poisoning is extremely varied and diverse. In typically developing cases, three stages are usually distinguished: 1. The stage of paralysis, in which after a series of severe symptoms (headache, feeling of pressure in the heart area, dizziness, noise in the ears, tendency to faintness) the first signs of paralysis develop, which are expressed first of all in weakness of the lower extremities. 2. The stage of motor irritations, in which various forms of muscle excitation (tremor, clonic and tonic convulsions, etc.) occur. 3. The stage of respiratory disorder (dyspnoe). Breathing becomes shallow and convulsive. Loss of consciousness occurs and at the same time an increase in body temperature to 40°. This stage, without timely help, usually ends in death. Such a typical course of poisoning is observed, however, not often; much more often various deviations from these typical forms are encountered. It is especially necessary to note the subsequent disorders that occur after acute poisoning and which mainly affect various parts of the nervous system: disorders of sensitivity (hyperesthesia, anesthesia, paresthesia), increased tendon reflexes, and sometimes even paralytic phenomena (hemiplegias and paraplegias). In chronic poisoning, first of all, various degrees and character of functional disorders of the nervous system (headaches, dizziness, irritability, mental disorders, psychoses) should be noted (Gelman), and sometimes more serious lesions (neuritis, vasomotor and trophic disorders), various disorders in the activity of the cardiovascular system (arrhythmia, pains in the heart area) and a decrease in the body's resistance to infection should be noted. Treatment. In cases of acute poisoning-immediate removal from the atmosphere containing CO. In case of respiratory arrest-immediate and prolonged artificial respiration. For the latter, oxygen or, much better, a gas mixture containing 93% O₂ and 7% CO₂ is used; the latter stimulates the respiratory center and, as research by a number of American authors has shown, when inhaling this mixture, recovery occurs faster and more completely.

With weak respiration, for stimulation of the respiratory center, intramuscular injection of lobeline (0.01) or intravenous injection (0.003-0.006) is recommended; in plethoric subjects in severe cases, bloodletting (200-300 cm³) is recommended, followed by administration of a saline solution; blood transfusion, according to the American commission, is absolutely contraindicated. Otherwise, treatment is symptomatic. In the subsequent period, a more or less prolonged rest in a rest home or sanatorium is required. Various formulas have been proposed by many authors for determining the degree of toxicity of air contaminated with carbon monoxide. The most famous is the formula of Henderson and Haggard: Cxt, where C is the volume content of CO in the air in percent, t is the exposure time, expressed in hours. The physiological effect of carbon monoxide is determined by Henderson from the following equation: Cxt= 300-no noticeable effect, Cxt= 600-quite noticeable effect, Cxt= 900-headache and nausea, Cxt= 1500-dangerous. In a practically more convenient form, these data are presented by the authors in the following table: Table 3. CO Concentrations Parts CO per 1 million parts air Concentration allowing exposure for several hours 400-500 600-700 1,000-1,200 1,500-2,000 4,000-and above Concentration at which inhalation for up to one hour is possible without noticeable effect Concentration causing quite noticeable effect after hourly exposure Concentration causing unpleasant but not dangerous symptoms after hourly exposure Concentration dangerous after hourly exposure Concentration dangerous with exposure for less than an hour. Both this formula and formulas proposed by other authors for establishing the degree of toxicity of air containing CO impurities have a very relative and conditional value, since first, the authors evaluate the entire complex of factors of CO's effect on man only from the point of view of the amount of carboxyhemoglobin that can form, completely not taking into account that with prolonged exposure to small doses, there is undoubtedly a layering of insignificant individual changes of a functional nature, not to mention the possibility of direct effect of CO on protoplasm. Secondly, the amount of CO₂ in the air is completely not taken into account, whose presence, according to a number of authors, increases the toxic effect of CO due to irritation of the respiratory center and corresponding decrease in oxygen content in the air. Thirdly, the nature of the work (degree of physical stress), the role of physical properties of the air, mainly temperature conditions, which have a serious effect both in terms of accelerating CO adsorption and in terms of slowing down CO dissociation, are not taken into account. According to Henderson and Haggard's data, with the same CO content in the air, for heavy work almost three times less time is required to form the same amount of carboxyhemoglobin than for light work. At the same time, according to their data, saturation of the blood with CO up to 10% is the limit, exceeding which may lead to some disturbance of the body's equilibrium; when blood saturation with CO exceeds 10%, signs (though weak) of poisoning may occur. In these experiments by Henderson and Haggard, the duration of exposure did not exceed one hour. In the experiments of Nickl, dogs were exposed to CO for a rather long period of time. The results of these experiments showed that when animals inhaled air containing 0.021% CO (about 0.25 mg per 1 liter of air), the blood was saturated with CO after 30 minutes-5%, after 1 hour-7%, after 2 hours-11%, after 3 hours-17%, after 4 hours-18%, after 6 hours-22%, after 7 hours-22%. Thus, during the first hours of CO exposure, the curve of carboxyhemoglobin formation grows quite rapidly, after the third hour the growth significantly slows down. In any case, after 6 hours of CO exposure, about 20% of the blood is saturated with carboxyhemoglobin. Consequently, even small doses (0.25 mg per 1 liter) with prolonged exposure cause the formation of such an amount of carboxyhemoglobin that can cause signs of poisoning. Under industrial conditions, where exposure to CO is prolonged, this can undoubtedly lead to a number of disturbances, mainly in the activity of the nervous system. Prevention. In the prevention of professional poisoning with carbon monoxide, main attention should be paid to eliminating the possibility of CO entering the air of work premises, which is achieved by proper equipment installation, its sealing, creating as complete as possible exhaust from the place of CO formation or - if this is impossible - by installing powerful supply and exhaust ventilation with a large number of air changes per hour, which makes it possible to reduce CO concentrations in the air of work premises to minimal, non-dangerous values. As such, the Institute of Labor Protection proposed a permissible maximum concentration of CO in the air of work premises of 0.01-0.02 mg per 1 liter, NKT established 0.03 mg per 1 liter. In this direction, significant successes have been achieved in recent years in a number of industries (foundries, forges); thanks to the introduction of improved equipment and ventilation installations, it was possible to achieve CO content in the air within the indicated values or even less, while in outdated and poorly equipped enterprises, values reaching tenths of mg/liter are quite often found.

3. Selyansky, N. Rozenbaum. Poisoning with carbon monoxide most often occurs accidentally; suicides are also observed, especially in France, and very rarely-even murders, mainly of children. In the RSFSR for 1924-25, according to court-medical experts, 325 accidental fatal poisonings with carbon monoxide were registered. It often happens that among persons exposed to the effect of carbon monoxide in the same room and for the same time, some are found dead, while others are only stunned. Here it is necessary to take into account the different susceptibility to carbon monoxide (for example, children are more resistant); in other cases, it was found that the survivors lay closer to the door, to the window, or were at a greater distance from the source of the poisonous gas. It is believed that corpses of persons who died from carbon monoxide poisoning decompose more slowly, muscular rigor mortis is sharply expressed. Postmortem spots are abundant and depending on the change in blood - light red, pink-red color; the dead body appears as if rouged. The blood is mostly liquid, light red, cherry or scarlet color, and therefore all organs take on the same coloration. The bloody dew appearing on the surface of brain section cuts seems almost the color of cinnabar. Small ecchymoses can be found in all organs. If death occurs after a longer time, then degenerative changes occur in parenchymatous organs, and in the brain extravasates and symmetrical anemic foci of "softening in the subcortical areas (in the lentiform nuclei). During court-medical examination of the corpse, the fact of carbon monoxide poisoning is established not only on the basis of autopsy data; chemical and spectral examination of the blood (see below) are also of essential importance. A characteristic spectrum can also be obtained when examining pieces of muscle (pectoral), crushed between glass slides. According to observations by Strassmann, spectral examination gives convincing results only when the blood contains at least 25% carbon monoxide. Cases occur when examination of the corpse gives a negative result, despite carbon monoxide poisoning. This is possible 1) when suffocation with vomit has already occurred in the first moments of poisoning-then during autopsy only signs of asphyxia are observed, the blood is liquid but dark; 2) in the case when death occurred after a long time, after the poisoned person had been removed from the harmful atmosphere; if artificial respiration etc. was applied; carbon monoxide is excreted by the lungs. In court-medical practice, carbon monoxide blood in a sealed tube can be presented as corpus delicti.

V. Vladimirsky. Discovery in legal cases and in professional poisonings. For the detection of O. u. in blood, recourse is had to spectroscopic and chemical investigations. For control in this case, a parallel investigation of 'normal' blood (e.g. from beef liver) is always performed. The blood is diluted with water until two absorption bands in the yellow and green parts of the spectrum are clearly visible upon spectroscopic examination (e.g. with a hand spectroscope of the Browning type or a microspectroscope), between the Fraunhofer lines B and E. In the case of 'normal' blood, these correspond to oxyhemoglobin. The addition of colorless ammonium sulfide produces the reduction of oxyhemoglobin to reduced Hb, which leads to the appearance of one wider band lying between the two former bands. In blood containing carboxyhemoglobin, two absorption bands of carboxyhemoglobin also appear, but comparison shows that the bands do not fully coincide with the bands of oxyhemoglobin. The addition of ammonium sulfide does not lead to the disappearance of the two absorption bands of carboxyhemoglobin, but usually a certain darkening appears between them due to the reduction of the oxyhemoglobin that still remains in the blood in greater or lesser quantity. The chemical investigation is based on the stability with which blood containing carboxyhemoglobin retains its pink (or light red) coloration in the diluted state after the addition of reagents that destroy the blood pigment of 'normal' blood (concentrated solution of caustic soda, solution of tannin, yellow blood salt, basic lead acetate, formalin, etc.). It is convenient to moisten filter paper with diluted blood and apply the corresponding reagents to it, making a comparison with normal blood. For the detection of O. u. in air, the latter is drawn through a diluted solution of beef blood, which is then examined by the methods described above. For the quantitative determination of O. u., numerous methods have been proposed, all leading to reliable results. For the quantitative determination of O. u. in blood, the O. u. is displaced by oxygen-free air (the latter is passed through washing bottles with a suspension of iron hydrate) and absorbed by appropriate reagents (see below) or the blood subjected to the action of reagents is compared with standard solutions of blood containing definite amounts of O. u. and mixed with the same amounts of reagents. There are methods based on measuring the displacement of the absorption band in the investigated and standard blood. Methods for the quantitative determination of O. u. in room air (and in the air displacing O. u. from blood) are based on the oxidation of O. u. to carbon dioxide and on the determination of the latter or on the reduction of metals from solutions of their salts (or oxides) by carbon monoxide. Such is the reduction of metallic silver from a titrated solution of silver nitrate upon the addition of caustic soda and an excess of pyridine (or ammonia), followed by the determination of the titer of the remaining silver in the solution.