Lead

Lead common (Plumbum), symbol Pb, a mixture of isotopes, atomic weight 207.22 (atomic weight of uranium lead 206.05, thorium 207.9). Besides these isotopes, there is also lead with atomic weight 207. The ratio of isotopes in ordinary lead is 206:207:208 = 100:75:175. In negligible quantities, there is apparently a fourth isotope with atomic weight 209. Its place in the periodic system is the 9th row, Group IV. Lead is found in nature mainly in the form of galena (PbS) of the regular system, less frequently in the form of cerussite or white lead ore (PbCO₃) of the rhombic system, pyromorphite or green lead ore [Pb₅(PO₄)₃Cl] of the hexagonal system, as well as mimetite {Pb₅(AsO₄)₃Cl} and vanadinite [Pb₅(VO₄)₃Cl]; wulfenite (PbMoO₄) of the square system, isomorphous with stolzite (PbWO₄), and crocoite (PbCrO₄) of the monoclinic system. In the USSR, lead is mined in the following deposits: in the North Caucasus region (Sadon mines), in Kazakhstan (Ridder mines). Near the village of Tetyukh in the Far Eastern region, metallic lead is obtained by smelting from pre-concentrated (in special "concentration" plants) ore. Commercial lead is almost entirely extracted from galena, which is roasted in a strong air stream along with limestone and quartz. PbS oxidizes according to the reactions: 2PbS + 3O₂ = 2PbO + 2SO₂; PbS + 2O₂ = PbSO₄; PbSO₄ with added quartz gives lead silicate PbSO₄ + SiO₂ = PbSiO₃ + SO₃. The resulting products and the lime formed from limestone are reduced with coke at high temperature; lead oxide gives lead, and lead silicate gives lead and calcium silicate PbO + CO = Pb + CO₂; PbSiO₃ + CaO + CO = CaSiO₃ + Pb + CO₂. In the electrolytic method, the anode is the bottom of lead plates containing dilute sulfuric acid, and the cathode is powdered galena. Hydrogen released at the cathode reduces lead, sulfur gives the gas H₂S. Physicochemical properties. Lead is a bluish-gray metal, its surface tarnishes quickly in air; lead is soft, can be cut with a knife, and has little ductility. Melting point 327°, boiling point 1540°, specific gravity 11.36-11.39; it crystallizes well, precipitating on a zinc or iron plate dipped in a solution of a lead salt. Lead dissolves in dilute nitric acid to form lead nitrate Pb(NO₃)₂ and nitrogen oxides. In air, in the presence of moisture, all acids act on lead slowly. Lead has wide applications: water pipes, numerous instruments for the chemical industry, and lead storage batteries are made from it. Lead sheets are used for the construction of sulfuric acid chambers, lead tubes for covering electrical cables; lead is a component of type metal, which contains, in addition to lead, about 25% antimony and small amounts of tin and bismuth. So-called solder contains about 50% tin and melts at a low temperature. Lead paints are common: white lead, red lead, etc. In compounds, lead is divalent and tetravalent. Of the divalent compounds, the most important are: 1) Lead oxide (PbO), formed by the oxidation of molten metal by atmospheric oxygen; in the solid, fused state it has a yellowish-red color and is called lead litharge; the yellow, powdery form of PbO is called massicot. The latter, when heated in air (at 470-480°), converts to Pb₃O₄, called red lead. At higher temperatures (above 550°), red lead decomposes in air with the release of free oxygen: 2Pb₃O₄ = 6PbO + O₂. 2) Lead nitrate Pb(NO₃)₂ is soluble in water: at 10°, 48 parts Pb(NO₃)₂ dissolve in 100 parts water; it easily forms basic, water-insoluble salts. 3) Lead acetate, white in color Pb(C₂H₃O₂)₂, when well dissolved in water, gives a sweet-tasting solution (lead sugar); when heated with lead hydroxide, it gives a basic salt Pb(OH)(C₂H₃O₂). 4) Lead sulfate (PbSO₄) - a white crystalline powder, found in nature as the mineral anglesite; insoluble in water, but noticeably soluble in concentrated H₂SO₄ and in concentrated NaOH solution; easily soluble in ammonium tartrate. 5) Lead carbonate (PbCO₃) - insoluble in water. In the form of a basic, finely ground salt [Pb(OH)₂ · 2PbCO₃], it is a component of white lead. 6) Lead chromate (PbCrO₄) - insoluble in water; a yellow pigment.--All lead paints in residential premises darken over time due to the formation of black lead sulfide (PbS). With the gas H₂S, lead compounds react, both in dry form and in solution, forming PbS, which is soluble in nitric acid. 7) Lead chloride (PbCl₂) - a white crystalline powder, slightly soluble in cold water and much more so in hot water. Tetravalent lead compounds are significantly less common. The most important of these is lead dioxide, or dioxide PbO₂ - a dark brown powder, easily decomposed by concentrated acids with the formation of divalent lead salts: 2PbO₂ + 2H₂SO₄ = 2PbSO₄ + H₂O + O₂. Tetravalent lead compounds are strong oxidizing agents. Qualitative reactions for the lead ion are the formation of lead sulfate, lead sulfide, and lead chromate. These same reactions are also used for quantitative determinations. Microchemical determination is carried out in the form of lead iodide PbI₂, precipitating when a crystal of KI is added to the solution in the form of lemon-yellow crystals of triangles with blunt angles. An even better reaction is the precipitation of lead in the form of the triple nitrite salt of potassium, copper, and lead-K₂PbCu(NO₂)₆, which forms as greenish-brown, almost black cubic crystals. Small amounts of lead are determined quantitatively: I. By the electrolysis method - by passing a current of about 0.5-1A at a voltage of 2-2.5V through a solution of lead nitrate acidified with nitric acid. At room temperature, the electrolysis lasts 2-3 hours. If there is a sufficient amount of nitric acid (20-30 cm³ of concentrated HNO₃ per 150-200 cm³ of solution containing not more than 0.5 g Pb), all lead is deposited as dioxide on the anode. II. Colorimetrically - in drinking and waste waters: after isolating lead as PbSO₄, it is dissolved by heating in a solution of ammonium acetate; it is acidified with acetic acid and transparent hydrogen sulfide water is added to the test liquid and to a standard solution of lead nitrate [1.6 g Pb(NO₃)₂ in 1 liter, i.e., 1 mg Pb in 1 cm³]. The resulting brown-colored liquids are compared in a colorimeter or in Gernov cylinders. III. Nephelometrically - in urine. The daily amount of urine is treated with heating with a 5% solution of soda (1 cm³ per 100 cm³ of urine). The precipitated flocculent sediment containing lead is filtered off, washed with a soda solution, and quantitatively transferred to a Kjeldahl flask. Mineralization is carried out by heating with a mixture of sulfuric (5 cm³) and nitric acids in the presence of perhydrol. After cooling, 6 cm³ of water and 20 cm³ of alcohol are added to the colorless liquid. After filtering and washing the lead sulfate with alcohol, it is dissolved in 5 cm³ of a 30% solution of ammonium acetate; after 30 minutes, it is filtered into a 25 cm³ volumetric flask, the filter is washed with water, the liquid is acidified with acetic acid, and 3 cm³ of a 5% solution of potassium chromate (K₂CrO₄) is added to it and to the standard solution (0.1570 g of lead acetate in 1 liter, i.e., 0.0001 g of Pb in 1 cm³). It is brought to volume with water and the degree of turbidity is compared in a nephelometer. The concentration of lead in the test solution is found by the formula: C_x = C_s · d/d_x, where C_s and C are the concentrations of lead in the test and standard solutions, d_x and d are the heights of the liquid columns in the nephelometer.

Lead. Sevorin. Lead preparations. In medicine, certain salts of lead are used. Pharmacologically, Lead belongs to the group of heavy metals and acts only in the form of ions. It has both local and general effects. For therapeutic purposes, organic acid salts of lead are used for local action. These salts are applied in solutions and ointments to mucous and wound surfaces for their astringent effect. Easily released Lead ions form insoluble albuminates with tissue proteins, covering the surface of the mucous membrane or wound with a thin film, causing constriction of nearby vessels. The surface becomes drier, serous infiltration of tissue disappears, swelling and pain sensation decrease. At the same time, the vital activity of bacteria is suppressed and cytolytic enzymes of inflammation are bound. Organic acid salts are used because their anion has almost no effect on tissues, whereas with inorganic acid salts, the effect of their anion must be taken into account. Having a well-expressed astringent effect even at solution concentrations of 0.01%, Lead salts have the weakest cauterizing effect among heavy metals: it is usually observed at concentrations not lower than 5%. Lead is usually not administered internally. Due to its weak irritating properties, when large quantities are taken, vomiting (reflex), diarrhea, and collapse may occur. The resorptive effect of Lead has no therapeutic value. Attempts to use lead intravenously for cancerous diseases must be considered unsuccessful. Preparations: 1) Saccharum Saturni, s. Plumbum aceticum depuratum, lead sugar (Ph. VII)-Pb(C2H3O2)2+3H2O-basic lead acetate. Colorless, translucent crystals smelling of vinegar. Soluble in water. Have a sweetish taste. Used for preparing ointments. Sometimes given internally for its astringent effect on the intestines, cautiously and for a short time due to the possibility of chronic Lead poisoning. Dose 0.06 (0.25). Externally for mouthwash (0.1:100.0); however, this is not recommended as Lead poisoning is possible; in the form of suppositories for hemorrhoids, in eye drops, lotions, and ointments. 2) Plumbum oxdatum, s. Lithargyrum (Ph. VII)-Lead oxide PbO. Used only externally for making plasters, poultices, and ointments. 3) Plumbum aceticum basicum solutum, s. Acetum Plumbi, s. Liquor Plumbi acetici-lead vinegar (ФУП). Composition: 180 parts lead sugar, 110 parts Lead oxide, water q.s.; colorless, transparent liquid, sp. gr. 1.248, alkaline reaction to litmus; contains 18% Lead. Turns cloudy on air from contact with CO2. Used for making lotions A°q. Plumbi. 4) Aqua Plumbi-1 part PI. acet. basici, 49 parts Aq. dest.; for lotions in pure form or mixed with water. 5) Emplastrum lithargyri, s. Empl. diachylon simplex, s. Empl. Plumbi simplex (ФУИ), diachylon plaster, or simple Lead plaster. Consists of equal parts of linseed oil, lard, Lead oxide, and water q.s. Used externally as a protective, non-irritating plaster, and also as a base for many other plaster mixtures; when Lead plaster is mixed with white vaseline (equal parts), Lead ointment of Hebra is obtained ex tempore, used in eczema, acne, and other skin lesions. 6) Emplastrum Plumbi compositum, s. lithargyri compos., s. diachylon compositum (Ph. VII)-compound Lead plaster, gummatous plaster. Composition: 85 parts simple Lead plaster, 10 parts rosin, 5 parts turpentine. Used in furunculosis and boils to accelerate the "ripening" of the boil by its irritating effect. 7) Emplastrum adhaesivum (Ph. VII) adhesive plaster. Composition: 100 parts Lead plaster, 10 parts yellow wax, 10 parts rosin, 10 parts anhydrous lanolin, 10 parts dammar resin, 10 parts larch turpentine. Used for securing bandages. 8) Emplastrum saponatum (Ph. VII), soap plaster. Composition: 70 parts Lead plaster, 10 parts white wax, 5 parts powdered medical soap, 1 part powdered camphor, 2 parts oil of Provence. Slightly irritating plaster; used for boils and bedsores. 9) Unguentum Plumbi subacetici, Lead ointment (Ph. VII). Composition: 55 parts wax ointment, 25 parts anhydrous lanolin, 10 parts solution of basic lead acetate, 10 parts glycerin. Protective ointment, reducing irritation, cooling; used in chilblains, bedsores, excoriations, etc. 10) Unguentum Plumbi tannici (Ph. VII), bed sore ointment. Composition: 5 parts tannin, 10 parts solution of basic lead acetate, 10 parts anhydrous lanolin, 40 parts yellow vaseline.

Vasiliev. Lead as an industrial poison. In industry, lead is used in its pure form, as well as in the form of various oxides and other compounds. During smelting of lead, massicot and litharge - lead oxide - are formed; when the latter is heated in closed furnaces, red lead is obtained; these compounds are widely used in a number of industries and in painting. Further used are: brown lead peroxide, lead sulfate, basic lead carbonate - lead white - of variable composition [approximately Pb(OH)₂·2PbCO₃], basic lead sulfate with varying Pb(OH)₂ content, lead chromate, lead acetate Pb(C₂H₃O₂)₂, halogen compounds - lead chloride, lead iodide, lead nitrate, recently introduced into use, possessing a specific effect on the organic compound of lead - tetraethyl lead, etc. The number of industries where lead and its compounds are used in one form or another is exceptionally large. As early as the 1880s, Layet listed about 150 industries; at present, their number is counted at about 120, while the number of workers dealing with lead amounts to many tens and hundreds of thousands. Among the industries where lead as an industrial poison plays the most important role, the following can be mentioned: work in mines - ores containing sulfur and carbon compounds of lead, which are more easily soluble in the body than sparingly soluble lead sulfide; but the latter also dissolves in the body's juices and causes poisoning of miners. The number of poisonings here is quite large: in Utah (USA) among workers in lead mines, 468 cases of poisoning were registered in 1919-20. - Smelting of lead and silver from ore. Almost all factory work involves the release of dust containing a lot (25-47%) of lead, evaporation of lead occurs from furnaces, etc. - Zinc smelting. In sphalerite there is 4-6% of lead, which is released along with smoke. In zinc plants in Silesia, American and others, cases of lead poisoning were observed, especially in previous years (e.g. in Opole for the years 1902-12, 28-69 cases annually). - Production of litharge and red lead - during roasting, sifting and packing, a large amount of dust is released. Many cases of poisoning occurred before the war in small-scale red lead factories of the Kostroma province (Glebovsky, Gurev, Gusev), in recent years the situation has significantly improved. - Production of lead white - one of the most dangerous industries (see Paints, professional hazards of paint production), painting - see Painters; production of accumulators - see Accumulators, accumulator production; porcelain and faience production and pottery production - see Ceramic production, professional hazards, see Printing industry. - Saw files. The linings used here until recently contained 20-85% lead. During sawing, dust is released, and when files are quenched in a lead bath (t° 850°), lead evaporates. Despite the small number of workers employed here, in England for 1900-09, 211 cases of poisoning were registered, of which 9 were fatal. - In recent years, a new work has emerged where many cases of poisoning occur, namely the scrapping of old ships; during autogenous cutting of the iron hull (t° 3,000°), the lead covering it evaporates (in Kiel, 56 mg of lead was found in 1 m³ of air). To the industries and works where a relatively small number of workers are exposed to poisoning hazards, sometimes quite significant, should be included galvanizing, soldering, tinning, glass production (grinding and faceting of special types of glass), shot production, production of lead chromate and other lead-containing paints, tin mining, production of lead plates and pipes, wind musical instruments, brass production, canneries, production of lead nitrite and many others. Tetraethyl lead is finding increasingly wider use recently as an additive to fuels used for internal combustion engines (automobiles, airplanes, etc.). It is an oily liquid that evaporates easily even at medium temperatures. It penetrates the body through the lungs and skin and is extremely toxic. The numerous poisonings observed when it was introduced into industry, many of them fatal, led in America even to a temporary ban on the use of this substance. In garages, ethyl fluid is used, consisting of 3 parts of tetraethyl lead and 1 part of ethylene bromide. This fluid is added to gasoline in the ratio of 1-2:1,300. In the last 2-3 years, tetraethyl lead has begun to find increasingly wider use in the automotive industry in our country as well and has already become the source of some observed poisonings. The toxicity of this compound is due to its volatility and solubility in lipoids, which ensures its rapid entry into the body (through the respiratory tract) and penetration without any delay into the great circle of circulation, and from there into the central nervous system. Therefore, in the clinic of tetraethyl lead poisoning, disturbances of the central nervous system come to the forefront. Statistics of professional lead poisoning. If one takes into account the prevalence of lead in industry, it becomes quite clear why the number of cases of lead poisoning ranks first among poisonings by industrial poisons everywhere, in some countries exceeding several times the number of poisonings by all other poisons taken together. We present some data on the most important European countries where mandatory registration of professional poisonings has been introduced. In England, where registration began in 1900, the number of lead poisoning cases in recent years fluctuates within 250-350 per year, with the number of fatal poisonings being 25-45. - Germany. Mandatory registration was introduced in 1925. The number of lead poisoning cases was: in 1926 - 3,129, in 1927 - 3,329, in 1928 - 3,424, in 1929 - 3,456, in 1930 - 2,055. The year 1930 showed a decrease compared to previous years due to a reduction in the number of workers due to the crisis. - Belgium. From July 1927 to 1928, 73 cases were registered, in 1929 - 55 cases, in 1931 - 75, in 1932 - 71 (the number of lead poisoning cases constitutes 95% of all cases of poisoning subject to compensation). - France. Mandatory registration was introduced in 1915. The number of lead poisoning cases was: in 1921 - 144 cases, in 1922 - 797, in 1923 - 1,095, in 1924 - 1,249, in 1925 - 1,343, in 1926 - 1,505, in 1927 - 1,040, in 1928 - 1,525, in 1929 - 1,846. Here there is a steady increase in the number of lead poisoning cases, and in 1929 their number constituted 90% of the total number of registered occupational diseases. In the USSR, mandatory registration of cases of occupational injuries and diseases was introduced in 1924. The number of lead poisonings was: in 1924/25 - 216 cases, in 1925/26 - 364, in 1926/27 - 354, in 1927/28 - 332, in 1928/29 - 316. In the first year of registration of poisoning cases in the USSR, it was very incomplete, and the established work in this direction by labor authorities gave a significant increase in the number of registered cases in the following year. However, starting from the second year of registration, thanks to the systematically conducted struggle in the USSR against occupational saturnism, we have a gradual decrease in the number of lead poisonings, despite the fact that from year to year the number of workers employed in production, and in particular in lead work, has increased enormously. These figures express the achievements in the field of combating occupational lead poisoning that we have in our Union. In recent years, a number of industries in the USSR have turned from so-called 'lead' industries into 'lead-free' ones due to the complete replacement of lead materials with harmless substances (in painting, file production, etc.). But it should be borne in mind that the above statistical data from all countries speak only about the number of registered poisonings, and the latter by no means corresponds to their actual number, which is undoubtedly much larger. The diagnosis of lead poisoning in chronic cases presents great difficulties, and mildly expressed cases are easily missed by doctors; besides clear forms, there are many metatoxic ones, often developing after cessation of work with lead, and the number of unaccounted lead poisonings in the USSR is undoubtedly less than in capitalist countries due to the specific features of the Soviet health care system. Besides occupational poisonings, lead also causes frequent individual and mass poisonings in domestic conditions. Sporadic and mass cases of lead poisoning have been described in persons using earthenware, the glaze of which contains a lot of lead - the latter can dissolve and pass into food, especially if the latter contains acid or alkali. Both in foreign and Russian literature, such cases have been described repeatedly (e.g. the article by Labinskaya - 1,410 cases in 2½ years, in Siberia - 102 cases, in Bryansk - 17 cases, etc.).

Furthermore, many cases of poisoning occur from using water that passes through lead pipes (in 1913 in Leipzig, about 1,000 people were poisoned), etc. Pathways of Lead entry into the body. Lead can enter the body through the skin, the digestive tract, and the respiratory organs. Under industrial conditions, the skin represents the least danger, since under normal conditions the absorption of Lead through intact skin is insignificant and has no practical significance (Siissmann). The digestive-tract as a gateway for Lead presents much greater danger. In an industrial setting, entry of Lead through the digestive tract occurs when dust is swallowed; furthermore, it is possible when food is taken in the workplace, when smoking, and when drinking. Lead compounds that enter the intestine are first converted into chlorides, and then into peptonates and albuminates. In addition to absorption in a dissolved state, Lead can enter the lymphatic system in the form of the smallest particles by impregnating the intestinal epithelium. As for the respiratory tract, based on numerous experimental works and clinical observations, the special danger of the respiratory tract as a gateway for the entry of Lead and its compounds into the body has been confirmed. Here there are the most favorable conditions for the absorption of Lead into the body both in terms of its dissolution and its direct entry into the systemic circulation. The entry of Lead into the deep parts of the lungs (bronchioles and alveoli) is of very great importance. The amount of Lead that reaches here depends on the size of the particles of lead dust: the finer the latter, the more of it penetrates into the deeper respiratory passages. However, it should be borne in mind that lead compounds are relatively well absorbed through the mucous membrane of the upper respiratory tract. The fate of Lead in the body. In the blood, Lead circulates in the form of colloidal albuminates and phosphates. From the blood it is deposited in various organs, mainly in the liver, spleen, lungs, kidneys, etc.; but from these organs a significant amount of Lead is eliminated from the body with feces and urine, and the remaining Lead is redistributed—the main amount is deposited in the bones, much smaller amounts—in the liver, spleen, and others. Kehoe and Thamann, when examining the organs of a number of people who worked with Lead and died from various diseases, found Lead throughout the body: in one who had stopped working with Lead 8 months before death—240 mg, 2 years before death—135 mg (the same amount—135 mg—was found in a young person who had never worked with Lead). Lead immobilized in the bones, deposited here in the form of insoluble trimetaphosphoric acid compounds, can be mobilized under the influence of metabolic disturbances; in particular, under the influence of a shift of the acid-base balance in the acidic direction, these compounds pass into soluble dimetaphosphoric acids, which again enter the bloodstream and can cause an outbreak of lead intoxication. This explains the very frequently observed cases of lead crises that develop after more or less a long time after the worker has left the lead production. Excretion of Lead from the body. Like all heavy metals, Lead is excreted from the body through the intestine, kidneys, and glands of the digestive tract. The amount of Lead excreted during the day is in close dependence on the amount of Lead introduced and therefore can fluctuate within wide limits: from 0.1-0.2 mg to 7.5 mg and more. With urine, no more than ¹/₁₀-₁/₅ of this amount is excreted, the rest is removed through the intestine with feces. Recent research has established that Lead is also excreted in healthy persons, and its source is Lead introduced with food (according to Kehoe and others, the amount of Lead introduced into the body of a resident of American cities with food and drink per day is 0.16-0.28 mg). The same authors established that if the amount of Lead in the daily feces does not exceed 0.2 mg and in 1 liter of urine 0.05 mg, all this Lead should be considered of food origin; with corresponding amounts exceeding 1.0 mg and 0.20 mg, the question of the professional origin of Lead can be answered affirmatively. Toxicity of various Lead compounds. Various lead compounds have different degrees of solubility; on this basis an attempt was made to establish their degree of toxicity and to isolate non-toxic compounds. However, such isolation is not sufficiently substantiated: lead compounds that are slightly soluble in water can easily become soluble in blood, lymph, tissue fluid, gastric and intestinal juice, etc. This applies to such compounds as lead sulfate, lead white, and lead red. Recently, the solubility in the lungs of very insoluble lead sulfide, etc., has been proven. The physical properties of the Lead entering the body and the pathways of entry play a very large role. The smaller the Lead particles, the greater the danger they represent to the body. In this respect, lead white is especially dangerous, the particles of which have a size of less than one micron; furthermore, particles of 'lead smoke' formed by processing at high temperatures, which oxidize in the air, turn into the finest colloidal suspension (particle size less than 0.5 μ).-Toxic doses. The question of the maximum allowable concentrations of Lead in the air of workplaces finds no resolution in the vast existing literature on Lead. According to different authors, Lead poisoning, which always occurs as a chronic condition, sets in at different concentrations at different times. However, none of the authors, except Gertner, mentions doses that are harmless to the body when Lead is systematically taken over a long period. Flury and Zanger consider this question insufficiently clarified. Nevertheless, they admit that on average the daily intake of 10-20 mg of Lead for several months leads to severe poisoning. Legge and Godby believe that when at least 2 mg of Lead is absorbed per day for a year, poisoning occurs. At the same time, they point out that even at very low concentrations of it in the air (less than 0.5 mg per 1 m³), cases of poisoning (colic) can be observed in workers. Teleki considers the absorption of 1 mg per day sufficient to get poisoning after several months; 10 mg, in his opinion, can cause poisoning after just a few weeks. The American National Safety Council has nevertheless set a limit for Lead at 0.6 mg/m³ for the air of a workplace. Taking into account the cumulative property of Lead, as well as the circumstance that workers are in contact with Lead for many years, and considering that among workers in lead productions, where the concentration of Lead in the room air is insignificant (printing houses, cable production, soldering, tinning), cases of poisoning are often observed, it should be recognized that the minimum content of lead (fractions of mg/m³) does not guarantee protection from lead poisoning for persons working under these conditions, and in this sense the permissible daily intake of 0.35 mg of Lead mentioned by Gertner cannot be considered harmless for workers. Chronic poisoning. Under industrial conditions, almost exclusively chronic lead poisoning occurs (which however can sometimes give acute crises). Lead acts on various organs and systems. From the combination of these effects the clinical picture of lead poisoning is formed. In the first place are changes in the blood. Lead is a hemolytic poison. It lowers the resistance of erythrocytes and shortens their existence. Increased breakdown of erythrocytes leads to the accumulation of hemolytic bilirubin in the blood, i.e., bilirubin giving an indirect reaction according to v. d. Bergh, which causes a subicteric coloration of the sclera. With sufficient intensity of hemolysis, an increased amount of urobilin is found in the urine. Breakdown products of Hb cause an enhanced regenerative function of the bone marrow, expressed by an increased number of reticulocytes (young forms of erythrocytes), which can reach 50-100 per 1,000 (instead of the normal 2-4%). Along with them, basophilic granular erythrocytes are found. In normal blood, the latter are encountered only rarely (according to Schmidt not more than 1:10,000 erythrocytes); in lead poisoning their number can reach 5-10 or more in each field of view. Basophilic granular erythrocytes are not absolutely pathognomonic for lead poisoning; they are also found in other poisonings—by arsine, benzene, etc., as well as in some diseases (hemolytic jaundice, pernicious anemia, malaria, etc.). However—in lead intoxication they usually appear early and in large numbers and serve as an important aid in the diagnosis of lead intoxication, especially in its early stage. Along with basophilic granular erythrocytes, polychromatophils and sometimes normoblasts are found in the blood. Despite hemolysis, the Hb level and the number of erythrocytes, with sufficient compensatory function of the bone marrow, can remain for a long time at a rather high level.

However, sooner or later the compensatory activity of the bone marrow becomes insufficient, and then we see a very pronounced lead anemia with a drop in Hb to 50% and less. Anemia always has an oligochromic character (the color index drops to 0.6-0.5). The very mechanism of the formation of basophilic erythrocytes is controversial. Some consider them a manifestation of impaired bone marrow function (pathological regeneration), while others believe they are the result of the harmful effect of lead on the erythrocytes themselves in the blood. Under the influence of lead, there is a quantitative but also qualitative disturbance of the pigment metamorphosis. In the urine of lead patients, hematoporphyrin appears, which under normal conditions does not form at all or forms only in small quantities (not exceeding 0.1 mg per 1 liter, according to Gunther). In lead patients, the amount can reach 3-4 mg per 1 liter. According to the scoring system proposed by Lavrovsky, the amount of hematoporphyrin in lead poisoning reaches 10-16 or more points instead of the highest normal limit of 4 points. Hematoporphyrin is also excreted with the feces, but its amount has not been determined here. In its nature, the hematoporphyrin excreted with the urine in lead poisoning can be characterized as coproporphyrin. Hematoporphyrinuria, indicating a severe disturbance of pigment metabolism, is one of the most important symptoms of lead poisoning. However, there is no complete parallelism between the accumulation of hematoporphyrin and the severity of lead poisoning. The difference between lead hematoporphyrinuria and genuine porphyria is the excretion of coproporphyrin in the former, while in the latter, along with coproporphyrin, uroporphyrin is excreted. However, this difference loses its fundamental significance after Fischer showed that in the body it is possible for coproporphyrin to be converted into uroporphyrin. Reitlinger and Kohle in an experiment on the isolated intestine of a cat, rabbit, and guinea pig showed that the most pronounced spasmogenic effect on the intestine belongs precisely to coproporphyrin. All this gives the right to include lead crises in the group of crises observed in other hematoporphyrinurias. From the side of the digestive organs, one should first note the very frequently encountered (however, by no means always) lead line. The latter represents a lilac-gray-gray stripe, 0.5-1.0 mm wide, running along the free edge of the gums. Sometimes it is found only on the projections of the gums between the teeth. On the mucous membranes of the cheeks and lips, gray-lilac spots similar to the lead line are often noted. The general color of the mucous membranes has the same gray-lilac tint. The lead line, as well as the gray-lilac color of the gums, is not an invariable symptom of lead poisoning: it may be absent in very severe forms of the latter, and conversely, be present in asymptomatic forms of lead invasion. It is formed due to the excretion of lead from the papillary capillaries; combining with hydrogen sulfide, which is always present in the oral cavity (especially in the presence of decayed teeth), lead turns into black insoluble lead sulfide, to which the peculiar color of the line is due. The lead line and the gray-lilac color of the gums are only a symptom of the circulation of lead in the body, of contact with it (invasion), and not of lead intoxication. Among other lesions of the oral cavity, alveolar pyorrhea and gum loosening have been noted in lead workers, which is also explained by the irritating effect of the excreted lead. From the side of the stomach, dyspeptic phenomena (loss of appetite, heaviness after eating, belching, etc.) and secretory disturbances, both in the direction of increased and decreased acidity, are often noted. Some researchers noted a somewhat higher frequency of stomach ulcers in lead workers, which can be explained by nervous-secretory disturbances. In chronic lead intoxication, intestinal disturbances are sometimes observed: abdominal pain, slight constipation, etc. However, these phenomena usually do not reach a significant degree. One of the most severe manifestations of lead intoxication is lead colic (colica saturnina). Lead colic mostly develops unexpectedly, like a real crisis. It is often preceded by prodromal phenomena: pain in the lower back, in the muscles, loss of appetite, metallic taste in the mouth, slight manifestations of stomatitis, increased salivation, insomnia. Following this, severe spasmodic pains appear, mainly in the upper and middle parts of the abdomen. The pains are somewhat relieved by pressure; the abdomen is drawn in, the abdominal walls are often board-like tense. Simultaneously with the pains, constipation appears, which does not yield to any measures. Vomiting is often observed. The pulse is slow and tense (40-50 per minute); blood pressure rises to 200 mm and higher. The amount of urine decreases, sometimes anuria develops: traces of protein, single cylinders in the urine. From the side of the neuropsychic sphere, headaches, insomnia, depressed state, sometimes muscle twitching and a slight increase in temperature (37.3-37.8°C) are noted. The duration of the attack varies from 3-5 days to 9-14. The end of the attack is marked by the appearance of a stool, first scanty, then abundant, after which all symptoms immediately disappear or sharply ease. Sometimes recurrences of lead colics are observed, which, however, have a shorter course. X-ray studies indicate a pronounced spastic-atonic state of the stomach and intestines. We do not always have to deal with such typical colic attacks. Often colics acquire a longer and less bright course. There are chronic intermittent colics that drag on for months, disappearing when leaving lead production. The less typical the course of lead colic, the more often there is a falling out of one symptom or another. Therefore, the absence of a rare pulse or elevated blood pressure does not rule out the possibility of lead colics in these atypical cases. Lead colic often gives rise to confusion with acute appendicitis, with gallstone and renal colics, acute spastic colitis, etc. The causes of lead colic have not been fully clarified. Some explain lead colic by vascular spasm leading to ischemic contracture of the intestinal walls, while others see its cause in inflammatory changes (endarteritis) and petechial hemorrhages (Legg and Godby). The effect of lead on the nervous system can go in two ways: peripheral lesions and lesions of the central nervous system. Peripheral disturbances are expressed in polyneuritis leading to paralysis. In most cases, these paralyses develop on the extensors of the fingers and hands, the latter acquiring the appearance of a 'hanging hand'. Usually, the process begins with paralysis of the extensors of the index finger and little finger, more often of the right hand than the left. The weakness of the extensors of the hand noted by many authors as an early symptom of saturnism does not have the significance attributed to it. Usually it develops together with polyneuritis, i.e., when there are already other more objective signs of saturnism. Paralyses can also involve other muscle groups: shoulder muscles (deltoid, biceps, long supinators, supra- and infraspinatus muscles). This is the so-called shoulder type of Remak. Aran-Duchenne distinguished a third type of lead paralysis (see Aran-Duchenne's hand). In children, paralysis of the peroneal muscles is observed. Neuritis of the optic nerve leads to a sharp deterioration of vision, amblyopia (see). Usually lead neuritis is not accompanied by pain. However, exceptions are possible. When removed from production, the paralyses mostly disappear, however, the period of recovery often drags on for weeks and even months. In addition to lesions of the peripheral mixed nerves, sometimes (rarely) lesions of the optic nerve leading to persistent or temporary blindness, lesions of the auditory nerve, etc., are observed. The most dangerous manifestation of lead intoxication is lead encephalopathy. Usually it develops after more or less prolonged prodromal phenomena: headache, irritability, poor sleep, deteriorating mood. Sometimes it is preceded by lead colic. In the most atypical cases, the onset of encephalopathy itself is acute. Consciousness is suddenly lost, seizures begin, periodically recurring. The disease ends within 2-3 days in a comatose state and death. In other cases, encephalopathy is expressed in epileptiform seizures. After one or more such seizures, complete recovery may occur. In some cases of lead encephalopathy, phenomena of psychic excitement are observed. The difference in the course of encephalopathy often depends, besides constitutional factors, on the additional effects of other poisons (alcohol). In recent years, due to the general improvement in working conditions and the introduction of a number of sanitary-technical measures, lead encephalopathy has become very rare.

Along with these clearly expressed severe forms of lead encephalopathy, which give a high percentage of mortality, mild chronic forms are often observed, proceeding according to the type of lead neurasthenia. The mechanism of development of lead encephalopathy has not been established. Apparently, there is a change in the chemistry of brain tissue, as well as the direct toxic effect of lead on nerve cells. The effect of Lead on the cardiovascular system. While Legg and Godby placed vascular changes at the center of all the pathology of lead poisoning—obliterating endarteritis of small vessels, pinpoint hemorrhages—the clinical picture rarely encounters clearly expressed cardiovascular changes that could be associated with the influence of lead. Of the violations observed in the clinic, one can note a tendency to spastic states, which can explain transient amauroses, dizziness, a special pallor with good hemoglobin (lead color). The hypertensions described by some authors, developing under the influence of prolonged exposure to Lead, we have not observed. On the contrary, there is even some tendency to hypotension. Hypertensions are only companions of lead colic and have a transient nature. There are many indications of the possibility of developing obliterating endarteritis, as well as early arteriosclerosis, especially of the brain, in lead workers. The effect of Lead on the kidneys can go in two ways: through the effect of excreted lead on the renal parenchyma and through the effect of lead circulating in the bloodstream on the vessels. Fahr and Folgard described shrunken lead kidneys. The arthralgias described earlier, which old authors called lead gout, now almost never occur. Acute poisonings are expressed in rapidly developing confusion, in a sharp loss of memory, ingenuity, a special childishness and primitiveness of the psyche and motor skills. Patients are poorly oriented, get to the wrong place where they are heading, cannot remember moments of the poisoning that occurred. They complain of headaches and suffocating nightmares and hypnagogic hallucinations at night. Along with this, from the somatic side, salivation, sweating, bradycardia, pallor of the skin are noted, not corresponding to the hemoglobin level. All this is suddenly interrupted by complete disorientation, severe psychic and motor agitation, often of a violent nature. After multiple such attacks, sometimes accompanied by prolonged convulsions, sudden death occurs. Often the course of poisoning takes a chronic character: headaches, special sensations (something is turning in the head), heavy nightmare dreams, often occurring immediately after the patient closes his eyes, memory loss, childishness of psychic manifestations, fussiness, tremor, decline in intellect. Among the somatic phenomena, pains under the xiphoid process are noted, sometimes of a colicky nature, however, not accompanied by constipation and less severe than in ordinary lead colics, weight loss, changes in blood (basophilic-granular erythrocytes), an increase in the number of reticulocytes with a slightly reduced Hb level. Changes in blood may not be sharply expressed even in severe poisonings; the amount of hematoporphyrin often remains at a low normal level. Lead is found in the urine. Sometimes the disease proceeds under the picture of schizophrenia. With a milder course, headaches, heavy dreams, weakness come to the forefront, which are the leading symptoms for the entire this group. Among the vegetative symptoms, one can note salivation, sweating, a decrease in temperature, especially in acute and subacute cases (35.5°C), bradycardia (40-50 beats per minute). The course of poisoning is very long, recovery occurs slowly and is often unstable. Prevention. The most radical health measure is the complete elimination of Lead, which for some productions can be carried out (and partly has been carried out) already at the present time. So for example in the production of files, lead linings, which caused a significant number of poisonings, since 1927-28 in the USSR have been replaced by zinc linings, as a result of which the danger of lead poisoning in this production immediately disappeared. The replacement of white lead with other—zinc, titanium, lithopone, etc.—is possible for most works, but to this day in capitalist countries, despite the decisions of a special conference of the Labor Bureau of the League of Nations, has not been carried out: in a number of countries mandatory regulations have been issued introducing this or that partial requirements. In the USSR at present the production and use of white lead is sharply limited: it constitutes only 10% of that produced before the war (white lead is used only for special works). In the porcelain-faience production for certain types of products, it is possible to completely eliminate lead from the glaze (see in detail Ceramic production). For productions where complete elimination of Lead (or partial replacement with other substances) is impossible, it is necessary to carry out measures that eliminate the possibility of workers coming into contact with lead and mainly the release of dust. In regard to carrying out measures for the mechanization of production processes, hermetization of equipment, isolation of harmful departments, installation of ventilation devices, etc., in the USSR there are significant achievements, thanks to which both the number of poisonings and the severity of the latter in a large number of productions (and moreover the most harmful) have sharply decreased (see above). In the USSR, a whole series of health measures has been further carried out, which have given a significant effect on many enterprises. Lead-smelting plants, where lead is smelted from ore, in recent years in our country have been re-equipped according to the latest technology (there are no data on poisonings in these plants). Further—the production of white lead, where a fully mechanized process has been introduced; the production of red lead and minium: instead of outdated semi-craft type plants, where the danger of poisoning workers was very great, plants have been built in Leningrad and Yaroslavl where the process from beginning to end is mechanized, the release of dust has sharply decreased; the production of storage batteries, where thanks to the isolation of dusty works, hermetization, etc., it was possible to sharply reduce the number of cases of poisoning; shot production, where a number of processes have been mechanized; in the galosh-chalk department of the 'Triangle' plant, briquetting of the mixture has been mechanized; on autogenous cutting of old ships, preliminary cleaning of the paint from the cutting lines has been introduced, etc. (For more on health measures for individual productions, see the corresponding words.)-Among general measures, legal legislation has special importance, in which the USSR naturally stands in the first place: reduction of the working day, additional vacations, additional nutrition (milk for a number of professions), etc. Individual hygiene has very great importance: special clothing, respirators, washstands, dressing rooms, restriction (and complete refusal) of alcohol consumption by workers, etc. Treatment. Therapeutic measures for lead poisoning are determined by the form and acuteness of clinical manifestations. In severe lead anemia (Hb amount less than 50%, a significant amount of basophilic-granular erythrocytes, increased amount of hematoporphyrin), it is necessary to transfer to work not associated with Lead; otherwise, strengthening treatment.-For lead colics, treatment consists in warmth, warming of the abdomen (compresses, hot-water bottles, diathermy), hot enemas, injections of atropine, morphine, intravenous administration of calcium chloride, glucose, 4-chamber sulfur baths.-For lead polyneuritis—removal from work, massage, electrotherapy, 4-chamber sulfur baths.-For encephalopathies—bloodletting followed by the introduction of physiological solution, 10% solution of sodium hyposulfite; intravenous administration of calcium chloride, in agitation—chloral hydrate orally or in enemas, morphine.-For acute and chronic forms of poisoning with tetraethyl lead—removal from work, bloodletting, intravenous injections of sodium hyposulfite (1%), subcutaneous injections of lipocerebrin, 4-chamber sulfur baths, enhanced nutrition, hydrotherapy; referral to a sanatorium. While in acute crises therapy aims to immobilize Lead in its depot, in chronic forms it aims to eliminate Lead. These purposes are served by sulfur baths (treatment in Pyatigorsk), iontophoresis with sulfur, long-term administration of acids (phosphoric and hydrochloric), a diet poor in calcium. Contraindications for assignment to work with Lead are kidney diseases, significant damage to the intestine, expressed arteriosclerosis, expressed anemia, hemolytic jaundice and liver diseases. Contraindications for return to work with lead after suffered lead poisoning are: suffered acute encephalopathy, repeated lead colics, severe anemia, lead paralyses.

"*%'. Gellman, D. Kagan, N. Rosenbaum. Discovery in legal cases and in professional poisonings. Objects of investigation in legal cases are parts of internal organs, contents of the stomach and intestines, vomit, and urine. After destruction of the organic substance of the objects with hydrochloric acid and potassium chlorate or with sulfuric acid and ammonium nitrate (nitric acid) (see Poisons, isolation) and dilution of the lead, lead sulfate is obtained as a precipitate. The precipitate is filtered, washed, and fused with soda and saltpeter, without allowing a flash. After cooling, the fusion is treated with the smallest possible amount of hot water. Carbon dioxide is passed into the turbid mixture. The precipitate is filtered and well washed with a saturated soda solution, then with distilled water, until the reaction for sulfate ions ceases (with barium chloride and hydrochloric acid). The washed precipitate is dissolved in nitric acid, the solution is evaporated to dryness on a water bath, and the residue is dissolved in a small amount of water. To a portion of the solution, saturated hydrogen sulfide water is added: a black precipitate or black coloration appears. To a portion of the solution, dilute sulfuric acid is added: a white precipitate or turbidity appears, which increases with the addition of alcohol. The precipitate dissolves in caustic soda as well as in ammonium acetate. A portion of the solution is made alkaline with caustic soda, then acidified with acetic acid: the addition of potassium dichromate causes a yellow precipitate. To a portion of the solution, a small amount of potassium iodide solution is added: a yellow precipitate appears, soluble in excess of the reagent. - Quantitative determination of lead is carried out either gravimetrically (for large amounts) as lead sulfate, or titrimetrically, by precipitating with a titrated solution of potassium dichromate and determining the excess of the latter by the liberation of iodine, or for extremely small amounts colorimetrically by comparing the color of lead sulfide in the form of a colloidal solution or suspension with the color of standard solutions. Discovery and determination of lead in food and flavor products are carried out in a similar manner. For the discovery of lead in dishes (more than the permissible 1%) and glaze (earthenware), the dishes are filled with vinegar (4% acetic acid) with the addition of 1% sodium chloride, boiled for an hour, the liquid is evaporated, the residue is dissolved in a small amount of water, and tested for lead by the methods described above. For the quantitative determination of lead in dishes, 1-2 g of the dish is treated in a flask on a water bath with concentrated nitric acid, the liquid is diluted with hot distilled water, and after filtering and washing the metastannic acid, the filtrate is evaporated, nitric acid is removed by evaporation with sulfuric acid, and lead is weighed as lead sulfate. For small amounts of lead, it is determined titrimetrically or colorimetrically. In the fight against professional poisonings, lead is determined in urine and in the air of industrial premises. In the latter case, a measured volume of air is drawn through absorption bottles with dilute nitric acid. The liquid is evaporated, the residue is dissolved, and the solution is examined for lead as described above, using quantitative determination.