Letheby found the trainmen of the London Underground Railroad little affected by the constant breathing of the tainted atmosphere. Experiments on rabbits, mice, and guinea-pigs showed 0.04 vol. per cent., sufficient to bring on marked symptoms of poisoning, while 0.3 per cent. proved fatal. Others claim that from 1 to 3 per cent. can be respired without ill effects (Hist). The gas produced the same effect whether breathed through the nose or by tube introduced in the trachea. The cornea becomes opaque, and there are dyspnea, cyanosis, and convulsions. Taken internally, there are catarrh of the stomach and chronic sulphuric acid poisoning. The effects on vegetation are greater than on animals. Suits for damages against works for the destruction of trees and other plants are frequent.3 Treatment. Proper prophylactic measures: masks for workmen containing a wet sponge; ventilation; restriction of quantity used to preserve food or drink. Mild alkalis serve as antidotes. Postmortem Appearances.-Those of asphyxia. The blood is very dark and has in part an acid reaction. The hemoglobin is changed first through loss of oxygen, then by decomposition, to hematin as with mineral acids. The respiratory tract is catarrhal or even croupous in aspect, due to the action of the acid. The lungs are partly edematous. Tests. Intense suffocating odor. Blue color with starch and iodic acid; sensitive to 1:3000. In foods and drinks it is tested for after being reduced to hydrogen sulphid by zine and hydrochloric acid.' NITROGEN MONOXID. = (Chemical formula, N2O 44. Synonyms, Nitrous Orid; Laughing-gas.) Laughing-gas is colorless, with a sweetish taste and smell. Water dissolves its own bulk. It supports combustion, but not life, as Davy supposed. It is eliminated from the blood unchanged. It has a specific gravity of 1.53. It becomes liquid at 7° C. and 40 atmospheres pressure; solidifies at -102° C. at common pressure. It is sold in a liquid state in wrought-iron containers, and is used from these as an anesthetic. It is prepared for this purpose by heating ammonium nitrate, and must be carefully purified. Symptoms. When breathed in small quantity it produces a delicious tingling sensation and tends to induce laughter, hence its names, "paradise gas" and "laughing-gas." Persons differ greatly in what they do when under the influence of the gas at this stage. Its anesthetic effect on a young man, Cooley, who bruised his shins while dancing under its influence yet felt no pain, was noticed by Dr. Horace Wells, of Hartford, and led to its use in dentistry. Gardiner Q. Colton administered the gas to Wells at the latter's request, and Dr. Riggs extracted 1 Ogata, Arch. f. Hygiene, 1884, vol. xi., p. 246. 2 Th. Weyl, Hygiene der chem. Gross-Industrie, Jena, 1896. 3 Schroeder and Reuss, Die Beschädigung der Vegetation durch Rauch und die Huettenrauch-Schaden, 1883; also Just and Blaine, Landw. Versuchsst., Jg. 1889, pt. ii. L. Hermann, Exp. Toxikologie, Berlin, 1874, p. 137. the first tooth without pain December 11, 1844. The gas fell into disuse, however, until 1863, when its use was revived by Colton. From February 4, 1864, the patients have inscribed their names on a scroll. The writer witnessed, January 17, 1898, gas administered to the 196,470th patient. No accidents have happened. By covering the nose and mouth with a respirator and keeping the patient's head slightly forward, the breathing is easy, unconsciousness speedy, the tint of the skin inclined to be blue, but not livid, insensibility complete, and recovery rapid. The use of the gas for prolonged surgical operations is growing, since there is rarely any subsequent vomiting. Access of air or 20 per cent. oxygen, or this mixture breathed under pressure, is employed, since nitrous oxid cannot replace oxygen for respiration. The brain is first paralyzed, then the center of sensation of pain, then consciousness. The action then extends to the spinal cord, medulla oblongata, and finally to the heart. Asphyxia follows prolonged inhalation without oxygen. The bloodpressure is much augmented, and it is dangerous, therefore, to use it on patients with a weakened vascular system. Arterial blood shaken with the gas becomes dark, and venous blood, though shaken, does not become arterial. It does not combine with the blood, though this is claimed. Death during the administration has not been due to poisonous action of the gas, but to asphyxia or other cause.2,3 Treatment. Fresh air, oxygen, and stimulants. Postmortem Appearances.-No changes observable in man or animals even after many hours' narcosis except that the blood is of dark color. Tests. Solubility of the gas in alcohol. Explosion with hydrogen leaves a residue of nitrogen and water. NITRIC OXID (NO = 30). Also NITROUS ANHYDRID (NO, 76); NITRIC PEROXID (NOg = 46). Nitric oxid is a highly poisonous, irrespirable gas. It is colorless, nearly insoluble in water, but turns red in air giving NO, and NO2, both of which dissolve. It is obtained by the deoxidation of nitric acid in voltaic batteries, or by the action of this acid on charcoal, metals, cotton, and vegetable fiber and by animal tissues. It is frequently evolved in great quantities in manufactures and laboratories, and must be especially guarded against by proper ventilation or by masks. Unfortunately, there is as yet no good absorbing respirator for these gases. Works, therefore, need constant supervision to protect employees. Symptoms. Habitually breathed in small quantities and great dilution it produces severe chronic diseases. In acute poisoning immediate dyspnea, tightness of chest, coughing, fainting, cyanosis, diarrhea, and collapse. Death within forty hours, though symptoms of slight poisoning are delayed, in which case the first symptoms are headache, desire for fresh air, thirst, and then suddenly symptoms of aggravated character— 1 L. Hermann, op. cit., p. 243. 2 Kobert, op. cit., p. 550; many citations of literature. distress of breathing, anxiety depicted on face, cold perspiration, protruding eyeballs, and spasmodic coughing, followed by vomiting. Blood drawn on venesection tarry, thick, black, and rapidly coagulating. It is of diminished alkalinity, and on dilution becomes red and shows the oxyhemoglobin spectrum. Although Hermann' was able to obtain a definite compound of nitric oxid and hemoglobin, ex corpus, Belky denies the possibility of its formation in poisoning by nitric oxid. Treatment.—Removal of the person from the vitiated atmosphere; in commencing edema of the lungs administer atropin. When edema is absent, inhalations of vapor of water and a little ammonia. In cyanosis, alkaline salt injections. Postmortem Appearances.-Congestion of the larynx and trachea and edema of the lungs. Brown-colored serum from any incision of the lungs. Veins of the pia mater full. The blood reacts acid. Tests. Starch and potassium iodid, after cautious acidulation with sulphuric acid, give blue color and detect traces. The color and odor of the gaseous mixture breathed are characteristic. 1865. 1 L. Hermann, op. cit., p. 112. Belky, Virchow's Arch., 1886, vol. clx., p. 160; Lehre der schädlichen Gase, FOOD-POISONING. THE term food-poisoning includes all forms of sickness caused by foods that contain organic poisons not added by human agency nor accidentally acquired through contact, but present in the tissues of the plant or animal during life, or developed during storage through decomposition changes wrought by various species of bacteria not connected with the usual diseases of man or animals. Poisoning by Vegetable Foods.-Poisoning due to abnormal vegetable foods is not common, and, in this country, is of minor interest and importance. It is restricted practically to ergotized rye and solanized potatoes. The former has long been known as a cause of chronic poisoning in those parts of Europe where rye constitutes the principal food of the poorer classes, the outbreaks occurring most commonly after the use of grain harvested after wet, bad seasons; the latter have been known, within recent years, to cause numerous outbreaks of acute poisoning among soldiers of the German army. It has long been known that potatoes contain normally a very small amount (about 0.06 per cent.) of the poisonous principle, solanin, but it is only within recent years that it has been discovered that, under certain conditions, they may contain the poison in amounts sufficient to cause grave disturbance of the system. The increase is due to the action of at least two species of bacteria, Bacterium solaniferum non-colorabile and Bacterium solaniferum colorabile, and occurs in those tubers that, during growth, have lain partially exposed above ground, and in those that, during storage, have become well sprouted. The most extensive outbreak of potato-poisoning recorded occurred in 1899 in a German regiment, fifty-six members of which, after eating sprouted potatoes, were seized with chills, fever, headache, vomiting, diarrhea, colic, and great prostration. Many showed more or less marked jaundice and several collapsed, but all recovered. Samples of the remaining potatoes yielded 0.38 per cent, of the poison, and this would indicate that a full portion must have contained nearly 5 grains. The most important forms of food-poisoning are those due to unwholesome foods of animal origin, as milk, cheese, meat, and meatproducts. In these the poisonous principles are products of bacterial action and may be divided into two classes-ptomains and toxalbumins. Poisoning by Ptomains.-Ptomains are alkaloidal bodies produced by the action of certain micro-organisms, mostly unidentified, on proteid material; they are decomposition products and always contain nitrogen. To the lay mind the word conveys the idea of deadly poison, 1 Deutsch. med. Wochenschr., 1899, p. 783. but all ptomains are not necessarily poisonous any more than all bacteria are necessarily pathogenic; in fact, only a very small minority are poisonous, and these include mytilotoxin, obtained by Salkowski and Brieger from mussels; tyrotoxicon, discovered by Vaughan in milk and cheese; and cholin, neuridin, neurin, cadaverin, and putrescin, isolated by Brieger from decomposing meat and fish. Whether, in any case of decomposition, any ptomains will be formed, and if any, what kinds, depends upon the species of organisms present, the nature of the material, temperature, access of air, and other conditions. It appears to be not always essential that tissues containing ptomains shall be dead, for in a number of cases of poisoning following the ingestion of freshly gathered mussels and oysters the cause has definitely been demonstrated to have been these bases. As a rule, however, ptomain-poisoning is due to contaminated milk or cheese or to meats or fish that have begun to decompose. The stage of the process of decomposition is of no great importance, for as they are only transition products, ptomains may be present or may have disappeared at any stage, and meat that is not perceptibly tainted may be very toxic, while that which is decidedly rotten may be perfectly innocuous. In point of fact, most ptomain-poisoning is due to foods not markedly decomposed, since those that are repugnant to the senses are commonly rejected at once. It is possible that some cases of poisoning attributed to ptomains may be due really to albumoses formed in the first stages of decomposition of meats. Ptomain-poisoning manifests itself, as a rule, within a short time after eating. The principal symptoms are those of more or less severe gastro-enteritis, but evidence of extensive involvement of the nervous system is by no means infrequent. The first outbreak of poisoning traced definitely to a ptomain was that which led to the discovery, by Professor Victor C. Vaughan, of the intensely poisonous benzene derivative, tyrotoxicon, which he isolated from a number of cheeses, which, during 1883 and 1884, caused no fewer than 300 cases of sickness. The symptoms included abdominal pain, vomiting, diarrhea, feeble and irregular pulse, dryness and constriction of the throat, and cyanosis. Later the same poison was isolated by Wallace from a cheese that caused poisoning in 50 of the 60 persons who ate of it. In this outbreak the symptoms, which appeared within four hours, included vomiting, purging, griping, chills, severe epigastric pain, cramps in the feet and legs, and very marked prostration, and were most severe in some who ate the least. 1886 Newton and Wallace1 isolated the poison from milk that caused extensive outbreaks in several hotels at Long Branch. In all, 73 guests were affected. They were seized soon after supper with nausea, vomiting, cramps, dryness of the throat, burning sensation in the esophagus, and collapse. Some had active diarrhea with no vomiting, and some had no diarrhea. As a rule, nausea and vomiting were persistent and were accompanied by a tendency to exhaustion and collapse. The most remarkable case of milk-poisoning on record was investi1 Medical News, September 25, 1886. In |