Sulphur is found in the native state in certain volcanic regions, or in the combined state as metal sulphides (pyrites, galena, blende, cinnabar), sulphates (anglesite, gypsum) or in the form of hydrogen sulphide in certain sources of water or natural gas. At one time, the mined sulphur-bearing rock was heated to melting point in primitive furnaces dug in the ground or in masonry furnaces open at the top (Sicilian calcaroni), the sulphur-bearing rock being covered with a layer of lag to prevent contact with the air. In both cases, some of the natural sulphur is itself consumed as fuel.
Elemental sulphur is largely extracted from petroleum refining. In some countries, sulphur is recovered as a by-product in the production of copper, lead and zinc, from their sulphur minerals; it is also obtained by roasting iron pyrites for the production of sulphuric acid.
Sulphur is used for the production of sulphuric acid, sulphates, hyposulphites, carbon disulphide and so on, in match manufacture, rubber vulcanization, electron melting and incendiary-bomb manufacture; it is used in agriculture to combat plant parasites and in the treatment of wine. It is also used as a bleaching agent for pulp and paper, textiles and dried fruit. Sulphur is a component of anti-dandruff shampoos, a binder and asphalt extender for road paving, an electric insulator, and a nucleating agent in photographic film.
Sulphur dioxide serves primarily as an intermediate in the production of sulphuric acid, but is also encountered in the production of paper pulp, starch, sulphites and thiosulphates. It is used as a bleaching agent for sugar, fibres, leather, glues and sugar liquor; in organic synthesis it is used as the starting point for numerous substances such as carbon disulphide, thiophene, sulphones and sulphonates; it is employed as a preservative in the wine and food industries. In combination with ammonia and atmospheric moisture, it forms artificial ammonium sulphite mists used to protect crops against night frost. Sulphur dioxide is used as a disinfectant in breweries, a depressant in the flotation of sulphide ores, an extractive solvent in oil refining, a cleaning agent for tile drains, and a tanning agent in the leather industry.
Sulphur trioxide is used as an intermediate in the manufacture of sulphuric acid and oleum for sulphonation, in particular, of dyes and dye-stuffs, and for the production of anhydrous nitric acid and explosives. Solid sulphur trioxide is marketed under such names as Sulphan and Triosul, and is used primarily for sulphonation of organic acids. Sulphur tetrafluoride is a fluorinating agent. Sulphur hexafluoride serves as a gaseous insulator in high-voltage electric installations. Sulphyryl fluoride is used as an insecticide and a fumigant.
Sulphur hexafluoride and trioxychlorofluoride are used in insulation material for high-voltage systems.
Many of these compounds are used in the dye-stuff, chemical, leather, photography, rubber and metalworking industries. Sodium metabisulphite, sodium trisulphite, sodium hydrosulphite, ammonium sulphate, sodium thiosulphate, calcium sulphate, sulphur dioxide, sodium sulphite and potassium metabisulphite are additives, preservatives and bleaching agents in the food industry. In the textile industry, sodium trisulphite and sodium sulphite are bleaching agents; ammonium sulphate and ammonium sulphamate are used for flameproofing; and sodium sulphite is used for printing cotton. Ammonium sulphate and carbon disulphide are used in the viscose silk industry, and sodium thiosulphate and sodium hydrosulphite are bleaching agents for pulp and paper. In addition, ammonium sulphate and sodium thiosulphate are tanning agents in the leather industry, and ammonium sulphamate is used for flameproofing wood and treating cigarette paper.
Carbon disulphide is a solvent for waxes, lacquers, oils and resins, as well as a flame lubricant for cutting glass. It is used for the cold vulcanization of rubber and for generating petroleum catalysts. Hydrogen sulphide is an additive in extreme-pressure lubricants and cutting oils, and a by-product of petroleum refining. It is used in ore reduction and for the purification of hydrochloric acid and sulphuric acid.
Hydrogen sulphide is a flammable gas which burns with a blue flame, giving rise to sulphur dioxide, a highly irritating gas with a characteristic odour. Mixtures of hydrogen sulphide and air in the explosive range may explode violently; since the vapours are heavier than air, they may accumulate in depressions or spread over the ground to a source of ignition and flash back. When exposed to heat, it decomposes to hydrogen and sulphur, and when in contact with oxidizing agents such as nitric acid, chlorine trifluoride and so on, it may react violently and ignite spontaneously. Extinguishing agents recommended for the fighting of hydrogen sulphide fires include carbon dioxide, chemical dry powder and water sprays.
Health hazards. Even at low concentrations, hydrogen sulphide has an irritant action on the eyes and respiratory tract. Intoxication may be hyperacute, acute, subacute or chronic. Low concentrations are readily detected by the characteristic rotten-egg odour; however, prolonged exposure dulls the sense of smell and makes the odour a very unreliable means of warning. High concentrations can rapidly deaden the sense of smell. Hydrogen sulphide enters the body through the respiratory system and is rapidly oxidized to form compounds of low toxicity; there are no accumulation phenomena, and elimination occurs through the intestine, urine and the expired air.
In cases of slight poisoning, following exposure to from 10 to 500 ppm, a headache may last several hours, pains in the legs may be felt and rarely there may be loss of consciousness. In moderate poisoning (from 500 to 700 ppm) there will be loss of consciousness lasting a few minutes, but no respiratory difficulty. In cases of severe poisoning the subject drops into a profound coma with dyspnoea, polypnoea and a slate-blue cyanosis until breathing restarts; there are tachycardia and tonic-clonic spasms.
Inhalation of massive quantities of hydrogen sulphide will rapidly produce anoxia resulting in death by asphyxia; epileptiform convulsions may occur and the individual falls apparently unconscious, and may die without moving again. This is a syndrome characteristic of hydrogen sulphide poisoning in sewer workers; however, in such cases, exposure is often due to a mixture of gases including methane, nitrogen, carbon dioxide and ammonia.
In subacute poisoning, the signs may be nausea, stomach distress, foetid eructations, characteristic “rotten-egg” breath, and diarrhoea. These digestive-system disorders may be accompanied by balance disorders, vertigo, dryness and irritation of the nose and throat with viscous and mucopurulent expectoration and diffuse rales and ronchi.
There have been reports of retrosternal pain similar to that found in angina pectoris, and the electrocardiogram may show the characteristic trace of myocardial infarction, which, however, disappears quite rapidly. The eyes are affected by palpebral oedema, bulbar conjunctivitis and mucopurulent secretion with, perhaps, a reduction in visual acuity—all of these lesions usually being bilateral. This syndrome is known to sugar and sewer workers as “gas eye”. A variety of other systemic effects have been reported, including headaches, asthenia, eye disorders, chronic bronchitis and a grey-green line on the gums; as in acute poisoning, the ocular lesions are said to predominate, with paralysis, meningitis, polyneuritis and even behavioural problems.
In rats, exposure to hydrogen sulphide has given rise to teratogenic effects.
Metabolism and pathology. Hydrogen sulphide has a general toxic action. It inhibits Warburg’s respiratory enzyme (cytochrome oxidase) by binding iron, and the oxydo-reduction processes are also blocked. This inhibition of enzymes essential for cellular respiration may be fatal. The substance has a local irritant action on the mucous membranes since, on contact with moisture, it forms caustic sulphides; this may also occur in the lung parenchyma as a result of combination with tissue alkalis. Experimental research has shown that these sulphides may enter into the circulation, producing respiratory effects such as polypnoea, bradycardia and hypertension, by their action on the vasosensitive, reflexogenic zones of the carotid nerves and Hering’s nerve.
Post-mortem examination in a number of cases of hyperacute poisoning has revealed pulmonary oedema and congestion of various organs. A characteristic autopsy feature is the odour of hydrogen sulphide that emanates from the dissected corpse. Other features of note are the haemorrhages of the gastric mucosae, and the greenish colour of the upper regions of the intestine and even of the brain.
The first cases of carbon disulphide poisoning were observed during the nineteenth century in France and Germany in connection with the vulcanization of rubber. After the First World War, the production of viscose rayon expanded, and with it the incidence of acute and chronic poisoning from carbon disulphide, which has remained a serious problem in some countries. Acute and, more often, chronic poisoning still occur, although improvements in technology and hygienic conditions in plants have virtually eliminated such problems in a number of countries.
Carbon disulphide is primarily a neurotoxic poison; therefore those symptoms indicating central and peripheral nervous system damage are the most important. It was reported that concentrations of 0.5 to 0.7 mg/l (160 to 230 ppm) caused no acute symptoms in humans, 1 to 1.2 mg/l (320 to 390 ppm) were bearable for several hours, with the appearance of headaches and unpleasant feelings after 8 hours of exposure; at 3.6 mg/l (1,150 ppm) giddiness set in; at 6.4 to 10 mg/l (2,000 to 3,000 ppm) light intoxication, paraesthesia and irregular breathing occurred within 1/2 to 1 hour. At concentrations of 15 mg/l (4,800 ppm), the dose was lethal after 30 minutes; and at even higher concentrations, unconsciousness occurred after several inhalations.
Acute poisoning occurs mainly after accidental exposures to very high concentrations. Unconsciousness, frequently rather deep, with extinction of cornea and tendon reflexes, occurs after only a short time. Death sets in by a blockage of the respiratory centre. If the patient regains consciousness, motor agitation and disorientation follow. If he or she recovers, frequently late sequellae include psychic disturbances as well as permanent damage to the central and peripheral nervous systems. Subacute cases of poisoning usually occur from exposure to concentrations of more than 2 mg/l. They are manifested mainly in mental disorders of the manic-depressive type; more frequent at lower concentrations, however, are cases of polyneuritis.
Chronic poisoning begins with weakness, fatigue, headache, sleep disturbances, often with frightening dreams, paraesthesia and weakness in the lower extremities, loss of appetite and stomach illness. Neurological symptoms are also seen, and impotence is rather frequent. Continued exposure may give rise to polyneuritis, which is said to appear after working in concentrations of 0.3 to 0.5 mg/l for several years; an early sign is the dissociation of tendon reflexes in lower extremities. Damage to the brain nerves is less frequent, but neuritis n. optici and vestibular and sense-of-smell disturbances have been observed.
In exposed workers, disorders occur in the male reproductive system (hypo- and asthenospermia), and excretion of 17-ketosteroids, 17-hydroxycorticosteroids and androsteron decreases during exposure. In women menstrual disturbances, metrorrhagia and more frequent abortions have been described. Carbon disulphide passes the placenta. Animals have demonstated foetotoxic and teratogenic effects at levels of 32 ppm and higher.
The relationship between carbon disulphide and atherosclerosis is a topic of special interest. Prior to the Second World War, not much attention was paid to this pattern, but thereafter, when classic carbon disulphide poisoning ceased to occur in many countries, several authors noted the development of atherosclerosis of the brain vessels in younger workers in viscose rayon plants.
Ophthalmodynamographic studies in young workers who were exposed to carbon disulphide concentrations of 0.2 to 0.5 mg/l for several years, showed that the retinal systolic and diastolic blood pressure was higher than that of the brachial artery. This increase was due to arterial hypertension in the brain, and it was reported that arterial spasms appeared before subjective complaints. Rheoencephalography has been recommended for assessment of brain vessel function. Changes in resistance are caused by arterial pulsation, especially of intracranial vessels, and could therefore lead to the discovery of possible increased rigidity or spasms of cranial vessels. In Japanese workers a higher incidence of small, round, retinal haemorrhages and microaneurysms was observed.
In chronically exposed men, arteriolocapillary hyalinosis was found, which represents a special type of carbon disulphide arteriosclerosis. Therefore, carbon disulphide may be assumed to be a contributing factor to the origin of this sclerosis, but not a direct cause. This hypothesis, as well as the results of biochemical examinations, seems to be supported further by reports about the significant increase of atherosclerosis, frequently in younger persons who were exposed to carbon disulphide. With regard to the kidneys, it seems that glomerulosclerosis of the Kimmelstiel-Wilson type is more frequent in persons exposed to carbon disulphide than in others. British, Finnish and other investigators have shown that there is increased mortality from coronary heart disease in male workers exposed for many years to relatively low carbon disulphide concentrations.
The absorption of carbon disulphide through the respiratory tract is rather high, and about 30% of the inhaled quantity is retained when a steady state of inhalation is reached. The time required for the establishment of this state varies in length from rather short, to several hours if light physical work is done. After termination of exposure, part of the carbon disulphide is rapidly excreted through the respiratory tract. The length of the desaturation period depends on the degree of exposure. Approximately 80 to 90% of the absorbed carbon disulphide is metabolized in the body with the formation of dithiocarbamates and possible further cyclization to thiazolidane. Owing to the nucleophilic character of carbon disulphide, which reacts especially with —SH, —CH, and —NH2 groups, perhaps other metabolites are formed too.
Carbon disulphide is also absorbed through the skin in considerable amounts, but less than through the respiratory tract. Dithiocarbamates easily chelate many metals such as copper, zinc, manganese, cobalt and iron. Increased zinc content has been demonstrated in the urine of animals and humans exposed to carbon disulphide. It is also believed that a direct reaction takes place with some of the metals contained in metalloenzymes.
Liver microsome tests have demonstrated the formation of carbon oxysulphide (COS) and atomic sulphur which is bound covalently to microsomal membranes. Other authors have found in rats that carbon disulphide after oxidative decomposition binds primarily to protein P-450. In urine it is excreted in a fraction of 1% as carbon disulphide; of the retained amount it is excreted to about 30% as inorganic sulphates, the remainder as organic sulphates and some unknown metabolites, one of which is thiourea.
It is assumed that the reaction of carbon disulphide with vitamin B6 is very important. B6 metabolism is impaired, which is manifested by enhanced excretion of xanthurenic acid and decreased excretion of 4-pyridoxine acid, and further in a reduced serum pyridoxine level. It appears that copper utilization is disturbed as indicated by the reduced level of ceruloplasmin in exposed animals and humans. Carbon disulphide interferes with serotonin metabolism in the brain by inhibiting certain enzymes. Furthermore, it has been reported that it inhibits the clearing factor (lipase activated by heparin in the presence of -lipoproteins), thus interfering with the clearing of fat from blood plasma. This may result in the accumulation of cholesterol and lipoid substances in vessel walls and stimulate the atherosclerotic process. However, not all reports about the inhibition of the clearing factor are so convincing. There are many, although often contradictory, reports about the behaviour of lipoproteins and cholesterol in the blood and organs of animals and humans exposed to carbon disulphide for a long time, or poisoned by it.
Impaired glucose tolerance of the chemical diabetes type has also been observed. It is elicited by the elevated level of xanthurenic acid in serum, which, as was demonstrated in experiments, forms a complex with insulin and reduces its biological activity. Neurochemical studies have demonstrated changed catecholamine levels in the brain as well as in other nervous tissues. These findings show that carbon disulphide changes the biosynthesis of catecholamines, probably by inhibiting dopamine hydroxylase by chelating enzymatic copper.
Examination of animals poisoned by carbon disulphide revealed a variety of neurologic changes. In humans the changes included serious degeneration of the grey matter in the brain and cerebellum, changes in the pyramid system of pons and spinal cord, degenerative changes of peripheral nerves and disintegration of their sheaths. Also described were atrophy, hypertrophy and hyalin degeneration of muscle fibres.
Sulphur and sulphur dioxide
Extraction of sulphur-bearing rock can lead to the inhalation of the high concentrations of sulphur dust in sulphur mines and may have harmful effects on the respiratory system. In sulphur mining, at the beginning of exposure, the miner suffers from upper respiratory tract catarrh, with cough, and expectoration which is mucoid and may even contain grains of sulphur. Asthma is a frequent complication.
The acute effects of inhalation of sulphur and its inorganic compounds include upper respiratory system effects (catarrhal inflammation of the nasal mucosae, which may lead to hyperplasia with abundant nasal secretion). Tracheobronchitis is a frequent occurrence, with shortness of breath (dyspnoea), persistent cough and expectoration which may sometimes be streaked with blood. There may also be irritation of the eyes, with lacrimation, photophobia, conjunctivitis and blepharoconjunctivitis; cases of damage to the crystalline lens have also been described, with the formation of opacities and even cataract and focal chorioretinitis.
The skin may be subject to erythematous and eczematous lesions and signs of ulceration, especially in the case of workers whose hands are in prolonged or repeated contact with powdered sulphur or sulphur compounds, as for example in bleaching and decolouring processes in the textile industry.
Sulphur dioxide is one of the most widely encountered contaminants in the workplace environment. It is released in considerable quantities in the manufacture of sulphuric acid, liquid sulphur dioxide and cast iron, in the refining of sulphur-rich minerals (copper, lead, zinc and so on) and from the combustion of sulphur-rich coal. It is also found as a contaminant in the production of cellulose, sugar and superphosphates, in food preserving, petroleum refining, bleaching, disinfecting and so on.
Sulphur dioxide is an irritant gas, and its effect is due to the formation of sulphurous and sulphuric acids on contact with moist mucosae. It may enter the body via the respiratory tract or, following dilution in the saliva, it may be swallowed and enter the gastro-intestinal tract in the form of sulphurous acid. Certain authors believe that it can enter the body via the skin. Due to its high solubility, sulphur dioxide is rapidly distributed throughout the body, producing metabolic acidosis with a reduction in the blood alkali reserve and compensatory elimination of ammonia in the urine and alkali in the saliva. The general toxic action is demonstrated by protein and carbohydrate metabolism disorders, vitamin B and C deficiency and oxidase inhibition. In the blood, sulphuric acid is metabolized to sulphates which are excreted in the urine. It is probable that the absorption of large quantities of sulphur dioxide has a pathological effect on the haemopoietic system and may produce methaemoglobin.
Acute poisoning results from the inhalation of very high concentrations of sulphur dioxide and is characterized by intense irritation of the conjunctivae and upper respiratory tract mucosae with dyspnoea and cyanosis followed rapidly by consciousness disorders. Death may ensue as a result of suffocation due to reflex spasm of the larynx, sudden circulatory arrest in the lungs, or shock.
In industry, sulphur dioxide poisoning is usually of a chronic nature. The substance’s local irritant action on the mucous membranes produces a sensation of burning, dryness and pain in the nose and throat, altered sense of smell, and causes secretion (which may be blood-streaked), nasal haemorrhage, and dry or productive cough, perhaps with bloody sputum. Gastric troubles have also been reported. Objective signs and symptoms include pronounced hyperaemia accompanied by oedema of the mucous membranes of the nose, pharyngeal walls, tonsils and, in some cases, also the larynx. Chronic conjunctivitis can be observed. In the more advanced stages, the process becomes atrophic, with dilation of the blood vessels in certain regions. Ulceration of the nasal septum, which bleeds readily, may also be observed. Persons who have a long history of exposure to high concentrations of sulphur dioxide may suffer from chronic bronchitis accompanied by emphysema. The initial symptoms are a reduction in vital capacity to the detriment of residual volume, compensatory hyperventilation and a reduction in oxygen consumption.
These manifestations often precede the radiological stage, which presents with dense and enlarged hilar shadows, gross reticulation produced by peribronchitis and, in some cases, bronchiectasis and even nodular appearances. These changes are bilateral and more evident in the median and basal regions.
Both behavioural and nervous system disorders may occur, probably due to the general toxic effect of sulphur dioxide on the body.
The mouth can be affected, with dental caries, peridontal and gingival disorders present. Patients may complain of rapid and painless dental destruction, loss of fillings, and increased tooth sensitivity to temperature changes. Objective symptoms include loss of brilliance, and enamel striation and yellowing.
Sulphur dioxide causes skin irritation which is aggravated by perspiration, and this may be attributed to the conversion of sulphur dioxide to sulphurous acid from contact with sweat.
The initial upper and lower respiratory tract symptoms may regress with suitable treatment and removal from exposure to all sources of respiratory tract inflammation; however, the prognosis is poor for the advanced forms—especially when accompanied by bronchiectasis and right heart deficiency.
The chronic effects consist mainly of bronchopulmonary disease which, after several years, may be complicated by emphysema and bronchiectasis. The maxillary and frontal sinuses may be affected; involvement is usually bilateral, and pansinusitis may be observed in some cases. X-ray examination of the respiratory system reveals irregular opacities, especially in the medial basal region; the apical regions are not usually affected. In certain cases, nodulation has been observed. Stratigraphy shows that the accentuation of pulmonary pattern depends on pulmonary vascular repletion.
Lung function examination has shown changes in pulmonary ventilation, increased oxygen consumption, reduced expiratory volume per second and increased residual volume. Pulmonary carbon dioxide diffusion capacity was also impaired. The disorders are often of a spasmodic nature. Levels of blood sulphur may be higher than normal; there is increased urinary excretion of sulphates and a rise in the ratio of total to organic sulphur.
Sulphur dust and sulphur dioxide are definitely at the origin of the chronic bronchitis. They irritate the mucous membranes and produce obstructive reactions. The possibility of sulphur-induced pulmonary sclerosis has been much discussed, and sulphur pneumoconiosis (“thiopneumoconiosis”) was described for the first time a century ago. However, experimental research and autopsy findings have shown that sulphur produces chronic bronchopulmonary disease without the formation of true nodular fibrosis and without any feature characteristic of silicosis.
Other sulphur compounds
Sulphur trioxide. The vapour pressure of sulphur trioxide rises rapidly with increasing temperatures and, when the a-form melts, the pressure rise is explosive; consequently transport and storage containers must withstand pressures of 10 to 15 atm. Sulphur trioxide reacts vigorously and highly exothermically with water to produce hydrosulphuric acid. When exposed to moist air, it fumes and forms a mist of sulphuric acid which eventually fills all the available space; it also corrodes metals. It is a powerful oxidizing agent and, in the liquid phase, carbonizes organic materials.
Wherever it is used in gaseous, liquid or solid form, or when oleum or hot sulphuric acid is being employed, sulphur trioxide will pollute the working environment. Sulphur dioxide in air will be oxidized by atmospheric oxygen to produce sulphur trioxide.
It enters the body through the respiratory tract and acts both as a local irritant and general toxic agent in a similar manner to sulphur dioxide, although its irritant action is more pronounced. It causes chronic respiratory tract damage and may degrade alkaline reserves and carbohydrate and protein metabolism; it is metabolized to sulphate in the blood and eliminated in the urine in the same way as sulphur dioxide.
The toxic action of oleum on the body is similar to that of sulphuric acid, but the objective signs and symptoms are more pronounced. Safety and health measures for sulphur trioxide are similar to those described for sulphur dioxide.
Carbonyl sulphide (COS). Carbonyl sulphide is encountered in the native state in volcanic gases and sulphurous waters. It is produced by the reaction of dilute sulphuric acid on ammonium thiocyanate. Carbonyl sulphide is known for its high toxicity. It has been found that it produces serious nervous-system impairment with narcotic effects in high concentrations and has an irritant action.
It is a potent oxidizing substance and should be handled appropriately.
Sulphur tetrafluoride, sulphur pentafluoride (S2F10), disulphur decafluoride, sulphuryl fluoride
(SO2F2), sulphuric oxyfluoride and thionyl fluoride (SOF2) are all irritant substances capable of causing pulmonary oedema in concentrations exceeding the exposure limits, because of their absence of water solubility. The most dangerous is sulphur pentafluoride, which in the presence of moisture hydrolyzes into hydrogen fluoride and sulphur dioxide; its irritant action is considered more severe than that of phosgene, not only as regards the dose, but also because pulmonary haemorrhages may be associated with lung oedema. Sulphuryl fluoride appears to act mainly as a convulsant agent on laboratory animals.
The safety and health measures to be taken in exposure to sulphur pentafluoride are the same as those recommended for the most severe irritant compounds. The other fluorinated sulphur compounds should be treated like sulphur dioxide.
Sulphur chloride is a flammable liquid which gives rise to a moderate fire hazard associated with the evolution of the dangerous decomposition products sulphur dioxide and hydrogen chloride. It is a fuming, corrosive liquid which is dangerous to the eyes; the vapour is irritating to the lungs and mucous membrane. In contact with the skin, the liquid can cause chemical burns. It should be handled under the maximum degree of enclosure and workers should be provided with personal protective equipment including eye protective equipment and respiratory protective equipment.
Sulphuryl chloride is formed by the direct combination of sulphur dioxide and chlorine in the presence of a catalyst which may be charcoal, camphor or acetic anydride. It is also obtained by heating chlorosulphonic acid, with mercuric sulphate, antimony or tin as catalyst. It is used in the manufacture of pharmaceuticals and dye-stuffs, and generally in organic synthesis as a chlorinating, dehydrating or acylating agent.
Sulphuryl chloride is a corrosive liquid which, in contact with the body, can cause burns; the vapour is a respiratory irritant. The precautions are similar to those recommended for sulphur chloride.
Safey and Health Management
Airborne sulphur dust is a fire and explosion hazard; there is also the danger of insidious release of sulphur dioxide leading to the inhalation of irritant vapours. Vapours given off during the melting of sulphur may contain sufficient hydrogen sulphide and carbon disulphide to permit ignition of the air/vapour mixture on contact with a hot surface; such an ignition may result in the transmission of flames to the molten sulphur.
The main hazards in the handling, transport and storage of molten sulphur are related to the flammability of the substance and the possible giving off, during cooling, of hydrogen sulphide, which is even more readily flammable and is explosible in air at concentrations ranging between 4.3 and 45%. Workers employed in sulphur extraction should have at their disposal suitable self-contained respiratory protective apparatus—in particular for rescue operations. Smoking should be prohibited during the transport and handling of sulphur and in sulphur storage areas. Contact of liquid or flowered sulphur with a source of ignition should be avoided, and sulphur stores should not be located in the vicinity of oxidizing agents. The loading and unloading of liquid sulphur necessitate special fire prevention and protection measures. Transport and storage of sulphur require proper grounding (earthing) procedures, exhaust of hydrogen sulphide and regular monitoring of its concentration, and protection of tanks against corrosion by hydrogen sulphide.
Sulphur is a poor conductor of electricity and tends to develop charges of static electricity during transport or processing; static discharges may lead to the ignition of sulphur dust. Pyrophoric deposits of ferrous sulphur which form on the tank wall are also a hazard. Fires in heaps of sulphur are frequent and insidious since they may break out again even after the original conflagration has ostensibly been extinguished.
Carbon disulphide is also highly flammable and explosive.
Sulphur dioxide management efforts should be directed primarily at reducing gas emission and ensuring sufficient ventilation to maintain sulphur dioxide concentrations at the workplace below maximum permissible levels. Total enclosure of processes is an effective and desirable technique. Respiratory protective equipment should be provided where workers may, under exceptional circumstances, be exposed to dangerous concentrations.
Precautions should be taken to prevent the emission of sulphur dust into the atmosphere, and the use of respirators is recommended if the atmospheric dust concentration exceeds the exposure level.
Pre-employment examination should ensure that persons suffering from bronchitis or asthma are not exposed to sulphur. In the periodic examination, clinical examination should be supplemented by chest x ray. These contraindications should also be borne in mind during the periodic medical examinations, which should be carried out at appropriate intervals.
Inorganic sulphur compounds tables
Table 1 - Chemical information.
Table 2 - Health hazards.
Table 3 - Physical and chemical hazards.
Table 4 - Physical and chemical properties.