ILO Content Manager

ILO Content Manager

Thursday, 10 February 2011 21:23

Haematopoietic and Lymphatic System

The lymphohaemopoietic system consists of the blood, the bone marrow, the spleen, the thymus, lymphatic channels and lymph nodes. The blood and bone marrow together are referred to as the haematopoietic system. The bone marrow is the site of cell production, continually replacing the cellular elements of the blood (erythrocytes, neutrophils and platelets). Production is under tight control of a group of growth factors. Neutrophils and platelets are used as they perform their physiological functions, and erythrocytes eventually become senescent and outlive their usefulness. For successful function, the cellular elements of the blood must circulate in proper numbers and retain both their structural and physiological integrity. Erythrocytes contain haemoglobin, which permits uptake and delivery of oxygen to tissues to sustain cellular metabolism. Erythrocytes normally survive in the circulation for 120 days while sustaining this function. Neutrophils are found in blood on their way to tissues to participate in the inflammatory response to microbes or other agents. Circulating platelets play a key role in haemostasis.

The production requirement of the bone marrow is a prodigious one. Daily, the marrow replaces 3 billion erythrocytes per kilogram of body weight. Neutrophils have a circulating half-life of only 6 hours, and 1.6 billion neutrophils per kilogram of body weight must be produced each day. The entire platelet population must be replaced every 9.9 days. Because of the need to produce large numbers of functional cells, the marrow is remarkably sensitive to any infectious, chemical, metabolic or environmental insult that impairs DNA synthesis or disrupts the formation of the vital subcellular machinery of the red blood cells, white blood cells or platelets. Further, since the blood cells are marrow progeny, the peripheral blood serves as a sensitive and accurate mirror of bone marrow activity. Blood is readily available for assay via venipuncture, and examination of the blood can provide an early clue of environmentally induced illness.

The haematological system can be viewed as both serving as a conduit for substances entering the body and as an organ system that may be adversely affected by occupational exposures to potentially harmful agents. Blood samples may serve as a biological monitor of exposure and provide a way to assess the effects of occupational exposure on the lymphohaematopoietic system and other body organs.

Environmental agents can interfere with the haematopoietic system in several ways, including inhibition of haemoglobin synthesis, inhibition of cell production or function, leukaemogenesis and increased red blood cell destruction.

Abnormality of blood cell number or function caused directly by occupational hazards can be divided into those for which the haematological problem is the most important health effect, such as benzene-induced aplastic anaemia, and those for which the effects on the blood are direct but of less significance than the effects on other organ systems, such as lead-induced anaemia. Sometimes haematological disorders are a secondary effect of a workplace hazard. For example, secondary polycythaemia can be the result of an occupational lung disease. Table 1 lists those hazards which are reasonably well accepted as having a direct effect on the haematological system.


Table 1. Selected agents implicated in environmentally and occupationally acquired methaemoglobinaemia

  • Nitrate-contaminated well water
  • Nitrous gases (in welding and silos)
  • Aniline dyes
  • Food high in nitrates or nitrites
  • Mothballs (containing naphthalene)
  • Potassium chlorate
  • Nitrobenzenes
  • Phenylenediamine
  • Toluenediamine


Examples of Workplace Hazards Primarily Affecting the Haematological System

Benzene

Benzene was identified as a workplace poison producing aplastic anaemia in the late 19th century (Goldstein 1988). There is good evidence that it is not benzene itself but rather one or more metabolites of benzene that is responsible for its haematological toxicity, although the exact metabolites and their subcellular targets have yet to be clearly identified (Snyder, Witz and Goldstein 1993).

Implicit in the recognition that benzene metabolism plays a role in its toxicity, as well as recent research on the metabolic processes involved in the metabolism of compounds such as benzene, is the likelihood that there will be differences in human sensitivity to benzene, based upon differences in metabolic rates conditioned by environmental or genetic factors. There is some evidence of a familial tendency towards benzene-induced aplastic anaemia, but this has not been clearly demonstrated. Cytochrome P-450(2E1) appears to play an important role in the formation of haematotoxic metabolites of benzene, and there is some suggestion from recent studies in China that workers with higher activities of this cytochrome are more at risk. Similarly, it has been suggested that Thalassaemia minor, and presumably other disorders in which there is increased bone marrow turnover, may predispose a person to benzene-induced aplastic anaemia (Yin et al. 1996). Although there are indications of some differences in susceptibility to benzene, the overall impression from the literature is that, in contrast to a variety of other agents such as chloramphenicol, for which there is a wide range in sensitivity, even including idiosyncratic reactions producing aplastic anaemia at relatively trivial levels of exposure, there is a virtual universal response to benzene exposure, leading to bone marrow toxicity and eventually aplastic anaemia in a dose-dependent fashion.

The effect of benzene on the bone marrow is thus analogous to the effect produced by chemotherapeutic alkylating agents used in the treatment of Hodgkin’s disease and other cancers (Tucker et al. 1988). With increasing dosage there is a progressive decline in all of the formed elements of the blood, which is sometimes manifested initially as anaemia, leucopenia or thrombocytopenia. It should be noted that it would be most unexpected to observe a person with thrombocytopenia that was not at least accompanied by a low normal level of the other formed blood elements. Further, such an isolated cytopenia would not be expected to be severe. In other words, an isolated white blood count of 2,000 per ml, where the normal range is 5,000 to 10,000, would suggest strongly that the cause of the leucopenia was other than benzene (Goldstein 1988).

The bone marrow has substantial reserve capacity. Following even a significant degree of hypoplasia of the bone marrow as part of a chemotherapeutic regimen, the blood count usually eventually returns to normal. However, individuals who have undergone such treatments cannot respond by producing as high a white blood cell count when exposed to a challenge to their bone marrow, such as endotoxin, as can individuals who have never previously been treated with such chemotherapeutic agents. It is reasonable to infer that there are dose levels of an agent such as benzene which can destroy bone marrow precursor cells and thus affect the reserve capability of the bone marrow without incurring sufficient damage to lead to a blood count that was lower than the laboratory range of normal. Because routine medical surveillance may not reveal abnormalities in a worker who may have indeed suffered from the exposure, the focus on worker protection must be preventive and employ basic principles of occupational hygiene. Although the extent of the development of bone marrow toxicity in relationship to benzene exposure at the workplace remains unclear, it does not appear that a single acute exposure to benzene is likely to cause aplastic anaemia. This observation might reflect the fact that bone marrow precursor cells are at risk only in certain phases of their cell cycle, perhaps when they are dividing, and not all the cells will be in that phase during a single acute exposure. The rapidity with which cytopenia develops depends in part on the circulating lifetime of the cell type. Complete cessation of bone marrow production would lead first to a leucopenia because white blood cells, particularly granulocytic blood cells, persist in circulation for less than a day. Next there would be a decrease in platelets, whose survival time is about ten days. Lastly there would be a decrease in red cells, which survive for a total of 120 days.

Benzene not only destroys the pluripotential stem cell, which is responsible for the production of red blood cells, platelets and granulocytic white blood cells, but it also has been found to cause a rapid loss in circulating lymphocytes in both laboratory animals and in humans. This suggests the potential for benzene to have an adverse effect on the immune system in exposed workers, an effect that has not been clearly demonstrated as yet (Rothman et al. 1996).

Benzene exposure has been associated with aplastic anaemia, which is frequently a fatal disorder. Death usually is caused by infection because the reduction in white blood cells, leucopenia, so compromises the body’s defence system, or by haemorrhage due to the reduction in platelets necessary for normal clotting. An individual exposed to benzene at a workplace who develops a severe aplastic anaemia must be considered to be a sentinel for similar effects in co-workers. Studies based on the discovery of a sentinel individual often have uncovered groups of workers who exhibit obvious evidence of benzene haematotoxicity. For the most part, those individuals who do not succumb relatively quickly to aplastic anaemia will usually recover following removal from the benzene exposure. In one follow-up study of a group of workers who previously had significant benzene-induced pancytopenia (decrease in all blood cell types) there were only minor residual haematological abnormalities ten years later (Hernberg et al. 1966). However, some workers in these groups, with initially relatively severe pancytopenia, progressed in their illnesses by first developing aplastic anaemia, then a myelodysplastic preleukaemic phase, and finally to the eventual development of acute myelogenous leukaemia (Laskin and Goldstein 1977). Such progression of disease is not unexpected since individuals with aplastic anaemia from any cause appear to have a higher-than-expected likelihood of developing acute myelogenous leukaemia (De Planque et al. 1988).

Other causes of aplastic anaemia

Other agents in the workplace have been associated with aplastic anaemia, the most notable being radiation. The effects of radiation on bone marrow stem cells have been employed in the therapy of leukaemia. Similarly, a variety of chemotherapeutic alkylating agents produce aplasia and pose a risk to workers responsible for producing or administering these compounds. Radiation, benzene and alkylating agents all appear to have a threshold level below which aplastic anaemia will not occur.

Protection of the production worker becomes more problematic when the agent has an idiosyncratic mode of action in which minuscule amounts may produce aplasia, such as chloramphenicol. Trinitrotoluene, which is absorbed readily through the skin, has been associated with aplastic anaemia in munition plants. A variety of other chemicals has been reported to be associated with aplastic anaemia, but it is often difficult to determine causality. An example is the pesticide lindane (gamma-benzene hexachloride). Case reports have appeared, generally following relatively high levels of exposure, in which lindane is associated with aplasia. This finding is far from being universal in humans, and there are no reports of lindane-induced bone marrow toxicity in laboratory animals treated with large doses of this agent. Bone marrow hypoplasia has also been associated with exposure to ethylene glycol ethers, various pesticides and arsenic (Flemming and Timmeny 1993).

 

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Thursday, 10 February 2011 03:00

Barium

Gunnar Nordberg

Occurrence and Uses

Barium (Ba) is abundant in nature and accounts for approximately 0.04% of the earth’s crust. The chief sources are the minerals barite (barium sulphate, BaSO4) and witherite (barium carbonate, BaCO3). Barium metal is produced in only limited quantities, by aluminium reduction of barium oxide in a retort.

Barium is used extensively in the manufacture of alloys for nickel barium parts found in ignition equipment for automobiles and in the manufacture of glass, ceramics and television picture tubes. Barite (BaSO4), or barium sulphate, is primarily used in the manufacture of lithopone, a white powder containing 20% barium sulphate, 30% zinc sulphide and less than 8% zinc oxide. Lithopone is widely employed as a pigment in white paints. Chemically precipitated barium sulphate—blanc fixe—is used in high-quality paints, in x-ray diagnostic work and in the glass and paper industries. It is also used in the manufacture of photographic papers, artificial ivory and cellophane. Crude barite is used as a thixotropic mud in oil-well drilling.

Barium hydroxide (Ba(OH)2) is found in lubricants, pesticides, the sugar industry, corrosion inhibitors, drilling fluids and water softeners. It is also used in glass manufacture, synthetic rubber vulcanization, animal and vegetable oil refining, and fresco painting. Barium carbonate (BaCO3) is obtained as a precipitate of barite and is used in the brick, ceramics, paint, rubber, oil-well drilling and paper industries. It also finds use in enamels, marble substitutes, optical glass and electrodes.

Barium oxide (BaO) is a white alkaline powder which is used to dry gases and solvents. At 450°C it combines with oxygen to produce barium peroxide (BaO2), an oxidizing agent in organic synthesis and a bleaching material for animal substances and vegetable fibres. Barium peroxide is used in the textile industry for dyeing and printing, in powder aluminium for welding and in pyrotechnics.

Barium chloride (BaCl2) is obtained by roasting barite with coal and calcium chloride, and is used in the manufacture of pigments, colour lakes and glass, and as a mordant for acid dyes. It is also useful for weighting and dyeing textile fabrics and in aluminium refining. Barium chloride is a pesticide, a compound added to boilers for softening water, and a tanning and finishing agent for leather. Barium nitrate (Ba(NO3)2) is used in pyrotechnics and the electronics industries.

Hazards

Barium metal has only limited use and presents an explosion hazard. The soluble compounds of barium (chloride, nitrate, hydroxide) are highly toxic; the inhalation of the insoluble compounds (sulphate) may give rise to pneumoconiosis. Many of the compounds, including the sulphide, oxide and carbonate, may cause local irritation to the eyes, nose, throat and skin. Certain compounds, particularly the peroxide, nitrate and chlorate, present fire hazards in use and storage.

Toxicity

When the soluble compounds enter by the oral route they are highly toxic, with a fatal dose of the chloride thought to be 0.8 to 0.9 g. However, although poisoning due to the ingestion of these compounds does occasionally occur, very few cases of industrial poisoning have been reported. Poisoning may result when workers are exposed to atmospheric concentrations of the dust of soluble compounds such as may occur during grinding. These compounds exert a strong and prolonged stimulant action on all forms of muscle, markedly increasing contractility. In the heart, irregular contractions may be followed by fibrillation, and there is evidence of a coronary constrictor action. Other effects include intestinal peristalsis, vascular constriction, bladder contraction and an increase in voluntary muscle tension. Barium compounds also have irritant effects on mucous membranes and the eye.

Barium carbonate, an insoluble compound, does not appear to have pathological effects from inhalation; however, it can cause severe poisoning from oral intake, and in rats it impairs the function of the male and female gonads; the foetus is sensitive to barium carbonate during the first half of pregnancy.

Pneumoconiosis

Barium sulphate is characterized by its extreme insolubility, a property which makes it non-toxic to humans. For this reason and due to its high radio-opacity, barium sulphate is used as an opaque medium in x-ray examination of the gastrointestinal, respiratory and urinary systems. It is also inert in the human lung, as has been demonstrated by its lack of adverse effects following deliberate introduction into the bronchial tract as a contrast medium in bronchography and by industrial exposure to high concentrations of fine dust.

Inhalation, however, may lead to deposition in the lungs in sufficient quantities to produce baritosis (a benign pneumoconiosis, which principally occurs in the mining, grinding and bagging of barite, but has been reported in the manufacture of lithopone). The first reported case of baritosis was accompanied by symptoms and disability, but these were associated later with other lung disease. Subsequent studies have contrasted the unimpressive nature of the clinical picture and the total absence of symptoms and abnormal physical signs with the well marked x-ray changes, which show disseminated nodular opacities throughout both lungs. The opacities are discrete but sometimes so numerous as to overlap and appear confluent. No massive shadows have been reported. The outstanding feature of the radiographs is the marked radio-opacity of the nodules, which is understandable in view of the substance’s use as a radio-opaque medium. The size of the individual elements may vary between 1 and 5 mm in diameter, although the average is about 3 mm or less, and the shape has been described variously as “rounded” and “dendritic”. In some cases, a number of very dense points have been found to lie in a matrix of lower density.

In one series of cases, dust concentrations of up to 11,000 particles/cm3 were measured at the workplace, and chemical analysis showed that the total silica content lay between 0.07 and 1.96%, quartz not being detectable by x-ray diffraction. Men exposed for up to 20 years and exhibiting x-ray changes were symptomless, had excellent lung function and were capable of carrying out strenuous work. Years after the exposure has ceased, follow-up examinations show a marked clearing of x-ray abnormalities.

Reports of post-mortem findings in pure baritosis are practically non-existent. However, baritosis may be associated with silicosis in mining due to contamination of barite ore by siliceous rock, and, in grinding, if siliceous millstones are used.

Safety and Health Measures

Adequate washing and other sanitary facilities should be provided for workers exposed to toxic soluble barium compounds, and rigorous personal hygiene measures should be encouraged. Smoking and consumption of food and beverages in workshops should be prohibited. Floors in workshops should be made of impermeable materials and frequently washed down. Employees working on such processes as barite leaching with sulphuric acid should be supplied with acid-resistant clothing and suitable hand and face protection. Although baritosis is benign, efforts should still be made to reduce atmospheric concentrations of barite dust to a minimum. In addition, particular attention should be paid to the presence of free silica in the airborne dust.

 

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Wednesday, 09 February 2011 04:36

Arsenic

Gunnar Nordberg

There are three major groups of arsenic (As) compounds:

  1. inorganic arsenic compounds
  2. organic arsenic compounds
  3. arsine gas and substituted arsines.

     

    Occurrence and Uses

    Arsenic is found widely in nature and most abundantly in sulphide ores. Arsenopyrite (FeAsS) is the most abundant one.

    Elemental arsenic

    Elemental arsenic is utilized in alloys in order to increase their hardness and heat resistance (e.g., alloys with lead in shot-making and battery grids). It is also used in the manufacture of certain types of glass, as a component of electrical devices and as a doping agent in germanium and silicon solid-state products.

    Trivalent inorganic compounds

    Arsenic trichloride (AsCl3) is used in the ceramics industry and in the manufacturing of chlorine-containing arsenicals. Arsenic trioxide (As2O3), or white arsenic, is useful in the purification of synthesis gas and as a primary material for all arsenic compounds. It is also a preservative for hides and wood, a textile mordant, a reagent in mineral flotation, and a decolourizing and refining agent in glass manufacture. Calcium arsenite (Ca(As2H2O4)) and cupric acetoarsenite (usually considered Cu(COOCH3)2 3Cu(AsO2)2) are insecticides. Cupric acetoarsenite is also used for painting ships and submarines. Sodium arsenite (NaAsO2) is employed as a herbicide, a corrosion inhibitor, and as a drying agent in the textile industry. Arsenic trisulphide is a component of infrared-transmitting glass and a dehairing agent in the tanning industry. It is also used in the manufacturing of pyrotechnics and semiconductors.

    Pentavalent inorganic compounds

    Arsenic acid (H3AsO4·½H2O) is found in the manufacture of arsenates, glass making and wood-treating processes. Arsenic pentoxide (As2O5), an herbicide and a wood preservative, is also used in the manufacture of coloured glass.

    Calcium arsenate (Ca3(AsO4)2) is used as an insecticide.

    Organic arsenic compounds

    Cacodylic acid ((CH3)2AsOOH) is used as a herbicide and a defoliant. Arsanilic acid (NH2C6H4AsO(OH)2) finds use as a grasshopper bait and as an additive in animal feeds. Organic arsenic compounds in marine organisms occur in concentrations corresponding to a concentration of arsenic in the range 1 to 100 mg/kg in marine organisms such as shrimp and fish. Such arsenic is mainly made up of arsenobetaine and arsenocholine, organic arsenic compounds of low toxicity.

    Arsine gas and the substituted arsines. Arsine gas is used in organic syntheses and in the processing of solid-state electronic components. Arsine gas may also be generated inadvertently in industrial processes when nascent hydrogen is formed and arsenic is present.

    The substituted arsines are trivalent organic arsenical compounds which, depending on the number of alkyl or phenyl groups that they have attached to the arsenic nucleus, are known as mono-, di- or tri-substituted arsines. Dichloroethylarsine (C2H5AsCl2), or ethyldichloroarsine, is a colourless liquid with an irritant odour. This compound, like the following one, was developed as a potential chemical warfare agent.

    Dichloro(2-chlorovinyl-)arsine (ClCH:CHAsCl2), or chlorovinyldichloroarsine (lewisite), is an olive-green liquid with a germanium-like odour. It was developed as a potential warfare agent but never used. The agent dimercaprol or British anti-lewisite (BAL) was developed as an antidote.

    Dimethyl-arsine (CH3)2AsH, or cacodyl hydride and trimethylarsine (CH3)3As), or trimethylarsenic, are both colourless liquids. These two compounds can be produced after metabolic transformation of arsenic compounds by bacteria and fungi.

    Hazards

    Inorganic arsenic compounds

    General aspects of toxicity. Although it is possible that very small amounts of certain arsenic compounds may have beneficial effects, as indicated by some animal studies, arsenic compounds, particularly the inorganic ones, are otherwise regarded as very potent poisons. Acute toxicity varies widely among compounds, depending on their valency state and solubility in biological media. The soluble trivalent compounds are the most toxic. Uptake of inorganic arsenic compounds from the gastrointestinal tract is almost complete, but uptake may be delayed for less soluble forms such as arsenic trioxide in particle form. Uptake after inhalation is also almost complete, since even less soluble material deposited on the respiratory mucosa, will be transferred to the gastrointestinal tract and subsequently taken up.

    Occupational exposure to inorganic arsenic compounds through inhalation, ingestion or skin contact with subsequent absorption may occur in industry. Acute effects at the point of entry may occur if exposure is excessive. Dermatitis may occur as an acute symptom but is more often the result of toxicity from long-term exposure, sometimes subsequent to sensitization (see the section “Long-term exposure (chronic poisoning)”).

    Acute poisoning

    Exposure to high doses of inorganic arsenic compounds by a combination of inhalation and ingestion may occur as a result of accidents in industries where large amounts of arsenic (e.g., arsenic trioxide), are handled. Depending on dose, various symptoms may develop, and when doses are excessive, fatal cases may occur. Symptoms of conjunctivitis, bronchitis and dyspnoea, followed by gastrointestinal discomfort with vomiting, and subsequently cardiac involvement with irreversible shock, may occur in a time course of hours. Arsenic in blood was reported to be above 3 mg/l in a case with fatal outcome.

    With exposure to sub-lethal doses of irritant arsenic compounds in air (e.g., arsenic trioxide), there may be symptoms related to acute damage to the mucous membranes of the respiratory system and acute symptoms from exposed skin. Severe irritation of the nasal mucosae, larynx and bronchi, as well as conjunctivitis and dermatitis, occur in such cases. Perforation of the nasal septum can be observed in some individuals only after a few weeks following exposure. A certain tolerance against acute poisoning is believed to develop upon repeated exposure. This phenomenon, however, is not well documented in the scientific literature.

    Effects due to accidental ingestion of inorganic arsenicals, mainly arsenic trioxide, have been described in the literature. However, such incidents are rare in industry today. Cases of poisoning are characterized by profound gastrointestinal damage, resulting in severe vomiting and diarrhoea, which may result in shock and subsequent oliguria and albuminuria. Other acute symptoms are facial oedema, muscular cramps and cardiac abnormalities. Symptoms may occur within a few minutes following exposure to the poison in solution, but may be delayed for several hours if the arsenic compound is in solid form or if it is taken with a meal. When ingested as a particulate, toxicity is also dependent on solubility and particle size of the ingested compound. The fatal dose of ingested arsenic trioxide has been reported to range from 70 to 180 mg. Death may occur within 24 hours, but the usual course runs from 3 to 7 days. Acute intoxication with arsenic compounds is usually accompanied by anaemia and leucopenia, especially granulocytopenia. In survivors these effects are usually reversible within 2 to 3 weeks. Reversible enlargement of the liver is also seen in acute poisoning, but liver function tests and liver enzymes are usually normal.

    In individuals surviving acute poisoning, peripheral nervous disturbances frequently develop a few weeks after ingestion.

    Long-term exposure (chronic poisoning)

    General aspects. Chronic arsenic poisoning may occur in workers exposed for a long time to excessive concentrations of airborne arsenic compounds. Local effects in the mucous membranes of the respiratory tract and the skin are prominent features. Involvement of the nervous and circulatory system and the liver may also occur, as well as cancer of the respiratory tract.

    With long-term exposure to arsenic via ingestion in food, drinking water or medication, symptoms are partly different from those after inhalation exposure. Vague abdominal symptoms—diarrhoea or constipation, flushing of the skin, pigmentation and hyperkeratosis—dominate the clinical picture. In addition, there may be vascular involvement, reported in one area to have given rise to peripheral gangrene.

    Anaemia and leucocytopenia often occur in chronic arsenic poisoning. Liver involvement has been more commonly seen in persons exposed for a long time via oral ingestion than in those exposed via inhalation, particularly in vineyard workers considered to have been exposed mainly through drinking contaminated wine. Skin cancer occurs with excess frequency in this type of poisoning.

    Vascular disorders. Long-term oral exposure to inorganic arsenic via drinking water may give rise to peripheral vascular disorders with Raynaud’s phenomenon. In one area of Taiwan, China, peripheral gangrene (so-called Blackfoot disease) has occurred. Such severe manifestations of peripheral vascular involvement have not been observed in occupationally exposed persons, but slight changes with Raynaud’s phenomenon and an increased prevalence of low peripheral blood presssure on cooling have been found in workers exposed for a long time to airborne inorganic arsenic (doses of absorbed arsenic are given below.

    Dermatological disorders. Arsenical skin lesions differ somewhat, depending on the type of exposure. Eczematoid symptoms of varying degrees of severity do occur. In occupational exposure to mainly airborne arsenic, skin lesions may result from local irritation. Two types of dermatological disorders may occur:

    1. an eczematous type with erythema (redness), swelling and papules or vesicles
    2. a follicular type with erythema and follicular swelling or follicular pustules.

       

      Dermatitis is primarily localized on the most heavily exposed areas, such as the face, back of the neck, forearms, wrists and hands. However, it may also occur on the scrotum, the inner surfaces of the thighs, the upper chest and back, the lower legs and around the ankles. Hyperpigmentation and keratoses are not prominent features of this type of arsenical lesions. Patch tests have demonstrated that the dermatitis is due to arsenic, not to impurities present in the crude arsenic trioxide. Chronic dermal lesions may follow this type of initial reaction, depending on the concentration and duration of exposure. These chronic lesions may occur after many years of occupational or environmental exposure. Hyperkeratosis, warts and melanosis of the skin are the conspicuous signs.

      Melanosis is most commonly seen on the upper and lower eyelids, around the temples, on the neck, on the areolae of the nipples and in the folds of the axillae. In severe cases arsenomelanosis is observed on the abdomen, chest, back and scrotum, along with hyperkeratosis and warts. In chronic arsenic poisoning, depigmentation (i.e., leukoderma), especially on the pigmented areas, commonly called “raindrop” pigmentation, also occurs. These chronic skin lesions, particularly the hyperkeratoses, may develop into pre-cancerous and cancerous lesions. A transverse striation of the nails (so-called Mees lines) also occurs in chronic arsenical poisoning. It should be noted that the chronic skin lesions may develop long after cessation of exposure, when arsenic concentrations in skin have returned to normal.

      Mucous membrane lesions in chronic arsenic exposure is most classically reported as perforation of the nasal septum after inhalation exposure. This lesion is a result of irritation of the mucous membranes of the nose. Such irritation also extends to the larynx, trachea and bronchi. Both in inhalation exposure and in poisoning caused by repeated ingestion, dermatitis of the face and eyelids sometimes extends to keratoconjunctivitis.

      Peripheral neuropathy. Peripheral nervous disturbances are frequently encountered in survivors of acute poisoning. They usually start within a few weeks after the acute poisoning, and recovery is slow. The neuropathy is characterized by both motor dysfunction and paresthaesia, but in less severe cases only sensory unilateral neuropathy may occur. Often the lower extremities are more affected than the upper ones. In subjects recovering from arsenical poisoning, Mees lines of the fingernails may develop. Histological examination has revealed Wallerian degeneration, especially in the longer axons. Peripheral neuropathy also may occur in industrial arsenic exposure, in most cases in a subclinical form that can be detected only by neurophysiological methods. In a group of smelter workers with long-term exposure corresponding to a mean cumulative total absorption of approximately 5 g (maximal absorption of 20 g), there was a negative correlation between cumulative absorption of arsenic and nerve conduction velocity. There were also some light clinical manifestations of peripheral vascular involvement in these workers (see above). In children exposed to arsenic, hearing loss has been reported.

      Carcinogenic effects. Inorganic arsenic compounds are classified by the International Agency for Research on Cancer (IARC) as lung and skin carcinogens. There is also some evidence to suggest that persons exposed to inorganic arsenic compounds suffer a higher incidence of angiosarcoma of the liver and possibly of stomach cancer. Cancer of the respiratory tract has been reported in excess frequency among workers engaged in the production of insecticides containing lead arsenate and calcium arsenate, in vine-growers spraying insecticides containing inorganic copper and arsenic compounds, and in smelter workers exposed to inorganic compounds of arsenic and a number of other metals. The latency time between onset of exposure and the appearance of cancer is long, usually between 15 and 30 years. A synergistic action of tobacco smoking has been demonstrated for lung cancer.

      Long-term exposure to inorganic arsenic via drinking water has been associated with an increased incidence of skin cancer in Taiwan and in Chile. This increase has been shown to be related to concentration in drinking water.

      Teratogenic effects. High doses of trivalent inorganic arsenic compounds may cause malformations in hamsters when injected intravenously. With regard to human beings there is no firm evidence that arsenic compounds cause malformations under industrial conditions. Some evidence, however, suggests such an effect in workers in a smelting environment who were exposed simultaneously also to a number of other metals as well as other compounds.

      Organic arsenic compounds

      Organic arsenicals used as pesticides or as drugs may also give rise to toxicity, although such adverse effects are incompletely documented in humans.

      Toxic effects on the nervous system have been reported in experimental animals following feeding with high doses of arsanilic acid, which is commonly used as a feed additive in poultry and swine.

      The organic arsenic compounds that occur in foodstuffs of marine origin, such as shrimp, crab and fish, are made up of arsinocholine and arsinobetaine. It is well known that the amounts of organic arsenic that are present in fish and shellfish can be consumed without ill effects. These compounds are quickly excreted, mainly via urine.

      Arsine gas and the substituted arsines. Many cases of acute arsine poisoning have been recorded, and there is a high fatality rate. Arsine is one of the most powerful haemolytic agents found in industry. Its haemolytic activity is due to its ability to cause a fall in erythrocyte-reduced glutathion content.

      Signs and symptoms of arsine poisoning include haemolysis, which develops after a latent period that is dependent on the intensity of exposure. Inhalation of 250 ppm of arsine gas is instantly lethal. Exposure to 25 to 50 ppm for 30 minutes is lethal, and 10 ppm may be lethal after longer exposures. The signs and symptoms of poisoning are those characteristic of an acute and massive haemolysis. Initially there is a painless haemoglobinuria, gastrointestinal disturbance such as nausea and possibly vomiting. There may also be abdominal cramps and tenderness. Jaundice accompanied by anuria and oliguria subsequently occurs. Evidence of bone marrow depression may be present. After acute and severe exposure, a peripheral neuropathy may develop and can still be present several months after poisoning. Little is known about repeated or chronic exposure to arsine, but since the arsine gas is metabolized to inorganic arsenic in the body, it can be assumed that there is a risk for symptoms similar to those in long-term exposure to inorganic arsenic compounds.

      The differential diagnosis should take account of acute haemolytic anaemias that could be caused by other chemical agents such as stibine or drugs, and secondary immunohaemolytic anaemias.

      The substituted arsines do not give rise to haemolysis as their main effect, but they act as powerful local and pulmonary irritants and systemic poisons. The local effect on the skin gives rise to sharply circumscribed blisters in the case of dichloro(2-chlorovinyl-)arsine (lewisite). The vapour induces marked spasmodic coughing with frowzy or blood-stained sputum, progressing to acute pulmonary oedema. Dimercaprol (BAL) is an effective antidote if given in the early stages of poisoning.

      Safety and Health Measures

      The most common type of occupational arsenic exposure is to inorganic arsenic compounds, and these safety and health measures are mainly related to such exposures. When there is a risk of exposure to arsine gas, particular attention needs to be paid to accidental leaks, since peak exposures for short intervals may be of special concern.

      The best means of prevention is to keep exposure well below accepted exposure limits. A programme of measurement of air-concentrations of arsenic is thus of importance. In addition to inhalation exposure, oral exposure via contaminated clothes, hands, tobacco and so on should be watched, and biological monitoring of inorganic arsenic in urine may be useful for evaluation of absorbed doses. Workers should be supplied with suitable protective clothing, protective boots and, when there is a risk that the exposure limit for airborne arsenic will be exceeded, respiratory protective equipment. Lockers should be provided with separate compartments for work and personal clothes, and adjacent sanitary facilities of a high standard should be made available. Smoking, eating and drinking at the workplace should not be allowed. Pre-employment medical examinations should be carried out. It is not recommended to employ persons with pre-existing diabetes, cardiovascular diseases, anaemia, allergic or other skin diseases, neurologic, hepatic or renal lesions, in arsenic work. Periodic medical examinations of all arsenic-exposed employees should be performed with special attention to possible arsenic-related symptoms.

      Determination of the level of inorganic arsenic and its metabolites in urine allows estimation of the total dose of inorganic arsenic taken up by various exposure routes. Only when inorganic arsenic and its metabolites can be specifically measured is this method useful. Total arsenic in urine may often give erroneous information about industrial exposure, since even a single meal of fish or other marine organisms (containing considerable amounts of non-toxic organic arsenic compound) may cause greatly elevated urinary arsenic concentrations for several days.

      Treatment

      Arsine gas poisoning. When there is reason to believe that there has been considerable exposure to arsine gas, or upon observation of the first symptoms (e.g., haemoglobinuria and abdominal pain), immediate removal of the individual from the contaminated environment and prompt medical attention are required. The recommended treatment, if there is any evidence of impaired renal function, consists of total-replacement blood transfusion associated with prolonged artificial dialysis. Forced diuresis has proved useful in some cases, whereas, in the opinion of most authors, treatment with BAL or other chelating agents seems to have only limited effect.

      Exposure to the substituted arsines should be treated in the same way as inorganic arsenic poisoning (see below).

      Poisoning by inorganic arsenic. If there has been exposure to doses that can be estimated to give rise to acute poisoning, or if severe symptoms from the respiratory system, the skin or the gastrointestinal tract occur in the course of long-term exposures, the worker should immediately be removed from exposure and treated with a complexing agent.

      The classical agent which has been used most widely in such situations is 2,3-dimercapto-1-propanol or British anti-lewisite (BAL, dimercaprol). Prompt administration in such cases is vital: to obtain maximal benefit such treatment should be given within 4 hours of poisoning. Other pharmaceuticals which may be used are sodium 2,3-dimercaptopropanesulphonate (DMPS or unithiol) or meso-2,3-dimercaptosuccinic acid (DMSA). These drugs are less likely to give side effects and are believed to be more effective than BAL. Intravenous administration of N-acetylcysteine has been reported in one case to be of value; in addition, general treatment, such as prevention of further absorption by removal from exposure and minimizing absorption from the gastrointestinal tract by gastric lavage and administration by gastric tube of chelating agents or charcoal, is mandatory. General supportive therapy, such as maintenance of respiration and circulation, maintenance of water and electrolyte balance, and control of nervous system effects, as well as elimination of absorbed poison through haemodialysis and exchange transfusion, may be used if feasible.

      Acute skin lesions such as contact dermatitis and mild manifestations of peripheral vascular involvement, such as Raynaud’s syndrome, usually do not require treatment other than removal from exposure.

       

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      Wednesday, 09 February 2011 04:31

      Antimony

      Gunnar Nordberg

      Antimony is stable at room temperature but, when heated, burns brilliantly, giving off dense white fumes of antimony oxide (Sb2O3) with a garlic-like odour. It is closely related, chemically, to arsenic. It readily forms alloys with arsenic, lead, tin, zinc, iron and bismuth.

      Occurrence and Uses

      In nature, antimony is found in combination with numerous elements, and the most common ores are stibnite (SbS3), valentinite (Sb2O3), kermesite (Sb2S2O) and senarmontite (Sb2O3).

      High-purity antimony is employed in the manufacture of semiconductors. Normal-purity antimony is used widely in the production of alloys, to which it imparts increased hardness, mechanical strength, corrosion resistance and a low coefficient of friction; alloys combining tin, lead and antimony are used in the electrical industry. Among the more important antimony alloys are babbitt, pewter, white metal, Britannia metal and bearing metal. These are used for bearing shells, storage battery plates, cable sheathing, solder, ornamental castings and ammunition. The resistance of metallic antimony to acids and bases is put to effect in the manufacture of chemical plants.

      Hazards

      The principal hazard of antimony is that of intoxication by ingestion, inhalation or skin absorption. The respiratory tract is the most important route of entry since antimony is so frequently encountered as a fine airborne dust. Ingestion may occur through swallowing dust or through contamination of beverages, food or tobacco. Skin absorption is less common, but may occur when antimony is in prolonged contact with skin.

      The dust encountered in antimony mining may contain free silica, and cases of pneumoconiosis (termed silico-antimoniosis) have been reported among antimony miners. During processing, the antimony ore, which is extremely brittle, is converted into fine dust more rapidly than the accompanying rock, leading to high atmospheric concentrations of fine dust during such operations as reduction and screening. Dust produced during crushing is relatively coarse, and the remaining operations—classification, flotation, filtration and so on—are wet processes and, consequently, dust free. Furnace workers who refine metallic antimony and produce antimony alloy, and workers setting type in the printing industry, are all exposed to antimony metal dust and fumes, and may present diffuse miliar opacities in the lung, with no clinical or functional signs of impairment in the absence of silica dust.

      Inhalation of antimony aerosols may produce localized reactions of the mucous membrane, respiratory tract and lungs. Examination of miners and concentrator and smelter workers exposed to antimony dust and fumes has revealed dermatitis, rhinitis, inflammation of upper and lower respiratory tracts, including pneumonitis and even gastritis, conjunctivitis and perforations of the nasal septum.

      Pneumoconiosis, sometimes in combination with obstructive lung changes, has been reported following long-term exposure in humans. Although antimony pneumoconiosis is regarded as benign, the chronic respiratory effects associated with heavy antimony exposure are not considered harmless. In addition, effects on the heart, even fatal, have been related to long-term occupational exposure to antimony trioxide.

      Pustular skin infections are sometimes seen in persons working with antimony and antimony salts. These eruptions are transient and primarily affect the skin areas in which heat exposure or sweating has occurred.

      Toxicology

      In its chemical properties and metabolic action, antimony has a close resemblance to arsenic, and, since the two elements are sometimes found in association, the action of antimony may be blamed on arsenic, especially in foundry workers. However, experiments with high-purity metallic antimony have shown that this metal has a completely independent toxicology; different authors have found the average lethal dose to be between 10 and 11.2 mg/100 g.

      Antimony may enter the body through the skin, but the principal route is through the lungs. From the lungs, antimony, and especially free antimony, is absorbed and taken up by the blood and tissues. Studies on workers and experiments with radioactive antimony have shown that the major part of the absorbed dose enters the metabolism within 48 hours and is eliminated in the faeces and, to a lesser extent, the urine. The remainder stays in the blood for some considerable time, with the erythrocytes containing several times more antimony than the serum. In workers exposed to pentavalent antimony, the urinary excretion of antimony is related to the intensity of exposure. It has been estimated that after 8 hours exposure to 500 µg Sb/m3, the increase in concentration of antimony excreted in the urine at the end of a shift amounts on average to 35 µg/g creatinine.

      Antimony inhibits the activity of certain enzymes, binds sulphydryl groups in the serum, and disturbs protein and carbohydrate metabolism and the production of glycogen by the liver. Prolonged animal experiments with antimony aerosols have led to the development of distinctive endogenous lipoid pneumonia. Cardiac injury and cases of sudden death have also been reported in workers exposed to antimony. Focal fibrosis of the lung and cardiovascular effects have also been observed in animal trials.

      The therapeutic use of antimonial drugs has made it possible to detect, in particular, the cumulative myocardial toxicity of the trivalent derivatives of antimony (which are excreted more slowly than pentavalent derivatives). Reduction in amplitude of T wave, increase of QT interval and arrhythmias have been observed in the electrocardiogram.

      Symptoms

      The symptoms of acute poisoning include violent irritation of the mouth, nose, stomach and intestines; vomiting and bloody stools; slow, shallow respiration; coma sometimes followed by death due to exhaustion and hepatic and renal complications. Those of chronic poisoning are: dryness of throat, nausea, headaches, sleeplessness, loss of appetite, and dizziness. Gender differences in the effects of antimony have been noted by some authors, but the differences are not well established.

      Compounds

      Stibine (SbH3), or antimony hydride (hydrogen antimonide), is produced by dissolving zinc-antimony or magnesium-antimony alloy in dilute hydrochloric acid. However, it occurs frequently as a by-product in the processing of metals containing antimony with reducing acids or in overcharging storage batteries. Stibine has been used as a fumigating agent. High-purity stibine is used as an n-type gas-phase dopant for silicon in semiconductors. Stibine is an extremely hazardous gas. Like arsine it may destroy blood cells and cause haemoglobinuria, jaundice, anuria and death. Symptoms include headache, nausea, epigastric pain and passage of dark red urine following exposure.

      Antimony trioxide (Sb2O3) is the most important of the antimony oxides. When airborne, it tends to remain suspended for an exceptionally long time. It is obtained from antimony ore by a roasting process or by oxidizing metallic antimony and subsequent sublimation, and is used for the manufacture of tartar emetic, as a paint pigment, in enamels and glazes, and as a flameproofing compound.

      Antimony trioxide is both a systemic poison and a skin disease hazard, although its toxicity is three times less than that of the metal. In long-term animal experiments, rats exposed to antimony trioxide via inhalation showed a high frequency of lung tumours. An excess of deaths due to cancer of the lung among workers engaged in antimony smelting for more than 4 years, at an average concentration in air of 8 mg/m3, has been reported from Newcastle. In addition to antimony dust and fumes, the workers were exposed to zircon plant effluents and caustic soda. No other experiences were informative on the carcinogenic potential of antimony trioxide. This has been classified by the American Conference of Governmental Industrial Hygienists (ACGIH) as a chemical substance associated with industrial processes which are suspected of inducing cancer.

      Antimony pentoxide (Sb2O5) is produced by the oxidation of the trioxide or the pure metal, in nitric acid under heat. It is used in the manufacture of paints and lacquers, glass, pottery and pharmaceuticals. Antimony pentoxide is noted for its low degree of toxic hazard.

      Antimony trisulphide (Sb2S3) is found as a natural mineral, antimonite, but can also be synthesized. It is used in the pyrotechnics, match and explosives industries, in ruby glass manufacture, and as a pigment and plasticizer in the rubber industry. An apparent increase in heart abnormalities has been found in persons exposed to the trisulphide. Antimony pentasulphide (Sb2S5) has much the same uses as the trisulphide and has a low level of toxicity.

      Antimony trichloride (SbCl3), or antimonous chloride (butter of antimony), is produced by the interaction of chlorine and antimony or by dissolving antimony trisulphide in hydrochloric acid. Antimony pentachloride (SbCl5) is produced by the action of chlorine on molten antimony trichloride. The antimony chlorides are used for blueing steel and colouring aluminium, pewter and zinc, and as catalysts in organic synthesis, especially in the rubber and pharmaceutical industries. In addition, antimony trichloride is used in the match and petroleum industries. They are highly toxic substances, act as irritants and are corrosive to the skin. The trichloride has an LD50 of 2.5 mg/100 g.

      Antimony trifluoride (SbF3) is prepared by dissolving antimony trioxide in hydrofluoric acid, and is used in organic synthesis. It is also employed in dyeing and pottery manufacture. Antimony trifluoride is highly toxic and an irritant to the skin. It has an LD50 of 2.3 mg/100 g.

      Safety and Health Measures

      The essence of any safety programme for the prevention of antimony poisoning should be the control of dust and fume formation at all stages of processing.

      In mining, dust prevention measures are similar to those for metal mining in general. During crushing, the ore should be sprayed or the process completely enclosed and fitted with local exhaust ventilation combined with adequate general ventilation. In antimony smelting the hazards of charge preparation, furnace operation, fettling and electrolytic cell operation should be eliminated, where possible, by isolation and process automation. Furnace workers should be provided with water sprays and effective ventilation.

      Where complete elimination of exposure is not possible, the hands, arms and faces of workers should be protected by gloves, dustproof clothing and goggles, and, where atmospheric exposure is high, respirators should be provided. Barrier creams should also be applied, especially when handling soluble antimony compounds, in which case they should be combined with the use of waterproof clothing and rubber gloves. Personal hygiene measures should be strictly observed; no food or beverages should be consumed in the workshops, and suitable sanitary facilities should be provided so that workers can wash before meals and before leaving work.

       

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      Wednesday, 09 February 2011 04:23

      Aluminium

      Gunnar Nordberg

      Occurrence and uses

      Aluminium is the most abundant metal in the earth’s crust, where it is found in combination with oxygen, fluorine, silica, etc., but never in the metallic state. Bauxite is the principal source of aluminium. It consists of a mixture of minerals formed by the weathering of aluminium-bearing rocks. Bauxites are the richest form of these weathered ores, containing up to 55% alumina. Some lateritic ores (containing higher percentages of iron) contain up to 35% Al2O3· Commercial deposits of bauxite are mainly gibbsite (Al2O3·3H2O) and boehmite (Al2O3·H2O) and are found in Australia, Guyana, France, Brazil, Ghana, Guinea, Hungary, Jamaica and Suriname. World production of bauxite in 1995 was 111,064 million tonnes. Gibbsite is more readily soluble in sodium hydroxide solutions than boehmite and is therefore preferred for aluminium oxide production.

      Aluminium is used widely throughout industry and in larger quantities than any other non-ferrous metal; worldwide primary metal production in 1995 was estimated at 20,402 million tonnes. It is alloyed with a variety of other material including copper, zinc, silicon, magnesium, manganese and nickel and may contain small amounts of chromium, lead, bismuth, titanium, zirconium and vanadium for special purposes. Aluminium and aluminium alloy ingots can be extruded or processed in rolling mills, wire-works, forges or foundries. The finished products are used in shipbuilding for internal fittings and superstructures; the electrical industry for wires and cables; the building industry for house and window frames, roofs and cladding; aircraft industry for airframes and aircraft skin and other components; automobile industry for bodywork, engine blocks and pistons; light engineering for domestic appliances and office equipment and in the jewellery industry. A major application of sheet is in beverage or food containers, while aluminium foil is used for packaging; a fine particulate form of aluminium is employed as a pigment in paints and in the pyrotechnics industry. Articles manufactured from aluminium are frequently given a protective and decorative surface finish by anodization.

      Aluminium chloride is used in petroleum cracking and in the rubber industry. It fumes in air to form hydrochloric acid and combines explosively with water; consequently, containers should be kept tightly closed and protected from moisture.

      Alkyl aluminium compounds. These are growing in importance as catalysts for the production of low-pressure polyethylene. They present a toxic, burn and fire hazard. They are extremely reactive with air, moisture and compounds containing active hydrogen and therefore must be kept under a blanket of inert gas.

      Hazards

      For the production of aluminium alloys, refined aluminium is melted in oil or gas-fired furnaces. A regulated amount of hardener containing aluminium blocks with a percentage of manganese, silicon, zinc, magnesium, etc. is added. The melt is then mixed and is passed into a holding furnace for degassing by passing either argon-chlorine or nitrogen-chlorine through the metal. The resultant gas emission (hydrochloric acid, hydrogen and chlorine) has been associated with occupational illnesses and great care should be taken to see that appropriate engineering controls capture the emissions and also prevent it from reaching the external environment, where it can also cause damage. Dross is skimmed off the surface of the melt and placed in containers to minimize exposure to air during cooling. A flux containing fluoride and/or chloride salts is added to the furnace to assist in separation of pure aluminium from the dross. Aluminium oxide and fluoride fumes may be given off so that this aspect of production must also be carefully controlled. Personal protective equipment (PPE) may be required. The aluminium smelting process is described in the chapter Metal processing and metal working industry. In the casting shops, exposure to sulphur dioxide may also occur.

      A wide range of different crystalline forms of aluminium oxide is used as smelter feed stock, abrasives, refractories and catalysts. A series of reports published in 1947 to 1949 described a progressive, non-nodular interstitial fibrosis in the aluminium abrasives industry in which aluminium oxide and silicon were processed. This condition, known as Shaver’s disease, was rapidly progressive and often fatal. The exposure of the victims (workers producing alundum) was to a dense fume comprising aluminium oxide, crystalline free-silica and iron. The particulates were of a size range that made them highly respirable. It is likely that the preponderence of disease is attributable to the highly damaging lung effects of the finely divided crystalline free-silica, rather than to the inhaled aluminium oxide, although the exact aetiology of the disease is not understood. Shaver’s disease is primarily of historical interest now, since no reports have been made in the second half of the 20th century.

      Recent studies of the health effects of high level exposures (100 mg/m3) to the oxides of aluminium amongst workers engaged in the Bayer process (described in the chapter Metal processing and metal working industry) have demonstrated that workers with more than twenty years of exposure can develop pulmonary alterations. These changes are clinically characterized by minor, predominantly asymptomatic degrees of restrictive pulmonary function changes. The chest x-ray examinations revealed small, scanty, irregular opacities, particularly at the lung bases. These clinical responses have been attributed to deposition of dust in the lung paraenchyma, which was the result of very high occupational exposures. These signs and symptoms cannot be compared to the extreme response of Shaver’s disease. It should be noted that other epidemiological studies in the United Kingdom regarding widespread alumina exposures in the pottery industry have produced no evidence that the inhalation of alumina dust produces chemical or radiographic signs of pulmonary disease or dysfunction.

      The toxicological effects of aluminium oxides remain of interest because of its commerical importance. The results of animal experiments are controversial. An especially fine (0.02 μm to 0.04 μm), catalytically active aluminium oxide, uncommonly used commercially, can cause lung changes in animals dosed by injection directly into the lung airways. Lower dose effects have not been observed.

      It should also be noted that so-called “potroom asthma” which has frequently been observed among workers in aluminium processing operations, is probably attributable to the exposures to fluoride fluxes, rather than to the aluminium dust itself.

      The production of aluminium has been classified as a Group 1, known human carcinogenic exposure situation, by the International Agency for Research on Cancer (IARC). As with the other diseases described above, the carcinogenicity is most likely attributable to the other substances present (e.g., polycyclic aromatic hydrocarbons (PAHs) and silica dust), although the exact role of the alumina dusts are simply not understood.

      Some data on the absorption of high levels of aluminium and nervous tissue damage are found among individuals requiring kidney dialysis. These high levels of aluminium have resulted in severe, even fatal brain damage. This response, however, has also been observed in other patients undergoing dialysis but who did not have similar elevated brain aluminium level. Animal experiments have been unsuccessful in replicating this brain response, or Alzheimer’s disease, which has also been postulated in the literature. Epidemiological and clinical follow-up studies on these issues have not been definitive and no evidence of such effects has been observed in the several large-scale epidemiological studies of aluminium workers.

       

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      Wednesday, 09 February 2011 04:19

      Acknowledgements

      The material presented here is based on an exhaustive review, revision and expansion of the data on metals found in the 3rd edition of the Encyclopaedia of Occupational Health and Safety. Members of the Scientific Committee on the Toxicology of Metals of the International Commission on Occupational Health carried out much of the review. They are listed below, along with other reviewers and authors.

      The reviewers are:

      L. Alessio

      Antero Aitio

      P. Aspostoli

      M. Berlin

      Tom W. Clarkson

      C-G. Elinder

      Lars Friberg

      Byung-Kook Lee

      N. Karle Mottet

      D.J. Nager

      Kogi Nogawa

      Tor Norseth

      C.N. Ong

      Kensaborv Tsuchiva

      Nies Tsukuab.

      The 4th edition contributors are:

      Gunnar Nordberg

      Sverre Langård.

      F. William Sunderman, Jr.

      Jeanne Mager Stellman

      Debra Osinsky

      Pia Markkanen

      Bertram D. Dinman

      Agency for Toxic Substances and Disease Registry (ATSDR).

      Revisions are based on the contributions of the following 3rd edition authors:
      A. Berlin, M. Berlin, P.L. Bidstrup, H.L. Boiteau, A.G. Cumpston, B.D. Dinman, A.T. Doig,
      J.L. Egorov, C-G. Elinder, H.B. Elkins, I.D. Gadaskina, J. Glrmme, J.R. Glover,
      G.A. Gudzovskij, S. Horiguchi, D. Hunter, Lars Järup, T. Karimuddin, R. Kehoe, R.K. Kye,
      Robert R. Lauwerys, S. Lee, C. Marti-Feced, Ernest Mastromatteo, O. Ja Mogilevskaja,
      L. Parmeggiani, N. Perales y Herrero, L. Pilat, T.A. Roscina, M. Saric, Herbert E. Stokinger,
      H.I. Scheinberg, P. Schuler, H.J. Symanski, R.G. Thomas, D.C. Trainor, Floyd A. van Atta,
      R. Wagg, Mitchell R. Zavon and R.L. Zielhuis.

       

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      Wednesday, 09 February 2011 04:02

      General Profile

      This chapter presents a series of short discussions of many metals. It contains a tabulation of major health effects, physical properties and physical and chemical hazards associated with these metals and many of their compounds (see table 1 and table 2). Not every metal is covered in this chapter. Cobalt and beryllium, for example, appear in the chapter Respiratory sytem. Other metals are discussed in more detail in articles that present information on the industries in which they predominate. The radioactive elements are discussed in the chapter Radiation, ionizing.

      Table 1. Physical and chemical hazards

      Chemical name

      CAS-number

      Molecular formula

      Physical and chemical hazards

      UN class/div/
subsidiary risks

      Aluminium chloride 
7446-70-0

      AICI3

       

      8

      Aluminium hydroxide
21645-51-2

      AI(OH)3

      • Forms gels (Al2·3H2O) on prolonged contact with water; absorbs acids and carbon dioxide
       

      Aluminium nitrate 
13473-90-0

      Al2(NO3)3

       

      5.1

      Aluminium phosphide 
20859-73-8

      AlP

      • Reacts with moist air, water, acids producing highly toxic fumes of phosphine
      • Reacts with water, moist air, acids causing fire and toxic (phosphine fumes) hazard

      4.3/ 6.1

      Diethylaluminium chloride 
96-10-6

      AlClC4H10

       

      4.2

      Ethylaluminium dichloride
563-43-9

      AlCl2C2H5

       

      4.2

      Ethylaluminium 
sesquichloride 
12075-68-2

      Al2Cl3C6H15

       

      4.2

      Sodium aluminate 
1302-42-7

       
      • The substance is a strong base, it reacts violently with acid and is corrosive
      • The solution in water is a strong base, it reacts violently with acid and is corrosive to aluminium and zinc

      8

      Triethylaluminium 
97-93-8

      AlC6H15

       

      4.2

      Triisobutylaluminium
100-99-2

      AlC12H27

       

      4.2

      Antimony 
7440-36-0

      Sb

      • On combustion, forms toxic fumes (antimony oxides) 
      • Reacts violently with strong oxidants (e.g., halogens, alkali permanganates and nitrates), causing fire and explosion hazard 
      • Reacts with nascent hydrogen in acid medium producing very toxic gas 
      • On contact with hot concentrated acids, emits toxic gas (stibine)

      6.1

      Antimony pentachloride 
7647-18-9

      SbCl5

       

      8

      Antimony pentafluoride 
7783-70-2

      SbF5

       

      3/ 6.1

      Antimony potassium tartrate
28300-74-5

      Sb2K2C8H4O12 ·
3H2O

       

      6.1

      Antimony trichloride 
10025-91-9

      SbCl3

       

      8

      Antimony trioxide 
1309-64-4

      Sb2O3

      • The substance decomposes on heating producing toxic fumes of antimony
      • Reacts under certain circumstances with hydrogen producing a very poisonous gas, stibine
       

      Stibine 
7803-52-3

      SbH3

      • The substance decomposes slowly at room temperature producing metallic antimony and hydrogen
      • Reacts violently with ozone and concentrated nitric 
acid causing fire and explosion hazard 
      • The substance decomposes on heating 
producing toxic fumes of antimony 
      • The gas is heavier than air and may travel along the ground; distant ignition possible

      2.3/ 2.1

      Arsenic 
7440-38-2

      As

      • Reacts with acids, oxidants, halogens 
      • The substance produces toxic fumes

      6.1

      Arsenic acid, copper salt
10103-61-4

      CuAsOH4

      • The substance decomposes on heating producing toxic fumes of arsenic by comparation with another compounds 
      • Reacts with acids releasing toxic arsine gas
       

      Arsenic acid, 
diammonium salt
7784-44-3

      (NH4)2AsOH4

      • The substance decomposes on heating producing toxic fumes including arsenic, nitrogen oxides and ammonia 
      • Reacts with acids producing toxic fumes of arsenic 
      • Attacks many metals, such as iron, aluminium and zinc, in presence of water releasing toxic fumes of arsenic and arsine
       

      Arsenic acid, 
disodium salt 
7778-43-0

      Na2AsOH4

      • The substance decomposes on heating producing toxic fumes of arsenic
      • Reacts with acids releasing toxic arsine gas 
      • Attacks many metals, such as iron, aluminium and zinc, in presence of water releasing toxic fumes of arsenic and arsine
       

      Arsenic acid, 
magnesium salt 
10103-50-1

      MgxAsO3H4

      • The substance decomposes on heating producing toxic fumes of arsenic 
      • Reacts with acids releasing toxic fumes of arsine gas

      6.1

      Arsenic acid, 
monopotassium salt 
7784-41-0

      KAsO2H4

      • The substance decomposes on heating producing toxic fumes of arsenic 
      • Reacts with acids releasing toxic arsine gas 
      • Attacks many metals, such as iron, aluminium and zinc, in presence of water releasing toxic fumes of arsenic and arsine
       

      Arsenic pentoxide
1303-28-2

      As2O5

      • The substance decomposes on heating above 300 °C producing toxic fumes (arsenic trioxide) and oxygen 
      • The solution in water is a medium strong acid, which may react with reducing substances producing very toxic gas (arsine) 
      • Reacts violently with bromine pentafluoride causing fire and explosion hazard 
      • Corrosive to metals in the presence of moisture

      6.1

      Arsenic trioxide 
1327-53-3

      As2O3

      • The substance is a strong reducing agent and reacts with oxidants 
      • The solution in water is a weak acid which may react with reducing substances producing very toxic gas (arsine) 
      • Gives off toxic fumes in a fire

      6.1

      Arsenious acid, 
copper(2+) salt(1:1)
10290-12-7

      CuAsH3

      • The substance decomposes on heating producing toxic fumes of arsenic 
      • Reacts with acids releasing toxic fumes of arsine gas

      6.1

      Arsenious acid, lead(II) salt
10031-13-7

      PbAs2O4

      • The substance decomposes on heating producing very toxic fumes of arsenic and lead
      • Reacts with oxidants · Reacts violently with strong acids
       

      Arsenious acid, 
potassium salt 
10124-50-2

      (KH3)x AsO3

      • The substance decomposes on heating producing toxic fumes of arsenic and potassium oxide
      • Reacts with acids releasing toxic arsine gas 
      • Decomposes on contact with air (by atmospheric carbon dioxide) and through the skin

      6.1

      Arsenous trichloride 
7784-34-1

      AsCl3

      • The substance decomposes on heating and under influence of light producing toxic fumes of hydrogen chloride and arsenic oxides 
      • Reacts violently with bases, strong oxidants and water, causing fire and toxic hazard 
      • On contact with air it emits corrosive fumes of hydrogen chloride
      • Attacks many metals forming combustible gas (hydrogen) in presence of moisture

      6.1

      Arsine 
7784-42-1

      AsH3

      • The substance decomposes on heating and under influence of light and moisture producing toxic arsenic fumes 
      • Reacts violently with strong oxidants, fluorine, chlorine, nitric acid, nitrogen trichloride, causing fire and explosion hazard 
      • The gas is heavier than air and may travel along the ground; distant ignition possible 
      • As a result of flow, agitation, etc., electrostatic charges can be generated, conductivity not checked

      2.3/ 2.1

      Calcium arsenate 
7778-44-1

      Ca3As2O8

      • The substance decomposes on heating producing toxic fumes of arsenic 
      • Reacts with acids releasing toxic arsine gas

      6.1

      Lead arsenate 
7784-40-9

      PbAsO4H

      • The substance decomposes on heating producing toxic fumes of lead, arsenic and its compounds, including arsine

      6.1

      Methylarsonic acid 
124-58-3

      AsCH503

      • The substance decomposes on heating or on burning producing toxic fumes (arsenic oxides)
      • The solution in water is a medium strong acid, which may react with reducing substances, active metals (i.e., iron, aluminium, zinc) producing toxic gas (methylarsine)
       

      Sodium arsenate
10048-95-0

      Na2AsO4H ·7H2O

      • The substance decomposes on heating producing toxic fumes including arsenic, arsenic oxides
      • Reacts violently with strong oxidants, strong acids and metals such as iron, aluminium and zinc causing explosion and toxic hazard

      6.1

      Barium 
7440-39-3

      Ba

      • The substance may spontaneously ignite on contact with air (if in powder form)
      • The substance is a strong reducing agent and reacts violently with oxidants and acids
      • Reacts with water, forming combustible gas (hydrogen) and barium hydroxide 
      • Reacts violently with halogenated solvents causing fire and explosion hazard

      4.3

      Barium carbonate 
513-77-9

      BaCO3

       

      6.1

      Barium chlorate 
13477-00-4

      BaCl2O6

      • Heating may cause violent combustion or explosion 
      • Shock-sensitive compounds are formed with organic compounds, reducing agents, ammonia-containing agents, metal powders, and sulphuric acid 
      • The substance decomposes violently on warming, on heating and on burning producing oxygen and toxic fumes, causing fire and explosion hazard
      • The substance is a strong oxidant and reacts with combustible and reducing materials
      • Dust explosion possible if in powder or granular form, mixed with air

      5.1/ 6.1

      Barium chloride 
10361-37-2

      BaCl2

      • The substance decomposes on heating producing toxic fumes

      6.1

      Barium chloride, dihydrate 
10326-27-9

      BaCl2·2H20

      • The substance decomposes on heating producing toxic fumes

      6.1

      Barium 
chromate (VI) 
10294-40-3

      BaCrH2O4

       

      6.1

      Barium hydroxide 
17194-00-2

      Ba(OH)2

       

      6.1

      Barium nitrate 
10022-31-8

      BaNO3

       

      5.1/ 6.1

      Barium oxide 
1304-28-5

      BaO

      • The solution in water is a medium strong base 
      • Reacts violently with water, hydrogen sulphide, hydroxylamine, and sulphur trioxide, causing fire and explosion hazard

      6.1

      Barium perchlorate 
13465-95-7

      BaCl2O8

       

      5.1/ 6.1

      Barium peroxide 
1304-29-6

      BaO2

      • The substance can presumably form explosive peroxides 
      • The substance is a strong oxidant and reacts with combustible and reducing materials 
      • The substance is a strong reducing agent and reacts with oxidants 
      • Reacts with water and acids forming hydrogen peroxide and barium oxide 
      • Mixtures with organic substances may be ignited or exploded on shock, friction or concussion

      5.1/ 6.1

      Barium sulphate 
7727-43-7

      BaSO4

      • The substance emits toxic fumes of sulphur oxides when heated to 
decomposition 
      • Reduction of barium sulphate by aluminium is attended by violent explosions

      6.1

      Beryllium 
7440-41-7

      Be

       

      6.1

      Beryllium oxide 
1304-56-9

      BeO

       

      6.1

      Cadmium 
7440-43-9

      Cd

      • Reacts with acids giving off flammable hydrogen gas 
      • Dust reacts with oxidants, hydrogen azide, zinc, selenium or tellurium, causing fire and explosion hazard
      • Dust explosion possible if in powder or granular form, mixed with air
       

      Cadmium acetate 
543-90-8

      Cd(C2H4O2)2

       

      6.1

      Cadmium chloride 
10108-64-2

      CdCl2

      • The substance decomposes on heating producing very toxic fumes of cadmium and chlorine
      • Solution in water is a weak acid · Reacts with strong oxidants
      • Reacts violently with fluoride, bromide and potassium and acids

      6.1

      Cadmium oxide 
1306-19-0

      CdO

      • The substance decomposes on heating producing toxic fumes of cadmium
      • Reacts violently with magnesium when heated causing fire and explosion hazard
      • Reacts with acids, oxidants

      6.1

      Cadmium suphate 
10124-36-4

      CdSO4

       

      6.1

      Cadmium sulphide 
1306-23-6

      CdS

      • Upon heating, toxic fumes are formed 
      • Reacts with strong oxidants 
      • Reacts with acids forming toxic gas (hydrogen sulphide) 
      • Gives off toxic fumes in a fire

      6.1

      Ammonium dichromate(VI)
7789-09-5

      (NH4)2Cr2H2O7

       

      5.1

      Chromic acid 
7738-94-5

      CrH2O4

       

      8

      Chromium 
7440-47-3

      Cr

       

      5.1

      Chromium trioxide 
1333-82-0

      CrO3

       

      5.1

      Chromyl chloride 
14977-61-8

      CrO2Cl2

      • The substance decomposes violently on contact with water producing toxic and corrosive fumes (hydrochloric acid, chlorine, chromium trioxide and chromium trichloride) 
      • The substance is a strong oxidant and reacts violently with combustible and reducing materials 
      • Reacts violently with water, non-metal halides, non-metal hydrides, ammonia and certain common solvents such as alcohol, ether, acetone, turpentine, causing fire and explosion hazard 
      • Attacks many metals in presence of water 
      • Incompatible with plastics 
      • Can ignite combustible substances

      8

      Cobalt 
7440-48-4

      Co

      • Reacts with strong oxidants (e.g., fused ammonium nitrate) causing fire and explosion hazard
      • Certain forms of cobalt metal powder can ignite spontaneously on contact with oxygen or air (pyrophoric) 
      • Can promote decomposition of various organic substances
       

      Cobalt chloride 
7646-79-9

      CoCl2

      • The substance decomposes on heating producing toxic fumes of chlorine and cobalt 
      • Reacts violently with alkali metals such as potassium or sodium causing fire and explosion hazard
       

      Cobalt (III) oxide 
1308-04-9

      Co2O3

      • Reacts violently with hydrogen peroxide 
      • Reacts with reducing agents
       

      Cobalt naphthenate 
61789-51-3

      CoC22H20O4

      • Upon heating, toxic fumes are formed 
      • As a result of flow, agitation, etc., electrostatic charges can be generated 
      • Dust explosion possible if in powder or granular form, mixed with air
       

      Copper 
7440-50-8

      Cu

      • Shock-sensitive compounds are formed with acetylenic compounds, ethylene oxides and azides 
      • Reacts with strong oxidants like chlorates, bromates and iodates, causing explosion hazard
       

      Copper (I) oxide 
1317-39-1

      Cu2O

      • Reacts with acids to form cupric salts · Corrodes aluminium
       

      Cupric acetate 
142-71-2

      CuC4H6O4

       

      6.1

      Cupric chloride 
7447-39-4

      CuCl2

       

      8

      Cupric hydroxide 
120427-59-2

      Cu(OH)2

       

      6.1

      Naphthenic acid, Cu-salt
1338-02-9

       
      • On combustion, forms toxic gases
       

      Ferric chloride 
7705-08-0

      FeCl3

       

      8

      Iron pentacarbonyl 
13463-40-6

      C5FeO5

       

      6.1/ 3

      Lead 
7439-92-1

      Pb

      • The substance decomposes on heating producing toxic fumes including lead oxides
      • The substance is a strong reducing agent
       

      Lead acetate 
301-04-2

      PbC4H6O4

      • The substance decomposes on heating and on burning producing toxic and corrosive fumes including lead, acetic acid 
      • Reacts violently with bromates, phosphates, carbonates, phenols 
      • Reacts with acids producing corrosive acetic acid

      6.1

      Lead chromate 
7758-97-6

      PbCrO4

      • The substance decomposes on heating producing toxic fumes including lead oxides
      • Reacts with strong oxidants, hydrogen peroxide, sodium and potassium
      • Reacts with aluminium dinitronaphthalene, iron (III) hexacyanoferrate(IV)
      • Reacts with organics at elevated temperature causing fire hazard
       

      Lead nitrate 
10099-74-8

      Pb(NO3)2

       

      5.1/ 6.1

      Lead dioxide 
1309-60-0

      PbO2

       

      5.1

      Lead(II) oxide 
1317-36-8

      PbO

      • Reacts violently with strong oxidants, aluminium powder and sodium 
      • Upon heating, toxic fumes of lead compounds are formed
       

      Naphthenic acid, Pb-salt
61790-14-5

       
      • On combustion, forms toxic fumes including lead oxide
       

      Tetraethyl lead 
78-00-2

      PbC8H20

      • The substance decomposes on heating above 110 °C and under influence of light producing toxic fumes: carbon monoxide, lead 
      • Reacts violently with strong oxidants, acids, halogens, oils and fats causing fire and explosion hazard 
      • Attacks rubber and some plastics and coatings
      • The vapour is heavier than air

      6.1

      Tetramethyl lead 
75-74-1

      PbC4H12

       

      6.1

      Lithium aluminium hydride
16853-85-3

      LiAlH4

       

      4.3

      Magnesium 
7439-95-4

      Mg

      • The substance may spontaneously ignite on contact with air or moisture producing irritating or poisonous gases including magnesium oxide 
      • Reacts violently with strong oxidants 
      • Reacts violently with many substances causing fire and explosion hazard
      • Reacts with acids or water forming flammable hydrogen gas, causing fire and explosion hazard
      • Dust explosion possible if in powder or granular form, mixed with air

      4.1

      Magnesium chloride 
7786-30-3

      MgCl2

      • The substance decomposes when slowly heated to 300 °C producing chlorine
      • Dissolution in water liberates a considerable amount of heat

      5.1

      Magnesium nitrate 
10377-60-3

      Mg(NO3)2

       

      5.1

      Magnesium oxide 
1309-48-4

      MgO

      • Readily absorbs moisture and carbon dioxide when exposed to air 
      • Reacts vigorously with halogens and strong acids
       

      Magnesium phosphide
12057-74-8

      Mg3P2

      • Reacts with water, air moisture, acids producing highly toxic fumes of phosphine
      • Reacts with water, air moisture, violently with acids causing fire and toxic (phosphine fumes) hazard

      4.3/ 6.1

      Mercuric acetate
1600-27-7

      HgC4H6O4

      • The substance decomposes on heating and under influence of light producing toxic fumes of mercury or mercuric oxide

      6.1

      Mercuric bromide 
7789-47-1

      HgBr2

       

      6.1

      Mercuric chloride 
7487-94-7

      HgCl2

      • The substance decomposes on heating producing toxic vapours of mercury and chloride
      • Reacts with light metals · Incompatible with formates, sulphites, hypophosphites, phosphates, sulphides, albumin, gelatin, alkalies, alkaloid salts, ammonia, lime water, antimony and arsenic, bromide, borax, carbonate, iron, copper, lead, silver salts

      6.1

      Mercuric nitrate 
10045-94-0

      Hg(NO3)2

      • The substance decomposes on heating producing toxic fumes (mercury, nitrogen oxides), or on exposure to light 
      • The substance is a strong oxidant and reacts violently with combustible and reducing materials 
      • Reacts with acetylene, alcohol, phosphine and sulphur to form shock-sensitive compounds 
      • Attacks most metals when in solution
      • Vigorous reaction with petroleum hydrocarbons

      6.1

      Mercuric oxide 
21908-53-2

      HgO

      • The substance decomposes on exposure to light, on heating above 500 °C, or on burning under influence of light producing highly toxic fumes including mercury and oxygen, which increases fire hazard 
      • Upon heating, toxic fumes are formed 
      • Reacts violently with chlorine, hydrogen peroxide, hypophosphorous acid, hydrazine hydrate, magnesium (when heated), disulphur dichloride and hydrogen trisulphide
      • Reacts explosively with acetyl nitrate, butadiene, ethanol, iodine 
(at 35 °C), chlorine, hydrocarbons, diboron tetrafluoride, hydrogen peroxide, traces of nitric acid, reducing agents 
      • Incompatible with reducing agents

      6.1

      Mercuric sulphate 
7783-35-9

      HgSO4

      • The substance decomposes on heating  or on exposure to light producing toxic fumes of mercury and sulphur oxides 
      • Reacts with water producing insoluble basic mercuric sulphate and sulphuric acid 
      • Reacts violently with hydrogen chloride

      6.1

      Mercuric thiocyanate 
592-85-8

      HgC2N2S2

       

      6.1

      Mercurous chloride 
10112-91-1

      Hg2Cl2

      • The substance decomposes on heating producing toxic fumes of chlorine and mercury, or on exposure to sunlight producing metallic mercury and mercuric chloride 
      • Reacts with bromides, iodides, sulphates, sulphites, carbonates, alkali chlorides, hydroxides, cyanides, lead salts, silver salts, soap, sulphides, copper salts, hydrogen peroxide, lime water, iodoform, ammonia, iodine
       

      Mercury 
7439-97-6

      Hg

      • Reacts violently with acetylene, chlorine, and ammonia 
      • Attacks copper and copper alloy materials 
      • Incompatible with acetylenes and ammonia gases 
      • Toxic vapours are formed on heating

      6.1

      Phenylmercuric acetate 
62-38-4

      C8H8HgO2

      • The substance decomposes on heating producing toxic vapours of mercury

      6.1

      Phenylmercuric nitrate 
55-68-5

      C6H5HgNO3

      • The substance decomposes on heating producing mercury vapours and other toxic fumes
      • Reacts with reducing agents

      6.1

      Nickel 
7440-02-0

      Ni

      • Reacts with strong oxidants 
      • Reacts violently, in powder form, with titanium powder and potassium perchlorate, and oxidants such as ammonium nitrate, causing fire and explosion hazard 
      • Reacts slowly with non-oxidizing acids and more rapidly with oxidizing acids 
      • Toxic gases and vapours (such as nickel carbonyl) may be released in a fire involving nickel 
      • Dust explosion possible if in powder or granular form, mixed with air
       

      Nickel (II) oxide 
1313-99-1

      NiO

      • Reacts violently with iodine and hydrogen sulphide causing fire and explosion hazard
       

      Nickel carbonate 
3333-67-3

      Ni2CO3

      • The substance decomposes on heating and on contact with acids producing carbon dioxide 
      • Reacts violently with aniline, hydrogen sulphide, flammable solvents, hydrazine and metal powders, especially zinc, aluminium and magnesium, causing fire and explosion hazard
       

      Nickel carbonyl 
13463-39-3

      NiC4O4

      • May explode on heating at 60 °C 
      • The substance may spontaneously ignite on contact with air
      • The substance decomposes on heating at 180 °C on contact with acids producing highly toxic carbon monoxide 
      • Reacts violently with oxidants, acids and bromine 
      • Reacts violently with oxidants causing fire and explosion hazard 
      • Oxidizes in air forming deposits which become peroxidized causing fire hazard 
      • The vapour is heavier than air and may travel along the ground; distant ignition possible

      6.1/ 3

      Nickel sulphide 
12035-72-2

      Ni3S2

      • The substance decomposes on heating to high temperatures producing sulphur oxides
       

      Nickel sulphate 
7786-81-4

      NiSO4

      • The substance decomposes on heating at 848 °C, producing toxic fumes of 
sulphur trioxide and nickel monoxide 
      • The solution in water is a weak acid
       

      Osmium tetroxide 
20816-12-0

      OsO4

      • The substance decomposes on heating producing fumes of osmium 
      • The substance is a strong oxidant and reacts with combustible and reducing materials
      • Reacts with hydrochloric acid to form toxic chlorine gas 
      • Forms unstable compounds with alkalis

      6.1

      Platinum tetrachloride 
13454-96-1

      PtCl4

      • On combustion, forms corrosive gases such as chlorine 
      • The substance decomposes on heating or on burning producing toxic fumes (chlorine) 
      • Reacts with strong oxidants
       

      Hydrogen selenide 
7783-07-5

      SeH2

      • The substance decomposes on heating above 100 °C producing toxic and flammable products including selenium and hydrogen 
      • The substance is a strong reducing agent and reacts violently with oxidants causing fire and explosion hazard 
      • On contact with air it emits toxic and corrosive fumes of selenium dioxide 
      • The gas is heavier than air and may travel along the ground; distant ignition possible

      2.3/ 2.1

      Selenious acid 
7783-00-8

      SeH2O3

      • The substance decomposes on heating producing water and toxic fumes of selenium oxides
      • Reacts on contact with acids producing toxic gaseous hydrogen selenide
       

      Selenious acid, disodium salt
10102-18-8

      Na2SeO3

      • On contact with hot surfaces or flames this substance decomposes forming toxic gases
      • The solution in water is a medium strong base 
      • Reacts with water, strong acids causing toxic hazard

      6.1

      Selenium 
7782-49-2

      Se

      • Upon heating, toxic fumes are formed 
      • Reacts violently with oxidants and strong acids 
      • Reacts with water at 50 °C forming flammable hydrogen and selenious acids 
      • Reacts with incandescence on gentle heating with phosphorous and metals such as nickel, zinc, sodium, potassium, platinum

      6.1

      Selenium dioxide 
7446-08-4

      SeO2

      • The substance decomposes on heating producing toxic fumes of selenium
      • The solution in water is a medium strong acid (selenious acid) 
      • Reacts with many substances giving off toxic vapours (selenium) 
      • Attacks many metals in presence of water
       

      Selenium hexafluoride 
7783-79-1

      SeF6

      • The substance decomposes on heating producing toxic and corrosive fumes including hydrogen fluoride, fluoride and selenium

      2.3/ 8

      Selenium oxychloride 
7791-23-3

      SeOCl2

      • The substance decomposes on heating producing toxic fumes of chloride and selenium
      • The solution in water is a strong acid, it reacts violently with bases and is corrosive
      • Reacts violently with white phosphorus and potassium causing fire and explosion hazard
      • Reacts violently with metal oxides

      3/ 6.1

      Selenium trioxide 
13768-86-0

      SeO3

      • The substance decomposes on heating producing toxic fumes of selenium
      • The substance is a strong oxidant and reacts with combustible and reducing materials
      • The solution in water is a strong acid, it reacts violently with bases and is corrosive
      • Reacts violently with water giving off selenic acid 
      • Attacks many metals when moisture is present
       

      Silver 
7440-22-4

      Ag

      • Shock-sensitive compounds are formed with acetylene 
      • Finely divided silver and strong hydrogen peroxide solution may explode (violent decomposition to oxygen gas) 
      • Contact with ammonia may cause formation of compounds that are explosive when dry 
      • Readily reacts with diluted nitric acid, hot concentrated sulphuric acid
       

      Silver nitrate 
7761-88-8

      AgNO3

      • Shock-sensitive compounds are formed with acetylene, alcohol, phosphine and sulphur
      • The substance decomposes on heating producing toxic fumes (nitrogen oxides) 
      • The substance is a strong oxidant and reacts violently with combustible and reducing materials
      • Reacts with incompatible substances such as acetylene, alkalis, halides and other compounds causing fire and explosion hazard 
      • Attacks some forms of plastics, rubber and coatings 
      • The substance decomposes on contact with organic contaminants when exposed to light

      5.1

      Strontium chromate 
7789-06-2

      SrCrH2O4

      • The substance decomposes on burning producing toxic fumes 
      • Reacts violently with hydrazine
      • Incompatible with combustible, organic or other readily oxidizable materials such as paper, wood, sulphur, aluminium, plastics
       

      Tellurium 
13494-80-9

      Te

      • Upon heating, toxic fumes are formed
      • Reacts vigorously with halogens or interhalogens causing flames hazard 
      • Reacts with zinc with incandescence
      • Lithium silicide attacks tellurium with incandescence

      6.1

      Tellurium hexafluoride 
7783-80-4

      TeF6

       

      2.3/ 8

      Thallium 
7440-28-0

      Tl

      • Reacts violently with fluorine 
      • Reacts with halogens at room temperature
      • Incompatible with strong acids, strong oxidants, and oxygen 
      • The substance forms toxic compounds on contact with moisture

      6.1

      Thallous sulphate 
7446-18-6

      Tl2 (SO4)3

      • The substance decomposes on heating producing highly toxic fumes of thallium and sulphur oxides

      6.1

      Thorium 
7440-29-1

      Th

       

      7

      Di-N-Butyltin dichloride 
683-18-1

      SnCl2C8H18

       

      6.1

      Di-N-Dibutyltin oxide 
818-08-6

      C8H18SnO

      • The substance decomposes on heating producing toxic fumes of tin, tin oxides
      • Reacts with oxidants 
      • Dust explosion possible if in powder or granular form, mixed with air
      • If dry, it can be charged electrostatically by swirling, pneumatic transport, pouring, etc.
       

      Dibutyltin dilaurate 
77-58-7

      SnC32H64O4

       

      6.1

      Stannic chloride 
7646-78-8

      SnCl4

      • The vapour is heavier than air 
      • The substance decomposes on heating producing toxic fumes
      • Reacts violently with water forming corrosive hydrochloric acid and tin oxide fumes 
      • Reacts with turpentine 
      • Attacks many metals, some forms of plastics, rubber and coatings 
      • Contact with alcohol and amines may cause fire and explosion hazard 
      • Reacts with moist air to form hydrochloric acid

      8

      Stannic oxide 
18282-10-5

      SnO

      • Reacts violently with chlorine trifluoride 
      • Contact with hydrogen trisulphide causes violent decomposition and ignition 
      • Violently reduced by magnesium on heating, with fire and explosion hazard
       

      Stannous chloride 
7772-99-8

      SnCl2

      • Upon heating, toxic fumes are formed 
      • The substance is a strong reducing agent and reacts violently with oxidants 
      • Reacts violently with bromine trifluoride, sodium and nitrates
       

      Stannous chloride dihydrate
10025-69-1

      SnCl2 ·2H2O

      • The substance is a strong reducing agent and reacts violently with oxidants
      • Upon heating, toxic and corrosive fumes are formed 
      • The substance absorbs oxygen from air and forms insoluble oxychloride
       

      Stannous fluoride 
7783-47-3

      SnF2

      • Reacts with acids; hydrogen fluoride fumes may be formed 
      • Reacts violently with 
chlorine 
      • Incompatible with alkaline substances and oxidizing agents
       

      Tin oxide 
21651-19-4

      SnO

      • On heating at 300 °C in air, oxidation to stannic oxide proceeds incandescently
      • Ignites in nitrous oxide at 400 °C and incandesces when heated in sulphur dioxide
       

      Titanium tetrachloride 
7550-45-0

      TiCl4

       

      8

      Titanium trichloride 
7705-07-9

      TiCl3

       

      8

      Vanadium pentoxide 
1314-62-1

      V2O5

      • Upon heating, toxic fumes are formed 
      • Acts as a catalyst in oxidation reactions

      6.1

      Vanadium tetrachloride 
7632-51-1

      VCl4

       

      8

      Vanadium trioxide 
1314-34-7

      V2O3

      • Ignites on heating in air 
      • The substance decomposes on heating or on burning producing irritating and toxic fumes (vanadium oxides)

      6.1

      Vanadyl trichloride 
7727-18-6

      VOCl3

       

      8

      Zinc 
7440-66-6

      Zn

       

      4.3/ 4.2

      Zinc chloride 
7646-85-7

      ZnCl2

       

      8

      Zinc nitrate 
7779-88-6

      Zn(NO3)2

       

      1.5

      Zinc phosphide 
1314-84-7

      Zn3P2

      • The substance decomposes on heating and on contact with acids or water producing toxic and flammable fumes of phosphorous and zinc oxides, and phosphine 
      • Reacts violently with strong oxidants causing fire hazard

      4.3/ 6.1

      Zinc stearate 
557-05-1

      ZnC36H70O4

      • The substance decomposes on heating producing acrid smoke and fumes of zinc oxide
      • Dust explosion possible if in powder or granular form, mixed with air 
      • If dry, it can be charged electrostatically by swirling, pneumatic transport, pouring, etc.
       

      The data on physical and chemical hazards are adapted from the International Chemical Safety Cards (ICSC) series produced by the International Programme on Chemical Safety (IPCS), a cooperative programme of the World Health Organization (WHO), the International Labour Organization (ILO) and the United Nations Environment Programme (UNEP).
The risk classification data are taken from Recommendations on the Transport of Dangerous Goods, 9th edition, developed by the United Nations Committee of Experts on the Transport of Dangerous Goods and published by the United Nations (1995).
In the UN risk classification, the following codes are used: 1.5 = very insensitive substances which have a mass explosion hazard; 2.1 = flammable gas; 2.3 = toxic gas; 
3 = flammable liquid; 4.1 = flammable solid; 4.2 = substance liable to spontaneous combustion; 4.3 = substance which in contact with water emits flammable gases; 
5.1 = oxidizing substance; 6.1 = toxic; 7 = radioactive; 8 = corrosive substance.

      Table 2. Health hazards

      Chemical 
name 
CAS-Number

      Short-term 
exposure

      Long-term
exposure

      Routes of 
exposure

      Symptoms

      Target organs, routes 
of entry

      Symptoms

      Aluminium phosphide
20859-73-8

      Eyes; skin; resp. tract

       

      Inhalation


Skin
Eyes
Ingestion

      Abdominal pain, burning sensation, 
cough, dizziness, dullness, headache, 
laboured breathing, nausea, sore throat
Redness, pain 
Redness, pain 
Abdominal pain, convulsions, nausea, 
unconsciousness, vomiting

         

      Antimony
7440-36-0

      Eyes; skin; resp. tract; lungs; heart

      Skin; lungs; resp. tract

      Inhalation


Skin
Eyes
Ingestion

      Cough, fever, shortness of breath, 
vomiting, soreness of upper respiratory 
tract; See Ingestion
Redness 
Redness, pain, conjunctivitis 
Abdominal pain, burning sensation, 
diarrhoea, nausea, shortness of breath, 
vomiting, cardiac arrhythmias

      Resp sys; CVS; skin; eyes 
Inh; ing; con

      Irrit eyes, skin, nose, throat, mouth; cough; dizz; head; nau, vomit, diarr; stomach cramps; insom; anor; unable to smell properly

      Antimony
trioxide 
1309-64-4

      Eyes; skin; resp. tract

      Skin; lungs

      Inhalation

Skin
Eyes
Ingestion

      Cough, fever, nausea, sore throat, 
vomiting 
Redness, pain, blisters 
Redness, pain 
Abdominal pain, diarrhoea, sore throat, 
vomiting, burning sensation

         

      Stibine 
7803-52-3

      Blood; kidneys; liver; CNS

       

      Inhalation

      Abdominal pain, headache, nausea, 
shortness of breath, vomiting, 
weakness, weak and irregular pulse, 
haematuria, shock

      Blood; liver; kidneys; resp. sys. 
Inh

      Head, weak; nau, abdom pain; lumbar pain, hemog, hema, hemolytic anemia; jaun; pulm irrit

      Arsenic 
7440-38-2

      Eyes; skin; resp. tract; liver; kidneys; 
GI tract

      Skin; liver; CNS; carcinogenic; may cause reproductive toxicity

      Inhalation

Skin
Eyes
Ingestion

      Chest pain, abdominal pain, cough, 
headache, weakness, giddiness 
May be absorbed, irritating 
Redness, irritating 
Diarrhoea, nausea, vomiting

      Liver; kidneys; skin; lungs; lymphatic sys (lung & lymphatic cancer) 
Inh; abs; con; ing

      Ulceration of nasal septum, derm, 
GI disturbances, peri neur, resp irrit, hyperpig of skin, (carc)

      Arsenic acid,
copper salt 
10103-61-4

      Eyes; resp. tract; CNS; digestive tract

      Skin; PNS; mucous membranes; liver

      Inhalation

Skin
Eyes
Ingestion

      Cough, headache, laboured breathing, 
weakness; See Ingestion
May be absorbed 
Redness pain 
Abdominal pain, diarrhoea, vomiting, 
burning sensation behind breastbone 
and in the mouth

         

      Arsenic acid,
diammonium 
salt 
7784-44-3

      Eyes; skin; resp. tract; CNS; digestive tract; circulatory system

      PNS; skin; mucous membranes; liver

      Inhalation

Skin
Eyes
Ingestion

      Cough, headache, laboured breathing, 
weakness; See Ingestion
May be absorbed, soluble, redness, pain
Redness, pain 
Abdominal pain, diarrhoea, vomiting, 
burning sensation behind breastbone 
and in the mouth

         

      Arsenic acid, 
disodium salt 
7778-43-0

      Eyes;skin; resp. tract; CNS; digestive tract; circulatory system

      PNS; skin; mucous membranes; liver

      Inhalation

Skin
Eyes
Ingestion

      Cough, headache, laboured breathing, 
weakness; See Ingestion
May be absorbed, soluble, redness, pain 
Redness, pain 
Abdominal pain, diarrhoea, vomiting, 
burning sensation behind breastbone 
and in the mouth

         

      Arsenic acid,
magnesium 
salt 
10103-50-1

      Eyes; resp. tract; CNS; digestive tract; circulatory system

      PNS; skin; mucous membranes; liver

      Inhalation

Skin
Eyes
Ingestion

      Cough, headache, laboured breathing, 
weakness; See Ingestion
May be absorbed 
Redness, pain 
Abdominal pain, diarrhoea, vomiting, 
burning sensation behind breastbone 
and in the mouth

         

      Arsenic acid, 
mono-
potassium 
salt
7784-41-0

      Eyes; skin; resp. tract; mucous 
mem-
branes

      Skin; PNS; mucous membranes; liver

      Inhalation

Skin
Eyes
Ingestion

      Cough, headache, laboured breathing, 
weakness; See Ingestion
May be absorbed, redness, pain
Redness, pain 
Abdominal pain, burning sensation, 
diarrhoea, vomiting

         

      Arsenic 
pentoxide 
1303-28-2

      Eyes; skin; resp. tract; kidneys; liver; CVS; CNS; blood

      Lungs; skin; bone marrow; CVS; CNS; carcinogenic; may cause reproductive toxicity

      Inhalation



Skin
Eyes
Ingestion

      Cough, headache, dizziness, weakness
shortness of breath, pain in chest, 
symptoms may be delayed; 
See Ingestion
Redness, skin burns, pain
Redness, pain, conjunctivitis
Constriction in throat, vomiting, 
abdominal pain, diarrhoea, severe thirst, 
muscular cramps, shock

         

      Arsenic 
trioxide 
1327-53-3

      Eyes; skin; resp. tract; kidneys; liver; CVS; CNS; hemato-
poietic

      Lungs; skin; bone marrow; PNS; CNS; CVS; heart; kidneys; liver; carcinogenic; may cause birth defects

      Inhalation



Skin
Eyes
Ingestion

      Cough, dizziness, headache, shortness 
of breath, weakness, pain in chest, 
symptoms may be delayed; 
See Ingestion
Redness, pain 
Redness, pain, conjunctivitis 
Constriction in throat, abdominal pain, 
diarrhoea, vomiting, severe thirst, 
muscular cramps, shock

         

      Arsenious acid, copper (2+) salt (1:1)
10290-12-7

      Eyes; skin; resp. tract.; CNS; digestive tract; circulatory system

      Skin; PNS; mucous membranes; liver

      Inhalation

Skin
Eyes
Ingestion

      Cough, headache, laboured breathing, 
weakness; See Ingestion
May be absorbed 
Redness, pain 
Abdominal pain, diarrhoea, vomiting, 
burning sensation behind breastbone 
and in the mouth

         

      Arsenious 
acid, lead (II)
salt 
10031-13-7

      Eyes; skin; resp. tract; CNS; GI tract; circulatory system

      Skin; PNS; mucous membranes; liver

      Inhalation

Skin
Eyes
Ingestion

      Cough, headache, laboured breathing, 
weakness; See Ingestion
Redness, pain 
Redness, pain 
Abdominal pain, diarrhoea, vomiting, 
burning sensation behind breastbone 
and in the mouth

         

      Arsenious 
acid, 
potassium 
salt 
10124-50-2

      Eyes; skin; resp. tract; CNS; digestive tract; circulatory system

       

      Inhalation

Skin

Eyes
Ingestion

      Cough, headache, laboured breathing, 
weakness; See Ingestion
May be absorbed, soluble, redness, 
pain 
Redness, pain 
Abdominal pain, diarrhoea, vomiting, 
burning sensation behind breastbone 
and in the mouth

         

      Arsenous 
trichloride 
7784-34-1

      Eyes; skin; resp. tract; lungs; CVS; CNS; GI tract

      Mucous membranes; skin; liver; kidneys; PNS

      Inhalation

Skin

Eyes
Ingestion

      Corrosive, cough, laboured breathing; See Ingestion
Corrosive, may be absorbed, redness, 
pain 
Corrosive, pain, severe deep burns
Corrosive, abdominal pain, burning 
sensation, diarrhoea, vomiting, collapse

         

      Arsine 
7784-42-1

      Lungs; blood; kidneys

       

      Inhalation


Skin
Eyes

      Abdominal pain, confusion, dizziness, 
headache, nausea, shortness of breath, 
vomiting, weakness 
On contact with liquid: frostbite 
On contact with liquid: frostbite, redness

      Blood; kidneys; liver (lung & lymphatic 
cancer)
Inh; con (liq)

      Head, mal, weak, dizz; dysp; abdom, back pain; nau, vomit, bronze skin; hema; jaun; peri neur, liq: frostbite; (carc)

      Calcium 
arsenate 
7778-44-1

      Eyes; skin; resp. tract; CNS; digestive tract; circulatory system

      PNS; skin; mucous membranes; liver

      Inhalation

Skin
Eyes
Ingestion

      Cough, headache, laboured breathing, 
weakness: See Ingestion
May be absorbed, redness, pain
Redness, pain 
Abdominal pain, diarrhoea, vomiting, 
burning sensation behind breastbone 
and in the mouth

      Eyes; resp sys; liver; skin; lymphatic sysrtem; CNS; (lymphatic & lung 
cancer) 
Inh; abs; ing; con

      Weak; GI dist; peri neur, skin hyperpig, palmar planter hyperkeratoses; derm; (carc); in animals: liver damage

      Lead arsenate
7784-40-9

      Intestines; CVS

      Skin; CNS; GI tract; liver; kidneys; blood; carcinogenic; may cause reproductive toxicity

      Inhalation



Skin
Eyes

      Abdominal cramps, diarrhoea, 
headache, nausea, vomiting, tightness 
of chest, constipation, excitation, 
disorientation 
Redness 
Redness

         

      Methylarsonic 
acid 
124-58-3

      Eyes; skin; resp. tract; lungs

      Bone marrow; PNS; kidneys; liver

      Inhalation
Skin
Eyes
Ingestion

      Cough 
Redness 
Redness 
Abdominal pain, diarrhoea, vomiting, 
burning sensation in throat

      Organic arsenic compounds: Skin, resp sys, kidneys, CNS, liver, GI tract, repro sys

      In animals: irrit skin, possible derm; resp. distress; diarr; kidney damage; musc tremor, sez; possible GI tract, terato, repro effects; possible liver damage

      Sodium 
arsenate 
10048-95-0

      Eyes; skin; resp. tract; digestive tract; heart; liver; kidneys; CNS

      Skin; CNS; CVS; blood; liver; carcinogenic

      Inhalation

Skin
Eyes
Ingestion

      Cough, headache, sore throat; 
See Ingestion
Redness, pain
Redness, pain 
Abdominal pain, burning sensation, 
diarrhoea, vomiting

         

      Barium 
7440-39-3

      Eyes; skin; resp. tract

       

      Inhalation
Skin
Eyes

      Cough, sore throat
Redness
Redness, pain

         

      Barium 
chlorate 
13477-00-4

      Eyes; skin; resp. tract; various tissues and organs

      Tissues and organs

      Inhalation


Eyes
Ingestion

      Abdominal pain, abdominal cramps, 
burning sensation, nausea, vomiting, 
weakness, paralysis 
Redness, pain
Abdominal cramps, abdominal pain, 
blue lips or fingernails, blue skin, 
burning sensation, diarrhoea, dizziness, 
nausea, sore throat, vomiting, 
weakness, cardiac dysrhythmia

         

      Barium 
chloride 
10361-37-2

      Eyes; skin; resp. tract; CNS; muscles

       

      Inhalation
Eyes
Ingestion

      Abdominal cramps, unconsciousness
Redness
Abdominal cramps, dullness, 
unconsciousness

      Heart; CNS; skin; resp sys; eyes 
Inh; ing; con

      Irrit eyes, skin, upper resp sys; skin burns, gastroenteritis; musc spasm; slow pulse, extrasystoles; hypokalaemia

      Barium 
chloride,
dihydrate 
10362-27-9

      Eyes; skin; resp. tract; CNS; muscles

       

      Inhalation
Eyes
Ingestion

      Abdominal cramps, unconsciousness
Redness 
Abdominal cramps, dullness, 
unconsciousness

         

      Barium oxide 
1304-28-5

      Eyes; skin; resp. tract; muscles

      Lungs

      Inhalation
Skin
Eyes
Ingestion

      Cough, shortness of breath, sore throat
Redness 
Redness, pain 
Abdominal pain, diarrhoea, dizziness, 
nausea, vomiting, muscle paralysis, 
cardiac arrhythmia, hypertension, death

         

      Barium
peroxide 
1304-29-6

       

      Skin

      Inhalation

Skin
Eyes
Ingestion

      Cough, nausea, shortness of breath, sore throat
Redness, skin burns, pain, bleaching
Redness, pain, severe deep burns
Abdominal pain, burning sensation, 
sore throat

         

      Barium 
sulphate 
7727-43-7

       

      Lungs

      Inhalation

      Cough

      Eyes; resp sys 
Inh; con

      Irrit eyes, nose, upper resp sys; 
benign pneumoconiosis (baritosis)

      Cadmium 
7440-43-9

      Eyes; resp. tract; lungs

      Lungs; kidneys

      Inhalation

Eyes
Ingestion

      Cough, headache, symptoms may be 
delayed 
Redness, pain 
Abdominal pain, diarrhoea, headache, 
nausea, vomiting

      Resp sys; kidneys; prostate; blood (prostatic & lung 
cancer)
Inh; ing

      Pulm oedema, dysp, cough, tight chest, subs pain; head; chills, musc aches; nau, vomit, diarr; anos, emphy, prot, mild anaemia; (carc)

      Cadmium 
chloride 
10108-64-2

      Resp. tract; digestive tract; lungs

      Lungs; kidneys; bone; probably carcinogenic

      Inhalation

Skin
Eyes
Ingestion

      Cough, laboured breathing, symptoms 
may be delayed 
Redness 
Redness, pain 
Abdominal pain, burning sensation, 
diarrhoea, nausea, vomiting

         

      Cadmium 
oxide 
1306-19-0

      Resp. tract; digestive tract; lungs

      Lungs; kidneys; carcinogenic

      Inhalation


Skin
Eyes
Ingestion

      Cough, laboured breathing, shortness 
of breath, 
symptoms may be delayed 
Redness 
Redness, pain 
Abdominal cramps, diarrhoea, nausea, 
vomiting

      Resp sys; kidneys; blood; (prostatic & lung cancer) 
Inh

      Pulm oedema, dysp, cough, tight chest, subs pain; head; chills, musc aches; nau, vomit, diarr; anos, emphy, prot, mild anaemia; (carc)

      Cadmium 
sulphide 
1306-23-6

       

      Lungs; kidneys; carcinogenic

             

      Chromium 
7440-47-3

      Eyes; skin; resp. tract; lungs; kidneys

      Skin; asthma; larynx; lungs

      Eyes
Ingestion

      Irritation 
Diarrhoea, nausea, unconsciousness, 
vomiting

      Resp sys; skin; eyes 
Inh; ing; con

      Irrit eyes, skin; lung fib (histologic)

      Chromyl 
chloride 
14977-61-8

      Eyes; skin; resp. tract; lungs; corrosive on ingestion

      Skin; asthma; probably carcinogenic

      Inhalation

Skin
Eyes
Ingestion

      Cough, laboured breathing, shortness 
of breath, sore throat 
Redness, skin burns, pain, blisters
Redness, pain, severe deep burns 
Abdominal pain

      Eyes; skin; resp sys (lung cancer) 
Inh; abs; ing; con

      Irrit eyes, skin, upper resp sys; eye, skin burns

      Lead 
chromate 
7758-97-6

      Resp. tract; may cause perforation of nasal septum

      Skin; inhalation may cause asthma; lungs

      Inhalation

Skin
Eyes
Ingestion

      Cough, headache, laboured breathing, 
nausea, metallic taste 
Skin burns, ulcers, blisters
Redness 
Abdominal pain, constipation, 
convulsions, cough, diarrhoea, 
vomiting, weakness, anorexia

         

      Cobalt 
7440-48-4

       

      Skin; resp. tract; lungs; heart

      Inhalation

Skin
Eyes
Ingestion

      Cough, laboured breathing, shortness 
of breath 
Redness 
Redness 
Abdominal pain, vomiting

      Resp sys; skin 
Inh; ing; con

      Cough, dysp, wheez, decr pulm func; low-wgt; derm; diffuse nodular fib; resp hypersensitivity, asthma

      Cobalt 
chloride 
7646-79-9

      Eyes; skin; resp. tract

      Skin; resp. tract ; heart

      Inhalation

Skin
Eyes
Ingestion

      Cough, laboured breathing, shortness 
of breath 
Redness 
Redness 
Abdominal pain, diarrhoea, nausea, 
vomiting

         

      Cobalt (III) 
oxide 
1308-04-9

      Eyes; skin; resp. tract

      Skin; may cause asthma; lungs; possibly carcinogenic

      Inhalation

Eyes

      Cough, laboured breathing, shortness 
of breath 
Redness

         

      Cobalt 
naphthenate 
61789-51-3

      Eyes; resp. tract

      Skin

      Inhalation
Skin
Eyes

      Cough, sore throat 
Redness, pain 
Redness, pain

         

      Copper 
7440-50-8

      Eyes

      Skin; lungs

      Inhalation

Skin
Eyes
Ingestion

      Cough, headache, shortness of breath, 
sore throat 
Redness 
Redness, pain
Abdominal pain, nausea, vomiting

      Eyes; resp sys; skin; liver; kidneys (incr risk with Wilsons disease)
Inh; ing; con

      Irrit eyes, nose, pharynx; nasal perf; metallic taste; derm; in animals: lung, liver, kidney damage; anaemia

      Copper (I) 
oxide 
1317-39-1

      Eyes; resp. tract

       

      Inhalation
Eyes
Ingestion

      Cough, metallic taste, metal fume fever
Redness 
Abdominal cramps, diarrhoea, nausea, 
vomiting

         

      Lead 
7439-92-1

       

      Nervous system; kidneys; may impair fertility; may cause retarded development of the newborn

      Inhalation
Ingestion

      Headache, nausea, abdominal spasm
Headache, nausea, sore throat, 
abdominal spasm

      Eyes; GI tract; CNS; kidneys; blood; gingival tissue 
Inh; ing; con

      Weak, lass, insom; facial pallor; pal eye, anor, low-wgt, malnut; constip, abdom pain, colic; anemia; gingival lead line; tremor; para wrist, ankles; encephalopathy; kidney disease; irrit eyes; hypotension

      Lead acetate 
301-04-2

      Eyes; skin; resp. tract; blood; CNS; kidneys

      Blood; bone marrow; CVS; kidneys; CNS

      Inhalation

Eyes
Ingestion

      Headache, chronic but not described as 
acute; See Ingestion
Redness, pain
Abdominal cramps, constipation, 
convulsions, headache, nausea, vomiting

         

      Tetraethyl 
lead 
78-00-2

      Eyes; skin; resp. tract; CNS

      Skin; CNS; may cause genetic damage; may cause reproductive toxicity

      Inhalation

Skin
Eyes
Ingestion

      Convulsions, dizziness, headache, 
unconsciousness, vomiting, weakness
May be absorbed, redness
Pain, blurred vision 
Convulsions, diarrhoea, dizziness, 
headache, unconsciousness, vomiting, 
weakness

      CNS; CVS; kidneys; eyes 
Inh; abs; ing; con

      Insom, lass, anxiety; tremor, hyper-reflexia, spasticity; bradycardia, hypotension, hypothermia, pallor, nau, anor, low-wgt; conf, disorientation, halu, psychosis, mania, convuls, coma; eye irrit

      Lead (II) 
oxide 
1317-36-8

       

      CNS; kidneys; blood

             

      Magnesium 
7439-95-4

         

      Inhalation
Eyes
Ingestion

      Cough, laboured breathing 
Redness, pain 
Abdominal pain, diarrhoea

         

      Magnesium 
chloride 
7786-30-3

      Eyes; resp. tract

       

      Inhalation
Eyes
Ingestion

      Cough 
Redness 
Diarrhoea

         

      Magnesium 
oxide 
1309-48-4

      Eyes; nose

       

      Inhalation
Eyes
Ingestion

      Cough 
Redness 
Diarrhoea

      Eyes; resp sys
Inh; con

      Irrit eyes, nose; metal fume fever, cough, chest pain, flu-like fever

      Magnesium 
phosphide 
12057-74-8

      Eyes; skin; resp. tract

       

      Inhalation


Skin
Eyes
Ingestion

      Abdominal pain, burning sensation, 
cough, dizziness, dullness, headache, 
laboured breathing, nausea, sore throat
Redness, pain
Redness, pain
Abdominal pain, convulsions, nausea, 
unconsciousness, vomiting

         

      Manganese 
sulphate 
10034-96-5

      Eyes; skin; resp. tract

      Lungs; CNS; liver; kidneys; testes

      Inhalation

Skin

Eyes
Ingestion

      Burning sensation, cough, laboured 
breathing 
May be absorbed, redness, burning 
sensation 
Redness, pain, blurred vision 
Abdominal cramps, nausea, sore throat

         

      Mercury 
7439-97-6

      Eyes; skin; lungs; CNS

      CNS; nervous system; kidneys

      Inhalation
Skin
Eyes

      Pulmonary irritation, cough 
May be absorbed 
Irritating

      Skin; resp sys; CNS; kidneys; eyes
Inh; abs; ing; con

      Irrit eyes, skin; cough, chest pain, dysp, bron pneuitis; tremor, insom, irrity, indecision, head, ftg, weak; stomatitis, salv; GI dist, anor, low-wgt; prot

      Mercuric 
acetate 
1600-27-7

      Eyes; skin; resp. tract; lungs; kidneys

      Skin; kidneys

      Inhalation



Skin
Eyes
Ingestion

      Cough, headache, laboured breathing, 
shortness of breath, sore throat, 
symptoms may be delayed;
See Ingestion
May be absorbed, skin burns, pain 
Pain, blurred vision, severe deep burns 
Abdominal pain, burning sensation, 
diarrhoea, vomiting, metallic taste

         

      Mercuric 
chloride 
7487-94-7

      Eyes; skin; resp. tract; lungs; kidneys

      Skin; kidneys

      Inhalation



Skin
Eyes
Ingestion

      Burning sensation, cough, laboured 
breathing, shortness of breath, sore 
throat, symptoms may be delayed; 
See Ingestion
May be absorbed, pain, blisters 
Pain, blurred vision, severe deep burns
Abdominal cramps, abdominal pain, 
burning sensation, diarrhoea, nausea, 
sore throat, vomiting, metallic taste

         

      Mercuric 
nitrate 
10045-94-0

      Skin; resp. tract; eyes; kidneys

      Kidneys

      Inhalation

Skin
Eyes
Ingestion

      Cough, headache, laboured breathing, 
shortness of breath, sore throat 
May be absorbed, redness, pain 
Pain, blurred vision, severe deep burns
Abdominal pain, diarrhoea, vomiting, 
metallic taste

         

      Mercuric 
oxide 
21908-53-2

      Eyes; skin; resp. tract

      Skin; kidneys; CNS

      Inhalation
Skin
Eyes
Ingestion

      Cough 
May be absorbed, redness 
Redness 
Abdominal pain, diarrhoea

         

      Mercuric 
sulphate 
7783-35-9

      Eyes; skin; resp. tract; lungs; GI tract; corrosive on ingestion

      Kidneys

      Inhalation



Skin

Eyes
Ingestion

      Burning sensation, cough, laboured 
breathing, shortness of breath, 
weakness, symptoms may be delayed;
See Ingestion
May be absorbed, redness, burning 
sensation, pain 
Pain, blurred vision, severe deep burns 
Abdominal pain, diarrhoea, nausea, 
vomiting, metallic taste

         

      Mercurous 
chloride 
10112-91-1

      Eyes

      Kidneys

      Eyes
Ingestion

      Redness
Weakness

         

      Mercury 
organoalkyl 
compound

             

      Eyes; skin; CNS; PNS; kidneys
Inh; abs; ing; con

      Pares; ataxia, dysarthria; vision, 
hearing dist; spasticity, jerking limbs; dizz; salv; lac; nau, vomit, diarr, 
constip; skin burns; emotional dist; 
kidney inj; possible terato effects

      Phenylmercuric acetate
62-38-4

      Eyes; skin; resp. tract; kidneys

      Skin; CNS; possibly causes toxic effects upon human reproduction

      Inhalation

Skin
Eyes
Ingestion

      Cough, laboured breathing, sore throat, 
symptoms may be delayed 
May be absorbed, redness, pain
Redness, pain, blurred vision 
Abdominal pain, diarrhoea, nausea, 
vomiting, weakness, symptoms of 
delayed effects

         

      Phenylmercuric nitrate
55-68-5

      Eyes; skin; resp. tract; kidneys

      Skin; CNS; possibly causes toxic effects on human reproduction

      Inhalation

Skin
Eyes
Ingestion

      Cough, laboured breathing, sore throat, 
symptoms may be delayed 
May be absorbed, redness, pain
Redness, pain, blurred vision 
Abdominal pain, diarrhoea, nausea, 
vomiting, symptoms of delayed effects

         

      Nickel 
7440-02-0

      Eyes; resp. tract

      Skin; inhalation may cause asthma; may effect conjuctiva; possibly carcinogenic

         

      Nasal cavities; lungs; skin (lung & nasal 
cancer)
Inh; ing; con

      Sens derm, allergic asthma, pneuitis; (carc)

      Nickel (II) 
oxide 
1313-99-1

      Eyes; resp. tract

      Skin; inhalation may cause asthma; carcinogenic

      Inhalation
Skin
Eyes

      Cough 
Redness 
Redness

         

      Nickel 
carbonate 
3333-67-3

      Eyes; resp. tract

      Skin; carcinogenic; asthma

      Inhalation
Skin
Eyes

      Cough 
Redness 
Redness

         

      Nickel 
carbonyl 
13463-39-3

      Eyes; skin; resp. tract; lungs; CNS

      Possibly carcinogenic; may cause defects on the unborn child

      Inhalation



Skin
Eyes
Ingestion

      Abdominal pain, blue skin, cough, 
dizziness, headache, nausea, shortness 
of breath, vomiting, symptoms may be 
delayed 
May be absorbed, redness, pain 
Redness, pain 
Abdominal pain, headache, nausea, 
vomiting

      Lungs; paranasal sinus; CNS; repro sys (lung & nasal cancer)
Inh; abs; ing; con

      Head, verti; nau, vomit, epigastric pain; subs pain; cough, hyperpnea; cyan; weak; leucyt; pneuitis; delirium; 
convuls; (carc); in animals: repro, terato effects

      Nickel 
sulphide 
12035-72-2

      Eyes; skin; resp. tract

      Skin; possibly carcinogenic

      Inhalation

      Cough, sore throat

         

      Nickel 
sulphate 
7786-81-4

      Eyes; skin; resp. tract; GI tract; CNS

      Skin; asthma; possibly carcinogenic

      Inhalation
Skin
Eyess
Ingestion

      Cough, sore throat 
May be absorbed, redness 
Redness 
Abdominal pain, dizziness, headache, 
nausea, vomiting

         

      Osmium 
tetroxide 
20816-12-0

      Eyes; skin; resp. tract; lungs

      Skin; kidneys

      Inhalation


Skin
Eyes
Ingestion

      Cough, headache, wheezing, shortness 
of breath, visual disturbances, 
symptoms may be delayed 
Redness, skin burns, skin discoloration 
Blurred vision, loss of vision 
Burning sensation

      Eyes; resp sys; skin Inh; ing; con

      Irrit eyes, resp sys; lac, vis dist; conj; head; cough, dysp; derm

      Platinium 
tetrachloride 
13454-96-1

      Eyes; skin; resp. tract

       

      Inhalation
Skin
Eyes

      Burning sensation, cough 
Redness 
Redness

      Eyes; skin; resp sys Inh; ing; con

      Irrit eyes, nose; cough; dysp, wheez, cyan; derm, sens skin; lymphocytosis

      Hydrogen 
selenide 
7783-07-5

      Eyes; resp. tract; lungs

      Skin; liver; spleen; kidneys

      Inhalation

Skin
Eyes

      Burning sensation, cough, laboured 
breathing, nausea, sore throat, 
weakness 
On contact with liquid: frostbite 
Redness, pain;

      Resp sys; eyes; liver Inh; con

      Irrit eyes, nose, throat; nau, vomit, diarr; metallic taste, garlic breathy; dizz, lass, ftg; liq: frostbite; in animals: pneuitis; liver damage

      Selenious acid 
7783-00-8

      Eyes; skin; resp. tract

      Skin

      Inhalation

Skin
Eyes

Ingestion

      Burning sensation, cough, laboured 
breathing, sore throat
May be absorbed, redness, pain, blisters 
Redness, pain, blurred vision, severe 
deep burns, puffy eyelids 
Abdominal pain, burning sensation, 
confusion, nausea, sore throat, 
weakness, low blood pressure

         

      Selenious 
acid, 
disodium salt 
10102-18-8

      Eyes; skin; resp. tract; lungs; liver; kidneys; heart; CNS; GI tract

      teeth; bone; blood

      Inhalation



Skin
Eyes

      Abdominal cramps, diarrhoea, dizziness, 
headache, hair loss, laboured breathing, 
nausea, vomiting, symptoms may be 
delayed 
Redness 
Redness

         

      Selenium 7782-49-2

      Lungs

      Skin; resp. tract; GI tract; integuments

      Inhalation



Skin

Eyes
Ingestion

      Irritation of nose, cough, dizziness, 
headache, laboured breathing, nausea, 
sore throat, vomiting, weakness, 
symptoms may be delayed 
Redness, skin burns, pain, 
discolouration 
Redness, pain, blurred vision 
Metallic taste, diarrhoea, chills, fever

      Resp sys; eyes; skin; liver; kidneys; blood; spleen 
Inh; ing; con

      Irrit eyes, skin, nose, throat; vis dist; head; chills, fever, dysp, bron; metallic taste, garlic breath, GI dist; derm, eye, skin burns; in animals: anemia; liver nec, cirr; kidney, spleen damage

      Selenium 
dioxide 
7446-08-4

      Eyes; skin; resp. tract; lungs

      Skin

      Inhalation

Skin
Eyes

Ingestion

      Burning sensation, cough, laboured 
breathing, sore throat 
May be absorbed, redness, pain, blisters 
Redness, pain, blurred vision, severe 
deep burns, puffy eyelids 
Abdominal pain, burning sensation, 
confusion, nausea, sore throat, 
weakness, low blood pressure

         

      Selenium 
hexafluoride 
7783-79-1

      Resp. tract; lungs

      Skin; CNS; liver; kidneys

      Inhalation

Skin

Eyes

      Corrosive, cough, headache, nausea, 
shortness of breath, sore throat 
Redness, pain, on contact with liquid: 
frostbite; corrosive 
Redness, pain, blurred vision;

      Resp sys
Inh

      In animals: plum irrit, edema

      Selenium 
oxychloride 
7791-23-3

      Eyes; skin; resp. tract; lungs

      Skin

      Inhalation

Skin

Eyes

Ingestion

      Burning sensation, cough, laboured 
breathing, sore throat 
Corrosive, may be absorbed, redness, 
pain, blisters 
Redness, pain, blurred vision, severe 
deep burns 
Abdominal cramps, confusion, nausea, 
sore throat, hypotension

         

      Selenium 
trioxide 
13768-86-0

      Eyes; skin; resp. tract

      Skin; lungs

      Inhalation

Skin
Eyes

Ingestion

      Burning sensation, cough, laboured 
breathing, sore throat 
May be absorbed, redness, pain 
Redness, pain, blurred vision, puffy 
eyelids 
Abdominal cramps, confusion, nausea, 
sore throat, weakness, low blood 
pressure

         

      Silver 
7740-22-4

       

      Eyes; nose; throat; skin

         

      Nasal septum; skin; eyes
Inh; ing; con

      Blue-gray eyes, nasal septum, throat, skin; irrit, ulceration skin; GI dist

      Silver nitrate 
7761-88-8

      Eyes; skin; resp. tract

      Blood; skin

      Inhalation

Skin
Eyes

Ingestion

      Burning sensation, cough, laboured 
breathing 
Redness, skin burns, pain
Redness, pain, loss of vision, severe 
deep burns 
Abdominal pain, burning sensation, 
weakness

         

      Strontium 
chromate 
7789-06-2

      Eyes; skin; resp. tract; kidneys; liver

      Skin; lungs; blood; liver; kidneys; brain; red and white blood cells; liver; kidneys; carcinogenic

      Inhalation
Skin
Ingestion

      Cough, hoarseness 
Redness, ulcerations 
Sore throat

         

      Tellurium 
13494-80-9

      Resp. tract; CNS

      Possibly causes malformations in human 
babies

      Inhalation

Skin
Eyes
Ingestion

      Drowsiness, headache, garlic odour, 
nausea 
May be absorbed 
Redness 
Abdominal pain, constipation, nausea, vomiting, garlic odour of the breath

      Skin; CNS; blood 
Inh; ing; con

      Garlic breath, sweat; dry mouth, metallic taste; som; anor, nau, no sweat; derm; in animals: CNS, red blood cell effects

      Thallium 
metal 
7440-28-0

      Nervous system

      Eyes; liver; lungs; may cause birth defects

      Inhalation


Skin
Eyes
Ingestion

      Nausea, vomiting, loss of hair, abdominal colic, pain in legs and chest, nervousness, irritability 
May be absorbed 
May be absorbed 
Abdominal pain, constipation, diarrhoea, headache, nausea, vomiting, loss of vision

      Eyes; CNS; lungs; liver; kidneys; GI tract, body hair; resp sys
Inh; abs; ing; con

      Nau, diarr, abdom pain, vomit; ptosis, strabismus; peri neuritis, tremor; retster tight, chest pain, pulm edema; sez, chorea, psychosis; liver, kidney damage; alopecia; pares legs

      Thallous 
sulphate 
7446-18-6

      Eyes; skin; CNS; CVS; kidneys; GI tract

       

      Inhalation
Skin

Eyes
Ingestion

      See Ingestion
May be absorbed, redness;
See Ingestion
Redness, pain 
Abdominal pain, convulsions, diarrhoea, headache, vomiting, weakness, delirium, tachycardia

         

      Di-N-Dibutyltin
oxide
818-08-6

      Eyes; skin; resp. tract; lungs

      Skin; PNS; liver; bile duct; lymphatic system;

      Inhalation

Skin
Eyes

      Headache, ringing in the ears, memory 
loss, disorientation
May be absorbed, skin burns, pain 
Redness, pain

         

      Stannic 
chloride 
7646-78-8

      Eyes; skin; resp. tract; lungs

      Skin

      Inhalation


Skin
Eyes
Ingestion

      Burning sensation, cough, laboured 
breathing, shortness of breath, sore 
throat 
Redness, skin burns, blisters 
Severe deep burns 
Abdominal cramps, vomiting

         

      Stannic oxide 
18282-10-5

      Resp. tract

      Lungs

      Inhalation

      Cough

      Resp sys
Inh; con

      Stannosis (benign pneumoconiosis): dysp, decr pulm func

      Stannous
chloride
7772-99-8

      Eyes; skin; resp. tract; CNS; blood

      Liver

      Inhalation
Skin
Eyes
Ingestion

      Cough, shortness of breath 
Redness 
Redness, pain 
Abdominal pain, diarrhoea, nausea, 
vomiting

         

      Stannous chloride 
dihydrate 
10025-69-1

      Eyes; skin; resp. tract; CNS; blood

      Liver

      Inhalation
Skin
Eyes
Ingestion

      Cough, shortness of breath 
Redness 
Redness pain 
Abdominal pain, diarrhoea, nausea, 
vomiting

         

      Stannous 
fluoride 
7783-47-3

      Skin; resp. tract; eyes

      Teeth; bone

      Inhalation
Skin
Eyes
Ingestion

      Cough 
Redness 
Redness, pain, severe deep burns 
Abdominal pain, nausea

         

      Tin oxide 
21651-19-4

      Resp. tract

      Lungs

      Inhalation

      Cough

      Resp sys
Inh; con

      Stannosis (benign pneumoconiosis): dysp, decr pulm func

      Titanium 
dioxide 
13463-67-7

      Eyes; lungs

      Lungs

      Inhalation
Eyes

      Cough 
Redness

      Resp sys (in animals: lung tumors)
Inh

      Lung fib; (carc)

      Vanadium 
pentoxide 
1314-62-1

      Eyes; resp. tract; lungs

      Skin; lungs; tongue

      Inhalation

Skin
Eyes
Ingestion

      Burning sensation, cough, shortness of 
breath 
Redness, burning sensation 
Redness, pain, conjunctivitis 
Abdominal pain, diarrhoea, drowsiness, 
unconsciousness, vomiting, symptoms of 
severe systemic poisoning and death

      Resp sys; skin; eyes
Inh; con

      Irrit eyes, skin, throat; green tongue, metallic taste, eczema; cough; fine râles, wheez, bron, dysp

      Vanadium 
trioxide 
1314-34-7

      Eyes; skin; resp. tract

      Resp. tract; may effect liver and cardiac function

      Inhalation



Skin
Eyes
Ingestion

      Runny nose, sneezing, cough, 
diarrhoea, laboured breathing, sore 
throat, weakness, pain in chest, green 
to black tongue 
Dry skin, redness 
Redness 
Headache, vomiting, weakness

         

      Zinc chromate 
13530-65-9

       

      Skin;  resp. tract

      Inhalation
Eyes
Ingestion

      Cough 
Redness 
Abdominal pain, diarrhoea, vomiting

         

      Zinc 
phosphide 
1314-84-7

      Resp. tract; lungs; liver; kidneys; heart; CNS

       

      Inhalation

Ingestion

      Cough, diarrhoea, headache, fatigue, 
nausea, vomiting 
Abdominal pain, cough, diarrhoea, 
dizziness, headache, laboured 
breathing, nausea, unconsciousness, 
vomiting, ataxia, fatigue

         

      The short-term and long-term exposure data area adapted from the International Chemical Safety Cards (ICSC) series produced by the International Programme on Chemical Safety (see notes to table 1). The abbreviations used are CNS = central nervous system; CVS = cardiovascular system; PNS = peripheral nervous system; resp. tract = respiratory tract.

      The remaining data are adapted from the NIOSH Pocket Guide to Chemical Hazards (NIOSH 1994). The following abbreviations are used:
abdom = abdominal; abnor = abnormal/abnormalities; album = albuminuria; anes = anesthesia; anor = anorexia; anos = anosmia (loss of the sense of smell); 
appre = apprehension; arrhy = arrhythmias; aspir = aspiration; asphy = asphyxia; BP = blood pressure; breath = breathing; bron = bronchitis; 
broncopneu = bronchopneumonia; bronspas = bronchospasm; BUN = blood urea nitrogen; (carc) = potential occupational carcinogen; card = cardiac; chol = cholinesterase; 
cirr = cirrhosis; CNS = central nervous system; conc = concentration; conf = confusion; conj = conjunctivitis; constip = constipation; convuls = convulsions; corn = corneal;
CVS = cardiovascular system; cyan = cyanosis; decr = decreased; depress = depressant/depression; derm = dermatitis; diarr = diarrhea; dist = disturbance; dizz = dizziness;
drow = drowsiness; dysfunc = dysfunction; dysp = dyspnea (breathing difficulty); emphy = emphysema; eosin = eosinophilia; epilep = epileptiform; epis = epistaxis 
(nosebleed); equi = equilibrium; eryt = erythema (skin redness); euph = euphoria; fail = failure; fasc = fasiculation; FEV = forced expiratory volume; fib = fibrosis; 
fibri = fibrillation; ftg = fatigue; func = function; GI = gastrointestinal; gidd = giddiness; halu = hallucinations; head = headache; hema = hematuria (blood in the urine); 
hemato = hematopoietic; hemog = hemoglobinuria; hemorr = hemorrhage; hyperpig = hyperpigmentation; hypox = hypoxemia (reduced oxygen in the blood); 
inco = incoordination; incr = increase(d); inebri = inebriation; inflamm = inflammation; inj = injury; insom = insomnia; irreg = irregularity/irregularities; irrit = irritation; 
irrty = irritability; jaun = jaundice; kera = keratitis (inflammation of the cornea); lac = lacrimation (discharge of tears); lar = laryngeal; lass = lassitude (weakness, exhaustion);
leth = lethargy (drowsiness or indifference); leucyt = leukocytosis (increased blood leukocytes); leupen = leukopenia (reduced blood leukocytes); li-head = lightheadedness; 
liq = liquid; local = localized; low-wgt = weight loss; mal = malaise (vague feeling of discomfort); malnut = malnutrition; methemo = methemoglobinemia; 
monocy = monocytosis (increased blood monocytes); molt = molten; muc memb = mucous membrane; musc = muscle; narco = narcosis; nau = nausea; nec = necrosis; 
nept = nephritis; ner = nervousness; numb = numbness; opac = opacity; palp = palpitations; para = paralysis; pares = paresthesia; perf = perforation; peri neur = peripheral neuropathy; periorb = periorbital (situated around the eye); phar = pharyngeal; photo = phtophobia (abnormal visual intolerance to); pneu = penumonia; 
pneuitis = pneumonitis; PNS = peripheral nervous system; polyneur = polyneuropathy; prot = proteinuria; pulm = pulmonary; RBC = red blood cell; repro = reproductive; 
resp = respiratory; restless = restlessness; retster = retrosternal (occurring behind the sternum); rhin = rhinorrhea (discharge of thin nasal mucus); salv = salivation; 
sens = sensitization; sez = seizure; short = shortness; sneez = sneezing; sol = solid; soln = solution; som = somnolence (sleepiness, unnatural drowsiness); subs = substernal
(occurring beneath the sternum); sweat = sweating; swell = swelling; sys = system; tacar = tachycardia; tend = tenderness; terato = teratogenic; throb = throbbing; 
tight = tightness; trachbronch = tracheobronchitis; twitch = twitching; uncon = unconsciousness; vap = vapor; venfib = ventricular fibrillation; vert = vertigo (an illusion of
movement); vesic = vesiculation; vis dist = viszal disturbance; vomit = vomiting; weak = weakness; wheez = wheezing.

      The reader is referred to the Guide to chemicals in Volume IV of this Encyclopaedia for additional information on the toxicity of related chemical substances and compounds. Calcium compounds and boron compounds, in particular, are to be found there. Specific information on biological monitoring is given in the chapter Biological monitoring.

       

      Back

      Wednesday, 09 February 2011 03:40

      Contents Page

      CONTENTS

      Chapter Editor                                                                                       Gunnar Nordberg

      • General Profile
      • Acknowledgements
      • Aluminium
      • Antimony
      • Arsenic
      • Barium
      • Bismuth
      • Cadmium
      • Chromium
      • Copper
      • Iron
      • Gallium
      • Germanium
      • Indium
      • Iridium
      • Lead
      • Magnesium
      • Manganese
      • Metal Carbonyls (especially Nickel Carbonyl)
      • Mercury
      • Molybdenum
      • Nickel
      • Niobium
      • Osmium
      • Palladium
      • Platinum
      • Rhenium
      • Rhodium
      • Ruthenium
      • Selenium
      • Silver
      • Tantalum
      • Tellurium
      • Thallium
      • Tin
      • Titanium
      • Tungsten
      • Vanadium
      • Zinc
      • Zirconium and Hafnium

       

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      Wednesday, 26 January 2011 00:49

      Traumatic Head Injuries

      Aetiological Factors

      Head trauma consists of skull injury, focal brain injury and diffuse brain tissue injury (Gennarelli and Kotapa 1992). In work-related head trauma falls account for the majority of the causes (Kraus and Fife 1985). Other job-related causes include being struck by equipment, machinery or related items, and by on-road motor vehicles. The rates of work-related brain injury are markedly higher among young workers than older ones (Kraus and Fife 1985).

      Occupations at Risk

      Workers involved in mining, construction, driving motor vehicles and agriculture are at higher risk. Head trauma is common in sportsmen such as boxers and soccer players.

      Neuropathophysiology

      Skull fracture can occur with or without damage to the brain. All forms of brain injury, whether resulting from penetrating or closed head trauma, can lead to the development of swelling of the cerebral tissue. Vasogenic and cytogenic pathophysiologic processes active at the cellular level result in cerebral oedema, increased intracranial pressure and cerebral ischaemia.

      Focal brain injuries (epidural, subdural or intracranial haematomas) may cause not only local brain damage, but a mass effect within the cranium, leading to midline shift, herniation and ultimately brain stem (mid-brain, pons and medulla oblongata) compression, causing, first a declining level of consciousness, then respiratory arrest and death (Gennarelli and Kotapa 1992).

      Diffuse brain injuries represent shearing trauma to innumerable axons of the brain, and may be manifested as anything from subtle cognitive dysfunction to severe disability.

      Epidemiological Data

      There are few reliable statistics on the incidence of head injury from work-related activities.

      In the United States, estimates of the incidence of head injury indicate that at least 2 million people incur such injuries each year, with nearly 500,000 resultant hospital admissions (Gennarelli and Kotapa 1992). Approximately half of these patients were involved in motor accidents.

      A study of brain injury in residents of San Diego County, California in 1981 showed that the overall work-related injury rate for males was 19.8 per 100,000 workers (45.9 per 100 million work hours). The incidence rates of work-related brain injuries for male civilian and military personnel were 15.2 and 37.0 per 100,000 workers, respectively. In addition, the annual incidence of such injuries was 9.9 per 100 million work hours for males in the work force (18.5 per 100 million hours for military personnel and 7.6 per 100 million hours for civilians) (Kraus and Fife 1985). In the same study, about 54% of the civilian work-related brain injuries resulted from falls, and 8% involved on-road motor vehicle accidents (Kraus and Fife 1985).

      Signs and Symptoms

      The signs and symptoms vary among different forms of head trauma (table 1) (Gennarelli and Kotapa 1992) and different locations of traumatic brain lesion (Gennarelli and Kotapa 1992; Gorden 1991). On some occasions, multiple forms of head trauma may occur in the same patient.

      Table 1. Classification of traumatic head injuries.

      Skull injuries

                            Brain tissue injuries


      Focal

      Diffuse

      Vault fracture

      Haematoma

      Concussion

      Linear

      Epidural

      Mild

      Depressed

      Subdural
      Intracranial

      Classical

      Basilar fracture

      Contusion

      Prolonged coma

      (diffuse axonal injury)

       

      Skull injuries

      Fractures of cerebral vault, either linear or depressed, can be detected by radiological examinations, in which the location and depth of the fracture are clinically most important.

      Fractures of the skull base, in which the fractures are usually not visible on conventional skull radiographs, can best be found by computed tomography (CT scan). It can also be diagnosed by clinical findings such as the leakage of cerebropinal fluid from the nose (CSF rhinorrhea) or ear (CSF otorrhea), or subcutaneous bleeding at the periorbital or mastoid areas, though these may take 24 hours to appear.

      Focal brain tissue injuries (Gennarelli and Kotapa 1992;Gorden 1991)

      Haematoma:

      Epidural haematoma is usually due to arterial bleeding and may be associated with a skull fracture. The bleeding is seen distinctly as a biconvex density on the CT scan. It is characterized clinically by transient loss of consciousness immediately after injury, followed by a lucid period. Consciousness may deteriorate rapidly due to increasing intracranial pressure.

      Subdural haematoma is the result of venous bleeding beneath the dura. Subdural haemorrhage may be classified as acute, subacute or chronic, based on the time course of the development of symptoms. Symptoms result from direct pressure to the cortex under the bleed. The CT scan of the head often shows a crescent-shaped deficit.

      Intracerebral haematoma results from bleeding within the parenchyma of the cerebral hemispheres. It may occur at the time of trauma or may appear a few days later (Cooper 1992). Symptoms are usually dramatic and include an acutely depressed level of consciousness and signs of increased intracranial pressure, such as headache, vomiting, convulsions and coma. Subarachnoid haemorrhage may occur spontaneously as the result of a ruptured berry aneurysm, or it may be caused by head trauma.

      In patients with any form of haematoma, deterioration of consciousness, ipsilateral dilated pupil and contralateral haemiparesis suggests an expanding haematoma and the need for immediate neurosurgical evaluation. Brain stem compression accounts for approximately 66% of deaths from head injuries (Gennarelli and Kotapa 1992).

      Cerebral contusion:

      This presents as temporary loss of consciousness or neurologic deficits. Memory loss may be retrograde—loss of memory a time period before the injury, or antegrade—loss of current memory. CT scans shows multiple small isolated haemorrhages in the cerebral cortex. Patients are at higher risk of subsequent intracranial bleeding.

      Diffuse brain tissue injuries (Gennarelli and Kotapa 1992;Gorden 1991)

      Concussion:

      Mild concussion is defined as a rapidly resolving (less than 24 hours) interruption of function (such as memory), secondary to trauma. This includes symptoms as subtle as memory loss and as obvious as unconsciousness.

      Classic cerebral concussion manifests as slowly resolving, temporary, reversible neurologic dysfunction such as memory loss, often accompanied by a significant loss of consciousness (more than 5 minutes, less than 6 hours). The CT scan is normal.

      Diffuse axonal injury: 

      This results in a prolonged comatose state (more than 6 hours). In the milder form, the coma is of 6 to 24 hours duration, and may be associated with long-standing or permanent neurologic or cognitive deficits. A coma of moderate form lasts for more than 24 hours and is associated with a mortality of 20%. The severe form shows brain stem dysfunction with the coma lasting for more than 24 hours or even months, because of the involvement of the reticular activating system.

      Diagnosis and Differential Diagnosis

      Apart from the history and serial neurologic examinations and a standard  assessment  tool  such  as  the  Glasgow  Coma  Scale (table 2), the radiological examinations are helpful in making a definitive diagnosis. A CT scan of the head is the most important diagnostic test to be performed in patients with neurologic findings after head trauma (Gennarelli and Kotapa 1992; Gorden 1991; Johnson and Lee 1992), and allows rapid and accurate assessment of surgical and nonsurgical lesions in the critically injured patients (Johnson and Lee 1992). Magnetic resonance (MR) imaging is complementary to the evaluation of cerebral head trauma. Many lesions are identified by MR imaging such as cortical contusions, small subdural haematomas and diffuse axonal injuries that may not be seen on CT examinations (Sklar et al. 1992).

      Table 2. Glasgow Coma Scale.

      Eyes

      Verbal

      Motor

      Does not open eyes

      Opens eyes to painful
      stimuli

      Opens eyes upon
      loud verbal command

      Opens eyes
      spontaneously

      Makes no noise

      Moans, makes unintelligible
      noises

      Talks but nonsensical


      Seems confused and
      disoriented

      Alert and oriented

      (1) No motor response to pain

      (2) Extensor response (decerebrate)


      (3) Flexor response (decorticate)


      (4) Moves parts of body but does not
      remove noxious stimuli

      (5) Moves away from noxious stimuli

      (6) Follows simple motor commands

       

      Treatment and Prognosis

      Patients with head trauma need to be referred to an emergency department, and a neurosurgical consultation is important. All patients known to be unconscious for more than 10 to 15 minutes, or with a skull fracture or a neurologic abnormality, require hospital admission and observation, because the possibility exists of delayed deterioration from expanding mass lesions (Gennarelli and Kotapa 1992).

      Depending on the type and severity of head trauma, provision of supplemental oxygen, adequate ventilation, decrease of brain water by intravenous administration of faster-acting hyperosmolar agents (e.g., mannitol), corticosteroids or diuretics, and surgical decompression may be necessary. Appropriate rehabilitation is advisable at a later stage.

      A multicentre study revealed that 26% of patients with severe head injury had good recovery, 16% were moderately disabled, and 17% were either severely disabled or vegetative (Gennarelli and Kotapa 1992). A follow-up study also found persistent headache in 79% of the milder cases of head injury, and memory difficulties in 59% (Gennarelli and Kotapa 1992).

      Prevention

      Safety and health education programmes for the prevention of work-related accidents should be instituted at the enterprise level for workers and management. Preventive measures should be applied to mitigate the occurrence and severity of head injuries due to work-related causes such as falls and transport accidents.

       

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      Wednesday, 26 January 2011 00:30

      First Aid

      First aid is the immediate care given to victims of accidents before trained medical workers arrive. Its goal is to stop and, if possible, reverse harm. It involves rapid and simple measures such as clearing the air passageway, applying pressure to bleeding wounds or dousing chemical burns to eyes or skin.

      The critical factors which shape first aid facilities in a workplace are work-specific risk and availability of definitive medical care. The care of a high-powered saw injury is obviously radically different from that of a chemical inhalation.

      From a first aid perspective, a severe thigh wound occurring near a surgical hospital requires little more than proper transport; for the same injury in a rural area eight hours from the nearest medical facility, first aid would include—among other things—debridement, tying off bleeding vessels and administration of tetanus immunoglobulin and antibiotics.

      First aid is a fluid concept not only in what (how long, how complex) must be done, but in who can do it. Though a very careful attitude is required, every worker can be trained in the top five or ten do’s and don’ts of first aid. In some situations, immediate action can save life, limb or eyesight. Co-workers of victims should not remain paralyzed while waiting for trained personnel to arrive. Moreover, the “top-ten” list will vary with each workplace and must be taught accordingly.

      Importance of First Aid

      In cases of cardiac arrest, defibrillation administered within four minutes yields survival rates of 40 to 50%, versus less than 5% if given later. Five hundred thousand people die of cardiac arrest every year in the United States alone. For chemical eye injuries, immediate flushing with water can save eyesight. For spinal cord injuries, correct immobilization can make the difference between full recovery and paralysis. For haemorrhages, the simple application of a fingertip to a bleeding vessel can stop life-threatening blood loss.

      Even the most sophisticated medical care in the world often cannot undo the effects of poor first aid.

      First Aid in the Context of the GeneralOrganization of Health and Safety

      The provision of first aid should always have a direct relationship to general health and safety organization, because first aid itself will not handle more than a small part of workers’ total care. First aid is a part of the total health care for workers. In practice, its application will depend to a large extent on persons present at the time of an accident, whether co-workers or formally trained medical personnel. This immediate intervention must be followed by specialized medical care whenever needed.

      First aid and emergency treatment in cases of accident and indisposition of workers at the workplace are listed as an important part of the functions of the occupational health services in the ILO Occupational Health Services Convention (No.  161), Article 5, and the Recommendation of the same name. Both adopted in 1985, they provide for the progressive development of occupational health services for all workers.

      Any comprehensive occupational safety and health programme should include first aid, which contributes to minimizing the consequences of accidents and is therefore one of the components of tertiary prevention. There is a continuum leading from the knowledge of the occupational hazards, their prevention, first aid, emergency treatment, further medical care and specialized treatment for reintegration into and readaptation to work. There are important roles that occupational health professionals can play along this continuum.

      It is not infrequent that several small incidents or minor accidents take place before a severe accident occurs. Accidents requiring only first aid represent a signal which should be heard and used by the occupational health and safety professionals to guide and promote preventive action.

      Relation to Other Health-Related Services

      The institutions which may be involved in the organization of first aid and provide assistance following an accident or illness at work include the following:

      • the occupational health service of the enterprise itself or other occupational health entities
      • other institutions which may provide services, such as: ambulance services; public emergency and rescue services; hospitals, clinics and health centres, both public and private; private physicians; poison centres; civil defence; fire departments; and police.

       

      Each of these institutions has a variety of functions and capabilities, but it must be understood that what applies to one type of institution—say a poison centre—in one country, may not necessarily apply to a poison centre in another country. The employer, in consultation with, for example, the factory physician or outside medical advisers, must ensure that the capabilities and facilities of neighbouring medical institutions are adequate to deal with the injuries expected in the event of serious accidents. This assessment is the basis for deciding which institutions will be entered into the referral plan.

      The cooperation of these related services is very important in providing proper first aid, particularly for small enterprises. Many of them may provide advice on the organization of first aid and on planning for emergencies. There are good practices which are very simple and effective; for example, even a shop or a small enterprise may invite the fire brigade to visit its premises. The employer or owner will receive advice on fire prevention, fire control, emergency planning, extinguishers, the first aid box and so on. Conversely, the fire brigade will know the enterprise and will be ready to intervene more rapidly and efficiently.

      There are many other institutions which may play a role, such as industrial and trade associations, safety associations, insurance companies, standards organizations, trade unions and other non-governmental organizations. Some of these organizations may be knowledgeable about occupational health and safety and can be a valuable resource in the planning and organization of first aid.

      An Organized Approach to First Aid

      Organization and planning

      First aid cannot be planned in isolation. First aid requires an organized approach involving people, equipment and supplies, facilities, support and arrangements for the removal of victims and non-victims from the site of an accident. Organizing first aid should be a cooperative effort, involving employers, occupational health and public health services, the labour inspectorate, plant managers and relevant non-governmental organizations. Involving workers themselves is essential: they are often the best source on the likelihood of accidents in specific situations.

      Whatever the degree of sophistication or the absence of facilities, the sequence of actions to be taken in the case of an unforeseen event must be determined in advance. This must be done taking due account of existing and potential occupational and non-occupational hazards or occurrences, as well as ways of obtaining immediate and appropriate assistance. Situations vary not only with the size of the enterprise but also with its location (in a town or a rural area) and with the development of the health system and of labour legislation at the national level.

      As regards the organization of first aid, there are several key variables to be considered:

      • type of work and associated level of risk
      • potential hazards
      • size and layout of the enterprise
      • other enterprise characteristics (e.g., configuration)
      • availability of other health services.

       

      Type of work and associated level of risk

      The risks of injury vary greatly from one enterprise and from one occupation to another. Even within a single enterprise, such as a metalworking firm, different risks exist depending on whether the worker is engaged in the handling and cutting of metal sheets (where cuts are frequent), welding (with the risk of burns and electrocution), the assembly of parts, or metal plating (which has the potential of poisoning and skin injury). The risks associated with one type of work vary according to many other factors, such as the design and age of the machinery used, the maintenance of the equipment, the safety measures applied and their regular control.

      The ways in which the type of work or the associated risks influence the organization of first aid have been fully recognized in most legislation concerning first aid. The equipment and supplies required for first aid, or the number of first aid personnel and their training, may vary in accordance with the type of work and the associated risks. Countries use different models for classifying them for the purpose of planning first aid and deciding whether higher or lower requirements are to be set. A distinction is sometimes made between the type of work and the specific potential risks:

      • low risk-for example, in offices or shops
      • higher risk-for example, in warehouses, farms and in some factories and yards
      • specific or unusual risks-for example, in steelmaking (especially when working on furnaces), coking, non-ferrous smelting and processing, forging, foundries; shipbuilding; quarrying, mining or other underground work; work in compressed air and diving operations; construction, lumbering and woodworking; abattoirs and rendering plants; transportation and shipping; most industries involving harmful or dangerous substances.

       

      Potential hazards

      Even in enterprises which seem clean and safe, many types of injury can occur. Serious injuries may result from falling, striking against objects or contact with sharp edges or moving vehicles. The specific requirements for first aid will vary depending on whether the following occur:

      • falls
      • serious cuts, severed limbs
      • crushing injuries and entanglements
      • high risks of spreading fire and explosions
      • intoxication by chemicals at work
      • other chemical exposure
      • electrocution
      • exposure to excessive heat or cold
      • lack of oxygen
      • exposure to infectious agents, animal bites and stings.

       

      The above is only a general guide. The detailed assessment of the potential risks in the working environment helps greatly to identify the need for first aid.

      Size and layout of the enterprise

      First aid must be available in every enterprise, regardless of size, taking into account that the frequency rate of accidents is often inversely related to the size of the enterprise.

      In larger enterprises, the planning and organization of first aid can be more systematic. This is because individual workshops have distinct functions and the workforce is more specifically deployed than in smaller enterprises. Therefore the equipment, supplies and facilities for first aid, and first aid personnel and their training, can normally be organized more precisely in response to the potential hazards in a large enterprise than in a smaller one. Nevertheless, first aid can also be effectively organized in smaller enterprises.

      Countries use different criteria for the planning of first aid in accordance with the size and other characteristics of the enterprise. No general rule can be set. In the United Kingdom, enterprises with fewer than 150 workers and involving low risks, or enterprises with fewer than 50 workers with higher risks, are considered small, and different criteria for the planning of first aid are applied in comparison with enterprises where the number of workers present at work exceeds these limits. In Germany, the approach is different: whenever there are fewer than 20 workers expected at work one set of criteria would apply; if the number of workers exceeds 20, other criteria will be used. In Belgium, one set of criteria applies to industrial enterprises with 20 or fewer workers at work, a second to those with between 20 and 500 workers, and a third to those with 1,000 workers and more.

      Other enterprise characteristics

      The configuration of the enterprise (i.e., the site or sites where the workers are at work) is important to the planning and organization of first aid. An enterprise might be located at one site or spread over several sites either within a town or region, or even a country. Workers may be assigned to areas away from the enterprise’s central establishment, such as in agriculture, lumbering, construction or other trades. This will influence the provision of equipment and supplies, the number and distribution of first aid personnel, and the means for the rescue of injured workers and their transportation to more specialized medical care.

      Some enterprises are temporary or seasonal in nature. This implies that some workplaces exist only temporarily or that in one and the same place of work some functions will be performed only at certain periods of time and may therefore involve different risks. First aid must be available whenever needed, irrespective of the changing situation, and planned accordingly.

      In some situations employees of more than one employer work together in joint ventures or in an ad hoc manner such as in building and construction. In such cases the employers may make arrangements to pool their provision of first aid. A clear allocation of responsibilities is necessary, as well as a clear understanding by the workers of each employer as to how first aid is provided. The employers must ensure that the first aid organized for this particular situation is as simple as possible.

      Availability of other health services

      The level of training and the extent of organization for first aid is, in essence, dictated by the proximity of the enterprise to, and its integration with, readily available health services. With close, good backup, avoiding delay in transport or calling for help can be more crucial to a good outcome than is skilful application of medical manoeuvres. Each workplace’s first aid programme must mold itself to—and become an extension of—the medical facility which provides the definitive care for its injured workers.

      Basic Requirements of a First Aid Programme

      First aid must be considered part of sound management and making work safe. Experience in countries where first aid is strongly established suggests that the best way to ensure effective first aid provision is to make it mandatory by legislation. In countries which have chosen this approach, the main requirements are set out in specific legislation or, more commonly, in national labour codes or similar regulations. In these cases, subsidiary regulations contain more detailed provisions. In most cases, the overall responsibility of the employer for providing and organizing first aid is laid down in the basic enabling legislation. The basic elements of a first aid programme include the following:

      Equipment, supplies and facilities

      • equipment to rescue the victim at the site of the accident so as to prevent further harm (e.g., in the case of fire, gassing, electrocution)
      • first aid boxes, first aid kits or similar containers, with a sufficient quantity of the materials and appliances required for the delivery of basic first aid
      • specialized equipment and supplies which may be required in enterprises involving specific or unusual risks at work
      • an adequately identified first aid room or a similar facility where first aid can be administered
      • provision of means of evacuation and emergency transportation of the injured persons to the first aid facility or the sites where further medical care is available
      • means of giving the alarm and communicating the alert

       

      Human resources

      • selection, training and retraining of suitable persons for administering first aid, their appointment and location at critical sites throughout the enterprise, and the assurance that they are permanently available and accessible
      • retraining, including practical exercises simulating emergency situations, with due account given to specific occupational hazards in the enterprise

       

      Other

      • establishment of a plan, including links between the relevant health or public health services, with a view to the delivery of medical care following first aid
      • education and information of all workers concerning the prevention of accidents and injuries, and the actions workers must themselves take following an injury (e.g., a shower immediately after a chemical burn)
      • information on the arrangements for first aid, and the periodic updating of this information
      • posting of information, visual guides (e.g., posters) and instruction about first aid, and plans with a view to the delivery of medical care after first aid
      • record keeping (the first aid treatment record is an internal report which will provide information concerning the health of the victim, as well as contributing to safety at work; it should include information on: the accident (time, location, occurrence), the type and severity of the injury, the first aid delivered, the additional medical care requested, the name of the casualty and the names of witnesses and other workers involved, especially those transporting the casualty)

       

      Although basic responsibility for implementing a first aid programme lies with the employer, without full participation of the workers, first aid cannot be effective. For example, workers may need to cooperate in rescue and first aid operations; they should thus be informed of first aid arrangements and should make suggestions, based on their knowledge of the workplace. Written instructions about first aid, preferably in the form of posters, should be displayed by the employer at strategic places within the enterprise. In addition, the employer should organize briefings for all workers. The following are essential parts of the briefing:

      • the organization of first aid in the enterprise, including the procedure for access to additional care
      • colleagues who have been appointed as first aid personnel
      • ways in which information about an accident should be communicated, and to whom
      • location of the first aid box
      • location of the first aid room
      • location of the rescue equipment
      • what the workers must do in case of an accident
      • location of the escape routes
      • workers’ actions following an accident
      • ways of supporting first aid personnel in their task.

       

      First Aid Personnel

      First aid personnel are persons on the spot, generally workers who are familiar with the specific conditions of work, and who might not be medically qualified but must be trained and prepared to perform very specific tasks. Not every worker is suitable to be trained for providing first aid. First aid personnel should be selected carefully, taking into account attributes such as reliability, motivation and the ability to cope with people in a crisis situation.

      Type and number

      National regulations for first aid vary with respect to both the type and number of first aid personnel required. In some countries the emphasis is on the number of persons employed in the workplace. In other countries, the overriding criteria are the potential risks at work. In yet others, both of these factors are taken into account. In countries with a long tradition of occupational safety and health practices and where the frequency of accidents is lower, more attention is usually given to the type of first aid personnel. In countries where first aid is not regulated, emphasis is normally placed on numbers of first aid personnel.

      A distinction may be made in practice between two types of first aid personnel:

      • the basic-level first-aider, who receives basic training as outlined below and who qualifies for appointment where the potential risk at work is low
      • the advanced-level first-aider, who will receive the basic and advanced training and will qualify for appointment where the potential risk is higher, special or unusual.

       

      The following four examples are indicative of the differences in approach used in determining the type and number of first aid personnel in different countries:

      United Kingdom

      • If the work involves relatively low hazards only, no first aid personnel are required unless there are 150 or more workers present at work; in this case a ratio of one first-aider per 150 workers is considered adequate. Even if fewer than 150 workers are at work, the employer should nevertheless designate an “appointed person” at all times when workers are present.
      • Should the work involve higher risk, one first-aider will normally be required when the number of workers at work is between 50 and 150. If more than 150 workers are at work, one additional first-aider for every 150 will be required and, if the number of workers at work is less than 50, an “appointed person” should be designated.
      • If the potential risk is unusual or special, there will be a need, in addition to the number of first aid personnel already required under the criteria set out above, for an additional person who will be trained specifically in first aid in case of accidents arising from these unusual or special hazards (the occupational first-aider).

       

      Belgium

      • One first-aider is usually required for every 20 workers present at work. However, a full-time occupational health staff member is required if there are special hazards and if the number of workers exceeds 500, or in the case of any enterprise where the number of workers on site is 1,000 or more.
      • Some degree of flexibility is possible in accordance with particular situations.

       

      Germany

      • One first-aider is required if there are 20 or fewer workers present at work.
      •  If more than 20 workers are present, the number of first-aiders should be 5% of those at work in offices or general trade, or 10% in all other enterprises. Depending on other measures which may have been taken by the enterprise to deal with emergencies and accidents, these numbers may be revised.
      • If work involves unusual or specific risks (for instance, if hazardous substances are involved), a special type of first aid personnel needs to be provided and trained; no specific number is stipulated for such personnel (i.e., the above-mentioned numbers apply).
      • If more than 500 workers are present and if unusual or special hazards exist (burns, poisonings, electrocutions, impairment of vital functions such as respiratory or cardiac arrest), specially trained full-time personnel must be made available to deal with cases where a delay in arrival of no more than 10 minutes may be allowable. This provision will apply in most larger construction sites where a number of enterprises often employ a workforce of several hundred workers.

       

      New Zealand

      • If more than five workers are present, an employee is appointed and put in charge of the equipment, supplies and facilities for first aid.
      • If more than 50 persons are present, the person appointed must be either a registered nurse or hold a certificate (issued by the St. John’s Ambulance Association or the New Zealand Red Cross Society).

       

      Training

      The training of first aid personnel is the single most important factor determining the effectiveness of organized first aid. Training programmes will depend on the circumstances within the enterprise, especially the type of work and the risks involved.

      Basic Training

      Basic training programmes are usually on the order of 10 hours. This is a minimum. Programmes can be divided into two parts, dealing with the general tasks to be performed and the actual delivery of first aid. They will cover the areas listed below.

      General tasks

      • how first aid is organized
      • how to assess the situation, the magnitude and severity of the injuries and the need for additional medical help
      • how to protect the casualty against further injury without creating a risk for oneself; the location and use of the rescue equipment
      • how to observe and interpret the victim’s general condition (e.g., unconsciousness, respiratory and cardiovascular distress, bleeding)
      • the location, use and maintenance of first aid equipment and facilities
      • the plan for access to additional care.

       

      Delivery of first aid

      The objective is to provide basic knowledge and delivery of first aid. At the basic level, this includes, for example:

      • wounds
      • bleeding
      • fractured bones or joints
      • crushing injuries (e.g., to the thorax or abdomen)
      • unconsciousness, especially if accompanied by respiratory difficulties or arrest
      • eye injuries
      • burns
      • low blood pressure, or shock
      • personal hygiene in dealing with wounds
      • care of amputated digits.

       

      Advanced Training

      The aim of advanced training is specialization rather than comprehensiveness. It is of particular importance in relation to the following types of situation (though specific programmes normally deal only with some of these, in accordance with needs, and their duration varies considerably):

      • cardiopulmonary resuscitation
      • poisoning (intoxication)
      • injuries caused by electric current
      • severe burns
      • severe eye injuries
      • skin injuries
      • contamination by radioactive material (internal, and skin or wound contamination)
      • other hazard-specific procedures (e.g., heat and cold stress, diving emergencies).

       

      Training Materials and Institutions

      A wealth of literature is available on training programmes for first aid. The national Red Cross and Red Crescent Societies and various organizations in many countries have issued material which covers much of the basic training programme. This material should be consulted in the design of actual training programmes, though it may need adaptation to the specific requirements of first aid at work (in contrast with first aid after traffic accidents, for instance).

      Training programmes should be approved by the competent authority or a technical body authorized to do so. In many cases, this may be the national Red Cross or Red Crescent Society or related institutions. Sometimes safety associations, industrial or trade associations, health institutions, certain non-governmental organizations and the labour inspectorate (or their subsidiary bodies) may contribute to the design and provision of the training programme to suit specific situations.

      This authority should also be responsible for testing first aid personnel upon completion of their training. Examiners independent of the training programmes should be designated. Upon successfully completing the examination, the candidates should be awarded a certificate upon which the employer or enterprise will base their appointment. Certification should be made obligatory and should also follow refresher training, other instruction or participation in field work or demonstrations.

      First Aid Equipment, Supplies and Facilities

      The employer is responsible for providing first aid personnel with adequate equipment, supplies and facilities.

      First aid boxes, first aid kits and similar containers

      In some countries, only the principal requirements are set out in regulations (e.g., that adequate amounts of suitable materials and appliances are included, and that the employer must determine what precisely may be required, depending on the type of work, the associated risks and the configuration of the enterprise). In most countries, however, more specific requirements have been set out, with some distinction made as to the size of the enterprise and the type of work and potential risks involved.

      Basic content

      The contents of these containers must obviously match the skills of the first aid personnel, the availability of a factory physician or other health personnel and the proximity of an ambulance or emergency service. The more elaborate the tasks of the first aid personnel, the more complete must be the contents of the containers. A relatively simple first aid box will usually include the following items:

      • individually wrapped sterile adhesive dressing
      • bandages (and pressure dressings, where appropriate)
      • a variety of dressings
      • sterile sheets for burns
      • sterile eye pads
      • triangular bandages
      • safety pins
      • a pair of scissors
      • antiseptic solution
      • cotton wool balls
      • a card with first aid instructions
      • sterile plastic bags
      • access to ice.

       

      Location

      First aid boxes should always be easily accessible, near areas where accidents could occur. They should be able to be reached within one to two minutes. They should be made of suitable materials, and should protect the contents from heat, humidity, dust and abuse. They need to be identified clearly as first aid material; in most countries, they are marked with a white cross or a white crescent, as applicable, on a green background with white borders.

      If the enterprise is subdivided into departments or shops, at least one first aid box should be available in each unit. However, the actual number of boxes required will be determined on the basis of the needs assessment made by the employer. In some countries the number of containers required, as well as their contents, has been established by law.

      Auxiliary kits

      Small first aid kits should always be available where workers are away from the establishment in such sectors as lumbering, agricultural work or construction; where they work alone, in small groups or in isolated locations; where work involves travelling to remote areas; or where very dangerous tools or pieces of machinery are used. The contents of such kits, which should also be readily available to self-employed persons, will vary according to circumstances, but they should always include:

      • a few medium-sized dressings
      • a bandage
      • a triangular bandage
      • safety pins.

       

      Specialized equipment and supplies

      Further equipment may be needed for the provision of first aid where there are unusual or specific risks. For example, if poisonings are a possibility, antidotes must be immediately available in a separate container, though it must be made clear that their administration is subject to medical instruction. Long lists of antidotes exist, many for specific situations. Potential risks will determine which antidotes are needed.

      Specialized equipment and material should always be located near the sites of potential accidents and in the first aid room. Transporting the equipment from a central location such as an occupational health service facility to the site of the accident may take too long.

      Rescue equipment

      In some emergency situations, specialized rescue equipment to remove or disentangle an accident victim may be necessary. Although it may not be easy to predict, certain work situations (such as working in confined spaces, at heights or above water) may have a high potential for this type of incident. Rescue equipment may include items such as protective clothing, blankets for fire-fighting, fire extinguishers, respirators, self-contained breathing apparatus, cutting devices and mechanical or hydraulic jacks, as well as equipment such as ropes, harnesses and specialized stretchers to move the victim. It must also include any other equipment required to protect the first aid personnel against becoming casualties themselves in the course of delivering first aid. Although initial first aid should be given before moving the patient, simple means should also be provided for transporting an injured or sick person from the scene of the accident to the first aid facility. Stretchers should always be accessible.

      The first aid room

      A room or a corner, prepared for administering first aid, should be available. Such facilities are required by regulations in many countries. Normally, first aid rooms are mandatory when there are more than 500 workers at work or when there is a potentially high or specific risk at work. In other cases, some facility must be available, even though this may not be a separate room—for example, a prepared corner with at least the minimum furnishings of a full-scale first aid room, or even a corner of an office with a seat, washing facilities and a first aid box in the case of a small enterprise. Ideally, a first aid room should:

      • be accessible to stretchers and must have access to an ambulance or other means of transportation to a hospital
      • be large enough to hold a couch, with space for people to work around it
      • be kept clean, well ventilated, well lit and maintained in good order
      • be reserved for the administration of first aid
      • be clearly identified as a first aid facility, be appropriately marked and be under the responsibility of first aid personnel
      • have clean running water, preferably both hot and cold, soap and a nail brush. If running water is not available, water should be kept in disposable containers near the first aid box for eye washing and irrigation
      • include towels, pillows and blankets, clean clothing for use by the first aid personnel, and a refuse container.

       

      Communication and Referral Systems

      Means for communicating the alert

      Following an accident or sudden illness, it is important that immediate contact be made with first aid personnel. This requires means of communication between work areas, the first aid personnel and the first aid room. Communications by telephone may be preferable, especially if distances are more than 200 metres, but this will not be possible in all establishments. Acoustic means of communication, such as a hooter or buzzer, may serve as a substitute as long as it can be assured that the first aid personnel arrive at the scene of the accident rapidly. Lines of communication should be pre-established. Requests for advanced or specialized medical care, or an ambulance or emergency service, are normally made by telephone. The employer should ensure that all relevant addresses, names and telephone numbers are clearly posted throughout the enterprise and in the first aid room, and that they are always available to the first aid personnel.

      Access to additional care

      The need for a referral of the victim to more advanced or specialized medical care must always be foreseen. The employer should have plans for such a referral, so that when the case arises everybody involved will know exactly what to do. In some cases the referral systems will be rather simple, but in others they may be elaborate, especially where unusual or special risks are involved at work. In the construction industry, for instance, referral may be required after serious falls or crushings, and the end point of referral will most probably be a general hospital, with adequate orthopaedic or surgical facilities. In the case of a chemical works, the end point of referral will be a poison centre or a hospital with adequate facilities for the treatment of poisoning. No uniform pattern exists. Each referral plan will be tailored to the needs of the enterprise under consideration, especially if higher, specific or unusual risks are involved. This referral plan is an important part of the enterprise’s emergency plan.

      The referral plan must be supported by a system of communication and means for transporting the casualty. In some cases, this may involve communication and transport systems organized by the enterprise itself, especially in the case of larger or more complex enterprises. In smaller enterprises, transport of the casualty may need to rely on outside capacity such as public transport systems, public ambulance services, taxis and so on. Stand-by or alternative systems should be set up.

      The procedures for emergency conditions must be communicated to everyone: workers (as part of their overall briefing on health and safety), first-aiders, safety officers, occupational health services, health facilities to which a casualty may be referred, and institutions which play a role in communications and the transport of the casualty (e.g., telephone services, ambulance services, taxi companies and so on).

       

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      Contents

      Preface
      Part I. The Body
      Part II. Health Care
      Part III. Management & Policy
      Part IV. Tools and Approaches
      Part V. Psychosocial and Organizational Factors
      Part VI. General Hazards
      Part VII. The Environment
      Part VIII. Accidents and Safety Management
      Part IX. Chemicals
      Part X. Industries Based on Biological Resources
      Part XI. Industries Based on Natural Resources
      Part XII. Chemical Industries
      Part XIII. Manufacturing Industries
      Part XIV. Textile and Apparel Industries
      Part XV. Transport Industries
      Part XVI. Construction
      Part XVII. Services and Trade
      Part XVIII. Guides