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

Gunner 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.

 

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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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In the following article, the term cardiovascular diseases (CVDs) refers to organic and functional disorders of the heart and circulatory system, including the resultant damage to other organ systems, which are classified under numbers 390 to 459 in the 9th revision of the International Classification of Diseases (ICD) (World Health Organization (WHO) 1975). Based essentially on international statistics assembled by the WHO and data collected in Germany, the article discusses the prevalence of CVDs, new disease rates, and frequency of deaths, morbidity and disability.

Definition and Prevalence in the Working-Age Population

Coronary artery disease (ICD 410-414) resulting in ischaemia of the myocardium is probably the most significant CVD in the working population, particularly in industrialized countries. This condition results from a constriction in the vascular system that supplies the heart muscle, a problem caused primarily by arteriosclerosis. It affects 0.9 to 1.5% of working-age men and 0.5 to 1.0% of women.

Inflammatory diseases (ICD 420-423) may involve the endocardium, the heart valves, the pericardium and/or the heart muscle (myocardium) itself. They are less common in industrialized countries, where their frequency is well below 0.01% of the adult population, but are seen more frequently in developing countries, perhaps reflecting the greater prevalence of nutritional disorders and infectious diseases.

Heart rhythm disorders (ICD 427) are relatively rare, although much media attention has been given to recent instances of disability and sudden death among prominent professional athletes. Although they can have a significant impact on the ability to work, they are often asymptomatic and transitory.

The myocardiopathies (ICD 424) are conditions which involve enlargement or thickening of the heart musculation, effectively narrowing the vessels and weakening the heart. They have attracted more attention in recent years, largely because of improved methods of diagnosis, although their pathogenesis is often obscure. They have been attributed to infections, metabolic diseases, immunologic disorders, inflammatory diseases involving the capillaries and, of particular importance in this volume, to toxic exposures in the workplace. They are divided into three types:

  • dilative—the most common form (5 to 15 cases per 100,000 people), which is associated with the functional weakening of the heart
  • hypertrophic—thickening and enlargement of the myocardium resulting in relative insufficiency of the coronary arteries
  • restrictive—a rare type in which myocardial contractions are limited.

 

Hypertension (ICD 401-405) (increased systolic and/or diastolic blood pressure) is the most common circulatory disease, being found among 15 to 20% of working people in industrialized countries. It is discussed in greater detail below.

Atherosclerotic changes in the major blood vessels (ICD 440), often associated with hypertension, cause disease in the organs they serve. Foremost among these is cerebrovascular disease (ICD 430-438), which may result in a stroke due to infarction and/or haemorrhage. This occurs in 0.3 to 1.0% of working people, most commonly among those aged 40 and older.

Atherosclerotic diseases, including coronary artery disease, stroke and hypertension, by far the most common cardiovascular diseases in the working population, are multifactorial in origin and have their onset early in life. They are of importance in the workplace because:

  • so large a proportion of the workforce has an asymptomatic or unrecognized form of cardiovascular disease
  • the development of that disease may be aggravated or acute symptomatic events precipitated by working conditions and job demands
  • the acute onset of a symptomatic phase of the cardiovascular disease is often attributed to the job and/or the workplace environment
  • most individuals with an established cardiovascular disease are capable of working productively, albeit, sometimes, only after effective rehabilitation and job retraining
  • the workplace is a uniquely propitious arena for primary and secondary preventive programmes.

 

Functional circulatory disorders in the extremities (ICD 443) include Raynaud’s disease, short-term pallor of the fingers, and are relatively rare. Some occupational conditions, such as frostbite, long-term exposure to vinyl chloride and hand-arm exposure to vibration can induce these disorders.

Varicosities in the leg veins (ICD 454), often improperly dismissed as a cosmetic problem, are frequent among women, especially during pregnancy. While a hereditary tendency to weakness of the vein walls may be a factor, they are usually associated with long periods of standing in one position without movement, during which the static pressure within the veins is increased. The resultant discomfort and leg oedema often dictate change or modification of the job.

Annual incidence rates

Among the CVDs, hypertension has the highest annual new case rate among working people aged 35 to 64. New cases develop in approximately 1% of that population every year. Next in frequency are coronary heart disease (8 to 92 new cases of acute heart attack per 10,000 men per year, and 3 to 16 new cases per 10,000 women per year) and stroke (12 to 30 cases per 10,000 men per year, and 6 to 30 cases per 10,000 women per year). As demonstrated by global data collected by the WHO-Monica project (WHO-MONICA 1994; WHO-MONICA 1988), the lowest new incidence rates for heart attack were found among men in China and women in Spain, while the highest rates were found among both men and women in Scotland. The significance of these data is that in the population of working age, 40 to 60% of heart attack victims and 30 to 40% of stroke victims do not survive their initial episodes.

Mortality

Within the primary working ages of 15 to 64, only 8 to 18% of deaths from CVDs occur prior to age 45. Most occur after age 45, with the annual rate increasing with age. The rates, which have been changing, vary considerably from country to country (WHO 1994b).

Table 3.1 [CAR01TE] shows the death rates for men and for women aged 45 to 54 and 55 to 64 for some countries. Note that the death rates for men are consistently higher than those for women of corresponding ages. Table 3.2 [CAR02TE] compares the death rates for various CVDs among people aged 55 to 64 in five countries.

Work Disability and Early Retirement

Diagnosis-related statistics on time lost from work represent an important perspective on the impact of morbidity on the working population, even though the diagnostic designations are usually less precise than in cases of early retirement because of disability. The case rates, usually expressed in cases per 10,000 employees, provide an index of the frequency of the disease categories, while the average number of days lost per case indicates the relative seriousness of particular diseases. Thus, according to statistics on 10 million workers in western Germany compiled by the Allgemeinen Ortskrankenkasse, CVDs accounted for 7.7% of the total disability in 1991-92, although the number of cases for that period was only 4.6% of the total (table 3.3 [CAR03TE]). In some countries, where early retirement is provided when work ability is reduced due to illness, the pattern of disability mirrors the rates for different categories of CVD.

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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Tuesday, 25 January 2011 20:15

Prevention

Occupational exposures account for only a minor proportion of the total number of cancers in the entire population. It has been estimated that 4% of all cancers can be attributed to occupational exposures, based on data from the United States, with a range of uncertainty from 2 to 8%. This implies that even total prevention of occupationally induced cancers would result in only a marginal reduction in national cancer rates.

However, for several reasons, this should not discourage efforts to prevent occupationally induced cancers. First, the estimate of 4% is an average figure for the entire population, including unexposed persons. Among people actually exposed to occupational carcinogens, the proportion of tumours attributable to occupation is much larger. Second, occupational exposures are avoidable hazards to which individuals are involuntarily exposed. An individual should not have to accept an increased risk of cancer in any occupation, especially if the cause is known. Third, occupationally induced cancers can be prevented by regulation, in contrast to cancers associated with lifestyle factors.

Prevention of occupationally induced cancer involves at least two stages: first, identification of a specific compound or occupational environment as carcinogenic; and second, imposing appropriate regulatory control. The principles and practice of regulatory control of known or suspected cancer hazards in the work environment vary considerably, not only among different parts of the developed and developing world, but also among countries of similar socio-economic development.

The International Agency for Research on Cancer (IARC) in Lyon, France, systematically compiles and evaluates epidemiological and experimental data on suspected or known carcinogens. The evaluations are presented in a series of monographs, which provide a basis for decisions on national regulations on the production and use of carcinogenic compounds (see “Occupational Carcinogens”, above.

Historical Background

The history of occupational cancer dates back to at least 1775, when Sir Percivall Pott published his classical report on scrotal cancer in chimney-sweeps, linking exposure to soot to the incidence of cancer. The finding had some immediate impact in that sweeps in some countries were granted the right to bathe at the end of the working day. Current studies of sweeps indicate that scrotal and skin cancer are now under control, although sweeps are still at increased risk for several other cancers.

In the 1890s, a cluster of bladder cancer was reported at a German dye factory by a surgeon at a nearby hospital. The causative compounds were later identified as aromatic amines, and these now appear in lists of carcinogenic substances in most countries. Later examples include skin cancer in radium-dial painters, nose and sinus cancer among woodworkers caused by inhalation of wood dust, and “mule-spinner’s disease”—that is, scrotal cancer among cotton industry workers caused by mineral oil mist. Leukaemia induced by exposure to benzene in the shoe repair and manufacturing industry also represents a hazard that has been reduced after the identification of carcinogens in the workplace.

In the case of linking asbestos exposure to cancer, this history illustrates a situation with a considerable time-lag between risk identification and regulatory action. Epidemiological results indicating that exposure to asbestos was associated with an increased risk of lung cancer were already starting to accumulate by the 1930s. More convincing evidence appeared around 1955, but it was not until the mid-1970s that effective steps for regulatory action began.

The identification of the hazards associated with vinyl chloride represents a different history, where prompt regulatory action followed identification of the carcinogen. In the 1960s, most countries had adopted an exposure limit value for vinyl chloride of 500 parts per million (ppm). In 1974, the first reports of an increased frequency of the rare tumour liver angiosarcoma among vinyl chloride workers were soon followed by positive animal experimental studies. After vinyl chloride was identified as carcinogenic, regulatory actions were taken for a prompt reduction of the exposure to the current limit of 1 to 5 ppm.

Methods Used for the Identificationof Occupational Carcinogens

The methods in the historical examples cited above range from observations of clusters of disease by astute clinicians to more formal epidemiological studies—that is, investigations of the disease rate (cancer rate) among human beings. Results from epidemiological studies are of high relevance for evaluations of the risk to humans. A major drawback of cancer epidemiological studies is that a long time period, usually at least 15 years, is necessary to demonstrate and evaluate the effects of an exposure to a potential carcinogen. This is unsatisfactory for surveillance purposes, and other methods must be applied for a quicker evaluation of recently introduced substances. Since the beginning of this century, animal carcinogenicity studies have been used for this purpose. However, the extrapolation from animals to humans introduces considerable uncertainty. The methods also have limitations in that a large number of animals must be followed for several years.

The need for methods with a more rapid response was partly met in 1971, when the short-term mutagenicity test (Ames test) was introduced. This test uses bacteria to measure the mutagenic activity of a substance (its ability to cause irreparable changes in the cellular genetic material, DNA). A problem in the interpretation of the results of bacterial tests is that not all substances causing human cancers are mutagenic, and not all bacterial mutagens are considered to be cancer hazards for human beings. However, the finding that a substance is mutagenic is usually taken as an indication that the substance might represent a cancer hazard for humans.

New genetic and molecular biology methods have been developed during the last 15 years, with the aim of detecting human cancer hazards. This discipline is termed “molecular epidemiology.” Genetic and molecular events are studied in order to clarify the process of cancer formation and thus develop methods for early detection of cancer, or indications of increased risk of the development of cancer. These methods include analysis of damage to the genetic material and the formation of chemical linkages (adducts) between pollutants and the genetic material. The presence of chromosomal aberrations clearly indicates effects on the genetic material which may be associated with cancer development. However, the role of molecular epidemiological findings in human cancer risk assessment remains to be settled, and research is under way to indicate more clearly exactly how results of these analyses should be interpreted.

Surveillance and Screening

The strategies for prevention of occupationally induced cancers differ from those applied for control of cancer associated with lifestyle or other environmental exposures. In the occupational field, the main strategy for cancer control has been reduction or total elimination of exposure to cancer-causing agents. Methods based on early detection by screening programmes, such as those applied for cervical cancer or breast cancer, have been of very limited importance in occupational health.

Surveillance

Information from population records on cancer rates and occupation may be used for surveillance of cancer frequencies in various occupations. Several methods to obtain such information have been applied, depending on the registries available. The limitations and possibilities depend largely on the quality of the information in the registries. Information on disease rate (cancer frequency) is typically obtained from local or national cancer registries (see below), or from death certificate data, while information on the age-composition and size of occupational groups is obtained from population registries.

The classical example of this type of information is the “Decennial supplements on occupational mortality,” published in the UK since the end of the nineteenth century. These publications use death certificate information on cause of death and on occupation, together with census data on frequencies of occupations in the entire population, to calculate cause-specific death rates in different occupations. This type of statistic is a useful tool to monitor the cancer frequency in occupations with known risks, but its ability to detect previously unknown risks is limited. This type of approach may also suffer from problems associated with systematic differences in the coding of occupations on the death certificates and in the census data.

The use of personal identification numbers in the Nordic countries has offered a special opportunity to link individual census data on occupations with cancer registration data, and to directly calculate cancer rates in different occupations. In Sweden, a permanent linkage of the censuses of 1960 and 1970 and the cancer incidence during subsequent years have been made available for researchers and have been used for a large number of studies. This Swedish Cancer-Environment Registry has been used for a general survey of certain cancers tabulated by occupation. The survey was initiated by a governmental committee investigating hazards in the work environment. Similar linkages have been performed in the other Nordic countries.

Generally, statistics based on routinely collected cancer incidence and census data have the advantage of ease in providing large amounts of information. The method gives information on the cancer frequencies regarding occupation only, not in relation to certain exposures. This introduces a considerable dilution of the associations, since exposure may differ considerably among individuals in the same occupation. Epidemiological studies of the cohort type (where the cancer experience among a group of exposed workers is compared with that in unexposed workers matched for age, sex and other factors) or the case-control type (where the exposure experience of a group of persons with cancer is compared to that in a sample of the general population) give better opportunities for detailed exposure description, and thus better opportunities for investigation of the consistency of any observed risk increase, for example by examining the data for any exposure-response trends.

The possibility of obtaining more refined exposure data together with routinely collected cancer notifications was investigated in a prospective Canadian case-control study. The study was set up in the Montreal metropolitan area in 1979. Occupational histories were obtained from males as they were added to the local cancer registry, and the histories were subsequently coded for exposure to a number of chemicals by occupational hygienists. Later, the cancer risks in relation to a number of substances were calculated and published (Siemiatycki 1991).

In conclusion, the continuous production of surveillance data based on recorded information provides an effective and comparatively easy way to monitor cancer frequency by occupation. While the main purpose achieved is surveillance of known risk factors, the possibilities for the identification of new risks are limited. Registry-based studies should not be used for conclusions regarding the absence of risk in an occupation unless the proportion of individuals significantly exposed is more precisely known. It is quite common that only a relatively small percentage of members of an occupation actually are exposed; for these individuals the substance may represent a substantial hazard, but this will not be observable (i.e., will be statistically diluted) when the entire occupational group is analysed as a single group.

Screening

Screening for occupational cancer in exposed populations for purposes of early diagnosis is rarely applied, but has been tested in some settings where exposure has been difficult to eliminate. For example, much interest has focused on methods for early detection of lung cancer among people exposed to asbestos. With asbestos exposures, an increased risk persists for a long time, even after cessation of exposure. Thus, continuous evaluation of the health status of exposed individuals is justified. Chest x rays and cytological investigation of sputum have been used. Unfortunately, when tested under comparable conditions neither of these methods reduces the mortality significantly, even if some cases may be detected earlier. One of the reasons for this negative result is that the prognosis of lung cancer is little affected by early diagnosis. Another problem is that the x rays themselves represent a cancer hazard which, while small for the individual, may be significant when applied to a large number of individuals (i.e., all those screened).

Screening also has been proposed for bladder cancer in certain occupations, such as the rubber industry. Investigations of cellular changes in, or mutagenicity of, workers’ urine have been reported. However, the value of following cytological changes for population screening has been questioned, and the value of the mutagenicity tests awaits further scientific evaluation, since the prognostic value of having increased mutagenic activity in the urine is not known.

Judgements on the value of screening also depend on the intensity of the exposure, and thus the size of the expected cancer risk. Screening might be more justified in small groups exposed to high levels of carcinogens than among large groups exposed to low levels.

To summarize, no routine screening methods for occupational cancers can be recommended on the basis of present knowledge. The development of new molecular epidemiological techniques may improve the prospects for early cancer detection, but more information is needed before conclusions can be drawn.

Cancer Registration

During this century, cancer registries have been set up at several locations throughout the world. The International Agency for Research on Cancer (IARC) (1992) has compiled data on cancer incidence in different parts of the world in a series of publications, “Cancer Incidence in Five Continents.” Volume 6 of this publication lists 131 cancer registries in 48 countries.

Two main features determine the potential usefulness of a cancer registry: a well-defined catchment area (defining the geographical area involved), and the quality and completeness of the recorded information. Many of those registries that were set up early do not cover a geographically well-defined area, but rather are confined to the catchment area of a hospital.

There are several potential uses of cancer registries in the prevention of occupational cancer. A complete registry with nationwide coverage and a high quality of recorded information can result in excellent opportunities for monitoring the cancer incidence in the population. This requires access to population data to calculate age-standardized cancer rates. Some registries also contain data on occupation, which therefore facilitates the monitoring of cancer risk in different occupations.

Registries also may serve as a source for the identification of cases for epidemiological studies of both the cohort and case-control types. In the cohort study, personal identification data of the cohort is matched to the registry to obtain information on the type of cancer (i.e., as in record linkage studies). This assumes that a reliable identifying system exists (for example, personal identification numbers in the Nordic countries) and that confidentiality laws do not prohibit use of the registry in this way. For case-control studies, the registry may be used as a source for cases, although some practical problems arise. First, the cancer registries cannot, for methodological reasons, be quite up to date regarding recently diagnosed cases. The reporting system, and necessary checks and corrections of the obtained information, results in some lag time. For concurrent or prospective case-control studies, where it is desirable to contact the individuals themselves soon after a cancer diagnosis, it usually is necessary to set up an alternative way of identifying cases, for example via hospital records. Second, in some countries, confidentiality laws prohibit the identification of potential study participants who are to be contacted personally.

Registries also provide an excellent source for calculating background cancer rates to use for comparison of the cancer frequency in cohort studies of certain occupations or industries.

In studying cancer, cancer registries have several advantages over mortality registries commonly found in many countries. The accuracy of the cancer diagnoses is often better in cancer registries than in mortality registries, which are usually based on death certificate data. Another advantage is that the cancer registry often holds information on histological tumour type, and also permits the study of living persons with cancer, and is not limited to deceased persons. Above all, registries hold cancer morbidity data, permitting the study of cancers that are not rapidly fatal and/or not fatal at all.

Environmental Control

There are three main strategies for reducing workplace exposures to known or suspected carcinogens: elimination of the substance, reduced exposure by reduced emission or improved ventilation, and personal protection of the workers.

It has long been debated whether a true threshold for carcinogen exposure exists, below which no risk is present. It is often assumed that the risk should be extrapolated linearly down to zero risk at zero exposure. If this is the case, then no exposure limit, no matter how low, would be considered entirely risk-free. Despite this, many countries have defined exposure limits for some carcinogenic substances, while, for others, no exposure limit value has been assigned.

Elimination of a compound may give rise to problems when replacement substances are introduced and when the toxicity of the replacement substance must be lower than that of the substance replaced.

Reducing the exposure at the source may be relatively easily accomplished for process chemicals by encapsulation of the process and ventilation. For example, when the carcinogenic properties of vinyl chloride were discovered, the exposure limit value for vinyl chloride was lowered by a factor of one hundred or more in several countries. Although this standard was at first considered impossible to achieve by industry, later techniques allowed compliance with the new limit. Reduction of exposure at the source may be difficult to apply to substances that are used under less controlled conditions, or are formed during the work operation (e.g., motor exhausts). The compliance with exposure limits requires regular monitoring of workroom air levels.

When exposure cannot be controlled either by elimination or by reduced emissions, the use of personal protection devices is the only remaining way to minimize the exposure. These devices range from filter masks to air-supplied helmets and protective clothing. The main route of exposure must be considered in deciding appropriate protection. However, many personal protection devices cause discomfort to the user, and filter masks introduce an increased respiratory resistance which may be very significant in physically demanding jobs. The protective effect of respirators is generally unpredictable and depends on several factors, including how well the mask is fitted to the face and how often filters are changed. Personal protection must be considered as a last resort, to be attempted only when more effective ways of reducing exposure fail.

Research Approaches

It is striking how little research has been done to evaluate the impact of programmes or strategies to reduce the risk to workers of known occupational cancer hazards. With the possible exception of asbestos, few such evaluations have been conducted. Developing better methods for control of occupational cancer should include an evaluation of how present knowledge is actually put to use.

Improved control of occupational carcinogens in the workplace requires the development of a number of different areas of occupational safety and health. The process of identification of risks is a basic prerequisite for reducing exposure to carcinogens in the workplace. Risk identification in the future must solve certain methodological problems. More refined epidemiological methods are required if smaller risks are to be detected. More precise data on exposure for both the substance under study and possible confounding exposures will be necessary. More refined methods for description of the exact dose of the carcinogen delivered to the specific target organ also will increase the power of exposure-response calculations. Today, it is not uncommon that very crude substitutes are used for the actual measurement of target organ dose, such as the number of years employed in the industry. It is quite clear that such estimates of dose are considerably misclassified when used as a surrogate for dose. The presence of an exposure-response relationship is usually taken as strong evidence of an aetiological relationship. However, the reverse, lack of demonstration of an exposure-response relationship, is not necessarily evidence that no risk is involved, especially when crude measures of target organ dose are used. If target organ dose could be determined, then actual dose-response trends would carry even more weight as evidence for causation.

Molecular epidemiology is a rapidly growing area of research. Further insight into the mechanisms of cancer development can be expected, and the possibility of the early detection of carcinogenic effects will lead to earlier treatment. In addition, indicators of carcinogenic exposure will lead to improved identification of new risks.

Development of methods for supervision and regulatory control of the work environment are as necessary as methods for the identification of risks. Methods for regulatory control differ considerably even among western countries. The systems for regulation used in each country depend largely on socio-political factors and the status of labour rights. The regulation of toxic exposures is obviously a political decision. However, objective research into the effects of different types of regulatory systems could serve as a guide for politicians and decision-makers.

A number of specific research questions also need to be addressed. Methods to describe the expected effect of withdrawal of a carcinogenic substance or reduction of exposure to the substance need to be developed (i.e., the impact of interventions must be assessed). The calculation of the preventive effect of risk reduction raises certain problems when interacting substances are studied (e.g., asbestos and tobacco smoke). The preventive effect of removing one of two interacting substances is comparatively greater than when the two have only a simple additive effect.

The implications of the multistage theory of carcinogenesis for the expected effect of withdrawal of a carcinogen also adds a further complication. This theory states that the development of cancer is a process involving several cellular events (stages). Carcinogenic substances may act either in early or late stages, or both. For example, ionizing radiation is believed to affect mainly early stages in inducing certain cancer types, while arsenic acts mainly at late stages in lung cancer development. Tobacco smoke affects both early and late stages in the carcinogenic process. The effect of withdrawing a substance involved in an early stage would not be reflected in a reduced cancer rate in the population for a long time, while the removal of a “late-acting” carcinogen would be reflected in a reduced cancer rate within a few years. This is an important consideration when evaluating the effects of risk-reduction intervention programmes.

Finally, the effects of new preventive factors have recently attracted considerable interest. During the last five years, a large number of reports have been published on the preventive effect on lung cancer of consuming fruits and vegetables. The effect seems to be very consistent and strong. For example, the risk of lung cancer has been reported as double among those with a low consumption of fruits and vegetables versus those with high intake. Thus, future studies of occupational lung cancer would have greater precision and validity if individual data on fruit and vegetable consumption can be included in the analysis.

In conclusion, improved prevention of occupational cancer involves both improved methods for risk identification and more research on the effects of regulatory control. For risk identification, developments in epidemiology should mainly be directed toward better exposure information, while in the experimental field, validation of the results of molecular epidemiological methods regarding cancer risk are needed.

 

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Tuesday, 25 January 2011 20:13

Environmental Cancer

Cancer is a common disease in all countries of the world. The probability that a person will develop cancer by the age of 70 years, given survival to that age, varies between about 10 and 40% in both sexes. On average, in developed countries, about one person in five will die from cancer. This proportion is about one in 15 in developing countries. In this article, environmental cancer is defined as cancer caused (or prevented) by non-genetic factors, including human behaviour, habits, lifestyle and external factors over which the individual has no control. A stricter definition of environmental cancer is sometimes used, comprising only the effect of factors such as air and water pollution, and industrial waste.

Geographical Variation

Variation between geographical areas in the rates of particular types of cancer can be much greater than that for cancer as a whole. Known variation in the incidence of the more common cancers is summarized in table 1. The incidence of nasopharyngeal carcinoma, for example, varies some 500-fold between South East Asia and Europe. This wide variation in frequency of the various cancers has led to the view that much of human cancer is caused by factors in the environment. In particular, it has been argued that the lowest rate of a cancer observed in any population is indicative of the minimum, possibly spontaneous, rate occurring in the absence of causative factors. Thus the difference between the rate of a cancer in a given population and the minimum rate observed in any population is an estimate of the rate of the cancer in the first population which is attributable to environmental factors. On this basis it has been estimated, very approximately, that some 80 to 90% of all human cancers are environmentally determined (International Agency for Research on Cancer 1990).

Table 1.  Variation between populations covered by cancer registration in the incidence of common cancers.1

Cancer (ICD9 code)

High-incidence area

CR2

Low-incidence area

CR2

Range of variation

Mouth (143-5)

France, Bas Rhin

2

Singapore (Malay)

0.02

80

Nasopharynx (147)

Hong Kong

3

Poland, Warsaw (rural)

0.01

300

Oesophagus (150)

France, Calvados

3

Israel (Israeli-born Jews)

0.02

160

Stomach (151)

Japan, Yamagata

11

USA, Los Angeles (Filipinos)

0.3

30

Colon (153)

USA, Hawaii (Japanese)

5

India, Madras

0.2

30

Rectum (154)

USA, Los Angeles (Japanese)

3

Kuwait (non-Kuwaiti)

0.1

20

Liver (155)

Thailand, Khon Khaen

11

Paraguay, Asuncion

0.1

110

Pancreas (157)

USA, Alameda County (Calif.) (Blacks)

2

India, Ahmedabad

0.1

20

Lung (162)

New Zealand (Maori)

16

Mali, Bamako

0.5

30

Melanoma of skin (172)

Australia, Capital Terr.

3

USA, Bay Area (Calif.)(Blacks)

0.01

300

Other skin cancers (173)

Australia, Tasmania

25

Spain, Basque Country

0.05

500

Breast (174)

USA, Hawaii (Hawaiian)

12

China, Qidong

1.0

10

Cervix uteri (180)

Peru, Trujillo

6

USA, Hawaii (Chinese)

0.3

20

Corpus uteri (182)

USA, Alameda County (Calif.) (Whites)

3

China, Qidong

0.05

60

Ovary (183)

Iceland

2

Mali, Bamako

0.09

20

Prostate (185)

USA, Atlanta (Blacks)

12

China, Qidong

0.09

140

Bladder (188)

Italy, Florence

4

India, Madras

0.2

20

Kidney (189)

France, Bas Rhin

2

China, Qidong

0.08

20

1 Data from cancer registries included in IARC 1992. Only cancer sites with cumulative rate larger or equal to 2% in the high-incidence area are included. Rates refer to males except for breast, cervix uteri, corpus uteri and ovary cancers.
2 Cumulative rate % between 0 and 74 years of age.
Source: International Agency for Research on Cancer 1992.

There are, of course, other explanations for geographical variation in cancer rates. Under-registration of cancer in some populations may exaggerate the range of variation, but certainly cannot explain differences of the size shown in table 1. Genetic factors also may be important. It has been observed, however, that when populations migrate along a gradient of cancer incidence they often acquire a rate of cancer which is intermediate between that of their home country and that of the host country. This suggests that a change in environment, without genetic change, has changed the cancer incidence. For example, when Japanese migrate to the United States their rates of colon and breast cancer, which are low in Japan, rise, and their rate of stomach cancer, which is high in Japan, falls, both tending more closely towards United States’ rates. These changes may be delayed until the first post-migration generation but they still occur without genetic change. For some cancers, change with migration does not occur. For example, the Southern Chinese retain their high rate of cancer of the nasopharynx wherever they live, thus suggesting that genetic factors, or some cultural habit which changes little with migration, are responsible for this disease.

Time Trends

Further evidence of the role of environmental factors in cancer incidence has come from the observation of time trends. The most dramatic and well-known change has been the rise in lung cancer rates in males and females in parallel with but occurring some 20 to 30 years after the adoption of cigarette use, which has been seen in many regions of the world; more recently in a few countries, such as the United States, there has been the suggestion of a fall in rates among males following a reduction in tobacco smoking. Less well understood are the substantial falls in incidence of cancers including those of the stomach, oesophagus and cervix which have paralleled economic development in many countries. It would be difficult to explain these falls, however, except in terms of reduction in exposure to causal factors in the environment or, perhaps, increasing exposure to protective factors—again environmental.

Main Environmental Carcinogenic Agents

The importance of environmental factors as causes of human cancer has been further demonstrated by epidemiological studies relating particular agents to particular cancers. The main agents which have been identified are summarized in table 10. This table does not contain the drugs for which a causal link with human cancer has been established (such as diethylstilboestrol and several alkylating agents) or suspected (such as cyclophosphamide) (see also Table 9). In the case of these agents, the risk of cancer has to be balanced with the benefits of the treatment. Similarly, Table 10 does not contain agents that occur primarily in the occupational setting, such as chromium, nickel and aromatic amines. For a detailed discussion of these agents see the previous article “Occupational Carcinogens.” The relative importance of the agents listed in table 8 varies widely, depending on the potency of the agent and the number of people involved. The evidence of carcinogenicity of several environmental agents has been evaluated within the IARC Monographs programme (International Agency for Research on Cancer 1995) (see again “Occupational Carcinogens” for a discussion of the Monographs programme); table 10 is based mainly on the IARC Monograph evaluations. The most important agents among those listed in table 10 are those to which a substantial proportion of the population is exposed in relatively large amounts. They include particularly: ultraviolet (solar) radiation; tobacco smoking; alcohol drinking; betel quid chewing; hepatitis B; hepatitis C and human papilloma viruses; aflatoxins; possibly dietary fat, and dietary fiber and vitamin A and C deficiency; reproductive delay; and asbestos.

Attempts have been made to estimate numerically the relative contributions of these factors to the 80 or 90% of cancers which might be attributed to environmental factors. The pattern varies, of course, from population to population according to differences in exposures and possibly in the genetic susceptibility to various cancers. In many industrialized countries, however, tobacco smoking and dietary factors are likely to be responsible each for roughly one-third of environmentally determined cancers (Doll and Peto 1981); while in developing countries the role of biological agents is likely to be large and that of tobacco relatively small (but increasing, following the recent increase in the consumption of tobacco in these populations).

Interactions between Carcinogens

An additional aspect to consider is the presence of interactions between carcinogens. Thus for example, in the case of alcohol and tobacco, and cancer of the oesophagus, it has been shown that an increasing consumption of alcohol multiplies manyfold the rate of cancer produced by a given level of tobacco consumption. Alcohol by itself may facilitate transport of tobacco carcinogens, or others, into the cells of susceptible tissues. Multiplicative interaction may also be seen between initiating carcinogens, as between radon and its decay products and tobacco smoking in miners of uranium. Some environmental agents may act by promoting cancers which have been initiated by another agent—this is the most likely mechanism for an effect of dietary fat on the development of breast cancer (probably through increased production of the hormones which stimulate the breast). The reverse may also occur, as, for example, in the case of vitamin A, which probably has an anti-promoting effect on lung and possibly other cancers initiated by tobacco. Similar interactions may also occur between environmental and constitutional factors. In particular, genetic polymorphism to enzymes implicated in the metabolism of carcinogenic agents or DNA repair is probably an important requirement of individual susceptibility to the effect of environmental carcinogens.

The significance of interactions between carcinogens, from the point of view of cancer control, is that withdrawal of exposure to one of two (or more) interacting factors may give rise to a greater reduction in cancer incidence than would be predicted from consideration of the effect of the agent when acting alone. Thus, for example, withdrawal of cigarettes may eliminate almost entirely the excess rate of lung cancer in asbestos workers (although rates of mesothelioma would be unaffected).

Implications for Prevention

The realization that environmental factors are responsible for a large proportion of human cancers has laid the foundation for primary prevention of cancer by modification of exposure to the factors identified. Such modification may comprise: removal of a single major carcinogen; reduction, as discussed above, in exposure to one of several interacting carcinogens; increasing exposure to protective agents; or combinations of these approaches. While some of this may be achieved by community-wide regulation of the environment through, for example, environmental legislation, the apparent importance of lifestyle factors suggests that much of primary prevention will remain the responsibility of individuals. Governments, however, may still create a climate in which individuals find it easier to take the right decision.

 

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