Wednesday, 09 February 2011 03:40

Contents Page

Written by

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

 

Back

Wednesday, 09 February 2011 04:02

General Profile

Written by

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

Table 1. Physical and chemical hazards

Chemical name

CAS-number

Molecular formula

Physical and chemical hazards

UN class/div/
subsidiary risks

Aluminium chloride 
7446-70-0

AICI3

 

8

Aluminium hydroxide
21645-51-2

AI(OH)3

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

Aluminium nitrate 
13473-90-0

Al2(NO3)3

 

5.1

Aluminium phosphide 
20859-73-8

AlP

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

4.3/ 6.1

Diethylaluminium chloride 
96-10-6

AlClC4H10

 

4.2

Ethylaluminium dichloride
563-43-9

AlCl2C2H5

 

4.2

Ethylaluminium 
sesquichloride 
12075-68-2

Al2Cl3C6H15

 

4.2

Sodium aluminate 
1302-42-7

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

8

Triethylaluminium 
97-93-8

AlC6H15

 

4.2

Triisobutylaluminium
100-99-2

AlC12H27

 

4.2

Antimony 
7440-36-0

Sb

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

6.1

Antimony pentachloride 
7647-18-9

SbCl5

 

8

Antimony pentafluoride 
7783-70-2

SbF5

 

3/ 6.1

Antimony potassium tartrate
28300-74-5

Sb2K2C8H4O12 ·
3H2O

 

6.1

Antimony trichloride 
10025-91-9

SbCl3

 

8

Antimony trioxide 
1309-64-4

Sb2O3

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

Stibine 
7803-52-3

SbH3

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

2.3/ 2.1

Arsenic 
7440-38-2

As

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

6.1

Arsenic acid, copper salt
10103-61-4

CuAsOH4

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

Arsenic acid, 
diammonium salt
7784-44-3

(NH4)2AsOH4

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

Arsenic acid, 
disodium salt 
7778-43-0

Na2AsOH4

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

Arsenic acid, 
magnesium salt 
10103-50-1

MgxAsO3H4

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

6.1

Arsenic acid, 
monopotassium salt 
7784-41-0

KAsO2H4

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

Arsenic pentoxide
1303-28-2

As2O5

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

6.1

Arsenic trioxide 
1327-53-3

As2O3

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

6.1

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

CuAsH3

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

6.1

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

PbAs2O4

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

Arsenious acid, 
potassium salt 
10124-50-2

(KH3)x AsO3

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

6.1

Arsenous trichloride 
7784-34-1

AsCl3

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

6.1

Arsine 
7784-42-1

AsH3

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

2.3/ 2.1

Calcium arsenate 
7778-44-1

Ca3As2O8

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

6.1

Lead arsenate 
7784-40-9

PbAsO4H

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

6.1

Methylarsonic acid 
124-58-3

AsCH503

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

Sodium arsenate
10048-95-0

Na2AsO4H ·7H2O

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

6.1

Barium 
7440-39-3

Ba

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

4.3

Barium carbonate 
513-77-9

BaCO3

 

6.1

Barium chlorate 
13477-00-4

BaCl2O6

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

5.1/ 6.1

Barium chloride 
10361-37-2

BaCl2

  • The substance decomposes on heating producing toxic fumes

6.1

Barium chloride, dihydrate 
10326-27-9

BaCl2·2H20

  • The substance decomposes on heating producing toxic fumes

6.1

Barium 
chromate (VI) 
10294-40-3

BaCrH2O4

 

6.1

Barium hydroxide 
17194-00-2

Ba(OH)2

 

6.1

Barium nitrate 
10022-31-8

BaNO3

 

5.1/ 6.1

Barium oxide 
1304-28-5

BaO

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

6.1

Barium perchlorate 
13465-95-7

BaCl2O8

 

5.1/ 6.1

Barium peroxide 
1304-29-6

BaO2

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

5.1/ 6.1

Barium sulphate 
7727-43-7

BaSO4

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

6.1

Beryllium 
7440-41-7

Be

 

6.1

Beryllium oxide 
1304-56-9

BeO

 

6.1

Cadmium 
7440-43-9

Cd

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

Cadmium acetate 
543-90-8

Cd(C2H4O2)2

 

6.1

Cadmium chloride 
10108-64-2

CdCl2

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

6.1

Cadmium oxide 
1306-19-0

CdO

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

6.1

Cadmium suphate 
10124-36-4

CdSO4

 

6.1

Cadmium sulphide 
1306-23-6

CdS

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

6.1

Ammonium dichromate(VI)
7789-09-5

(NH4)2Cr2H2O7

 

5.1

Chromic acid 
7738-94-5

CrH2O4

 

8

Chromium 
7440-47-3

Cr

 

5.1

Chromium trioxide 
1333-82-0

CrO3

 

5.1

Chromyl chloride 
14977-61-8

CrO2Cl2

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

8

Cobalt 
7440-48-4

Co

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

Cobalt chloride 
7646-79-9

CoCl2

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

Cobalt (III) oxide 
1308-04-9

Co2O3

  • Reacts violently with hydrogen peroxide 
  • Reacts with reducing agents
 

Cobalt naphthenate 
61789-51-3

CoC22H20O4

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

Copper 
7440-50-8

Cu

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

Copper (I) oxide 
1317-39-1

Cu2O

  • Reacts with acids to form cupric salts · Corrodes aluminium
 

Cupric acetate 
142-71-2

CuC4H6O4

 

6.1

Cupric chloride 
7447-39-4

CuCl2

 

8

Cupric hydroxide 
120427-59-2

Cu(OH)2

 

6.1

Naphthenic acid, Cu-salt
1338-02-9

 
  • On combustion, forms toxic gases
 

Ferric chloride 
7705-08-0

FeCl3

 

8

Iron pentacarbonyl 
13463-40-6

C5FeO5

 

6.1/ 3

Lead 
7439-92-1

Pb

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

Lead acetate 
301-04-2

PbC4H6O4

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

6.1

Lead chromate 
7758-97-6

PbCrO4

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

Lead nitrate 
10099-74-8

Pb(NO3)2

 

5.1/ 6.1

Lead dioxide 
1309-60-0

PbO2

 

5.1

Lead(II) oxide 
1317-36-8

PbO

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

Naphthenic acid, Pb-salt
61790-14-5

 
  • On combustion, forms toxic fumes including lead oxide
 

Tetraethyl lead 
78-00-2

PbC8H20

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

6.1

Tetramethyl lead 
75-74-1

PbC4H12

 

6.1

Lithium aluminium hydride
16853-85-3

LiAlH4

 

4.3

Magnesium 
7439-95-4

Mg

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

4.1

Magnesium chloride 
7786-30-3

MgCl2

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

5.1

Magnesium nitrate 
10377-60-3

Mg(NO3)2

 

5.1

Magnesium oxide 
1309-48-4

MgO

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

Magnesium phosphide
12057-74-8

Mg3P2

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

4.3/ 6.1

Mercuric acetate
1600-27-7

HgC4H6O4

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

6.1

Mercuric bromide 
7789-47-1

HgBr2

 

6.1

Mercuric chloride 
7487-94-7

HgCl2

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

6.1

Mercuric nitrate 
10045-94-0

Hg(NO3)2

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

6.1

Mercuric oxide 
21908-53-2

HgO

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

6.1

Mercuric sulphate 
7783-35-9

HgSO4

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

6.1

Mercuric thiocyanate 
592-85-8

HgC2N2S2

 

6.1

Mercurous chloride 
10112-91-1

Hg2Cl2

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

Mercury 
7439-97-6

Hg

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

6.1

Phenylmercuric acetate 
62-38-4

C8H8HgO2

  • The substance decomposes on heating producing toxic vapours of mercury

6.1

Phenylmercuric nitrate 
55-68-5

C6H5HgNO3

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

6.1

Nickel 
7440-02-0

Ni

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

Nickel (II) oxide 
1313-99-1

NiO

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

Nickel carbonate 
3333-67-3

Ni2CO3

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

Nickel carbonyl 
13463-39-3

NiC4O4

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

6.1/ 3

Nickel sulphide 
12035-72-2

Ni3S2

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

Nickel sulphate 
7786-81-4

NiSO4

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

Osmium tetroxide 
20816-12-0

OsO4

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

6.1

Platinum tetrachloride 
13454-96-1

PtCl4

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

Hydrogen selenide 
7783-07-5

SeH2

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

2.3/ 2.1

Selenious acid 
7783-00-8

SeH2O3

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

Selenious acid, disodium salt
10102-18-8

Na2SeO3

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

6.1

Selenium 
7782-49-2

Se

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

6.1

Selenium dioxide 
7446-08-4

SeO2

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

Selenium hexafluoride 
7783-79-1

SeF6

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

2.3/ 8

Selenium oxychloride 
7791-23-3

SeOCl2

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

3/ 6.1

Selenium trioxide 
13768-86-0

SeO3

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

Silver 
7440-22-4

Ag

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

Silver nitrate 
7761-88-8

AgNO3

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

5.1

Strontium chromate 
7789-06-2

SrCrH2O4

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

Tellurium 
13494-80-9

Te

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

6.1

Tellurium hexafluoride 
7783-80-4

TeF6

 

2.3/ 8

Thallium 
7440-28-0

Tl

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

6.1

Thallous sulphate 
7446-18-6

Tl2 (SO4)3

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

6.1

Thorium 
7440-29-1

Th

 

7

Di-N-Butyltin dichloride 
683-18-1

SnCl2C8H18

 

6.1

Di-N-Dibutyltin oxide 
818-08-6

C8H18SnO

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

Dibutyltin dilaurate 
77-58-7

SnC32H64O4

 

6.1

Stannic chloride 
7646-78-8

SnCl4

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

8

Stannic oxide 
18282-10-5

SnO

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

Stannous chloride 
7772-99-8

SnCl2

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

Stannous chloride dihydrate
10025-69-1

SnCl2 ·2H2O

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

Stannous fluoride 
7783-47-3

SnF2

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

Tin oxide 
21651-19-4

SnO

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

Titanium tetrachloride 
7550-45-0

TiCl4

 

8

Titanium trichloride 
7705-07-9

TiCl3

 

8

Vanadium pentoxide 
1314-62-1

V2O5

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

6.1

Vanadium tetrachloride 
7632-51-1

VCl4

 

8

Vanadium trioxide 
1314-34-7

V2O3

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

6.1

Vanadyl trichloride 
7727-18-6

VOCl3

 

8

Zinc 
7440-66-6

Zn

 

4.3/ 4.2

Zinc chloride 
7646-85-7

ZnCl2

 

8

Zinc nitrate 
7779-88-6

Zn(NO3)2

 

1.5

Zinc phosphide 
1314-84-7

Zn3P2

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

4.3/ 6.1

Zinc stearate 
557-05-1

ZnC36H70O4

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

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

Table 2. Health hazards

Chemical 
name 
CAS-Number

Short-term 
exposure

Long-term
exposure

Routes of 
exposure

Symptoms

Target organs, routes 
of entry

Symptoms

Aluminium phosphide
20859-73-8

Eyes; skin; resp. tract

 

Inhalation


Skin
Eyes
Ingestion

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

   

Antimony
7440-36-0

Eyes; skin; resp. tract; lungs; heart

Skin; lungs; resp. tract

Inhalation


Skin
Eyes
Ingestion

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

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

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

Antimony
trioxide 
1309-64-4

Eyes; skin; resp. tract

Skin; lungs

Inhalation

Skin
Eyes
Ingestion

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

   

Stibine 
7803-52-3

Blood; kidneys; liver; CNS

 

Inhalation

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

Blood; liver; kidneys; resp. sys. 
Inh

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

Arsenic 
7440-38-2

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

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

Inhalation

Skin
Eyes
Ingestion

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

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

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

Arsenic acid,
copper salt 
10103-61-4

Eyes; resp. tract; CNS; digestive tract

Skin; PNS; mucous membranes; liver

Inhalation

Skin
Eyes
Ingestion

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

   

Arsenic acid,
diammonium 
salt 
7784-44-3

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

PNS; skin; mucous membranes; liver

Inhalation

Skin
Eyes
Ingestion

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

   

Arsenic acid, 
disodium salt 
7778-43-0

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

PNS; skin; mucous membranes; liver

Inhalation

Skin
Eyes
Ingestion

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

   

Arsenic acid,
magnesium 
salt 
10103-50-1

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

PNS; skin; mucous membranes; liver

Inhalation

Skin
Eyes
Ingestion

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

   

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

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

Skin; PNS; mucous membranes; liver

Inhalation

Skin
Eyes
Ingestion

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

   

Arsenic 
pentoxide 
1303-28-2

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

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

Inhalation



Skin
Eyes
Ingestion

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

   

Arsenic 
trioxide 
1327-53-3

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

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

Inhalation



Skin
Eyes
Ingestion

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

   

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

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

Skin; PNS; mucous membranes; liver

Inhalation

Skin
Eyes
Ingestion

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

   

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

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

Skin; PNS; mucous membranes; liver

Inhalation

Skin
Eyes
Ingestion

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

   

Arsenious 
acid, 
potassium 
salt 
10124-50-2

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

 

Inhalation

Skin

Eyes
Ingestion

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

   

Arsenous 
trichloride 
7784-34-1

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

Mucous membranes; skin; liver; kidneys; PNS

Inhalation

Skin

Eyes
Ingestion

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

   

Arsine 
7784-42-1

Lungs; blood; kidneys

 

Inhalation


Skin
Eyes

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

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

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

Calcium 
arsenate 
7778-44-1

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

PNS; skin; mucous membranes; liver

Inhalation

Skin
Eyes
Ingestion

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

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

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

Lead arsenate
7784-40-9

Intestines; CVS

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

Inhalation



Skin
Eyes

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

   

Methylarsonic 
acid 
124-58-3

Eyes; skin; resp. tract; lungs

Bone marrow; PNS; kidneys; liver

Inhalation
Skin
Eyes
Ingestion

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

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

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

Sodium 
arsenate 
10048-95-0

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

Skin; CNS; CVS; blood; liver; carcinogenic

Inhalation

Skin
Eyes
Ingestion

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

   

Barium 
7440-39-3

Eyes; skin; resp. tract

 

Inhalation
Skin
Eyes

Cough, sore throat
Redness
Redness, pain

   

Barium 
chlorate 
13477-00-4

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

Tissues and organs

Inhalation


Eyes
Ingestion

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

   

Barium 
chloride 
10361-37-2

Eyes; skin; resp. tract; CNS; muscles

 

Inhalation
Eyes
Ingestion

Abdominal cramps, unconsciousness
Redness
Abdominal cramps, dullness, 
unconsciousness

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

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

Barium 
chloride,
dihydrate 
10362-27-9

Eyes; skin; resp. tract; CNS; muscles

 

Inhalation
Eyes
Ingestion

Abdominal cramps, unconsciousness
Redness 
Abdominal cramps, dullness, 
unconsciousness

   

Barium oxide 
1304-28-5

Eyes; skin; resp. tract; muscles

Lungs

Inhalation
Skin
Eyes
Ingestion

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

   

Barium
peroxide 
1304-29-6

 

Skin

Inhalation

Skin
Eyes
Ingestion

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

   

Barium 
sulphate 
7727-43-7

 

Lungs

Inhalation

Cough

Eyes; resp sys 
Inh; con

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

Cadmium 
7440-43-9

Eyes; resp. tract; lungs

Lungs; kidneys

Inhalation

Eyes
Ingestion

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

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

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

Cadmium 
chloride 
10108-64-2

Resp. tract; digestive tract; lungs

Lungs; kidneys; bone; probably carcinogenic

Inhalation

Skin
Eyes
Ingestion

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

   

Cadmium 
oxide 
1306-19-0

Resp. tract; digestive tract; lungs

Lungs; kidneys; carcinogenic

Inhalation


Skin
Eyes
Ingestion

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

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

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

Cadmium 
sulphide 
1306-23-6

 

Lungs; kidneys; carcinogenic

       

Chromium 
7440-47-3

Eyes; skin; resp. tract; lungs; kidneys

Skin; asthma; larynx; lungs

Eyes
Ingestion

Irritation 
Diarrhoea, nausea, unconsciousness, 
vomiting

Resp sys; skin; eyes 
Inh; ing; con

Irrit eyes, skin; lung fib (histologic)

Chromyl 
chloride 
14977-61-8

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

Skin; asthma; probably carcinogenic

Inhalation

Skin
Eyes
Ingestion

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

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

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

Lead 
chromate 
7758-97-6

Resp. tract; may cause perforation of nasal septum

Skin; inhalation may cause asthma; lungs

Inhalation

Skin
Eyes
Ingestion

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

   

Cobalt 
7440-48-4

 

Skin; resp. tract; lungs; heart

Inhalation

Skin
Eyes
Ingestion

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

Resp sys; skin 
Inh; ing; con

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

Cobalt 
chloride 
7646-79-9

Eyes; skin; resp. tract

Skin; resp. tract ; heart

Inhalation

Skin
Eyes
Ingestion

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

   

Cobalt (III) 
oxide 
1308-04-9

Eyes; skin; resp. tract

Skin; may cause asthma; lungs; possibly carcinogenic

Inhalation

Eyes

Cough, laboured breathing, shortness 
of breath 
Redness

   

Cobalt 
naphthenate 
61789-51-3

Eyes; resp. tract

Skin

Inhalation
Skin
Eyes

Cough, sore throat 
Redness, pain 
Redness, pain

   

Copper 
7440-50-8

Eyes

Skin; lungs

Inhalation

Skin
Eyes
Ingestion

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

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

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

Copper (I) 
oxide 
1317-39-1

Eyes; resp. tract

 

Inhalation
Eyes
Ingestion

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

   

Lead 
7439-92-1

 

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

Inhalation
Ingestion

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

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

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

Lead acetate 
301-04-2

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

Blood; bone marrow; CVS; kidneys; CNS

Inhalation

Eyes
Ingestion

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

   

Tetraethyl 
lead 
78-00-2

Eyes; skin; resp. tract; CNS

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

Inhalation

Skin
Eyes
Ingestion

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

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

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

Lead (II) 
oxide 
1317-36-8

 

CNS; kidneys; blood

       

Magnesium 
7439-95-4

   

Inhalation
Eyes
Ingestion

Cough, laboured breathing 
Redness, pain 
Abdominal pain, diarrhoea

   

Magnesium 
chloride 
7786-30-3

Eyes; resp. tract

 

Inhalation
Eyes
Ingestion

Cough 
Redness 
Diarrhoea

   

Magnesium 
oxide 
1309-48-4

Eyes; nose

 

Inhalation
Eyes
Ingestion

Cough 
Redness 
Diarrhoea

Eyes; resp sys
Inh; con

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

Magnesium 
phosphide 
12057-74-8

Eyes; skin; resp. tract

 

Inhalation


Skin
Eyes
Ingestion

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

   

Manganese 
sulphate 
10034-96-5

Eyes; skin; resp. tract

Lungs; CNS; liver; kidneys; testes

Inhalation

Skin

Eyes
Ingestion

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

   

Mercury 
7439-97-6

Eyes; skin; lungs; CNS

CNS; nervous system; kidneys

Inhalation
Skin
Eyes

Pulmonary irritation, cough 
May be absorbed 
Irritating

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

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

Mercuric 
acetate 
1600-27-7

Eyes; skin; resp. tract; lungs; kidneys

Skin; kidneys

Inhalation



Skin
Eyes
Ingestion

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

   

Mercuric 
chloride 
7487-94-7

Eyes; skin; resp. tract; lungs; kidneys

Skin; kidneys

Inhalation



Skin
Eyes
Ingestion

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

   

Mercuric 
nitrate 
10045-94-0

Skin; resp. tract; eyes; kidneys

Kidneys

Inhalation

Skin
Eyes
Ingestion

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

   

Mercuric 
oxide 
21908-53-2

Eyes; skin; resp. tract

Skin; kidneys; CNS

Inhalation
Skin
Eyes
Ingestion

Cough 
May be absorbed, redness 
Redness 
Abdominal pain, diarrhoea

   

Mercuric 
sulphate 
7783-35-9

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

Kidneys

Inhalation



Skin

Eyes
Ingestion

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

   

Mercurous 
chloride 
10112-91-1

Eyes

Kidneys

Eyes
Ingestion

Redness
Weakness

   

Mercury 
organoalkyl 
compound

       

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

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

Phenylmercuric acetate
62-38-4

Eyes; skin; resp. tract; kidneys

Skin; CNS; possibly causes toxic effects upon human reproduction

Inhalation

Skin
Eyes
Ingestion

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

   

Phenylmercuric nitrate
55-68-5

Eyes; skin; resp. tract; kidneys

Skin; CNS; possibly causes toxic effects on human reproduction

Inhalation

Skin
Eyes
Ingestion

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

   

Nickel 
7440-02-0

Eyes; resp. tract

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

   

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

Sens derm, allergic asthma, pneuitis; (carc)

Nickel (II) 
oxide 
1313-99-1

Eyes; resp. tract

Skin; inhalation may cause asthma; carcinogenic

Inhalation
Skin
Eyes

Cough 
Redness 
Redness

   

Nickel 
carbonate 
3333-67-3

Eyes; resp. tract

Skin; carcinogenic; asthma

Inhalation
Skin
Eyes

Cough 
Redness 
Redness

   

Nickel 
carbonyl 
13463-39-3

Eyes; skin; resp. tract; lungs; CNS

Possibly carcinogenic; may cause defects on the unborn child

Inhalation



Skin
Eyes
Ingestion

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

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

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

Nickel 
sulphide 
12035-72-2

Eyes; skin; resp. tract

Skin; possibly carcinogenic

Inhalation

Cough, sore throat

   

Nickel 
sulphate 
7786-81-4

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

Skin; asthma; possibly carcinogenic

Inhalation
Skin
Eyess
Ingestion

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

   

Osmium 
tetroxide 
20816-12-0

Eyes; skin; resp. tract; lungs

Skin; kidneys

Inhalation


Skin
Eyes
Ingestion

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

Eyes; resp sys; skin Inh; ing; con

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

Platinium 
tetrachloride 
13454-96-1

Eyes; skin; resp. tract

 

Inhalation
Skin
Eyes

Burning sensation, cough 
Redness 
Redness

Eyes; skin; resp sys Inh; ing; con

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

Hydrogen 
selenide 
7783-07-5

Eyes; resp. tract; lungs

Skin; liver; spleen; kidneys

Inhalation

Skin
Eyes

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

Resp sys; eyes; liver Inh; con

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

Selenious acid 
7783-00-8

Eyes; skin; resp. tract

Skin

Inhalation

Skin
Eyes

Ingestion

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

   

Selenious 
acid, 
disodium salt 
10102-18-8

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

teeth; bone; blood

Inhalation



Skin
Eyes

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

   

Selenium 7782-49-2

Lungs

Skin; resp. tract; GI tract; integuments

Inhalation



Skin

Eyes
Ingestion

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

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

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

Selenium 
dioxide 
7446-08-4

Eyes; skin; resp. tract; lungs

Skin

Inhalation

Skin
Eyes

Ingestion

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

   

Selenium 
hexafluoride 
7783-79-1

Resp. tract; lungs

Skin; CNS; liver; kidneys

Inhalation

Skin

Eyes

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

Resp sys
Inh

In animals: plum irrit, edema

Selenium 
oxychloride 
7791-23-3

Eyes; skin; resp. tract; lungs

Skin

Inhalation

Skin

Eyes

Ingestion

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

   

Selenium 
trioxide 
13768-86-0

Eyes; skin; resp. tract

Skin; lungs

Inhalation

Skin
Eyes

Ingestion

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

   

Silver 
7740-22-4

 

Eyes; nose; throat; skin

   

Nasal septum; skin; eyes
Inh; ing; con

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

Silver nitrate 
7761-88-8

Eyes; skin; resp. tract

Blood; skin

Inhalation

Skin
Eyes

Ingestion

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

   

Strontium 
chromate 
7789-06-2

Eyes; skin; resp. tract; kidneys; liver

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

Inhalation
Skin
Ingestion

Cough, hoarseness 
Redness, ulcerations 
Sore throat

   

Tellurium 
13494-80-9

Resp. tract; CNS

Possibly causes malformations in human 
babies

Inhalation

Skin
Eyes
Ingestion

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

Skin; CNS; blood 
Inh; ing; con

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

Thallium 
metal 
7440-28-0

Nervous system

Eyes; liver; lungs; may cause birth defects

Inhalation


Skin
Eyes
Ingestion

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

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

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

Thallous 
sulphate 
7446-18-6

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

 

Inhalation
Skin

Eyes
Ingestion

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

   

Di-N-Dibutyltin
oxide
818-08-6

Eyes; skin; resp. tract; lungs

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

Inhalation

Skin
Eyes

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

   

Stannic 
chloride 
7646-78-8

Eyes; skin; resp. tract; lungs

Skin

Inhalation


Skin
Eyes
Ingestion

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

   

Stannic oxide 
18282-10-5

Resp. tract

Lungs

Inhalation

Cough

Resp sys
Inh; con

Stannosis (benign pneumoconiosis): dysp, decr pulm func

Stannous
chloride
7772-99-8

Eyes; skin; resp. tract; CNS; blood

Liver

Inhalation
Skin
Eyes
Ingestion

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

   

Stannous chloride 
dihydrate 
10025-69-1

Eyes; skin; resp. tract; CNS; blood

Liver

Inhalation
Skin
Eyes
Ingestion

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

   

Stannous 
fluoride 
7783-47-3

Skin; resp. tract; eyes

Teeth; bone

Inhalation
Skin
Eyes
Ingestion

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

   

Tin oxide 
21651-19-4

Resp. tract

Lungs

Inhalation

Cough

Resp sys
Inh; con

Stannosis (benign pneumoconiosis): dysp, decr pulm func

Titanium 
dioxide 
13463-67-7

Eyes; lungs

Lungs

Inhalation
Eyes

Cough 
Redness

Resp sys (in animals: lung tumors)
Inh

Lung fib; (carc)

Vanadium 
pentoxide 
1314-62-1

Eyes; resp. tract; lungs

Skin; lungs; tongue

Inhalation

Skin
Eyes
Ingestion

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

Resp sys; skin; eyes
Inh; con

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

Vanadium 
trioxide 
1314-34-7

Eyes; skin; resp. tract

Resp. tract; may effect liver and cardiac function

Inhalation



Skin
Eyes
Ingestion

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

   

Zinc chromate 
13530-65-9

 

Skin;  resp. tract

Inhalation
Eyes
Ingestion

Cough 
Redness 
Abdominal pain, diarrhoea, vomiting

   

Zinc 
phosphide 
1314-84-7

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

 

Inhalation

Ingestion

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

   

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

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

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

 

Back

Wednesday, 09 February 2011 04:19

Acknowledgements

Written by

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.

 

Back

Wednesday, 09 February 2011 04:23

Aluminium

Written by

Gunnar Nordberg

Occurrence and uses

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

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

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

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

Hazards

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

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

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

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

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

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

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

 

Back

Wednesday, 09 February 2011 04:31

Antimony

Written by

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.

 

Back

Wednesday, 09 February 2011 04:36

Arsenic

Written by

Gunnar Nordberg

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

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

 

Occurrence and Uses

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

Elemental arsenic

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

Trivalent inorganic compounds

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

Pentavalent inorganic compounds

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

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

Organic arsenic compounds

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

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

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

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

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

Hazards

Inorganic arsenic compounds

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

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

Acute poisoning

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

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

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

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

Long-term exposure (chronic poisoning)

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

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

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

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

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

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

 

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

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

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

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

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

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

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

Organic arsenic compounds

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

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

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

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

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

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

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

Safety and Health Measures

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

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

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

Treatment

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

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

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

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

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

 

Back

Thursday, 10 February 2011 03:00

Barium

Written by

Gunnar Nordberg

Occurrence and Uses

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

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

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

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

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

Hazards

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

Toxicity

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

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

Pneumoconiosis

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

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

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

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

Safety and Health Measures

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

 

Back

Friday, 11 February 2011 03:48

Bismuth

Written by

Gunnar Nordberg

Occurrence and Uses

In nature, bismuth (Bi) occurs both as the free metal and in ores such as bismutite (carbonate) and bismuthinite (double bismuth and tellurium sulphide), where it is accompanied by other elements, mainly lead and antimony.

Bismuth is used in metallurgy for the manufacture of numerous alloys, especially alloys with a low melting point. Some of these alloys are used for welding. Bismuth also finds use in safety devices in fire detection and extinguishing systems, and in the production of malleable irons. It acts as a catalyst for making acrylic fibres.

Bismuth telluride is used as a semiconductor. Bismuth oxide, hydroxide, oxychloride, trichloride and nitrate are employed in the cosmetics industry. Other salts (e.g., succinate, orthoxyquinoleate, subnitrate, carbonate, phosphate and so on) are used in medicine.

Hazards

There have been no reports of occupational exposure during the production of metallic bismuth and the manufacture of pharmaceuticals, cosmetics and industrial chemicals. Because bismuth and its compounds do not appear to have been responsible for poisoning associated with work, they are regarded as the least toxic of the heavy metals currently used in industry.

Bismuth compounds are absorbed through the respiratory and gastrointestinal tracts. The main systemic effects in humans and animals are exerted in the kidney and liver. The organic derivatives cause alterations of the convoluted tubules and may result in serious, and sometimes fatal, nephrosis.

Gum discolouration has been reported with exposure to bismuth dusts. The insoluble mineral salts, taken orally over prolonged periods in doses generally exceeding 1 per day, may provoke brain disease characterized by mental disorders (confused state), muscular disorders (myoclonia), motor coordination disorders (loss of balance, unsteadiness) and dysarthria. These disorders stem from an accumulation of bismuth in the nerve centres which manifests itself when bismuthaemia exceeds a certain level, estimated at around 50 mg/l. In most cases, bismuth-linked encephalopathy gradually disappears without medication within a period of from 10 days to 2 months, during which time the bismuth is eliminated in the urine. Fatal cases of encephalopathy have, however, been recorded.

Such effects have been observed in France and Australia since 1973. They are caused by a factor not yet fully investigated which encourages the absorption of bismuth through the intestinal mucous membrane and leads to an increase in bismuthaemia to a level as high as several hundred mg/l. The danger of encephalopathy caused by inhaling metallic dust or oxide smoke in the workplace is very remote. The poor solubility of bismuth and bismuth oxide in blood plasma and its fairly rapid elimination in the urine (its half-life is about 6 days) argue against the likelihood of a sufficiently acute impregnation of the nerve centres to reach pathological levels.

In animals, inhalation of insoluble compounds such as bismuth telluride provokes the usual lung response of an inert dust. However, long-term exposure to bismuth telluride “doped” with selenium sulphide can produce in various species a mild reversible granulomatous reaction of the lung.

Some bismuth compounds decompose into dangerous chemicals. Bismuth pentafluoride decomposes on heating and emits highly toxic fumes.

 

Back

Friday, 11 February 2011 03:51

Cadmium

Written by

Gunnar Nordberg

Occurrence and Uses

Cadmium (Cd) has many chemical and physical similarities to zinc and occurs together with zinc in nature. In minerals and ores, cadmium and zinc generally have a ratio of 1:100 to 1:1,000.

Cadmium is highly resistant to corrosion and has been widely used for electroplating of other metals, mainly steel and iron. Screws, screw nuts, locks and various parts for aircraft and motor vehicles are frequently treated with cadmium in order to withstand corrosion. Nowadays, however, only 8% of all refined cadmium is used for platings and coatings. Cadmium compounds (30% of the use in developed countries) are used as pigments and stabilizers in plastics, and cadmium is also used in certain alloys (3%). Rechargeable, small portable cadmium-containing batteries, used, for example, in mobile telephones, comprise a rapidly increasing usage of cadmium (55% of all cadmium in industrialized countries in 1994 was used in batteries).

Cadmium occurs in various inorganic salts. The most important is cadmium stearate, which is used as a heat stabilizer in polyvinyl chloride (PVC) plastics. Cadmium sulphide and cadmium sulphoselenide are used as yellow and red pigments in plastics and colours. Cadmium sulphide is also used in photo- and solar cells. Cadmium chloride acts as a fungicide, an ingredient in elecroplating baths, a colourant for pyrotechnics, an additive to tinning solution and a mordant in dyeing and printing textiles. It is also used in the production of certain photographic films and in the manufacture of special mirrors and coatings for electronic vacuum tubes. Cadmium oxide is an elecroplating agent, a starting material for PVC heat stabilizers and a component of silver alloys, phosphors, semiconductors and glass and ceramic glazes.

Cadmium can represent an environmental hazard, and many countries have introduced legislative actions aimed towards decreasing the use and subsequent environmental spread of cadmium.

Metabolism and accumulation

Gastrointestinal absorption of ingested cadmium is about 2 to 6% under normal conditions. Individuals with low body iron stores, reflected by low concentrations of serum ferritin, may have considerably higher absorption of cadmium, up to 20% of a given dose of cadmium. Significant amounts of cadmium may also be absorbed via the lung from the inhalation of tobacco smoke or from occupational exposure to atmospheric cadmium dust. Pulmonary absorption of inhaled respirable cadmium dust is estimated at 20 to 50%. After absorption via the gastrointestinal tract or the lung, cadmium is transported to the liver, where production of a cadmium-binding low-molecular-weight protein, metallothionein, is initiated.

About 80 to 90% of the total amount of cadmium in the body is considered to be bound to metallothionein. This prevents the free cadmium ions from exerting their toxic effects. It is likely that small amounts of metallothionein-bound cadmium are constantly leaving the liver and being transported to the kidney via the blood. The metallothionein with the cadmium bound to it is filtered through the glomeruli into the primary urine. Like other low-molecular-weight proteins and amino acids, the metallothionein-cadmium complex is subsequently reabsorbed from the primary urine into the proximal tubular cells, where digestive enzymes degrade the engulfed proteins into smaller peptides and amino acids. Free cadmium ions in the cells result from degradation of metallothionein and initiate a new synthesis of metallothionein, binding the cadmium, and thus protecting the cell from the highly toxic free cadmium ions. Kidney dysfunction is considered to occur when the metallothionein-producing capacity of the tubular cells is exceeded.

The kidney and liver have the highest concentrations of cadmium, together containing about 50% of the body burden of cadmium. The cadmium concentration in the kidney cortex, before cadmium-induced kidney damage occurs, is generally about 15 times the concentration in liver. Elimination of cadmium is very slow. As a result of this, cadmium accumulates in the body, the concentrations increasing with age and length of exposure. Based on organ concentration at different ages the biological half-life of cadmium in humans has been estimated in the range of 7 to 30 years.

Acute toxicity

Inhalation of cadmium compounds at concentrations above 1 mg Cd/m3 in air for 8 hours, or at higher concentrations for shorter periods, may lead to chemical pneumonitis, and in severe cases pulmonary oedema. Symptoms generally occur within 1 to 8 hours after exposure. They are influenza-like and similar to those in metal fume fever. The more severe symptoms of chemical pneumonitis and pulmonary oedema may have a latency period up to 24 hours. Death may occur after 4 to 7 days. Exposure to cadmium in the air at concentrations exceeding 5 mg Cd/m3 is most likely to occur where cadmium alloys are smelted, welded or soldered. Ingestion of drinks contaminated with cadmium at concentrations exceeding 15 mg Cd/l gives rise to symptoms of food poisoning. Symptoms are nausea, vomiting, abdominal pains and sometimes diarrhoea. Sources of food contamination may be pots and pans with cadmium-containing glazing and cadmium solderings used in vending machines for hot and cold drinks. In animals parenteral administration of cadmium at doses exceeding 2 mg Cd/kg body weight causes necrosis of the testis. No such effect has been reported in humans.

Chronic toxicity

Chronic cadmium poisoning has been reported after prolonged occupational exposure to cadmium oxide fumes, cadmium oxide dust and cadmium stearates. Changes associated with chronic cadmium poisoning may be local, in which case they involve the respiratory tract, or they may be systemic, resulting from absorption of cadmium. Systemic changes include kidney damage with proteinuria and anaemia. Lung disease in the form of emphysema is the main symptom at heavy exposure to cadmium in air, whereas kidney dysfunction and damage are the most prominent findings after long-term exposure to lower levels of cadmium in workroom air or via cadmium-contaminated food. Mild hypochromic anaemia is frequently found among workers exposed to high levels of cadmium. This may be due to both increased destruction of red blood cells and to iron deficiency. Yellow discolouration of the necks of teeth and loss of sense of smell (anosmia) may also be seen in cases of exposure to very high cadmium concentrations.

Pulmonary emphysema is considered a possible effect of prolonged exposure to cadmium in air at concentrations exceeding 0.1 mg Cd/m3. It has been reported that exposure to concentrations of about 0.02 mg Cd/m3 for more than 20 years can cause certain pulmonary effects. Cadmium-induced pulmonary emphysema can reduce working capacity and may be the cause of invalidity and life shortening. With long-term low-level cadmium exposure the kidney is the critical organ (i.e., the organ first affected). Cadmium accumulates in renal cortex. Concentrations exceeding 200 µg Cd/g wet weight have previously been estimated to cause tubular dysfunction with decreased reabsorption of proteins from the urine. This causes tubular proteinuria with increased excretion of low-molecular-weight proteins such as
α,α-1-microglobulin (protein HC), β-2-microglobulin and retinol binding protein (RTB). Recent research suggests, however, that tubular damage may occur at lower levels of cadmium in kidney cortex. As the kidney dysfunction progresses, amino acids, glucose and minerals, such as calcium and phosphorus, are also lost into the urine. Increased excretion of calcium and phosphorous may disturb bone metabolism, and kidney stones are frequently reported by cadmium workers. After long-term medium-to-high levels of exposure to cadmium, the kidney’s glomeruli may also be affected, leading to a decreased glomerular filtration rate. In severe cases uraemia may develop. Recent studies have shown the glomerular dysfunction to be irreversible and dose dependent. Osteomalacia has been reported in cases of severe chronic cadmium poisoning.

In order to prevent kidney dysfunction, as manifested by β-2-microglobulinuria, particularly if the occupational exposure to cadmium fumes and dust is likely to last for 25 years (at 8 hours workday and 225 workdays/year), it is recommended that the average workroom concentration of respirable cadmium should be kept below 0.01 mg/m3.

Excessive cadmium exposure has occurred in the general population through ingestion of contaminated rice and other foodstuffs, and possibly drinking water. The itai-itai disease, a painful type of osteomalacia, with multiple fractures appearing together with kidney dysfunction, has occurred in Japan in areas with high cadmium exposure. Though the pathogenesis of itai-itai disease is still under dispute, it is generally accepted that cadmium is a necessary aetiological factor. It should be stressed that cadmium-induced kidney damage is irreversible and may grow worse even after exposure has ceased.

Cadmium and cancer

There is strong evidence of dose-response relationships and an increased mortality from lung cancer in several epidemiological studies on cadmium-exposed workers. The interpretation is complicated by concurrent exposures to other metals which are known or suspected carcinogens. Continuing observations of cadmium-exposed workers have, however, failed to yield evidence of increased mortality from prostatic cancer, as initially suspected. The IARC in 1993 assessed the risk of cancer from exposure to cadmium and concluded that it should be regarded as a human carcinogen. Since then additional epidemiological evidence has come forth with somewhat contradictory results, and the possible carcinogenicity of cadmium thus remains unclear. It is nevertheless clear that cadmium possesses strong carcinogenic properties in animal experiments.

Safety and Health Measures

The kidney cortex is the critical organ with long-term cadmium exposure via air or food. The critical concentration is estimated at about 200 µg Cd/g wet weight, but may be lower, as stated above. In order to keep the kidney cortex concentration below this level even after lifelong exposure, the average cadmium concentration in workroom air (8 hours per day) should not exceed 0.01 mg Cd/m3.

Work processes and operations which may release cadmium fumes or dust into the atmosphere should be designed to keep concentration levels to a minimum and, if practicable, be enclosed and fitted with exhaust ventilation. When adequate ventilation is impossible to maintain (e.g., during welding and cutting), respirators should be carried and air should be sampled to determine the cadmium concentration. In areas with hazards of flying particles, chemical splashes, radiant heat and so on (e.g., near electroplating tanks and furnaces), workers should wear appropriate safety equipment, such as eye, face, hand and arm protection and impermeable clothing. Adequate sanitary facilities should be supplied, and workers should be encouraged to wash before meals and to wash thoroughly and change clothes before leaving work. Smoking, eating and drinking in work areas should be prohibited. Tobacco contaminated with cadmium dust from workrooms can be an important exposure route. Cigarettes and pipe tobacco should not be carried in the workroom. Contaminated exhaust air should be filtered, and persons in charge of dust collectors and filters should wear respirators while working on the equipment.

To ensure that excessive accumulation of cadmium in the kidney does not occur, cadmium levels in blood and in urine should be checked regularly. Cadmium levels in blood are mainly an indication of the last few months exposure, but can be used to assess body burden a few years after exposure has ceased. A value of 100 nmol Cd/l whole blood is an approximate critical level if exposure is regular for long periods. Cadmium values in urine can be used to estimate the cadmium body burden, providing kidney damage has not occurred. It has been estimated by the WHO that 10 nmol/mmol creatinine is the concentration below which kidney dysfunction should not occur. Recent research has, however, shown that kidney dysfunction may occur already at around 5 nmol/mmol creatinine.

Since the mentioned blood and urinary levels are levels at which action of cadmium on kidney has been observed, it is recommended that control measures be applied whenever the individual concentrations of cadmium in urine and/or in blood exceed 50 nmol/l whole blood or
3 nmol/mmol creatinine respectively. Pre-employment medical examinations should be given to workers who will be exposed to cadmium dust or fumes. Persons with respiratory or kidney disorders should avoid such work. Medical examination of cadmium-exposed workers should be carried out at least once every year. In workers exposed to cadmium for longer periods, quantitative measurements of ß-2-microglobulin or other relevant low-molecular-weight proteins in urine should be made regularly. Concentrations of ß-2-microglobulin in urine should normally not exceed 34 µg/mmol creatinine.

Treatment of cadmium poisoning

Persons who have ingested cadmium salts should be made to vomit or given gastric lavage; persons exposed to acute inhalation should be removed from exposure and given oxygen therapy if necessary. No specific treatment for chronic cadmium poisoning is available, and symptomatic treatment has to be relied upon. As a rule the administration of chelating agents such as BAL and EDTA is contraindicated since they are nephrotoxic in combination with cadmium.

 

Back

Friday, 11 February 2011 03:52

Chromium

Written by

Gunnar Nordberg

Occurrence and Uses

Elemental chromium (Cr) is not found free in nature, and the only ore of any importance is the spinel ore, chromite or chrome iron stone, which is ferrous chromite (FeOCr2O3), widely distributed over the earth’s surface. In addition to chromic acid, this ore contains variable quantities of other substances. Only ores or concentrates containing more than 40% chromic oxide (Cr2O3) are used commercially, and countries having the most suitable deposits are the Russian Federation, South Africa, Zimbabwe, Turkey, the Philippines and India. The prime consumers of chromites are the United States, the Russian Federation, Germany, Japan, France and the United Kingdom.

Chromite may be obtained from both underground and open cast mines. The ore is crusted and, if necessary, concentrated.

The most significant usage of pure chromium is for electroplating of a wide range of equipment, such as automobile parts and electric equipment. Chromium is used extensively for alloying with iron and nickel to form stainless steel, and with nickel, titanium, niobium, cobalt, copper and other metals to form special-purpose alloys.

Chromium Compounds

Chromium forms a number of compounds in various oxidation states. Those of II (chromous), III (chromic) and VI (chromate) states are most important; the II state is basic, the III state is amphoteric and the VI state is acidic. Commercial applications mainly concern compounds in the VI state, with some interest in III state chromium compounds.

The chromous state (CrII) is unstable and is readily oxidized to the chromic state (CrIII). This instability limits the use of chromous compounds. The chromic compounds are very stable and form many compounds which have commercial use, the principal of which are chromic oxide and basic chromium sulphate.

Chromium in the +6 oxidation state (CrVI) has its greatest industrial application as a consequence of its acidic and oxidant properties, as well as its ability to form strongly coloured and insoluble salts. The most important compounds containing chromium in the CrVI state are sodium dichromate, potassium dichromate and chromium trioxide. Most other chromate compounds are produced industrially using dichromate as the source of CrVI.

Production

Sodium mono- and dichromate are the starting materials from which most of the chromium compounds are manufactured. Sodium chromate and dichromate are prepared directly from chrome ore. Chrome ore is crushed, dried and ground; soda ash is added and lime or leached calcine may also be added. After thorough mixing the mixture is roasted in a rotary furnace at an optimum temperature of about 1,100°C; an oxidizing atmosphere is essential to convert the chromium to the CrVI state. The melt from the furnace is cooled and leached and the sodium chromate or dichromate is isolated by conventional processes from the solution.

ChromiumIII compounds

Technically, chromium oxide (Cr2O3, or chromic oxide), is made by reducing sodium dichromate either with charcoal or with sulphur. Reduction with sulphur is usually employed when the chromic oxide is to be used as a pigment. For metallurgical purposes carbon reduction is normally employed.

The commercial material is normally basic chromic sulphate [Cr(OH)(H2O)5]SO4, which is prepared from sodium dichromate by reduction with carbohydrate in the presence of sulphuric acid; the reaction is vigorously exothermic. Alternatively, sulphur dioxide reduction of a solution of sodium dichromate will yield basic chromic sulphurate. It is used in the tanning of leather, and the material is sold on the basis of Cr2O3 content, which ranges from 20.5 to 25%.

ChromiumVI compounds

Sodium dichromate can be converted into the anhydrous salt. It is the starting point for preparation of chromium compounds.

Chromium trioxide or chromium anhydride (sometimes referred to as “chromic acid”, although true chromic acid cannot be isolated from solution) is formed by treating a concentrated solution of a dichromate with strong sulphuric acid excess. It is a violent oxidizing agent, and the solution is the principal constituent of chromium plating.

Insoluble chromates

Chromates of weak bases are of limited solubility and more deeply coloured than the oxides; hence their use as pigments. These are not always distinct compounds and may contain mixtures of other materials to provide the right pigment colour. They are prepared by the addition of sodium or potassium dichromate to a solution of the appropriate salt.

Lead chromate is trimorphic; the stable monoclinic form is orange-yellow, “chrome yellow”, and the unstable orthombic form is yellow, isomorphous with lead sulphate and stabilized by it. An orange-red tetragonal form is similar and isomorphous with lead molybdate (VI) PbMoO4 and stabilized by it. On these properties depends the versatility of lead chromate as a pigment in producing a variety of yellow-orange pigments.

Uses

Compounds containing CrVI are used in many industrial operations. The manufacture of important inorganic pigments such as lead chromes (which are themselves used to prepare chrome greens), molybdate-oranges, zinc chromate and chromium-oxide green; wood preservation; corrosion inhibition; and coloured glasses and glazes. Basic chromic sulphates are widely used for tanning.

The dyeing of textiles, the preparation of many important catalysts containing chromic oxide and the production of light-sensitive dichromated colloids for use in lithography are also well-known industrial uses of chromium-containing chemicals.

Chromic acid is used not only for “decorative” chromium plating but also for “hard” chromium plating, where it is deposited in much thicker layers to give an extremely hard surface with a low coefficient of friction.

Because of the strong oxidizing action of chromates in acid solution, there are many industrial applications particularly involving organic materials, such as the oxidation of trinitrotoluene (TNT) to give phloroglucinol and the oxidation of picoline to give nicotine acid.

Chromium oxide is also used for the production of pure chromium metal that is suitable for incorporation in creep-resistant, high-temperature alloys, and as a refractory oxide. It may be included in a number of refractory compositions with advantage—for example, in magnetite and magnetite-chromate mixtures.

Hazards

Compounds with CrIII oxidation states are considerably less hazardous than are CrVI compounds. Compounds of CrIII are poorly absorbed from the digestive system. These CrIII compounds may also combine with proteins in the superficial layers of the skin to form stable complexes. Compounds of CrIII do not cause chrome ulcerations and do not generally initiate allergic dermatitis without prior sensitization by CrVI compounds.

In the CrVI oxidation state, chromium compounds are readily absorbed after ingestion as well as during inhalation. The uptake through intact skin is less well elucidated. The irritant and corrosive effects caused by CrVI occur readily after uptake through mucous membranes, where they are readily absorbed. Work-related exposure to CrVI compounds may induce skin and mucous membrane irritation or corrosion, allergic skin reactions or skin ulcerations.

The untoward effects of chromium compounds generally occur among workers in workplaces where CrVI is encountered, in particular during manufacture or use. The effects frequently involve the skin or respiratory system. Typical industrial hazards are inhalation of the dust or fumes arising during the manufacture of dichromate from chromite ore and the manufacture of lead and zinc chromates, inhalation of chromic acid mists during electroplating or surface treatment of metals, and skin contact with CrVI compounds in manufacture or use. Exposure to CrVI-containing fumes may also occur during welding of stainless steels.

Chrome ulcerations. Such lesions used to be common after work-related exposure to CrVI compounds. The ulcers result from the corrosive action of CrVI, which penetrates the skin through cuts or abrasions. The lesion usually begins as a painless papule, commonly on the hands, forearms or feet, resulting in ulcerations. The ulcer may penetrate deeply into soft tissue and may reach underlying bone. Healing is slow unless the ulcer is treated at an early stage, and atrophic scars remain. There are no reports about skin cancer following such ulcers.

Dermatitis. The CrVI compounds may cause both primary skin irritation and sensitization. In chromate-producing industries, some workers may develop skin irritation, particularly at the neck or wrist, soon after starting work with chromates. In the majority of cases, this clears rapidly and does not recur. However, sometimes it may be necessary to recommend a change of work.

Numerous sources of exposure to CrVI have been listed (e.g., contact with cement, plaster, leather, graphic work, work in match factories, work in tanneries and various sources of metal work). Workers employed in wet sandpapering of car bodies have also been reported with allergy. Affected subjects react positively to patch testing with 0.5% dichromate. Some affected subjects had only erythema or scattered papules, and in others the lesions resembled dyshidriotic pompholyx; nummular eczema may lead to misdiagnosis of genuine cases of occupational dermatitis.

It has been shown that CrVI penetrates the skin through the sweat glands and is reduced to CrIII in the corium. It is shown that the CrIII then reacts with protein to form the antigen-antibody complex. This explains the localization of lesions around sweat glands and why very small amounts of dichromate can cause sensitization. The chronic character of the dermatitis may be due to the fact that the antigen-antibody complex is removed more slowly than would be the case if the reaction occurred in the epidermis.

Acute respiratory effects. Inhalation of dust or mist containing CrVI is irritating to mucous membranes. At high concentrations of such dust, sneezing, rhinorrhoea, lesions of the nasal septum and redness of the throat are documented effects. Sensitization has also been reported, resulting in typical asthmatic attacks, which may recur on subsequent exposure. At exposure for several days to chromic acid mist at concentrations of about 20 to 30 mg/m3, cough, headache, dyspnoea and substernal pain have also been reported after exposure. The occurrence of bronchospasm in a person working with chromates should suggest chemical irritation of the lungs. Treatment is only symptomatic.

Ulcerations of the nasal septum. In previous years, when the exposure levels to CrVI compounds could be high, ulcerations of the nasal septum were frequently seen among exposed workers. This untoward effect results from deposition of CrVI-containing particulates or mist droplets on the nasal septum, resulting in ulceration of the cartilaginous portion followed, in many cases, by perforation at the site of ulceration. Frequent nose-picking may enhance the formation of perforation. The mucosa covering the lower anterior part of the septum, known as the Kiesselbach’s and Little’s area, is relatively avascular and closely adherent to the underlying cartilage. Crusts containing necrotic debris from the cartilage of the septum continue to form, and within a week or two the septum becomes perforated. The periphery of the ulceration remains active for up to several months, during which time the perforation may increase in size. It heals by the formation of vascular scar tissue. Sense of smell is almost never impaired. During the active phase, rhinorrhoea and nose-bleeding may be troublesome symptoms. When soundly healed, symptoms are rare and many persons are unaware that the septum is perforated.

Effects in other organs. Necrosis of the kidneys has been reported, starting with tubular necrosis, leaving the glomeruli undamaged. Diffuse necrosis of the liver and subsequent loss of architecture has also been reported. Soon after the turn of the century there were a number of reports on human ingestion of CrVI compounds resulting in major gastro-intestinal bleeding from ulcerations of the intestinal mucosa. Sometimes such bleedings resulted in cardiovascular shock as a possible complication. If the patient survived, tubular necrosis of the kidneys or liver necrosis could occur.

Carcinogenic effects. Increased incidence of lung cancer among workers in manufacture and use of CrVI compounds has been reported in a great number of studies from France, Germany, Italy, Japan, Norway, the United States and the United Kingdom. Chromates of zinc and calcium appear to be among the most potent carcinogenic chromates, as well as among the most potent human carcinogens. Elevated incidence of lung cancer has also been reported among subjects exposed to lead chromates, and to fumes of chromium trioxides. Heavy exposures to CrVI compounds have resulted in very high incidence of lung cancer in exposed workers 15 or more years after first exposure, as reported in both cohort studies and case reports.

Thus, it is well established that an increase in the incidence of lung cancer of workers employed in the manufacture of zinc chromate and the manufacture of mono- and dichromates from chromite ore is a long-term effect of work-related heavy exposure to CrVI compounds. Some of the cohort studies have reported measurements of exposure levels among the exposed cohorts. Also, a small number of studies have indicated that exposure to fumes generated from welding on Cr-alloyed steel may result in elevated incidence of lung cancer among these welders.

There is no firmly established “safe” level of exposure. However, most of the reports on association between CrVI exposure and cancer of the respiratory organs and exposure levels report on air levels exceeding 50 mg CrVI/m3 air.

The symptoms, signs, course, x-ray appearance, method of diagnosis and prognosis of lung cancers resulting from exposure to chromates differ in no way from those of cancer of the lung due to other causes. It has been found that the tumours often originate in the periphery of the bronchial tree. The tumours may be of all histological types, but a majority of the tumours seem to be anaplastic oat-celled tumours. Water-soluble, acid soluble and water insoluble chromium is found in the lung tissues of chromate workers in varying amounts.

Although it has not been firmly established, some studies have indicated that exposure to chromates may result in increased risk of cancer in the nasal sinuses and the alimentary tract. The studies that indicate excess cancer of the alimentary tract are case reports from the 1930s or cohort studies that reflect exposure at high levels than generally encountered today.

Safety and Health Measures

On the technical side, avoidance of exposure to chromium depends on appropriate design of processes, including adequate exhaust ventilation and the suppression of dust or mist containing chromium in the hexavalent state. Built-in control measures are also necessary, requiring the least possible action by either process operators or maintenance staff.

Wet methods of cleaning should be used where possible; at other sites, the only acceptable alternative is vacuum cleaning. Spill of liquids or solids must be removed to prevent dispersion as airborne dust. The concentration in the work environment of chromium-containing dust and fumes should preferably be measured at regular intervals by individual and area sampling. Where unacceptable concentration levels are found by either method, the sources of dust or fumes should be identified and controlled. Dust masks, preferably with an efficiency of more than 99% in retaining particles of 0.5 µm size, should be worn in situations above non-hazardous levels, and it may be necessary to provide air-supplied respiratory protective equipment for jobs considered to be hazardous. Management should ensure that dust deposits and other surface contaminants should be removed by washing down or suction before work of this type begins. Providing laundering overalls daily may help in avoiding skin contamination. Hand and eye protection is generally recommended, as is repair and replacement of all personal protective equipment (PPE).

The medical surveillance of workers on processes in which CrVI compounds may be encountered should include education in toxic and the carcinogenic properties of both CrVI and CrIII compounds, as well as on the differences between the two groups of compounds. The nature of the exposure hazards and subsequent risks of various diseases (e.g., lung cancer) should be given at job entry as well as at regular intervals during employment. The need to observe a high standard of personal hygiene should be emphasized.

All untoward effects of exposure to chromium can be avoided. Chrome ulcers of the skin can be prevented by eliminating sources of contact and by preventing injury to the skin. Skin cuts and abrasions, however slight, should be cleaned immediately and treated with 10% sodium EDTA ointment. Together with the use of a frequently renewed impervious dressing, this will enhance rapid healing for any ulcer that may develop. Although EDTA does not chelate CrVI compounds at room temperature, it reduces the CrVI to CrIII rapidly, and the excess EDTA chelates CrIII. Both the direct irritant and corrosive action of CrVI compounds and the formation of protein/CrIII complexes are thus prevented. After accidental ingestion of CrVI compounds, immediate swallowing of ascorbic acid may also quickly reduce the CrVI.

Careful washing of the skin after contact and care to avoid friction and sweating are important in the prevention and the control of primary irritation due to chromates. In previous years an ointment containing 10% sodium EDTA was applied regularly to the nasal septum before exposure. This preventive treatment could assist in keeping the septum intact. Soreness of the nose and early ulceration were also treated by regular application of this ointment, and healing could be achieved without perforation.

Results from research indicate that workers exposed to high air concentrations of CrVI could be monitored successfully by monitoring the excretion of chromium in the urine. Such results, however, bear no relation to the hazard of skin allergy. As of today, with the very long latent period of CrVI-related lung cancer, hardly anything can be said regarding the cancer hazard on the basis of urinary levels of Cr.

 

Back