61. Using, Storing and Transporting Chemicals
Chapter Editors: Jeanne Mager Stellman and Debra Osinsky
Safe Handling and Usage of Chemicals
Case Study: Hazard Communication: The Chemical Safety Data Sheet or the Material Safety Data Sheet (MSDS)
Classification and Labelling Systems for Chemicals
Konstantin K. Sidorov and Igor V. Sanotsky
Case Study: Classification Systems
Safe Handling and Storage of Chemicals
A.E. Quinn
Compressed Gases: Handling, Storage and Transport
A. Türkdogan and K.R. Mathisen
Laboratory Hygiene
Frank Miller
Methods for Localized Control of Air Contaminants
Louis DiBernardinis
The GESTIS Chemical Information System: A Case Study
Karlheinz Meffert and Roger Stamm
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62. Minerals and Agricultural Chemicals
Chapter Editors: Debra Osinsky and Jeanne Mager Stellman
Table of Contents
Minerals
Agricultural Chemicals
Gary A. Page
The WHO Guidelines to Classification of Pesticides by Hazard (Slightly Hazardous)
The WHO Guidelines to Classification of Pesticides by Hazard (Unlikely to Present Acute Hazard)
The WHO Guidelines to Classification of Pesticides by Hazard (Present Acute Hazard continued)
The WHO Guidelines to Classification of Pesticides by Hazard (Obsolete or Discontinued)
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63. Metals: Chemical Properties and Toxicity
Chapter Editor: Gunnar Nordberg
Table of Contents
GENERAL PROFILE
ACKNOWLEDGEMENTS
Aluminium
Antimony
Arsenic
Barium
Bismuth
Cadmium
Chromium
Copper
Iron
Gallium
Germanium
Indium
Iridium
Lead
Magnesium
Manganese
Metal Carbonyls (especially Nickel Carbonyl)
Mercury
Molybdenum
Nickel
Niobium
Osmium
Palladium
Platinum
Rhenium
Rhodium
Ruthenium
Selenium
Silver
Tantalum
Tellurium
Thallium
Tin
Titanium
Tungsten
Vanadium
Zinc
Zirconium and Hafnium
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Table 5. List of technical products unlikely to present acute hazard in normal use
Name |
Status |
Main use |
Chemical type |
Physical state |
Route |
LD50 (mg/kg) |
Remarks |
Aclonifen |
N(B) |
H |
S |
O |
+5,000 |
||
Acrinathrin |
ISO |
MT |
S |
O |
+5,000 |
||
Alloxydim |
ISO |
H |
S |
O |
2,260 |
||
Aminotriazole |
N(F) |
See amitrole |
|||||
Amitrole |
ISO |
H |
T |
S |
O |
5,000 |
EHC 158, DS 79; HSG 85 |
Ammonium sulfamate |
ISO |
H |
S |
O |
3,900 |
||
Ancymidol |
ISO |
PGR |
S |
O |
4,500 |
||
Anilazine |
ISO |
F |
T |
S |
O |
2,710 |
Irritant to eyes and skin |
Anthraquinone |
ISO |
RP (birds) |
S |
O |
+5,000 |
||
Asulam |
ISO |
H |
TC |
S |
O |
+4,000 |
|
Atrazine |
ISO |
H |
T |
S |
O |
c2,000 |
DS 82; HSG 47 |
Aziprotryne |
ISO |
H |
T |
S |
O |
3,600 |
|
Benalaxyl |
ISO |
F |
S |
O |
c4,200 |
||
Benazolin |
ISO |
H |
S |
O |
3,200 |
Irritant to skin and eyes |
|
Benefin |
N(A) |
See benfluralin |
|||||
Benfluralin |
ISO |
H |
S |
O |
+10,000 |
||
Benfuresate |
ISO |
H |
S |
O |
2,031 |
||
Benomyl |
ISO |
F |
TC |
S |
O |
+10,000 |
EHC 148, DS 87; HSG 81 |
Benoxacor |
ISO |
H |
S |
O |
+5,000 |
||
Bensulfuron |
N(B) |
H |
S |
O |
+5,000 |
||
Benthrodine |
N(J) |
See benfluralin |
|||||
Benzamizole |
See isoxaben |
||||||
Benzoximate |
ISO |
AC |
S |
O |
+10,000 |
||
Bifenox |
ISO |
H |
S |
O |
+6,400 |
||
Bioresmethrin |
ISO |
I |
PY |
L |
O |
+7,000 |
DS 34 |
Biphenyl |
ISO |
F |
S |
O |
3,280 |
||
Bispyribac |
ISO |
H |
S |
O |
2,635 |
||
Bitertanol |
ISO |
F |
S |
O |
+5,000 |
||
Borax |
ISO |
F |
S |
O |
4,500 |
||
Bromacil |
ISO |
H |
S |
O |
5,200 |
||
Bromobutide |
ISO |
H |
S |
O |
+5,000 |
||
Bromocyclen |
ISO |
I,AC |
S |
O |
+10,000 |
||
Bromopropylate |
ISO |
AC |
S |
O |
+5,000 |
||
Bupirimate |
ISO |
F |
S |
O |
c4,000 |
||
Buprofezin |
ISO |
I |
S |
O |
2,200 |
||
Butachlor |
ISO |
H |
L |
O |
3,300 |
||
Buthiobate |
ISO |
F |
L |
O |
3,200 |
||
Butopyronoxyl |
N(A) |
RP (insects) |
L |
O |
7,840 |
||
Butralin |
ISO |
H |
S |
O |
+10,000 |
||
Buturon |
ISO |
H |
S |
O |
3,000 |
||
Butylate |
ISO |
F |
TC |
L |
O |
+4,000 |
|
Captan |
ISO |
F |
S |
O |
9,000 |
Irritant to skin; DS 9; HSG 50 |
|
Carbendazim |
ISO |
F |
S |
O |
+10,000 |
DS 89; EHC 149; HSG 82 |
|
Carbetamide |
ISO |
H |
S |
O |
+10,000 |
||
Carboxin |
ISO |
FST |
S |
O |
3,820 |
||
Chinomethionat |
ISO |
AC,F |
S |
O |
2,500 |
||
Chlomethoxyfen |
N(B) |
H |
S |
O |
+10,000 |
||
Chloramben |
ISO |
H |
S |
O |
5,620 |
||
Chlorbromuron |
ISO |
H |
S |
O |
+5,000 |
||
Chlorbufam |
ISO |
H |
S |
O |
2,500 |
||
Chlorfenidim |
N(U) |
See monuron |
|||||
Chlorfluazuron |
ISO |
IGR |
S |
O |
8,500 |
||
Chlorflurecol |
N(B) |
See chlorflurenol |
|||||
Chlorflurenol |
ISO |
PGR |
OC |
S |
O |
+10,000 |
|
Chloridazon |
ISO |
H |
S |
O |
2,420 |
||
Chlorimuron |
N(B) |
H |
S |
O |
4,102 |
||
Chlornitrofen |
ISO |
H |
S |
O |
+10,000 |
||
Chloromethiuron |
ISO |
Ix |
S |
O |
2,500 |
||
Chloroneb |
ISO |
H |
OC |
S |
O |
+10,000 |
|
Chloropropylate |
ISO |
AC |
OC |
S |
O |
+5,000 |
|
Chlorothalonil |
ISO |
F |
S |
O |
+10,000 |
||
Chlorotoluron |
ISO |
H |
S |
O |
+10,000 |
||
Chloroxifenidim |
N(U) |
See chloroxuron |
|||||
Chloroxuron |
ISO |
H |
S |
O |
+3,000 |
||
Chlorphoxim |
ISO |
I |
OP |
S |
O |
+2,500 |
DS 32 |
Chlorpropham |
ISO |
H |
S |
O |
+5,000 |
||
Chlorpyrifos methyl |
ISO |
I |
OP |
L |
O |
+3,000 |
DS 33 |
Chlorsulfuron |
ISO |
H |
S |
O |
5,545 |
||
Chlorthal-dimethyl |
ISO |
H |
S |
O |
+3,000 |
||
Chlozolinate |
N(B) |
F |
S |
O |
+4,000 |
||
Cinmethylin |
ISO |
H |
L |
O |
3,960 |
||
Cinosulfuron |
ISO |
H |
S |
O |
+5,000 |
||
Clofentezine |
N(B) |
AC |
S |
O |
+5,200 |
||
Clomeprop |
ISO |
H |
S |
O |
+5,000 |
||
Clonitralide |
N(A) |
See niclosamide |
|||||
Clopyralid |
N(B) |
H |
S |
O |
4,300 |
Severe irritant to eyes |
|
Cloxyfonac |
ISO |
PGR |
S |
O |
+5,000 |
||
CNA |
N(J) |
See dicloran |
|||||
COMU |
N(J) |
See cycluron |
|||||
Credazine |
N(J) |
H |
S |
O |
3,090 |
||
Cryolite |
C |
I |
S |
O |
+10,000 |
||
Cycloprothrin |
ISO |
I |
PY |
L |
O |
+5,000 |
|
Cycloxydim |
N(B) |
H |
S |
O |
3,900 |
||
Cycluron |
ISO |
H |
S |
O |
2,600 |
||
Cyometrinil |
N(B) |
H |
S |
O |
2,277 |
||
Cyromazine |
ISO |
L |
S |
O |
3,300 |
||
Caimuron |
ISO |
H |
S |
O |
+5,000 |
||
Dalapon |
N(A,B,F) |
H |
S |
O |
9,330 |
||
Daminozide |
ISO |
H |
S |
O |
8,400 |
||
Desmedipham |
ISO |
H |
S |
O |
+9,600 |
||
Diafenthiuron |
ISO |
AC |
S |
O |
2,068 |
||
Dichlobenil |
ISO |
H |
S |
O |
3,160 |
||
Dichlorfenidim |
N(U) |
See diuron |
|||||
Dichlofluanid |
ISO |
F |
S |
O |
+5,000 |
||
Dichloropicolinic acid |
See clopyralid |
||||||
Diclobutrazol |
ISO |
F |
T |
S |
O |
+4,000 |
|
Diclomezine |
ISO |
F |
S |
O |
+10,000 |
||
Dicloran |
N(B) |
F |
S |
O |
4,000 |
||
Diethatyl |
ISO |
H |
S |
O |
2,300 |
||
Diethofencarb |
ISO |
F |
S |
O |
+5,000 |
||
Difenoxuron |
ISO |
H |
S |
O |
+7,750 |
||
Diflubenzuron |
ISO |
L |
S |
O |
+4,640 |
DS 77 |
|
Diflufenican |
N(B) |
H |
S |
O |
+2,000 |
||
Dikegulac |
ISO |
PGR |
S |
O |
+10,000 |
||
Dimefuron |
ISO |
H |
S |
O |
+2,000 |
||
Dimethirimol |
ISO |
F |
S |
O |
2,350 |
||
Dimethomorph |
ISO |
F |
S |
O |
+5,000 |
||
Dimethyl phthalate |
C |
RP (insect) |
L |
O |
8,200 |
||
Dinitramine |
ISO |
H |
S |
O |
3,000 |
||
Diphenyl |
See biphenyl |
||||||
Dipropetryn |
ISO |
H |
T |
S |
O |
4,050 |
|
Dipropyl isocinchomerate |
C |
RP (fly) |
L |
O |
5,230 |
||
Disodium octaborate |
See borax |
||||||
Ditalmifos |
ISO |
F |
OP |
S |
O |
5,660 |
Irritant to skin; allergenic |
Dithiopyr |
ISO |
H |
O |
+5,000 |
|||
Diuron |
ISO |
H |
S |
O |
3,400 |
||
Dodemorph |
ISO |
H |
L |
O |
4,500 |
||
Eglinazine |
ISO |
H |
S |
O |
+10,000 |
||
Ethalfluralin |
ISO |
H |
S |
O |
+10,000 |
||
Ethephon |
N(A) |
PGR |
S |
O |
+4,000 |
||
Ethidimuron |
ISO |
H |
S |
O |
+5,000 |
||
Ethirimol |
ISO |
FST |
S |
O |
6,340 |
||
Ethofumesate |
ISO |
H |
S |
O |
+6,400 |
||
Etofenprox |
N(B) |
I |
S |
O |
+10,000 |
||
Fenarimol |
ISO |
F |
S |
O |
2,500 |
||
Fenbutatin oxide |
ISO |
MT |
OT |
S |
O |
2,630 |
EHC 15 |
Fenchlorazole |
ISO |
H |
S |
O |
+5,000 |
||
Fenclorim |
ISO |
H |
S |
O |
+5,000 |
||
Fenfuram |
ISO |
FST |
S |
O |
+10,000 |
||
Fenidim |
N(U) |
See fenuron |
|||||
Fenitropan |
ISO |
F |
S |
O |
3,230 |
||
Fenoxaprop-ethyl |
N(B) |
H |
S |
O |
2,350 |
||
Fenoxycarb |
ISO |
I |
C |
S |
O |
+10,000 |
|
Fenpiclonil |
ISO |
FST |
S |
O |
+5,000 |
||
Fenpropimorph |
ISO |
F |
oil |
O |
3,515 |
||
Fenuron |
ISO |
H |
S |
O |
6,400 |
||
Fenuron-TCA |
(ISO) |
H |
S |
O |
4,000 |
||
Ferbam |
ISO |
F |
TC |
S |
O |
+10,000 |
|
Flamprop-M |
ISO |
H |
S |
O |
+3,000 |
||
Fluazifop |
ISO |
H |
P |
L |
O |
3,330 |
|
Flubenzimine |
ISO |
AC |
S |
O |
3,000 |
||
Flucycloxuron |
ISO |
AC |
S |
O |
+5,000 |
||
Flufenoxuron |
ISO |
I |
S |
O |
+3,000 |
||
Flumetralin |
N(B) |
PGR |
S |
O |
+5,000 |
||
Flumetsulam |
ISO |
H |
S |
O |
+5,000 |
||
Fluometuron |
ISO |
H |
S |
O |
+8,000 |
||
Fluorodifen |
ISO |
H |
S |
O |
9,000 |
||
Fluoromide |
N(J) |
F |
S |
O |
+10,000 |
||
Flupropanate |
ISO |
H |
S |
O |
+10,000 |
||
Flurecol butyl |
See flurenol |
||||||
Flurenol |
ISO |
PGR |
S |
O |
+5,000 |
||
Fluridone |
ISO |
H |
S |
O |
+10,000 |
||
Flurochloridone |
ISO |
H |
S |
O |
4,000 |
||
Fluthiacet |
ISO |
H |
S |
O |
+5,000 |
||
Fluroxypyr |
N(B) |
H |
S |
O |
+5,000 |
||
Fluthiacet |
ISO |
H |
S |
O |
+5,000 |
||
Flutolanil |
ISO |
F |
S |
O |
+10,000 |
||
Tau-fluvalinate |
ISO |
I |
PY |
oil |
O |
+3,000 |
Skin and eye irritant |
Folpet |
ISO |
F |
S |
O |
+10,000 |
HSG 72 |
|
Fosamine |
ISO |
H |
S |
O |
2,400 |
||
Fosetyl |
N(B) |
F |
S |
O |
5,800 |
||
Furmecyclox |
N(B) |
FST |
S |
O |
3,780 |
||
Gibberellic acid |
N(B) |
PGR |
S |
O |
+10,000 |
||
Glyphosate |
ISO |
H |
S |
O |
4,230 |
EHC 159, DS 91 |
|
Glyphosine |
ISO |
H |
S |
O |
3,920 |
Continues on next page.
Table 5. List of of technical products unlikely to present acute hazard in normal use (continued)
Name | Status | Main use | Chemical type | Physical state | Route | LD50 (mg/kg) | Remarks |
Hexaconazole |
N(B) |
F |
S |
O |
2,180 |
||
Hexaflumuron |
ISO |
I |
S |
O |
+5,000 |
||
Hexythiazox |
N(B) |
AC |
S |
O |
+5,000 |
||
Hydroprene |
N(A) |
IGR |
L |
O |
+10,000 |
||
2-Hydroxyethyl octyl sulphide |
C |
RP (insect) |
L |
O |
8,530 |
||
Hydroxyisoxazole |
N(J) |
See hymexazol |
|||||
Hymexazol |
N(B) |
FST |
S |
O |
3,900 |
||
Imazamethabenz-methyl |
(ISO) |
H |
S |
O |
+5,000 |
||
Imazapyr |
ISO |
H |
S |
O |
+5,000 |
Irritant to eyes |
|
Imazaquin |
ISO |
H |
S |
O |
+5,000 |
||
Imazethapyr |
N(B) |
H |
S |
O |
+5,000 |
||
Imibenconazole |
ISO |
F |
S |
O |
+5,000 |
||
Inabenfide |
ISO |
PGR |
S |
O |
+10,000 |
||
Iodofenphos |
N(A,B) |
See jodfenphos |
|||||
Iprodione |
ISO |
F |
S |
O |
3,500 |
||
Isopropalin |
ISO |
H |
L |
O |
+5,000 |
||
Isoxaben |
N(B) |
H |
S |
O |
+10,000 |
||
Jodfenphos |
ISO |
I |
OP |
S |
O |
2,100 |
DS 43 |
Karbutilate |
ISO |
H |
S |
O |
3,000 |
||
Kasugamycin |
N(J) |
F |
S |
O |
+10,000 |
||
Kinoprene |
ISO |
IGR |
S |
O |
4,900 |
||
Lenacil |
ISO |
H |
S |
O |
+10,000 |
||
Linuron |
ISO |
H |
S |
O |
4,000 |
||
Maleic hydrazide |
ISO |
PGR |
S |
O |
6,950 |
||
Mancozeb |
ISO |
F |
TC |
S |
O |
+8,000 |
Irritant to skin on multiple exposure; DS 94 |
Maneb |
ISO |
F |
TC |
S |
O |
6,750 |
Irritant to skin on multiple exposure; DS 94 |
Mefenacet |
ISO |
H |
S |
O |
+5,000 |
||
Mepanipyrim |
ISO |
F |
S |
O |
+5,000 |
||
Mepronil |
N(J) |
F |
S |
O |
+10,000 |
||
Metamitron |
ISO |
H |
S |
O |
3,343 |
||
Metazachlor |
ISO |
H |
S |
O |
2,150 |
||
Methabenzthiazuron |
ISO |
H |
S |
O |
+2,500 |
||
Methoprene |
ISO |
IGR |
L |
O |
+10,000 |
DS 47 |
|
Methoprotryne |
ISO |
H |
S |
O |
+5,000 |
||
Methoxychlor |
ISO |
I |
OC |
S |
O |
6,000 |
DS 28 |
Methoxyphenone |
N(J) |
H |
S |
O |
+4,000 |
||
Methyldymron |
N(J) |
H |
S |
O |
3,948 |
||
Metiram |
N(J) |
F |
S |
O |
+10,000 |
||
Metobromuron |
ISO |
H |
S |
O |
2,500 |
||
Metosulam |
ISO |
H |
S |
O |
+5,000 |
||
Metoxuron |
ISO |
H |
S |
O |
+3,200 |
||
Metribuzin |
ISO |
H |
T |
S |
O |
2,200 |
|
Metsulfovax |
ISO |
F |
S |
O |
3,929 |
||
Metsulfuron |
N(A,B) |
H |
S |
O |
+5,000 |
||
Monalide |
ISO |
H |
S |
O |
+4,000 |
||
Monolinuron |
ISO |
H |
S |
O |
2,250 |
||
Monuron |
ISO |
H |
S |
O |
3,600 |
||
Monuron-TCA |
N(A) |
H |
S |
O |
3,700 |
||
Naphthalene |
C |
F |
S |
O |
2,200 |
||
Naphthalic anhydride |
C |
PGR |
S |
O |
+10,000 |
||
2-(1-naphthyl) acetamide |
ISO |
PGR |
S |
O |
6,400 |
||
1-naphthylacetic acid |
ISO |
PGR |
S |
O |
c3,000 |
||
Napropamide |
ISO |
H |
S |
O |
5,000 |
||
Naptalam |
ISO |
PGR |
S |
O |
8,200 |
||
Neburon |
ISO |
H |
S |
O |
+10,000 |
||
Niclosamide |
ISO |
M |
S |
O |
5,000 |
DS 63 |
|
Nicosulfuron |
ISO |
H |
S |
O |
+5,000 |
Irritant to eyes |
|
Nitralin |
ISO |
H |
S |
O |
+2,000 |
||
Nitrothal-isopropyl |
ISO |
F |
S |
O |
6,400 |
||
Norflurazon |
ISO |
H |
S |
O |
+8,000 |
||
(octylthio)ethanol |
C |
See 2-hydroxyethyl octyl sulphide |
|||||
Ofurace |
ISO |
F |
S |
O |
2,600 |
||
Oryzalin |
ISO |
H |
S |
O |
+10,000 |
||
Oxabetrinil |
ISO |
H |
S |
O |
+5,000 |
||
Oxadiazon |
ISO |
H |
S |
O |
+8,000 |
||
Oxine copper |
ISO |
F |
S |
O |
10,000 |
||
Oxycarboxin |
ISO |
F |
S |
O |
2,000 |
||
Oxyfluorfen |
ISO |
H |
S |
O |
+5,000 |
||
Penconazole |
N(B) |
F |
S |
O |
2,120 |
||
Pencycuron |
ISO |
F |
S |
O |
+5,000 |
||
Pentanochlor |
ISO |
H |
S |
O |
+10,000 |
||
Phenisobromolate |
N(J) |
See bromopropylate |
|||||
Phenisopham |
ISO |
H |
S |
O |
+4,000 |
||
Phenmedipham |
ISO |
H |
S |
O |
+8,000 |
||
Phenothrin |
ISO |
I |
PY |
L |
O |
+5,000 |
DS 85; EHC 96; HSG 32 |
2-Phenylphenol |
ISO |
F |
S |
O |
2,480 |
||
Phosdiphen |
N(J) |
F |
L |
O |
6,200 |
||
Phthalide |
N(J) |
F |
S |
O |
+10,000 |
||
Picloram |
ISO |
H |
S |
O |
8,200 |
||
Piperonyl butoxide |
N(A) |
SY |
oil |
O |
+7,500 |
||
Pretilachlor |
ISO |
H |
L |
O |
6,100 |
||
Primisulfuron |
ISO |
H |
S |
O |
+5,050 |
||
Probenazole |
N(J) |
F |
S |
O |
2,030 |
||
Procymidone |
ISO |
F |
S |
O |
6,800 |
||
Prodiamine |
ISO |
H |
S |
O |
+5,000 |
||
Profluralin |
ISO |
H |
S |
O |
c10,000 |
||
Proglinazine |
ISO |
H |
S |
O |
+8,000 |
||
Prometon |
ISO |
H |
T |
S |
O |
2,980 |
|
Prometryn |
ISO |
H |
T |
S |
O |
3,150 |
|
Pronamide |
N(A) |
See propyzamide |
|||||
Propamocarb |
ISO |
F |
S |
O |
8,600 |
||
Propaquizafop |
ISO |
H |
S |
O |
+5,000 |
||
Propazine |
ISO |
H |
T |
S |
O |
+5,000 |
|
Propham |
ISO |
H |
S |
O |
5,000 |
||
Propineb |
ISO |
H |
TC |
S |
O |
8,500 |
|
Propyzamide |
ISO |
H |
S |
O |
5,620 |
||
Pyracarbolid |
ISO |
F |
S |
O |
+10,000 |
||
Pyrazolynate |
ISO |
H |
S |
O |
9,550 |
||
Pyrazon |
N(A) |
See chloridazon |
|||||
Pyrazosulfuron |
ISO |
H |
S |
O |
+5,000 |
||
Pyrimethanil |
ISO |
F |
S |
O |
4,150 |
||
Pyriminobac |
ISO |
H |
S |
O |
+5,000 |
||
Pyriproxyfen |
N(B) |
I |
S |
O |
+5,000 |
||
Quinclorac |
ISO |
H |
S |
O |
2,680 |
||
Quinmerac |
ISO |
H |
S |
O |
+5,000 |
||
Quinomethinoate |
N(B) |
See chinomethionat |
|||||
Quinonamid |
ISO |
F |
S |
O |
+10,000 |
||
Quintozene |
ISO |
F |
S |
O |
+10,000 |
EHC 41 |
|
Rimsulfuron |
C |
H |
S |
O |
+5,000 |
||
Secbumeton |
ISO |
H |
T |
S |
O |
2,680 |
|
Siduron |
ISO |
H |
S |
O |
+7,500 |
||
Simazine |
ISO |
H |
T |
S |
O |
+5,000 |
|
Sodium metaborate |
C |
See borax |
|||||
Sodium trichloracetate |
The data shown refer to sodium trichloroacetic acid. In many countries, the term TCA refers to the free acid (now accepted by ISO): this is a solid with an oral LD50 of 400 mg/kg and if used as a pesticide is placed in Class II. It is highly corrosive to skin |
||||||
Solan |
N(A) |
See pentanochlor |
|||||
Stirofos |
N(A) |
See tetrachlorvinphos |
|||||
Sulfometuron |
N(B) |
H |
S |
O |
+5,000 |
||
Sulfur |
N(A,J) |
See sulphur |
|||||
Sulphur |
ISO |
F,I |
S |
O |
+3,000 |
Irritant to skin and mucous membranes. Sulphur dust can spontaneously ignite unless diluted about 50% with inert material |
|
TCA |
ISO |
H |
S |
O |
3,200 |
Irritant to skin and eyes; see sodium trichloracetate |
|
Tebuconazole |
ISO |
F |
S |
O |
4,000 |
||
Tebutam |
ISO |
H |
oil |
O |
6,210 |
||
Tecnazene |
ISO |
F |
S |
O |
+10,000 |
EHC 42; HSG 12 |
|
Tedion |
N(U) |
See tetradifon |
|||||
Teflubenzuron |
N(B) |
I |
S |
O |
+5,000 |
||
Temephos |
ISO |
I |
OP |
L |
O |
8,600 |
DS 8 |
Terbacil |
ISO |
H |
S |
O |
+5,000 |
||
Terbuthylazine |
ISO |
H |
T |
S |
O |
2,160 |
|
Terbutryn |
ISO |
H |
T |
S |
O |
2,400 |
|
Tetrachlorvinphos |
ISO |
I |
OP |
S |
O |
4,000 |
|
Tetradifon |
ISO |
AC |
S |
O |
+10,000 |
EHC 67; HSG 11 |
|
Tetramethrin |
ISO |
O |
PY |
S |
O |
+5,000 |
EHC 98; HSG 31 |
Tetrasul |
ISO |
AC |
S |
O |
6,810 |
||
Thiabendazole |
ISO |
F |
S |
O |
3,330 |
||
Thidiazuron |
ISO |
PGR |
S |
O |
+4,000 |
||
Thifensulfuron |
N(B) |
H |
S |
O |
+5,000 |
||
Thiophanate |
ISO |
F |
S |
O |
+10,000 |
||
Thiophanate-methyl |
ISO |
F |
S |
O |
+6,000 |
||
Tiocarbazil |
ISO |
H |
TC |
L |
O |
10,000 |
|
Tolclofos-methyl |
ISO |
F-S |
S |
O |
c5,000 |
||
Tolyfluanid |
ISO |
F |
S |
O |
+5,000 |
||
Transfluthrin |
ISO |
I |
PY |
S |
O |
+5,000 |
|
Triasulfuron |
ISO |
H |
S |
O |
+5,000 |
||
Tribenuron |
N(B) |
H |
S |
O |
+5,000 |
||
Trichlamide |
ISO |
F |
S |
O |
+5,000 |
||
Trietazine |
ISO |
H |
T |
S |
O |
2,830 |
|
Trifluralin |
ISO |
H |
S |
O |
+10,000 |
||
Triflumuron |
ISO |
PGR |
S |
O |
+5,000 |
||
Triforine |
ISO |
F |
S |
O |
+6,000 |
||
Triticonazole |
N(B) |
F |
triazole |
S |
O |
+2,000 |
|
Validamycin |
N(J) |
F |
S |
O |
+10,000 |
||
Vinclozolin |
ISO |
F |
S |
O |
10,000 |
||
Zineb |
ISO |
F |
S |
O |
+5,000 |
DS 94 |
Source: WHO 1996.
Table 6. Technical products not included in the WHO Classification and believed to be obsolete or discontinued for use as pesticides
Allyxycarb |
Dinex |
Methacarbate |
Table 7. List of gaseous or volatile fumigants not classified under the WHO Recommended Classification of Pesticides by Hazard
Acrylonitrile (EHC 28; HSG 1) |
Ethylene dichloride (EHC 176) |
Note: The WHO Classification does not set out any criteria for air concentrations on which classification could be based. Most of these compounds are of high hazard and recommended exposure limits for occupational exposure have been adopted by national authorities in many countries.
Source: WHO 1996.
The entries and abbrevations used in the tables’ various columns are explained here under the corresponding heading.
Name
The first column in the tables list the approved name of active ingredients. Trade names are not listed since there are many of these.
Status
The following abbreviations are used:
Main use
In most cases only a single use is given. This is only for identification purposes and does not exclude other uses. The following abbreviations are used:
Chemical type
A limited number of chemical types are shown in this column. Most have some significance in the sense that they may have a common antidote or may be confused in the nomenclature with other chemical types. For example, thiocarbamates are not cholinesterase inhibitors and do not have the same effects as carbamates. The following abbreviations are used:
These chemical classification are included only for convenience and do not represent a recommendation on the part of the WHO as to the way in which pesticides should be classified. It should, furthermore, be understood that some pesticides may fall into more than one type.
Chemical type is not shown where it is apparent from the name.
Physical state
This refers only to the technical compound. The following are used:
It may happen in a few cases that where the technical product is a solid, highly concentrated liquid formulations may need to be classified in a more hazardous class. In most cases, oils have been classified as liquids unless very viscous at ordinary temperatures.
Route
Oral route values are used unless the dermal route values place the compound in a hazardous class or the dermal values are significantly lower than the oral values, although in the same class. The following abbreviations are used:
LD50 (mg/kg)
The LD50 value is a statistical estimate of the number of mg of toxicant per kg of body weight required to kill 50% of a large population of test animals; the rat is used unless otherwise states. A single value is given: “c” preceding the value indicates that it is a value within a wider than usual range, adopted for classification purposes; “+” preceding the value indicates that the kill at the stated dose was less than 50% of the test animals.
The toxicity data for pyrethroids are highly variable according to isomer ratios, the vehicle for oral administration and the husbandry of the test animals. The variability is reflected in the prefix “c”. The single LD50 value now chosen for classification purposes is based on administration in corn oil and is much lower than that in aqueous solutions. This has resulted in considerable changes in the classification of some products and also underlines the need for classification by formulation if labelling is to reflect true hazard.
The figures in this column are not median values; rather, a safety margin is incorporated by choosing the lower confidence limit in most cases. Where a sex difference occurs in LD50 values, the value for the more sensitive sex is used. A number of classification adjustments have been made in respect of some pesticides and these are explained. A borderline case has been classified in the more or less hazardous class after consideration of its toxicology and use experience.
In table 5, a number of pesticides are listed as unlikely to present any acute hazard in normal use. The WHO Classification is open-ended but it is clear that there must be a point at which the acute hazard posed by the use of these compounds is so low as to be negligible provided that the necessary precautions are taken. For the purposes of this table, it has been assumed that this point is an oral LD50 of 2,000 mg/kg for solids and 3,000 mg/kg for liquids. However, it should not be overlooked that in formulations of these technical products, solvents or vehicles may present a greater hazard than the actual pesticide and therefore classification of a formulation in one of the higher hazard classes may be necessary.
Biological pesticides are not included in the WHO Classification because the methods of the safety testing of live biological agents are not appropriate to classification procedures applied to chemical compounds.
Remarks
Where the classification of a technical product has been adjusted, the basis for this is indicated in this column. Major irritant properties are noted; these do not affect classification. Where the name of a technical product is cross-referenced, the referenced product will be found in the same table. Abbreviations are used to indicate that a WHO/FAO Data Sheet (DS) or an issue of International Programme on Chemical Safety (IPCS) Environmental Health Criteria (EHC) Series or Health and Safety Guide contains further information on the product; the relevant issue numbers follow the abbreviations.
CONTENTS
Chapter Editor Gunnar Nordberg
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 |
|
|
Aluminium nitrate 13473-90-0 |
Al2(NO3)3 |
5.1 |
|
Aluminium phosphide 20859-73-8 |
AlP |
|
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 |
|
8 |
|
Triethylaluminium 97-93-8 |
AlC6H15 |
4.2 |
|
Triisobutylaluminium 100-99-2 |
AlC12H27 |
4.2 |
|
Antimony 7440-36-0 |
Sb |
|
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 |
|
|
Stibine 7803-52-3 |
SbH3 |
|
2.3/ 2.1 |
Arsenic 7440-38-2 |
As |
|
6.1 |
Arsenic acid, copper salt 10103-61-4 |
CuAsOH4 |
|
|
Arsenic acid, diammonium salt 7784-44-3 |
(NH4)2AsOH4 |
|
|
Arsenic acid, disodium salt 7778-43-0 |
Na2AsOH4 |
|
|
Arsenic acid, magnesium salt 10103-50-1 |
MgxAsO3H4 |
|
6.1 |
Arsenic acid, monopotassium salt 7784-41-0 |
KAsO2H4 |
|
|
Arsenic pentoxide 1303-28-2 |
As2O5 |
|
6.1 |
Arsenic trioxide 1327-53-3 |
As2O3 |
|
6.1 |
Arsenious acid, copper(2+) salt(1:1) 10290-12-7 |
CuAsH3 |
|
6.1 |
Arsenious acid, lead(II) salt 10031-13-7 |
PbAs2O4 |
|
|
Arsenious acid, potassium salt 10124-50-2 |
(KH3)x AsO3 |
|
6.1 |
Arsenous trichloride 7784-34-1 |
AsCl3 |
|
6.1 |
Arsine 7784-42-1 |
AsH3 |
|
2.3/ 2.1 |
Calcium arsenate 7778-44-1 |
Ca3As2O8 |
|
6.1 |
Lead arsenate 7784-40-9 |
PbAsO4H |
|
6.1 |
Methylarsonic acid 124-58-3 |
AsCH503 |
|
|
Sodium arsenate 10048-95-0 |
Na2AsO4H ·7H2O |
|
6.1 |
Barium 7440-39-3 |
Ba |
|
4.3 |
Barium carbonate 513-77-9 |
BaCO3 |
6.1 |
|
Barium chlorate 13477-00-4 |
BaCl2O6 |
|
5.1/ 6.1 |
Barium chloride 10361-37-2 |
BaCl2 |
|
6.1 |
Barium chloride, dihydrate 10326-27-9 |
BaCl2·2H20 |
|
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 |
|
6.1 |
Barium perchlorate 13465-95-7 |
BaCl2O8 |
5.1/ 6.1 |
|
Barium peroxide 1304-29-6 |
BaO2 |
|
5.1/ 6.1 |
Barium sulphate 7727-43-7 |
BaSO4 |
|
6.1 |
Beryllium 7440-41-7 |
Be |
6.1 |
|
Beryllium oxide 1304-56-9 |
BeO |
6.1 |
|
Cadmium 7440-43-9 |
Cd |
|
|
Cadmium acetate 543-90-8 |
Cd(C2H4O2)2 |
6.1 |
|
Cadmium chloride 10108-64-2 |
CdCl2 |
|
6.1 |
Cadmium oxide 1306-19-0 |
CdO |
|
6.1 |
Cadmium suphate 10124-36-4 |
CdSO4 |
6.1 |
|
Cadmium sulphide 1306-23-6 |
CdS |
|
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 |
|
8 |
Cobalt 7440-48-4 |
Co |
|
|
Cobalt chloride 7646-79-9 |
CoCl2 |
|
|
Cobalt (III) oxide 1308-04-9 |
Co2O3 |
|
|
Cobalt naphthenate 61789-51-3 |
CoC22H20O4 |
|
|
Copper 7440-50-8 |
Cu |
|
|
Copper (I) oxide 1317-39-1 |
Cu2O |
|
|
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 |
|
||
Ferric chloride 7705-08-0 |
FeCl3 |
8 |
|
Iron pentacarbonyl 13463-40-6 |
C5FeO5 |
6.1/ 3 |
|
Lead 7439-92-1 |
Pb |
|
|
Lead acetate 301-04-2 |
PbC4H6O4 |
|
6.1 |
Lead chromate 7758-97-6 |
PbCrO4 |
|
|
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 |
|
|
Naphthenic acid, Pb-salt 61790-14-5 |
|
||
Tetraethyl lead 78-00-2 |
PbC8H20 |
|
6.1 |
Tetramethyl lead 75-74-1 |
PbC4H12 |
6.1 |
|
Lithium aluminium hydride 16853-85-3 |
LiAlH4 |
4.3 |
|
Magnesium 7439-95-4 |
Mg |
|
4.1 |
Magnesium chloride 7786-30-3 |
MgCl2 |
|
5.1 |
Magnesium nitrate 10377-60-3 |
Mg(NO3)2 |
5.1 |
|
Magnesium oxide 1309-48-4 |
MgO |
|
|
Magnesium phosphide 12057-74-8 |
Mg3P2 |
|
4.3/ 6.1 |
Mercuric acetate 1600-27-7 |
HgC4H6O4 |
|
6.1 |
Mercuric bromide 7789-47-1 |
HgBr2 |
6.1 |
|
Mercuric chloride 7487-94-7 |
HgCl2 |
|
6.1 |
Mercuric nitrate 10045-94-0 |
Hg(NO3)2 |
|
6.1 |
Mercuric oxide 21908-53-2 |
HgO |
|
6.1 |
Mercuric sulphate 7783-35-9 |
HgSO4 |
|
6.1 |
Mercuric thiocyanate 592-85-8 |
HgC2N2S2 |
6.1 |
|
Mercurous chloride 10112-91-1 |
Hg2Cl2 |
|
|
Mercury 7439-97-6 |
Hg |
|
6.1 |
Phenylmercuric acetate 62-38-4 |
C8H8HgO2 |
|
6.1 |
Phenylmercuric nitrate 55-68-5 |
C6H5HgNO3 |
|
6.1 |
Nickel 7440-02-0 |
Ni |
|
|
Nickel (II) oxide 1313-99-1 |
NiO |
|
|
Nickel carbonate 3333-67-3 |
Ni2CO3 |
|
|
Nickel carbonyl 13463-39-3 |
NiC4O4 |
|
6.1/ 3 |
Nickel sulphide 12035-72-2 |
Ni3S2 |
|
|
Nickel sulphate 7786-81-4 |
NiSO4 |
|
|
Osmium tetroxide 20816-12-0 |
OsO4 |
|
6.1 |
Platinum tetrachloride 13454-96-1 |
PtCl4 |
|
|
Hydrogen selenide 7783-07-5 |
SeH2 |
|
2.3/ 2.1 |
Selenious acid 7783-00-8 |
SeH2O3 |
|
|
Selenious acid, disodium salt 10102-18-8 |
Na2SeO3 |
|
6.1 |
Selenium 7782-49-2 |
Se |
|
6.1 |
Selenium dioxide 7446-08-4 |
SeO2 |
|
|
Selenium hexafluoride 7783-79-1 |
SeF6 |
|
2.3/ 8 |
Selenium oxychloride 7791-23-3 |
SeOCl2 |
|
3/ 6.1 |
Selenium trioxide 13768-86-0 |
SeO3 |
|
|
Silver 7440-22-4 |
Ag |
|
|
Silver nitrate 7761-88-8 |
AgNO3 |
|
5.1 |
Strontium chromate 7789-06-2 |
SrCrH2O4 |
|
|
Tellurium 13494-80-9 |
Te |
|
6.1 |
Tellurium hexafluoride 7783-80-4 |
TeF6 |
2.3/ 8 |
|
Thallium 7440-28-0 |
Tl |
|
6.1 |
Thallous sulphate 7446-18-6 |
Tl2 (SO4)3 |
|
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 |
|
|
Dibutyltin dilaurate 77-58-7 |
SnC32H64O4 |
6.1 |
|
Stannic chloride 7646-78-8 |
SnCl4 |
|
8 |
Stannic oxide 18282-10-5 |
SnO |
|
|
Stannous chloride 7772-99-8 |
SnCl2 |
|
|
Stannous chloride dihydrate 10025-69-1 |
SnCl2 ·2H2O |
|
|
Stannous fluoride 7783-47-3 |
SnF2 |
|
|
Tin oxide 21651-19-4 |
SnO |
|
|
Titanium tetrachloride 7550-45-0 |
TiCl4 |
8 |
|
Titanium trichloride 7705-07-9 |
TiCl3 |
8 |
|
Vanadium pentoxide 1314-62-1 |
V2O5 |
|
6.1 |
Vanadium tetrachloride 7632-51-1 |
VCl4 |
8 |
|
Vanadium trioxide 1314-34-7 |
V2O3 |
|
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 |
|
4.3/ 6.1 |
Zinc stearate 557-05-1 |
ZnC36H70O4 |
|
|
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. |
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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.
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.
Gunner Nordberg
Occurrence and uses
Aluminium is the most abundant metal in the earth’s crust, where it is found in combination with oxygen, fluorine, silica, etc., but never in the metallic state. Bauxite is the principal source of aluminium. It consists of a mixture of minerals formed by the weathering of aluminium-bearing rocks. Bauxites are the richest form of these weathered ores, containing up to 55% alumina. Some lateritic ores (containing higher percentages of iron) contain up to 35% Al2O3· Commercial deposits of bauxite are mainly gibbsite (Al2O3·3H2O) and boehmite (Al2O3·H2O) and are found in Australia, Guyana, France, Brazil, Ghana, Guinea, Hungary, Jamaica and Suriname. World production of bauxite in 1995 was 111,064 million tonnes. Gibbsite is more readily soluble in sodium hydroxide solutions than boehmite and is therefore preferred for aluminium oxide production.
Aluminium is used widely throughout industry and in larger quantities than any other non-ferrous metal; worldwide primary metal production in 1995 was estimated at 20,402 million tonnes. It is alloyed with a variety of other material including copper, zinc, silicon, magnesium, manganese and nickel and may contain small amounts of chromium, lead, bismuth, titanium, zirconium and vanadium for special purposes. Aluminium and aluminium alloy ingots can be extruded or processed in rolling mills, wire-works, forges or foundries. The finished products are used in shipbuilding for internal fittings and superstructures; the electrical industry for wires and cables; the building industry for house and window frames, roofs and cladding; aircraft industry for airframes and aircraft skin and other components; automobile industry for bodywork, engine blocks and pistons; light engineering for domestic appliances and office equipment and in the jewellery industry. A major application of sheet is in beverage or food containers, while aluminium foil is used for packaging; a fine particulate form of aluminium is employed as a pigment in paints and in the pyrotechnics industry. Articles manufactured from aluminium are frequently given a protective and decorative surface finish by anodization.
Aluminium chloride is used in petroleum cracking and in the rubber industry. It fumes in air to form hydrochloric acid and combines explosively with water; consequently, containers should be kept tightly closed and protected from moisture.
Alkyl aluminium compounds. These are growing in importance as catalysts for the production of low-pressure polyethylene. They present a toxic, burn and fire hazard. They are extremely reactive with air, moisture and compounds containing active hydrogen and therefore must be kept under a blanket of inert gas.
Hazards
For the production of aluminium alloys, refined aluminium is melted in oil or gas-fired furnaces. A regulated amount of hardener containing aluminium blocks with a percentage of manganese, silicon, zinc, magnesium, etc. is added. The melt is then mixed and is passed into a holding furnace for degassing by passing either argon-chlorine or nitrogen-chlorine through the metal. The resultant gas emission (hydrochloric acid, hydrogen and chlorine) has been associated with occupational illnesses and great care should be taken to see that appropriate engineering controls capture the emissions and also prevent it from reaching the external environment, where it can also cause damage. Dross is skimmed off the surface of the melt and placed in containers to minimize exposure to air during cooling. A flux containing fluoride and/or chloride salts is added to the furnace to assist in separation of pure aluminium from the dross. Aluminium oxide and fluoride fumes may be given off so that this aspect of production must also be carefully controlled. Personal protective equipment (PPE) may be required. The aluminium smelting process is described in the chapter Metal processing and metal working industry. In the casting shops, exposure to sulphur dioxide may also occur.
A wide range of different crystalline forms of aluminium oxide is used as smelter feed stock, abrasives, refractories and catalysts. A series of reports published in 1947 to 1949 described a progressive, non-nodular interstitial fibrosis in the aluminium abrasives industry in which aluminium oxide and silicon were processed. This condition, known as Shaver’s disease, was rapidly progressive and often fatal. The exposure of the victims (workers producing alundum) was to a dense fume comprising aluminium oxide, crystalline free-silica and iron. The particulates were of a size range that made them highly respirable. It is likely that the preponderence of disease is attributable to the highly damaging lung effects of the finely divided crystalline free-silica, rather than to the inhaled aluminium oxide, although the exact aetiology of the disease is not understood. Shaver’s disease is primarily of historical interest now, since no reports have been made in the second half of the 20th century.
Recent studies of the health effects of high level exposures (100 mg/m3) to the oxides of aluminium amongst workers engaged in the Bayer process (described in the chapter Metal processing and metal working industry) have demonstrated that workers with more than twenty years of exposure can develop pulmonary alterations. These changes are clinically characterized by minor, predominantly asymptomatic degrees of restrictive pulmonary function changes. The chest x-ray examinations revealed small, scanty, irregular opacities, particularly at the lung bases. These clinical responses have been attributed to deposition of dust in the lung paraenchyma, which was the result of very high occupational exposures. These signs and symptoms cannot be compared to the extreme response of Shaver’s disease. It should be noted that other epidemiological studies in the United Kingdom regarding widespread alumina exposures in the pottery industry have produced no evidence that the inhalation of alumina dust produces chemical or radiographic signs of pulmonary disease or dysfunction.
The toxicological effects of aluminium oxides remain of interest because of its commerical importance. The results of animal experiments are controversial. An especially fine (0.02 μm to 0.04 μm), catalytically active aluminium oxide, uncommonly used commercially, can cause lung changes in animals dosed by injection directly into the lung airways. Lower dose effects have not been observed.
It should also be noted that so-called “potroom asthma” which has frequently been observed among workers in aluminium processing operations, is probably attributable to the exposures to fluoride fluxes, rather than to the aluminium dust itself.
The production of aluminium has been classified as a Group 1, known human carcinogenic exposure situation, by the International Agency for Research on Cancer (IARC). As with the other diseases described above, the carcinogenicity is most likely attributable to the other substances present (e.g., polycyclic aromatic hydrocarbons (PAHs) and silica dust), although the exact role of the alumina dusts are simply not understood.
Some data on the absorption of high levels of aluminium and nervous tissue damage are found among individuals requiring kidney dialysis. These high levels of aluminium have resulted in severe, even fatal brain damage. This response, however, has also been observed in other patients undergoing dialysis but who did not have similar elevated brain aluminium level. Animal experiments have been unsuccessful in replicating this brain response, or Alzheimer’s disease, which has also been postulated in the literature. Epidemiological and clinical follow-up studies on these issues have not been definitive and no evidence of such effects has been observed in the several large-scale epidemiological studies of aluminium workers.
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.
Gunnar Nordberg
There are three major groups of arsenic (As) compounds:
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:
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.
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.
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.
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.
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.
Gunnar Nordberg
Copper (Cu) is malleable and ductile, conducts heat and electricity exceedingly well and is very little altered in its functional capacity by exposure to dry air. In a moist atmosphere containing carbon dioxide it becomes coated with a green carbonate. Copper is an essential element in human metabolism.
Occurrence and Uses
Copper occurs principally as mineral compounds in which 63Cu constitutes 69.1% and 65Cu, 30.9% of the element. Copper is widely distributed in all continents and is present in most living organisms. Although some natural deposits of metallic copper have been found, it is generally mined either as sulphide ores, including covellite (CuS), chalcocite (Cu2S), chalcopyrite (CuFeS2) and bornite (Cu3FeS3); or as oxides, including malachite (Cu2CO3(OH)2); chrysocolla
(CuSiO3·2H2O) and chalcanthite (CuSO4·5H2O).
Because of its electrical properties, more than 75% of copper output is used in the electrical industries. Other applications for copper include water piping, roofing material, kitchenware, chemical and pharmaceutical equipment, and the production of copper alloys. Copper metal is also used as a pigment, and as a precipitant of selenium.
Alloys and Compounds
The most widely used non-ferrous copper alloys are those of copper and zinc (brass), tin (bronze), nickel (monel metal), aluminium, gold, lead, cadmium, chromium, beryllium, silicon or phosphorus.
Copper sulphate is used as an algicide and molluscicide in water; with lime, as a plant fungicide; as a mordant; in electroplating; as a froth flotation agent for the separation of zinc sulphide ore; and as an agent for leather tanning and hide preservation. Copper sulphate neutralized with hydrated lime, known as Bordeaux mixture, is used for the prevention of mildew in vineyards.
Cupric oxide has been used as a component of paint for ship bottoms and as a pigment in glass, ceramics, enamels, porcelain glazes and artificial gems. It is also used in the manufacture of rayon and other copper compounds, and as an optical glass polishing agent and a solvent for chromic iron ores. Cupric oxide is a component of flux in copper metallurgy, pyrotechnic compositions, welding fluxes for bronze and agricultural products such as insecticides and fungicides. Black cupric oxide is used for correcting copper-deficient soils and as a feed supplement.
Copper chromates are pigments, catalysts for liquid-phase hydrogenation and potato fungicides. A solution of cupric hydroxide in excess ammonia is a solvent for cellulose used in the manufacture of rayon (viscose). Cupric hydroxide is used in the manufacture of battery electrodes and for treating and staining paper. It is also a pigment, a feed additive, a mordant in dyeing and an ingredient in fungicides and insecticides.
Hazards
Amine complexes of cupric chlorate, cupric dithionate, cupric azide and cuprous acetylide are explosive but are of no industrial or public health importance. Copper acetylide was found to be the cause of explosions in acetylene plants and has caused the abandonment of the use of copper in the construction of such plants. Fragments of metallic copper or copper alloys that lodge in the eye, a condition known as chalcosis, may lead to uveitis, abscess and loss of the eye. Workers who spray vineyards with Bordeaux mixture may suffer from pulmonary lesions (sometimes called “vineyard sprayer’s lung”) and copper-laden hepatic granulomas.
Accidental ingestion of soluble copper salts is generally innocuous since the vomiting induced rids the patient of much of the copper. The possibility of copper-induced toxicity may occur in the following situations:
Acute toxicity
Although some chemical reference works contain statements to the effect that soluble salts of copper are poisonous, in practical terms this is true only if such solutions are used with misguided or suicidal intent, or as topical treatment of extensively burned areas. When copper sulphate, known as bluestone or blue vitriol, is ingested in gram quantities, it induces nausea, vomiting, diarrhoea, sweating, intravascular haemolysis and possible kidney failure; rarely, convulsions, coma and death may result. Drinking of carbonated water or citrus fruit juices which have been in contact with copper vessels, pipes, tubing or valves can cause gastrointestinal irritation, which is seldom serious. Such beverages are acidic enough to dissolve irritating levels of copper. There is a report of corneal ulcers and skin irritation, but little other toxicity, in a copper-mine worker who fell into an electrolytic bath, but the acidity, rather than the copper, may have been the cause. In some instances where copper salts have been used in the treatment of burns, high concentrations of serum copper and toxic manifestations have ensued.
The inhalation of dusts, fumes and mists of copper salts can cause congestion of the nasal and mucous membranes and ulceration with perforation of the nasal septum. Fumes from the heating of metallic copper can cause metal fume fever, nausea, gastric pain and diarrhoea.
Chronic toxicity
Chronic toxic effects in human beings attributable to copper appears only to be found in individuals who have inherited a particular pair of abnormal autosomal recessive genes and in whom, as a consequence, hepatolenticular degeneration (Wilson’s disease) develops. This is a rare occurrence. Most daily human diets contain 2 to 5 mg of copper, almost none of which is retained. The adult human body copper content is quite constant at about 100 to 150 mg. In normal individuals (without Wilson’s disease), almost all of the copper is present as an integral and functional moiety of one of perhaps a dozen proteins and enzyme systems including, for example, cytochrome oxidase, dopa-oxidase and serum ceruloplasmin.
Tenfold, or more, increases in the daily intake of copper can occur in individuals who eat large quantities of oysters (and other shellfish), liver, mushrooms, nuts and chocolate—all rich in copper; or in miners who may work and eat meals, for 20 years or more, in an atmosphere laden with 1 to 2% copper ores dusts. Yet evidence of primary chronic copper toxicity (well defined from observations of patients with inherited chronic copper toxicosis—Wilson’s disease—as dysfunction of and structural damage to the liver, central nervous system, kidney, bones and eyes) has never been found in any individuals except those with Wilson’s disease. However, the excessive copper deposits that are found in the livers of patients with primary biliary cirrhosis, cholestasis and Indian childhood cirrhosis may be one contributing factor to the severity of the hepatic disease that is characteristic of these conditions.
Safety and Health Measures
Workers exposed to copper dusts or mists should be provided with adequate protective clothing to prevent repeated or prolonged skin contact. Where dust conditions cannot be sufficiently controlled, appropriate respirators and eye protection are necessary. Housekeeping and the provision of adequate sanitary facilities is essential since eating, drinking and smoking should be prohibited at the worksite. In mines where there are water-soluble ores such as chalcanthite, workers should be particularly careful to wash their hands with water before eating.
The prevention of metal fume fever is a matter of keeping exposure below the level of concentration currently accepted as satisfactory for working with copper in industry. The employment of local exhaust ventilation (LEV) is a necessary measure to collect copper fumes at the source.
People with Wilson’s disease should avoid employment in copper industries. The serum concentration of ceruloplasmin is a screen for this condition, since unaffected individuals have levels which range from 20 to 50 mg/100 cm3 of this copper protein whereas 97% of patients with Wilson’s disease have less than 20 mg/100 cm3. This is a relatively expensive procedure for broad-based screening programmes.
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