International
Agencyfor Research on Cancer
International
Agency
Group 1: The agent (mixture) is carcinogenic to humans. The exposure circumstance entails exposures that are carcinogenic to humans.
Group 2 (two classifications):
Group 2A: The agent (mixture) is probably carcinogenic to
humans. The exposure circumstance entails exposures that are probably carcinogenic to
humans.
Group 2B: The agent (mixture) is possibly carcinogenic to humans.
The exposure circumstance entails exposures that are possibly carcinogenic to humans.
Group 3: The agent (mixture, or exposure circumstance) is unclassifiable as to carcinogenicity in humans.
Group 4: The agent (mixture, exposure circumstance) is probably not carcinogenic to humans.
This list contains all agents, mixtures and exposures evaluated as being in Group 1 to
date.
Where appropriate, chemical abstract numbers are given [in square brackets]. For details
of the evaluation, the relevant Monograph should be consulted (volume number given in
round brackets, followed by year of publication of latest evaluation). Use a free-text
search to find a particular compound
Aflatoxins, naturally occurring [1402-68-2] (Vol. 56; 1993)
4-Aminobiphenyl [92-67-1] (Vol. 1, Suppl. 7; 1987)
Arsenic [7440-38-2] and arsenic compounds (Vol. 23, Suppl. 7; 1987)
(NB: This evaluation applies to the group of compounds as a whole and not necessarily to
all individual compounds within the group)
Asbestos [1332-21-4] (Vol. 14, Suppl. 7; 1987)
Azathioprine [446-86-6] (Vol. 26, Suppl. 7; 1987)
Benzene [71-43-2] (Vol. 29, Suppl. 7; 1987)
Benzidine [92-87-5] (Vol. 29, Suppl. 7; 1987)
Beryllium [7440-41-7] and beryllium compounds (Vol. 58; 1993)
(NB: Evaluated as a group)
N,N-Bis(2-chloroethyl)-2-naphthylamine (Chlornaphazine) [494-03-1] (Vol. 4, Suppl. 7; 1987)
Bis(chloromethyl)ether [542-88-1] and chloromethyl methyl ether [107-30-2]
(technical-grade)
(Vol. 4, Suppl. 7; 1987)
1,4-Butanediol dimethanesulfonate (Busulphan; Myleran) [55-98-1] (Vol. 4, Suppl. 7; 1987)
Cadmium [7440-43-9] and cadmium compounds (Vol. 58; 1993)
(NB: Evaluated as a group)
Chlorambucil [305-03-3] (Vol. 26, Suppl. 7; 1987)
1-(2-Chloroethyl)-3-(4-methylcyclohexyl)-1-nitrosourea (Methyl-CCNU; Semustine) [13909-09-6] (Suppl. 7; 1987)
Chromium[VI] compounds (Vol. 49; 1990)
(NB: Evaluated as a group)
Ciclosporin [79217-60-0] (Vol. 50; 1990)
Cyclophosphamide [50-18-0] [6055-19-2] (Vol. 26, Suppl. 7; 1987)
Diethylstilboestrol [56-53-1] (Vol. 21, Suppl. 7; 1987)
Epstein-Barr virus (Vol. 70; 1997)
Erionite [66733-21-9] (Vol. 42, Suppl. 7; 1987)
Ethylene oxide [75-21-8] (Vol. 60; 1994)
(NB: Overall evaluation upgraded from 2A to 1 with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Helicobacter pylori (infection with) (Vol. 61; 1994)
Hepatitis B virus (chronic infection with) (Vol. 59; 1994)
Hepatitis C virus (chronic infection with) (Vol. 59; 1994)
Human immunodeficiency virus type 1 (infection with) (Vol. 67; 1996)
Human papillomavirus type 16 (Vol. 64; 1995)
Human papillomavirus type 18 (Vol. 64; 1995)
Human T-cell lymphotropic virus type I (Vol. 67; 1996)
Melphalan [148-82-3] (Vol. 9, Suppl. 7; 1987)
8-Methoxypsoralen (Methoxsalen) [298-81-7] plus ultraviolet A radiation (Vol. 24, Suppl. 7; 1987)
MOPP and other combined chemotherapy including alkylating agents (Suppl. 7; 1987)
Mustard gas (Sulfur mustard) [505-60-2] (Vol. 9, Suppl. 7; 1987)
2-Naphthylamine [91-59-8] (Vol. 4, Suppl. 7; 1987)
Nickel compounds (Vol. 49; 1990)
(NB: Evaluated as a group)
Oestrogen replacement therapy (Suppl. 7; 1987)
Oestrogens, nonsteroidal (Suppl. 7; 1987)
(NB: This evaluation applies to the group of compounds as a whole and not necessarily to
all individual compounds within the group)
Oestrogens, steroidal (Suppl. 7; 1987)
(NB: This evaluation applies to the group of compounds as a whole and not necessarily to
all individual compounds within the group)
Opisthorchis viverrini (infection with) (Vol. 61; 1994)
Oral contraceptives, combined (Suppl. 7; 1987)
(NB: There is also conclusive evidence that these agents have a protective effect against
cancers of the ovary and endometrium)
Oral contraceptives, sequential (Suppl. 7; 1987)
Radon [10043-92-2] and its decay products (Vol. 43; 1988)
Schistosoma haematobium (infection with) (Vol. 61; 1994)
Silica [14808-60-7], crystalline (inhaled in the form of quartz or cristobalite from
occupational sources)
(Vol. 68; 1997)
Solar radiation (Vol. 55; 1992)
Talc containing asbestiform fibres (Vol. 42, Suppl. 7; 1987)
Tamoxifen [10540-29-1] (Vol. 66; 1996)
(NB: There is also conclusive evidence that this agent (tamoxifen) reduces the risk of
contralateral breast cancer)
2,3,7,8-Tetrachlorodibenzo-para-dioxin [1746-01-6] (Vol. 69; 1997)
(NB: Overall evaluation upgraded from 2A to 1 with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Thiotepa [52-24-4] (Vol. 50; 1990)
Treosulfan [299-75-2] (Vol. 26, Suppl. 7; 1987)
Vinyl chloride [75-01-4] (Vol. 19, Suppl. 7; 1987)
Alcoholic beverages (Vol. 44; 1988)
Analgesic mixtures containing phenacetin (Suppl. 7; 1987)
Betel quid with tobacco (Vol. 37, Suppl. 7; 1987)
Coal-tar pitches [65996-93-2] (Vol. 35, Suppl. 7; 1987)
Coal-tars [8007-45-2] (Vol. 35, Suppl. 7; 1987)
Mineral oils, untreated and mildly treated (Vol. 33, Suppl. 7; 1987)
Salted fish (Chinese-style) (Vol. 56; 1993)
Shale-oils [68308-34-9] (Vol. 35, Suppl. 7; 1987)
Soots (Vol. 35, Suppl. 7; 1987)
Tobacco products, smokeless (Vol. 37, Suppl. 7; 1987)
Tobacco smoke (Vol. 38, Suppl. 7; 1987)
Wood dust (Vol. 62; 1995)
Aluminium production (Vol. 34, Suppl. 7; 1987)
Auramine, manufacture of (Suppl. 7; 1987)
Boot and shoe manufacture and repair (Vol. 25, Suppl. 7; 1987)
Coal gasification (Vol. 34, Suppl. 7; 1987)
Coke production (Vol. 34, Suppl. 7; 1987)
Furniture and cabinet making (Vol. 25, Suppl. 7; 1987)
Haematite mining (underground) with exposure to radon (Vol. 1, Suppl. 7; 1987)
Iron and steel founding (Vol. 34, Suppl. 7; 1987)
Isopropanol manufacture (strong-acid process) (Suppl. 7; 1987)
Magenta, manufacture of (Vol. 57; 1993)
Painter (occupational exposure as a) (Vol. 47; 1989)
Rubber industry (Vol. 28, Suppl. 7; 1987)
Strong-inorganic-acid mists containing sulfuric acid (occupational exposure to) (Vol. 54; 1992)
This list contains all agents, mixtures and exposures evaluated as being in Group 2A to
date.
Where appropriate, chemical abstract numbers are given [in square brackets]. For details
of the evaluation, the relevant Monograph should be consulted (volume number given in
round brackets, followed by year of publication of latest evaluation). Use a free-text
search to find a particular compound.
Acrylamide [79-06-1] (Vol. 60; 1994)
(NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Adriamycin [23214-92-8] (Vol. 10, Suppl. 7; 1987)
(NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Androgenic (anabolic) steroids (Suppl. 7; 1987)
Azacitidine [320-67-2] (Vol. 50; 1990)
(NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Benz[a]anthracene [56-55-3] (Vol. 32, Suppl. 7; 1987)
(NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Benzidine-based dyes (Suppl. 7; 1987)
(NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Benzo[a]pyrene [50-32-8] (Vol. 32, Suppl. 7; 1987)
(NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Bischloroethyl nitrosourea (BCNU) [154-93-8] (Vol. 26, Suppl. 7; 1987)
1,3-Butadiene [106-99-0] (Vol. 71; 1998)
Captafol [2425-06-1] (Vol. 53; 1991)
(NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Chloramphenicol [56-75-7] (Vol. 50; 1990)
(NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
a-Chlorinated toluenes (benzal chloride, benzotrichloride, benzyl chloride) and benzoyl chloride (combined exposures) (Vol. 29, Suppl. 7, Vol. 71; 1998)
1-(2-Chloroethyl)-3-cyclohexyl-1-nitrosourea (CCNU) [13010-47-4] (Vol. 26, Suppl. 7;
1987)
(NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
para-Chloro-ortho-toluidine [95-69-2] and its strong acid salts (Vol. 48;
1990)
(NB: Evaluated as a group)
Chlorozotocin [54749-90-5] (Vol. 50; 1990)
(NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Cisplatin [15663-27-1] (Vol. 26, Suppl. 7; 1987)
(NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Clonorchis sinensis (infection with) (Vol. 61; 1994)
(NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Dibenz[a,h]anthracene [53-70-3] (Vol. 32, Suppl. 7; 1987)
(NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Diethyl sulfate [64-67-5] (Vol. 54, Vol. 71; 1998)
Dimethylcarbamoyl chloride [79-44-7] (Vol. 12, Suppl. 7, Vol. 71; 1998)
(NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
1,2-Dimethylhydrazine [540-73-8] (Vol. 4, Vol. 71; 1998)
Dimethyl sulfate [77-78-1] (Vol. 4, Suppl. 7, Vol. 71; 1998)
(NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Epichlorohydrin [106-89-8] (Vol. 11, Suppl. 7, Vol. 71; 1998)
(NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Ethylene dibromide [106-93-4] (Vol. 15, Suppl. 7, Vol. 71; 1998)
(NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
N-Ethyl-N-nitrosourea [759-73-9] (Vol. 17, Suppl. 7; 1987)
(NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Formaldehyde [50-00-0] (Vol. 62; 1995)
Human papillomavirus type 31 (Vol. 64; 1995)
Human papillomavirus type 33 (Vol. 64; 1995)
IQ (2-Amino-3-methylimidazo[4,5-f]quinoline) [76180-96-6] (Vol. 56; 1993)
(NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Kaposi's sarcoma herpesvirus/human herpesvirus 8 (Vol. 70; 1997)
5-Methoxypsoralen [484-20-8] (Vol. 40, Suppl. 7; 1987)
(NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
4,4´-Methylene bis(2-chloroaniline) (MOCA) [101-14-4] (Vol. 57; 1993)
(NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Methyl methanesulfonate [66-27-3] (Vol. 7, Vol. 71; 1998)
N-Methyl-N´-nitro-N-nitrosoguanidine (MNNG) [70-25-7] (Vol. 4,
Suppl. 7; 1987)
(NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
N-Methyl-N-nitrosourea [684-93-5] (Vol. 17, Suppl. 7; 1987)
(NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Nitrogen mustard [51-75-2] (Vol. 9, Suppl. 7; 1987)
N-Nitrosodiethylamine [55-18-5] (Vol. 17, Suppl. 7; 1987)
(NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
N-Nitrosodimethylamine [62-75-9] (Vol. 17, Suppl. 7; 1987)
(NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Phenacetin [62-44-2] (Vol. 24, Suppl. 7; 1987)
Procarbazine hydrochloride [366-70-1] (Vol. 26, Suppl. 7; 1987)
(NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Styrene-7,8-oxide [96-09-3] (Vol. 60; 1994)
(NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Tetrachloroethylene [127-18-4] (Vol. 63; 1995)
Trichloroethylene [79-01-6] (Vol. 63; 1995)
1,2,3-Trichloropropane [96-18-4] (Vol. 63; 1995)
Tris(2,3-dibromopropyl)phosphate [126-72-7] (Vol. 20, Suppl. 7, Vol. 71; 1998)
(NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Ultraviolet radiation A (Vol. 55; 1992)
(NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Ultraviolet radiation B (Vol. 55; 1992)
(NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Ultraviolet radiation C (Vol. 55; 1992)
(NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Vinyl bromide [593-60-2] (Vol. 39, Suppl. 7, Vol. 71; 1998)
(NB: Overall evaluation upgraded from 2B to 2A with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Vinyl fluoride [75-02-5] (Vol. 63; 1995)
Creosotes [8001-58-9] (Vol. 35, Suppl. 7; 1987)
Diesel engine exhaust (Vol. 46; 1989)
Hot mate (Vol. 51; 1991)
Non-arsenical insecticides (occupational exposures in spraying and application of) (Vol. 53; 1991)
Polychlorinated biphenyls [1336-36-3] (Vol. 18, Suppl. 7; 1987)
Art glass, glass containers and pressed ware (manufacture of) (Vol. 58; 1993)
Hairdresser or barber (occupational exposure as a) (Vol. 57; 1993)
Petroleum refining (occupational exposures in) (Vol. 45; 1989)
Sunlamps and sunbeds (use of) (Vol. 55; 1992)
This list contains all agents, mixtures and exposures evaluated as being in Group 2B. Where appropriate, chemical abstract numbers are given [in square brackets]. For details of the evaluation, the relevant Monograph should be consulted (volume number given in round brackets, followed by year of publication of latest evaluation). Use a free-text search to find a particular compound.
A-a-C (2-Amino-9H-pyrido[2,3-b]indole) [26148-68-5] (Vol. 40, Suppl. 7; 1987)
Acetaldehyde [75-07-0] (Vol. 36, Suppl. 7, Vol. 71; 1998)
Acetamide [60-35-5] (Vol. 7, Suppl. 7, Vol. 71; 1998)
Acrylonitrile [107-13-1] (Vol. 71; 1998)
AF-2 [2-(2-Furyl)-3-(5-nitro-2-furyl)acrylamide] [3688-53-7] (Vol. 31, Suppl. 7; 1987)
Aflatoxin M1 [6795-23-9] (Vol. 56; 1993)
para-Aminoazobenzene [60-09-3] (Vol. 8, Suppl. 7; 1987)
ortho-Aminoazotoluene [97-56-3] (Vol. 8, Suppl. 7; 1987)
2-Amino-5-(5-nitro-2-furyl)-1,3,4-thiadiazole [712-68-5] (Vol. 7, Suppl. 7; 1987)
Amitrole [61-82-5] (Vol. 41, Suppl. 7; 1987)
ortho-Anisidine [90-04-0] (Vol. 27, Suppl. 7; 1987)
Antimony trioxide [1309-64-4] (Vol. 47; 1989)
AramiteŽ [140-57-8] (Vol. 5, Suppl. 7; 1987)
Atrazine [1912-24-9] (Vol. 53; 1991)
(NB: Overall evaluation upgraded from 3 to 2B with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Auramine [492-80-8] (technical-grade) (Vol. 1, Suppl. 7; 1987)
Azaserine [115-02-6] (Vol. 10, Suppl. 7; 1987)
Aziridine [151-56-4] (Vol. 9, Vol. 71; 1998)
Benzo[b]fluoranthene [205-99-2] (Vol. 32, Suppl. 7; 1987)
Benzo[j]fluoranthene [205-82-3] (Vol. 32, Suppl. 7; 1987)
Benzo[k]fluoranthene [207-08-9] (Vol. 32, Suppl. 7; 1987)
Benzofuran [271-89-6] (Vol. 63; 1995)
Benzyl violet 4B [1694-09-3] (Vol. 16, Suppl. 7; 1987)
Bleomycins [11056-06-7] (Vol. 26, Suppl. 7; 1987)
(NB: Overall evaluation upgraded from 3 to 2B with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Bracken fern (Vol. 40, Suppl. 7; 1987)
Bromodichloromethane [75-27-4] (Vol. 52, Vol. 71; 1998)
Butylated hydroxyanisole (BHA) [25013-16-5] (Vol. 40, Suppl. 7; 1987)
b-Butyrolactone [3068-88-0] (Vol. 11, Suppl. 7, Vol. 71; 1998)
Caffeic acid [331-39-5] (Vol. 56; 1993)
Carbon black [1333-86-4] (Vol. 65; 1996)
Carbon tetrachloride [56-23-5] (Vol. 20, Suppl. 7, Vol. 71; 1998)
Catechol [120-80-9] (Vol. 15, Vol. 71; 1998)
Ceramic fibres (Vol. 43; 1988)
Chlordane [57-74-9] (Vol. 53; 1991)
Chlordecone (Kepone) [143-50-0] (Vol. 20, Suppl. 7; 1987)
Chlorendic acid [115-28-6] (Vol. 48; 1990)
para-Chloroaniline [106-47-8] (Vol. 57; 1993)
Chloroform [67-66-3] (Vol. 20, Suppl. 7; 1987)
1-Chloro-2-methylpropene [513-37-1] (Vol. 63; 1995)
Chlorophenoxy herbicides (Vol. 41, Suppl. 7; 1987)
4-Chloro-ortho-phenylenediamine [95-83-0] (Vol. 27, Suppl. 7; 1987)
Chloroprene [126-99-8] (Vol. 71; 1998)
CI Acid Red 114 [6459-94-5] (Vol. 57; 1993)
CI Basic Red 9 [569-61-9] (Vol. 57; 1993)
CI Direct Blue 15 [2429-74-5] (Vol. 57; 1993)
Citrus Red No. 2 [6358-53-8] (Vol. 8, Suppl. 7; 1987)
Cobalt [7440-48-4] and cobalt compounds (Vol. 52; 1991)
(NB: Evaluated as a group)
para-Cresidine [120-71-8] (Vol. 27, Suppl. 7; 1987)
Cycasin [14901-08-7] (Vol. 10, Suppl. 7; 1987)
Dacarbazine [4342-03-4] (Vol. 26, Suppl. 7; 1987)
Dantron (Chrysazin; 1,8-Dihydroxyanthraquinone) [117-10-2] (Vol. 50; 1990)
Daunomycin [20830-81-3] (Vol. 10, Suppl. 7; 1987)
DDT [p,p'-DDT, 50-29-3] (Vol. 53; 1991)
N,N'-Diacetylbenzidine [613-35-4] (Vol. 16, Suppl. 7; 1987)
2,4-Diaminoanisole [615-05-4] (Vol. 27, Suppl. 7; 1987)
4,4'-Diaminodiphenyl ether [101-80-4] (Vol. 29, Suppl. 7; 1987)
2,4-Diaminotoluene [95-80-7] (Vol. 16, Suppl. 7; 1987)
Dibenz[a,h]acridine [226-36-8] (Vol. 32, Suppl. 7; 1987)
Dibenz[a,j]acridine [224-42-0] (Vol. 32, Suppl. 7; 1987)
7H-Dibenzo[c,g]carbazole [194-59-2] (Vol. 32, Suppl. 7; 1987)
Dibenzo[a,e]pyrene [192-65-4] (Vol. 32, Suppl. 7; 1987)
Dibenzo[a,h]pyrene [189-64-0] (Vol. 32, Suppl. 7; 1987)
Dibenzo[a,i]pyrene [189-55-9] (Vol. 32, Suppl. 7; 1987)
Dibenzo[a,l]pyrene [191-30-0] (Vol. 32, Suppl. 7; 1987)
1,2-Dibromo-3-chloropropane [96-12-8] (Vol. 20, Suppl. 7, Vol. 71; 1998)
para-Dichlorobenzene [106-46-7] (Vol. 29, Suppl. 7; 1987)
3,3'-Dichlorobenzidine [91-94-1] (Vol. 29, Suppl. 7; 1987)
3,3'-Dichloro-4,4'-diaminodiphenyl ether [28434-86-8] (Vol. 16, Suppl. 7; 1987)
1,2-Dichloroethane [107-06-2] (Vol. 20, Vol. 71; 1998)
Dichloromethane (methylene chloride) [75-09-2] (Vol. 71; 1998)
1,3-Dichloropropene [542-75-6] (technical-grade) (Vol. 41, Suppl. 7, Vol. 71; 1998)
Dichlorvos [62-73-7] (Vol. 53; 1991)
Di(2-ethylhexyl)phthalate [117-81-7] (Vol. 29, Suppl. 7; 1987)
1,2-Diethylhydrazine [1615-80-1] (Vol. 4, Vol. 71; 1998)
Diglycidyl resorcinol ether [101-90-6] (Vol. 36, Vol. 71; 1998)
Dihydrosafrole [94-58-6] (Vol. 10, Suppl. 7; 1987)
Diisopropyl sulfate [2973-10-6] (Vol. 54, Vol. 71; 1998)
3,3'-Dimethoxybenzidine (ortho-Dianisidine) [119-90-4] (Vol. 4, Suppl. 7; 1987)
para-Dimethylaminoazobenzene [60-11-7] (Vol. 8, Suppl. 7; 1987)
trans-2-[(Dimethylamino)methylimino]-5-[2-(5-nitro-2-furyl)-vinyl]-1,3,4-oxadiazole
[25962-77-0]
(Vol. 7, Suppl. 7; 1987)
2,6-Dimethylaniline (2,6-Xylidine) [87-62-7] (Vol. 57; 1993)
3,3'-Dimethylbenzidine (ortho-Tolidine) [119-93-7] (Vol. 1, Suppl. 7; 1987)
1,1-Dimethylhydrazine [57-14-7] (Vol. 4, Vol. 71; 1998)
3,7-Dinitrofluoranthene [105735-71-5] (Vol. 65; 1996)
3,9-Dinitrofluoranthene [22506-53-2] (Vol. 65; 1996)
1,6-Dinitropyrene [42397-64-8] (Vol. 46; 1989)
1,8-Dinitropyrene [42397-65-9] (Vol. 46; 1989)
2,4-Dinitrotoluene [121-14-2] (Vol. 65; 1996)
2,6-Dinitrotoluene [606-20-2] (Vol. 65; 1996)
1,4-Dioxane [123-91-1] (Vol. 11, Suppl. 7, Vol. 71; 1998)
Disperse Blue 1 [2475-45-8] (Vol. 48; 1990)
1,2-Epoxybutane [106-88-7] (Vol. 47, Vol. 71; 1998)
(NB: Overall evaluation upgraded from 3 to 2B with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Ethyl acrylate [140-88-5] (Vol. 39, Suppl. 7, Vol. 71; 1998)
Ethylene thiourea [96-45-7] (Vol. 7, Suppl. 7; 1987)
Ethyl methanesulfonate [62-50-0] (Vol. 7, Suppl. 7; 1987)
2-(2-Formylhydrazino)-4-(5-nitro-2-furyl)thiazole [3570-75-0] (Vol. 7, Suppl. 7; 1987)
Furan [110-00-9] (Vol. 63; 1995)
Glasswool (Vol. 43; 1988)
Glu-P-1 (2-Amino-6-methyldipyrido[1,2-a:3',2'-d]imidazole) [67730-11-4] (Vol. 40, Suppl. 7; 1987)
Glu-P-2 (2-Aminodipyrido[1,2-a:3',2'-d]imidazole) [67730-10-3] (Vol. 40, Suppl. 7; 1987)
Glycidaldehyde [765-34-4] (Vol. 11, Vol. 71, 1998)
Griseofulvin [126-07-8] (Vol. 10, Suppl. 7; 1987)
HC Blue No. 1 [2784-94-3] (Vol. 57; 1993)
Heptachlor [76-44-8] (Vol. 53; 1991)
Hexachlorobenzene [118-74-1] (Vol. 20, Suppl. 7; 1987)
Hexachlorocyclohexanes (Vol. 20, Suppl. 7; 1987)
Hexamethylphosphoramide [680-31-9] (Vol. 15, Vol. 71; 1998)
Human immunodeficiency virus type 2 (infection with) (Vol. 67; 1996)
Human papillomaviruses: some types other than 16, 18, 31 and 33 (Vol. 64; 1995)
Hydrazine [302-01-2] (Vol. 4, Suppl. 7, Vol. 71; 1998)
Indeno[1,2,3-cd]pyrene [193-39-5] (Vol. 32, Suppl. 7; 1987)
Iron-dextran complex [9004-66-4] (Vol. 2, Suppl. 7; 1987)
Isoprene [78-79-5] (Vol. 60, Vol. 71; 1998)
Lasiocarpine [303-34-4] (Vol. 10, Suppl. 7; 1987)
Lead [7439-92-1] and lead compounds, inorganic (Vol. 23, Suppl. 7; 1987)
(NB: Evaluated as a group)
Magenta [632-99-5] (containing CI Basic Red 9) (Vol. 57; 1993)
MeA-a-C (2-Amino-3-methyl-9H-pyrido[2,3-b]indole) [68006-83-7] (Vol. 40, Suppl. 7; 1987)
Medroxyprogesterone acetate [71-58-9] (Vol. 21, Suppl. 7; 1987)
MeIQ (2-Amino-3,4-dimethylimidazo[4,5-f]quinoline) [77094-11-2] (Vol. 56; 1993)
MeIQx (2-Amino-3,8-dimethylimidazo[4,5-f]quinoxaline) [77500-04-0] (Vol. 56; 1993)
Merphalan [531-76-0] (Vol. 9, Suppl. 7; 1987)
2-Methylaziridine (Propyleneimine) [75-55-8] (Vol. 9, Vol. 71; 1998)
Methylazoxymethanol acetate [592-62-1] (Vol. 10, Suppl. 7; 1987)
5-Methylchrysene [3697-24-3] (Vol. 32, Suppl. 7; 1987)
4,4'-Methylene bis(2-methylaniline) [838-88-0] (Vol. 4, Suppl. 7; 1987)
4,4'-Methylenedianiline [101-77-9] (Vol. 39, Suppl. 7; 1987)
Methylmercury compounds (Vol. 58; 1993)
(NB: Evaluated as a group)
2-Methyl-1-nitroanthraquinone [129-15-7] (uncertain purity) (Vol. 27, Suppl. 7; 1987)
N-Methyl-N-nitrosourethane [615-53-2] (Vol. 4, Suppl. 7; 1987)
Methylthiouracil [56-04-2] (Vol. 7, Suppl. 7; 1987)
Metronidazole [443-48-1] (Vol. 13, Suppl. 7; 1987)
Mirex [2385-85-5] (Vol. 20, Suppl. 7; 1987)
Mitomycin C [50-07-7] (Vol. 10, Suppl. 7; 1987)
Monocrotaline [315-22-0] (Vol. 10, Suppl. 7; 1987)
5-(Morpholinomethyl)-3-[(5-nitrofurfurylidene)amino]-2-oxazolidinone [3795-88-8] (Vol. 7, Suppl. 7; 1987)
Nafenopin [3771-19-5] (Vol. 24, Suppl. 7; 1987)
Nickel, metallic [7440-02-0] and alloys (Vol. 49; 1990)
Niridazole [61-57-4] (Vol. 13, Suppl. 7; 1987)
Nitrilotriacetic acid [139-13-9] and its salts (Vol. 48; 1990)
(NB: Evaluated as a group)
5-Nitroacenaphthene [602-87-9] (Vol. 16, Suppl. 7; 1987)
2-Nitroanisole [91-23-6] (Vol. 65; 1996)
Nitrobenzene [98-95-3] (Vol. 65; 1996)
6-Nitrochrysene [7496-02-8] (Vol. 46; 1989)
Nitrofen [1836-75-5] (technical-grade) (Vol. 30, Suppl. 7; 1987)
2-Nitrofluorene [607-57-8] (Vol. 46; 1989)
1-[(5-Nitrofurfurylidene)amino]-2-imidazolidinone [555-84-0] (Vol. 7, Suppl. 7; 1987)
N-[4-(5-Nitro-2-furyl)-2-thiazolyl]acetamide [531-82-8] (Vol. 7, Suppl. 7; 1987)
Nitrogen mustard N-oxide [126-85-2] (Vol. 9, Suppl. 7; 1987)
2-Nitropropane [79-46-9] (Vol. 29, Vol. 71; 1998)
1-Nitropyrene [5522-43-0] (Vol. 46; 1989)
4-Nitropyrene [57835-92-4] (Vol. 46; 1989)
N-Nitrosodi-n-butylamine [924-16-3] (Vol. 17, Suppl. 7; 1987)
N-Nitrosodiethanolamine [1116-54-7] (Vol. 17, Suppl. 7; 1987)
N-Nitrosodi-n-propylamine [621-64-7] (Vol. 17, Suppl. 7; 1987)
3-(N-Nitrosomethylamino)propionitrile [60153-49-3] (Vol. 37, Suppl. 7; 1987)
4-(N-Nitrosomethylamino)-1-(3-pyridyl)-1-butanone (NNK) [64091-91-4] (Vol. 37, Suppl. 7; 1987)
N-Nitrosomethylethylamine [10595-95-6] (Vol. 17, Suppl. 7; 1987)
N-Nitrosomethylvinylamine [4549-40-0] (Vol. 17, Suppl. 7; 1987)
N-Nitrosomorpholine [59-89-2] (Vol. 17, Suppl. 7; 1987)
N'-Nitrosonornicotine [16543-55-8] (Vol. 37, Suppl. 7; 1987)
N-Nitrosopiperidine [100-75-4] (Vol. 17, Suppl. 7; 1987)
N-Nitrosopyrrolidine [930-55-2] (Vol. 17, Suppl. 7; 1987)
N-Nitrososarcosine [13256-22-9] (Vol. 17, Suppl. 7; 1987)
Ochratoxin A [303-47-9] (Vol. 56; 1993)
Oil Orange SS [2646-17-5] (Vol. 8, Suppl. 7; 1987)
Oxazepam [604-75-1] (Vol. 66; 1996)
Palygorskite (attapulgite) [12174-11-7] (long fibres, > 5 micrometers) (Vol. 68; 1997)
Panfuran S (containing dihydroxymethylfuratrizine [794-93-4]) (Vol. 24, Suppl. 7; 1987)
Phenazopyridine hydrochloride [136-40-3] (Vol. 24, Suppl. 7; 1987)
Phenobarbital [50-06-6] (Vol. 13, Suppl. 7; 1987)
Phenoxybenzamine hydrochloride [63-92-3] (Vol. 24, Suppl. 7; 1987)
Phenyl glycidyl ether [122-60-1] (Vol. 47, Vol. 71; 1998)
Phenytoin [57-41-0] (Vol. 66; 1996)
PhIP (2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine) [105650-23-5] (Vol. 56; 1993)
Polychlorophenols and their sodium salts (mixed exposures) (Vol. 41, Suppl. 7, Vol. 53, Vol. 71; 1998)
Ponceau MX [3761-53-3] (Vol. 8, Suppl. 7; 1987)
Ponceau 3R [3564-09-8] (Vol. 8, Suppl. 7; 1987)
Potassium bromate [7758-01-2] (Vol. 40, Suppl. 7; 1987)
Progestins (Suppl. 7; 1987)
1,3-Propane sultone [1120-71-4] (Vol. 4, Vol. 71; 1998)
b-Propiolactone [57-57-8] (Vol. 4, Vol. 71; 1998)
Propylene oxide [75-56-9] (Vol. 60; 1994)
Propylthiouracil [51-52-5] (Vol. 7, Suppl. 7; 1987)
Rockwool (Vol. 43; 1988)
Saccharin [81-07-2] (Vol. 22, Suppl. 7; 1987)
Safrole [94-59-7] (Vol. 10, Suppl. 7; 1987)
Schistosoma japonicum (infection with) (Vol. 61; 1994)
Slagwool (Vol. 43; 1988)
Sodium ortho-phenylphenate [132-27-4] (Vol. 30, Suppl. 7; 1987)
Sterigmatocystin [10048-13-2] (Vol. 10, Suppl. 7; 1987)
Streptozotocin [18883-66-4] (Vol. 17, Suppl. 7; 1987)
Styrene [100-42-5] (Vol. 60; 1994)
(NB: Overall evaluation upgraded from 3 to 2B with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Sulfallate [95-06-7] (Vol. 30, Suppl. 7; 1987)
Tetrafluoroethylene [116-14-3] (Vol. 19, Vol. 71; 1998)
Tetranitromethane [509-14-8] (Vol. 65; 1996)
Thioacetamide [62-55-5] (Vol. 7, Suppl. 7; 1987)
4,4'-Thiodianiline [139-65-1] (Vol. 27, Suppl. 7; 1987)
Thiourea [62-56-6] (Vol. 7, Suppl. 7; 1987)
Toluene diisocyanates [26471-62-5] (Vol. 39, Vol. 71; 1998)
ortho-Toluidine [95-53-4] (Vol. 27, Suppl. 7; 1987)
Toxins derived from Fusarium moniliforme (Vol. 56; 1993)
Trichlormethine (Trimustine hydrochloride) [817-09-4] (Vol. 50; 1990)
Trp-P-1 (3-Amino-1,4-dimethyl-5H-pyrido[4,3-b]indole) [62450-06-0] (Vol. 31, Suppl. 7; 1987)
Trp-P-2 (3-Amino-1-methyl-5H-pyrido[4,3-b]indole) [62450-07-1] (Vol. 31, Suppl. 7; 1987)
Trypan blue [72-57-1] (Vol. 8, Suppl. 7; 1987)
Uracil mustard [66-75-1] (Vol. 9, Suppl. 7; 1987)
Urethane [51-79-6] (Vol. 7, Suppl. 7; 1987)
Vinyl acetate [108-05-4] (Vol. 63; 1995)
4-Vinylcyclohexene [100-40-3] (Vol. 60; 1994)
4-Vinylcyclohexene diepoxide [106-87-6] (Vol. 60; 1994)
Bitumens [8052-42-4], extracts of steam-refined and air-refined (Vol. 35, Suppl. 7; 1987)
Carrageenan [9000-07-1], degraded (Vol. 31, Suppl. 7; 1987)
Chlorinated paraffins of average carbon chain length C12 and average degree of chlorination approximately 60% (Vol. 48; 1990)
Coffee (urinary bladder) (Vol. 51; 1991)
(NB: There is some evidence of an inverse relationship between coffee drinking and cancer
of the large bowel; coffee drinking could not be classified as to its carcinogenicity to
other organs)
Diesel fuel, marine (Vol. 45; 1989)
(NB: Overall evaluation upgraded from 3 to 2B with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Engine exhaust, gasoline (Vol. 46; 1989)
Fuel oils, residual (heavy) (Vol. 45; 1989)
Gasoline (Vol. 45; 1989)
(NB: Overall evaluation upgraded from 3 to 2B with supporting evidence from other data
relevant to the evaluation of carcinogenicity and its mechanisms)
Pickled vegetables (traditional in Asia) (Vol. 56; 1993)
Polybrominated biphenyls [Firemaster BP-6, 59536-65-1] (Vol. 41, Suppl. 7; 1987)
Toxaphene (Polychlorinated camphenes) [8001-35-2] (Vol. 20, Suppl. 7; 1987)
Welding fumes (Vol. 49; 1990)
Carpentry and joinery (Vol. 25, Suppl. 7; 1987)
Dry cleaning (occupational exposures in) (Vol. 63; 1995)
Printing processes (occupational exposures in) (Vol. 65; 1996)
Textile manufacturing industry (work in) (Vol. 48; 1990)
This list contains all agents, mixtures and exposures evaluated as Group 3 carcinogens
to date.
Where appropriate, chemical abstract numbers are given [in square brackets]. For details
of the evaluation, the relevant Monograph should be consulted (volume number given in
round brackets, followed by year of publication of latest evaluation). Use a free-text
search to find a particular compound.
Acridine orange [494-38-2] (Vol. 16, Suppl. 7; 1987)
Acriflavinium chloride [8018-07-3] (Vol. 13, Suppl. 7; 1987)
Acrolein [107-02-8] (Vol. 63; 1995)
Acrylic acid [79-10-7] (Vol. 19, Vol. 71; 1998)
Acrylic fibres (Vol. 19, Suppl. 7; 1987)
Acrylonitrile-butadiene-styrene copolymers (Vol. 19, Suppl. 7; 1987)
Actinomycin D [50-76-0] (Vol. 10, Suppl. 7; 1987)
Agaritine [2757-90-6] (Vol. 31, Suppl. 7; 1987)
Aldicarb [116-06-3] (Vol. 53; 1991)
Aldrin [309-00-2] (Vol. 5, Suppl. 7; 1987)
Allyl chloride [107-05-1] (Vol. 36, Vol. 71; 1998)
Allyl isothiocyanate [57-06-7] (Vol. 36, Suppl. 7; 1987)
Allyl isovalerate [2835-39-4] (Vol. 36, Vol. 71; 1998)
Amaranth [915-67-3] (Vol. 8, Suppl. 7; 1987)
5-Aminoacenaphthene [4657-93-6] (Vol. 16, Suppl. 7; 1987)
2-Aminoanthraquinone [117-79-3] (Vol. 27, Suppl. 7; 1987)
para-Aminobenzoic acid [150-13-0] (Vol. 16, Suppl. 7; 1987)
1-Amino-2-methylanthraquinone [82-28-0] (Vol. 27, Suppl. 7; 1987)
2-Amino-4-nitrophenol [99-57-0] (Vol. 57; 1993)
2-Amino-5-nitrophenol [121-88-0] (Vol. 57; 1993)
4-Amino-2-nitrophenol [119-34-6] (Vol. 16, Suppl. 7; 1987)
2-Amino-5-nitrothiazole [121-66-4] (Vol. 31, Suppl. 7; 1987)
11-Aminoundecanoic acid [2432-99-7] (Vol. 39, Suppl. 7; 1987)
Ampicillin [69-53-4] (Vol. 50; 1990)
Anaesthetics, volatile (Vol. 11, Suppl. 7; 1987)
Angelicin [523-50-2] plus ultraviolet A radiation (Vol. 40, Suppl. 7; 1987)
Aniline [62-53-3] (Vol. 27, Suppl. 7; 1987)
para-Anisidine [104-94-9] (Vol. 27, Suppl. 7; 1987)
Anthanthrene [191-26-4] (Vol. 32, Suppl. 7; 1987)
Anthracene [120-12-7] (Vol. 32, Suppl. 7; 1987)
Anthranilic acid [118-92-3] (Vol. 16, Suppl. 7; 1987)
Antimony trisulfide [1345-04-6] (Vol. 47; 1989)
Apholate [52-46-0] (Vol. 9, Suppl. 7; 1987)
para-Aramid fibrils [24938-64-5] (Vol. 68; 1997)
Aurothioglucose [12192-57-3] (Vol. 13, Suppl. 7; 1987)
2-(1-Aziridinyl)ethanol [1072-52-2] (Vol. 9, Suppl. 7; 1987)
Aziridyl benzoquinone [800-24-8] (Vol. 9, Suppl. 7; 1987)
Azobenzene [103-33-3] (Vol. 8, Suppl. 7; 1987)
Benz[a]acridine [225-11-6] (Vol. 32, Suppl. 7; 1987)
Benz[c]acridine [225-51-4] (Vol. 32, Suppl. 7; 1987)
Benzo[ghi]fluoranthene [203-12-3] (Vol. 32, Suppl. 7; 1987)
Benzo[a]fluorene [238-84-6] (Vol. 32, Suppl. 7; 1987)
Benzo[b]fluorene [243-17-4] (Vol. 32, Suppl. 7; 1987)
Benzo[c]fluorene [205-12-9] (Vol. 32, Suppl. 7; 1987)
Benzo[ghi]perylene [191-24-2] (Vol. 32, Suppl. 7; 1987)
Benzo[c]phenanthrene [195-19-7] (Vol. 32, Suppl. 7; 1987)
Benzo[e]pyrene [192-97-2] (Vol. 32, Suppl. 7; 1987)
para-Benzoquinone dioxime [105-11-3] (Vol. 29, Vol. 71; 1998)
Benzoyl peroxide [94-36-0] (Vol. 36, Vol. 71; 1998)
Benzyl acetate [140-11-4] (Vol. 40, Vol. 71; 1998)
Bis(1-aziridinyl)morpholinophosphine sulfide [2168-68-5] (Vol. 9, Suppl. 7; 1987)
Bis(2-chloroethyl)ether [111-44-4] (Vol. 9, Vol. 71; 1998)
1,2-Bis(chloromethoxy)ethane [13483-18-6] (Vol. 15; Vol. 71; 1998)
1,4-Bis(chloromethoxymethyl)benzene [56894-91-8] (Vol. 15, Vol. 71; 1998)
Bis(2-chloro-1-methylethyl)ether [108-60-1] (Vol. 41, Vol. 71; 1998)
Bis(2,3-epoxycyclopentyl)ether [2386-90-5] (Vol. 47, Vol. 71; 1998)
Bisphenol A diglycidyl ether [1675-54-3] (Vol. 47, Vol. 71; 1998)
Bisulfites (Vol. 54; 1992)
Blue VRS [129-17-9] (Vol. 16, Suppl. 7; 1987)
Brilliant Blue FCF, disodium salt [3844-45-9] (Vol. 16, Suppl. 7; 1987)
Bromochloroacetonitrile [83463-62-1] (Vol. 52, Vol. 71; 1998)
Bromoethane [74-96-4] (Vol. 52, Vol. 71; 1998)
Bromoform [75-25-2] (Vol. 52, Vol. 71; 1998)
n-Butyl acrylate [141-32-2] (Vol. 39, Vol. 71; 1998)
Butylated hydroxytoluene (BHT) [128-37-0] (Vol. 40, Suppl. 7; 1987)
Butyl benzyl phthalate [85-68-7] (Vol. 29, Suppl. 7; 1987)
g-Butyrolactone [96-48-0] (Vol. 11, Vol. 71; 1998)
Caffeine [58-08-2] (Vol. 51; 1991)
Cantharidin [56-25-7] (Vol. 10, Suppl. 7; 1987)
Captan [133-06-2] (Vol. 30, Suppl. 7; 1987)
Carbaryl [63-25-2] (Vol. 12, Suppl. 7; 1987)
Carbazole [86-74-8] (Vol. 32, Vol. 71; 1998)
3-Carbethoxypsoralen [20073-24-9] (Vol. 40, Suppl. 7; 1987)
Carmoisine [3567-69-9] (Vol. 8, Suppl. 7; 1987)
Carrageenan [9000-07-1], native (Vol. 31, Suppl. 7; 1987)
Chloral [75-87-6] (Vol. 63; 1995)
Chloral hydrate [302-17-0] (Vol. 63; 1995)
Chlordimeform [6164-98-3] (Vol. 30, Suppl. 7; 1987)
Chlorinated drinking-water (Vol. 52; 1991)
Chloroacetonitrile [107-14-2] (Vol. 52, Vol. 71; 1998)
Chlorobenzilate [510-15-6] (Vol. 30, Suppl. 7; 1987)
Chlorodibromomethane [124-48-1] (Vol. 52, Vol. 71; 1998)
Chlorodifluoromethane [75-45-6] (Vol. 41, Vol. 71; 1998)
Chloroethane [75-00-3] (Vol. 52, Vol. 71; 1998)
Chlorofluoromethane [593-70-4] (Vol. 41, Vol. 71; 1998)
3-Chloro-2-methylpropene [563-47-3] (Vol. 63; 1995)
4-Chloro-meta-phenylenediamine [5131-60-2] (Vol. 27, Suppl. 7; 1987)
Chloronitrobenzenes [88-73-3; 121-73-3; 100-00-5] (Vol. 65; 1996)
Chloropropham [101-21-3] (Vol. 12, Suppl. 7; 1987)
Chloroquine [54-05-7] (Vol. 13, Suppl. 7; 1987)
Chlorothalonil [1897-45-6] (Vol. 30, Suppl. 7; 1987)
2-Chloro-1,1,1-trifluoroethane [75-88-7] (Vol. 41, Vol. 71; 1998)
Cholesterol [57-88-5] (Vol. 31, Suppl. 7; 1987)
Chromium[III] compounds (Vol. 49; 1990)
Chromium [7440-47-3], metallic (Vol. 49; 1990)
Chrysene [218-01-9] (Vol. 32, Suppl. 7; 1987)
Chrysoidine [532-82-1] (Vol. 8, Suppl. 7; 1987)
CI Acid Orange 3 [6373-74-6] (Vol. 57; 1993)
Cimetidine [51481-61-9] (Vol. 50; 1990)
Cinnamyl anthranilate [87-29-6] (Vol. 31, Suppl. 7; 1987)
CI Pigment Red 3 [2425-85-6] (Vol. 57; 1993)
Citrinin [518-75-2] (Vol. 40, Suppl. 7; 1987)
Clofibrate [637-07-0] (Vol. 66; 1996)
Clomiphene citrate [50-41-9] (Vol. 21, Suppl. 7; 1987)
Coal dust (Vol. 68; 1997)
Copper 8-hydroxyquinoline [10380-28-6] (Vol. 15, Suppl. 7; 1987)
Coronene [191-07-1] (Vol. 32, Suppl. 7; 1987)
Coumarin [91-64-5] (Vol. 10, Suppl. 7; 1987)
meta-Cresidine [102-50-1] (Vol. 27, Suppl. 7; 1987)
Crotonaldehyde [4170-30-3] (Vol. 63; 1995)
Cyclamates [sodium cyclamate, 139-05-9] (Vol. 22, Suppl. 7; 1987)
Cyclochlorotine [12663-46-6] (Vol. 10, Suppl. 7; 1987)
Cyclohexanone [108-94-1] (Vol. 47, Vol. 71; 1998)
Cyclopenta[cd]pyrene [27208-37-3] (Vol. 32, Suppl. 7; 1987)
D & C Red No. 9 [5160-02-1] (Vol. 57; 1993)
Dapsone [80-08-0] (Vol. 24, Suppl. 7; 1987)
Decabromodiphenyl oxide [1163-19-5] (Vol. 48, Vol. 71; 1998)
Deltamethrin [52918-63-5] (Vol. 53; 1991)
Diacetylaminoazotoluene [83-63-6] (Vol. 8, Suppl. 7; 1987)
Diallate [2303-16-4] (Vol. 30, Suppl. 7; 1987)
1,2-Diamino-4-nitrobenzene [99-56-9] (Vol. 16, Suppl. 7; 1987)
1,4-Diamino-2-nitrobenzene [5307-14-2] (Vol. 57; 1993)
2,5-Diaminotoluene [95-70-5] (Vol. 16, Suppl. 7; 1987)
Diazepam [439-14-5] (Vol. 66; 1996)
Diazomethane [334-88-3] (Vol. 7, Suppl. 7; 1987)
Dibenz[a,c]anthracene [215-58-7] (Vol. 32, Suppl. 7; 1987)
Dibenz[a,j]anthracene [224-41-9] (Vol. 32, Suppl. 7; 1987)
Dibenzo-para-dioxin (Vol. 69; 1997)
Dibenzo[a,e]fluoranthene [5385-75-1] (Vol. 32, Suppl. 7; 1987)
Dibenzo[h,rst]pentaphene [192-47-2] (Vol. 3, Suppl. 7; 1987)
Dibromoacetonitrile [3252-43-5] (Vol. 52, Vol. 71; 1998)
Dichloroacetic acid [79-43-6] (Vol. 63; 1995)
Dichloroacetonitrile [3018-12-0] (Vol. 52, Vol. 71; 1998)
Dichloroacetylene [7572-29-4] (Vol. 39, Vol. 71; 1998)
ortho-Dichlorobenzene [95-50-1] (Vol. 29, Suppl. 7; 1987)
trans-1,4-Dichlorobutene [110-57-6] (Vol. 15, Vol. 71; 1998)
2,6-Dichloro-para-phenylenediamine [609-20-1] (Vol. 39, Suppl. 7; 1987)
1,2-Dichloropropane [78-87-5] (Vol. 41, Vol. 71; 1998)
Dicofol [115-32-2] (Vol. 30, Suppl. 7; 1987)
Dieldrin [60-57-1] (Vol. 5, Suppl. 7; 1987)
Di(2-ethylhexyl)adipate [103-23-1] (Vol. 29, Suppl. 7; 1987)
Dihydroxymethylfuratrizine [794-93-4] (Vol. 24, Suppl. 7; 1987)
Dimethoxane [828-00-2] (Vol. 15, Suppl. 7; 1987)
3,3'-Dimethoxybenzidine-4,4'-diisocyanate [91-93-0] (Vol. 39, Suppl. 7; 1987)
para-Dimethylaminoazobenzenediazo sodium sulfonate [140-56-7] (Vol. 8, Suppl. 7; 1987)
4,4'-Dimethylangelicin [22975-76-4] plus ultraviolet A radiation (Suppl. 7; 1987)
4,5'-Dimethylangelicin [4063-41-6] plus ultraviolet A radiation (Suppl. 7; 1987)
N,N-Dimethylaniline [121-69-7] (Vol. 57; 1993)
Dimethylformamide [68-12-2] (Vol. 47; Vol. 71; 1998)
Dimethyl hydrogen phosphite [868-85-9] (Vol. 48, Vol. 71; 1998)
1,4-Dimethylphenanthrene [22349-59-3] (Vol. 32, Suppl. 7; 1987)
1,3-Dinitropyrene [75321-20-9] (Vol. 46; 1989)
3,5-Dinitrotoluene [618-85-9] (Vol. 65; 1996)
Dinitrosopentamethylenetetramine [101-25-7] (Vol. 11, Suppl. 7; 1987)
2,4'-Diphenyldiamine [492-17-1] (Vol. 16, Suppl. 7; 1987)
Disperse Yellow 3 [2832-40-8] (Vol. 48; 1990)
Disulfiram [97-77-8] (Vol. 12, Suppl. 7; 1987)
Dithranol [1143-38-0] (Vol. 13; Suppl. 7; 1987)
Doxefazepam [40762-15-0] (Vol. 66; 1996)
Droloxifene [82413-20-5] (Vol. 66; 1996)
Dulcin [150-69-6] (Vol. 12, Suppl. 7; 1987)
Endrin [72-20-8] (Vol. 5, Suppl. 7; 1987)
Eosin [15086-94-9] (Vol. 15, Suppl. 7; 1987)
3,4-Epoxy-6-methylcyclohexylmethyl-3,4-epoxy-6-methylcyclo-hexane carboxylate
[141-37-7]
(Vol. 11, Vol. 71; 1998)
cis-9,10-Epoxystearic acid [2443-39-2] (Vol. 11, Vol. 71; 1998)
Estazolam [29975-16-4] (Vol. 66; 1996)
Ethionamide [536-33-4] (Vol. 13, Suppl. 7; 1987)
Ethylene [74-85-1] (Vol. 60; 1994)
Ethylene sulfide [420-12-2] (Vol. 11, Suppl. 7; 1987)
2-Ethylhexyl acrylate [103-11-7] (Vol. 60; 1994)
Ethyl selenac [5456-28-0] (Vol. 12, Suppl. 7; 1987)
Ethyl tellurac [20941-65-5] (Vol. 12, Suppl. 7; 1987)
Eugenol [97-53-0] (Vol. 36, Suppl. 7; 1987)
Evans blue [314-13-6] (Vol. 8, Suppl. 7; 1987)
Fast Green FCF [2353-45-9] (Vol. 16, Suppl. 7; 1987)
Fenvalerate [51630-58-1] (Vol. 53; 1991)
Ferbam [14484-64-1] (Vol. 12, Suppl. 7; 1987)
Ferric oxide [1309-37-1] (Vol. 1, Suppl. 7; 1987)
Fluometuron [2164-17-2] (Vol. 30, Suppl. 7; 1987)
Fluoranthene [206-44-0] (Vol. 32, Suppl. 7; 1987)
Fluorene [86-73-7] (Vol. 32, Suppl. 7; 1987)
Fluorescent lighting (Vol. 55; 1992)
Fluorides (inorganic, used in drinking-water) (Vol. 27, Suppl. 7; 1987)
5-Fluorouracil [51-21-8] (Vol. 26, Suppl. 7; 1987)
Furazolidone [67-45-8] (Vol. 31, Suppl. 7; 1987)
Furfural [98-01-1] (Vol. 63; 1995)
Furosemide (Frusemide) [54-31-9] (Vol. 50; 1990)
Gemfibrozil [25812-30-0] (Vol. 66; 1996)
Glass filaments (Vol. 43; 1988)
Glycidyl oleate [5431-33-4] (Vol. 11, Suppl. 7; 1987)
Glycidyl stearate [7460-84-6] (Vol. 11, Suppl. 7; 1987)
Guinea Green B [4680-78-8] (Vol. 16, Suppl. 7; 1987)
Gyromitrin [16568-02-8] (Vol. 31, Suppl. 7; 1987)
Haematite [1317-60-8] (Vol. 1, Suppl. 7; 1987)
HC Blue No. 2 [33229-34-4] (Vol. 57; 1993)
HC Red No. 3 [2871-01-4] (Vol. 57; 1993)
HC Yellow No. 4 [59820-43-8] (Vol. 57; 1993)
Hepatitis D virus (Vol. 59; 1994)
Hexachlorobutadiene [87-68-3] (Vol. 20, Suppl. 7; 1987)
Hexachloroethane [67-72-1] (Vol. 20, Suppl. 7; 1987)
Hexachlorophene [70-30-4] (Vol. 20, Suppl. 7; 1987)
Human T-cell lymphotropic virus type II (Vol. 67; 1996)
Hycanthone mesylate [23255-93-8] (Vol. 13, Suppl. 7; 1987)
Hydralazine [86-54-4] (Vol. 24, Suppl. 7; 1987)
Hydrochloric acid [7647-01-0] (Vol. 54; 1992)
Hydrochlorothiazide [58-93-5] (Vol. 50; 1990)
Hydrogen peroxide [7722-84-1] (Vol. 36, Vol. 71; 1998)
Hydroquinone [123-31-9] (Vol. 15, Vol. 71; 1998)
4-Hydroxyazobenzene [1689-82-3] (Vol. 8, Suppl. 7; 1987)
8-Hydroxyquinoline [148-24-3] (Vol. 13, Suppl. 7; 1987)
Hydroxysenkirkine [26782-43-4] (Vol. 10, Suppl. 7; 1987)
Hypochlorite salts (Vol. 52; 1991)
Iron-dextrin complex [9004-51-7] (Vol. 2, Suppl. 7; 1987)
Iron sorbitol-citric acid complex [1338-16-5] (Vol. 2, Suppl. 7; 1987)
Isatidine [15503-86-3] (Vol. 10, Suppl. 7; 1987)
Isonicotinic acid hydrazide (Isoniazid) [54-85-3] (Vol. 4, Suppl. 7; 1987)
Isophosphamide [3778-73-2] (Vol. 26, Suppl. 7; 1987)
Isopropanol [67-63-0] (Vol. 15, Suppl. 7, Vol. 71; 1998)
Isopropyl oils (Vol. 15, Suppl. 7, Vol. 71; 1998)
Isosafrole [120-58-1] (Vol. 10, Suppl. 7; 1987)
Jacobine [6870-67-3] (Vol. 10, Suppl. 7; 1987)
Kaempferol [520-18-3] (Vol. 31, Suppl. 7; 1987)
Lauroyl peroxide [105-74-8] (Vol. 36, Vol. 71; 1998)
Lead, organo [75-74-1], [78-00-2] (Vol. 23, Suppl. 7; 1987)
Light Green SF [5141-20-8] (Vol. 16, Suppl. 7; 1987)
d-Limonene [5989-27-5] (Vol. 56; 1993)
Luteoskyrin [21884-44-6] (Vol. 10, Suppl. 7; 1987)
Malathion [121-75-5] (Vol. 30, Suppl. 7; 1987)
Maleic hydrazide [123-33-1] (Vol. 4, Suppl. 7; 1987)
Malonaldehyde [542-78-9] (Vol. 36, Vol. 71; 1998)
Maneb [12427-38-2] (Vol. 12, Suppl. 7; 1987)
Mannomustine dihydrochloride [551-74-6] (Vol. 9, Suppl. 7; 1987)
Medphalan [13045-94-8] (Vol. 9, Suppl. 7; 1987)
Melamine [108-78-1] (Vol. 39, Suppl. 7; 1987)
6-Mercaptopurine [50-44-2] (Vol. 26, Suppl. 7; 1987)
Mercury [7439-97-6] and inorganic mercury compounds (Vol. 58; 1993)
Metabisulfites (Vol. 54; 1992)
Methotrexate [59-05-2] (Vol. 26, Suppl. 7; 1987)
Methoxychlor [72-43-5] (Vol. 20, Suppl. 7; 1987)
Methyl acrylate [96-33-3] (Vol. 39, Vol. 71; 1998)
5-Methylangelicin [73459-03-7] plus ultraviolet A radiation (Suppl. 7; 1987)
Methyl bromide [74-83-9] (Vol. 41, Suppl. 7, Vol. 71; 1998)
Methyl carbamate [598-55-0] (Vol. 12, Suppl. 7; 1987)
Methyl chloride [74-87-3] (Vol. 41, Suppl. 7, Vol. 71; 1998)
1-Methylchrysene [3351-28-8] (Vol. 32, Suppl. 7; 1987)
2-Methylchrysene [3351-32-4] (Vol. 32, Suppl. 7; 1987)
3-Methylchrysene [3351-31-3] (Vol. 32, Suppl. 7; 1987)
4-Methylchrysene [3351-30-2] (Vol. 32, Suppl. 7; 1987)
6-Methylchrysene [1705-85-7] (Vol. 32, Suppl. 7; 1987)
N-Methyl-N,4-dinitrosoaniline [99-80-9] (Vol. 1, Suppl. 7; 1987)
4,4'-Methylene bis(N,N-dimethyl)benzenamine [101-61-1] (Vol. 27, Suppl. 7; 1987)
4,4'-Methylenediphenyl diisocyanate [101-68-8] (Vol. 19, Vol. 71; 1998)
2-Methylfluoranthene [33543-31-6] (Vol. 32, Suppl. 7; 1987)
3-Methylfluoranthene [1706-01-0] (Vol. 32, Suppl. 7; 1987)
Methylglyoxal [78-98-8] (Vol. 51; 1991)
Methyl iodide [74-88-4] (Vol. 41, Vol. 71; 1998)
Methyl methacrylate [80-62-6] (Vol. 60; 1994)
N-Methylolacrylamide [90456-67-0] (Vol. 60; 1994)
Methyl parathion [298-00-0] (Vol. 30, Suppl. 7; 1987)
1-Methylphenanthrene [832-69-9] (Vol. 32, Suppl. 7; 1987)
7-Methylpyrido[3,4-c]psoralen [85878-63-3] (Vol. 40, Suppl. 7; 1987)
Methyl red [493-52-7] (Vol. 8, Suppl. 7; 1987)
Methyl selenac [144-34-3] (Vol. 12, Suppl. 7; 1987)
Modacrylic fibres (Vol. 19, Suppl. 7; 1987)
Monuron [150-68-5] (Vol. 53; 1991)
Morpholine [110-91-8] (Vol. 47, Vol. 71; 1998)
Musk ambrette [83-66-9] (Vol. 65; 1996)
Musk xylene [81-15-2] (Vol. 65; 1996)
1,5-Naphthalenediamine [2243-62-1] (Vol. 27, Suppl. 7; 1987)
1,5-Naphthalene diisocyanate [3173-72-6] (Vol. 19, Vol. 71; 1998)
1-Naphthylamine [134-32-7] (Vol. 4, Suppl. 7; 1987)
1-Naphthylthiourea (ANTU) [86-88-4] (Vol. 30, Suppl. 7; 1987)
Nithiazide [139-94-6] (Vol. 31, Suppl. 7; 1987)
5-Nitro-ortho-anisidine [99-59-2] (Vol. 27, Suppl. 7; 1987)
9-Nitroanthracene [602-60-8] (Vol. 33, Suppl. 7; 1987)
7-Nitrobenz[a]anthracene [20268-51-3] (Vol. 46; 1989)
6-Nitrobenzo[a]pyrene [63041-90-7] (Vol. 46; 1989)
4-Nitrobiphenyl [92-93-3] (Vol. 4, Suppl. 7; 1987)
3-Nitrofluoranthene [892-21-7] (Vol. 33, Suppl. 7; 1987)
Nitrofural (Nitrofurazone) [59-87-0] (Vol. 50; 1990)
Nitrofurantoin [67-20-9] (Vol. 50; 1990)
1-Nitronaphthalene [86-57-7] (Vol. 46; 1989)
2-Nitronaphthalene [581-89-5] (Vol. 46; 1989)
3-Nitroperylene [20589-63-3] (Vol. 46; 1989)
2-Nitropyrene [789-07-1] (Vol. 46; 1989)
N'-Nitrosoanabasine [37620-20-5] (Vol. 37, Suppl. 7; 1987)
N'-Nitrosoanatabine [71267-22-6] (Vol. 37, Suppl. 7; 1987)
N-Nitrosodiphenylamine [86-30-6] (Vol. 27, Suppl. 7; 1987)
para-Nitrosodiphenylamine [156-10-5] (Vol. 27, Suppl. 7; 1987)
N-Nitrosofolic acid [29291-35-8] (Vol. 17, Suppl. 7; 1987)
N-Nitrosoguvacine [55557-01-2] (Vol. 37, Suppl. 7; 1987)
N-Nitrosoguvacoline [55557-02-3] (Vol. 37, Suppl. 7; 1987)
N-Nitrosohydroxyproline [30310-80-6] (Vol. 17, Suppl. 7; 1987)
3-(N-Nitrosomethylamino)propionaldehyde [85502-23-4] (Vol. 37, Suppl. 7; 1987)
4-(N-Nitrosomethylamino)-4-(3-pyridyl)-1-butanal (NNA) [64091-90-3] (Vol. 37, Suppl. 7; 1987)
N-Nitrosoproline [7519-36-0] (Vol. 17, Suppl. 7; 1987)
Nitrotoluenes [88-72-2; 99-08-1; 99-99-0] (Vol. 65; 1996)
5-Nitro-ortho-toluidine [99-55-8] (Vol. 48; 1990)
Nitrovin [804-36-4] (Vol. 31, Suppl. 7; 1987)
Nylon 6 [25038-54-4] (Vol. 19, Suppl. 7; 1987)
Oestradiol mustard [22966-79-6] (Vol. 9, Suppl. 7; 1987)
Oestrogen-progestin replacement therapy (Suppl. 7; 1987)
Opisthorchis felineus (infection with) (Vol. 61; 1994)
Orange I [523-44-4] (Vol. 8, Suppl. 7; 1987)
Orange G [1936-15-8] (Vol. 8, Suppl. 7; 1987)
Oxyphenbutazone [129-20-4] (Vol. 13, Suppl. 7; 1987)
Palygorskite (attapulgite) [12174-11-7] (short fibres, < 5 micrometers) (Vol. 68; 1997)
Paracetamol (Acetaminophen) [103-90-2] (Vol. 50; 1990)
Parasorbic acid [10048-32-5] (Vol. 10, Suppl. 7; 1987)
Parathion [56-38-2] (Vol. 30, Suppl. 7; 1987)
Patulin [149-29-1] (Vol. 40, Suppl. 7; 1987)
Penicillic acid [90-65-3] (Vol. 10, Suppl. 7; 1987)
Pentachloroethane [76-01-7] (Vol. 41, Vol. 71; 1998)
Permethrin [52645-53-1] (Vol. 53; 1991)
Perylene [198-55-0] (Vol. 32, Suppl. 7; 1987)
Petasitenine [60102-37-6] (Vol. 31, Suppl. 7; 1987)
Phenanthrene [85-01-8] (Vol. 32, Suppl. 7; 1987)
Phenelzine sulfate [156-51-4] (Vol. 24, Suppl. 7; 1987)
Phenicarbazide [103-03-7] (Vol. 12, Suppl. 7; 1987)
Phenol [108-95-2] (Vol. 47, Vol. 71; 1998)
Phenylbutazone [50-33-9] (Vol. 13, Suppl. 7; 1987)
meta-Phenylenediamine [108-45-2] (Vol. 16, Suppl. 7; 1987)
para-Phenylenediamine [106-50-3] (Vol. 16, Suppl. 7; 1987)
N-Phenyl-2-naphthylamine [135-88-6] (Vol. 16, Suppl. 7; 1987)
ortho-Phenylphenol [90-43-7] (Vol. 30, Suppl. 7; 1987)
Picloram [1918-02-1] (Vol. 53; 1991)
Piperonyl butoxide [51-03-6] (Vol. 30, Suppl. 7; 1987)
Polyacrylic acid [9003-01-4] (Vol. 19, Suppl. 7; 1987)
Polychlorinated dibenzo-para-dioxins (other than 2,3,7,8-tetrachlorodibenzo-para-dioxin) (Vol. 69; 1997)
Polychlorinated dibenzofurans (Vol. 69; 1997)
Polychloroprene [9010-98-4] (Vol. 19, Suppl. 7; 1987)
Polyethylene [9002-88-4] (Vol. 19, Suppl. 7; 1987)
Polymethylene polyphenyl isocyanate [9016-87-9] (Vol. 19, Suppl. 7; 1987)
Polymethyl methacrylate [9011-14-7] (Vol. 19, Suppl. 7; 1987)
Polypropylene [9003-07-0] (Vol. 19, Suppl. 7; 1987)
Polystyrene [9003-53-6] (Vol. 19, Suppl. 7; 1987)
Polytetrafluoroethylene [9002-84-0] (Vol. 19, Suppl. 7; 1987)
Polyurethane foams [9009-54-5] (Vol. 19, Suppl. 7; 1987)
Polyvinyl acetate [9003-20-7] (Vol. 19, Suppl. 7; 1987)
Polyvinyl alcohol [9002-89-5] (Vol. 19, Suppl. 7; 1987)
Polyvinyl chloride [9002-86-2] (Vol. 19, Suppl. 7; 1987)
Polyvinyl pyrrolidone [9003-39-8] (Vol. 19, Suppl. 7; 1987)
Ponceau SX [4548-53-2] (Vol. 8, Suppl. 7; 1987)
Potassium bis(2-hydroxyethyl)dithiocarbamate [23746-34-1] (Vol. 12, Suppl. 7; 1987)
Prazepam [2955-38-6] (Vol. 66; 1996)
Prednimustine [29069-24-7] (Vol. 50; 1990)
Prednisone [53-03-2] (Vol. 26, Suppl. 7; 1987)
Proflavine salts (Vol. 24, Suppl. 7; 1987)
Pronetalol hydrochloride [51-02-5] (Vol. 13, Suppl. 7; 1987)
Propham [122-42-9] (Vol. 12, Suppl. 7; 1987)
n-Propyl carbamate [627-12-3] (Vol. 12, Suppl. 7; 1987)
Propylene [115-07-1] (Vol. 60; 1994)
Ptaquiloside [87625-62-5] (Vol. 40, Suppl. 7; 1987)
Pyrene [129-00-0] (Vol. 32, Suppl. 7; 1987)
Pyrido[3,4-c]psoralen [85878-62-2] (Vol. 40, Suppl. 7; 1987)
Pyrimethamine [58-14-0] (Vol. 13, Suppl. 7; 1987)
Quercetin [117-39-5] (Vol. 31, Suppl. 7; 1987)
para-Quinone [106-51-4] (Vol. 15, Vol. 71; 1998)
Quintozene (Pentachloronitrobenzene) [82-68-8] (Vol. 5, Suppl. 7; 1987)
Reserpine [50-55-5] (Vol. 24, Suppl. 7; 1987)
Resorcinol [108-46-3] (Vol. 15, Vol. 71, 1998)
Retrorsine [480-54-6] (Vol. 10, Suppl. 7; 1987)
Rhodamine B [81-88-9] (Vol. 16, Suppl. 7; 1987)
Rhodamine 6G [989-38-8] (Vol. 16, Suppl. 7; 1987)
Riddelliine [23246-96-0] (Vol. 10, Suppl. 7; 1987)
Rifampicin [13292-46-1] (Vol. 24, Suppl. 7; 1987)
Ripazepam [26308-28-1] (Vol. 66; 1996)
Rugulosin [23537-16-8] (Vol. 40, Suppl. 7; 1987)
Saccharated iron oxide [8047-67-4] (Vol. 2, Suppl. 7; 1987)
Scarlet Red [85-83-6] (Vol. 8, Suppl. 7; 1987)
Schistosoma mansoni (infection with) (Vol. 61; 1994)
Selenium [7782-49-2] and selenium compounds (Vol. 9, Suppl. 7; 1987)
Semicarbazide hydrochloride [563-41-7] (Vol. 12, Suppl. 7; 1987)
Seneciphylline [480-81-9] (Vol. 10, Suppl. 7; 1987)
Senkirkine [2318-18-5] (Vol. 31, Suppl. 7; 1987)
Sepiolite [15501-74-3] (Vol. 68; 1997)
Shikimic acid [138-59-0] (Vol. 40, Suppl. 7; 1987)
Silica [7631-86-9], amorphous (Vol. 68; 1997)
Simazine [122-34-9] (Vol. 53; 1991)
Sodium chlorite [7758-19-2] (Vol. 52; 1991)
Sodium diethyldithiocarbamate [148-18-5] (Vol. 12, Suppl. 7; 1987)
Spironolactone [52-01-7] (Vol. 24, Suppl. 7; 1987)
Styrene-acrylonitrile copolymers [9003-54-7] (Vol. 19, Suppl. 7; 1987)
Styrene-butadiene copolymers [9003-55-8] (Vol. 19, Suppl. 7; 1987)
Succinic anhydride [108-30-5] (Vol. 15, Suppl. 7; 1987)
Sudan I [842-07-9] (Vol. 8, Suppl. 7; 1987)
Sudan II [3118-97-6] (Vol. 8, Suppl. 7; 1987)
Sudan III [85-86-9] (Vol. 8, Suppl. 7; 1987)
Sudan Brown RR [6416-57-5] (Vol. 8, Suppl. 7; 1987)
Sudan Red 7B [6368-72-5] (Vol. 8, Suppl. 7; 1987)
Sulfafurazole (Sulfisoxazole) [127-69-5] (Vol. 24, Suppl. 7; 1987)
Sulfamethoxazole [723-46-6] (Vol. 24, Suppl. 7; 1987)
Sulfites (Vol. 54; 1992)
Sulfur dioxide [7446-09-5] (Vol. 54; 1992)
Sunset Yellow FCF [2783-94-0] (Vol. 8, Suppl. 7; 1987)
Symphytine [22571-95-5] (Vol. 31, Suppl. 7; 1987)
Talc [14807-96-6], not containing asbestiform fibres (Vol. 42, Suppl. 7; 1987)
Tannic acid [1401-55-4] and tannins (Vol. 10, Suppl. 7; 1987)
Temazepam [846-50-4] (Vol. 66; 1996)
2,2',5,5'-Tetrachlorobenzidine [15721-02-5] (Vol. 27, Suppl. 7; 1987)
1,1,1,2-Tetrachloroethane [630-20-6] (Vol. 41, Vol. 71; 1998)
1,1,2,2-Tetrachloroethane [79-34-5] (Vol. 20, Vol. 71; 1998)
Tetrachlorvinphos [22248-79-9] (Vol. 30, Suppl. 7; 1987)
Tetrakis(hydroxymethyl)phosphonium salts (Vol. 48, Vol. 71; 1998)
Theobromine [83-67-0] (Vol. 51; 1991)
Theophylline [58-55-9] (Vol. 51; 1991)
Thiouracil [141-90-2] (Vol. 7, Suppl. 7; 1987)
Thiram [137-26-8] (Vol. 53; 1991)
Titanium dioxide [13463-67-7] (Vol. 47; 1989)
Toluene [108-88-3] (Vol. 47, Vol. 71; 1998)
Toremifene [89778-26-7] (Vol. 66; 1996)
Toxins derived from Fusarium graminearum, F. culmorum and F. crookwellense (Vol. 56; 1993)
Toxins derived from Fusarium sporotrichioides (Vol. 56; 1993)
Trichlorfon [52-68-6] (Vol. 30, Suppl. 7; 1987)
Trichloroacetic acid [76-03-9] (Vol. 63; 1995)
Trichloroacetonitrile [545-06-2] (Vol. 52, Vol. 71; 1998)
1,1,1-Trichloroethane [71-55-6] (Vol. 20, Vol. 71; 1998)
1,1,2-Trichloroethane [79-00-5] (Vol. 52, Vol. 71; 1998)
Triethylene glycol diglycidyl ether [1954-28-5] (Vol. 11, Vol. 71; 1998)
Trifluralin [1582-09-8] (Vol. 53; 1991)
4,4',6-Trimethylangelicin [90370-29-9] plus ultraviolet A radiation (Suppl. 7; 1987)
2,4,5-Trimethylaniline [137-17-7] (Vol. 27, Suppl. 7; 1987)
2,4,6-Trimethylaniline [88-05-1] (Vol. 27, Suppl. 7; 1987)
4,5',8-Trimethylpsoralen [3902-71-4] (Vol. 40, Suppl. 7; 1987)
2,4,6-Trinitrotoluene [118-96-7] (Vol. 65; 1996)
Triphenylene [217-59-4] (Vol. 32, Suppl. 7; 1987)
Tris(aziridinyl)-para-benzoquinone (Triaziquone) [68-76-8] (Vol. 9, Suppl. 7; 1987)
Tris(1-aziridinyl)phosphine oxide [545-55-1] (Vol. 9, Suppl. 7; 1987)
2,4,6-Tris(1-aziridinyl)-s-triazine [51-18-3] (Vol. 9, Suppl. 7; 1987)
Tris(2-chloroethyl) phosphate [115-96-8] (Vol. 48, Vol. 71; 1998)
1,2,3-Tris(chloromethoxy)propane [38571-73-2] (Vol. 15, Vol. 71; 1998)
Tris(2-methyl-1-aziridinyl)phosphine oxide [57-39-6] (Vol. 9, Suppl. 7; 1987)
Vat Yellow 4 [128-66-5] (Vol. 48; 1990)
Vinblastine sulfate [143-67-9] (Vol. 26, Suppl. 7; 1987)
Vincristine sulfate [2068-78-2] (Vol. 26, Suppl. 7; 1987)
Vinyl chloride-vinyl acetate copolymers [9003-22-9] (Vol. 19, Suppl. 7; 1987)
Vinylidene chloride [75-35-4] (Vol. 39, Suppl. 7, Vol. 71; 1998)
Vinylidene chloride-vinyl chloride copolymers [9011-06-7] (Vol. 19, Suppl. 7; 1987)
Vinylidene fluoride [75-38-7] (Vol. 39, Vol. 71; 1998)
N-Vinyl-2-pyrrolidone [88-12-0] (Vol. 19, Vol. 71; 1998)
Vinyl toluene [25013-15-4] (Vol. 60; 1994)
Wollastonite [13983-17-0] (Vol. 68; 1997)
Xylene [1330-20-7] (Vol. 47, Vol. 71; 1998)
2,4-Xylidine [95-68-1] (Vol. 16, Suppl. 7; 1987)
2,5-Xylidine [95-78-3] (Vol. 16, Suppl. 7; 1987)
Yellow AB [85-84-7] (Vol. 8, Suppl. 7; 1987)
Yellow OB [131-79-3] (Vol. 8, Suppl. 7; 1987)
Zectran [315-18-4] (Vol. 12, Suppl. 7; 1987)
Zeolites [1318-02-1] other than erionite (clinoptilolite, phillipsite, mordenite, non-fibrous Japanese zeolite, synthetic zeolites) (Vol. 68; 1997)
Zineb [12122-67-7] (Vol. 12, Suppl. 7; 1987)
Ziram [137-30-4] (Vol. 53; 1991)
Betel quid, without tobacco (Vol. 37, Suppl. 7; 1987)
Bitumens [8052-42-4], steam-refined, cracking-residue and air-refined (Vol. 35, Suppl. 7; 1987)
Crude oil [8002-05-9] (Vol. 45; 1989)
Diesel fuels, distillate (light) (Vol. 45; 1989)
Fuel oils, distillate (light) (Vol. 45; 1989)
Jet fuel (Vol. 45; 1989)
Mate (Vol. 51; 1991)
Mineral oils, highly-refined (Vol. 33, Suppl. 7; 1987)
Petroleum solvents (Vol. 47; 1989)
Printing inks (Vol. 65; 1996)
Tea (Vol. 51; 1991)
Terpene polychlorinates (StrobaneŽ) [8001-50-1] (Vol. 5, Suppl. 7; 1987)
Flat-glass and specialty glass (manufacture of) (Vol. 58; 1993)
Hair colouring products (personal use of) (Vol. 57; 1993)
Leather goods manufacture (Vol. 25, Suppl. 7; 1987)
Leather tanning and processing (Vol. 25, Suppl. 7; 1987)
Lumber and sawmill industries (including logging) (Vol. 25, Suppl. 7; 1987)
Paint manufacture (occupational exposure in) (Vol. 47; 1989)
Pulp and paper manufacture (Vol. 25, Suppl. 7; 1987)
This list contains all agents, mixtures and exposures evaluated as being in Group 4 to
date.
Where appropriate, chemical abstract numbers are given [in square brackets]. For details
of the evaluation, the relevant Monograph should be consulted (volume number given in
round brackets, followed by year of publication of latest evaluation). Use a free-text
search to find a particular compound.
Caprolactam [105-60-2] (Vol. 39, Suppl. 7, Vol. 71; 1998)
The Preamble to the Monographs sets out the objective and scope of the evaluation programme, the procedures used when making assessments, and the types of evidence considered and criteria used in reaching the final evaluations. The list of contents is followed by the full text of the Preamble, which should always be used when referring to the list of evaluations provided.
1. Background
2. Objectives and Scope
3. Selection of Topics for the
Monographs
4. Data for the Monographs
5. The Working Group
6. Working Procedures
7. Exposure Data
8. Studies of Cancer in Humans
9. Studies of Cancer in
Experimental Animals
10. Other Data Relevant to an Evaluation of Carcinogenicity
and its Mechanisms
11. Summary of Data Reported
12. Evaluation
References
In 1969, the International Agency for Research on Cancer (IARC) initiated a programme to evaluate the carcinogenic risk of chemicals to humans and to produce monographs on individual chemicals. The Monographs programme has since been expanded to include consideration of exposures to complex mixtures of chemicals (which occur, for example, in some occupations and as a result of human habits) and of exposures to other agents, such as radiation and viruses. With Supplement 6 (IARC, 1987a), the title of the series was modified from IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans to IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, in order to reflect the widened scope of the programme.
The criteria established in 1971 to evaluate carcinogenic risk to humans were adopted by the working groups whose deliberations resulted in the first 16 volumes of the IARC Monographs series. Those criteria were subsequently updated by further ad-hoc working groups (IARC, 1977, 1978, 1979, 1982, 1983, 1987b, 1988, 1991a; Vainio et al., 1992).
The objective of the programme is to prepare, with the help of international working groups of experts, and to publish in the form of monographs, critical reviews and evaluations of evidence on the carcinogenicity of a wide range of human exposures. The Monographs may also indicate where additional research efforts are needed.
The Monographs represent the first step in carcinogenic risk assessment, which involves examination of all relevant information in order to assess the strength of the available evidence that certain exposures could alter the incidence of cancer in humans. The second step is quantitative risk estimation. Detailed, quantitative evaluations of epidemiological data may be made in the Monographs, but without extrapolation beyond the range of the data available. Quantitative extrapolation from experimental data to the human situation is not undertaken.
The term 'carcinogen' is used in these monographs to denote an exposure that is capable of increasing the incidence of malignant neoplasms; the induction of benign neoplasms may in some circumstances (see p. 16) contribute to the judgement that the exposure is carcinogenic. The terms 'neoplasm' and 'tumour' are used interchangeably.
Some epidemiological and experimental studies indicate that different agents may act at different stages in the carcinogenic process, and several different mechanisms may be involved. The aim of the Monographs has been, from their inception, to evaluate evidence of carcinogenicity at any stage in the carcinogenesis process, independently of the underlying mechanisms. Information on mechanisms may, however, be used in making the overall evaluation (IARC, 1991a; Vainio et al., 1992; see also pp. 26-29).
The Monographs may assist national and international authorities in making risk assessments and in formulating decisions concerning any necessary preventive measures. The evaluations of IARC working groups are scientific, qualitative judgements about the evidence for or against carcinogenicity provided by the available data. These evaluations represent only one part of the body of information on which regulatory measures may be based. Other components of regulatory decisions may vary from one situation to another and from country to country, responding to different socioeconomic and national priorities. Therefore, no recommendation is given with regard to regulation or legislation, which are the responsibility of individual governments and/or other international organizations.
The IARC Monographs are recognized as an authoritative source of information on the carcinogenicity of a wide range of human exposures. A users' survey, made in 1988, indicated that the Monographs are consulted by various agencies in 57 countries. Each volume is generally printed in 4000 copies for distribution to governments, regulatory bodies and interested scientists. The Monographs are also available via the Distribution and Sales Service of the World Health Organization.
Topics are selected on the basis of two main criteria: (a) there is evidence of human exposure, and (b) there is some evidence or suspicion of carcinogenicity. The term 'agent' is used to include individual chemical compounds, groups of related chemical compounds, physical agents (such as radiation) and biological factors (such as viruses). Exposures to mixtures of agents may occur in occupational exposures and as a result of personal and cultural habits (like smoking and dietary practices). Chemical analogues and compounds with biological or physical characteristics similar to those of suspected carcinogens may also be considered, even in the absence of data on a possible carcinogenic effect in humans or experimental animals.
The scientific literature is surveyed for published data relevant to an assessment of carcinogenicity. The IARC directories of agents being tested for carcinogenicity (IARC, 1973-1996) and directories of on-going research in cancer epidemiology (IARC, 1976-1996) often indicate those exposures that may be scheduled for future meetings. Ad-hoc working groups convened by IARC in 1984, 1989, 1991 and 1993 gave recommendations as to which agents should be evaluated in the IARC Monographs series (IARC, 1984, 1989, 1991b, 1993).
As significant new data on subjects on which monographs have already been prepared become available, re-evaluations are made at subsequent meetings, and revised monographs are published.
The Monographs do not necessarily cite all the literature concerning the subject of an evaluation. Only those data considered by the Working Group to be relevant to making the evaluation are included.
With regard to biological and epidemiological data, only reports that have been published or accepted for publication in the openly available scientific literature are reviewed by the working groups. In certain instances, government agency reports that have undergone peer review and are widely available are considered. Exceptions may be made on an ad-hoc basis to include unpublished reports that are in their final form and publicly available, if their inclusion is considered pertinent to making a final evaluation (see pp. 22-29). In the sections on chemical and physical properties, on analysis, on production and use and on occurrence, unpublished sources of information may be used.
Reviews and evaluations are formulated by a working group of experts. The tasks of the group are: (i) to ascertain that all appropriate data have been collected; (ii) to select the data relevant for the evaluation on the basis of scientific merit; (iii) to prepare accurate summaries of the data to enable the reader to follow the reasoning of the Working Group; (iv) to evaluate the results of epidemiological and experimental studies on cancer; (v) to evaluate data relevant to the understanding of mechanism of action; and (vi) to make an overall evaluation of the carcinogenicity of the exposure to humans.
Working Group participants who contributed to the considerations and evaluations within a particular volume are listed, with their addresses, at the beginning of each publication. Each participant who is a member of a working group serves as an individual scientist and not as a representative of any organization, government or industry. In addition, nominees of national and international agencies and industrial associations may be invited as observers.
Approximately one year in advance of a meeting of a working group, the topics of the monographs are announced and participants are selected by IARC staff in consultation with other experts. Subsequently, relevant biological and epidemiological data are collected by IARC from recognized sources of information on carcinogenesis, including data storage and retrieval systems such as MEDLINE and TOXLINE, and EMIC and ETIC for data on genetic and related effects and reproductive and developmental effects, respectively.
For chemicals and some complex mixtures, the major collection of data and the preparation of first drafts of the sections on chemical and physical properties, on analysis, on production and use and on occurrence are carried out under a separate contract funded by the United States National Cancer Institute. Representatives from industrial associations may assist in the preparation of sections on production and use. Information on production and trade is obtained from governmental and trade publications and, in some cases, by direct contact with industries. Separate production data on some agents may not be available because their publication could disclose confidential information. Information on uses may be obtained from published sources but is often complemented by direct contact with manufacturers. Efforts are made to supplement this information with data from other national and international sources.
Six months before the meeting, the material obtained is sent to meeting participants, or is used by IARC staff, to prepare sections for the first drafts of monographs. The first drafts are compiled by IARC staff and sent, prior to the meeting, to all participants of the Working Group for review.
The Working Group meets in Lyon for seven to eight days to discuss and finalize the texts of the monographs and to formulate the evaluations. After the meeting, the master copy of each monograph is verified by consulting the original literature, edited and prepared for publication. The aim is to publish monographs within six months of the Working Group meeting.
The available studies are summarized by the Working Group, with particular regard to the qualitative aspects discussed below. In general, numerical findings are indicated as they appear in the original report; units are converted when necessary for easier comparison. The Working Group may conduct additional analyses of the published data and use them in their assessment of the evidence; the results of such supplementary analyses are given in square brackets. When an important aspect of a study, directly impinging on its interpretation, should be brought to the attention of the reader, a comment is given in square brackets.
Sections that indicate the extent of past and present human exposure, the sources of exposure, the people most likely to be exposed and the factors that contribute to the exposure are included at the beginning of each monograph.
Most monographs on individual chemicals, groups of chemicals or complex mixtures include sections on chemical and physical data, on analysis, on production and use and on occurrence. In monographs on, for example, physical agents, occupational exposures and cultural habits, other sections may be included, such as: historical perspectives, description of an industry or habit, chemistry of the complex mixture or taxonomy. Monographs on biological agents have sections on structure and biology, methods of detection, epidemiology of infection and clinical disease other than cancer.
For chemical exposures, the Chemical Abstracts Services Registry Number, the latest Chemical Abstracts Primary Name and the IUPAC Systematic Name are recorded; other synonyms are given, but the list is not necessarily comprehensive. For biological agents, taxonomy and structure are described, and the degree of variability is given, when applicable.
Information on chemical and physical properties and, in particular, data relevant to identification, occurrence and biological activity are included. For biological agents, mode of replication, life cycle, target cells, persistence and latency and host response are given. A description of technical products of chemicals includes trades names, relevant specifications and available information on composition and impurities. Some of the trade names given may be those of mixtures in which the agent being evaluated is only one of the ingredients.
The purpose of the section on analysis or detection is to give the reader an overview of current methods, with emphasis on those widely used for regulatory purposes. Methods for monitoring human exposure are also given, when available. No critical evaluation or recommendation of any of the methods is meant or implied. The IARC publishes a series of volumes, Environmental Carcinogens: Methods of Analysis and Exposure Measurement (IARC, 1978-93), that describe validated methods for analysing a wide variety of chemicals and mixtures. For biological agents, methods of detection and exposure assessment are described, including their sensitivity, specificity and reproducibility.
The dates of first synthesis and of first commercial production of a chemical or mixture are provided; for agents which do not occur naturally, this information may allow a reasonable estimate to be made of the date before which no human exposure to the agent could have occurred. The dates of first reported occurrence of an exposure are also provided. In addition, methods of synthesis used in past and present commercial production and different methods of production which may give rise to different impurities are described.
Data on production, international trade and uses are obtained for representative regions, which usually include Europe, Japan and the United States of America. It should not, however, be inferred that those areas or nations are necessarily the sole or major sources or users of the agent. Some identified uses may not be current or major applications, and the coverage is not necessarily comprehensive. In the case of drugs, mention of their therapeutic uses does not necessarily represent current practice nor does it imply judgement as to their therapeutic efficacy.
Information on the occurrence of an agent or mixture in the environment is obtained from data derived from the monitoring and surveillance of levels in occupational environments, air, water, soil, foods and animal and human tissues. When available, data on the generation, persistence and bioaccumulation of the agent are also included. In the case of mixtures, industries, occupations or processes, information is given about all agents present. For processes, industries and occupations, a historical description is also given, noting variations in chemical composition, physical properties and levels of occupational exposure with time and place. For biological agents, the epidemiology of infection is described.
Statements concerning regulations and guidelines (e.g. pesticide registrations, maximal levels permitted in foods, occupational exposure limits) are included for some countries as indications of potential exposures, but they may not reflect the most recent situation, since such limits are continuously reviewed and modified. The absence of information on regulatory status for a country should not be taken to imply that that country does not have regulations with regard to the exposure. For biological agents, legislation and control, including vaccines and therapy, are described.
(a) Types of studies considered
Three types of epidemiological studies of cancer contribute to the assessment of carcinogenicity in humans-cohort studies, case-control studies and correlation (or ecological) studies. Rarely, results from randomized trials may be available. Case series and case reports of cancer in humans may also be reviewed.
Cohort and case-control studies relate individual exposures under study to the occurrence of cancer in individuals and provide an estimate of relative risk (ratio of incidence or mortality in those exposed to incidence or mortality in those not exposed) as the main measure of association.
In correlation studies, the units of investigation are usually whole populations (e.g. in particular geographical areas or at particular times), and cancer frequency is related to a summary measure of the exposure of the population to the agent, mixture or exposure circumstance under study. Because individual exposure is not documented, however, a causal relationship is less easy to infer from correlation studies than from cohort and case-control studies. Case reports generally arise from a suspicion, based on clinical experience, that the concurrence of two events-that is, a particular exposure and occurrence of a cancer-has happened rather more frequently than would be expected by chance. Case reports usually lack complete ascertainment of cases in any population, definition or enumeration of the population at risk and estimation of the expected number of cases in the absence of exposure. The uncertainties surrounding interpretation of case reports and correlation studies make them inadequate, except in rare instances, to form the sole basis for inferring a causal relationship. When taken together with case-control and cohort studies, however, relevant case reports or correlation studies may add materially to the judgement that a causal relationship is present.
Epidemiological studies of benign neoplasms, presumed preneoplastic lesions and other end-points thought to be relevant to cancer are also reviewed by working groups. They may, in some instances, strengthen inferences drawn from studies of cancer itself.
(b) Quality of studies considered
The Monographs are not intended to summarize all published studies. Those that are judged to be inadequate or irrelevant to the evaluation are generally omitted. They may be mentioned briefly, particularly when the information is considered to be a useful supplement to that in other reports or when they provide the only data available. Their inclusion does not imply acceptance of the adequacy of the study design or of the analysis and interpretation of the results, and limitations are clearly outlined in square brackets at the end of the study description.
It is necessary to take into account the possible roles of bias, confounding and chance in the interpretation of epidemiological studies. By 'bias' is meant the operation of factors in study design or execution that lead erroneously to a stronger or weaker association than in fact exists between disease and an agent, mixture or exposure circumstance. By 'confounding' is meant a situation in which the relationship with disease is made to appear stronger or to appear weaker than it truly is as a result of an association between the apparent causal factor and another factor that is associated with either an increase or decrease in the incidence of the disease. In evaluating the extent to which these factors have been minimized in an individual study, working groups consider a number of aspects of design and analysis as described in the report of the study. Most of these considerations apply equally to case-control, cohort and correlation studies. Lack of clarity of any of these aspects in the reporting of a study can decrease its credibility and the weight given to it in the final evaluation of the exposure.
Firstly, the study population, disease (or diseases) and exposure should have been well defined by the authors. Cases of disease in the study population should have been identified in a way that was independent of the exposure of interest, and exposure should have been assessed in a way that was not related to disease status.
Secondly, the authors should have taken account in the study design and analysis of other variables that can influence the risk of disease and may have been related to the exposure of interest. Potential confounding by such variables should have been dealt with either in the design of the study, such as by matching, or in the analysis, by statistical adjustment. In cohort studies, comparisons with local rates of disease may be more appropriate than those with national rates. Internal comparisons of disease frequency among individuals at different levels of exposure should also have been made in the study.
Thirdly, the authors should have reported the basic data on which the conclusions are founded, even if sophisticated statistical analyses were employed. At the very least, they should have given the numbers of exposed and unexposed cases and controls in a case-control study and the numbers of cases observed and expected in a cohort study. Further tabulations by time since exposure began and other temporal factors are also important. In a cohort study, data on all cancer sites and all causes of death should have been given, to reveal the possibility of reporting bias. In a case-control study, the effects of investigated factors other than the exposure of interest should have been reported.
Finally, the statistical methods used to obtain estimates of relative risk, absolute rates of cancer, confidence intervals and significance tests, and to adjust for confounding should have been clearly stated by the authors. The methods used should preferably have been the generally accepted techniques that have been refined since the mid-1970s. These methods have been reviewed for case-control studies (Breslow & Day, 1980) and for cohort studies (Breslow & Day, 1987).
(c) Inferences about mechanism of action
Detailed analyses of both relative and absolute risks in relation to temporal variables, such as age at first exposure, time since first exposure, duration of exposure, cumulative exposure and time since exposure ceased, are reviewed and summarized when available. The analysis of temporal relationships can be useful in formulating models of carcinogenesis. In particular, such analyses may suggest whether a carcinogen acts early or late in the process of carcinogenesis, although at best they allow only indirect inferences about the mechanism of action. Special attention is given to measurements of biological markers of carcinogen exposure or action, such as DNA or protein adducts, as well as markers of early steps in the carcinogenic process, such as proto-oncogene mutation, when these are incorporated into epidemiological studies focused on cancer incidence or mortality. Such measurements may allow inferences to be made about putative mechanisms of action (IARC, 1991a; Vainio et al., 1992).
(d) Criteria for causality
After the quality of individual epidemiological studies of cancer has been summarized and assessed, a judgement is made concerning the strength of evidence that the agent, mixture or exposure circumstance in question is carcinogenic for humans. In making their judgement, the Working Group considers several criteria for causality. A strong association (i.e. a large relative risk) is more likely to indicate causality than a weak association, although it is recognized that relative risks of small magnitude do not imply lack of causality and may be important if the disease is common. Associations that are replicated in several studies of the same design or using different epidemiological approaches or under different circumstances of exposure are more likely to represent a causal relationship than isolated observations from single studies. If there are inconsistent results among investigations, possible reasons are sought (such as differences in amount of exposure), and results of studies judged to be of high quality are given more weight than those of studies judged to be methodologically less sound. When suspicion of carcinogenicity arises largely from a single study, these data are not combined with those from later studies in any subsequent reassessment of the strength of the evidence.
If the risk of the disease in question increases with the amount of exposure, this is considered to be a strong indication of causality, although absence of a graded response is not necessarily evidence against a causal relationship. Demonstration of a decline in risk after cessation of or reduction in exposure in individuals or in whole populations also supports a causal interpretation of the findings.
Although a carcinogen may act upon more than one target, the specificity of an association (i.e. an increased occurrence of cancer at one anatomical site or of one morphological type) adds plausibility to a causal relationship, particularly when excess cancer occurrence is limited to one morphological type within the same organ.
Although rarely available, results from randomized trials showing different rates among exposed and unexposed individuals provide particularly strong evidence for causality.
When several epidemiological studies show little or no indication of an association between an exposure and cancer, the judgement may be made that, in the aggregate, they show evidence of lack of carcinogenicity. Such a judgement requires first of all that the studies giving rise to it meet, to a sufficient degree, the standards of design and analysis described above. Specifically, the possibility that bias, confounding or misclassification of exposure or outcome could explain the observed results should be considered and excluded with reasonable certainty. In addition, all studies that are judged to be methodologically sound should be consistent with a relative risk of unity for any observed level of exposure and, when considered together, should provide a pooled estimate of relative risk which is at or near unity and has a narrow confidence interval, due to sufficient population size. Moreover, no individual study nor the pooled results of all the studies should show any consistent tendency for relative risk of cancer to increase with increasing level of exposure. It is important to note that evidence of lack of carcinogenicity obtained in this way from several epidemiological studies can apply only to the type(s) of cancer studied and to dose levels and intervals between first exposure and observation of disease that are the same as or less than those observed in all the studies. Experience with human cancer indicates that, in some cases, the period from first exposure to the development of clinical cancer is seldom less than 20 years; latent periods substantially shorter than 30 years cannot provide evidence for lack of carcinogenicity.
All known human carcinogens that have been studied adequately in experimental animals have produced positive results in one or more animal species (Wilbourn et al., 1986; Tomatis et al., 1989). For several agents (aflatoxins, 4-aminobiphenyl, azathioprine, betel quid with tobacco, BCME and CMME (technical grade), chlorambucil, chlornaphazine, ciclosporin, coal-tar pitches, coal-tars, combined oral contraceptives, cyclophosphamide, diethylstilboestrol, melphalan, 8-methoxypsoralen plus UVA, mustard gas, myleran, 2-naphthylamine, nonsteroidal oestrogens, oestrogen replacement therapy/steroidal oestrogens, solar radiation, thiotepa and vinyl chloride), carcinogenicity in experimental animals was established or highly suspected before epidemiological studies confirmed the carcinogenicity in humans (Vainio et al., 1995). Although this association cannot establish that all agents and mixtures that cause cancer in experimental animals also cause cancer in humans, nevertheless, in the absence of adequate data on humans, it is biologically plausible and prudent to regard agents and mixtures for which there is sufficient evidence (see p. 24) of carcinogenicity in experimental animals as if they presented a carcinogenic risk to humans. The possibility that a given agent may cause cancer through a species-specific mechanism which does not operate in humans (see p. 28) should also be taken into consideration.
The nature and extent of impurities or contaminants present in the chemical or mixture being evaluated are given when available. Animal strain, sex, numbers per group, age at start of treatment and survival are reported.
Other types of studies summarized include: experiments in which the agent or mixture was administered in conjunction with known carcinogens or factors that modify carcinogenic effects; studies in which the end-point was not cancer but a defined precancerous lesion; and experiments on the carcinogenicity of known metabolites and derivatives.
For experimental studies of mixtures, consideration is given to the possibility of changes in the physicochemical properties of the test substance during collection, storage, extraction, concentration and delivery. Chemical and toxicological interactions of the components of mixtures may result in nonlinear dose-response relationships.
An assessment is made as to the relevance to human exposure of samples tested in experimental animals, which may involve consideration of: (i) physical and chemical characteristics, (ii) constituent substances that indicate the presence of a class of substances, (iii) the results of tests for genetic and related effects, including genetic activity profiles, DNA adduct profiles, proto-oncogene mutation and expression and suppressor gene inactivation. The relevance of results obtained, for example, with animal viruses analogous to the virus being evaluated in the monograph must also be considered. They may provide biological and mechanistic information relevant to the understanding of the process of carcinogenesis in humans and may strengthen the plausibility of a conclusion that the biological agent that is being evaluated is carcinogenic in humans.
(a) Qualitative aspects
An assessment of carcinogenicity involves several considerations of qualitative importance, including (i) the experimental conditions under which the test was performed, including route and schedule of exposure, species, strain, sex, age, duration of follow-up; (ii) the consistency of the results, for example, across species and target organ(s); (iii) the spectrum of neoplastic response, from preneoplastic lesions and benign tumours to malignant neoplasms; and (iv) the possible role of modifying factors.
As mentioned earlier (p. 9), the Monographs are not intended to summarize all published studies. Those studies in experimental animals that are inadequate (e.g. too short a duration, too few animals, poor survival; see below) or are judged irrelevant to the evaluation are generally omitted. Guidelines for conducting adequate long-term carcinogenicity experiments have been outlined (e.g. Montesano et al., 1986).
Considerations of importance to the Working Group in the interpretation and evaluation of a particular study include: (i) how clearly the agent was defined and, in the case of mixtures, how adequately the sample characterization was reported; (ii) whether the dose was adequately monitored, particularly in inhalation experiments; (iii) whether the doses and duration of treatment were appropriate and whether the survival of treated animals was similar to that of controls; (iv) whether there were adequate numbers of animals per group; (v) whether animals of both sexes were used; (vi) whether animals were allocated randomly to groups; (vii) whether the duration of observation was adequate; and (viii) whether the data were adequately reported. If available, recent data on the incidence of specific tumours in historical controls, as well as in concurrent controls, should be taken into account in the evaluation of tumour response.
When benign tumours occur together with and originate from the same cell type in an organ or tissue as malignant tumours in a particular study and appear to represent a stage in the progression to malignancy, it may be valid to combine them in assessing tumour incidence (Huff et al., 1989). The occurrence of lesions presumed to be preneoplastic may in certain instances aid in assessing the biological plausibility of any neoplastic response observed. If an agent or mixture induces only benign neoplasms that appear to be end-points that do not readily undergo transition to malignancy, it should nevertheless be suspected of being a carcinogen and requires further investigation.
(b) Quantitative aspects
The probability that tumours will occur may depend on the species, sex, strain and age of the animal, the dose of the carcinogen and the route and length of exposure. Evidence of an increased incidence of neoplasms with increased level of exposure strengthens the inference of a causal association between the exposure and the development of neoplasms.
The form of the dose-response relationship can vary widely, depending on the particular agent under study and the target organ. Both DNA damage and increased cell division are important aspects of carcinogenesis, and cell proliferation is a strong determinant of dose-response relationships for some carcinogens (Cohen & Ellwein, 1990). Since many chemicals require metabolic activation before being converted into their reactive intermediates, both metabolic and pharmacokinetic aspects are important in determining the dose-response pattern. Saturation of steps such as absorption, activation, inactivation and elimination may produce nonlinearity in the dose-response relationship, as could saturation of processes such as DNA repair (Hoel et al., 1983; Gart et al., 1986).
(c) Statistical analysis of long-term experiments in animals
Factors considered by the Working Group include the adequacy of the information given for each treatment group: (i) the number of animals studied and the number examined histologically, (ii) the number of animals with a given tumour type and (iii) length of survival. The statistical methods used should be clearly stated and should be the generally accepted techniques refined for this purpose (Peto et al., 1980; Gart et al., 1986). When there is no difference in survival between control and treatment groups, the Working Group usually compares the proportions of animals developing each tumour type in each of the groups. Otherwise, consideration is given as to whether or not appropriate adjustments have been made for differences in survival. These adjustments can include: comparisons of the proportions of tumour-bearing animals among the effective number of animals (alive at the time the first tumour is discovered), in the case where most differences in survival occur before tumours appear; life-table methods, when tumours are visible or when they may be considered 'fatal' because mortality rapidly follows tumour development; and the Mantel-Haenszel test or logistic regression, when occult tumours do not affect the animals' risk of dying but are 'incidental' findings at autopsy.
In practice, classifying tumours as fatal or incidental may be difficult. Several survival-adjusted methods have been developed that do not require this distinction (Gart et al., 1986), although they have not been fully evaluated.
In coming to an overall evaluation of carcinogenicity in humans (see p. 26), the Working Group also considers related data. The nature of the information selected for the summary depends on the agent being considered.
For chemicals and complex mixtures of chemicals such as those in some occupational situations and involving cultural habits (e.g. tobacco smoking), the other data considered to be relevant are divided into those on absorption, distribution, metabolism and excretion; toxic effects; reproductive and developmental effects; and genetic and related effects.
Concise information is given on absorption, distribution (including placental transfer) and excretion in both humans and experimental animals. Kinetic factors that may affect the dose-response relationship, such as saturation of uptake, protein binding, metabolic activation, detoxification and DNA repair processes, are mentioned. Studies that indicate the metabolic fate of the agent in humans and in experimental animals are summarized briefly, and comparisons of data from humans and animals are made when possible. Comparative information on the relationship between exposure and the dose that reaches the target site may be of particular importance for extrapolation between species. Data are given on acute and chronic toxic effects (other than cancer), such as organ toxicity, increased cell proliferation, immunotoxicity and endocrine effects. The presence and toxicological significance of cellular receptors is described. Effects on reproduction, teratogenicity, fetotoxicity and embryotoxicity are also summarized briefly.
Tests of genetic and related effects are described in view of the relevance of gene mutation and chromosomal damage to carcinogenesis (Vainio et al., 1992). The adequacy of the reporting of sample characterization is considered and, where necessary, commented upon; with regard to complex mixtures, such comments are similar to those described for animal carcinogenicity tests on pp. 13-14. The available data are interpreted critically by phylogenetic group according to the end-points detected, which may include DNA damage, gene mutation, sister chromatid exchange, micronucleus formation, chromosomal aberrations, aneuploidy and cell transformation. The concentrations employed are given, and mention is made of whether use of an exogenous metabolic system in vitro affected the test result. These data are given as listings of test systems, data and references; bar graphs (activity profiles) and corresponding summary tables with detailed information on the preparation of the profiles (Waters et al., 1987) are given in appendices.
Positive results in tests using prokaryotes, lower eukaryotes, plants, insects and cultured mammalian cells suggest that genetic and related effects could occur in mammals. Results from such tests may also give information about the types of genetic effect produced and about the involvement of metabolic activation. Some end-points described are clearly genetic in nature (e.g. gene mutations and chromosomal aberrations), while others are to a greater or lesser degree associated with genetic effects (e.g. unscheduled DNA synthesis). In-vitro tests for tumour-promoting activity and for cell transformation may be sensitive to changes that are not necessarily the result of genetic alterations but that may have specific relevance to the process of carcinogenesis. A critical appraisal of these tests has been published (Montesano et al., 1986).
Genetic or other activity manifest in experimental mammals and humans is regarded as being of greater relevance than that in other organisms. The demonstration that an agent or mixture can induce gene and chromosomal mutations in whole mammals indicates that it may have carcinogenic activity, although this activity may not be detectably expressed in any or all species. Relative potency in tests for mutagenicity and related effects is not a reliable indicator of carcinogenic potency. Negative results in tests for mutagenicity in selected tissues from animals treated in vivo provide less weight, partly because they do not exclude the possibility of an effect in tissues other than those examined. Moreover, negative results in short-term tests with genetic end-points cannot be considered to provide evidence to rule out carcinogenicity of agents or mixtures that act through other mechanisms (e.g. receptor-mediated effects, cellular toxicity with regenerative proliferation, peroxisome proliferation) (Vainio et al., 1992). Factors that may lead to misleading results in short-term tests have been discussed in detail elsewhere (Montesano et al., 1986).
When available, data relevant to mechanisms of carcinogenesis that do not involve structural changes at the level of the gene are also described.
The adequacy of epidemiological studies of reproductive outcome and genetic and related effects in humans is evaluated by the same criteria as are applied to epidemiological studies of cancer.
Structure-activity relationships that may be relevant to an evaluation of the carcinogenicity of an agent are also described.
For biological agents-viruses, bacteria and parasites-other data relevant to carcinogenicity include descriptions of the pathology of infection, molecular biology (integration and expression of viruses, and any genetic alterations seen in human tumours) and other observations, which might include cellular and tissue responses to infection, immune response and the presence of tumour markers.
In this section, the relevant epidemiological and experimental data are summarized. Only reports, other than in abstract form, that meet the criteria outlined on p. 4 are considered for evaluating carcinogenicity. Inadequate studies are generally not summarized: such studies are usually identified by a square-bracketed comment in the preceding text.
(a) Exposures
Human exposure to chemicals and complex mixtures is summarized on the basis of elements such as production, use, occurrence in the environment and determinations in human tissues and body fluids. Quantitative data are given when available. Exposure to biological agents is described in terms of transmission, and prevalence of infection.
(b) Carcinogenicity in humans
Results of epidemiological studies that are considered to be pertinent to an assessment of human carcinogenicity are summarized. When relevant, case reports and correlation studies are also summarized.
(c) Carcinogenicity in experimental animals
Data relevant to an evaluation of carcinogenicity in animals are summarized. For each animal species and route of administration, it is stated whether an increased incidence of neoplasms or preneoplastic lesions was observed, and the tumour sites are indicated. If the agent or mixture produced tumours after prenatal exposure or in single-dose experiments, this is also indicated. Negative findings are also summarized. Dose-response and other quantitative data may be given when available.
(d) Other data relevant to an evaluation of carcinogenicity and its mechanisms
Data on biological effects in humans that are of particular relevance are summarized. These may include toxicological, kinetic and metabolic considerations and evidence of DNA binding, persistence of DNA lesions or genetic damage in exposed humans. Toxicological information, such as that on cytotoxicity and regeneration, receptor binding and hormonal and immunological effects, and data on kinetics and metabolism in experimental animals are given when considered relevant to the possible mechanism of the carcinogenic action of the agent. The results of tests for genetic and related effects are summarized for whole mammals, cultured mammalian cells and nonmammalian systems.
When available, comparisons of such data for humans and for animals, and particularly animals that have developed cancer, are described.
Structure-activity relationships are mentioned when relevant.
For the agent, mixture or exposure circumstance being evaluated, the available data on end-points or other phenomena relevant to mechanisms of carcinogenesis from studies in humans, experimental animals and tissue and cell test systems are summarized within one or more of the following descriptive dimensions:
(i) Evidence of genotoxicity (i.e. structural changes at the level of the gene): for example, structure-activity considerations, adduct formation, mutagenicity (effect on specific genes), chromosomal mutation/aneuploidy
(ii) Evidence of effects on the expression of relevant genes (i.e. functional changes at the intracellular level): for example, alterations to the structure or quantity of the product of a proto-oncogene or tumour suppressor gene, alterations to metabolic activation/inactivation/DNA repair
(iii) Evidence of relevant effects on cell behaviour (i.e. morphological or behavioural changes at the cellular or tissue level): for example, induction of mitogenesis, compensatory cell proliferation, preneoplasia and hyperplasia, survival of premalignant or malignant cells (immortalization, immunosuppression), effects on metastatic potential
(iv) Evidence from dose and time relationships of carcinogenic effects and interactions between agents: for example, early/late stage, as inferred from epidemiological studies; initiation/promotion/progression/malignant conversion, as defined in animal carcinogenicity experiments; toxicokinetics
These dimensions are not mutually exclusive, and an agent may fall within more than one of them. Thus, for example, the action of an agent on the expression of relevant genes could be summarized under both the first and second dimension, even if it were known with reasonable certainty that those effects resulted from genotoxicity.
Evaluations of the strength of the evidence for carcinogenicity arising from human and experimental animal data are made, using standard terms.
It is recognized that the criteria for these evaluations, described below, cannot encompass all of the factors that may be relevant to an evaluation of carcinogenicity. In considering all of the relevant scientific data, the Working Group may assign the agent, mixture or exposure circumstance to a higher or lower category than a strict interpretation of these criteria would indicate.
(a) Degrees of evidence for carcinogenicity in humans and in experimental animals and supporting evidence
These categories refer only to the strength of the evidence that an exposure is carcinogenic and not to the extent of its carcinogenic activity (potency) nor to the mechanisms involved. A classification may change as new information becomes available.
An evaluation of degree of evidence, whether for a single agent or a mixture, is limited to the materials tested, as defined physically, chemically or biologically. When the agents evaluated are considered by the Working Group to be sufficiently closely related, they may be grouped together for the purpose of a single evaluation of degree of evidence.
(i) Carcinogenicity in humans
The applicability of an evaluation of the carcinogenicity of a mixture, process, occupation or industry on the basis of evidence from epidemiological studies depends on the variability over time and place of the mixtures, processes, occupations and industries. The Working Group seeks to identify the specific exposure, process or activity which is considered most likely to be responsible for any excess risk. The evaluation is focused as narrowly as the available data on exposure and other aspects permit.
The evidence relevant to carcinogenicity from studies in humans is classified into one of the following categories:
Sufficient evidence of carcinogenicity: The Working Group considers that a causal relationship has been established between exposure to the agent, mixture or exposure circumstance and human cancer. That is, a positive relationship has been observed between the exposure and cancer in studies in which chance, bias and confounding could be ruled out with reasonable confidence.
Limited evidence of carcinogenicity: A positive association has been observed between exposure to the agent, mixture or exposure circumstance and cancer for which a causal interpretation is considered by the Working Group to be credible, but chance, bias or confounding could not be ruled out with reasonable confidence.
Inadequate evidence of carcinogenicity: The available studies are of insufficient quality, consistency or statistical power to permit a conclusion regarding the presence or absence of a causal association, or no data on cancer in humans are available.
Evidence suggesting lack of carcinogenicity: There are several adequate studies covering the full range of levels of exposure that human beings are known to encounter, which are mutually consistent in not showing a positive association between exposure to the agent, mixture or exposure circumstance and any studied cancer at any observed level of exposure. A conclusion of 'evidence suggesting lack of carcinogenicity' is inevitably limited to the cancer sites, conditions and levels of exposure and length of observation covered by the available studies. In addition, the possibility of a very small risk at the levels of exposure studied can never be excluded.
In some instances, the above categories may be used to classify the degree of evidence related to carcinogenicity in specific organs or tissues.
(ii) Carcinogenicity in experimental animals
The evidence relevant to carcinogenicity in experimental animals is classified into one of the following categories:
Sufficient evidence of carcinogenicity: The Working Group considers that a causal relationship has been established between the agent or mixture and an increased incidence of malignant neoplasms or of an appropriate combination of benign and malignant neoplasms in (a) two or more species of animals or (b) in two or more independent studies in one species carried out at different times or in different laboratories or under different protocols.
Exceptionally, a single study in one species might be considered to provide sufficient evidence of carcinogenicity when malignant neoplasms occur to an unusual degree with regard to incidence, site, type of tumour or age at onset.
Limited evidence of carcinogenicity: The data suggest a carcinogenic effect but are limited for making a definitive evaluation because, e.g. (a) the evidence of carcinogenicity is restricted to a single experiment; or (b) there are unresolved questions regarding the adequacy of the design, conduct or interpretation of the study; or (c) the agent or mixture increases the incidence only of benign neoplasms or lesions of uncertain neoplastic potential, or of certain neoplasms which may occur spontaneously in high incidences in certain strains.
Inadequate evidence of carcinogenicity: The studies cannot be interpreted as showing either the presence or absence of a carcinogenic effect because of major qualitative or quantitative limitations, or no data on cancer in experimental animals are available.
Evidence suggesting lack of carcinogenicity: Adequate studies involving at least two species are available which show that, within the limits of the tests used, the agent or mixture is not carcinogenic. A conclusion of evidence suggesting lack of carcinogenicity is inevitably limited to the species, tumour sites and levels of exposure studied.
(b) Other data relevant to the evaluation of carcinogenicity and its mechanisms
Other evidence judged to be relevant to an evaluation of carcinogenicity and of sufficient importance to affect the overall evaluation is then described. This may include data on preneoplastic lesions, tumour pathology, genetic and related effects, structure-activity relationships, metabolism and pharmacokinetics, physicochemical parameters and analogous biological agents.
Data relevant to mechanisms of the carcinogenic action are also evaluated. The strength of the evidence that any carcinogenic effect observed is due to a particular mechanism is assessed, using terms such as weak, moderate or strong. Then, the Working Group assesses if that particular mechanism is likely to be operative in humans. The strongest indications that a particular mechanism operates in humans come from data on humans or biological specimens obtained from exposed humans. The data may be considered to be especially relevant if they show that the agent in question has caused changes in exposed humans that are on the causal pathway to carcinogenesis. Such data may, however, never become available, because it is at least conceivable that certain compounds may be kept from human use solely on the basis of evidence of their toxicity and/or carcinogenicity in experimental systems.
For complex exposures, including occupational and industrial exposures, the chemical composition and the potential contribution of carcinogens known to be present are considered by the Working Group in its overall evaluation of human carcinogenicity. The Working Group also determines the extent to which the materials tested in experimental systems are related to those to which humans are exposed.
(c) Overall evaluation
Finally, the body of evidence is considered as a whole, in order to reach an overall evaluation of the carcinogenicity to humans of an agent, mixture or circumstance of exposure.
An evaluation may be made for a group of chemical compounds that have been evaluated by the Working Group. In addition, when supporting data indicate that other, related compounds for which there is no direct evidence of capacity to induce cancer in humans or in animals may also be carcinogenic, a statement describing the rationale for this conclusion is added to the evaluation narrative; an additional evaluation may be made for this broader group of compounds if the strength of the evidence warrants it.
The agent, mixture or exposure circumstance is described according to the wording of one of the following categories, and the designated group is given. The categorization of an agent, mixture or exposure circumstance is a matter of scientific judgement, reflecting the strength of the evidence derived from studies in humans and in experimental animals and from other relevant data.
This category is used when there is sufficient evidence of carcinogenicity in humans. Exceptionally, an agent (mixture) may be placed in this category when evidence in humans is less than sufficient but there is sufficient evidence of carcinogenicity in experimental animals and strong evidence in exposed humans that the agent (mixture) acts through a relevant mechanism of carcinogenicity.
This category includes agents, mixtures and exposure circumstances for which, at one extreme, the degree of evidence of carcinogenicity in humans is almost sufficient, as well as those for which, at the other extreme, there are no human data but for which there is evidence of carcinogenicity in experimental animals. Agents, mixtures and exposure circumstances are assigned to either group 2A (probably carcinogenic to humans) or group 2B (possibly carcinogenic to humans) on the basis of epidemiological and experimental evidence of carcinogenicity and other relevant data.
This category is used when there is limited evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals. In some cases, an agent (mixture) may be classified in this category when there is inadequate evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals and strong evidence that the carcinogenesis is mediated by a mechanism that also operates in humans. Exceptionally, an agent, mixture or exposure circumstance may be classified in this category solely on the basis of limited evidence of carcinogenicity in humans.
This category is used for agents, mixtures and exposure circumstances for which there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of carcinogenicity in experimental animals. In some instances, an agent, mixture or exposure circumstance for which there is inadequate evidence of carcinogenicity in humans but limited evidence of carcinogenicity in experimental animals together with supporting evidence from other relevant data may be placed in this group.
This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals.
Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans.
Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.
This category is used for agents or mixtures for which there is evidence suggesting lack of carcinogenicity in humans and in experimental animals. In some instances, agents or mixtures for which there is inadequate evidence of carcinogenicity in humans but evidence suggesting lack of carcinogenicity in experimental animals, consistently and strongly supported by a broad range of other relevant data, may be classified in this group.
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Vol. 1. Analysis of Volatile Nitrosamines in Food (IARC Scientific Publications No. 18). Edited by R. Preussmann, M. Castegnaro, E.A. Walker & A.E. Wasserman (1978)
Vol. 2. Methods for the Measurement of Vinyl Chloride in Poly(vinyl chloride), Air, Water and Foodstuffs (IARC Scientific Publications No. 22). Edited by D.C.M. Squirrell & W. Thain (1978)
Vol. 3. Analysis of Polycyclic Aromatic Hydrocarbons in Environmental Samples (IARC Scientific Publications No. 29). Edited by M. Castegnaro, P. Bogovski, H. Kunte & E.A. Walker (1979)
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Vol. 5. Some Mycotoxins (IARC Scientific Publications No. 44). Edited by L. Stoloff, M. Castegnaro, P. Scott, I.K. O'Neill & H. Bartsch (1983)
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Vol. 7. Some Volatile Halogenated Hydrocarbons (IARC Scientific Publications No. 68). Edited by L. Fishbein & I.K. O'Neill (1985)
Vol. 8. Some Metals: As, Be, Cd, Cr, Ni, Pb, Se, Zn (IARC Scientific Publications No. 71). Edited by I.K. O'Neill, P. Schuller & L. Fishbein (1986)
Vol. 9. Passive Smoking (IARC Scientific Publications No. 81). Edited by I.K. O'Neill, K.D. Brunnemann, B. Dodet & D. Hoffmann (1987)
Vol. 10. Benzene and Alkylated Benzenes (IARC Scientific Publications No. 85). Edited by L. Fishbein & I.K. O'Neill (1988)
Vol. 11. Polychlorinated Dioxins and Dibenzofurans) (IARC Scientific Publications No. 108). Edited by C. Rappe, H.R. Buser, B. Dodet & I.K. O'Neill (1991)
Vol. 12. Indoor Air (IARC Scientific Publications No. 109). Edited by B. Seifert, H. van de Wiel, B. Dodet & I.K. O'Neill (1993)
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Last updated: 12 March 1998
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