● Chlorella pigment 　（クロレラ色素） 　　
　　 CAS: 　Food/Natural dye　 MW:

CA

CHL/IU

Max( 4.0 mg/ml, -S9), 24h

△

1)

1) Sofuni T. (Ed.): Data Book of Chromosomal Aberration Test In Vitro,, LIC, Tokyo (1998）  (Tables in English)

● Chlorfluazuron 　（アタプロン）　
　　 　71422-67-8 　　Pesticide　　 540.66

REC	B. subtilis	Max( 5 mg/disk)	□	1)
AM	Sal./E. coli	Max( 5 mg/plate, ±S9)	□	1)
CA	CHL/IU	Max( 3.3 x 10-6M, ±S9)	□	1)

1) Ishihara Sangyo Co. Ltd., J. Pesticide Science, 20, 225-228 (1995)

● Chloridazon （ピラミン;　アリセップ;　レナパック）
　　 　 1698-60-8　　Pesticide　　 221.6

REC	B. subtilis	Max( 2 mg/disk)	□	1)
AM	Sal./E. coli	Max( 1-3 mg/ml, ±S9)	□	1)
CA	Human LY	Max( 5.0 μg/ml, ±S9)	□	1)

1) BASF Japan: J. Pesticide Science, 17, S171-S176 (1992)

● Chlorinated camphene　（トキサフェン） (Toxaphene)　　　
　　　 8001-35-2　Insecticide　　 414 (average)

AM	Sal./E. coli	Min(?)	○	1)
DLv	Mice	Max (?)	□	2)

1) Hooper NK., et al.: Science, 205, 591-593 (1979)
2) Epstein SS., et al. :Toxicol. Appl. Pharmacol., 23, 288-325 (1972)

  US-NTP Genotoxicity Screening：
 ○ Ames Test: 　○

 IARC Carcinogenicity Criteria：
  Group 2B (Possibly carcinogenic to humans)

● Chlorinated naphthalenes (polychlorinated naphthalenes, or PCNs)
     Industry   C₁₀H_8anCl_n, where n = 1-8.

【Note】　(Cited from CICADs Documents, 34, 2001)

1,2,3,4-Tetrachloronaphthalene was not mutagenic in the Ames test with or without metabolic (S-9) activation in Salmonella typhimurium strains TA98, TA100, TA1535, and TA1537 at concentrations of 100-10 000 μg/plate; toxic effects were not reported (Haworth et al., 1983). There was also no mutagenic activity of 1-monochloronaphthalene in the Ames test with or without metabolic (S-9) activation in Salmonella typhimurium strains TA98 and TA100 at concentrations ranging from 0.1 to 100 μg/plate. 1-Monochloronaphthalene exerted a toxic effect in strain TA100 at a concentration of 100 μg/plate and in both strains tested at a concentration of 1000 μg/plate (Lofroth et al., 1985).    There are no data available for any other PCNs or from any other in vitro or in vivo test system on genotoxicity or related end-points. References ・Haworth S, Lawlor T, Mortelmans K, Speck W, Zeiger E (1983) Salmonella mutagenicity test results for 250 chemicals. Environmental mutagenesis, Supplement 1: 3-142. ・Lofroth G, Nilsson L, Agurell E, Sugiyama T (1985) Salmonella/ microsome mutagenicity of monochloro derivatives of some di- and tri- and tetracyclic aromatic hydrocarbons. Mutation research, 155: 91-94.

● Chlorine dioxide, 4% solution　（クロリンジオキサイド 4%溶液) (ClO2)　
　　 10049-04-4　 Industrial /Food　　　 67.46

AM	Sal./E. coli	Min (?)	○	1)
COM	Hum. Ly.	Min (0.2 ppm)	○w	4)
CA	CHL/IU	(4% Aqueous solution): Min ( 0.1 mg/ml, -S9), 24-48h	□	2)
MNv	Mice/ddY	Min ( 12.5 mg/kg, ip) 18h	○	3)

1) Smith RP. & Willhite CC.: Regul. Toxicol. Pharmacol., 11, 42-62 (1990)
2) Sofuni T. (Ed.): Data Book of Chromosomal Aberration Test In Vitro,, LIC, Tokyo (1998）  (Tables in English)
3) Hayashi M., et al., Food Chem. Toxic., 26, 487-500 (1988)
4) Buschini. A. et. al., Mutagenesis, 19, 157-162 (2004)

【Note】　Cited from CICADs Documents, 37, 2002)

Studies in bacteria     In a modified Ames test, 10, 100, and 1000 mg/litre of an aqueous extract from chlorine dioxide gas sterilization of a medical device was tested against Salmonella typhimurium TA1535 only, with and without S9 (Jeng & Woodworth, 1990). A negative result was obtained, although there are considerable doubts about whether or not the extract tested contained any chlorine dioxide.    The same authors (Jeng & Woodworth, 1990) performed another Ames test again using only TA1535 apparently against 10, 100, and 1000 mg chlorine dioxide gas/litre with and without metabolic activation. No further details of the techniques used were reported, and, although a negative result was claimed, no details were recorded. In vitro studies in mammalian systems    In an unpublished but well conducted in vitro cytogenetics assay, Chinese hamster ovary cells were treated with 0, 2.5, 5, 10, 15, 30, or 60 μg 0.2% chlorine dioxide/ml in phosphate-buffered saline solution in the absence of metabolic activation and 0, 6, 13, 25, 50, or 75 μg/ml in the presence of metabolic activation (Ivett & Myhr, 1986). Cell toxicity was observed at 60 μg/ml (-S9), and there was an absence of mitotic cells at 30 μg/ml. At 2.5-15 μg/ml, there was a marked dose-related, statistically significant increase in the number of metaphases with chromosome aberrations. In the presence of metabolic activation, cell toxicity and an absence of mitotic cells were observed at 75 μg/ml. A statistically significant increase in the number of metaphases with chromosome aberrations was noted at 50 μg/ml.    In a mouse lymphoma forward mutation assay using the L5178Y TK+/? system, cells were treated with 0-65 μg chlorine dioxide/ml in phosphate-buffered saline in the presence and absence of metabolic activation (Cifone & Myhr, 1986). In the absence of metabolic activation, marked toxicity was observed at the highest concentration used, 37 μg/ml. The relative growth (compared with control cultures) at the next two concentrations (15 and 24 μg/ml) was 13?18%. There was a dose-related increase in mutant frequency. Similarly, in the presence of metabolic activation, marked toxicity was observed at the highest concentration, 65 μg/ml, and there was also a dose-related increase in mutant frequency, indicating positive results both with and without metabolic activation in this test system.    An unpublished in vitro cell transformation assay is available in which BALB/3T3 cells were administered 0?6 μg aqueous chlorine dioxide/ml (Rundell & Myhr, 1986). The frequency of transformed foci was within the range of spontaneous transformations observed in historical controls, indicating a negative result. In vivo studies in mammalian systems    In a bone marrow cytogenetics assay, groups of five male and five female CD-1 mice received a single intraperitoneal injection of approximately 0, 2, 5, or 15 mg aqueous chlorine dioxide/kg body weight (Ivett & Myhr, 1984a). Bone marrow cells were analysed for chromosome aberrations at 6, 24, and 48 h. There were no clear effects on the mitotic index, but two males receiving approximately 15 mg chlorine dioxide/kg body weight died, and other signs of toxicity (poor grooming) were also observed at the highest dose level. There were no increases in the frequency of chromosome aberrations among treated animals at any of the sacrifice times when compared with controls.    Groups of five male and five female CD-1 mice received five daily oral gavage doses of approximately 0, 5, 10, or 20 mg aqueous chlorine dioxide/kg body weight (Meier et al., 1985). Animals were killed 6 h after the last administration, and 1000 polychromatic erythrocytes from the bone marrow of each animal were analysed for micronucleus formation. In addition, groups of four male and four female CD-1 mice were used for analysis of chromosome aberrations from bone marrow samples. Animals were exposed to the same doses as above, either as a single administration or using a repeated-exposure regime. Following single exposure, animals were killed at 6, 24, and 48 h post-administration and 50 metaphase cells taken from the bone marrow of each animal for analysis of chromosome aberrations. A negative result was obtained for micronucleus formation, and there were no increases in the number of structural or numerical chromosome aberrations (including an assessment of hyperploidy and polyploidy). Apparently, there were no overt signs of general toxicity.    Groups of five male ICR mice received a single intraperitoneal injection of approximately 0, 9, 21, 28, or 39 mg aqueous chlorine dioxide/kg body weight (Ivett & Myhr, 1984b). Following subcutaneous implantation of bromodeoxyuridine and 26 h after chlorine dioxide administration, approximately 25 bone marrow metaphase cells from each animal were assessed for sister chromatid exchange. Shortly after administration of aqueous chlorine dioxide, all animals showed hyperactive behaviour. There were no significant increases in sister chromatid exchange among any of the chlorine dioxide-treated groups. Studies in germ cells    The only study available (an unpublished dominant lethal assay in rats; Moore & Myhr, 1984) employed the intraperitoneal route of administration using up to 20 mg aqueous chlorine dioxide/kg body weight. This study did not show any mutagenic effects on male germ cells, and the result does provide some reassurance, in that even at levels affecting fertility and producing mortality, no evidence of mutagenic activity is seen. However, in addition, the results of in vivo mutagenicity studies conducted using this exposure route showed no evidence for effects in the bone marrow; hence, effects in the germ cells would not be expected. Other studies    Positive results for chlorine dioxide were claimed in various test systems (e.g., Ames test, in vitro cytogenetics, in vivo bone marrow micronucleus, in vivo chromosome aberrations). However, in general, the conduct of these tests was poorly described, and it has subsequently emerged that aqueous sodium chlorite solutions were tested rather than chlorine dioxide (Ishidate et al., 1984; Hayashi et al., 1988; Fujie & Aoki, 1989). References ・Jeng D, Woodworth A (1990a) Chlorine dioxide gas sterilisation of oxygenators in an industrial scale sterilizer: a successful model. Artificial organs, 14(5): 361-368. ・Ivett J, Myhr B (1984) Mutagenicity evaluation of chlorine dioxide in the mouse bone marrow cytogenetic assay. Kensington, MD, Litton Bionetics Inc. (Report No. 22202). ・Ivett J, Myhr B (1984b) Mutagenicity evaluation of chlorine dioxide in the sister chromatid exchange assay in vivo in the bone marrow. Kensington, MD, Litton Bionetics Inc. (Report No. 22204).・Ivett J, Myhr B (1986) Mutagenicity evaluation of chlorine dioxide in an in vitro cytogenetic assay. Kensington, MD, Litton Bionetics Inc. (Report No. 20990 ・Cifone M, Myhr B (1986) Mutagenicity evaluation of chlorine dioxide in the mouse lymphoma forward mutationassay. Kensington, MD, Litton Bionetics Inc. (Report No. 20989). ・Rundell J, Myhr B (1986) Evaluation of chlorine dioxide in the in vitro cell transformation of BALB/3T3 cells. Kensington, MD, Litton Bionetics Inc. (Report No. 20992). ・Meier J, Bull R, Stober J, Cimino M (1985) Evaluation of chemicals used for drinking water disinfection for production of chromosomal damage and sperm-head abnormalities in mice. Environmental mutagenesis, 7: 201-211 .・Moore M, Myhr B (1984) Evaluation of chlorine dioxide in the mouse dominant lethal assay. Kensington, MD, Litton Bionetics Inc. (Report No. 22203). ・Ishidate M Jr, Sofuni T, Yoshikawa K, Hayashi M, Nohmi T, Sawada M, Matsuoka A (1984) Primary mutagenicity screening of food additives currently used in Japan. Food and chemical toxicology, 22(8) :623-636. ・Hayashi M, Kishi M, Sofuni T, Ishidate M Jr (1988) Micronucleus tests in mice on 39 food additives and 8 miscellaneous chemicals. Food and chemical toxicology, 26(6): 487-500.; ・Fujie K, Aoki T (1989) Acute cytogenetic effects of alternative disinfectants on rat bone marrow cells in vivo. Mutation research, 216(6): 359.

● Chlornaphazine
　　 494-03-1　 Industrial /Food　　　 268.19

CA

CHL/IU

Min (0.005 mg/ml, -S9); D20= 0.0032mg/ml; TR= 8400

◎

1)

1) Sofuni T. (Ed.): Data Book of Chromosome Aberration Test in vitro, LIC, Tokyo (1998）  (Tables in English)

● Chloroacetaldehyde （クロロアセトアルデヒド）　　
　　　　 107-20-0　(Industrial use/ Fungicide)　　 78.50

AM	Sal./E. coli	Min (?)	○	1)
MB	A. nidulans (コウジカビ）	Min (?)	○	2)
MB	S. coelicolor (放線菌）	Min (?)	○	2)
MB	CHL/IU	Min (0.8 μg/ml, -S9), 24h; Poly also; D20= 0.00033	◎	5)
DNA	Sal./Repair	(hisG/TS24); Min ( 1.2 mg)	○	3)
SM	V79	Min( 6.4 μM)	○	4)

１）McCann J., et al. : Proc. Natl Acad. Sci. (USA), 72, 5135-5139 (1975)
2) Bignami M., et al: Chem. Biol. Interact., 30, 9-23 (1980)
3) Waskell L.: Mutation Res., 57, 141 (1978)
4) Kelly-Garvert F. & Legator MS.: Mutation Res., 21, 101-105 (1973)
5) Ministry of Labour, Japan: Mutagen. Test Data of Exist. Chem. Sub.; JETOC (1996)  (Tables in English)

●　Chloroacetic acid 　（クロロ酢酸; クロロエタン酸；モノクロロ酢酸））
　 　　 79-11-8　Industry 　 94.5

AM	Sal.	Max (5.0 mg/plate, ±Ｓ９）	□	1)
AM	E. coli	Max (?)	□	2, 3)
SCE	CHO	Min (?), -S9	○	2, 3)
MLA	L5178Y	Min (?), -S9	○	2, 3, 4)
SM	V79	Max (?), -S9	□	2, 3)
DNA	E. coli	Max (?),±Ｓ９	□	3)
CAv	Mice	Min (?), ip	○	2, 3, 4)
SLRLv	Drosophila	Min ( 900 ppm)	○	2, 3)

1)Ministry of Labour, Japan: Mutagen. Test Data of Exist. Chem. Sub.; JETOC (1996)  (Tables in English)
2) IUCLID (International Uniform Chemical Information Data Base), Data Sheet.,  EU (1995)
3) BUA Rep., 127 (1993)
4) Hazardous Substances Data Bank (HSDS), U.S. Natl Library Medicine (1996)

●　Chloroacetone　（クロロアセトン）
　 　　 78-95-5　Industry/Fungicide 　 92.53

AM	Sal.	Max (?)	□	1)
SLRL	Drosophila	(ih)Min (?)	○	2)

１） Sargent　EV., et al.: Am. Ind. Hyg. Assoc. J. 47, 375 (1986)
2) Auerbach C., et al.: Proc. R. Soc. Edinburgh, 62B, 284 (1947)

● α-Chloroacetophenone 　（α-クロロアセトフェノン）
　　　523-27-4　Lactimating agent　　 154.59

AM	Sal	Max (?)	□	1)
SCE	CHO	Max (?)	□	2)
CA	CHO	Min (?), -S9	○	2)

1) Zeiger E., et al.: Environ. Mutagen. 9 (Suppl.9)1-110 (1987)　
2) NTP: Technical Report No. 379. NIH, Research Triangle Park, NC (1990)

  US-NTP Genotoxicity Screening：
  ○ Ames Test (±S9): 　□
 ○ CA Test with CHO Cells:　○ｗ
  ○ SCE Test with CHO Cells: 　□

● Chloroacetyl chloride　（クロロアセチルクロライド) (CAC)
　　　 79-04-9　Industry/Intermediate　 112.95

AM	Sal.	Max (?)　±S9	□	1)
CA/SCE	CHL/IU	Max ( 0.5 mg/ml, ±S9), 6-18h	□	2)
UDSv	Rat/Hepatocytes	Min (4 g/kg, po, 17h):	○	1)

１） Simmon　VF.: Interium Report, Stanford Res. Inst. Report for the Dow Chemical Comapny, Midland, MI (1976)
2)　Sawada M., et al.: Mutation Res. , 187,157-163 (1987)

 (Additional Ref.)
1) Hazardous Substances Data Bank (HSDB), U.S. Natl Library of Medicine (1998)

●Top Page　（トップページ）

●Abbreviation 　（省略記号）

●Mutagenicity 　（変異原性）

●Test Systems　(試験法の種類）

●Technical Problems　（技術的問題点）

●List of　Compounds（化合物リスト）

●Evaluation of Results　（試験結果の評価）