NITE - Chemical Management Field

GHS Classification Results by the Japanese Government

GENERAL INFORMATION

Item	Information
CAS RN	108-95-2
Chemical Name	Phenol
Substance ID	R03-B-007-METI, MOE
Classification year (FY)	FY2021
Ministry who conducted the classification	Ministry of Economy, Trade and Industry (METI)/Ministry of the Environment (MOE)
New/Revised	Revised
Classification result in other fiscal year	FY2014 FY2006
Download of Excel format	Excel file

REFERENCE INFORMATION

Item	Information
Guidance used for the classification (External link)	GHS Classification Guidance for the Japanese Government (FY2019 revised edition (Ver. 2.0))
UN GHS document (External link)	UN GHS document
Definitions/Abbreviations (Excel file)	Definitions/Abbreviations
Model Label by MHLW (External link)	MHLW Website (in Japanese Only)
Model SDS by MHLW (External link)	MHLW Website (in Japanese Only)
OECD/eChemPortal (External link)	eChemPortal

PHYSICAL HAZARDS

Hazard class		Classification	Pictogram Signal word	Hazard statement (code)	Precautionary statement (code)	Rationale for the classification
1	Explosives	Not classified (Not applicable)	- -	-	-	There are no chemical groups associated with explosive properties present in the molecule.
2	Flammable gases	Not classified (Not applicable)	- -	-	-	Solid (GHS definition)
3	Aerosols	Not classified (Not applicable)	- -	-	-	Not aerosol products.
4	Oxidizing gases	Not classified (Not applicable)	- -	-	-	Solid (GHS definition)
5	Gases under pressure	Not classified (Not applicable)	- -	-	-	Solid (GHS definition)
6	Flammable liquids	Not classified (Not applicable)	- -	-	-	Solid (GHS definition). Besides, it is a substance with a low melting point, and there is information on a flash point of 82 deg C (closed cup) (GESTIS (Accessed July 2021)).
7	Flammable solids	Classification not possible	- -	-	-	No data available. There is information on a flash point of 82 deg C (closed cup) (GESTIS (Accessed July 2021)).
8	Self-reactive substances and mixtures	Not classified (Not applicable)	- -	-	-	There are no chemical groups present in the molecule associated with explosive or self-reactive properties.
9	Pyrophoric liquids	Not classified (Not applicable)	- -	-	-	Solid (GHS definition)
10	Pyrophoric solids	Not classified	- -	-	-	It is estimated that it does not ignite at normal temperatures from an autoignition temperature of 595 deg C (GESTIS (Accessed July 2021)).
11	Self-heating substances and mixtures	Classification not possible	- -	-	-	Test methods applicable to solid (melting point <= 140 deg C) substances are not available.
12	Substances and mixtures which, in contact with water, emit flammable gases	Not classified (Not applicable)	- -	-	-	The chemical structure of the substance does not contain metals or metalloids (B, Si, P, Ge, As, Se, Sn, Sb, Te, Bi, Po, At).
13	Oxidizing liquids	Not classified (Not applicable)	- -	-	-	Solid (GHS definition)
14	Oxidizing solids	Not classified (Not applicable)	- -	-	-	The substance is an organic compound containing oxygen (but not fluorine or chlorine) which is chemically bonded only to carbon or hydrogen.
15	Organic peroxides	Not classified (Not applicable)	- -	-	-	Organic compounds containing no bivalent -O-O- structure in the molecule.
16	Corrosive to metals	Classification not possible	- -	-	-	It is a solid with a melting point of 55 deg C or lower, but the classification is not possible due to no data.
17	Desensitized explosives	Not classified (Not applicable)	- -	-	-	There are no chemical groups associated with explosive properties present in the molecule.

HEALTH HAZARDS

Hazard class		Classification	Pictogram Signal word	Hazard statement (code)	Precautionary statement (code)	Rationale for the classification
1	Acute toxicity (Oral)	Category 4	Warning	H302	P301+P312 P264 P270 P330 P501	[Rationale for the Classification] Based on (1) to (7), it was classified in Category 4. [Evidence Data] (1) LD50 for rats: 414 mg/kg (Environmental Risk Assessment for Chemical Substances (Ministry of the Environment, 2002)) (2) LD50 for rats: between 340 to 650 mg/kg (Initial Risk Assessment Report (NITE, CERI, NEDO, 2008)) (3) LD50 for rats: 400 mg/kg (EPA Pesticides RED (2009)) (4) LD50 for rats: 650 mg/kg (EPA Pesticides RED (2009)) (5) LD50 for rats: 1,030 mg/kg (EPA Pesticides RED (2009)) (6) LD50 for rats: between 340 to 530 mg/kg (EFSA (2013), AICIS IMAP (2014)) (7) LD50 for rats: 530 mg/kg (ACGIH (2001))
1	Acute toxicity (Dermal)	Category 3	Danger	H311	P302+P352 P361+P364 P280 P312 P321 P405 P501	[Rationale for the Classification] Based on (1) to (8), it was classified in Category 3. [Evidence Data] (1) LD50 for rats: 669 mg/kg (Environmental Risk Assessment for Chemical Substances (Ministry of the Environment, 2002)) (2) LD50 for rats: between 525 to 714 mg/kg (Initial Risk Assessment Report (NITE, CERI, NEDO, 2008)) (3) LD50 for rats (non-occlusive application): 0.68 mL/kg (converted value at the density of 1.071 g/cm3: 728 mg/kg) (EPA Pesticides RED (2009)) (4) LD50 for rats (occlusive application): 0.50 mL/kg (converted value at the density of 1.071 g/cm3: 536 mg/kg) (EPA Pesticides RED (2009)) (5) LD50 for rats: 669.4 mg/kg (EPA Pesticides RED (2009)) (6) LD50 for rabbits: 850 mg/kg (Environmental Risk Assessment for Chemical Substances (Ministry of the Environment, 2002)) (7) LD50 for rabbits: 630 mg/kg (EPA Pesticides RED (2009)) (8) LD50 for rabbits: between 850 to 1,400 mg/kg (Initial Risk Assessment Report (NITE, CERI, NEDO, 2008))
1	Acute toxicity (Inhalation: Gases)	Not classified	- -	-	-	[Rationale for the Classification] Solid (GHS definition). It was classified as "Not classified."
1	Acute toxicity (Inhalation: Vapours)	Classification not possible	- -	-	-	[Rationale for the Classification] Based on (1) and (2), it does not correspond to category 1, but no category could be identified. Therefore, classification was not possible. Also, since the exposure concentration was lower than 90% (414 ppm) of the saturated vapor pressure concentration, it was judged to be in a vapor state and classified based on the reference value in units of ppmV. [Evidence Data] (1) LC50 (8 hours) for rats: > 900 mg/m3 (converted 4-hour equivalent value: 1,800 mg/m3 (330.7 ppm)) (EPA Pesticides RED (2009), Hazard Assessment Report (CERI, NITE, 2008), AICIS IMAP (2014)) (2) The vapor pressure of this substance was 0.35 mmHg (25℃) (HSDB (Accessed July 2021)).
1	Acute toxicity (Inhalation: Dusts and mists)	Classification not possible	- -	-	-	[Rationale for the Classification] Classification not possible due to lack of data.
2	Skin corrosion/irritation	Category 1	Danger	H314	P301+P330+P331 P303+P361+P353 P305+P351+P338 P304+P340 P260 P264 P280 P310 P321 P363 P405 P501	[Rationale for the Classification] Based on (1) to (5), it was classified in Category 1. [Evidence Data] (1) An administration of drugs containing this substance to the local skin caused the incidence of irritant dermatitis, and a local skin exposure caused bleaching action or erythema in that site, resulting in corrosion or necrosis in some cases (Hazard Assessment Report (CERI, NITE, 2008), Environmental Risk Assessment for Chemical Substances (Ministry of the Environment, 2002)). (2) This substance showed strong irritation to the skin, eye, and mucosa when humans were orally or dermally exposed to it (Hazard Assessment Report (CERI, NITE, 2008)). (3) This substance showed corrosivity to the skin of rabbits (EPA Pesticides RED (2009)). (4) It was reported that, as a result of an application of this substance to the eye or skin of rabbits, rats, mice, and pigs, reddening, inflammations, discoloration, rash, ulceration, necrosis, and corrosivity were observed, and this substance was considered to show strong irritation or corrosivity to the eyes and skin (Hazard Assessment Report (CERI, NITE, 2008), CEPA PSAR (2000), EHC (1994)). (5) It was reported that, in an in vitro skin corrosion test (OECD TG 431), corrosive property to the skin was observed (AICIS IMAP (2014)). [Reference Data, etc.] (6) In the Ministry of Labour Notification No. 33 issued in 1996 (revised by the Ministry of Health, Labour and Welfare Notification No. 316 in 2013), this substance is designated as "phenol (carbolic acid)" in simple chemical substances or compounds (including alloys) designated by the Minister of Health, Labour and Welfare based on Appended Table 1-2, (iv) 1 of the Ordinance for Enforcement of the Labor Standards Act, and diseases (subjective symptoms such as headache, dizziness, and vomiting, skin disorders, disorders in the anterior part of the eye, respiratory tract and lung disorders) with specific symptoms or disorders caused by occupations exposed to this substance as main symptoms or disorders, are designated as occupational diseases.
3	Serious eye damage/eye irritation	Category 1	Danger	H318	P305+P351+P338 P280 P310	[Rationale for the Classification] Based on (1) to (5), it was classified in Category 1. [Evidence Data] (1) It was classified in Category 1 for skin corrosion/irritation. (2) Phenol showed strong irritation to the skin, eyes, and mucosa when humans were orally or dermally exposed to it (Hazard Assessment Report (CERI, NITE, 2008)). (3) This substance caused severe damage to the cornea of rabbits in a 15% solution and lesser damage to the cornea in a 5% solution (EPA Pesticides RED (2009)). (4) It was reported that, in an acute eye irritation/corrosion test (equivalent to OECD TG 405, 14-day observation) with rabbits, severe conjunctivitis, iritis, and corneal opacities, and ulcerations were observed, and those symptoms did not disappear even after 14 days (EPA Pesticides RED (2009), Hazard Assessment Report (CERI, NITE, 2008), AICIS IMAP (2014), REACH registration dossier (Accessed July 2021)). (5) It was reported that, as a result of an application of phenol to the eye or skin of rabbits, rats, mice, and pigs, reddening, inflammations, discoloration, rash, ulceration, necrosis, and corrosivity were observed, and this substance was considered to show strong irritation or corrosivity to the eyes and skin (Hazard Assessment Report (CERI, NITE, 2008)). [Reference Data, etc.] (6) In the Ministry of Labour Notification No. 33 issued in 1996 (revised by the Ministry of Health, Labour and Welfare Notification No. 316 in 2013), this substance is designated as "phenol (carbolic acid)" in simple chemical substances or compounds (including alloys) designated by the Minister of Health, Labour and Welfare based on Appended Table 1-2, (iv) 1 of the Ordinance for Enforcement of the Labor Standards Act, and diseases (subjective symptoms such as headache, dizziness, and vomiting, skin disorders, disorders in the anterior part of the eye, respiratory tract and lung disorders) with specific symptoms or disorders caused by occupations exposed to this substance as main symptoms or disorders, are designated as occupational diseases.
4	Respiratory sensitization	Classification not possible	- -	-	-	[Rationale for the Classification] Classification not possible due to lack of data.
4	Skin sensitization	Not classified	- -	-	-	[Rationale for the Classification] Based on (1) to (3), it was classified as "Not classified." [Evidence Data] (1) It was reported that two volunteers were skin-induced with 2% phenol in solution and challenged with 1% solution, but no sensitization was observed (Hazard Assessment Report (CERI, NITE, 2008)). (2) It was reported that, in a maximization test, 24 volunteers were induced with 2% phenol solution and then later challenged with 1% phenol solution, and no sensitization reactions were observed (AICIS IMAP (2014), REACH registration dossier (Accessed July 2021)). (3) It was reported that, in a modified Buehler test (equivalent to OECD TG 406, local administration: 10% solution) with guinea pigs (n=10), the positive rate at 24 hours after the patch was removed was 0% (0/9 animals) (Hazard Assessment Report (CERI, NITE, 2008), CEPA PSAR (2000), AICIS IMAP (2014), EHC (1994), SIAP (2004), REACH registration dossier (Accessed July 2021)).
5	Germ cell mutagenicity	Category 2	Warning	H341	P308+P313 P201 P202 P280 P405 P501	[Rationale for the Classification] Based on (1) to (6), the biological relevance of the micronucleus induction in the oral route was low, however, since effects on the contact sites in other routes were considered, it was classified in Category 2. Also, the positive findings of the chromosomal aberration test using germ cells, which were considered to be the basis for the previous classification 1B, were considered to be insufficient, and therefore, they were not adopted as evidence of the classification. [Evidence Data] (1) As for in vivo, positive results were obtained in a chromosomal aberration test (oral (drinking water) administration) using spermatogonia/primary spermatocytes, which was carried out as a part of a reproduction study with mice; negative results were obtained in a chromosomal aberration test (oral administration and intraperitoneal injection) using the bone marrow cells of rats; positive or negative results were obtained in a micronucleus test (oral administration or intraperitoneal injection) using the bone marrow cells of mice; and positive results were obtained both in the bone marrow of dams and in the liver of fetuses in a micronucleus test (oral administration) using pregnant mice. In addition, negative results were obtained in both a DNA single-strand break test, which targeted the testis cells of rats and the bone marrow cells of mice, and a DNA adduct formation test, which targeted various organs of rats (Hazard Assessment Report (CERI, NITE, 2008)). (2) As for in vitro, in a bacterial reverse mutation assay, negative results were obtained as a whole, and in a mammalian cell gene mutation test, many positive results were reported, but many of them were weakly positive at high concentrations at which cytotoxicity occurred. In addition, in a mammalian chromosomal aberration test, a micronucleus assay, etc., positive results were obtained mainly at cytotoxic concentrations in chromosome mutation assays (REACH registration dossier (Accessed July 2021)). (3) Among the in vivo data in (1), positive results in a chromosomal aberration test using germ cells of mice, which were mentioned at the beginning, were not adopted in the assessment by the EU. According to the EHC 161 (1994), the original source was the report of 1977 which was the results of an unconventional study that was carried out as a part of a five-generation test, and the description was also insufficient. In addition, as another mammalian germ cell mutagenicity test described in the EHC, negative results were obtained in studies of DNA strand breakage (5-day intraperitoneal injection) using the testis of rats (EHC 161 (1994)). The EU avoided the assessment for the germ cell mutagenicity of phenol, considering that there were no sufficient test data, and assessed the substance as a somatic cell mutagenic substance (EU REACH CoRAP (2015), EU RAR (2006), REACH registration dossier (Accessed July 2021)). (4) The EU was also skeptical about the somatic cell mutagenicity of phenol. In an in vivo micronucleus test, contradictory results (positive and negative) were obtained, but the positive results were observed only at high doses, and the results were also borderline positive, inducing 2 -2.5-fold increases of micronuclei in polychromatic erythrocytes. Furthermore, it was pointed out that the increase of micronuclei in animals receiving high doses may be an effect due to phenol-induced hypothermia, which may affect the fidelity of chromosome segregation, causing a disturbance of mitotic segregation, and by controlling the body temperature to prevent hypothermia, an effect of reducing micronuclei was obtained (REACH registration dossier (Accessed July 2021), EU RAR (2006), EFSA (2013)). (5) The EFSA experts' panel concluded that orally administered phenol was devoid of biologically relevant genotoxicity in vivo (EFSA (2013)). For the classification of phenol in Muta. Category 2, the EU commented that phenol did not have relevant genotoxicity in vivo for the oral route of exposure, but the possibility of mutagenicity still remained for other routes of exposure, and there was no change in the positioning of phenol as a germ cell mutagenic substance (EU REACH CoRAP (2015)). (6) The ATSDR indicated that phenol had been tested for genotoxicity in a variety of in vivo and in vitro tests, but the results of these assays had been equivocal. It indicated that phenol itself appeared to be potentially genotoxic, although this might be a result of the action of its metabolites, and additional genotoxicity studies of phenol were not necessary (ATSDR (2008)).
6	Carcinogenicity	Not classified	- -	-	-	[Rationale for the Classification] Based on (1) and (2), it was classified as "Not classified." [Evidence Data] (1) As for the classification results by domestic and international organizations, the IARC classified this substance in Group 3 (IARC 71 (1999)), ACGIH classified it in A4 (ACGIH (7th, 2001)), and the EPA classified it in Group D (IRIS (2002)). (2) In a carcinogenicity study with rats and mice dosed by drinking water for two years, in a test with mice, there was no increase in the incidence of tumor by the administration in either males or females at doses up to 5,000 ppm. In a test with rats, increases in the incidence of adrenal medulla pheochromocytoma, thyroid C-cell carcinoma, and testicular interstitial cell tumors were observed in males of a group dosed at or above 2,500 ppm, but the incidence of tumors was not found as dose-dependent, and leukemia and lymphomas, which were observed in males of a 2,500 ppm group, were also observed in the control group. Therefore, there was no incidence of dose-dependent tumors by the administration in this test. Phenol was not carcinogenic for either male or female rats, or for male or female mice (Environmental Risk Assessment for Chemical Substances (Ministry of the Environment, 2002), Hazard Assessment Report (CERI, NITE, 2008), ACGIH (7th, 2001), EPA Pesticides RED (2007), EFSA (2013), AICIS IMAP (2014)). [Reference Data, etc.] (3) It was reported that, in a two-step carcinogenicity study using DMBA and benzopyrene as an initiator, phenol showed the promotion action by repeated oral or dermal administration to mice (Hazard Assessment Report (CERI, NITE, 2008), Environmental Risk Assessment for Chemical Substances (Ministry of the Environment, 2002), ACGIH (7th, 2001)).
7	Reproductive toxicity	Category 1B	Danger	H360	P308+P313 P201 P202 P280 P405 P501	[Rationale for the Classification] Based on (1) to (3), it was classified in Category 1B. In (1), a decrease in pup survival was observed in offspring at a dose at which no severe general toxic effects were observed in parent animals. [Evidence Data] (1) It was reported that, in a two-generation reproduction toxicity study by oral administration of drinking water to rats (OECD TG416, GLP, approximately 16 weeks from 10 weeks prior to mating), at 5,000 ppm, a decrease in body weight or reduced body weight gain, and decreases in food and water consumption were observed in F0 and F1 parent animals, and a decrease in pup survival (F1 and F2), and delayed days of vaginal opening and preputial separation (F1) were observed in offspring (Hazard Assessment Report (CERI, NITE, 2008), US AEGL (2009), EFSA (2013), REACH registration dossier (Accessed June 2021), Ryan et al. (2001)). (2) It was reported that, in two developmental toxicity studies with rats dosed by gavage (days 6 to 15 of gestation), no developmental toxicity was observed (Hazard Assessment Report (CERI, NITE, 2008), Environmental Risk Assessment for Chemical Substances (Ministry of the Environment, 2002), US AEGL (2009), EFSA (2013)). (3) It was reported that, in a developmental toxicity study with rats dosed by gavage (days 6 to 15 of gestation), at 360 mg/kg/day, a decrease in body weight, reduced body weight gain, decreases in food consumption, salivation, tachypnea, and death (1 animal) were observed in parent animals, and reduced body weight, and delayed ossification of the metatarsal were observed in offspring, but there were no malformations (Hazard Assessment Report (CERI, NITE, 2008), EFSA (2013), AICIS IMAP (2014)). [Reference Data, etc.] (4) This substance was classified in Group 3 of reproductive toxicants by the Japan Society For Occupational Health (JSOH) (OEL Documentations (Reproductive toxicant classification) (Japan Society For Occupational Health (JSOH)) , 2014)). (5) It was reported that, in a developmental toxicity study with mice dosed by gavage (days 6 to 15 of gestation), reduced body weight, decreased survival, and cleft palate (due to stress) were observed in fetuses at a dose at which noticeable general toxic effects (death (4/36 animals), tremor, ataxia, etc.) were observed in parent animals (Hazard Assessment Report (CERI, NITE, 2008), US AEGL (2009), REACH registration dossier (Accessed June 2021), AICIS IMAP (2014)). (6) In a developmental toxicity study with rats dosed by gavage (days 6-19 of gestation), a decrease in the number of births was observed in parent animals at or above 40 mg/kg/day, and reduced body weight gain in parent animals, and increases in death at birth and kinked tails in offspring were observed at 53 mg/kg/day (Hazard Assessment Report (CERI, NITE, 2008), Environmental Risk Assessment for Chemical Substances (Ministry of the Environment, 2002), US AEGL (2009), EFSA (2013)). However, a decrease in the number of births or an increase in kinked tails in offspring was considered to be due to severe effects on dams because respiratory syndrome was observed in the dams, and therefore, it was considered that the findings could not be used for the assessment of developmental toxicity (EFSA (2013)).
8	Specific target organ toxicity - Single exposure	Category 1 (nervous system, respiratory organs, cardiovascular system, kidney)	Danger	H370	P308+P311 P260 P264 P270 P321 P405 P501	[Rationale for the Classification] Based on (1) to (5), it was classified in Category 1 (nervous system, respiratory organs, cardiovascular system, kidney). [Evidence Data] (1) It was reported that, after oral ingestion (57 g/person), severe irritation to the digestive tract such as the stomach, etc. were observed, and effects on the heart, blood vessels, and respiratory organs were observed (Hazard Assessment Report (CERI, NITE, 2008), EHC (1994)). (2) It was reported that, as acute intoxication of phenol due to inhalation exposure, anorexia, weight loss, headache, vertigo, salivation, and dark urine were known, but there was no death (Hazard Assessment Report (CERI, NITE, 2008), Environmental Risk Assessment for Chemical Substances (Ministry of the Environment, 2002), EHC (1994)). (3) It was reported that, as a result of dermal absorption of phenol in large amounts, toxic symptoms appeared rapidly, and hyperventilation, respiratory distress, cardiac dysrhythmias, cardiovascular shock, severe metabolic acidosis, methemoglobinemia, acute renal failure, renal damage, dark urine, neurological effects such as convulsions, coma, death, etc. were observed (Hazard Assessment Report (CERI, NITE, 2008), Environmental Risk Assessment for Chemical Substances (Ministry of the Environment, 2002), EHC (1994)). (4) It was reported that, as acute symptoms which were observed in animal studies of phenol, depression of the central nervous system, spasms, and hyperexcitability of the nervous and muscular systems, irregular heart rate increase followed by decrease, the blood pressure which at first increased then fell, salivation, dyspnea, a decrease in the body temperature, etc. were observed irrespective of the route of administration, and after oral ingestion, the mucous membranes of the throat and esophagus showed swelling, corrosion, and necrosis, with hemorrhages, and toxicity to the liver, kidney, adrenal gland, and thymus were observed (Hazard Assessment Report (CERI, NITE, 2008)). (5) In the Ministry of Labour Notification No. 33 issued in 1996 (revised by the Ministry of Health, Labour and Welfare Notification No. 316 in 2013), this substance is designated as "phenol (carbolic acid)" in simple chemical substances or compounds (including alloys) designated by the Minister of Health, Labour and Welfare based on Appended Table 1-2, (iv) 1 of the Ordinance for Enforcement of the Labor Standards Act, and diseases (subjective symptoms such as headache, dizziness, and vomiting, skin disorders, disorders in the anterior part of the eye, respiratory tract and lung disorders) with specific symptoms or disorders caused by occupations exposed to this substance as main symptoms or disorders, are designated as occupational diseases.
9	Specific target organ toxicity - Repeated exposure	Category 1 (central nervous system, cardiovascular system, blood system, liver, kidney)	Danger	H372	P260 P264 P270 P314 P501	[Rationale for the Classification] Based on the effects on humans in (1), the cardiovascular system was considered to be the target organ, and based on (2) to (7), effects on the central nervous system, blood system, kidney, and liver were observed within the dose range for Category 1. Therefore, it was classified in Category 1 (central nervous system, cardiovascular system, blood system, liver, kidney). Also, among the target organs which were adopted as the target organs by the previous classification, the spleen and thymus were not adopted for the classification because details of the symptoms were not clear and less reliable and the findings of the digestive tract were judged to be due to irritation. [Evidence Data] (1) It was reported that a cardiovascular disease (CVD) mortality study was conducted for rubber manufacturing workers during the 15-year follow-up period, and as a result, an increase in the mortality due to cardiovascular diseases, which was dependent on the exposure period, was observed in workers who might have been exposed to phenol (Hazard Assessment Report (CERI, NITE, 2008), EHC (1994)). (2) It was reported that, in a repeated dose 2-week oral toxicity study with rats, atrophy and necrosis of the spleen and thymus (details were unknown) were observed in 1 animal at or above 12 mg/kg/day (converted guidance value: 1.85 mg/kg/day, within the range for Category 1), and behavioral changes (reduced locomotor activity, increased rearing), effects on the kidney (necrosis of the renal tubules, papillary hemorrhage, protein cast of the renal tubules), and atrophy and necrosis of the spleen and thymus (details were unknown) in 2 animals were observed at or above 40 mg/kg/day (converted guidance value: 6.2 mg/kg/day, within the range for Category 1) (Hazard Assessment Report (CERI, NITE, 2008)). (3) It was reported that, in another repeated dose 2-week oral toxicity study with rats, tremor, and effects on the kidney (protein cast and necrosis of the renal tubules, papillary hemorrhage) were observed at 4 to 120 mg/kg/day or below (converted guidance value: 0.62 to 18.7 mg/kg/day, within the range for Category 1 and Category 2) (Hazard Assessment Report (CERI, NITE, 2008)). (4) It was reported that, in a repeated dose 4-week oral toxicity study with mice dosed by drinking water, a dose-dependent significant decrease in the red blood cell count was observed, and concentrations of neurotransmitters such as dopamine, noradrenaline, etc. and their metabolites decreased in the hypothalamus of the brain, midbrain striatum, etc. at or above 4.7 ppm (converted guidance value: 0.55 mg/kg/day, within the range for Category 1) (Hazard Assessment Report (CERI, NITE, 2008)). (5) It was reported that, in a repeated dose 3.5-month oral toxicity study with guinea pigs, thrombocytopenia, the incidence of slight eosinophilia and reticulocytosis, and a decrease in the erythroblast maturation index of the bone marrow were observed at 0.5 mg/kg/day (within the range for Category 1) (Hazard Assessment Report (CERI, NITE, 2008)). (6) It was reported that, in a 15-day repeated inhalation (vapor) exposure test with rats, effects on the central nervous system (inclined plane test), and effects on the liver (increases in AST and ALT, liver damage, etc.) were observed at or above 100 mg/m3 (0.1 mg/L, within the range for Category 1) (Hazard Assessment Report (CERI, NITE, 2008)). (7) It was reported that, in a 61-day repeated inhalation (vapor) exposure test with rats, neurological effects (shortened muscle extension time value), and increased blood cholinesterase activities were observed at or above 0.012 mg/m3 (0.000012 mg/L, within the range for Category 1) (Hazard Assessment Report (CERI, NITE, 2008)). [Reference Data, etc.] (8) As a report on occupational exposure before 1900, there was a case of chronic poisoning due to inhalation of phenol called phenol marasmus (carbol marasmus) in physicians and their helpers, and it was reported that marasmus with anorexia, weight loss, headache, vertigo, salivation, dark urine, etc. developed among workers in a laboratory using boiled phenol solutions (Hazard Assessment Report (CERI, NITE, 2008), EHC (1994)). (9) It was reported that 100 residents who used groundwater, which was contaminated due to an accidental phenol spill (US Wisconsin, 1974), as drinking water (estimated ingestion amount: 10 to 240 mg/person) complained of health effects (diarrhea, mouth sores, dark urine, burning of the mouth), but no abnormalities were found in physical examinations or clinical biochemical examinations 6 months after the accident (Hazard Assessment Report (CERI, NITE, 2008), EHC (1994)). (10) It was reported that, as a result of comparison of a group of 20 male workers who were exposed to phenol alone while working in an oil refining plant (Group I: mean duration of exposure 13.2 ± 6.6 years, time-weighted average exposure concentration: 5.4 ppm), a group of 32 male workers who were exposed to mixtures of phenol (4.7 ppm), benzene (0.7 ppm), toluene (220 ppm), and methyl ethyl ketone (90 ppm) (Group II: mean duration of exposure 14.3 ± 6.1 years), and a group of subjects who were employees from the administrative departments located far away from any exposure to phenol (Group III: n = 30), a significant increase in serum ALT and AST activity, prolonged blood clotting time, and lower serum creatinine were observed in exposed groups (Group I and II) (US AEGL (2009)). (11) In the Ministry of Labour Notification No. 33 issued in 1996 (revised by the Ministry of Health, Labour and Welfare Notification No. 316 in 2013), this substance is designated as "phenol (carbolic acid)" in simple chemical substances or compounds (including alloys) designated by the Minister of Health, Labour and Welfare based on Appended Table 1-2, (iv) 1 of the Ordinance for Enforcement of the Labor Standards Act, and diseases (subjective symptoms such as headache, dizziness, and vomiting, skin disorders, disorders in the anterior part of the eye, respiratory tract and lung disorders) with specific symptoms or disorders caused by occupations exposed to this substance as main symptoms or disorders, are designated as occupational diseases.
10	Aspiration hazard	Classification not possible	- -	-	-	[Rationale for the Classification] Classification not possible due to lack of data.

ENVIRONMENTAL HAZARDS

Hazard class		Classification	Pictogram Signal word	Hazard statement (code)	Precautionary statement (code)	Rationale for the classification
11	Hazardous to the aquatic environment Short term (Acute)	Category 2	- -	H401	P273 P501	It was classified in Category 2 from 48-hour LC50 = 3.1 mg/L for crustacea (Ceriodaphnia dubia) (EU RAR (2006), SIAP (2004), EHC (1994), Initial Risk Assessment (NITE, CERI, NEDO, 2007), Environmental Risk Assessment for Chemical Substances (Ministry of the Environment, 2002)).
11	Hazardous to the aquatic environment Long term (Chronic)	Category 2	-	H411	P273 P391 P501	It was classified in Category 2 because it was rapidly degradable (a degradation rate by BOD: 85% (Biodegradation and Bioconcentration Results of Existing Chemical Substances under the Chemical Substances Control Law, METI, 1979)), and due to 60-day NOEC = 0.077 mg/L for fish (Cirrhina mrigala) (SIAP (2004)). The classification result was changed from the previous classification by using new information.
12	Hazardous to the ozone layer	Classification not possible	- -	-	-	This substance is not listed in the Annexes to the Montreal Protocol.

NOTE:

GHS Classification Result by the Japanese Government is intended to provide a reference for preparing a GHS label or SDS for users. To include the same classification result in a label or SDS for Japan is NOT mandatory.
Users can cite or copy this classification result when preparing a GHS label or SDS. Please be aware, however, that the responsibility for a label or SDS prepared by citing or copying this classification result lies with users.
This GHS classification was conducted based on the information sources and the guidance for classification and judgement which are described in the GHS Classification Guidance for the Japanese Government etc. Using other literature, test results etc. as evidence and including different content from this classification result in a label or SDS are allowed.
Hazard statement and precautionary statement will show by hovering the mouse cursor over a code in the column of "Hazard statement" and "Precautionary statement," respectively. In the excel file, both the codes and statements are provided.
A blank or "-" in the column of "Classification" denotes that a classification for the hazard class was not conducted in the year.
An asterisk “*” in the column of “Classification” denotes that “Not classified (or No applicable)” and/or “Classification not possible” is applicable. Details are described in the column of “Rationale for the classification”. If no English translation is available for “Rationale for the classification,” please refer to the Japanese version of the results.

To GHS Information