Substances Included Synonyms

Therapeutic Toxic Class

A)

Specific Substances

1) Cum
2) Cumol
3) Isopropylbenzene
4) Isopropylbenzol
5) Propane, 2-phenyl
6) RCRA WASTE NUMBER: UO55
7) 1-methylethylbenzene
8) 2-Fenilpropano (Italian)
9) 2-phenylpropane
10) CAS 98-82-8

1.2.1) MOLECULAR FORMULA
1) C9-H12
2) C6H5CH(CH3)2

Available Forms Sources

A)

1) Cumene is a colorless, flammable liquid with a sharp, aromatic, or gasoline-like odor (Bingham et al, 2001). Cumene is produced in technical, research, and pure grades (HSDB , 2001).

a) Impurities that may occur in cumene are sulfur compounds at a maximum of 2 ppm, and olefinic materials from 200-700 ppm (HSDB , 2001).

B)

1) Propylene + benzene, utilizing an acid catalyst such as phosphoric acid; Friedel-Crafts alkylation (Ashford, 1994; Clayton & Clayton, 1994; Lewis, 1997; Bingham et al, 2001).
2) Fractional distillation is employed to recover cumene from petroleum (Clayton & Clayton, 1994; Lewis, 1997; Bingham et al, 2001).
3) Cumene is produced through distillation of coal tap naptha fractions (Lewis, 1997).
4) The release of cumene from the following sources has been estimated to total 21 million pounds annually (Howard, 1997):

a) Manufacturing and processing plants release cumene; releases also occur during transport of the compound.
b) Because it is a component of both finished fuels and crude oil, cumene is released through incomplete fossil fuel combustion, evaporation from motor vehicle fueling stations, distribution of motor vehicle fuels, and oil spills.
c) Cumene is released in consumption of cigarette tobacco.

5) Other human-made sources of cumene release include jet engine exhaust, outboard motor function, use of solvents, building materials, vulcanization of rubber, and manufacture of paint, textiles, and pharmaceuticals (Howard, 1997).
6) Additional anthropogenic cumene releases are caused by steel and iron manufacturing, roofing and paving, ore and coal mining, manufacture of plastics and organics, pesticide production, leather tanning, ink formulation, publishing and printing, pulp and paper manufacture, and electroplating (Howard, 1997).
7) Natural sources of cumene include essential oils from plants, various foodstuffs, and marsh grasses (Howard, 1997).

C)

1) Cumene is used in the production of acetone, phenol, acetophenone, alpha-methylstyrene, and styrene (ACGIH, 1991; Sittig, 1991; Ashford, 1994; Clayton & Clayton, 1994; Hathaway et al, 1996; ITI, 1995; Lewis, 1997; Bingham et al, 2001).

a) According to Howard (1997), approximately 98% of cumene produced in the United States is used in manufacture of acetone and phenol.

2) Cumene is used in the synthesis of polymerization catalysts, diisopropylbenzene, and dicumyl peroxide (HSDB , 2001).
3) This compound serves as a raw material for oxidation-catalysts and peroxides (ITI, 1995) and is a constituent of naptha (HSDB , 2001).
4) Cumene is commonly used as a thinner for paints, enamels, and lacquers, and as a constituent for petroleum-based solvents (ACGIH, 1991; Sittig, 1991; Ashford, 1994; Clayton & Clayton, 1994; Hathaway et al, 1996; Bingham et al, 2001).
5) Additionally, it is a high-octane aviation fuel component (ACGIH, 1991; Hathaway et al, 1996; ITI, 1995; Sittig, 1991), a catalyst for polyester and acrylic type resins (HSDB , 2001), and it is used in perfume manufacture (Clayton & Clayton, 1994; Bingham et al, 2001).
6) In 1993, the U.S. production of cumene was estimated to be 4.49 billion pounds (HSDB , 2001).
7) Cumene is 0.16% by weight in gasoline (HSDB , 2001).

Overview

Life Support

A)

Clinical Effects

0.2.1)

A) USES: Cumene is a colorless, flammable liquid with a gasoline-like odor, commonly used as a thinner for paints, enamels, and lacquers, a constituent for petroleum-based solvents, and in the production of acetone, phenol, acetophenone, alpha-methylstyrene, and styrene.
B) TOXICOLOGY: The primary action of cumene is similar to that of other aromatic hydrocarbons, manifesting as CNS depression.
C) EPIDEMIOLOGY: Poisoning is rare, with no reports of acute intoxication in humans.
D) WITH POISONING/EXPOSURE

1) MILD TO MODERATE TOXICITY: Cumene is considered a primary skin and eye irritant.
2) SEVERE TOXICITY: Although there are no reports of acute intoxication in humans, inhalation of high concentrations of vapors may result in dizziness, incoordination, and loss of consciousness. In experimental animals, acute exposure resulted in vasodilation, CNS depression, ataxia, lethargy, and respiratory depression.

0.2.20)

A) Cumene has been reported to be teratogenic and to decrease neonatal viability in rats. It did not affect spermatogenesis in rats exposed by inhalation.

0.2.21)

A) No excess overall mortality or deaths from cancer were seen in cumene workers.

Laboratory Monitoring

A)

B)

Treatment Overview

0.4.2)

A) MANAGEMENT OF MILD TO MODERATE TOXICITY

1) Treatment is symptomatic and supportive.

B) MANAGEMENT OF SEVERE TOXICITY

1) Severe toxicity is very rare; symptoms are expected to be self-limiting. Treatment is symptomatic and supportive.

C) DECONTAMINATION

1) PREHOSPITAL/HOSPITAL: Cumene is an aromatic hydrocarbon and GI decontamination is not indicated due to the risk of aspiration.

D) AIRWAY MANAGEMENT

1) There are no reports of a patient needing an advanced airway due to the exposure of this chemical; however, cumene is a hydrocarbon and airway compromise is theoretically possible, therefore endotracheal intubation should be performed early in patients with significant CNS or respiratory depression.

E) ANTIDOTE

1) None

F) ENHANCED ELIMINATION

1) Given the expectation that symptoms are self-limiting, hemodialysis and other forms of enhanced elimination are not required.

G) PATIENT DISPOSITION

1) HOME CRITERIA: Asymptomatic patients can be managed at home. Any patient with weakness or altered mental status should be evaluated at a healthcare facility.
2) OBSERVATION CRITERIA: Patients with altered mental status, weakness, or syncope should be evaluated at a healthcare facility until symptoms resolve or are clearly improving.
3) ADMISSION CRITERIA: Patients with persistent ataxia or other severe systemic symptoms should be admitted to a medical floor.
4) CONSULT CRITERIA: Consult a poison center or medical toxicologist if patients develop respiratory failure, hemodynamic instability or other symptoms not expected with this exposure.

H) PITFALLS

1) Common errors for managing these patients include failing to look for other exposures, and not identifying other similar presenting conditions.

I) DIFFERENTIAL DIAGNOSIS

1) Other causes of altered mental status and ataxia include other poisonings (eg, carbon monoxide, anticonvulsants), CNS and systemic infections, hypoglycemia, liver failure, and substance intoxication and withdrawal.

0.4.3)

A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.

0.4.4)

A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.

0.4.5)

A) OVERVIEW

1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

A)

Clinical Effects

Summary Of Exposure

A)

B)

C)

D)

1) MILD TO MODERATE TOXICITY: Cumene is considered a primary skin and eye irritant.
2) SEVERE TOXICITY: Although there are no reports of acute intoxication in humans, inhalation of high concentrations of vapors may result in dizziness, incoordination, and loss of consciousness. In experimental animals, acute exposure resulted in vasodilation, CNS depression, ataxia, lethargy, and respiratory depression.

Heent

3.4.3)

A) CONJUNCTIVITIS: Cumene is a primary eye irritant (Bingham et al, 2001; HSDB , 2001; Material Safety Data Sheet, 1998; ACGIH, 1991). Placed undiluted in rabbit eyes, it produced slight conjunctival irritation (Sandmeyer, 1981; (Clayton & Clayton, 1994).
B) EXCITATION OF VESTIBULO-OCULOMOTOR REFLEX has been reported in rats (Tham et al, 1984).

3.4.5)

A) Cumene is irritating to the mucous membranes (ACGIH, 1991) Hathaway et al, 1991).

Cardiovascular

3.5.3)

A) ANIMAL STUDIES

1) VASODILATATION

a) MICE: Vasodilation was noted in mice exposed to the vapors (ACGIH, 1991).

Respiratory

3.6.2)

A) DISORDER OF RESPIRATORY SYSTEM

1) UNSPECIFIED CHANGES IN THE RESPIRATORY SYSTEM have been reported as part of the human systemic effects expected following inhalation of 200 ppm (Lewis, 1992).

3.6.3)

A) ANIMAL STUDIES

1) RESPIRATORY DEPRESSION

a) MICE: Respiratory depression was seen in mice exposed to vapors (ACGIH, 1991). The cumene concentration necessary to depress the respiratory rate by 50% was estimated to be 2,490 ppm (Nielsen & Alarie, 1982).

Neurologic

3.7.2)

A) CENTRAL NERVOUS SYSTEM DEFICIT

1) Concentrations lethal to humans are not expected to be encountered at room temperature because of the low volatility of cumene.

a) If inhalation of high concentrations of the vapor occurs, dizziness, incoordination, and unconsciousness would be expected (Bingham et al, 2001; HSDB , 2001; Baselt, 2000; Material Safety Data Sheet, 1998) Hathaway et al, 1991).

3.7.3)

A) ANIMAL STUDIES

1) CNS DEPRESSION

a) Animal studies indicate slow induction and long duration of narcosis after vapor exposure, suggesting a cumulative action (ACGIH, 1991) Hathaway et al, 1991).

1) The narcotic dose in mice was between 4,000 and 5,000 ppm (Lazarew, 1929).

b) MICE: Narcosis developed in mice at concentrations below 2,000 ppm, with maximal narcosis occurring toward the end of a 7 hour exposure (Werner et al, 1944).

2) ATAXIA

a) Ataxia and lethargy were observed following repeated exposure of rabbits and rats to 2,000 ppm (Sandmeyer, 1981; Hathaway et al, 1991).

3) LACK OF EFFECT

a) RATS: No neurotoxicity or ototoxicity were seen in Fischer 344 rats exposed to levels of cumene as high as 1200 ppm for 5 hours per day, 6 days per week for 13 weeks (Cushman et al, 1995).

Hepatic

3.9.2)

A) ABNORMAL LIVER FUNCTION

1) Inhalation, especially chronic, may result in spleen and liver damage (Material Safety Data Sheet, 1998).
2) CASE SERIES: 48% of 102 workers exposed to cumene vapors over 7 to 10 years had increased bilirubin concentration, alterations of enzymatic activity, lipid metabolism, liver and hepatobiliary functions, and dyskinesia (Putalova, 1979).

3.9.3)

A) ANIMAL STUDIES

1) LIVER FATTY

a) Edematous and fatty liver changes were noted in chronically exposed animals (Snyder, 1987; Werner et al, 1944).

Genitourinary

3.10.3)

A) ANIMAL STUDIES

1) RENAL FUNCTION ABNORMAL

a) RATS: RENAL HYPEREMIA has been reported in rats following exposure to 500 ppm daily for 150 days (Fabre et al, 1955).
b) INCREASED KIDNEY WEIGHT was observed in animals when exposed to cumene at 462 mg/kg (Wolf et al, 1956). Increased weights were also seen in Fischer 344 rats exposed to 500 or 1200 ppm for 6 hours per day, 5 days per week for 13 weeks (Cushman et al, 1995).

2) RENAL TUBULAR DISORDER

a) MICE: BASOPHILIC CASTS AND FAT GLOBULES were noted in the tubules and kidney cortex of exposed mice (Werner et al, 1944).
b) RATS: Renal proximal tubular cell hypertrophy, hyperplasia, and hyaline drop formation were seen in male Fisher 344 rats exposed to 500 or 1200 ppm cumene for 6 hours per day, 5 days per week for 13 weeks (Cushman et al, 1995).

Hematologic

3.13.2)

A) HEMOLYSIS

1) If cumene is allowed to oxidize to the peroxide, a hemolytic effect may be seen (Sandmeyer, 1981).

B) LACK OF EFFECT

1) Although cumene has a structure similar to that of benzene, there is NO evidence that it causes hematopoietic damage (Hathaway et al, 1991; Snyder, 1987; Raffle et al, 1987).

3.13.3)

A) ANIMAL STUDIES

1) WBC ABNORMAL

a) Chronic exposure of rats and rabbits to cumene caused decreased osmotic resistance of leukocytes with decreased glycogen and peroxidase content, and lipid accumulation in neutrophils (Makar'eva, 1972).

Dermatologic

3.14.2)

A) DERMATITIS

1) Cumene is a primary skin irritant (Bingham et al, 2001; HSDB , 2001) Hathaway et al, 1991; Lewis, 1992; (ACGIH, 1991). It may be absorbed through intact skin (ACGIH, 1991).
2) Skin contact with the liquid causes erythema, dryness and irritation (Material Safety Data Sheet, 1998) Gerarde, 1959). Placed undiluted on rabbit skin, it produces moderate irritation and slight narcosis (Sandmeyer, 1981; (Clayton & Clayton, 1994).

3.14.3)

A) ANIMAL STUDIES

1) VASODILATATION

a) MICE: Dilation of cutaneous blood vessels were noted in mice following exposure to cumene vapors at 2,000 ppm (Werner et al, 1944).

Immunologic

3.19.3)

A) ANIMAL STUDIES

1) IMMUNE SYSTEM DISORDER

a) RABBITS: Immunological changes were seen in rabbits after exposure to 0.5 mg/L, 4 h/day for 4 months (HSDB, 1995; Samedav et al, 1978).

Reproductive

3.20.1)

A) Cumene has been reported to be teratogenic and to decrease neonatal viability in rats. It did not affect spermatogenesis in rats exposed by inhalation.

3.20.2)

A) FETOTOXICITY

1) ANIMAL STUDIES

a) RATS - In rats, no adverse effects on the offspring were found when males and females were exposed to a cumene airborne concentration of 500 ppm, although toxicity did occur in adult animals (International Research & Development Corp, 1989). When pregnant rats and rabbits were exposed to airborne concentrations of 1200 ppm and 2300 ppm, respectively, no adverse effects were noted in the offspring although maternal toxicity occurred (Darmer et al, 1997).
b) RATS - Decreased neonatal viability was seen in offspring of rats exposed to 1500 ppm, but not 500 ppm, of cumene (American Petroleum Institute, 1986; International Research & Development Corp, 1989). These doses produced toxicity in the adult animals.

Carcinogenicity

3.21.1)

A) IARC Carcinogenicity Ratings for CAS98-82-8 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):

1) Not Listed

3.21.2)

A) No excess overall mortality or deaths from cancer were seen in cumene workers.

3.21.3)

A) LACK OF EFFECT

1) No excess overall deaths or cancer mortality were seen from 1952 to 1978 in a retrospective study of persons working in the cumene unit of a large refinery (Tsai et al, 1983).

Genotoxicity

A)

Laboratory Monitoring

Monitoring Parameters Levels

4.1.1)

A) Hematologic, hepatic, and renal function tests may be useful in both acute and chronic exposure.
B) Cumene concentrations are not readily available and are unlikely to be useful for the clinical management of patients.

4.1.2)

A) BLOOD/SERUM CHEMISTRY

1) Cumene concentrations are not readily available and are unlikely to be useful for the clinical management of patients.
2) Liver and renal function tests may be useful in both acute and chronic exposure.

B) HEMATOLOGIC

1) Peripheral smears and leukocyte fragility and enzyme studies may be helpful in chronic toxicity.

Methods

A)

1) A gas chromatographic method to determine the urinary metabolite, dimethylphenylcarbinol, is available (Sandmeyer, 1981).
2) Dimethylphenylcarbinol may be measured in urine by flame-ionization gas chromatography (Baselt, 1988).
3) Cumene and other aromatic hydrocarbons can be detected in forensic medicine with the use of a solvent extraction method combined with GC/MS (Kimura et al, 1988).
4) The major urinary metabolites, 2-phenylpropan-1-ol and 2-phenylpropan-2-ol, can be determined by extraction in methylene chloride followed by gas chromatography. The lower limit of detection is 3 to 6 mg/L urine (Goenechea et al, 1978).
5) Cumene was analyzed in extracts of blood by gas-liquid chromatography; the lower limit of detection was 0.4 mg/L serum (Goenechea et al, 1980).
6) Gas chromatography-mass spectrometry with headspace sampling has been used to measure cumene in blood (Baselt, 2000).

Treatment

Life Support

A)

Patient Disposition

6.3.1)

6.3.1.1) ADMISSION CRITERIA/ORAL

A) Patients with persistent ataxia or other severe systemic symptoms should be admitted to a medical floor.

6.3.1.2) HOME CRITERIA/ORAL

A) Asymptomatic patients can be managed at home. Any patient with weakness or altered mental status should be evaluated at a healthcare facility.

6.3.1.3) CONSULT CRITERIA/ORAL

A) Consult a poison center or medical toxicologist if patients develop respiratory failure, hemodynamic instability or other symptoms not expected with this exposure.

6.3.1.5) OBSERVATION CRITERIA/ORAL

A) Patients with altered mental status, weakness, or syncope should be evaluated at a healthcare facility until symptoms resolve or are clearly improving.

Monitoring

A)

B)

Oral Exposure

6.5.1)

A) This is an aromatic hydrocarbon, and GI decontamination is not indicated due to the risk of aspiration. Dermal exposures should be irrigated with water to remove the product.

6.5.2)

A) SUMMARY

1) This is an aromatic hydrocarbon, and GI decontamination should generally NOT be performed because of the risk of aspiration.

6.5.3)

A) SUPPORT

1) There are no specific antidotes for cumene toxicity. Treatment is supportive, with special attention to respiratory support.

B) MONITORING OF PATIENT

1) Hematologic, hepatic, and renal function tests may be useful in both acute and chronic exposure.
2) Cumene concentrations are not readily available and are unlikely to be useful for the clinical management of patients.

Inhalation Exposure

6.7.1)

A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.

Eye Exposure

6.8.1)

A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).

Dermal Exposure

6.9.1)

A) DERMAL DECONTAMINATION

1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Enhanced Elimination

A)

1) Given the expectation that symptoms are self-limiting, hemodialysis and other forms of enhanced elimination are not required.

Abstracts

Range Of Toxicity

Summary

A)

Minimum Lethal Exposure

A)

1) The minimum lethal human dose to this agent has not been delineated.
2) Due to the low volatility of cumene, concentrations lethal to humans are not expected to exist at room temperature (Hathaway et al, 1996).
3) Although there is no information on the minimum lethal dose of cumene for humans, the lowest published toxic concentration of cumene for humans is 200 ppm (RTECS , 2001).
4) According to Raffle et al (1994), there are "no well-documented reports of toxic effects on exposed workers."

Maximum Tolerated Exposure

A)

1) The following are symptoms of acute cumene exposure (HSDB , 2001):

a) Ingestion results in:

1) A burning sensation of the mouth and stomach along with salivation, nausea, and vomiting. Hematemesis is possible;
2) Possibly hoarseness, cough, and substernal pain;
3) During either ingestion or due to vomiting or eructations, aspiration into the tracheobronchial tree is possible, and may cause severe hemorrhagic pneumonitis.

b) Cumene liquid contact can lead to:

1) Erythema; blisters result from prolonged contact;
2) If the liquid contacts mucous membranes, hemorrhagic inflammatory lesions may develop.

c) Exposure to cumene vapor may cause:

1) Transient euphoria, along with headache, giddiness, vertigo, ataxia, and tinnitus;
2) Confusion, stupefaction, and coma may result. Commonly associated with a cumene-induced coma are tremors, hypertonus and hyperactive reflexes, and motor restlessness;
3) Sudden ventricular fibrillation or respiratory failure may cause death.

2) If high concentrations of cumene were to be inhaled, dizziness, incoordination, and unconsciousness would be expected results (Hathaway et al, 1996).
3) Unconsciousness may result from cumene levels of 4000 ppm (Sittig, 1991).
4) Mildly toxic by inhalation, human effects include: an antipsychotic and non-specific changes in the respiratory system and sense of smell (Lewis, 1996).
5) Cumene is an irritant and toxic by all routes (OHM/TADS , 2000).
6) Of 102 workers exposed to cumene vapors for a 7-10 year span, 48% experienced altered enzymatic activity, heightened bilirubin concentrations, altered liver and hepatobiliary functions and lipid metabolism, and dyskinesia (HSDB , 2001).
7) Cumene vapor has the potential to cause narcosis, that is induced slowly and lasts for a long period of time (Baselt, 1997; Clayton & Clayton, 1994; Lewis, 1996).
8) A central nervous depressant (Baselt, 2000; Lewis, 1996), cumene is 2 and 3 times more potent than toluene and benzene, respectively (Baselt, 2000; Clayton & Clayton, 1994).
9) Cumene has only a slight to moderate toxicity when directly applied to skin/mucous membranes (Baselt, 2000; Lewis, 1996). Skin rashes may result from prolonged skin contact (Clayton & Clayton, 1994).
10) Cumene is irritating to the eyes and skin (Lewis, 1996).
11) According to Raffle et al (1994), there are "no well-documented reports of toxic effects on exposed workers."

Workplace Standards

A)

1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.

a) Adopted Value

1) Cumene

a) TLV:

1) TLV-TWA: 50 ppm
2) TLV-STEL:
3) TLV-Ceiling:

b) Notations and Endnotes:

1) Carcinogenicity Category: Not Listed
2) Codes: Not Listed
3) Definitions: Not Listed

c) TLV Basis - Critical Effect(s): Eye, skin, and URT irr; CNS impair
d) Molecular Weight: 120.19

1) For gases and vapors, to convert the TLV from ppm to mg/m(3):

a) [(TLV in ppm)(gram molecular weight of substance)]/24.45

2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:

a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance

e) Additional information:

B) NIOSH REL and IDLH Values for CAS98-82-8 (National Institute for Occupational Safety and Health, 2007):

1) Listed as: Cumene
2) REL:

a) TWA: 50 ppm (245 mg/m(3))
b) STEL:
c) Ceiling:
d) Carcinogen Listing: (Not Listed) Not Listed
e) Skin Designation: [skin]

1) Indicates the potential for dermal absorption; skin exposure should be prevented as necessary through the use of good work practices and gloves, coveralls, goggles, and other appropriate equipment.

f) Note(s):

3) IDLH:

a) IDLH: 900 ppm
b) Note(s): [10%LEL]

1) [10%LEL]: The 10%LEL designation is provided where the IDLH was based on 10% of the lower explosive limit. This is used for safety purposes in some cases even though toxicity is not indicative of irreversible health effects or impairment of escape exists only at higher concentrations.

C) Carcinogenicity Ratings for CAS98-82-8 :

1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Cumene
2) EPA (U.S. Environmental Protection Agency, 2011): D ; Listed as: Cumene

a) D : Not classifiable as to human carcinogenicity.

3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Cumene
5) MAK (DFG, 2002): Not Listed
6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

D) OSHA PEL Values for CAS98-82-8 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

1) Listed as: Cumene
2) Table Z-1 for Cumene:

a) 8-hour TWA:

1) ppm: 50

a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.

2) mg/m3: 245

a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.

3) Ceiling Value:
4) Skin Designation: Yes
5) Notation(s): Not Listed

Toxicity Information

7.7.1)

A) References: ACGIH, 1991 Budavari, 1996 Clayton & Clayton, 1994 Hathaway et al, 1996 ITI, 1995 Lewis, 1996 RTECS, 2001

1) LD50- (ORAL)MOUSE:

a) 12.8 g/kg (Clayton & Clayton, 1994)
b) 12,750 mg/kg

2) LD50- (ORAL)RAT:

a) 1400 mg/kg -- Gastritis
b) 2.91 g/kg (Budavari, 1996)
c) Male, 1.4 g/kg (ACGIH, 1991)

3) TCLo- (INHALATION)HUMAN:

a) 200 ppm -- Somnolence (general depression), antipsychotic, irritability
b) 200 ppm -- Nose, CNS, and pulmonary effects (Lewis, 1996)

4) TCLo- (INHALATION)RAT:

a) 1200 ppm for 6H/13W-I -- Effects on sense organs/senses, motor activity change, nucleated or pigmented red blood cells

Pharmacology Toxicology

Toxicologic Mechanism

A)

B)

C)

D)

Physicochemical

Physical Characteristics

A)

B)

Molecular Weight

A)

Animal Toxicology

References

General Bibliography

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CUMENE

Classification | Detailed evidence-based information

Therapeutic Toxic Class

Specific Substances

Available Forms Sources

Life Support

Clinical Effects

Laboratory Monitoring

Treatment Overview

Range Of Toxicity

Summary Of Exposure

Heent

Cardiovascular

Respiratory

Neurologic

Hepatic

Genitourinary

Hematologic

Dermatologic

Immunologic

Reproductive

Carcinogenicity

Genotoxicity

Monitoring Parameters Levels

Methods

Life Support

Patient Disposition

Monitoring

Oral Exposure

Inhalation Exposure

Eye Exposure

Dermal Exposure

Enhanced Elimination

Summary

Minimum Lethal Exposure

Maximum Tolerated Exposure

Workplace Standards

Toxicity Information

Toxicologic Mechanism

Physical Characteristics

Molecular Weight

General Bibliography