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음 .. 갈뜽 .. 이다 ..

 

Report on Carcinogens, Twelfth Edition (2011)

National Toxicology Program, Department of Health and Human Services

Isoprene

CAS No. 78-79-5

Reasonably anticipated to be a human carcinogen

First listed in the Ninth Report on Carcinogens (2000)

HCCH2CCH2CH3

Carcinogenicity

Isoprene is reasonably anticipated to be a human carcinogen based on sufficient evidence of carcinogenicity from studies in experimental animals.

Cancer Studies in Experimental Animals

Exposure to isoprene by inhalation caused tumors at several different tissue sites in mice and rats. In mice of both sexes, isoprene caused blood-vessel cancer (hemangiosarcoma) and benign or malignant tumors of the Harderian gland (adenoma or carcinoma) and the lung (alveolar/bronchiolar adenoma or carcinoma). In male mice, it also caused cancer of the hematopoietic system (histiocytic sarcoma) and benign or malignant tumors of the liver (hepatocellular adenoma or carcinoma) and forestomach (squamous-cell papilloma or carcinoma). In rats of both sexes, isoprene caused benign or malignant tumors of the mammary gland (fibroadenoma or carcinoma) and kidney (renal-cell adenoma or carcinoma). In male rats, it also caused benign tumors of the testis (adenoma) (NTP 1995, Placke et al. 1996, Melnick and Sills 2001).

Studies on Mechanisms of Carcinogenesis

Isoprene is the 2-methyl analog of 1,3‑butadiene, an industrial chemical that has been identified as a carcinogen in humans and experimental animals (Gervasi et al. 1985, NTP 1999a,b). The isoprene analogue isopentenyl pyrophosphate is a building block of cholesterol synthesis, and levels of exhaled isoprene correlate with cholesterol synthesis (IARC 1994, Rieder et al. 2001). Isoprene and butadiene are metabolized to monoepoxide and diepoxide intermediates by liver microsomal cytochrome P450-dependent monooxygenases from several species, including humans (Gervasi et al. 1985, IARC 1994, NTP 1999a). These intermediates may be detoxified by hydrolysis (catalyzed by epoxide hydrolase) or conjugation with glutathione (catalyzed by glutathione S-transferase).

The diepoxide intermediates of isoprene and butadiene caused mutations in Salmonella typhimurium, whereas the monoepoxides of isoprene and parent compounds did not. In mammalian cells in vitro, isoprene did not cause sister chromatid exchange, chromosomal aberrations, or micronucleus formation (NTP 1995, 1999a), but did cause DNA damage in human peripheral-blood mononuclear cells and human leukemia cells when incubated with microsomal enzymes (Fabiani et al. 2007). In mice exposed in vivo, isoprene and 1,3-butadiene caused sister chromatid exchange in bone-marrow cells and micronucleus formation in peripheral-blood erythrocytes (Tice 1988, Tice et al. 1988). Sites at which both isoprene and butadiene caused tumors in rodents include the liver, lung, Harderian gland, forestomach, hematopoietic tissue, and circulatory system in mice and the mammary gland, kidney, and testis in rats (NTP 1999a,b). Harderian-gland tumors caused by isoprene in mice had a high frequency of unique mutations of the K‑ras protooncogene (A to T transversions at codon 61) (Hong et al. 1997).

There is no evidence to suggest that mechanisms by which isoprene causes tumors in experimental animals would not also operate in humans.

Cancer Studies in Humans

No epidemiological studies were identified that evaluated the relationship between human cancer and exposure specifically to isoprene.

Properties

Isoprene is structurally similar to 1,3‑butadiene and exists as a colorless, volatile liquid at room temperature (NTP 1999a). It occurs frequently in nature and is emitted to the environment by plants and trees. Isoprene is practically insoluble in water, but is soluble in ethanol, diethyl ether, benzene, and acetone. It is stable under normal conditions, but it is very flammable and will polymerize vigorously or decompose with abrupt changes in temperature or pressure (IARC 1994, Akron 2009). Physical and chemical properties of isoprene are listed in the following table.

Property Information

Molecular weight 68.1

Specific gravity 0.681 at 20°C/4°C

Melting point –145.95°C

Boiling point 34.07°C at 760 mm Hg

Log Kow 2.42

Water solubility 0.642 g/L at 25°C

Vapor pressure 550 mm Hg at 25°C

Vapor density relative to air 2.4

Source: HSDB 2009.

Use

The majority of isoprene produced commercially is used to make synthetic rubber (cis-polyisoprene), most of which is used to produce vehicle tires. The second- and third-largest uses are in the production of styrene-isoprene-styrene block polymers and butyl rubber (isobutene-isoprene copolymer) (IARC 1994).

Production

Isoprene is recovered as a by-product of thermal cracking of naphtha or gas oil from C5 streams (IARC 1994, NTP 1999a). The isoprene yield is about 2% to 5% of the ethylene yield. U.S. demand for isoprene grew 6.5% annually from 1985 to 1992 (NTP 1999a). In 1994, isoprene production in the United States was about 619 million pounds, almost 29% more than in 1992. Estimated isoprene production capacity for eight facilities was 598 million pounds in 1996, based on estimates of isoprene content of product stream available from ethylene production via heavy liquids. In 2009, isoprene was produced by 22 manufacturers worldwide, including 12 U.S. producers (SRI 2009), and was available from 23 suppliers, including 12 U.S. suppliers (ChemSources 2009). U.S. imports of isoprene (purity ≥ 95% by weight) increased from zero in 1989 to a peak of 144 million pounds in 2003. Imports declined to 19.6 million pounds in 2004, the lowest level since 1992, but remained near 32 million pounds from 2005 through 2008. During this period, U.S. exports of isoprene ranged from 7.9 million to 39.6 million pounds (in 2006) (USITC 2009). Reports filed from 1986 to 2002 under the U.S. Environmental Protection Agency’s Toxic Substances Control Act Inventory Update Rule indicated that U.S. production plus imports of isoprene totaled 100 million to 500 million pounds (EPA 2004).

Exposure

Isoprene is formed endogenously in humans at a rate of 0.15 μmol/kg of body weight per hour, equivalent to approximately 2 to 4 mg/kg per

National Toxicology Program, Department of Health and Human Services

day (Taalman 1996), and is the major hydrocarbon in human breath

(accounting for up to 70% of exhaled hydrocarbons) (Gelmont et al.

1981). Concentrations in human blood range from 1.0 to 4.8 μg/L

(Cailleux et al. 1992). Isoprene is produced at higher rates in males

than females. The rate of isoprene production increases with age up

to the age of 29 (Lechner et al. 2006); it is lower in young children

than adults by a factor of about 2.4 (Taucher et al. 1997). In a study

of 30 adult volunteers, the mean isoprene concentration measured in

alveolar breath was 118 ppb, with a range of 0 to 474 ppb (Turner et

al. 2006). After 20 to 30 minutes of exercise, isoprene concentration

in exhaled air decreased to a range of 0 to 40 ppb (Senthilmohan et

al. 2000). Smoking one cigarette increased the concentration of isoprene

in exhaled air by 70% (Senthilmohan et al. 2001). Isoprene is

also produced endogenously by other animals. Production rates reported

for rats and mice were 1.9 and 0.4 μmol/kg of body weight

per hour, respectively (Peter et al. 1987).

Foods of plant origin would be expected to be a source of daily

exposure to isoprene, since isoprene is emitted by agricultural crops

and is the basic structural unit in countless natural products found in

foods, such as terpenes and vitamins A and K (NTP 1999a). Isoprene

has been reported to occur in the essential oil of oranges, the fruit of

hops, carrot roots, and roasted coffee (Taalman 1996, NTP 1999a).

Isoprene is emitted from plants and trees and is present in the

general environment at low concentrations (Taalman 1996). Isoprene

emissions from many types of plants have been estimated under various

climatic conditions, to evaluate their importance in global climate

change (Mayrhofer et al. 2004, Parra et al. 2004, Schnitzler et al. 2004,

2005, Pegoraro et al. 2005, Sasaki et al. 2005, Sharkey 2005, Moukhtar

et al. 2006, Simon et al. 2006, Tambunan et al. 2006). Annual global

isoprene emissions, estimated at 175 billion to 503 billion kilograms

(386 billion to 1,109 billion pounds), account for an estimated 57% of

total global natural volatile organic compound emissions (Guenther

et al. 1995). The average biogenic emission rate factor for isoprene in

U.S. woodlands is 3 mg/m2 per hour (compared with 5.1 mg/m2 for

total volatile organic compounds) (Guenther et al. 1994). Isoprene

concentrations in biogenic emissions range from 8% to 91% of total

volatile organic compounds, averaging 58%. Because isoprene biosynthesis

is associated with photosynthesis, isoprene emissions are

negligible at night (Lamb et al. 1993). Because isoprene is emitted

primarily by deciduous trees, emissions are seasonal, being highest

in the summer and lowest in the winter (Guenther et al. 1994, Fuentes

and Wang 1999). The south central and southeastern areas of the

United States have the highest biogenic emissions (Lamb et al. 1993,

Guenther et al. 1994). The half-life of atmospheric isoprene has been

estimated at 0.5 hours by reaction with nitric oxide, 4 hours by reaction

with hydroxyl radicals, and 19 hours by reaction with ozone

(HSDB 2009).

Anthropogenic sources of isoprene in the atmosphere include ethylene

production by cracking naphtha, wood pulping, oil fires, woodburning

stoves and fireplaces, other biomass combustion, tobacco

smoking (200 to 400 μg per cigarette), gasoline, and exhaust from

turbines and automobiles (Adam et al. 2006, HSDB 2009). Isoprene

has been measured as one of the volatile organic compounds in the

ambient air in regions with industrial pollution, and in urban, residential,

and rural areas as an indicator of the potential for ozone formation.

Thus, isoprene is a key indicator for regional air quality, as

well as being a component of the global carbon cycle (Borbon et al.

2004, Guo et al. 2004, Kuster et al. 2004, Warneke et al. 2005, Hellen

et al. 2006).

The reported concentration of isoprene in U.S. ambient air ranges

from 1 to 21 parts per billion carbon (ppbC) and generally is less than

10 ppbC. Isoprene accounts for less than 10% of non-methane hydrocarbons

in ambient air. Biogenic hydrocarbons may contribute more

to total atmospheric hydrocarbons under stagnant atmospheric conditions

(Altschuller 1983, Hagerman et al. 1997). The major sources

of isoprene in ambient air appear to be biogenic emissions at rural

sites and vehicular emissions in urban areas (Borbon et al. 2001, So

and Wang 2004). Where the source is primarily biogenic, the isoprene

concentration slowly increases during the day, reaching a peak

in the middle of the day, when photosynthesis is greatest. Where vehicular

emissions are the primary source, the isoprene concentration

peaks during the morning and evening rush hours and is low in the

middle of the day (Borbon et al. 2002). One study concluded that in

summer, at least 80% of the isoprene at a rural site was due to biogenic

emissions, but that in winter, more than 90% of residual isoprene

was from urban air-mass mixing (Borbon et al. 2004). Where

industrial emissions are the primary source of isoprene, the concentration

may peak at night, or there may be no peak at all (Zhao et al.

2004, Chiang et al. 2007).

The primary source of isoprene in indoor air is environmental

tobacco smoke. Isoprene was found to be the major component of

Hydrocarbons in the air of a smoky café (10 patrons smoking, 10 not

smoking) (16.7%) and in sidestream smoke (29.2%) (Barrefors and

Petersson 1993). A monitoring survey in November 1992 in homes

and workplaces in the greater Philadelphia area found mean isoprene

concentrations in personal air samples of 4.65 μg/m3 in 60 nonsmoking

homes, 18.15 μg/m3 in 29 homes with smokers, 5.29 μg/m3 in 51

nonsmoking workplaces, and 22.80 μg/m3 in 28 workplaces that allowed

smoking (Heavner 1996). A survey in the Lower Rio Grande

Valley of Texas reported a median summertime isoprene concentration

of 2.90 μg/m3 for three indoor air samples (it was not reported

whether the occupants were smokers or nonsmokers), compared with

0.40 μg/m3 for three outdoor air samples (Mukerjee 1997).

Air-monitoring data were collected at three U.S. facilities that

produced isoprene monomers or polymers; 98.5% of the samples

showed concentrations of less than 10 ppm, and 91.3% of less than

1 ppm (Leber 2001, Lynch 2001). The National Occupational Hazard

Survey (conducted from 1972 to 1974) estimated that 58,000 workers

in over 30 industries potentially were exposed to isoprene (NIOSH

1976). The National Occupational Exposure Survey (conducted from

1981 to 1983) estimated in a more limited survey that 3,700 workers

in four industries, including 578 women, potentially were exposed

to isoprene (NIOSH 1990).

Regulations

Coast Guard, Department of Homeland Security

Minimum requirements have been established for safe transport of isoprene on ships and barges.

Department of Transportation (DOT)

Isoprene is considered a hazardous material, and special requirements have been set for marking, labeling, and transporting this material.

Environmental Protection Agency (EPA)

Clean Air Act

New Source Performance Standards: Manufacture of isoprene is subject to certain provisions for the control of volatile organic compound emissions.

Prevention of Accidental Release: Threshold quantity (TQ) = 10,000 lb.

Clean Water Act

Isoprene has been designated a hazardous substance.

Comprehensive Environmental Response, Compensation, and Liability Act

Reportable quantity (RQ) = 100 lb.