Benzo(G)chrysene

SRP: Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in air, soil or water; effects on animal, aquatic and plant life; and conformance with environmental and public health regulations. If it is possible or reasonable use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination.

SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.

The worker should wash daily at the end of each work shift, and prior to eating, drinking, smoking, etc. /Coal tar pitch volatiles/

Workers whose clothing may have become contaminated should change into uncontaminated clothing before leaving the work premises. /Coal tar pitch volatiles/

SRP: Contaminated protective clothing should be segregated in a manner such that there is no direct personal contact by personnel who handle, dispose, or clean the clothing. The completeness of the cleaning procedures should be considered before the decontaminated protective clothing is returned for reuse by the workers. Contaminated clothing should not be taken home at the end of shift, but should remain at employee's place of work for cleaning.

8 Hr Time Weighted Avg (TWA): 0.2 mg/cu m. /Coal tar pitch volatiles, as benzene soluble aerosol/

Peak Exposure Recommendation: Transient increases in workers' exposure levels may exceed 3 times the value of the TLV-TWA level for no more than 15 minutes at a time, on no more than 4 occasions spaced 1 hour apart during a workday, and under no circumstances should they exceed 5 times the value of the TLV-TWA level. In addition, the 8-hour TWA is not to be exceeded for an 8-hour work period. /Coal tar pitch volatiles, as benzene soluble aerosol/

A1; Confirmed human carcinogen. /Coal tar pitch volatiles, as benzene soluble aerosol/

Biological Exposure Index (BEI): Determinant: 1-Hydroxypyrene (1-HP) in urine (with hydrolysis); Sampling Time: end of shift at end of workweek. BEI: None.; Biological monitoring should be considered for this compound based on the review; however, a specific BEI could not be determined due to insufficient data. /Polycyclic aromatic hydrocarbons/

For more Threshold Limit Values (TLV) (Complete) data for Benzo(g)chrysene (6 total), please visit the HSDB record page.

Respirator Recommendations: At concentrations above the NIOSH REL, or where there is no REL, at any detectable concentration: /Coal tar pitch volatiles/[Table#4729]

Respirator Recommendations: Escape conditions: /Coal tar pitch volatiles/[Table#4730]

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 2.0X10+6(SRC), determined from a structure estimation method(2), indicates that benzo(g)chrysene is expected to be immobile in soil(SRC). Volatilization of benzo(g)chrysene from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 1.2X10-7 atm-cu m/mole(SRC), using a fragment constant estimation method(3). Benzo(g)chrysene is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 2.0X10-8 mm Hg at 25 °C(SRC), determined from a fragment constant method(2). In general, polycyclic aromatic hydrocarbons (PAHs) with four or more benzene rings do not biodegrade readily(7).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 2.0X10+6(SRC), determined from a structure estimation method(2), indicates that benzo(g)chrysene is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 1.2X10-7 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(5), an estimated BCF of 1.2X10+4(SRC), from an estimated log Kow of 6.70(2) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is very high, provided the compound is not metabolized by the organism. Benzo(g)chrysene may not bioconcentrate in aquatic organisms which contain microsomal oxidase, such as fish, as this enzyme enables the rapid metabolism of certain polycyclic aromatic hydrocarbons(6). In general, polycyclic aromatic hydrocarbons(PAHs) with four or more benzene rings do not biodegrade readily(7).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), benzo(g)chrysene, which has an estimated vapor pressure of 2.0X10-8 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase benzo(g)chrysene is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 0.2 days(SRC), calculated from its rate constant of 5.0X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase benzo(g)chrysene may be removed from the air by wet and dry deposition(SRC). Benzo(g)chrysene contains chromophores that absorb at wavelengths >290 nm(4) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).

IDENTIFICATION AND USE: Benzo(g)chrysene (B(g)C) is a polynuclear aromatic hydrocarbon (PAH). It is not produced commercially, and it is used mostly in biochemical research. PAHs are ubiquitous in combustion products of organic matter, including cigarette smoke. HUMAN EXPOSURE AND TOXICITY: Four major DNA adducts were detected in human fibroblasts. ANIMAL STUDIES: B(g)C is a moderate carcinogen. B(g)C is metabilically activated in mouse skin and forms DNA adducts. The adenine adducts accounted for 64% of the total major adducts formed in B[g]C-treated mouse skin. B(g)C metabolites formed also DNA adducts in Chinese hamster V79 cell.

Using a structure estimation method based on molecular connectivity indices(1), the Koc of benzo(g)chrysene can be estimated to be 2.0X10+6(SRC). According to a classification scheme(2), this estimated Koc value suggests that benzo(g)chrysene is expected to be immobile in soil(SRC).

Benzo(g)chrysene is one of many polycyclic aromatic hydrocarbons (PAH), a group of chemicals that are formed during the incomplete burning of coal, oil, gas, wood, garbage, or other organic substances. PAHs generally occur as complex mixtures, for example as part of combustion products such as soot, not as single compounds. PAHs occur naturally in volcanoes and forest fires. They can also be found in substances such as crude oil and coal. They are found throughout the environment in the air, water, and soil(1). /Polycyclic aromatic hydrocarbons/

/GENOTOXICITY-DNA ADDUCTS/ Benzo(g)chrysene is a widespread environmental contaminant and potent carcinogen. We have measured the formation and nucleotide excision repair of covalent DNA adducts formed by the DNA-reactive metabolite of this compound in human fibroblasts, in which expression of the p53 tumor suppressor gene could be controlled by a tetracycline-inducible promoter. Cells were exposed for 1 hr to 0.01, 0.1, or 1.2 uM (+/-)-anti-benzo(g)chrysene diol-epoxide, and DNA adducts were assessed at various post-treatment times by subjecting isolated DNA to (32)P-postlabeling analysis. Four major DNA adducts were detected, corresponding to the reaction of either the (+)- or (-)-anti-benzo(g)chrysene diol-epoxide stereoisomer with adenine or guanine. Treatment with 1.2 uM resulted in a level of 1100 total adducts/10(8) nucleotides for both p53-proficient and -deficient cells; removal of adducts was not observed in either case. In cells treated with 0.1 uM, the maximum level of total adducts at 24 hr was 150/10(8) nucleotides in p53-proficient cells and 210 adducts/10(8) nucleotides in p53-deficient cells. A concentration of 0.01 microM resulted in a maximum of 20 adducts/10(8) nucleotides in p53-proficient cells at 4 hr, but 40 adducts/10(8) nucleotides persisted in p53-deficient cells at 24 hr. Whereas there were clear differences in the time course of adduct levels in p53-proficient compared with p53-deficient cells treated with 0.1 uM or 0.01 uM, these levels did not decrease extensively over 3 days. This is likely because of the stabilization of the diol-epoxide in cells, and consequent exposure and formation of adducts for many hours after the initial treatment. Furthermore, despite minor quantitative differences, all 4 of the adducts behaved similarly with respect to the effect of p53 expression on their removal. p53 appears to minimize the appearance of benzo(g)chrysene adducts in human cells by up-regulating global nucleotide excision repair and reducing the maximum adduct levels achieved. The fact that this p53-dependent effect is noted at levels of DNA adducts that are commonly found in human tissues (i.e., <100 adducts/10(8) nucleotides) because of environmental factors such as smoking is particularly significant with respect to human carcinogenesis related to environmental exposure. /(+/-)-Anti-benzo(g)chrysene diol-epoxide, metabolite/

/GENOTOXICITY-DNA ADDUCTS/ Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous in combustion products of organic matter, including cigarette smoke. Metabolically activated diol epoxides of these compounds, including benzo[a]pyrene diol epoxide (B[a]PDE), have been suggested as causative agents in the development of lung cancer. We previously mapped the distribution of B[a]PDE adducts within the p53 tumor suppressor gene (also known as TP53), which is mutated in 60% of human lung cancers, and found that B[a]PDE adducts preferentially form at lung cancer mutational hotspots (codons 154, 157, 158, 245, 248, and 273). Other PAHs may be important in lung cancer as well. Here we have mapped the distribution of adducts induced by diol epoxides of additional PAHs: chrysene (CDE), 5-methylchrysene (5-MCDE), 6-methylchrysene (6-MCDE), benzo[c]phenanthrene (B[c]PDE), and benzo[g]chrysene (B[g]CDE) within exons 5, 7, and 8 of the p53 gene in human bronchial epithelial cells. CDE exposure produced only low levels of adducts. Exposure of cells to the other activated PAHs resulted in DNA damage patterns similar to those previously observed with B[a]PDE but with some distinct differences. 5-MCDE, 6-MCDE, B[g]CDE, and B[c]PDE efficiently induced adducts at guanines within codons 154, 156, 157, 158, and 159 of exon 5, codons 237, 245 and 248 of exon 7, and codon 273 of exon 8, but the relative levels of adducts at each site varied for each compound. B[g]CDE, B[c]PDE, and 5-MCDE induced damage at codon 158 more selectively than 6-MCDE or B[a]PDE. The sites most strongly involved in PAH adduct formation were also the sites of highest mutation frequency (codons 157, 158, 245, 248, and 273). The data suggest that PAHs contribute to the mutational spectrum in human lung cancer.

Polycyclic aromatic hydrocarbons (PAHs), such as benzo(g)chrysene, occur as ubiquitous products of incomplete combustion of fossil fuels, wood, diesel oils and gasoline fuels(1). PAHs generally occur as complex mixtures, for example as part of combustion products such as soot, not as single compounds. /Polycyclic aromatic hydrocarbons/

Benzo[g]chrysene

Group 3: Not classifiable as to its carcinogenicity to humans

Volume 92: (2010) Some Non-heterocyclic Polycyclic Aromatic Hydrocarbons and Some Related Exposures

2010

2005

An estimated BCF of 1.2X10+4 was calculated in fish for benzo(g)chrysene(SRC), using an estimated log Kow of 6.70(1) and a regression-derived equation(1) ). According to a classification scheme(2), this BCF suggests the potential for bioconcentration in aquatic organisms is very high(SRC), provided the compound is not metabolized by the organism(SRC). Benzo(g)chrysene may not bioconcentrate in aquatic organisms which contain microsomal oxidase, such as fish, as this enzyme enables the rapid metabolism of certain polycyclic aromatic hydrocarbons(3).

The Henry's Law constant for benzo(g)chrysene is estimated as 1.2X10-7 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that benzo(g)chrysene is expected to be essentially nonvolatile from water and moist soil surfaces(2). Benzo(g)chrysene is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 2.0X10-8 mm Hg(SRC), determined from a fragment constant method(3).

/GENOTOXICITY-DNA ADDUCTS/ The metabolic activation in mouse skin of benzo[g]chrysene (B[g]C), a moderately carcinogenic polycyclic aromatic hydrocarbon (PAH) present in coal tar, was investigated. Male Parkes mice were treated topically with 0.5 umol B[g]C and DNA was isolated from the treated areas of skin at various times after treatment and analyzed by 32P-post-labelling. Seven major adduct spots were detected, at a maximum level of 6.55 fmol adducts/ug DNA. Mouse skin treated with the PAH benzo[c]phenanthrene (B[c]Ph) gave a total of 0.24 fmol adducts/ug DNA. B[g]C-DNA adducts persisted in skin for at least 3 weeks. Treatment of mice with 0.5 umol of the optically pure putative proximate carcinogens, the (+)- and (-)-trans benzo[g]chrysene-11,12-dihydrodiols, led to the formation of adducts which comigrated on TLC and HPLC with those formed in B[g]C-treated mice, which suggested that the detected adducts were formed by the fjord region B[g]C-11,12-dihydrodiol-13,14-epoxides (B[g]CDEs). To test this, the four optically pure synthetic B[g]CDEs were reacted in vitro with DNA and the heteroco-polymers poly(dA x dT) and poly(dG x dC) and these samples 32P-postlabelled. Co-chromatography, on both TLC and HPLC, of in vitro and in vivo adducts indicated that B[g]C is activated in mouse skin through formation of the (-)-anti-(11R,12S,l3S,14R) and (+)-syn-(11S,12R,13S,14R) B[g]CDEs. (-)-anti-B[g]CDE formed five adducts with DNA, two of them with adenine and three with guanine bases. (+)-syn-B[g]CDE formed one adduct with each of these bases in DNA. The adenine adducts accounted for 64% of the total major adducts formed in B[g]C-treated mouse skin. The route of metabolic activation or B[g]C is similar to that reported for B[c]Ph, but the extent of activation to the fjord region diol-epoxides is significantly greater in the case of B[g]C, as demonstrated by the higher levels of adduct formation in vivo.

/GENOTOXICITY-DNA ADDUCTS/ Chinese hamster V79 cells were treated with the anti- and syn-diastereomers of the bay- or fjord-region diol-epoxides of four polycyclic aromatic hydrocarbons, namely benzo[a]pyrene (BP), benzo[c]chrysene (BcC), benzo[g]chrysene (BgC) and benzo[c]phenanthrene (BcPh). The frequency of induction of 6-thioguanine-resistant mutations was determined, and the extent of formation of DNA adducts was measured by 32P-postlabelling. When expressed as mutation frequency per nanomoles compound per millilitre incubation medium, this group of chemicals expressed a 160-fold range in potency. In agreement with previous experimental studies, the anti-diol-epoxide of BcC was highly mutagenic, inducing in excess of 3 x 10(4) mutations/10(6) cells per nmol compound/ml. The mutagenic activities of the anti- and syn-diol-epoxides of BP were 10- and 100-fold lower, respectively. Both diol-epoxides of BgC, the syn-BcC and the anti-BcPh derivatives were also highly mutagenic, and only the syn-BcPh diol-epoxide was less mutagenic than the anti-diol-epoxide of BP. Determination of the levels of DNA adducts formed by the diol-epoxides indicated that the most mutagenic compounds were the most DNA reactive, although the fjord-region diol-epoxides gave rise to more complex patterns of adducts than those of the BP diol-epoxides. When the mutagenicity results were expressed as mutations per femtomoles total adducts formed, all compounds showed similar activities. Thus the potent mutagenicity of the fjord region diol-epoxides appears to be due to the high frequency with which they form DNA adducts in V79 cells, rather than to formation of adducts with greater mutagenic potential.

Toxic pollutant designated pursuant to section 307(a)(1) of the Federal Water Pollution Control Act and is subject to effluent limitations. /Polynuclear aromatic hydrocarbons (including benzanthracenes, benzopyrenes, benzofluoranthene, chrysenes, dibenz-anthracenes, and indenopyrenes)/

For the maximum protection of human health from the potential carcinogenic effects of exposure to polynuclear aromatic hydrocarbons through ingestion of contaminated water and contaminated aquatic organisms, the ambient water concentration should be zero, based on the nonthreshold assumption for this chemical. However, zero level may not be attainable at the present time. Therefore, the levels which may result in incremental increase of cancer risk over the lifetime are estimated at 1X10-5, 1X10-6, and 1X10-7. The corresponding recommended criteria are 28.0 ng/L, 2.8 ng/L, and 0.28 ng/L, respectively. If these estimates are made for consumption of aquatic organisms only, excluding consumption of water, the levels are 311.0 ng/L, 31.1 ng/L, and 3.11 ng/L, respectively. /Polynuclear aromatic hydrocarbons/.

Used as a research chemical; Not commercially produced in the US; [HSDB]

BIOCHEMICAL RESEARCH

(1975) NOT PRODUCED COMMERCIALLY IN US

(1977) NOT PRODUCED COMMERCIALLY IN US