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EC number: 200-753-7 | CAS number: 71-43-2
- Life Cycle description
- Uses advised against
- Endpoint summary
- Appearance / physical state / colour
- Melting point / freezing point
- Boiling point
- Density
- Particle size distribution (Granulometry)
- Vapour pressure
- Partition coefficient
- Water solubility
- Solubility in organic solvents / fat solubility
- Surface tension
- Flash point
- Auto flammability
- Flammability
- Explosiveness
- Oxidising properties
- Oxidation reduction potential
- Stability in organic solvents and identity of relevant degradation products
- Storage stability and reactivity towards container material
- Stability: thermal, sunlight, metals
- pH
- Dissociation constant
- Viscosity
- Additional physico-chemical information
- Additional physico-chemical properties of nanomaterials
- Nanomaterial agglomeration / aggregation
- Nanomaterial crystalline phase
- Nanomaterial crystallite and grain size
- Nanomaterial aspect ratio / shape
- Nanomaterial specific surface area
- Nanomaterial Zeta potential
- Nanomaterial surface chemistry
- Nanomaterial dustiness
- Nanomaterial porosity
- Nanomaterial pour density
- Nanomaterial photocatalytic activity
- Nanomaterial radical formation potential
- Nanomaterial catalytic activity
- Endpoint summary
- Stability
- Biodegradation
- Bioaccumulation
- Transport and distribution
- Environmental data
- Additional information on environmental fate and behaviour
- Ecotoxicological Summary
- Aquatic toxicity
- Endpoint summary
- Short-term toxicity to fish
- Long-term toxicity to fish
- Short-term toxicity to aquatic invertebrates
- Long-term toxicity to aquatic invertebrates
- Toxicity to aquatic algae and cyanobacteria
- Toxicity to aquatic plants other than algae
- Toxicity to microorganisms
- Endocrine disrupter testing in aquatic vertebrates – in vivo
- Toxicity to other aquatic organisms
- Sediment toxicity
- Terrestrial toxicity
- Biological effects monitoring
- Biotransformation and kinetics
- Additional ecotoxological information
- Toxicological Summary
- Toxicokinetics, metabolism and distribution
- Acute Toxicity
- Irritation / corrosion
- Sensitisation
- Repeated dose toxicity
- Genetic toxicity
- Carcinogenicity
- Toxicity to reproduction
- Specific investigations
- Exposure related observations in humans
- Toxic effects on livestock and pets
- Additional toxicological data
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Endpoint summary
Administrative data
Key value for chemical safety assessment
Genetic toxicity in vitro
Endpoint conclusion
- Endpoint conclusion:
- adverse effect observed (positive)
Genetic toxicity in vivo
Description of key information
The available data in animals and humans indicate that benzene and/or its metabolites are indirect genotoxicants rather than direct mutagens (Schnatter et al. 2020).
The Mode of Action of benzene and benzene metabolites aligns with a number of threshold mechanisms described by North et al. (2020a), which are initiated by the reactive oxygen species, protein cross-linking, and protein adduct formation.
Link to relevant study records
- Endpoint:
- genetic toxicity in vivo, other
- Remarks:
- chromosome aberration and micronucleus
- Type of information:
- experimental study
- Adequacy of study:
- key study
- Study period:
- 1980-2018
- Reliability:
- 1 (reliable without restriction)
- Rationale for reliability incl. deficiencies:
- test procedure in accordance with generally accepted scientific standards and described in sufficient detail
- Qualifier:
- no guideline required
- Principles of method if other than guideline:
- Quality review of epidemiological (genotoxicity) studies for Occupational Exposure Limit Derivation.
- GLP compliance:
- no
- Remarks:
- Not applicable
- Type of assay:
- other: a number of genetic toxicity assays
- Species:
- other: human exposure studies
- Route of administration:
- inhalation
- Key result
- Sex:
- male/female
- Genotoxicity:
- negative
- Toxicity:
- no effects
- Vehicle controls validity:
- not applicable
- Negative controls validity:
- not applicable
- Positive controls validity:
- not applicable
- Remarks on result:
- other: OEL 0.25 ppm
- Key result
- Sex:
- male/female
- Genotoxicity:
- negative
- Toxicity:
- no effects
- Vehicle controls validity:
- not applicable
- Negative controls validity:
- not applicable
- Positive controls validity:
- not applicable
- Remarks on result:
- other:
- Remarks:
- NOAEC: 0.69 ppm
- Key result
- Sex:
- male/female
- Genotoxicity:
- positive
- Toxicity:
- not specified
- Vehicle controls validity:
- not applicable
- Negative controls validity:
- not applicable
- Positive controls validity:
- not applicable
- Remarks on result:
- other:
- Remarks:
- LOAEC = 2 ppm
- Conclusions:
- The data presented by Schnatter et al 2020 define a benzene LOAEC of 2 ppm (8 h TWA) and a NOAEC of 0.5 ppm (8 h TWA). However, the use of peripheral blood measures of bone marrow effects introduces some scientific uncertainty, thus until the issue of bone marrow sensitivity compared to that of peripheral blood is resolved an extra assessment factor of two is applied. An OEL of 0.25 ppm (8 h TWA) for benzene is the best estimate based on available human data.
- Executive summary:
This paper derives an occupational exposure limit for benzene using quality assessed data. Seventy-seven genotoxicity studies in workers were scored for study quality with an adapted tool based on that of Vlaanderen et al., 2008 (Environ Health. Perspect. 116 1700−5). Genotoxicity endpoint (as well as haematotoxicity) was selected as one of most sensitive and relevant endpoints to the proposed mode of action (MOA) and protecting against it will protect against benzene carcinogenicity. Lowest and No- Adverse Effect Concentrations (LOAECs and NOAECs) were derived from the highest quality studies (i.e. those ranked in the top tertile or top half) and further assessed as being “more certain” or “less certain”. Several sensitivity analyses were conducted to assess whether alternative “high quality” constructs affected conclusions. Genotoxicity, studies showed effects near 2 ppm and showed no effects at about 0.69 ppm (the findings supported the haematotoxicity results). Several sensitivity analyses supported these observations. These data define a benzene LOAEC of 2 ppm (8 h TWA) and a NOAEC of 0.5 ppm (8 h TWA). Allowing for possible subclinical effects in bone marrow not apparent in studies of peripheral blood endpoints, an OEL of 0.25 ppm (8 h TWA) is proposed.
Reference
Results
Quality scoring results for genotoxic studies
Among 56 genotoxicity study populations the top score was 20 (of a possible 24), which was due to the (Qu et al., 2003) study. Genotoxicity studies showed a wide range (6–20) indicating marked differences in study quality for each body of literature.
LOAECs and NOAECs for high quality studies
Factory workers
Of the 21 studies in the top tertile, ten studies were among factory workers, five among fuel handlers and six among workers exposed to traffic and ambient air. In factory workers, the five studies with more certain LOAECs were (Qu et al., 2003) (LOAEC=3.07 ppm), (Xing et al., 2010)(LOAEC>1.6 ppm), (Zhang et al., 2012) (LOAEC>2.64 ppm), (Zhang et al., 2007) (LOAEC=13.6 ppm) and (Zhang et al., 2014) (LOAEC=2 ppm). The top tertile study generating a less certain LOAEC (>0.56 ppm) was (Kim et al., 2004a) due to the presence of PAH co-exposures.
Fuel workers
Three studies (Carere et al., 1995; Pandey et al., 2008 and Rekhadevi et al., 2010) in the top tertile were associated with a more certain LOAEC and none with a less certain LOAEC. The three studies showed similar LOAECs of 2 ppm, 2 ppm, and > 1 ppm, respectively. A NOAEC in the Carere study for micronuclei is 0.47 ppm and in the Pandey study∼0.9 ppm. The quality scores of the first tertile fuel studies (14.5) are lower than those from the factory
setting (17.25).
Traffic/ambient air
There were only two studies (Leopardi et al., NOAEC=0.003 ppm; Maffei et al., LOAEC=0.008 ppm) in the top tertile which produced a more certain LOAEC or NOAEC. Violante et al. (15.5) has a less certain NOAEC of 0.005 ppm and Angelini (14.5) has a less certain LOAEC of 0.006 ppm. Since the exposure concentrations present in the traffic/ambient air studies are lower than other NOAECs based on fuel and factory studies, this group of studies does not add meaningful information to the NOAEC analysis.
Since the single top tertile study that showed a more certain LOAEC is of lower quality (13.5) than studies from the factory and fuel sectors (average=16.07), this group of studies also does not add meaningful information to the LOAEC analysis. Thus, these studies are not subsequently considered.
Derivation of LOAECs
The highest quality studies (i.e. first tertile) that generated a more certain LOAEC originated from the factory and fuel study scenarios. There were five such studies from the factory scenario: Qu et al. (LOAEC=3.07 ppm), Xing et al. (LOAEC>1.6 ppm), Zhang et al. (2012) (LOAEC>2.64 ppm), Zhang et al., 2007(LOAEC=13.6 ppm), and Zhang 2014 (LOAEC=2 ppm).
Zhang et al., 2007 studied mainly higher exposures, and can therefore be excluded. The four remaining high-quality factory studies result in an average LOAEC of 2.33 ppm. This is the best supported LOAEC (leading case) since it is a weighted average of the highest quality studies, with an average quality score of 17.25. When the three additional studies from the fuel scenario: Carere et al. (2 ppm), Rekhadavi et al. (1 ppm), and Pandey et al. (2 ppm) are added, the resulting LOAEC is 2.04 ppm, which can be regarded as the sensitivity analysis based on the next highest quality studies.
If high quality is defined more inclusively as studies above the median, adding the one additional study from the factory setting with a more certain LOAEC (Eastmond et al., 1.29 ppm) with the other first tertile more certain factory studies, results in an average LOAEC of 2.12 ppm. The average quality score in this sensitivity analysis decreases to 16.3 (from 17.25), but still supports a LOAEC of approximately 2 ppm. There were no additional studies from the fuel nor ambient scenarios which generated more certain LOAECs above the median score of 12.5. All high certainty LOAECs above the median score from the factory and fuel sector combined, result in a LOAEC of 1.95 ppm (average score – 14.85). Although average quality score has decreased, this also supports an aggregate LOAEC of∼2ppm.
Consideration of the Less certain LOAECs included Kim et al., 2004a, >0.56 ppm, potential confounding by PAH exposure; average LOAEC for all factory studies in the first tertile was 1.97 ppm, quality score of 17.10); Factory studies with a less certain LOAEC (Bogadi-Sare et al., 2003 LOAEC=13 ppm, Holz et al., 1995, LOAEC=0.6–1 ppm). The LOAECs from Bogardi-Sare and Holz differ by more than two orders of magnitude, thus sensitivity analyses are not warranted.
The leading case LOAEC of 2.33 ppm is supported by the leading sensitivity analyses which account for more studies with a lower quality score and suggest slightly lower LOAECs near 2 ppm. Interpreted with due regard to quality, in aggregate the literature supports a LOAEC of 2 ppm.
Derivation of NOAECs. Three studies from the factory scenario that suggest NOAECs: Bogadi-Sare et al. 1997a (8 ppm), Zhang et al., 2011 (4.95 ppm) and Basso et al., 2011
(0.029 ppm). These studies differ by more than two orders of magnitude and as such, do not offer a good “base case” on which to justify a NOAEC. We face the problem of a NOAEC that is higher than the LOAEC. Despite the difficulty in isolating an effect of benzene in impure fuel and (especially) ambient studies, they are the best avenue at present for estimating a NOAEC for genotoxicity. In the fuel scenario, two studies scored in the first tertile and were characterized by more certain NOAECs: Carere et al. (1995) (0.47 ppm) and Pandey et al. (2008) (0.9 ppm). Combining these gives an average NOAEC of 0.69 ppm for genotoxicity. There are three other studies: Fracasso et al. (2010) (0.012 ppm), Pitarque et al. (1996) (0.3 ppm) and Göethel et al. (2014) (0.6 ppm) from the fuel sector that score above the median with more certain NOAECs. Using this set of studies as a sensitivity analysis a NOAEC of 0.45 ppm results. These analyses suggest that a NOAEC of 0.5 ppm is justified.
OEL derivation
Method 1: (Use of the LOAEC)
POINT OF DEPARTURE FOR GENOTOXIC EFFECTS: >2.33 ppm.
This preferred approach is based on four studies (Table 6) in the factory setting with a more certain LOAEC that are high quality (top tertile). A fifth study (Zhang et al., 2007) which showed a higher LOAEC of 13.6 ppm was not considered. This preferred derivation is supported by additional sensitivity analyses summarized previously which consider the fuel sector as well as the factory sector, and the alternative definition of “high quality” using studies above the median rather than the top tertile.
POTENTIAL ASSESSMENT FACTORS:
• Dose-response (LOAEC to NOAEC).>2.33 ppm is the lowest level of exposure among four high quality (top tertile). Subsequently, a NOAEC of 0.69 ppm was calculated (see below). Other NOAECs which were near or greater than the LOAEC were not considered. In addition, the preferred LOAEC is noted as greater than 2.33, thus 2.33 should be regarded as the minimum preferred value. Given the degree of potential overlap in LOAECs and NOAECs, and the fact that there is some uncertainty in the inequality >2.33 ppm, the factor should be lower than the usual value of 3. A value of 2 is recommended.
• Intraspecies. A factor lower than 3 is recommended when a reasonably large human study is used in which a range of sensitivities are already present and extrapolations from the study data are to other occupational populations. In aggregate, the LOAEC studies considered included >2700 benzene exposed individuals. In addition, all the LOAECs are based on Chinese workers, who may be a more sensitive population. Thus, a value of 2 is recommended. A value of 1 could also be considered since a possibly more sensitive population generates the LOAEC, thus, sensitive sub-populations may have already been accounted for in the selection of this LOAEC.
OEL=2.33 ppm / 4 (=2×2)=0.58 ppm METHOD 1
Method 2: (Use of NOAECs)
Method 2 is derived from the NOAECs of two studies of high quality in the fuel sector since studies in the factory sector showed higher NOAECs when compared to the preferred LOAEC. NOAECs that are
near or above the LOAEC from above are not considered, thus this could be considered a conservative approach.
POINT OF DEPARTURE FOR GENOTOXIC EFFECTS:
NOAECs from two high quality studies are used as the basis for a weighted NOAEC of 0.69 ppm. Studies of Zhang et al., 2011 (NOAEC=4.95) and Bogadi-Šare et al., 2003 (NOAEC=8) were not considered, thus the value of 0.69 may be conservative. On the other hand, only two studies are used to calculate the aggregate NOAEC, which could balance the conservative nature of the selection of studies that were included. Concordance with method 1, arguably based on stronger data (average quality score of LOAEC studies=17.25, average quality score of NOAEC studies=14.5) would also justify an intra-species factor of 1.
OEL=0.69 ppm. METHOD 2.
Given that the haematology data suggest an OEL of 0.5 ppm, the genotoxicity based OELs of 0.58 ppm (Method 1), and 0.69 ppm (Method 2) it can be agreed that both datasets would support an OEL of 0.5 ppm (8 h TWA).
As was the case for haematotoxicity, the data supporting this position are mainly derived from worker studies examining effects in peripheral blood (except for (Xing et al., 2010). An additional factor of two is proposed for possible subclinical effects in the bone marrow until additional research clarifies the sensitivity of peripheral blood versus bone marrow effects. This additional factor would support an OEL of 0.25 ppm (8 h TWA) for both haematotoxicity and genotoxicity endpoints.
Endpoint conclusion
- Endpoint conclusion:
- adverse effect observed (positive)
Additional information
in vitro data
Benzene has been extensively examined for the core endpoints of gene mutation in bacteria, gene mutation in mammalian cells and chromosomal damage in mammalian cells in a number of laboratories (EHC/IPCS, 1993). The results have been conflicting, with predominantly negative results being reported from earlier studies, especially with bacterial systems. However, a number of positive results have been reported with these core endpoints, including studies with enclosed systems together with auxiliary metabolic activation. Positive results have been reported for bacterial mutation (Glatt et al, 1989), mammalian cell gene mutation (Tsutsui et al, 1997) and mammalian cell chromosomal damage (Ishidate and Sofuni, 1985). A similar profile of mixed results has been reported for additional endpoints including DNA repair, DNA strand breaks and cell transformation (Ashby et al 1985, Tsutsui et al, 1997; EHC/ IPCS, 1993). It is considered that containment of the material in contact with the target cells, together with an appropriate source of metabolism is required to allow the identification of a mutagenic response.
in vivo data
The key studies in animal in vivo systems are considered to be cytogenetic studies in the bone marrow and germ cells Ciranni et al, 1991; Farris et al, 1996. A gene mutation study in somatic cells Mullin et al, 1995) has been reported but this and other similar studies have been observed to have limitations.
Of the in vivo cytogenetic studies benzene was studied in a rodent bone marrow cytogenetic assay in which male Swiss SD1 mice were exposed to a single oral dose of 0, 88, 440 or 880 mg/kg and samples of bone marrow cells taken for cytogenetic analysis. Samples of differentiating spermatagonia were similarly taken after 0, 220, 440 or 880 mg/kg benzene exposure. Dose-related significant increases in chromosomal aberrations were found in both tissues. Benzene was mutagenic in this assay in both the bone marrow and germ cells (Ciranni et al, 1991). Additionally, in a bone marrow micronucleus assay, male B6C3F1 mice were exposed to benzene by the inhalation route at atmospheres of 0, 1, 10, 100, 200, 400 ppm over an 8 week exposure period. A dose-related increase in micronucleus incidence was reported (Farris et al, 1996). A number of other studies have confirmed the clastogenicity of benzene in both rats and mice (EU RAR, 2008). Benzene was also active in a comet assay in mice measuring DNA strand breaks, but only showed marginal activity for sister chromatid exchange induction in rats and mice (EU RAR, 2008).
Whilst there are reports of findings of mutation in transgenic rodents exposed to benzene (Mullin et al 1995, Mullin et al 1998, and Provost et al 1996) these studies variously have design limitations (e.g. sample size, species differences in organs affected by cancer compared to man, limitations in statistical analysis) marginal findings and inappropriate delays in sampling periods which have led to their outcome being discounted (Whysner et al 2004, DECOS 2013).
Human information
In a review by Schnatter et al 2020, seventy-seven repeat dose studies addressing genotoxic and cytogenetic effects of benzene in exposed human worker populations, focussing on micronuclei formation and chromosomal aberrations were scored for study quality with an adapted tool based on that of Vlaanderen et al., 2008 (Environ Health. Perspect. 116 1700−5). Genotoxicity endpoint (as well as haematotoxicity) was selected as one of most sensitive and relevant endpoints to the proposed mode of action (MOA) and protecting against it will protect against benzene carcinogenicity. Lowest and No- Adverse Effect Concentrations (LOAECs and NOAECs) were derived from the highest quality studies (i.e. those ranked in the top tertile or top half) and further assessed as being “more certain” or “less certain”. Several sensitivity analyses were conducted to assess whether alternative “high quality” constructs affected conclusions. Genotoxicity, studies showed effects near 2 ppm and showed no effects at about 0.69 ppm (the findings supported the haematotoxicity results). Several sensitivity analyses supported these observations. These data define a benzene LOAEC of 2 ppm (8 h TWA) and a NOAEC of 0.5 ppm (8 h TWA). Allowing for possible subclinical effects in bone marrow not apparent in studies of peripheral blood endpoints, an OEL of 0.25 ppm (8 h TWA) is proposed.
Mode of Action
There is significant32P-postlabelling assay data suggesting that exposure to benzene does not result in the formation of DNA adducts. Animal models (Li et al., 1996), where 32P-postlabelling is used, the extreme conditions (twice daily intraperitoneal injections totalling 880 mg/kg/d) resulting in a response, support the notion that such a mechanism is unlikely to operate in carcinogenic exposures as the 32P-postlabelling was only higher following treatments that were significantly above the carcinogenic exposure (50 mg/kg/d oral exposure). This result strongly indicates that genotoxicity of benzene and/or its metabolites rather than direct mutagenicity is likely a key event the carcinogenic process of benzene. This is further supported by human data, because historical exposures resulting in excess leukaemia are associated with gene duplication, but not gene inactivation (Rothman et al., 1995). Indirectly acting clastogens/aneugens are linked to gene duplication, whereas direct-acting mutagens are linked to gene inactivation.
The MoA of benzene and benzene metabolites aligns with a number of threshold mechanisms described by North et al. (2020a), which are initiated by the reactive oxygen species, protein cross-linking, and protein adduct formation.
REFERENCES
Ashby et al (1985). Assays to measure the induction of unscheduled DNA synthesis in cultured hepatocytes, (Eds) Progress in Mutation Research, Vol 5, pp 371-373
Ciranni R et al (1991). Dose related clastogenic effects induced by benzene in bone marrow cells and in differentiating spermatogonia of Swiss CD1 mice, Mutagenesis .6(5) 417-421
DECOS (2014). Benzene- Health-based recommended occupational exposure limit. Health Council of the Netherlands, Publication no.2014 /3 The Hague
IPCS (1993). Environmental Health Criteria No. 150. Benzene.
EU RAR (2008). Risk Assessment. Benzene.
Farris GM et al (1996). Benzene-induced micronuclei in erythrocytes: an inhalation concentration -response study in B6C3F1 mice, Mutagenesis. 11(5) 455-462
Glatt et al (1989). Multiple activation pathways of benzene leading to products with varying genotoxic characteristics, Environmental Health Perspectives. 82, 81-89
Li G et al (1996). Tissue distribution of DNA adducts and their persistence in blood of mice exposed to benzene, Environ. Health Perspect.104 suppl. 6 1337-8
Mullin AH et al (1995). Inhalation of benzene leads to an increase in the mutant frequencies of alacItransgene in lung and spleen tissues of mice, Mutat Res. 327 121-129
Mullin AH et al (1998). Inhaled benzene increases the frequency and length oflacIdeletion mutations in lung tissues of mice, Carcinogenesis. 19(10) 1723-1733
North CM et al (2020a) Modes of Action Considerations in Threshold Expectations for Health Effects of Benzene. Toxicology Letters Volume 334: 78-86.
Pathak DN et al (1995). DNA adduct formation in the bone marrow of B6C3F1 mice treated with benzene, Carcinogenesis. 16(8) 1803-8
Provost GS et al (1996). Mutagenic response to benzene and tris(2.3-dibromopropyl)-phosphate in the lambda lacI transgenic mouse mutation assay: a standardized approach to in vivo mutation analysis, Environ Mol Mutagen. 28(4) 342-7
Qu et al (2003). Validation and evaluation of biomarkers in workers exposed to benzene in China, Res Rep Health Eff Inst. (115) 1-72
Rothman N et al (1995). Benzene induces gene-duplicating but not gene-inactivating mutations at the glycophorin A locus in exposed humans, Proc. Natl. Acad. Sci. 92 4069-4073
Schnatter AR, Rooseboom M, Kocabas NA, North CM, Dalzell A, Twisk J, Faulhammer F, Rushton E, Boogaard PJ, Ostapenkaite V, Williams SD. Derivation of an occupational exposure limit for benzene using epidemiological study quality assessment tools. Toxicology Letters Volume 334: 117-144. https://doi.org/10.1016/j.toxlet.2020.05.036
Smith MT et al (1998). Increased translocations and aneusomy in chromosomes 8 and 21 among workers exposed to benzene, Cancer Research. 58 2176-2181
Tsutsui T et al (1997). Benzene, catechol, hydroquinone and phenol induced cell transformation, gene mutations, chromosome aberrations, aneuploidy, sister chromatid exchanges and unscheduleded DNA synthesis in Syrian Hamster embryo cells, Mutat Res. 373 (1) 113-23
Whysner J et al (2004). Genetic toxicology of benzene and its metabolites, Mutat Res. 566(2) 99-130
Zhang L et al (1996). Interphase cytogenetics of workers exposed to benzene Environ. Health Perspect. 104 suppl. 6 1325-1329
Zhang et al (1998). Increased Translocations and Aneusomy in Chromosomes 8 and 21 Among workers exposed to Benzene, Cancer Research. 58 2176-2181
Justification for classification or non-classification
Benzene is an in vivo mutagen in mammals and Humans, inducing chromosomal aberrations and micronuclei. Benzene is therefore classified as Mutagenic Cat 1B (H340) under Regulation (EC) No 1272/2008 of the European Parliament.
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