-
British Journal of Industrial Medicine Jul 1991Benzene, a common industrial chemical and a component of gasoline, is radiomimetic and exposure may lead progressively to aplastic anaemia, leukaemia, and multiple... (Review)
Review
Benzene, a common industrial chemical and a component of gasoline, is radiomimetic and exposure may lead progressively to aplastic anaemia, leukaemia, and multiple myeloma. Although benzene has been shown to cause many types of genetic damage, it has consistently been classified as a non-mutagen in the Ames test, possibly because of the inadequacy of the S9 microsomal activation system. The metabolism of benzene is complex, yielding glucuronide and sulphate conjugates of phenol, quinol, and catechol, L-phenylmercapturic acid, and muconaldehyde and trans, trans-muconic acid by ring scission. Quinol is oxidised to p-benzoquinone, which binds to vital cellular components or undergoes redox cycling to generate oxygen radicals; muconaldehyde, like p-benzoquinone, is toxic through depletion of intracellular glutathione. Exposure to benzene may also induce the microsomal mixed function oxidase, cytochrome P450 IIE1, which is probably responsible for the oxygenation of benzene, but also has a propensity to generate oxygen radicals. The radiomimetic nature of benzene and its ability to induce different sites of neoplasia indicate that formation of oxygen radicals is a major cause of benzene toxicity, which involves multiple mechanisms including synergism between arylating and glutathione-depleting reactive metabolites and oxygen radicals. The occupational exposure limit in the United Kingdom (MEL) and the United States (PEL) was 10 ppm based on the association of benzene exposure with aplastic anaemia, but recently was lowered to 5 ppm and 1 ppm respectively, reflecting a concern for the risk of neoplasia. The American Conference of Governmental Industrial Hygienists (ACGIH) has even more recently recommended that, as benzene is considered an A1 carcinogen, the threshold limit value (TLV) should be decreased to 0.1 ppm. Only one study in man, based on nine cases of benzene associated fatal neoplasia, has been considered suitable for risk assessment. Recent re-evaluation of these data indicated that past assessments may have overestimated the risk, and different authors have considered that lifetime exposure to benzene at 1 ppm would result in an excess of leukaemia deaths of 9.5 to 1.0 per 1000. Although in this study, deaths at low levels of benzene exposure were associated with multiple myeloma and a long latency period, instead of leukaemia, which might justify further lowering of the exposure limit, the risk assessment model has been found to be non-significant for response at low levels of exposure. The paucity of data for man, the complexity of the metabolic activation of benzene, the interactive and synergistic mechanisms of benzene toxicity and carcinogenicity, the different disease endpoints (aplastic anaemia, leukaemia, and multiple myeloma), and different individual susceptibilities, all indicate that in such a complex scenario, regulators should proceed with caution before making further changes to the exposure limit for this chemical.
Topics: Anemia, Aplastic; Animals; Benzene; Bone Marrow; Chemical Phenomena; Chemistry; Humans; Leukemia; Maximum Allowable Concentration; Multiple Myeloma; Neoplasms; Occupational Exposure; Risk
PubMed: 1854646
DOI: 10.1136/oem.48.7.437 -
Sensors (Basel, Switzerland) Nov 2021The presence of benzene and similar aromatic compounds in civil environments is due to anthropic actions but also to natural sources. Natural gas consists of a gas...
The presence of benzene and similar aromatic compounds in civil environments is due to anthropic actions but also to natural sources. Natural gas consists of a gas mixture where benzene and related compounds are usually presents. Thus, the detection of these compounds in natural gas pipelines is of the utmost importance as well as the control of the concentration level, which must remain below the limits consented by law. In this regard, it is of striking interest to engineer devices able to detect these compounds by automatic and continuous remote control. Here, we discuss the application of an optical device designed for the measurement of sulfured odorizing agents in natural gas pipelines aiming at the detection and the measurement of benzene, toluene, and xylenes (BTX) in the same contexts. The instrument consists of a customized UV spectrophotometer connected to an automatic control system able to provide in-field detections of BTX through a continuous and remote check of the gaseous mixture. Relatively to benzene, the instrument is characterized by values of LOD (level of detection) and LOQ (level of quantification) equal to 0.55 and 1.84 mg/Sm3, respectively. Similar limits are found for toluene and xylenes (LOD of 0.81, 1.05, 1.41, and 1.00 mg/Sm3 for toluene, meta-, ortho-, and para-xylene, respectively).
Topics: Benzene; Benzene Derivatives; Natural Gas; Toluene; Xylenes
PubMed: 34833651
DOI: 10.3390/s21227575 -
International Journal of Environmental... May 2023(1) Background: Benzene, toluene, and xylene isomers (BTX) are present in gasoline. Exposure to benzene may lead to the appearance of a series of signs, symptoms, and...
(1) Background: Benzene, toluene, and xylene isomers (BTX) are present in gasoline. Exposure to benzene may lead to the appearance of a series of signs, symptoms, and complications, which are characterized by benzene poisoning, which is an occupational disease. This study evaluated the presence of signs and symptoms related to occupational exposure and whether occupational exposure to BTX is associated with the development of hematological changes. (2) Material and Methods: This cross-sectional epidemiological study included 542 participants, in which 324 were gas station workers (GSWs) and 218 were office workers (OWs) with no occupational exposure to benzene. To characterize the type of exposure (exposed and not exposed), trans,trans-Muconic acid (tt-MA), Hippuric acid (HA), and Methylhippuric acid (MHA) were used as exposure biomarkers. The tt-MA analysis revealed that the GSWs had 0.29 mg/g of urinary creatinine and the OWs had 0.13 mg/g of urinary creatinine. For HA, the GSWs presented 0.49 g/g of creatinine while the OWs presented 0.07. MHA analysis revealed that the GSWs had 1.57 g/g creatinine and the OWs had 0.01 g/g creatinine. Occupation habits and clinical symptoms were collected by questionnaire and blood samples were analyzed for hematological parameters. The persistence of hematological changes was evaluated with three serial blood collections every 15 days followed by laboratory hematological analysis. A descriptive analysis by the Chi-square test method was performed to evaluate the association between occupational exposure to fuels and the occurrence of changes in hematological parameters. (3) Results: In the GSWs, the most described signs and symptoms were somnolence (45.1%), headache (38.3%), dizziness (27.5%), tingling (25.4%), and involuntary movement (25%). Twenty GSWs that presented hematological alterations performed serial collections fifteen days apart. In addition, these workers presented total leukocyte counts above the upper limit and lymphocyte counts close to the lower limit. Leukocytosis and lymphopenia are hematological alterations present in chronic benzene poisoning. (4) Conclusions: The results found an initial change in different hematological parameters routinely used in clinics to evaluate health conditions. These findings reveal the importance of valuing clinical changes, even in the absence of disease, during the health monitoring of gas station workers and other groups that share the same space.
Topics: Humans; Benzene; Environmental Monitoring; Creatinine; Cross-Sectional Studies; Occupational Exposure
PubMed: 37239622
DOI: 10.3390/ijerph20105896 -
Journal of Immunology Research 2014Benzene represents an ubiquitous pollutant both in the workplace and in the general environment. Health risk and stress posed by benzene have long been a concern because... (Review)
Review
Benzene represents an ubiquitous pollutant both in the workplace and in the general environment. Health risk and stress posed by benzene have long been a concern because of the carcinogenic effects of the compound which was classified as a Group 1 carcinogen to humans and animals. There is a close correlation between leukemia, especially acute myeloid leukemia, and benzene exposure. In addition, exposure to benzene can cause harmful effects on immunological, neurological, and reproductive systems. Benzene can directly damage hematopoietic progenitor cells, which in turn could lead to apoptosis or may decrease responsiveness to cytokines and cellular adhesion molecules. Alternatively, benzene toxicity to stromal cells or mature blood cells could disrupt the regulation of hematopoiesis, including hematopoietic commitment, maturation, or mobilization, through the network of cytokines, chemokines, and adhesion molecules. Today there is mounting evidence that benzene may alter the gene expression, production, or processing of several cytokines in vitro and in vivo. The purpose of this review was to systematically analyze the published cases of cytokine effects on human benzene exposure, particularly hematotoxicity, and atopy, and on lungs.
Topics: Benzene; Cytokines; Environmental Pollutants; Hematopoiesis; Humans; Hypersensitivity, Immediate; Lung; Signal Transduction
PubMed: 25202711
DOI: 10.1155/2014/937987 -
Regulatory Toxicology and Pharmacology... Dec 2018Exposure to benzene has many sources, from gasoline refueling to tobacco combustion. Although the toxicology of benzene is well studied, the potential for environmental... (Review)
Review
Exposure to benzene has many sources, from gasoline refueling to tobacco combustion. Although the toxicology of benzene is well studied, the potential for environmental exposure and a heightened interest in identifying substances that may cause toxicity by interacting with the endocrine systems of humans and wildlife resulted in benzene being placed on the second list of chemicals for possible screening under the USEPA's Endocrine Disruptor Screening Program. Therefore, we conducted a thorough, systematic literature search and used a weight-of-evidence methodology to test hypotheses regarding the potential for benzene to act via estrogen, androgen, thyroid, and steroidogenic pathways. The methodology included an assessment of data quality and a semi-quantitative weighting of endocrine-responsive endpoints measured in various types of studies according to their relevance for evaluating each hypothesis. This maximized use of all relevant and reliable literature on benzene and enabled a transparent comparison of evidence supporting and opposing each hypothesized mode of action. While benzene affected reproductive organ weights and histopathology in a few studies, there was no consistent pattern of effects suggestive of an estrogen, androgen, thyroid or steroidogenic mode of action. Based on data from multiple animal species, benzene appears to lack endocrine activity by these pathways.
Topics: Animals; Benzene; Endocrine System; Humans
PubMed: 30273620
DOI: 10.1016/j.yrtph.2018.09.027 -
Chemico-biological Interactions Mar 2010Benzene has been measured throughout the environment and is commonly emitted in several industrial and transportation settings leading to widespread environmental and... (Review)
Review
Benzene has been measured throughout the environment and is commonly emitted in several industrial and transportation settings leading to widespread environmental and occupational exposures. Inhalation is the most common exposure route but benzene rapidly penetrates the skin and can contaminant water and food resulting in dermal and ingestion exposures. While less toxic solvents have been substituted for benzene, it still is a component of petroleum products, including gasoline, and is a trace impurity in industrial products resulting in continued sub to low ppm occupational exposures, though higher exposures exist in small, uncontrolled workshops in developing countries. Emissions from gasoline/petrochemical industry are its main sources to the ambient air, but a person's total inhalation exposure can be elevated from emissions from cigarettes, consumer products and gasoline powered engines/tools stored in garages attached to homes. Air samples are collected in canisters or on adsorbent with subsequent quantification by gas chromatography. Ambient air concentrations vary from sub-ppb range, low ppb, and tens of ppb in rural/suburban, urban, and source impacted areas, respectively. Short-term environmental exposures of ppm occur during vehicle fueling. Indoor air concentrations of tens of ppb occur in microenvironments containing indoor sources. Occupational and environmental exposures have declined where regulations limit benzene in gasoline (<1%) and cigarette smoking has been banned from public and work places. Similar controls should be implemented worldwide to reduce benzene exposure. Biomarkers of benzene used to estimate exposure and risk include: benzene in breath, blood and urine; its urinary metabolites: phenol, t,t-muconic acid (t,tMA) and S-phenylmercapturic acid (sPMA); and blood protein adducts. The biomarker studies suggest benzene environmental exposures are in the sub to low ppb range though non-benzene sources for urinary metabolites, differences in metabolic rates compared to occupational or animal doses, and the presence of polymorphisms need to be considered when evaluating risks from environmental exposures to individuals or potentially susceptible populations.
Topics: Animals; Benzene; Biomarkers; Environmental Exposure; Humans; Occupational Exposure
PubMed: 20056112
DOI: 10.1016/j.cbi.2009.12.030 -
Carcinogenesis Jan 2013Benzene is a ubiquitous air pollutant that causes human leukemia and hematotoxic effects. Although the mechanism by which benzene causes toxicity is unclear, metabolism... (Review)
Review
Benzene is a ubiquitous air pollutant that causes human leukemia and hematotoxic effects. Although the mechanism by which benzene causes toxicity is unclear, metabolism is required. A series of articles by Kim et al. used air and biomonitoring data from workers in Tianjin, China, to investigate the dose-specific metabolism (DSM) of benzene over a wide range of air concentrations (0.03-88.9 p.p.m.). Kim et al. concluded that DSM of benzene is greatest at air concentrations <1 p.p.m. This provocative finding motivated the American Petroleum Institute to fund a study by Price et al. to reanalyze the original data. Although their formal 'reanalysis' reproduced Kim's finding of enhanced DSM at sub-p.p.m. benzene concentrations, Price et al. argued that Kim's methods were inappropriate for assigning benzene exposures to low exposed subjects (based on measurements of urinary benzene) and for adjusting background levels of metabolites (based on median values from the 60 lowest exposed subjects). Price et al. then performed uncertainty analyses under alternative approaches, which led them to conclude that '… the Tianjin data appear to be too uncertain to support any conclusions …' regarding the DSM of benzene. They also argued that the apparent low-dose metabolism of benzene could be explained by 'lung clearance.' In addressing these criticisms, we show that the methods and arguments presented by Price et al. are scientifically unsound and that their results are unreliable.
Topics: Air Pollutants, Occupational; Benzene; Environmental Monitoring; Humans; Models, Statistical; Occupational Exposure
PubMed: 23222815
DOI: 10.1093/carcin/bgs382 -
Microbial Biotechnology Nov 2011Benzene is a widespread and toxic contaminant. The fate of benzene in contaminated aquifers seems to be primarily controlled by the abundance of oxygen: benzene is... (Review)
Review
Benzene is a widespread and toxic contaminant. The fate of benzene in contaminated aquifers seems to be primarily controlled by the abundance of oxygen: benzene is aerobically degraded at high rates by ubiquitous microorganisms, and the oxygen-dependent pathways for its breakdown were elucidated more than 50 years ago. In contrast, benzene was thought to be persistent under anoxic conditions until 25 years ago. Nevertheless, within the last 15 years, several benzene-degrading cultures have been enriched under varying electron acceptor conditions in laboratories around the world, and organisms involved in anaerobic benzene degradation have been identified, indicating that anaerobic benzene degradation is a relevant environmental process. However, only a few benzene degraders have been isolated in pure culture so far, and they all use nitrate as an electron acceptor. In some highly enriched strictly anaerobic cultures, benzene has been described to be mineralized cooperatively by two or more different organisms. Despite great efforts, the biochemical mechanism by which the aromatic ring of benzene is activated in the absence of oxygen is still not fully elucidated; methylation, hydroxylation and carboxylation are discussed as likely reactions. This review summarizes the current knowledge about the 'key players' of anaerobic benzene degradation under different electron acceptor conditions and the possible pathway(s) of anaerobic benzene degradation.
Topics: Anaerobiosis; Bacteria; Benzene; Biotransformation; Electron Transport; Environmental Pollutants; Oxidation-Reduction
PubMed: 21450012
DOI: 10.1111/j.1751-7915.2011.00260.x -
Environmental Health Perspectives Dec 1996Benzene toxicity involves both bone marrow depression and leukemogenesis caused by damage to multiple classes of hematopoietic cells and a variety of hematopoietic cell... (Review)
Review
Benzene toxicity involves both bone marrow depression and leukemogenesis caused by damage to multiple classes of hematopoietic cells and a variety of hematopoietic cell functions. Study of the relationship between the metabolism and toxicity of benzene indicates that several metabolites of benzene play significant roles in generating benzene toxicity. Benzene is metabolized, primarily in the liver, to a variety of hydroxylated and ring-opened products that are transported to the bone marrow where subsequent secondary metabolism occurs. Two potential mechanisms by which benzene metabolites may damage cellular macromolecules to induce toxicity include the covalent binding of reactive metabolites of benzene and the capacity of benzene metabolites to induce oxidative damage. Although the relative contributions of each of these mechanisms to toxicity remains unestablished, it is clear that different mechanisms contribute to the toxicities associated with different metabolites. As a corollary, it is unlikely that benzene toxicity can be described as the result of the interaction of a single metabolite with a single biological target. Continued investigation of the metabolism of benzene and its metabolites will allow us to determine the specific combination of metabolites as well as the biological target(s) involved in toxicity and will ultimately lead to our understanding of the relationship between the production of benzene metabolites and bone marrow toxicity.
Topics: Animals; Benzene; Biotransformation; Bone Marrow; DNA Adducts; Humans; In Vitro Techniques; Leukemia; Microsomes, Liver; Molecular Structure; Oxidative Stress
PubMed: 9118888
DOI: 10.1289/ehp.961041165 -
International Journal of Hygiene and... Mar 2022The fire service has become more aware of the potential for adverse health outcomes due to occupational exposure to hazardous combustion byproducts. Because of these...
The fire service has become more aware of the potential for adverse health outcomes due to occupational exposure to hazardous combustion byproducts. Because of these concerns, personal protective equipment (PPE) manufacturers have developed new protection concepts like particulate-blocking hoods to reduce firefighters' exposures. Additionally, fire departments have implemented exposure reduction interventions like routine laundering of PPE after fire responses. This study utilized a fireground exposure simulator (FES) with 24 firefighters performing firefighting activities on three consecutive days wearing one of three PPE ensembles (stratified by hood design and treatment of PPE): 1) new knit hood, new turnout jacket and new turnout pants 2) new particulate-blocking hood, new turnout jacket and new turnout pants or 3) laundered particulate-blocking hood, laundered turnout jacket and laundered turnout pants. As firefighters performed the firefighting activities, personal air sampling on the outside and inside the turnout jacket was conducted to quantify exposures to volatile organic compounds (VOCs) and naphthalene. Pre- and immediately post-fire exhaled breath samples were collected to characterize the absorption of VOCs. Benzene, toluene, and naphthalene were found to diffuse through and/or around the turnout jacket, as inside jacket benzene concentrations were often near levels reported outside the turnout jacket (9.7-11.7% median benzene reduction from outside the jacket to inside the jacket). The PPE ensemble did not appear to affect the level of contamination found inside the jacket for the compounds evaluated here. Benzene concentrations in exhaled breath increased significantly from pre to post-fire for all three groups (p-values < 0.05). The difference of pre-to post-fire benzene exhaled breath concentrations were positively associated with inside jacket and outside jacket benzene concentrations, even though self-contained breathing apparatus (SCBA) were worn during each response. This suggests the firefighters can absorb these compounds via the dermal route.
Topics: Air Pollutants, Occupational; Benzene; Firefighters; Humans; Naphthalenes; Occupational Exposure; Personal Protective Equipment; Polycyclic Aromatic Hydrocarbons; Toluene
PubMed: 34902715
DOI: 10.1016/j.ijheh.2021.113900