Abstract
Simple SummaryBenzene is produced by diverse petroleum transformation processes and it is widely employed in industry despite its oncogenic effects. In fact, occupational exposure to benzene may cause hematopoietic malignancy. The leukemogenic action of benzene is particularly complex. Possible processes of onset of hematological malignancies have been recognized as a genotoxic action and the provocation of immunosuppression. However, benzene can induce modifications that do not involve alterations in the DNA sequence, the so-called epigenetics changes. Acquired epigenetic modification may also induce leukemogenesis, as benzene may alter nuclear receptors, and cause changes at the protein level, thereby modifying the function of regulatory proteins, including oncoproteins and tumor suppressor proteins.Benzene carcinogenic ability has been reported, and chronic exposure to benzene can be one of the risk elements for solid cancers and hematological neoplasms. Benzene is acknowledged as a myelotoxin, and it is able to augment the risk for the onset of acute myeloid leukemia, myelodysplastic syndromes, aplastic anemia, and lymphomas. Possible mechanisms of benzene initiation of hematological tumors have been identified, as a genotoxic effect, an action on oxidative stress and inflammation and the provocation of immunosuppression. However, it is becoming evident that genetic alterations and the other causes are insufficient to fully justify several phenomena that influence the onset of hematologic malignancies. Acquired epigenetic alterations may participate with benzene leukemogenesis, as benzene may affect nuclear receptors, and provoke post-translational alterations at the protein level, thereby touching the function of regulatory proteins, comprising oncoproteins and tumor suppressor proteins. DNA hypomethylation correlates with stimulation of oncogenes, while the hypermethylation of CpG islands in promoter regions of specific tumor suppressor genes inhibits their transcription and stimulates the onset of tumors. The discovery of the systems of epigenetic induction of benzene-caused hematological tumors has allowed the possibility to operate with pharmacological interventions able of stopping or overturning the negative effects of benzene.
Highlights
It begins with oxidation to benzene oxide principally by cytochrome P450 2E1, and this substance rapidly is transformed to phenol, and into catechol and hydroquinone metabolites, both of which can be commuted into noxious elements [18]
It is logical to assume that benzene and its metabolites exert different actions on different elements of the hematopoietic system able to provoke haemato-toxicity and malignancy
The possible mechanisms conducting to the onset and progression of the hematologic malignancies are described as a “multi-hit” model
Summary
Benzene is a ubiquitous environmental contaminant (air, soil, water), classified in group 1 by the International Agency for research on cancer [1]. It comes from both natural, such as volcanoes and forest fires, and anthropogenic sources that include combustible fuel emissions, vehicles exhaust, hazardous waste sites or industry. The main sources of benzene exposure for the general population include vehicle exhaust and cigarette smoke [3,4], while considerably lower exposures to benzene can occur from consumption of food, water and beverages [5]. Occupational exposure to benzene occurs in the petroleum and chemical industries and as a result of exposure to gasoline engine emissions and combustion products. Recent studies showed that the occupational exposures to benzene in Europe decreased and are usually below 0.1 ppm, exposures above 0.1 ppm have been reported for some tasks such as gasoline pump repair and maintenance, or for fuel-tanker drivers or work in refineries [7,8,9,10,11,12]
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