Comment on Zheng et al. Association between Promoter Methylation of Gene ERCC3 and Benzene Hematotoxicity. Int. J. Environ. Res. Public Health 2017, 14, 921

Benzene is an established carcinogenic substance [1,2]. Benzene displays rather low acute toxicityin various animal species [1], and benzene itself is not mutagenic in the classical bacterial tests.In mammal cell systems and after metabolic activation it is genotoxic due to oxidation mediatedby Cytochrome P450 ([2] and references therein]). Although the International Agency for Researchon Cancer (IARC) [2] provides a lengthy discussion on the mechanisms and tries to explain whygenotoxicity in men is almost exclusively observed in the hemopoetic system, it still is surprising thatother organs with high metabolic activity like the liver do not seem to be affected. Some epidemiologicalstudies indicate also other target organs [3], but the findings are not as clear as with leukemia.Indeed, there is a need for more complex explanation of causative pathways leading to leukemiatargeting several pathways, including epigenetics [4]. Zheng et al. [5] report about epigenetic effects ofbenzene exposure and propose that the promoter region of the ERCC3 gene plays an important role inbenzene hematoxicity.