of action for FA carcinogenesis. Currently available data strongly indicate that genotoxicity plays an important role in the carcinogenicity of FA in humans. Numerous experiments have demonstrated that FA exposure can induce mutations in a variety of test systems ranging from bacteria to laboratory animals [10; 11]. Moreover, micronucleus formation has been repeatedly reported to occur in cells of the nasal and oral mucosa of FA-exposed humans [3; 12; 13]. Formaldehyde is a highly reactive compound. It can covalently bind to DNA and proteins inducing adducts formation and cross-linking [8]. FA reacts with lysine residues to produce N(6)-formyl-lysine adducts with proteins in vitro and in vivo [14; 15], and FA protein adducts have been described for albumin [16], insulin [17], and hemoglobin [18; 19]. Such alterations may function as sensitive and specific exposure biomarkers (dose metric) and potential effect indicators, as they are involved in mutations and subsequent cancer development [20].  
However, exposure to genotoxic carcinogens, in addition to their genetic effects, might involve a variety of non-genotoxic changes in cells [21]. In this perspective, it cannot be excluded that epigenetic mechanisms may contribute to the FA toxicity [22]. Epigenetics is defined as the study of heritable phenotypes that do not alter the DNA sequence, able to control development, tissue differentiation, and cellular responsiveness [23; 24]. DNA methylation, post-translational histone modifications, and changes in microRNA expression are the most used mechanisms able to initiate and sustain epigenetic information. These effects may all contribute to regulate gene expression profiles, affecting chromatin structure, chromosome integrity, gene transcription, and genomic imprinting therefore possibly contributing to the risk of disease development [25]. An altered epigenetic status may cause genomic instability and loss of controlled growth signals, as typically observed in cancer cells [26]. Epigenetic alterations, rather than specific genetic mutations per se are reported for the clonal expansion of altered preneoplastic foci and tumor development [27]. Therefore, it seems important to verify if epigenetic modifications may function as early cellular events in response to genotoxic carcinogens with well-known modes of action.  
Considering the ubiquitous nature of FA pollutant and the great number of job categories potentially exposed in workplaces, the aim of our review is to provide a comprehensive overview on possible epigenetic changes induced by FA exposure in humans, animals, and cellular models and to address the potential health impact derived from such effects. This may allow to deeply understand the molecular mechanisms underlying FA-induced toxicity and carcinogenicity and to define novel, early biological alterations that may function as possible future biomarkers of effect or susceptibility in exposed subjects. Overall, this review may provide deep insight into the relationship between genome, FA chemical exposure, and disease risk and may be helpful to point out biological mechanisms that should be carefully considered in future public and occupational risk assessment and management approaches.