However, in this scenario of lower cancer risk some specific cancers show an incidence higher than expected. Soft tissue sarcoma, Hodgkin’s and non-Hodgkin’s lymphoma, leukemia, multiple myeloma, stomach, brain, prostate, pancreatic, breast and ovarian cancer have been associated with various degrees of consistency to pesticides exposure (Bassil et al., 2007, Blair Selleckchem Ceritinib et al., 1992 and Dich et al., 1997). The strongest epidemiological associations reported, are those concerning hematological malignancies and pesticides
exposure (Bassil et al., 2007 and Chiu and Blair, 2009). While acute toxic effects of pesticides are well known, uncertainties still remain regarding chronic and long term effects. For some pesticides, mechanisms such as the endocrine disruption (De Coster and van Larebeke, 2012) have been hypothesizes. Moreover, it has been speculated that health effects observed in agricultural population may be related to the mutagenic effect of solar radiation (Nordby et al., 2004). To date, however, the specific molecular mechanisms linking exposure to health effects are still lacking. It is also necessary taking into account that pesticide market is quickly changing in the so-called “developed countries”, also as a consequence of new and more stringent legislation regarding authorization procedures, and oganophosphates and carbamates are being replaced
by the less toxic pyrethroids and the more efficient, selective and more expensive new compounds. Conversely in the developing Natural Product Library mouse countries, the old generation compounds are Phloretin still largely used. The complexity of the field, makes extremely difficult to formulate a unifying theory, able to explain at what level pesticides exert their toxic function. Recently some environmental factors have been linked to aberrant changes in epigenetic pathways both in experimental and epidemiological studies (Baccarelli and Bollati, 2009). In addition, epigenetic mechanisms may mediate specific mechanisms of toxicity
and responses to certain chemicals (Marsit et al., 2006). In this context, we will review the current evidences which seem to indicate epigenetics as a possible link between pesticides exposure and health effects. Epigenetic modifications include DNA methylation, histone modifications, and microRNAs (Chuang and Jones, 2007). DNA methylation is a covalent modification, involved in regulating many cellular processes including chromatin structure and remodeling, X-chromosome inactivation, genomic imprinting, chromosome stability, and gene transcription (Grewal and Moazed, 2003 and Reik et al., 2001). DNA methylation is heritable by somatic cells after cell division. The 5-methyl-cytosine (5MeC) represents 2–5% of all cytosines in mammalian genomes and is found primarily on CpG dinucleotides (Millar et al., 2003).