The presence of pesticides in fruits, vegetables, cereals, other food products and even breast milk is of grave concern (Munshi et al. 2001; FAO/WHO 2005; Damgaard et al 2006; Cok et al. 2007; There are many other studies describing the presence of pesticides as residues in food materials above established maximum residue limits (MRLs). (Bajpai et al. 2007; Devanathan et al. 2009; Srivastava et al. 2011). Of the 267 vegetable samples collected from the farmer's field, 225 samples contained detectable residues representing 84% contamination rate (Ahmed et al. al. 2007). In 1999, 4,700 samples of peppers, cauliflowers and grains were analyzed of wheat and melons (European Commission 2001). Methamidophos residues exceeded the MRLs most often in all vegetables (8.7%), followed by the maneb group (1.1%), thiabendazole (0.57%), acephate. (0.41%) and benomyl group (0.35%). In Brazil, more than 90% of composite milk samples contained organochlorine pesticide residues. Out of 100 composite samples, 44% of the samples contained aldrin followed by DDT (36%), mirex (34%), endosulfan (32%), chlordane (17%), dicofol (14%), heptachlor (11%), and dieldrin (11%) (Avancini et al. 2012). Approximately 20% of Indian food products were found to be contaminated with pesticide residues above the tolerance level compared to only 2% globally (TERI 2000). Pesticide Toxicity The entry of pesticides into the human body through contaminated food or any other mode has been directly associated with health risks. Although pesticides were formulated to kill target pests, they were also toxic to non-target species, and humans were no exception. Many accidents have been reported in different parts of the world...... middle of paper ......cide. In this mode of action, pesticides structurally similar to the cognate ligand bind with the active NR causing conformational changes leading to the release of inappropriate signals (Ruegg et al. 2009). The indirect mechanism of endocrine disruption can occur through inhibition of steroidogenic enzymes and binding to steroid transport proteins (Tebourbi et al. 2011). In this mode of action, pesticides compete for common cofactors and indirectly disrupt the activity of nuclear NRs. Other possible mechanisms of indirect endocrine disruption include xenosensor-induced receptor ubiquitination followed by targeted degradation of NR in the proteasome; transcription of enzymes involved in hormone metabolism induced by xenosensors; blocking genetic regulation through nuclear receptor elements by binding xenohormones to inhibitory elements of the xenobiotic response (Ruegg et al. 2009).