Colorectal cancer (CRC) is the fourth most common cause of death from cancer worldwide. CRC is a multistep and progressive disease where genetic factors are important in the initiation, the development and the progression of the disease. Then, CRCs can arise from sequential steps including the acquisition of mutations in the adenomatous polyposis coli (APC), followed by the mutational activation of oncogene KRAS and the inactivation of the tumor suppressor gene, TP53. The occurrence of colorectal cancer is largely influenced by the environment, including food contaminants, lifestyle and nutrition. However, the influence of mutations on the response to environmental pollutants is poorly evaluated. Environmental carcinogenesis lacks robust models to explore the interaction between genes and environment and to determine whether genetic mutations associated with colon carcinogenesis generate a particular susceptibility to the harmful effects of pollutants.