How do the revised Guidelines incorporate our knowledge of how an agent causes cancer into the risk assessment process?
Cancer refers to a group of diseases involving abnormal, malignant tissue growth. Research has revealed that the development of cancer involves a complex series of steps and that carcinogens may operate in a number of different ways. Ultimately, cancer results from a series of defects in genes controlling cell growth, division, and differentiation. Genetic defects leading to cancer may occur because a chemical (or other carcinogenic agent) damages DNA directly. Alternatively, an agent may have indirect effects that increase the likelihood, or accelerate the onset, of cancer without directly interacting with DNA. For example, an agent might interfere with DNA repair mechanisms; thereby increasing the likelihood that cell division will give rise to cells with damaged DNA. An agent might also increase rates of cell division, thus increasing the potential for genetic errors to be introduced as cells replicate their DNA in preparation for division.
Related Questions
- How were the cancer risk estimates affected by EPAs recently revised Guidelines for Carcinogen Risk Assessment (EPA/630/P-03/001F) and new Supplemental Guidance for Assessing Susceptibility from Early-Life Exposure to Carcinogens (EPA/630/R-03/003F)?
- How do the revised Guidelines incorporate our knowledge of how an agent causes cancer into the risk assessment process?
- How does the cancer risk identified in this assessment compare to lifetime cancer risk from all causes?
