Humans cancer risk assessment

Williams GM. Mechanisms of chemical carcinogenesis and applications to human cancer risk assessment. Toxicology 2001 166 3-10. 

Poirier MC, Beland FA. 1992. DNA adduct measurements and tumor incidence during chronic carcinogen exposure in animal models implications for DNA adduct-based human cancer risk assessment. Chem. Res. Toxicol. 5 749-55... 

Paules RS, Aubrecht J, Corvi R, Garthoff B, Kleinjans JC (2011) Moving forward in human cancer risk assessment. Environ Health Perspect 119 739-743... 

Dietrich, D. R. (1995). Alpha 2u-globuhn Species- and sex-specific protein synthesis and excretion, association with chemically induced renal toxicity and neoplasia in the male rat and relevance in human cancer risk assessment. Rev Biochem Toxicol 11, 115-180. 

Estimated Upper-Bound Human Cancer Risk Levels This is the range associated with the upper-bound for lifetime cancer risk of 1 in 10,000 to 1 in 10,000,000. These risk levels are derived from the EPA s Human Health Assessment Group s upper-bound estimates of the slope of the cancer dose response curve at low dose levels (qi ). 

In animal experiments exposures can be carefully controlled, and dose-response curves can be formally estimated. Extrapolating such information to the human situation is often done for regulatory purposes. There are several models for estimating a lifetime cancer risk in humans based on extrapolation from animal data. These models, however, are premised on empirically unverified assumptions that limit their usefulness for quantitative purposes. While quantitative cancer risk assessment is widely used, it is by no means universally accepted. Using different models, one can arrive at estimates of potential cancer incidence in humans that vary by several orders of magnitude for a given level of exposure. Such variations make it rather difficult to place confidence intervals around benefits estimations for regulatory purposes. Furthermore, low dose risk estimation methods have not been developed for chronic health effects other than cancer. The... 

The Corley model (Corley et al. 1990) was the first chloroform PBPK model to describe and ultimately predict the fate of chloroform in several species (including humans) under a variety of exposure conditions. Many subsequent PBPK models for chloroform (Chinery and Gleason 1993 McKone 1993) are based on the Corley model. The Corley model has been used for cancer risk assessment (Reitz et al. 1990). 

Cancer risk assessment is basically a two-step procedure, involving a qualitative assessment of how likely it is that a compound is a human carcinogen, and a quantitative assessment of the cancer risk that is likely to occur at given exposure levels and duration of exposure. 

Bnrmaster DE, Lloyd KJ, Thompson KM. 1995. The need for new methods to backcalculate soil cleannp targets in interval and probabilistic cancer risk assessments. Human Ecol Risk Assess 1 89-100. 

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