Perfluorooctanoic acid (PFOA), a widely used synthetic chemical, is a growing public health concern. Detectable serum levels can be found in most residents of the U.S. The purpose of this thesis is to convert the environmental PFOA exposures to internal doses in a specific population and to extrapolate the internal dose into estimates of individual risk.
Because exposure to PFOA is suspected to cause a number of human health effects, in order to better understand the impact of environmental PFOA exposure, this thesis first reviewed major epidemiology studies on the most frequently reported cancer and non-cancer human health effects. Though evidence remains limited and clear associations have not been established for most of the outcomes, the association between PFOA and kidney cancer is the most robust and is thus selected as the outcome of interest for this study.
To evaluate exposure and effects, I then evaluated the pharmacokinetics of PFOA. It is almost completely absorbed and it is not metabolized in human, so its fate is determined by elimination. Most human studies used compartmental pharmacokinetic models to approximate that elimination, but results have been inconsistent. I next considered some of the likely reasons for that. Finally, I compared one-compartment models using pharmacokinetic parameters from different human studies, and applied them to drinking water data from the State of Colorado. This thesis demonstrates the utility of pharmacokinetic models and their dependency on the available parameters for model building.