Cronin W J, Oswald E J, Shelley M L, Fisher J W, Flemming C D
Air Force Institute of Technology, Department of Engineering and Environmental Management, Wright-Patterson Air Force Base, Ohio 45433, USA.
Risk Anal. 1995 Oct;15(5):555-65. doi: 10.1111/j.1539-6924.1995.tb00752.x.
A Monte Carlo simulation is incorporated into a risk assessment for trichloroethylene (TCE) using physiologically-based pharmacokinetic (PBPK) modeling coupled with the linearized multistage model to derive human carcinogenic risk extrapolations. The Monte Carlo technique incorporates physiological parameter variability to produce a statistically derived range of risk estimates which quantifies specific uncertainties associated with PBPK risk assessment approaches. Both inhalation and ingestion exposure routes are addressed. Simulated exposure scenarios were consistent with those used by the Environmental Protection Agency (EPA) in their TCE risk assessment. Mean values of physiological parameters were gathered from the literature for both mice (carcinogenic bioassay subjects) and for humans. Realistic physiological value distributions were assumed using existing data on variability. Mouse cancer bioassay data were correlated to total TCE metabolized and area-under-the-curve (blood concentration) trichloroacetic acid (TCA) as determined by a mouse PBPK model. These internal dose metrics were used in a linearized multistage model analysis to determine dose metric values corresponding to 10(-6) lifetime excess cancer risk. Using a human PBPK model, these metabolized doses were then extrapolated to equivalent human exposures (inhalation and ingestion). The Monte Carlo iterations with varying mouse and human physiological parameters produced a range of human exposure concentrations producing a 10(-6) risk.
采用基于生理的药代动力学(PBPK)模型结合线性化多阶段模型,将蒙特卡罗模拟纳入三氯乙烯(TCE)的风险评估中,以推导人类致癌风险外推值。蒙特卡罗技术纳入了生理参数变异性,以产生一系列基于统计得出的风险估计值,从而量化与PBPK风险评估方法相关的特定不确定性。该评估涵盖了吸入和摄入两种暴露途径。模拟的暴露场景与美国环境保护局(EPA)在其TCE风险评估中使用的场景一致。从小鼠(致癌生物测定对象)和人类的文献中收集了生理参数的平均值。利用现有的变异性数据假设了现实的生理值分布。通过小鼠PBPK模型确定,小鼠癌症生物测定数据与代谢的总TCE以及曲线下面积(血药浓度)三氯乙酸(TCA)相关。这些内部剂量指标用于线性化多阶段模型分析,以确定对应于10^(-6)终身超额癌症风险的剂量指标值。然后,使用人类PBPK模型,将这些代谢剂量外推至等效的人类暴露量(吸入和摄入)。对小鼠和人类生理参数进行变化的蒙特卡罗迭代产生了一系列导致10^(-6)风险的人类暴露浓度。