ABSTRACT

This review is intended to provide risk assessors and risk managers with a better understanding of issues associated with total exposures of human populations to ethylene oxide from endogenous and exogenous pathways. Biomonitoring of human populations and lab animals exposed to ethylene oxide has relied upon the detection of hemoglobin adducts such as 2-hydroxyethylvaline (HEV), which provides a useful measure of total exposure to ethylene oxide from all pathways. Recent biomonitoring data from CDC provide an excellent characterization of total exposure to ethylene oxide to the general U.S. population by demographic factors such as age, gender, and race as well as smoking habit, which might be comparable to previous measurements reported for humans and lab animals. The biochemical pathways including gastrointestinal (production by bacteria) and systemic (enzymatic production) pathways by which endogenous ethylene is generated and converted to ethylene oxide are described. The relative importance of endogenous pathways and exogenous pathways via ambient air or tobacco smoke was quantified based upon available data to characterize their relative importance to total exposure. Considerable variation was noted for HEV measurements in human populations, and important sources of variation for all pathways are discussed. Issues related to risk assessment and risk management of human populations exposed to ethylene oxide are provided within the context of characterizing total exposure, and data needs for supporting future risk assessment identified.

摘要

本综述旨在让风险评估人员和风险管理人员更好地了解与人群从内源性和外源性途径中总暴露于环氧乙烷相关的问题。对暴露于环氧乙烷的人群和实验室动物的生物监测依赖于血红蛋白加合物的检测，例如 2-羟乙基缬氨酸 (HEV)，它提供了一种有用的测量方法，可以测量所有途径中环氧乙烷的总暴露量。CDC 最近的生物监测数据通过年龄、性别和种族以及吸烟习惯等人口统计因素提供了美国一般人群对环氧乙烷的总暴露量的极好表征，这可能与之前为人类和实验室动物报告的测量结果相当. 描述了生化途径，包括胃肠道（由细菌产生）和全身（酶促产生）途径，通过这些途径产生内源性乙烯并将其转化为环氧乙烷。内源性途径和通过环境空气或烟草烟雾的外源性途径的相对重要性根据可用数据进行量化，以表征它们对总暴露的相对重要性。注意到人类人群中 HEV 测量的相当大的变化，并讨论了所有途径的重要变异来源。在表征总暴露量的背景下提供了与暴露于环氧乙烷的人群的风险评估和风险管理相关的问题，并确定了支持未来风险评估的数据需求。