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首页> 外文会议>Annual conference of the International Society of Exposure Science >A Computational Framework for Modeling Multisystem Biological Effects of Multiroute Human Exposures to Ozone and Associated Air Pollutants
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A Computational Framework for Modeling Multisystem Biological Effects of Multiroute Human Exposures to Ozone and Associated Air Pollutants

机译：用于模拟多途径人体暴露于臭氧和相关空气污染物的多系统生物效应的计算框架

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Human exposures to ozone and associated photochemical air pollutants constitute a persisting and widespread problem around the globe. In addition to causing respiratory effects, photochemical pollution also impacts the cardiovascular, immune, integumentary and other physiological systems. Dermal contact can be a significant exposure route, with skin being both a barrier and target organ for pollutants. Reactive contaminants such as ozone often exert their detrimental effects via the generation of reactive oxygen species (ROS). For example, ROS result from reactions of ozone with skin lipids during dermal contact and from reactions with lung lining fluid components following inhalation. These secondary ROS initiate series of cascading events, such as release of pro-inflammatory mediators, infiltration of immune cells, activation of aryl hydrocarbon receptor (AhR) pathways, etc. Other physiological systems are subsequently affected: for example, the respiratory-originated pro-inflammation mediators can enter the circulatory system, initiate neuroendocrine-immune crosstalk and subsequently affect heart rate variability. The present work demonstrates new interconnected modules for the exposure biology of ozone and associated photochemical pollutants in the human integumentary, respiratory and cardiovascular systems. These modules are designed as components of the MENTOR (Modeling Environment for Total Risk) multiscale computational platform for whole-body human exposure, dosimetry, toxicokinetics and toxicodynamics. MENTOR has been under continuing development at the Computational Chemodynamics Laboratory (CCL) of EOHSI and employs a spectrum of systems dynamics modeling approaches, combining differential equation and agent-based methods to quantify overlapping Adverse Outcome Pathways (AOPs) involving multiple scales (biomolecular, cellular, histological, organ) and physiological systems and endpoints, resulting from multiple exposure routes.
机译：人类暴露于臭氧和相关的光化学空气污染物构成了全球范围内持续存在且普遍存在的问题。除了造成呼吸作用外，光化学污染还影响心血管，免疫，皮肤和其他生理系统。皮肤接触可能是重要的接触途径，皮肤既是污染物的屏障，又是目标器官。诸如臭氧之类的反应性污染物通常通过产生反应性氧（ROS）发挥其有害作用。例如，ROS是由于臭氧在皮肤接触过程中与皮肤脂质的反应以及吸入后与肺里的液体成分的反应引起的。这些继发性ROS引发一系列级联事件，例如促炎性介质的释放，免疫细胞的浸润，芳基碳氢化合物受体（AhR）途径的激活等。随后，其他生理系统也受到影响：例如，呼吸道起源的促红细胞生成素-炎症介质可进入循环系统，引发神经内分泌免疫串扰，进而影响心率变异性。目前的工作演示了新的相互连接的模块，用于在人类皮肤，呼吸系统和心血管系统中暴露臭氧和相关的光化学污染物。这些模块被设计为MENTOR（总风险建模环境）多尺度计算平台的组成部分，用于全身人体暴露，剂量测定，毒物动力学和毒物动力学。 MENTOR已在EOHSI的计算化学动力学实验室（CCL）进行持续开发，并采用了一系列系统动力学建模方法，结合了微分方程和基于代理的方法来量化涉及多个尺度（生物分子，细胞，细胞和细胞）的重叠不良结果途径（AOP）。 ，组织学，器官）以及生理系统和终点，这是由多种暴露途径导致的。

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