Toxicology Program, North Carolina State University, Raleigh, NC 27695-7617, United States of America; Bioinformatics Research Center, North Carolina State University, Raleigh, NC 27695-7617, United States of America; Department of Biological Sciences, North Carolina State University, Raleigh, NC 27695-7617, United States of America.
Toxicology Program, North Carolina State University, Raleigh, NC 27695-7617, United States of America; Bioinformatics Research Center, North Carolina State University, Raleigh, NC 27695-7617, United States of America; Department of Biological Sciences, North Carolina State University, Raleigh, NC 27695-7617, United States of America; Center for Human Health and the Environment, North Carolina State University, Raleigh, NC 27695-7617, United States of America.
Toxicol Appl Pharmacol. 2019 Sep 15;379:114674. doi: 10.1016/j.taap.2019.114674. Epub 2019 Jul 16.
Traditional methods for chemical risk assessment are too time-consuming and resource-intensive to characterize either the diversity of chemicals to which humans are exposed or how that diversity may manifest in population susceptibility differences. The advent of novel toxicological data sources and their integration with bioinformatic databases affords opportunities for modern approaches that consider gene-environment (GxE) interactions in population risk assessment. Here, we present an approach that systematically links multiple data sources to relate chemical risk values to diseases and gene-disease variants. These data sources include high-throughput screening (HTS) results from Tox21/ToxCast, chemical-disease relationships from the Comparative Toxicogenomics Database (CTD), hazard data from resources like the Integrated Risk Information System, exposure data from the ExpoCast initiative, and gene-variant-disease information from the DisGeNET database. We use these integrated data to identify variants implicated in chemical-disease enrichments and develop a new value that estimates the risk of these associations toward differential population responses. Finally, we use this value to prioritize chemical-disease associations by exploring the genomic distribution of variants implicated in high-risk diseases. We offer this modular approach, termed DisQGOS (Disease Quotient Genetic Overview Score), for relating overall chemical-disease risk to potential for population variable responses, as a complement to methods aiming to modernize aspects of risk assessment.
传统的化学风险评估方法既耗时又耗资源,无法描述人类接触的化学物质的多样性,也无法说明这种多样性可能如何体现在人群易感性差异上。新型毒理学数据资源的出现及其与生物信息数据库的整合,为考虑人群风险评估中的基因-环境(GxE)相互作用的现代方法提供了机会。在这里,我们提出了一种系统地将多个数据源联系起来的方法,将化学风险值与疾病和基因-疾病变异联系起来。这些数据源包括来自 Tox21/ToxCast 的高通量筛选(HTS)结果、来自比较毒理学基因组数据库(CTD)的化学-疾病关系、来自综合风险信息系统等资源的危害数据、来自 ExpoCast 计划的暴露数据以及来自 DisGeNET 数据库的基因变异-疾病信息。我们利用这些综合数据来识别与化学-疾病富集相关的变异,并开发一种新的价值来估计这些关联对人群不同反应的风险。最后,我们通过探索与高风险疾病相关的变异的基因组分布,利用该值来对化学-疾病关联进行优先级排序。我们提出了一种名为 DisQGOS(疾病分数遗传概览评分)的模块化方法,用于将整体化学-疾病风险与人群可变反应的潜力联系起来,作为对旨在使风险评估现代化的方法的补充。