啮齿动物吸入研究表明苯乙烯是一种小鼠肺部特异性致癌物。作用模式（MOA）分析表明，由于在啮齿动物和人类中检测到共同的氧化代谢物，因此不能排除肺肿瘤与人类的定量相关性较弱。然而，苯乙烯在体内给药后也不具有遗传毒性。本次综述的目的是通过保守地假设小鼠肺部肿瘤与人类相关但由非基因毒性 MOA 操作来描述职业和一般人群癌症风险的特征。各职业和一般人群暴露的吸入性癌症值参考浓度（RfCcar-ocup 和 RfCcar-genpop）源自小鼠吸入性肿瘤剂量反应数据的初始基准剂量 (BMD) 模型。肺部肿瘤的总体最低 BMDL10 为 4.7 ppm，通过基于生理学的药代动力学 (PBPK) 模型进一步调整持续时间和剂量，以分别得出 6.2 ppm 和 0.8 ppm 的 RfCcar-ocup/genpop 值。除了不使用个人防护装备 (PPE) 的开模纤维增强复合材料工人外，RfCcar-ocup/genpop 值大于典型职业和一般人群的人类暴露量，因此表明苯乙烯暴露导致人类肺癌的可能性较低风险。与这一结论一致，对苯乙烯职业流行病学的回顾并不支持苯乙烯暴露与肺癌发生之间存在关联的结论，并且进一步支持了保守推导的 RfCcar-ocup 对肺癌具有保护作用的结论。

Rodent inhalation studies indicate styrene is a mouse lung-specific carcinogen. Mode-of-action (MOA) analyses indicate that the lung tumors cannot be excluded as weakly quantitatively relevant to humans due to shared oxidative metabolites detected in rodents and humans. However, styrene also is not genotoxic following in vivo dosing. The objective of this review was to characterize occupational and general population cancer risks by conservatively assuming mouse lung tumors were relevant to humans but operating by a non-genotoxic MOA. Inhalation cancer values reference concentrations for respective occupational and general population exposures (RfCcar-occup and RfCcar-genpop) were derived from initial benchmark dose (BMD) modeling of mouse inhalation tumor dose-response data. An overall lowest BMDL10 of 4.7 ppm was modeled for lung tumors, which was further duration- and dose-adjusted by physiologically based pharmacokinetic (PBPK) modeling to derive RfCcar-occup/genpop values of 6.2 ppm and 0.8 ppm, respectively. With the exception of open-mold fiber reinforced composite workers not using personal protective equipment (PPE), the RfCcar-occup/genpop values are greater than typical occupational and general population human exposures, thus indicating styrene exposures represent a low potential for human lung cancer risk. Consistent with this conclusion, a review of styrene occupational epidemiology did not support a conclusion of an association between styrene exposure and lung cancer occurrence, and further supports a conclusion that the conservatively derived RfCcar-occup is lung cancer protective.