Parodi S, Lutz W K, Colacci A, Mazzullo M, Taningher M, Grilli S
Centro Interuniversitario per la Ricerca sul Cancro, Istituto di Oncologia Clinica e Sperimentale, Università di Genova, Italy.
Environ Health Perspect. 1989 Jul;82:171-6. doi: 10.1289/ehp.8982171.
Considering the very large industrial usage of benzene, studies in risk assessment aimed at the evaluation of carcinogenic risk at low levels of exposure are important. Animal data can offer indications about what could happen in humans and provide more diverse information than epidemiological data with respect to dose-response consideration. We have considered experiments investigating metabolism, short-term genotoxicity tests, DNA adduct formation, and carcinogenicity long-term tests. According to the different experiments, a saturation of benzene metabolism and benzene effects in terms of genotoxicity seems evident above 30 to 100 ppm. Below 30 to 60 ppm the initiating effect of benzene seems to be linear for a large interval of dosages, at least judging from DNA adduct formation. Potential lack of a promoting effect of benzene (below 10 ppm) could generate a sublinear response at nontoxic levels of exposure. This possibility was suggested by epidemiological data in humans and is not confirmed or excluded by our observations with animals.
考虑到苯在工业上的大量使用，旨在评估低水平暴露致癌风险的风险评估研究很重要。动物数据可以提供关于人类可能发生情况的线索，并且在剂量反应考量方面比流行病学数据提供更多样化的信息。我们考虑了研究代谢、短期遗传毒性试验、DNA加合物形成以及长期致癌性试验的实验。根据不同的实验，在30至100 ppm以上，苯代谢和苯在遗传毒性方面的影响似乎明显饱和。在30至60 ppm以下，至少从DNA加合物形成判断，苯的起始作用在很大剂量区间内似乎呈线性。苯（低于10 ppm）潜在缺乏促进作用可能会在无毒暴露水平产生亚线性反应。人类的流行病学数据提示了这种可能性，而我们对动物的观察既未证实也未排除这种可能性。
