Suvorov Alexander, Takser Larissa
Département Obstétrique Gynécologie, Faculté de Médecine et des sciences de la Santé, Université de Sherbrooke, Sherbrooke, Québec, Canada.
Environ Health. 2008 Nov 13;7:58. doi: 10.1186/1476-069X-7-58.
A well-documented fact for a group of persistent, bioaccumulating organohalogens contaminants, namely polychlorinated biphenyls (PCBs), is that appropriate regulation was delayed, on average, up to 50 years. Some of the delay may be attributed to the fact that the science of toxicology was in its infancy when PCBs were introduced in 1920's. Nevertheless, even following the development of modern toxicology this story repeats itself 45 years later with polybrominated diphenyl ethers (PBDEs) another compound of concern for public health. The question is why? One possible explanation may be the low coherence between experimental studies of toxic effects in animal models and human studies. To explore this further, we reviewed a total of 807 PubMed abstracts and full texts reporting studies of toxic effects of PCB and PBDE in animal models. Our analysis documents that human epidemiological studies of PBDE stand to gain little from animal studies due to the following: 1) the significant delay between the commercialisation of a substance and studies with animal models; 2) experimental exposure levels in animals are several orders of magnitude higher than exposures in the general human population; 3) the limited set of evidence-based endocrine endpoints; 4) the traditional testing sequence (adult animals--neonates--foetuses) postpones investigation of the critical developmental stages; 5) limited number of animal species with human-like toxicokinetics, physiology of development and pregnancy; 6) lack of suitable experimental outcomes for the purpose of epidemiological studies. Our comparison of published PCB and PBDE studies underscore an important shortcoming: history has, unfortunately, repeated itself. Broadening the crosstalk between the various branches of toxicology should therefore accelerate accumulation of data to enable timely and appropriate regulatory action.
对于一组持久性、生物累积性有机卤素污染物,即多氯联苯(PCBs),一个有充分记录的事实是,适当的监管平均延迟了长达50年。部分延迟可能归因于这样一个事实:20世纪20年代多氯联苯问世时,毒理学尚处于起步阶段。然而,即使在现代毒理学发展之后,这个故事在45年后又重演了,涉及另一种公众健康关注的化合物——多溴二苯醚(PBDEs)。问题是为什么?一种可能的解释可能是动物模型中毒性效应的实验研究与人体研究之间的一致性较低。为了进一步探讨这一点,我们总共查阅了807篇PubMed摘要和全文,这些文献报道了多氯联苯和多溴二苯醚在动物模型中的毒性效应研究。我们的分析表明,由于以下原因,多溴二苯醚的人体流行病学研究从动物研究中获益甚微:1)一种物质商业化与动物模型研究之间存在显著延迟;2)动物实验暴露水平比一般人群的暴露水平高出几个数量级;3)基于证据的内分泌终点有限;4)传统的测试顺序(成年动物——新生儿——胎儿)推迟了对关键发育阶段的研究;5)具有类似人类毒代动力学、发育生理学和妊娠生理学的动物物种数量有限;6)缺乏适用于流行病学研究目的的合适实验结果。我们对已发表的多氯联苯和多溴二苯醚研究的比较突出了一个重要缺点:不幸的是,历史重演了。因此,扩大毒理学各分支之间的相互交流应能加速数据积累,以便及时采取适当的监管行动。