Abstract
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.
Highlights
The history of research on a group of persistent, bioaccumulating organohalogen environmental contaminants, namely polychlorinated biphenyls (PCBs), shows serious delays in the accumulation of necessary data for the purpose of toxic-substance policy making and regulatory action [1]
Could delays in regulatory action be at least partly attributable to the low coherence between experimental studies of toxic effects in animal models and human studies? In other words, to what extent the outputs of animal studies aid in the design of human studies? Animal models play an important role in studying the toxic effects of hazardous substances, determining dose-response relationships, and pinpointing the most susceptible developmental stages
Critical analysis of reports of PCB and polybrominated diphenyl ether (PBDE) toxicity testing in animal models shows that the logistics of toxicological experiments makes animal data difficult to transfer to human studies
Summary
The history of research on a group of persistent, bioaccumulating organohalogen environmental contaminants, namely polychlorinated biphenyls (PCBs), shows serious delays in the accumulation of necessary data for the purpose of toxic-substance policy making and regulatory action [1]. We considered that the internal dose had been estimated if there was any type of measurement of residuals or metabolites of administered congeners done at any time point in any tissues of directly exposed animals or their offspring, in the case of developmental exposures We used these basic requirements in order to "harmonize" reports of animal experiments for the purpose of data transfer to human studies. Milk, and tissues, total PBDE levels have increased exponentially over the past 30 years, doubling every 5 years [42] Their health effects, especially at low doses, need to be studied further, PBDEs are known to be associated with neurodevelopmental toxicity and thyroid hormone imbalance in rodents [18,43,44,45,46,47]. PCB and PBDE studies seem to be at odds with respect to route of exposure
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