Summary of Public Comments received on the Draft Human Health State of Science Report on Decabromodiphenyl ether (decaBDE)
Comments on the draft State of the Science Report on decabromodiphenyl ether or decaBDE (hereafter referred to as the SOS) were provided by Albemarle Corporation, the Boeing Company, and the Bromine Science and Environmental Forum (BSEF). The table contains a condensed version of each comment and a response in non-technical terms. The summarized comments and responses are organized by topic:
Condensed version of each comment and a response in non-technical terms: General, Exposure Assessment, Health Effects and Risk Characterization
| Topic | Comment | Response |
|---|---|---|
| General | The submitted comments supported the SOS's conclusion that decaBDE does not pose a risk to human health at the current estimated levels of exposure. | Health Canada acknowledges the comments. |
| Exposure Assessment | A recently published study by Siddique et al. (2012) shows the total Polybrominated diphenylether (PBDE) concentrations in Canadian breast milk. | The Siddique et al. (2012) study has been added to the final SOS. The breast milk calculations were also corrected and updated. |
| A United Kingdom report recommends caution when applying the Viberg et al. (2003) developmental neurotoxicity results due to concerns in the study design and because no neurotoxicity was observed in the Biesemier et al. (2011) study. | The developmental neurotoxicity studies being referred to are presented in the SOS. Additionally, the critical effect level in the SOS is based upon consideration of several studies of different durations with relevant endpoints, not a single study. |
| A European Union (EU) risk evaluation concluded that a developmental neurotoxicity study in mice or rats was needed to adequately characterize the risks. | The 2003 EU study was considered in the preparation of the draft SOS, as well as several more recent studies on developmental neurotoxicity, including information on the developmental neurotoxicity endpoint presented in the 2008 review of decaBDE by the US Environmental Protection Agency (EPA). | |
| An independent group of toxicologists, Toxicological Excellence for Risk Assessment (TERA), stated that non-guideline developmental neurotoxicity studies (Viberg et al. and Rice et al.) should not be used to determine the critical health effect. | The references presented in TERA (2011), including the source document by Hardy et al. (2009) are presented in the SOS. The critical effect level was based upon consideration of several studies of different durations with relevant endpoints, not a single study. Health effects characterization took into account both guideline and non-guideline studies. The TERA (2011) report has been added to the SOS. | |
| Consideration should be given to decaBDE’s pharmacokinetics. DecaBDE is highly unlikely to exert neurological effects because of its low absorption, low systemic distribution, and negligible distribution to the brain. | In the SOS, the toxicokinetics of decaBDE is summarized. It is recognized that a model for human metabolism has not been established. Taking into consideration this uncertainty, the potential neurological effects of decaBDE are considered relevant for risk characterization. | |
| Clarification on loss of rat offspring exposed to decaBDE during developmental toxicity tests conducted by Biesemeier et al. (2011) should be included. | Table 3 Summary of New Health Effects Information for decaBDE in the SOS provides clarification regarding the loss of rat pups as shown in the Biesemeier et al. (2011) study. Cannibalization was taken into account in Table 3 in the discussion of the increased number of pups found dead or missing at 100 and 1000 mg/kg bw/day. | |
| There was disagreement with Health Canada's analysis of brain morphometric measures of offspring in the developmental neurotoxicity study conducted by Biesemeier et al. (2011). | Health Canada was aware of the discussion on historical control data in the Biesemeier et al. (2011) developmental neurotoxicity study. As stated in the SOS, Shibutani et al. (2011) also noted the significant differences in the brain morphometric analyses at 1000 mg/kg-bw per day and stated that morphometric changes should first be discussed in relation to cellular morphology and function of the brain area measured, which was missing in Beisemeier et al.’s (2011) article. Although historical control data were missing in the supplementary data, the concurrent data were considered adequate for making comparisons with exposed animals. | |
| Results of motor activity tests in offspring of the developmental neurotoxicity study conducted by Biesemeier et al. (2011) were incorrectly summarized and interpreted. | It has been confirmed that the text of this study in Table 3 of the SOS is an accurate reflection of effects observed. The text in the SOS has been clarified to state significant differences in a number of motor activity parameters all occurred at the same time point (PND 180). | |
| Effects in the SOS that are declared to occur at 1000 mg/kg bw/day in the developmental neurotoxicity study conducted by Biesemeier et al. (2011) do not correlate with similar plasma concentrations of decaBDE at all dose levels in this study and do not describe a dose-response relationship. | No reference was made to a dose response relationship in the summary of the Biesemeier et al. (2011) developmental neurotoxicity study. Effects were noted at both 100 and 1000 mg/kg bw/day, leading to the determination of a LOAEL of 100 mg/kg bw/day in the SOS. Toxicokinetic information summarized in the SOS indicates that a small percentage of the oral dose will remain in the body of rodents as parent compound and metabolites. | |
| There was disagreement with the acute toxicity critical effect level. | The determination of the LOAEL for acute oral toxicity (2.22 mg/kg bw) was based not only on the Johansson et al. (2008) study, but also on several studies following similar protocols, discussed under nervous system effects in the SOS. | |
| Certain studies were not reviewed as part of the SOS e.g. by the U.S. National Toxicology Program (NTP) (1986), and by Schroeder (2000) and published as Hardy et al. (2002). | These studies were considered in the Health Canada State of Science (SOS) report on PBDEs (2006). The decaBDE SOS “… focuses on new studies on the human health effects of decaBDE identified since the publication of the SOS report for PBDEs (Health Canada 2006), in particular those related to development, neurological effects and potential endocrine and immune system effects". Table 3 of the SOS presents a summary of the new health effects studies associated with decaBDE. | |
| Comments questioned the validity, quality and / or choice of studies cited in Table 3 of the SOS (e.g. Rice et al. (2007), Viberg et al. (2003, 2007) and Johansson et al. 2008). | The reliability of individual studies were taken into consideration when characterizing health effects associated with decaBDE. All the studies cited in Table 3 of the SOS were from the peer reviewed literature. Reviews by international jurisdictions (i.e., US EPA) were taken into consideration. The SOS has undergone external peer review/ consultation. Weight of evidence was applied in characterizing health effects associated with decaBDE, | |
| Health Canada should revise the SOS to correctly reflect decaBDE's toxicology / critical effect level. Specifically:
| Weight of evidence was applied in characterizing health effects associated with decaBDE. The critical effect level of 2.22 mg/kg-bw is based on not one, but several studies of different durations with relevant endpoints, and the US EPA used the same critical effect level as the basis for setting their revised regulatory reference dose for decaBDE. Health Canada acknowledges the scientific debate related to the referenced studies. |
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