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US HBB Annex F

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US HBB Annex FUS H

     Secretariat of the Stockholm Convention page 1

    Annex F Questionnaire (one per chemical) Chemical name

    (as used by the POPs

    Review Committee Hexabromobiphenyl (HBB)

    (POPRC))

Introductory information

     Name of the United States of America submitting Party/observer

    Ellie Clark Contact details Office of Pollution Prevention & Toxics (name, telephone, U.S. Environmental Protection Agency e-mail) of the 202-564-2962 submitting clark.ellie@epa.gov Party/observer

Date of submission February 9, 2007

Additional Annex E information

    (i) Production data, Hexabromobiphenyl (HBB) production was voluntarily including quantity discontinued in the U.S. in 1975.

    and location

(ii) Uses

     (iii) Releases, such as discharges, losses and emissions

    A. Efficacy and efficiency of possible control measures in meeting risk reduction goals (provide summary information and relevant references):

    HBB production was voluntarily discontinued in the U.S. in 1975

    (ATSDR, 2004. Toxicological Profile for Polybrominated

    Biphenyls and Polybrominated Diphenyl Ethers. http://www.atsdr.cdc.gov/toxprofiles/tp68.html ). (i) Describe possible control measures HBB is subject to a Toxic Substances Control Act (TSCA) Significant New Use Rule which would require notification to

    EPA prior to re-initiation of manufacture or import for any use (63

    FR 45955, August 28, 1998; 40 CFR 721.1790).

     (ii) Technical feasibility

     Office location: International Environment House, 11-13 chemin des Anémones, Châtelaine, 1219, Geneva, Switzerland

     Secretariat of the Stockholm Convention page 2

     (iii) Costs, including environmental and health costs

B. Alternatives (products and processes) (provide summary information and relevant

    references):

    At time of regulatory action, polybromodiphenyl ethers were the

    preferred alternatives; however, alternatives are now being (i) Describe

    developed for them. alternatives

     (ii) Technical feasibility

     (iii) Costs, including environmental and health costs

     (iv) Efficacy

     (v) Risk

     (vi) Availability

     (vii) Accessibility

C. Positive and/or negative impacts on society of implementing possible control measures

    (provide summary information and relevant references):

     (i) Health, including public, environmental

    and occupational health

     (ii) Agriculture, including aquaculture and forestry

     (iii) Biota (biodiversity)

     (iv) Economic aspects

(v) Movement towards sustainable development

     (vi) Social costs

     Office location: International Environment House, 11-13 chemin des Anémones, Châtelaine, 1219, Geneva, Switzerland

     Secretariat of the Stockholm Convention page 3

    D. Waste and disposal implications (in particular, obsolete stocks of pesticides and

    clean-up of contaminated sites) (provide summary information and relevant references):

    Approximately 11.8 million pounds (5.4 million kg) of HBB were

    used in commercial and consumer products in the U.S., mostly in

    plastic products with an estimated use life of 5-10 years. It is

    assumed that most of these products, such as TV cabinet and (i) Technical business machine housings must have been disposed of by land feasibility filling or incineration. (ATSDR, 2004).

    The sole U.S. producer depleted their remaining stocks in April

    1975 (IARC Monographs, 1972 to present, V. 18, p. 110, quoted in

    TOXNET entry, http://toxnet.nlm.nih.gov)

     (ii) Costs

    E. Access to information and public education (provide summary information and relevant references):

F. Status of control and monitoring capacity (provide summary information and relevant

    references):

G. Any national or regional control actions already taken, including information on

    alternatives, and other relevant risk management information:

    HBB is subject to a TSCA Significant New Use Rule which would require notification to EPA prior to re-initiation of manufacture or import for any use (63 FR 45955, August 28,

    1998; 40 CFR 721.1790).

H. Other relevant information for the risk management evaluation:

I. Other information requested by the POPRC:

    Additional information requested on aquatic toxicity of HBB via dietary exposure:

    Several factors obviate the need for aquatic toxicity data based on dietary exposures:

    (1) The availability of tissue-based toxicity data. For highly bioaccumulative chemicals

    such as HBB, dietary exposures are considered to be significant and more important than waterborne exposures. For this reason, toxicity values based on tissue concentration are

    considered to be more credible for highly bioaccumulative chemicals. Hence, the tissue concentration-based LD50 determined by Hornung et al. (1996) is a credible and

     Office location: International Environment House, 11-13 chemin des Anémones, Châtelaine, 1219, Geneva, Switzerland

     Secretariat of the Stockholm Convention page 4

    ecologically relevant toxicity endpoint for fish.

    (2) Salmonids (trout) early life stages are the aquatic organisms most sensitive to toxicity mediated by the Ah receptor. It is well established that early life stage

    exposures are the most critical for causing AhR-mediated toxicity to sensitive aquatic

    organisms (i.e. developmental toxicity is the critical endpoint of concern). Further, of approximately 25 species of fish tested, salmonids are the most sensitive and are among

    the most sensitive of all vertebrates to AhR-mediated toxicity. Hence, the available

    aquatic toxicity data for early life stage toxicity in trout (Hornung et al. 1996) sufficiently represents credible and ecologically relevant toxicity of HBB in aquatic vertebrates.

    (3) The existing toxicity data for trout also shows that they are very insensitive to some HBB congeners (PBB-153). The finding of Hornung et al. (1996) that trout are

    insensitive to HBB (PBB-153) is consistent with the established structure-activity

    relationship for chlorinated biphenyls in fish, wherein sensitivity dramatically decreases (to essentially non-toxic) when halogen substitution occurs in a di-ortho pattern, as it does

    in PBB-153, whereas aquatic dependent wildlife (birds and mammals) maintain sensitivity to di-ortho PCBs and PBBs, albeit lower sensitivity. Given that fish are very insensitive to di-ortho polyhalogenated biphenyls and that invertebrates do not possess an active AhR, it

    is not necessary to generate additional information on the toxicity of PBB-153 to aquatic

    organisms. However, toxicity to fish is greater for co-planar congeners such as PBB-169.

Comments on aquatic toxicity discussion in the draft risk profile:

    (1) The aquatic toxicity values reported for rainbow trout in the draft risk profile

    should reference both HBB congeners used in the study. The only aquatic toxicity

    value reported in the draft risk profile (LD of 3910 ug/kg) attributed to Hornung et al. 50

    (1996) is for PBB-169. However, the Hornung et al. paper also reports information for

    PBB-153, in which no toxicity occurred at the highest concentration tested, which was 230,000 μg/kg. Hence, the value reported in the draft risk profile for HBB should be a

    range of NOECs from 3910 - 230,000 μg/kg.

    (2) The information request specifically mentions “under environmentally relevant conditions”. Although Hornung et al (1996) has been characterized as “untraditional” in

    the draft risk profile, a number of other studies have established that the injection exposure route is both valid and more credible for chemicals such as HBB (i.e. high log Kow; bioaccumulative; significant biomagnification). “Traditional” waterborne exposures were

    found to be problematic for these types of chemicals, due to solubility issues. Hence,

    researchers moved to exposing aquatic organisms to these types of compounds via injection or maternal transfer. Furthermore, studies have been conducted that demonstrate

    no difference in effect concentrations on early life stages of salmonids exposed via water, injection and maternal transfer (the most „environmentally relevant‟ route). Finally, while “traditional” fish toxicity tests are conducted with juvenile fish, it was established earlier in the 1980s-1990s that fish early life stages are the most sensitive to AhR-mediated

    toxicity, hence, testing of early life stages of fish represents the critical, and most ecologically relevant, exposure period for these types of compounds, including HBB (PBB-153).

    (3) The citation for Hornung et al (1996) in the draft risk profile is incorrect. The

    correct citation for the study discussed in the draft risk profile is: Hornung, M.W., E.W.

    Zabel & R.E. Peterson (1996): Toxic Equivalency Factors of Polybrominated Dibenzo-p-

    dixon, Dibenzofuran, Biphenyl and Polyhalogenated Diphenyl Ether Based on Rainbow Trout Early Life Stage Mortality. Toxicology and Applied Pharmacology, 140: 227-234.

Additional data requested on critical body burdens:

    Tissue-based toxicity data (i.e. critical body burden) for sensitive aquatic species is available. The study by Hornung et al. (1996) defines a critical body burden for the most sensitive life stage of the genus of fish species that is most sensitive to AhR agonists.

    For reasons provided above the focus of gathering information on toxicity via dietary exposures and critical body burdens data should be on birds and mammals.

     Office location: International Environment House, 11-13 chemin des Anémones, Châtelaine, 1219, Geneva, Switzerland

     Secretariat of the Stockholm Convention page 5

    Comments on request for additional lab or field food-chain studies:

    For these types of chemicals (non-ionic organics) the use of food chain modeling to

    estimate bioaccumulation and trophic transfer within aquatic food chains is well established (e.g. Gobas model). Such modeling could be conducted to estimate trophic

    transfer and biomagnification. However, given that accumulation of HBB in higher trophic level organisms has been well documented, it is unclear what this type of information would provide. Furthermore, there would be great difficulty in conducting

    laboratory study to provide food chain bioaccumulation information for the top predators for which empirical data exist (e.g., predatory birds, seals, polar bear, moose, reindeer)

Comments on request for additional toxicokinetic information:

    The tissue-based toxicity values for fish and birds obviate the need for toxicokinetic data.

Comments on request for additional mammalian toxicity data:

    As stated on page 21 of the Draft Risk Profile, “The studies included in Annex A, Table

    A.3 have been selected from the very large database on toxicological studies on hexabromobiphenyl. The relatively recent (2004) ATSDR Toxicological Profile for PBBs and PBDEs corroborates this statement. For example, Figure 5-6 in the ATSDR

    shows that health effects data (e.g. chronic, neurologic, reproductive) is available for humans exposed via inhalation, oral and dermal routes. Health effects data for laboratory

    mammals are available for additional toxicity endpoints and routes of exposure.

    Laboratory mammal studies can be used to establish toxicity thresholds for wildlife mammals. U.S. EPA has used laboratory mammal test data in establishing Wildlife Criteria for the Great Lakes Water Quality Initiative and for developing Wildlife Toxicity

    Reference Values in the Superfund Program.

Some additional recent references not already included in the draft risk profile regarding

    mammalian toxicity, critical body burdens and toxicokinetics include:

     Carvan MJ, Solis WA, Gedamu L, Nebert DW. Activation of transcription

    factors in zebra fish cell cultures by environmental pollutants. Arch. Biochem

    Biophys. 2000 Apr 15 ; 376 (2): 320-7.

     Curran CP, Miller KA, Dalton,TP, Vorhees VC, Miller ML, Shertzer HG, Nebert,

    DW. Genetic differences in lethality of newborn mice treated in utero with coplanar

    versus non-coplanar hexabromobiphenyl. Toxicol. Sci. 2006. Feb; 89(2): 454-64.

     Brown DJ, Van Overmeire I, Goeyens L, Denison MS, DeVito MJ, Clark GC.

    Analysis of Ah receptor pathway activation by brominated flame retardants.

    Chemosphere. 2004. June; 55(11):1509-18.

     Sjodin A, Jones RS, Focant JF, Lapeza C, Wang RY, McGahee EE, Zhang Y,

    Turner WE, Slazyk B, Needham LL, Patterson DG. Retrospective time-trend study of

    polybrominated diphenyl ether and polybrominated and polychlorinated biphenyl

    levels in human serum from the United States. Environ Health Perspect. 2004 May;

    112 (6): 654-8.

     Sjodin A, Patterson DG, Bergman A. Brominated flame retardants in serum from

    U.S. blood donors. Environ Sci Technol. 2001. Oct 1; 35 (19): 3830-3.

     Tuey DB, and Mattews DH. Distribution and excretion of 2,2,4,4,5,5-

    hexabromobiphenyls in rats and man: pharmacokinetic model predictions. 1980.

    Toxicology and Applied Pharmacology 53, 420-430.

     Wolff MS, et al. A Amer Med Assoc 15: 2112-16. 1982. Body Burden - -

    Polybrominated biphenyls (PBB) detected in blood and adipose tissue of 1788 persons

    in Michigan

Additional data is still needed to show the potential effects on humans and/or the

    environment as a result of long-range environmental transport, particularly on the higher

    levels of the trophic chain.

     Office location: International Environment House, 11-13 chemin des Anémones, Châtelaine, 1219, Geneva, Switzerland

Secretariat of the Stockholm Convention page 6

Office location: International Environment House, 11-13 chemin des Anémones, Châtelaine, 1219, Geneva, Switzerland

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