Swedish Statute Book

Annex 1

1. ------IND- 2005 0649 S-- EN------20051208 ------PROJET Swedish Statute Book

SFS Published on

Order amending the Order (1998:994) on bans etc. in certain cases in connection with the handling, import and export of chemical products issued on xx 2006.

Having regard to the Order (1998:994) on bans etc. in certain cases in connection with the handling, import and export of chemical products, the government lays down1 the following: - Section 1 shall be worded as follows; - three new Sections, Sections 4a - c, shall be inserted into the Order, and immediately before Section 4a a new heading shall be inserted worded as set out below.

Section 12This Order shall apply alongside the Order (1998:941) on chemical products and biotechnical organisms with regard to 1. cadmium compounds, 2. decabromodiphenyl ether, 3. chlorinated solvents, 4. mercury, 5. cadmium, mercury, lead, hexavalent chromium and other chemical products contained in electrical and electronic products, 6. heavy metals in packaging,

1 Cf. Directive 98/34/EC of 22 June 1998 laying down a procedure for the provision of information in the field of technical standards and regulations and of rules on information society services (OJ L 204, 21.7.1998, p. 37, Celex 398L0034), most recently amended by the Act concerning the conditions of accession of the Czech Republic, the Republic of Estonia, the Republic of Cyprus, the Republic of Latvia, the Republic of Lithuania, the Republic of Hungary, the Republic of Malta, the Republic of Poland, the Republic of Slovenia and the Slovak Republic and the adjustments to the Treaties on which the European Union is founded (OJ L 236, 23.9.2003, p. 68, Celex 12003TN02/01/H). 2 Most recent wording 2005:217. 1 Évid 2,7 vid 2,85

SFS 1993:1399 7. ammunition containing lead, and 8. certain other chemical products and goods that are harmful to health or the environment. The Order shall not apply to the chemical products and biotechnical organisms that are covered by the Foodstuffs Act (1971:511), the Medicinal Products Act (1992:859) or the Act (1985:295) on feedingstuffs.

Decabromodiphenyl ether

Section 4 a Decabromodiphenyl ether (CAS number 1163-19-5) must not be placed onto the market or used as a substance or be contained in a substance or preparation at levels higher than 0.1% by weight. Goods, or flame-protected parts thereof, containing decabromodiphenyl ether at levels higher than 0.1% by weight must not be placed on the market.

Section 4 b The prohibition in Section 4 a shall not apply to 1. vehicles as referred to in the Act (2001:559) on road traffic definitions; 2. products covered by Section 11 a.

Section 4 c Under special circumstances the Swedish Chemicals Inspectorate may issue administrative provisions on exemption from the ban in accordance with Section 4 a. In exceptional circumstances, the Swedish Chemicals Inspectorate may grant dispensation in individual cases from the ban in Section 4 a up to 31 December 2009.

2 Memorandum Annex 3

08.11.2005

Ministry of Sustainable Development SFS

Impact assessment for a national ban on decabromodiphenyl ether

Introduction This impact assessment has been performed in the light of the fact that a national ban should include use and placing on the market of decabromodiphenyl ether (decaBDE) both as a substance and contained in products or parts of products.

Use of decaBDE within the EU According to information in a revised EU risk assessment, which followed the environmental and health risk assessment of decaBDE published in 2002 by the United Kingdom (Risk-Assessment Report Vol.17, 2002, on decabromodiphenyl ether), the world-wide production of decaBDE in 2001 was 56 100 tonnes. However, no

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SFS 1993:1399 decaBDE is produced in the EU today. It is produced primarily in Japan and the USA. In the revised EU risk assessment it was estimated that during 2003 around 1 300 tonnes of decaBDE was imported into the EU in products, mainly electrical and electronic products such as television sets.

The European Brominated Flame Retardant Industry Panel (EBFRIP) estimates the quantity of decaBDE used in 2003 within the EU for the manufacture of products or parts thereof to be 7 300 tonnes. The majority is used to provide flame protection to plastics and other polymers used within the electronics industry (80%). The remaining 20% (1 460 tonnes) is used mainly in textiles, furniture upholstery, cables, protective clothing and various bed products. Of this 20%, half (730 tonnes) is used in the United Kingdom. How use of the remaining 730 tonnes is distributed between the various EU Member States or exported in products manufactured within the EU has not been reported. DecaBDE is no longer used in Sweden. However, the import of products results in the import of a certain amount of decaBDE. The undertakings and trade organisations in Sweden which import products from other EU countries have not been able to provide information to enable the possible proportion of the 730 tonnes that might be imported into Sweden in products to be quantified.

The effect of a national ban The draft does not cover the use of decaBDE in electrical and electronic products. Use is regulated by Directive 2002/95/EC on the restriction of the use of certain hazardous substances in electrical and electronic products (RoHS Directive). Council Directive 70/156/EEC of 6 February 1970 on the approximation of the laws of the Member States relating to the type-approval of motor vehicles and their trailers does not allow the possibility of prohibiting type-approved vehicles containing decaBDE by means of national legislation. Therefore, vehicles are not covered by the draft Order either.

4 As regards the remaining areas of application, a national ban SFS may reduce any new supplies and prevent decaBDE being used in new areas of application, thus helping to prevent increases in exposure in the future.

Compliance and control are more difficult with regard to imported products, as there is no system for providing information on chemicals contained in products. The fact that the supervisory authority does not have a clear picture of which, and how many, undertakings may be affected by a ban hampers effective supervision.

The supervisory authority may lay down requirements for reporting the substances contained in a product and issue an order, possibly associated with a fine. The supplier will then have a certain period of time to produce the desired information. Where the Swedish importer does not receive information from his foreign supplier it may lead to the importer choosing to cease selling the product or opting for a different supplier who is able to declare the content of the product. The importer may also choose to perform his own analyses on the product.

It is uncertain to what extent decaBDE is imported into Sweden in products from another EU country. Theoretically, decaBDE could be found as a component or part of a product used in a context with a very high requirement for fire protection. Such an example, which has been noted with regard to the common EU ban on pentaBDE, is the use of pentaBDE in emergency equipment in aircraft. Conversion to alternatives to pentaBDE for this application, e.g. decaBDE, takes time to implement on account of extensive test requirements. Therefore, in order to safeguard deliveries of new aircraft and spare parts for old aircraft Sweden is not introducing an absolute national ban on decaBDE. The opportunity is provided to lay down general exemptions or grant dispensation in individual cases. This provides adequate opportunity to permit the use of decaBDE within areas in which it would prove difficult to replace the substance for Swedish requirements.

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SFS 1993:1399 Benefits to the environment and human health DecaBDE is considered to be very persistent. There are even indications that decaBDE causes damage during brain development as well as suspicions that decaBDE may bioaccumulate. DecaBDE has also been shown to be capable of degrading to lower brominated and probably more toxic diphenyl ethers. There is insufficient information at present to classify decaBDE as a PBT substance (Persistent, Bioaccumulative and Toxic), but further studies relating to this issue are planned at EU level. On the basis of the precautionary principle and of the available studies of the substances it is justified to prevent further release of decaBDE to the environment.

A national ban may have a positive effect with regard to the possibility of achieving objective 3 of Sweden’s national environmental objectives, Giftfri miljö [A non-toxin environment], and provide an increased level of protection for consumers as regards the supply of new quantities of decaBDE. Since it is not possible to quantify the extent to which decaBDE enters Sweden via imported products it is also not possible to identify a particular area of application where a phase-out would have the most positive effects on health and the environment. It can therefore be considered justified to produce general provisions.

The quantity of decaBDE that has already accumulated in the environment or which escapes from the products already in use will not be limited by a ban.

The assessment of benefits to the environment and human health applies provided that alternatives to decaBDE do not comprise other substances with properties that are similar to or more dangerous than decaBDE, such as hexabromocyclododecane (HBCD). The Swedish Chemicals Inspectorate’s inspection project “Flamskydd i varor 2003”[Flame protection in products 2003] indicates however that the flame retardants used most are organic phosphorous and nitrogen compounds as well as inorganic salts such as aluminium and magnesium salts.

6 Alternatives to decaBDE as a flame retardant SFS Alternative flame retardants already exist in the applications that should be affected by a national ban on decaBDE. The fire protection standards in existence do not specify a particular type of flame retardant or technique for complying with the requirements laid down. It is therefore entirely possibly to meet the requirements for fire protection using alternatives to decaBDE.

Current alternatives to decaBDE used in textile applications are mostly inorganic phosphorous and nitrogen compounds as well as halogenated compounds. Intumescent (expansive) systems based on the formation of expanded coal tar are also used to a certain extent. The coal tar acts both as an insulating barrier to heat and as a waste gas trap. The intumescent systems are still in the developmental stages but increased use of these is predicted for the future, the same being the case for the use of flame-resistant fibres. For construction products made of wood fibres and recycled paper, borax or boric acid are normally used. For pipes made of various plastics, pressed graphite is used, for example. Plastic and rubber polymers for cables can be flame-protected using magnesium or aluminium hydroxide and antimony trioxide, among others.

A national ban will not therefore affect the possibility of meeting the fire protection requirements in force.

Economic and competitive conditions In order to be neutral as regards competition, a national ban should not only cover the use of the substance decaBDE, but also products containing decaBDE imported from another EU Member State or a non-EU country.

A national ban could prevent products entering the country if the foreign supplier cannot or will not state whether decaBDE is contained in the product. A Swedish supplier who does not receive this information can choose another supplier or cease to sell the product. In connection with

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SFS 1993:1399 supervision by the authorities, the supplier may have to pay for an analysis of the product. Such an analysis, carried out using gas chromatography, costs SEK 3 000 – 5 000, provided that the polymer that the product is made of is known. Where it is not known, the cost may rise to SEK 20 000 in order to develop a new method. The costs of analyses rest primarily with the first link in the chain, i.e. the party importing the product into Sweden. In this respect, smaller companies in particular, which do not have the same ability as large companies to influence foreign suppliers, could be faced with higher costs.

In the event of a ban, the subsequent links in the product chain will require information from the party importing a product from another EU Member State. Thus, there may be a shift in the market, with the domestic undertakings that are able to supply a product which they can show with certainty does not contain decaBDE taking over a large share of the market. The overall market for such products will therefore be the same, but the market structure may change.

The most common scenario is for a customer to require a product to comply with flame retardancy requirements in accordance with a particular standard. Where the supplier can produce a certificate to show that the product complies with the requirement, the customer is generally satisfied. However, if a foreign customer expressly wishes to have a product flame-protected using decaBDE there is a risk of loss of income. Such a product group could be upholstered furniture, for which British test institutes recommend the use of decaBDE as a flame retardant. The United Kingdom is the largest user of decaBDE within the EU. However, exports to the United Kingdom are very limited and sporadic. Only 2% of the production value for upholstered furniture relates to exports to the United Kingdom. A large decrease in orders is not therefore anticipated.

Neither is there a risk of Swedish manufacturers moving production to another country, as Swedish manufacturers no longer use decaBDE. The costs arising as a result of the conversion to other flame retardants or techniques were in 8 most cases incurred by undertakings several years ago. The SFS initial increase in costs was calculated to be in the region of 15-30% and has already been written off. There is currently no price difference. However, a foreign supplier may incur increased costs for product development and verification, which may lead to a higher price for the product for Swedish suppliers.

Summary The ban does not include electrical and electronic products or vehicles. DecaBDE is neither produced nor used in Sweden. A national ban will therefore have no effect at all on Sweden’s trade with other countries within the EU as regards the substance decaBDE.

Imports of products from other EU Member States or non- EU countries means that a certain amount of decaBDE is brought in. However, it is not possible to fully quantify the benefits of a national ban to human health and the environment, as there is no system within the EU or Sweden for providing information on the substances contained in products. If the importer cannot obtain information from the supplier as to whether or not decaBDE is contained in the product, the importer can opt to change supplier or have the product analysed. The Swedish importer could also choose to influence the supplier to change agent or technique. A national ban may therefore be important for reducing the supply of new quantities of decaBDE and preventing use in any new applications.

There are currently good alternatives to using decaBDE in the applications that are to be covered by a national regulation. This assessment is valid, provided that the alternatives to decaBDE do not comprise other substances with properties that are similar to or more dangerous than decaBDE, such as other halogenated substances. The Swedish Chemicals Inspectorate’s inspection project “Flamskydd i varor 2003”[Flame protection in products 2003] indicates however that the flame retardants used most

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SFS 1993:1399 are organic phosphorous and nitrogen compounds as well as inorganic salts such as aluminium and magnesium salts.

References: KEMI Rapport 5/04 Dekabromdifenyleter (dekaBDE) – underlag till ett nationellt förbud [Decabromodiphenyl ether (decaBDE) – basis for a national ban], Swedish Chemicals Inspectorate, Stockholm, November 2004, order no. 360 799.

KEMI PM no. 2/04, Flammskydd 2003 [Flame protection 2003], Swedish Chemicals Inspectorate, Stockholm, June 2004, order no. 510 784.

The Swedish Chemicals Inspectorate’s reports can be ordered on fax number +46-8 735 76 98, or by e-mail [email protected]. The reports can also be obtained from www.kemi.se under “trycksaker” [publications] and then “rapporter” [reports].

10 SFS

11 Memorandum Annex 2

Évid 2,7 vid 2,85 08.11.2005

SFS 1993:1399 Ministry of Sustainable Development

Risk assessment for decabromodiphenyl ether (decaBDE)

12 SFS Contents

1. Background 14 2. Status of the existing risk assessment and summary of the conclusions 14 3. Further studies and risk-reducing measures 17 4. Summary of the EU’s existing risk assessment for decaBDE 18 4.1 Physico-chemical properties of decaBDE 18 4.2 Environment 19 4.3 Health 32

13 SFS Risks to health and the environment 1. Background This risk assessment aims to provide a picture of the risks to health and the environment posed by decaBDE. A risk assessment of decaBDE has been carried out within the EU’s programme for existing substances3 and was published in 2002 (EU, 2002). The United Kingdom is the Rapporteur Member State for environmental risks and France is the Rapporteur Member State for health risks. When the risk assessment was revised in September 2005, the conclusion was that even though it has not yet been possible to identify clear risks to health or the environment the level of uncertainty is so high that there is a need for new studies. After carrying out such studies the risk assessment will be revised.

This assessment will summarise the revised risk assessment and report on its current status. The ongoing work with decaBDE within the EU as a result of the risk assessment will also be described.

2. Status of the existing risk assessment and summary of the conclusions DecaBDE is considered to be very slow to degrade (persistent). It has also been found that decaBDE can be converted to lower brominated compounds and it was not possible to determine the extent of this in the risk assessment. In the long term this may pose a risk.

At present there is insufficient information to give a clear picture of the health and environmental risks associated with decaBDE. Therefore, in the environmental risk assessment, conclusion (i) according to the EU TGD4 applies, i.e. “there is a need for further information and/or testing” with regard

3 Council Regulation (EEC) No 793/93 on the evaluation and control of the risks of existing substances. 4 European Technical Guidance Document 14 to a number of points that are very important primarily for SFS the assessment of decaBDE as a possible PBT substance (Persistent, Bioaccumulative, Toxic). These are:

• Potential neurotoxicity In experiments on neonatal mice, decaBDE was found to be capable of interfering with brain development when the mice were exposed during a critical period resulting in behavioural disturbances in adulthood. This may also pose a risk to bird embryos, as decaBDE has been found in bird eggs. However, the quality of the study has been called into question, and in order to check the reliability of the study it will be necessary to carry out a new study.

• Uptake by mammals The extent to which decaBDE is taken up by mammals is uncertain. More recent studies have shown a higher uptake than previous studies, and the uptake also appears to depend on how decaBDE is administered.

• Sporadic occurrence high up in the food chain DecaBDE has been found in, among others, peregrine falcons and their eggs. It is not known whether this is a result of the fact that decaBDE is bioaccumulative in falcons or whether they are exposed to higher levels than other species. There is no information available on trends over time. DecaBDE has also been found in Arctic polar bears but it is not known how it has spread to there.

• Degradation to more toxic substances DecaBDE has been found to be capable of degrading in the environment and in living organisms to lower brominated (and probably more toxic) diphenyl ethers. These include, for example, pentaBDE and octaBDE, which are prohibited on account of their properties that are harmful to health and the environment, as well as brominated dibenzofurans. It is also known that chlorinated and brominated dibenzodioxins and dibenzofurans can form on incineration and recovery of material containing polybrominated diphenyl ethers (PBDEs). The extent of the formation of these substances 15 SFS from decaBDE in the environment, living organisms and in connection with incineration is not yet known.

In all other respects, conclusion (ii) in accordance with the EU TGD has been reached, i.e. “there is at present no need for further information and/or testing and no need for risk reduction measures beyond those which are being applied already”. This applies to direct exposure of organisms via air, water, sediment and soil as well as the exposure of mammals and birds via their food.

In connection with the health risk assessment, conclusion (i) in accordance with the EU TGD “there is a need for further information and/or testing” applies as regards the following points:

• Potential neurotoxicity The interference with brain development observed in mice may also be considered to include humans and constitute a risk. However, the results are regarded as being somewhat uncertain due to the fact that the quality of the study has been called into question and it is necessary to carry out a new study.

• Concentrations in blood and breast milk DecaBDE has been found in blood and breast milk in humans. More information is required concerning the levels in humans and whether they show an upward or downward trend over time.

In other respects, conclusion (ii) in accordance with the EU TGD is thought to apply “there is at present no need for further information and/or testing and no need for risk reduction measures beyond those which are being applied already”, as no other risks to workers or the general public (consumers and humans exposed indirectly via the environment) have been identified. This applies to acute toxicity, toxicity on long-term exposure, carcinogenicity, mutagenicity, reproductive toxicity and irritation and sensitisation. 16 SFS 3. Further studies and risk-reducing measures On account of the uncertainties surrounding the existing environmental and health risk assessment, the collection of more data is deemed necessary. The following studies are therefore planned at EU level:

• An extended repeat of the neurotoxicity study on mice This study is crucial for the significance of the toxicity of decaBDE and affects the conclusions regarding health and environmental risks.

• Monitoring of decaBDE and its degradation products in the environment in order to identify a possible trend A programme for monitoring concentrations in the European environment is planned. This shall last for at least six years with a possible extension to ten years and with reports being drawn up every two years. The programme has not been confirmed but the plan is for it to include measurements of the concentration of decaBDE and degradation products in: - sediment - sludge at waste water treatment plants - sparrowhawk eggs in the United Kingdom and glaucous gull eggs in the Norwegian Arctic (Svalbard or Bjørnøya)

Measurements of decaBDE in the air will probably also be included.

• Monitoring of decaBDE in blood and breast milk in humans for continued analysis of concentrations and possible trends A programme for monitoring levels in humans is planned, but no details are available yet.

17 SFS A final decision regarding the risks associated with decaBDE cannot be taken until one or some of the following points have been satisfied:

• a clear trend can be seen with regard to concentrations in the environment • a clear NOAEL5 has been established for neurotoxic effects • we have knowledge of whether or not bioaccumulation occurs • the significance of conversion to similar lower substances has been investigated

As it has not been possible at the present time to identify a clear risk with regard to decaBDE, no risk reduction strategy has been developed yet. The industry using this substance will instead implement a voluntary programme for reducing emissions of decaBDE within the plastics and textiles sectors by means of a code of good practice. The industry using the substance aims to reduce its emissions to almost zero, which is to be achieved primarily through changes to processes and the handling of decaBDE. As things stand it has not yet been decided how this programme will be evaluated and monitored, but this will probably be done by means of mass balance calculations of use in processes supplemented by chemical analyses of emissions.

4. Summary of the EU’s existing risk assessment for decaBDE Below is a summary of the EU’s revised health and environmental risk assessment. Some new studies that did not form part of this risk assessment have also be included and references to them have been given. Otherwise, all information has been taken from the EU’s risk assessment.

4.1 Physico-chemical properties of decaBDE

Table 1. Physico-chemical properties of decaBDE

5 No Observed Adverse Effect Level. 18 SFS

Synonyms Decabromobiphenyl oxide Decabromodiphenyl ether CAS number 1163-19-5

Molecular formula C12Br10O Structural formula [see original above] Molecular weight 959.2 g/mol Particle size Usually < 5 μm Melting point 300 – 310 °C Boiling point Decomposes at > 320 °C Solubility in water < 0.1 μm/l (25 °C)

Log Kow Uncertain. The result varies between 6.27 and 9.97 Vapour pressure 4.63 x 10-6 Pa (21 °C) Henry’s Law constant 44.4 Pa m3 mol-1

4.2 Environment Emissions and dissemination Emissions of decaBDE can occur throughout its life cycle. Locally, this can occur during its manufacture, handling, 19 SFS incorporation into plastics and during treatment of textiles. More diffuse emissions can occur via evaporation, combustion or leakage of/from the products in which decaBDE is used. Emissions are also assumed to occur from landfill sites, for example, after the product has been used and can therefore result in increases in levels in the environment over time.

In the revised risk assessment the emissions of decaBDE within the EU are estimated to be approximately 38 tonnes/year (Table 2), the overwhelming majority of which, 37.5 tonnes, is believed to originate from impregnated textiles after disposal. There is currently no production of decaBDE within the EU and the industrial emissions, which are assumed to constitute only a small proportion of the total emissions, come primarily from the impregnation of textiles and the incorporation of decaBDE into plastics. However, it should be pointed out that these are estimated emissions and that there is considerable uncertainty in these data.

Table 2 Estimated emissions of decaBDE into the European environment (tonnes/year)

Air Surface Waste water treatment Soil Total water plants 0.014 – 0.123 9.4 0.14 28.2 ~ 38

Based on the properties of decaBDE (high log Kow, slow degradation in sediment and long atmospheric half-life), decaBDE is expected primarily to bind to and accumulate in sediment, waste water treatment plant sludge and soil.

Available data indicates that decaBDE can be degraded by sunlight (photolysis) to lower polybrominated diphenyl ethers and to polybrominated dibenzofurans (PBDFs). Studies have shown that photolytic degradation of decaBDE occurs first to nona- then to octa-, hepta- and hexabromodiphenyl ether. These are the dominant degradation products. Formation of pentaBDE has been observed, but in small quantities and in an artificial medium,

20 as well as the formation of PBDFs. These degradation SFS products will in turn be degraded further by photolysis. It is extremely difficult to predict the rate of their formation and degradation in the environment. If they are degraded more slowly than they are formed, an increase in these substances can be assumed to occur. The studies carried out have shown that the degradation rate falls with decreasing bromination and, in an environment with a constant supply of decaBDE, this results in a build-up of lower PBDEs. In one study (Bezares-Cruz et al, 2004) which looked at the degradation of decaBDE in sunlight in an artificial medium, pentaBDE, among others, could be detected after 365 and 2028 minutes’ exposure to sunlight in July and October, respectively, in West Lafayette, USA. Preliminary data indicate that the degradation rate in a more natural medium is significantly slower. Conversion of decaBDE in the environment is, however, assumed to be relatively limited, based on the fact that decaBDE binds to particles and then accumulates in sediment and soil where exposure to sunlight is judged to be low. The concentrations of pentaBDE and octaBDE found in the environment today are believed to be the result mainly of historical emissions.

DecaBDE has also be found to be capable of forming polybrominated dibenzodioxins (PBDDs) and dibenzofurans at high temperatures. These compounds can therefore be formed as by-products during the incineration of material containing decaBDE (waste incineration, unintentional fires) and during recycling. During incineration of decaBDE together with material containing chlorine, polychlorinated dibenzodioxins (PCDD) and dibenzofurans (PCDF) as well as polyhalogenated dibenzodioxins (PHDD) and dibenzofurans (PHDF) can also be formed. In one study (Hayakawa et al, 2004) a connection could be seen between levels of PBDEs and PBDD/PBDFs in the atmosphere, which may indicate that these dioxins and furans were formed from PBDEs. It is currently not known how great the contribution of decaBDEs is to the formation of dioxins and furans. However, it appears to be limited in relation to the contribution from lower brominated diphenyl ethers. Under controlled conditions, emissions can be reduced, for 21 SFS example, by means of an efficient incineration process and waste gas cleaning.

Levels in the environment Levels of decaBDE in water have been measured in the United Kingdom, the Netherlands, Finland and Japan, among others. The results showed that the levels were most often below the detection limits (5 - 2500 ng/l), but concentrations between 15 and 400 ng/l were detected.

In sediment, where decaBDE is expected to accumulate, concentrations have been measured in several countries, the highest measured concentrations of which are shown in Table 3. It should be pointed out that these are extremely high in relation to other measured concentrations and derive from areas connected to industrial activity in which decaBDE is used; they are shown in order to describe the “worst case” concentrations. In the majority of the studies carried out concentrations vary from below the detection limit (varying between < 0.6 and 500 µg/kg) to approximately 100 µg/kg dry weight. A study of the sediment in five estuaries in England and the Netherlands showed that the concentrations of decaBDE increased by 50 – 100% between 1995 and 2001 in three of these estuaries.

Concentrations of decaBDE were measured in sludge in European waste water treatment plants (Table 3). In a Swiss study of eight treatment plants, the concentrations of decaBDE increased from an average of 220 µg/kg dry weight to 1100 µg/kg during the period from 1993 to 2002, which is equivalent to a percentage increase of 150 – 1700% in the individual treatment plants.

22 Table 3. Highest measured concentrations of decaBDE in SFS sediment and sludge in waste water treatment plants

Country Highest Highest concentration in concentration in sediment (µg/kg waste water dry weight) treatment plants (µg/kg dry weight) The Netherlands 4600 920 United Kingdom 3190 1950* Finland 2697 - Sweden 1205* 390 Switzerland - 1100 (mean value from 8 treatment plants) USA 14000 1470 Japan 6000 - * = converted from µg/kg wet weight

The presence of nine different PBDEs was measured in precipitation (rain, particles) over a two-week period in Lund in 2000. The results showed that decaBDE was the dominant of these and occurred in rainwater at a mean concentration of 0.209 ng/l. The total precipitation of decaBDE was calculated to be 1 ng/m2/day.

No concentrations of decaBDE have been measured in soil, but decaBDE is expected to occur in soil on account of the supply from sludge from waste water treatment plants and via deposition from the atmosphere in the form of rainwater and particles.

Concentrations in living organisms Uptake of decaBDE by living organisms has been judged to be low based on its high molecular weight. However, this has been contradicted by decaBDE being detected in particular in birds of prey and their eggs. The original risk assessment noted a biological uptake of decaBDE by mammals of 6% via food. This has now been re-evaluated, as significantly higher uptake has been observed and 23 SFS appears to be dependent on how decaBDE is supplied to the animals. DecaBDE has also be found to be capable of transformation in living organisms. In studies of fish, decaBDE has been found to be capable of giving rise to lower brominated diphenyl ethers similar to, among others, pentaBDE and octaBDE. In one study, two hexaBDE congeners could be observed as well as five different unknown diphenyl ethers varying from pentaBDE to octaBDE. An increase in the lower brominated diphenyl ethers was observed during the study, which indicates that this shift is caused by metabolism. In studies on rats, metabolites similar to PBDEs from pentaBDE to nonaBDE were detected.

As regards aquatic organisms within Europe, decaBDE has been detected mainly in fish and mussels, but also in mammals such as dolphins, porpoises and seals. In the Netherlands 0.9 µg/kg dry weight was measured in the muscles of fish and 4.9 µg/kg dry weight was measured in the whole body homogenate of mussels, which corresponds to a wet weight of 0.16 and 0.98 µg/kg respectively, based on an 80% water content in these organisms. However, it cannot be ruled out that the high concentrations in mussels is partly due to particles in their digestive tract that have decaBDE bound to them.

As regards terrestrial animals, decaBDE has been detected in a large number of species such as birds, polar bears, lynx, elk and deer. The highest concentrations have been found in predatory animals, particularly in birds of prey and their eggs, with concentrations up to 24 µg/kg wet weight. In a study of three populations of peregrine falcons (Falco peregrinus), a wild population from northern Sweden, a wild population from southern Sweden and a population reared in captivity, it was possible to ascertain that the wild peregrine falcons had significantly higher concentrations of decaBDE in their eggs. This shows that they have been exposed to decaBDE in the environment. However, it is difficult to determine where this exposure has occurred, as both peregrine falcons and the birds that constitute their

24 prey overwinter in southern Europe, where they may also be SFS exposed to decaBDE.

In a study carried out in 2002 on account of more data being considered necessary in the original risk assessment, the presence of decaBDE was investigated in fourteen bird species from the United Kingdom and the Netherlands. The results showed that decaBDE could be detected in ten of these species and in 35% of the samples. The concentrations in peregrine falcons at the 90th percentile were 14.2 µg/kg wet weight in eggs, 4.6 µg/kg wet weight in liver and 4 µg/kg wet weight in muscle. The highest concentration of 24 µg/kg wet weight was measured in a peregrine falcon egg.

In a recently concluded study, decaBDE was detected in glaucous gulls and their eggs as well as polar bears in the Norwegian Arctic. The fact that decaBDE can be detected in predatory animals in the Arctic environment illustrates its potential for both long-distance transport and possibly also for bioaccumulation.

An analysis of concentrations of decaBDE measured in the muscles of sparrowhawks and the eggs of peregrine falcons in the United Kingdom from 1975 to 2001 has been carried out with a view to clarifying time trends. The conclusion reached was that, in general, the concentrations are clearly higher now than they were at the end of the 1970s. A contributory cause of this is the increased use of decaBDE. However, no significant change was observed during the period from 1995 to 2001/2002.

The fact that decaBDE can be detected in different animal species and in different environments, particularly in Arctic environments, shows that it is wide-spread. This is unexpected, as previous opinion has been that decaBDE does not have the physico-chemical properties for this. Neither was it expected that decaBDE would accumulate in tissues on account of its properties and based on results of earlier animal studies. Nor has it been established whether the concentrations show an upward or downward trend, and 25 SFS continued monitoring is to be carried out to try to answer this question.

Toxicity The toxicity of decaBDE has been tested on aquatic and terrestrial organisms.

Determinations of toxic concentrations in water were complicated by the fact that decaBDE has very limited solubility in water (< 0.1 µg/l). Effects of decaBDE on direct exposure have only been demonstrated in algae, although with an added quantity greatly exceeding its water solubility, which should therefore be regarded as unlikely to be attained under normal conditions in the environment. The effect on fish has been observed in a study on carp (Cyprinus carpio) with a view to studying the metabolism of decaBDE given via their food. Toxic effects were, however, observed in the form of reduced growth and a reduced amount of body fat. Seven different lower brominated diphenyl ethers would be detected in the tissues of the fish and their levels increased during the course of the study. This is interpreted as proof of the fact that decaBDE has been metabolised. This study used only one concentration of decaBDE, 940 µg/kg, making it impossible to determine a NOEC6 value for toxicity.

No effects were observed in the terrestrial environment in a study on earth worms and likewise in a study on six different species of plant.

Two studies have been used to assess the risks to mammals exposed to decaBDE via the food chain. A chronic study on rats observed, among other things, the effect on the liver at a concentration of decaBDE in food of 25 000 mg/kg. In another study on mice, neurotoxic effects were seen after a single dose of 2.22 mg/kg body weight during a critical period of brain development.

See Table 4 for a summary of the toxicity of decaBDE in aquatic and terrestrial environments.

6 No Observed Effect Concentration 26 SFS Table 4 Summary of the toxicity of decaBDE in aquatic and terrestrial environments

Matrix Species Toxicity 36 Algae (S. Costatum, EC50 > 1 mg/l* T. Pseudonana, Chlorella sp.) Fresh- and saltwater Water fleas (Daphnia NOEC > 2 µg/l* magna) 37 Medaka (Oryzias LC50 > 500 mg/l* latipes) Carp (Cyprinus LOEC38 = 940 µg/kg carpio) Oligochaete Sediment (Lumbriculus NOEC > 1480 mg/kg variegatus) Waste water treatment Microorganisms NOEC > 15 mg/l plant sludge Soil Earthworm (Eisenia NOEC > 4910 mg/kg fetida) dry weight Soil Plants NOEC > 5349 mg/kg dry weight Indirect toxicity via Rats NOEC > 25 000 the food chain mg/kg Mice LOAEL39 = 2.22 mg/kg bw * = concentration higher than the water solubility of decaBDE ------36 Effective Concentration 50 per cent. 37 Lethal Concentration 50 per cent. 38 Lowest Observed Effect Concentration. 39 Lowest Observed Adverse Effect Level.

Risk characterisation It has not been possible to carry out a risk characterisation for fresh- and saltwater environments, as decaBDE has shown no toxicity up the limit of its solubility in water.

In sediment, levels in the European environment have been measured up to a maximum of 4600 µg/kg dry weight, which corresponds to a concentration of approximately 920 µg/kg wet weight. However, the revised risk assessment 27 SFS only uses theoretical modelled values of which the highest is 31 mg/kg wet weight. As this is used as a PEC7 and is weighed against the toxicity of decaBDE (which with an assessment factor of 10 gives a PNEC8 value of ≥ 148 mg/kg), a ratio of < 0.21 is obtained. As this value is less than 1 there is considered to be no risk to sediment-dwelling organisms.

The highest concentration of decaBDE measured in sludge from a European treatment plant is 1100 µg/kg dry weight, which corresponds to approximately 9 µg/kg wet weight. The revised risk assessment uses theoretical values, the highest of which being 1.25 mg/kg. As the PNEC is determined to be > 1.5 mg/kg for microorganisms this results in a PEC/PNEC ratio of < 0.83 and there is thought to be no risk of an effect on waste water treatment processes.

No measurements have been taken of the presence of decaBDE in soil. However, concentrations up to 11.6 mg/kg have been estimated by calculation. When this concentration is compared against the PNEC (> 87 mg/kg, based on toxicity to earthworms) a PEC/PNEC ratio of < 0.13 is obtained. There is therefore considered to be no risk to terrestrial organisms.

Direct emissions of decaBDE to the atmosphere are judged to be very low. Based on this and on the low volatility of decaBDE an effect on biota (living organisms) or abiota (in this case the ozone layer, greenhouse effect, etc.) is considered unlikely.

Indirect poisoning of mammals and birds via the food chain may be possible as a result of their consumption of food containing decaBDE. The NOAEL in a chronic study on rats was determined to be 25 000 mg/kg, which according to the EU TGD gives a PNEC value of 833 mg/kg. In fish and mussels concentrations equivalent to up to 0.16 µg/kg wet weight and 0.98 µg/kg wet weight, respectively, have been

7 Predicted Environmental Concentration. 8 Predicted No-Effect Concentration. 28 measured. However, the revised risk assessment uses SFS theoretical values, the highest of which in fish and earthworms are 0.2 µg/kg and 0.17 mg/kg, respectively. When these PEC values are weighed against the PNEC value, ratios of 2.4 x 10-7 and 2.0 x 10-4, respectively, are obtained. As these values are less than 1 there is considered to be no risk of poisoning via the food chain in this scenario.

Neurotoxic effects in mice have been observed at significantly lower concentrations of decaBDE than in the chronic study, at as low as 2.22 mg/kg. The uptake of decaBDE in these mice was estimated to be at least 13.4%. However, this study has been called into question by certain Member States and is not therefore used in the revised risk assessment for toxic effects via the food chain. If these effects were taken into account the safety margins would be reduced significantly and would indicate a risk at the theoretical levels of decaBDE in earthworms.

Of great significance is the discovery of decaBDE in the eggs of birds of prey in which a developing foetus can be thought to experience a high level of exposure. If the uptake in mice is considered to be 13.4%, the internal dose in mice would be 300 µg/kg. The highest measured concentrations in a bird of prey egg is 24 µg/kg wet weight and the 90th percentile is represented by a concentration of 14.2 µg/kg wet weight. When these measured concentrations are weighed against the internal dose in mice the margins of safety of 12 and 21, respectively, are obtained. In accordance with the TGD, there shall be a margin of safety of not less than 30 in toxicity data and where the margins of safety are lower than this it will cause concern for the effects on the developing foetus. Furthermore, these ratios are based on the LOAEL values and not the NOAEL values. However, it should be pointed out that extrapolation of data from mice to birds is uncertain and that the study is thought to be deficient as regards its design.

Poisoning via the food chain may also be considered to include fish. As already mentioned, effects on fish in the form of reduced growth and reduced body weight were 29 SFS observed at a concentration of decaBDE in food of 940 µg/kg. However, since this was the only dose tested no PNEC value could be determined. Nevertheless, this value can be compared directly with the highest concentrations measured in fish or mussels (approximately 5 µg/kg), which gives a margin of 188. This leads to the conclusion that there is no risk.

A PBT assessment has also been carried out for decaBDE. PBT is a term used in risk assessment in accordance with the EU TGD. It aims to determine whether a substance exhibits such inherent properties that on the basis of these alone it can be deemed to pose a risk. In order for a substance to be classified as a PBT substance, it shall be:

 persistent (P criterion)  able to bioaccumulate (B criterion)  toxic (T criterion)

A substance which exhibits a very high persistence and ability to bioaccumulate may meet the requirements for a vPvB9 substance. Toxicity is not considered to be relevant for such a substance. The EU TGD contains requirements for meeting the criteria described.

DecaBDE is considered to meet the vP criterion. This is based on a 32 week study in which no degradation of decaBDE could be observed in sediment.

The B criterion is currently not thought to be met, according to the EU TGD, based on data relating to fish. In a study on seals, approximately 11 – 15% of an administered dose of decaBDE was present in adipose tissue 30 days after exposure had ceased, which indicates bioaccumulative properties. The presence of decaBDE in top predators is also an indication that bioaccumulation and biomagnification can occur. However, this is still not known, as it has not been established how these predators are exposed. The levels in birds and their eggs may be the result of a high level of exposure. More data is needed to investigate this.

9 Very Persistent, very Bioaccumulative. 30 SFS DecaBDE is currently not considered to meet the T criterion according to the EU TGD, based on its toxicity to aquatic and terrestrial organisms and mammals and the fact that it has not been shown to be carcinogenic, mutagenic or toxic for reproduction. However, the study that shows that decaBDE is neurotoxic may be decisive with regard to meeting the T criterion if the result of this study can be reproduced.

The conclusion of the PBT assessment is that decaBDE cannot currently be regarded as a PBT substance. However, the assessment is complicated by a number of facts and more data is required. DecaBDE has been found in top predators, which is unexpected based on its physico- chemical properties. It is also unclear whether these levels show an upward or downward trend. DecaBDE has shown suspected neurotoxic properties, something which is very important with regard to its toxicity and may entail a risk to bird embryos at the concentrations that can be measured in eggs. DecaBDE has also proven to be capable of degrading to lower brominated compounds such as pentaBDE and octaBDE, which are classed as PBT substances.

4.3 Health Metabolism and pharmacokinetics Uptake of decaBDE may occur via inhalation, via the skin and via the digestive tract. It has been studied predominantly in the digestive tract. The original risk assessment assumed this to be between 6 and 9% of an administered oral dose. However, more recent studies indicate a higher uptake, which appears to be largely dependent on the medium in which decaBDE is administered. In a metabolism study on rats, an uptake of at least 26% was observed, but it may be higher as metabolites could also be detected. Uptake via the skin has been estimated to be around 1-2% based on a study in vitro10. Uptake via the lungs may also be considered to

10 Term within biomedical science to indicate that experiments have been carried out or observations made in reaction vessels, test tubes, culture dishes, etc., i.e. in an artificial environment and not in a living body (in vivo). 31 SFS occur, due to the particle size of decaBDE (< 5 µm), but no studies have been done on this.

After uptake, decaBDE has been found to be distributed primarily to the plasma and to organs with a good blood supply (liver, kidneys, heart, adrenal glands, intestine wall). However, decaBDE does not accumulate in adipose tissue, which might be expected based on its high fat solubility and because lower PBDEs have done so.

The half-life for elimination from plasma has been determined in rats to be approximately 2.5 days. DecaBDE is excreted predominantly in faeces. In one study, after three days > 90% of an administered dose of decaBDE had been excreted in faeces and only a small amount in the urine (< 0.05%). 65% of this dose was excreted as metabolites, which shows that decaBDE is extensively metabolised. 10% of these metabolites were excreted via the bile, which means that 55% of the metabolites originate from other sources. Active transport to the intestine lumen via P-glycoproteins has been suggested, as well as first pass metabolism in the intestine wall. However, it cannot be ruled out that a certain amount of microbial degradation also occurs in the intestines. Another study showed a concentration of metabolites four times higher than the concentration of decaBDE three days after oral administration.

Debromination is believed to occur as the first step in the metabolism of decaBDE. Oxidation is also assumed to occur, which results directly or indirectly (via a reactive metabolite) in hydroxylation. Metabolites that have been detected and are believed to originate from decaBDE include lower brominated diphenyl ethers such as nonaBDE and monohydroxylated metabolites, including nonaBDE and octaBDE, as well as phenolic metabolites with five to seven bromine atoms. The fact that a concentration of metabolites four times higher than the concentration of decaBDE was detected may indicate that exposure to these is higher than exposure to decaBDE. One reason for the high concentrations of metabolites may be that they are retained by binding to a transport protein in the blood, transthyretin, 32 which has been shown to bind substances with a similar SFS structure to decaBDE, such as polychlorinated biphenyls (PBCs).

Exposure The highest exposure is assumed to occur in connection with the occupational handling of decaBDE. This includes manufacture, handling, incorporation in plastics and textiles and the use of products that are flame-protected using decaBDE. Inhalation of particles and skin contact with decaBDE are considered to constitute the largest source of exposure. When decaBDE is heated it can be assumed that a certain amount of vapour will be inhaled. Exposure via treated plastics or textiles is assumed to be very low. It should be mentioned that decaBDE is no longer produced within the EU.

In an analysis of levels in the air from a plant for recycling electronic equipment concentrations of decaBDE of up to 200 ng/m3 were measured. In an analysis of dust from, among others, offices of various European authorities, levels of decaBDE of between 0.26 and 6.9 mg/kg were measured. The highest theoretical concentration of decaBDE in air that is used in the revised risk assessment for occupational exposure is 5 mg/m3. For skin exposure, a theoretical maximum exposure of 1 mg/cm2/day is assumed.

In an analysis of blood from Swedish workers, decaBDE could be detected in serum at levels between < 0.7 and 278 µg/kg lipid weight. The highest level was detected in workers at a plant for the manufacture of cables (see Table 5).

Table 5. Measured levels of decaBDE in serum from Swedish workers.

Sample Concentration of decaBDE in serum (µg/kg lipid weight) Exposed group Median Variation Dismantlers of electronics 4.8 0.29 – 9.5 equipment (N = 19) 33 SFS Recyclers of circuit boards (N = 2.3 < 0.96 – 5.6 9) Rubber mixers (N = 7) 28.1 1.2 – 144 Rubber cable producers (N = 12) 35 6.7 – 278 Computer engineers (N = 19) 1.5 <0.96 – 6.8 Office workers (N = 20) < 0.7 < 0.7 – 7.7 Non-exposed group Median Variation Hospital cleaners (N = 20) < 0.7 < 0.7 – 3.7 Slaughterhouse workers N = 17) 2.4 0.92 – 9.3

There are no clear exposure sources of decaBDE for the general public (consumers and people exposed indirectly via the environment). Exposure is therefore assumed to be low and occurs in a diffuse manner via, for example, food, inhalation of dust and skin contact with flame-protected products. In a recently published study (Schecter et al, 2004) the presence of decaBDE was detected in a large number of food products in the US, the highest concentrations of which could be measured, for example, in fish, calf liver and cheese. The highest measured concentration in fish, 1.27 µg/kg, shows that exposure via food is low. It is interesting to note that decaBDE occurs at relatively high levels in cheese but low levels in milk, something that may indicate that decaBDE is conveyed via the packaging or in the manufacturing process.

DecaBDE has been detected in indoor air in a number of studies. In the United Kingdom, decaBDE dust from vacuum cleaners was measured at concentrations with a mean value of 9.8 mg/kg (3.8 – 19.9 mg/kg). In comparison, the levels in one sample from Finland and one from Denmark were 0.1 and 0.26 mg/kg respectively. A similar study in the US indicated levels with a mean of 4.6 mg/kg (0.6 – 16.4 mg/kg). An estimate of the exposure of children to decaBDE in the US gave levels between 0.0012 and 0.76 mg/kg/day. The theoretically estimated uptake in humans according to the revised risk assessment is assumed to be 0.05 – 12 µg/kg/day for the general public.

In an analysis of blood from the general public in the United Kingdom, decaBDE could be detected in 7% (11/155) of the 34 samples at levels up to 241 µg/kg lipid weight with a SFS median of 83 µg/kg lipid weight. In a follow-up study on Members of the European Parliament, decaBDE could be detected in serum from 34% (16/47) of the individuals tested and at levels up to 2400 µg/kg lipid weight with a median of 53 µg/kg lipid weight. These two studies concluded that a there is a large variation in levels of decaBDE in the general population. The reason for this is not known, but there may have been occupationally exposed individuals in these two studies. The collection of more data concerning concentrations in humans is considered necessary and a monitoring programme for measuring levels in humans will therefore be initiated.

In a study on breast milk from American women, decaBDE could be detected in 7 of 23 samples at levels between 0.48 – 8.24 µg/kg lipid weight with a median of 0.92 µg/kg lipid weight. In a follow-up study, decaBDE was detected in 80% (16/20) of the samples with a mean of 0.24 µg/kg lipid weight (0.08 – 1.23 µg/kg).

Toxicity DecaBDE has in general demonstrated low toxicity in the animals studies carried out. However, it should be pointed out that in later studies it was found that uptake via the digestive tract may depend on how decaBDE is given to the animals and that may mean that the toxicity was underestimated in earlier studies.

DecaBDE has demonstrated low acute toxicity on oral11 and 12 13 dermal exposure and on inhalation. The LD50 on oral exposure has been determined as > 5000 mg/kg. No signs of toxicity have been observed on oral exposure up to 2000 mg/kg. On dermal exposure, no mortality or signs of toxicity have been reported at levels up to 2000 mg/kg. In an inhalation study on rats, a small effect on breathing could be detected at a dose of 2 mg/l air and higher.

11 Via the mouth. 12 Via the skin. 13 Lethal Dose 50%- the dose resulting in 50% mortality. 35 SFS DecaBDE has not been found to irritate the skin or eyes or be sensitising.

On repeated exposure, the lowest NOAEL for systemic toxicity was determined to be 1120 mg/kg/day and was observed in a two-year dietary study on rats. At the higher dose tested in this study (2240 mg/kg/day) effects on the liver (thrombosis, fibrosis), spleen (fibrosis) and tonsils (hyperplasia) were observed. Local effects in the form of effects on the stomach would be observed in a few individuals at a dose of 1120 mg/kg/day.

DecaBDE is not considered to be mutagenic, based on studies in vitro and in vivo. In the aforementioned chronic two-year study on rats, a significant and dose-related increase in the number of liver tumours could be observed in males and females. As effects could be seen at the lowest dose tested (1120 mg/kg/day) this is the LOAEL for carcinogenicity. As regards carcinogenicity, decaBDE has been assigned by IARC14 to group 3 “the agent is unclassifiable as to carcinogenicity in humans”.

DecaBDE is not considered to be toxic for reproduction. No effects were seen in rat foetuses at a maternal dose of up to 1000 mg/kg/day. No fertility-disrupting effects could be observed in a reproduction study on rats at doses up to 100 mg/kg/day and no histological changes to the reproductive organs were observed in a chronic study at doses corresponding to 7780 mg/kg/day.

DecaBDE has been found to give rise to neurotoxic effects in a study on mice. In this study, mice were given an oral dose of decaBDE of 2.22 and 20.1 mg/kg bw; 1.34 13.4 and 20.1 mg/kg bw and 2.22 and 20.1 mg/kg bw respectively 3, 10 or 19 days after birth. Radioactive decaBDE was also given to study uptake in the brain. Behaviour tests were then performed on the different groups 2, 4 and 6 months after exposure. The behaviour test measures the activity in the mice, which are placed in a new cage, and is based on the fact that normal mice exhibit habituation, i.e. reduced

14 International Agency for Research on Cancer. 36 activity with time as they become more familiar with their SFS new environment.

The results at 2, 4 and 6 months showed that the mice exposed to a dose of 20.1 mg/kg bw during day 3 did not exhibit the normal habituation behaviour, but were instead hyperactive compared with the control group. This behaviour also grew worse with increasing age. The study also showed that decaBDE was taken up in the brain and that the level there was highest 7 days after exposure. A weak effect could possibly also be discerned at a dose of 2.22 mg/kg bw given on day 3. The reason for these behavioural disturbances is believed to be that decaBDE interferes with the development of the brain during a critical period referred to as the brain growth spurt. This occurs around 10 days after birth in mice and is characterised by rapid growth and maturing of nerve cells in the brain. Corresponding results have been seen in earlier studies on mice exposed to the lower brominated diphenyl ethers tetra-, penta- and hexaBDE. However, the effect in these studies was greatest in the mice exposed on day 10. This leads to the suspicion that metabolites of decaBDE may be the cause of the effects observed in this study.

The results of this study have been called into question, but not completely rejected, by a number of Member States. This is due, among other things, to the fact that the method used has not been standardised and on account of the dosing method, how the choice of individuals for the behaviour tests was made, the fact that few individuals were used in the dosage groups, which provides little statistical basis, and that no analysis of metabolites was carried out. Since this study is of very great importance as regards the view of the toxicity of decaBDE a decision has been taken to repeat this study. Discussions are currently underway concerning the design of the new study and it is unclear when it will be started, but this will probably happen during the spring of 2005.

Risk characterisation

37 SFS The risk characterisation took toxicity on repeated exposure, carcinogenic effects, reproductive toxic effects (only the general public) and neurotoxic effects into account. As regards other effects, conclusion (ii) in accordance with the EU TGD was reached, i.e. “There is at present no need for further information and/or testing and no need for risk reduction measures beyond those which are being applied already”.

With regard to neurotoxic effects, conclusion (i) in accordance with the EU TGD was reached “there is a need for further information and/or testing” for both occupationally exposed people and the general public. This is based on the fact that it has not been possible to determine a NOAEL value for this effect and that the results are considered to be sufficiently meaningful. However, the study has been criticised and is to be repeated in a more standardised manner with a view to obtaining a NOAEL value.

For workers, exposure to decaBDE is considered to consist primarily of skin contact and dust inhalation. Oral exposure is not considered to be relevant. For workers, the highest exposure is estimated to occur during production or handling of decaBDE, with exposure to 0.7 mg/kg/day via the air and 0.1 mg/kg/day via the skin.

As regards toxicity on repeated exposure, an internal dose of 291.2 mg/kg/day was obtained based on an NOAEL of 1120 mg/kg/day and assuming an absorption of 26%. When this is compared with the exposure on inhalation of 0.7 mg/kg/day, a margin of safety of 416 is obtained, which is considered satisfactory. On skin exposure a corresponding margin of safety of 2427 is obtained. For combined exposure a margin of safety of 355 is obtained. As no risk can be identified in these scenarios, conclusion (ii) is considered to apply.

Conclusion (ii) also applies as regards cancer. This is based on the same internal effect concentration as on repeated exposure (291.2 mg/kg/day) and results in an identical margin of safety. However, in this case the internal effect 38 concentration is based on an LOAEL value, but in the risk SFS assessment it is nevertheless regarded as satisfactory, as the calculations were conservative.

For the general public (consumers and people exposed indirectly via the environment) a theoretical maximum intake of decaBDE of 12 µg/kg/day is estimated. When this is compared with the internal dose at the NOAEL for repeated exposure and carcinogenicity (291.2) a margin of safety of 93333 is obtained. Since this margin of safety is considered to be satisfactory, no risk can be identified and conclusion (ii) is deemed to apply.

For reproductive toxic effects an NOAEL of > 100 mg/kg/day has been determined. When this is compared with the highest theoretical intake (12 µg/kg/day), a margin of safety of 8333 is obtained. No risk can be identified, which leads to conclusion (ii).

For children, the daily intake of decaBDE via breast milk is estimated to be 0.0052 µg/kg/day. This will result in a higher margin of safety than in the above scenarios.

Despite no direct risk being identified for the general public, conclusion (i) “there is a need for further information and/or testing” is nevertheless reached as regards levels of decaBDE in blood and breast milk. This is due to the large variations that occur. A programme for measuring levels and time trends in blood and breast milk is planned at EU level.

Based on the above scenarios that have been investigated there is also considered to be no risk in connection with combined occupational and environmental exposure.

References

KEMI Rapport 5/04 Dekabromdifenyleter (dekaBDE) – underlag till ett nationellt förbud [Decabromodiphenyl ether (deBDE) – basis for a national ban], order no. 360 799, 39 SFS Stockholm, November 2004. Published by: Swedish Chemicals Inspectorate. Order address: fax 08 735 76 98, e- mail [email protected]. The report can also be obtained from the website www.kemi.se under “trycksaker” [publications] and then “rapporter” [reports].

Bezares-Cruz J, Jafvert CT, Hua I (2004). Solar decomposition of decabromodiphenylether: Products and Quantum yield. Environmental Science & Technology 2004, Vol.38 No 15 pp. 4149-4156.

Hayakawa K, Takatsuki H, Watanabe I, Sakai S-I (2004). Poly brominated diphenylethers (PBDEs), polybrominated dibenzo-p-dioxins/furans (PBDD/Fs) monobromo- polychlorinated dibenzo-p-dioxins/dibenzofurans (MoBPXDD/Fs) in the atmosphere and bulk deposition in Kyoto. Japan. Chemosphere 57:343-356.

Schecter A, Päpke O, Tung K-C, Staskal D, Birnbaum L (2004) Polybrominated diphenylethers contamination of United States food. Environmental Science and Technology. In press.