BBP ANNEX XV ?IDENTIFICATION OF SVHC FORMAT
Annex XV dossier
PROPOSAL FOR IDENTIFICATION OF A SUBSTANCE AS A
CMR CAT 1 OR 2, PBT, vPvB OR A SUBSTANCE OF AN
EQUIVALENT LEVEL OF CONCERN
Substance Name: benzyl butyl phthalate
EC Number: 201-622-7
CAS Number: 85-68-7
? It is proposed to identify the substance as a CMR according to Article 57 (c).
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BBP ANNEX XV ?IDENTIFICATION OF SVHC FORMAT
CONTENTS
PROPOSAL FOR IDENTIFICATION OF A SUBSTANCE AS A CMR CAT 1 OR 2, PBT, VPVB OR A
SUBSTANCE OF AN EQUIVALENT LEVEL OF CONCERN................................................................................5
JUSTIFICATION .........................................................................................................................................................7
1 IDENTITY OF THE SUBSTANCE AND PHYSICAL AND CHEMICAL PROPERTIES.................................7
1.1 Name and other identifiers of the substance...................................................................................................7
1.2 Composition of the substance.........................................................................................................................7
1.3 Physico-chemical properties...........................................................................................................................8
2 MANUFACTURE AND USES..............................................................................................................................8
3 CLASSIFICATION AND LABELLING ...............................................................................................................8
3.1 Classification in Annex I of Directive 67/548/EEC .......................................................................................8
3.2 Self classification(s) .......................................................................................................................................9
4 ENVIRONMENTAL FATE PROPERTIES ..........................................................................................................10
4.1 Degradation ....................................................................................................................................................10
4.1.1 Stability ...............................................................................................................................................10
4.1.2 Biodegradation ....................................................................................................................................10
4.1.2.1 Biodegradation estimation.....................................................................................................10
4.1.2.2 Screening tests.......................................................................................................................10
4.1.2.3 Simulation tests .....................................................................................................................10
4.1.3 Summary and discussion of persistence ..............................................................................................10
4.2 Environmental distribution .............................................................................................................................10
4.2.1 Adsorption/desorption.........................................................................................................................10
4.2.2 Volatilisation .......................................................................................................................................10
4.2.3 Distribution modelling ........................................................................................................................10
4.3 Bioaccumulation.............................................................................................................................................10
4.3.1 Aquatic bioaccumulation.....................................................................................................................10
4.3.1.1 Bioaccumulation estimation ..................................................................................................10
4.3.1.2 Measured bioaccumulation data............................................................................................10
4.3.2 Terrestrial bioaccumulation.................................................................................................................10
4.3.3 Summary and discussion of bioaccumulation .....................................................................................10
4.4 Secondary poisoning ......................................................................................................................................10
5 HUMAN HEALTH HAZARD ASSESSMENT ....................................................................................................11
5.1 Toxicokinetics (absorption, metabolism, distribution and elimination) .........................................................11
5.2 Acute toxicity .................................................................................................................................................11
5.2.1 Acute toxicity: oral..............................................................................................................................11
5.2.2 Acute toxicity: inhalation ....................................................................................................................11
5.2.3 Acute toxicity: dermal .........................................................................................................................11
5.2.4 Acute toxicity: other routes .................................................................................................................11
5.2.5 Summary and discussion of acute toxicity ..........................................................................................11
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ANNEX XV ?IDENTIFICATION OF SVHC FORMAT BBP
5.3 Irritation..........................................................................................................................................................11
5.4 Corrosivity......................................................................................................................................................11
5.5 Sensitisation....................................................................................................................................................11
5.6 Repeated dose toxicity....................................................................................................................................11
5.6.1 Repeated dose toxicity: oral ................................................................................................................11
5.6.2 Repeated dose toxicity: inhalation ......................................................................................................11
5.6.3 Repeated dose toxicity: dermal ...........................................................................................................11
5.6.4 Other relevant information ..................................................................................................................11
5.6.5 Summary and discussion of repeated dose toxicity:............................................................................11
5.7 Mutagenicity...................................................................................................................................................12
5.7.1 In vitro data .........................................................................................................................................12
5.7.2 In vivo data..........................................................................................................................................12
5.7.3 Human data .........................................................................................................................................12
5.7.4 Other relevant information ..................................................................................................................12
5.7.5 Summary and discussion of mutagenicity...........................................................................................12
5.8 Carcinogenicity...............................................................................................................................................12
5.8.1 Carcinogenicity: oral ...........................................................................................................................12
5.8.2 Carcinogenicity: inhalation .................................................................................................................12
5.8.3 Carcinogenicity: dermal ......................................................................................................................12
5.8.4 Carcinogenicity: human data...............................................................................................................12
5.8.5 Other relevant information ..................................................................................................................12
5.8.6 Summary and discussion of carcinogenicity .......................................................................................12
5.9 Toxicity for reproduction ...............................................................................................................................12
5.9.1 Effects on fertility................................................................................................................................12
5.9.2 Developmental toxicity .......................................................................................................................12
5.9.3 Human data .........................................................................................................................................12
5.9.4 Other relevant information ..................................................................................................................12
5.9.5 Summary and discussion of reproductive toxicity ..............................................................................14
5.10 Other effects ...................................................................................................................................................15
5.11 Derivation of DNEL(s) or other quantitative or qualitative measure for dose response ................................15
5.11.1 Overview of typical dose descriptors for all endpoints .......................................................................15
5.11.2 Correction of dose descriptors if needed (for example route-to-route extrapolation) .........................15
5.11.3 Application of assessment factors .......................................................................................................15
5.11.4 Selection/ identification of the critical DNEL(s)/ the leading health effect ........................................15
6 HUMAN HEALTH HAZARD ASSESSMENT OF PHYSICO-CHEMICAL PROPERTIES..............................16
7 ENVIRONMENTAL HAZARD ASSESSMENT..................................................................................................17
7.1 Aquatic compartment (including sediment) ...................................................................................................17
7.1.1 Toxicity test results .............................................................................................................................19
7.1.1.1 Fish........................................................................................................................................19
Short-term toxicity to fish .....................................................................................................19
Long-term toxicity to fish .....................................................................................................19
7.1.1.2 Aquatic invertebrates ............................................................................................................19
Short-term toxicity to aquatic invertebrates ..........................................................................19
Long-term toxicity to aquatic invertebrates ..........................................................................19
7.1.1.3 Algae and aquatic plants .......................................................................................................19
7.1.1.4 Sediment organisms ..............................................................................................................19
7.1.1.5 Other aquatic organisms........................................................................................................19
7.1.2 Calculation of Predicted No Effect Concentration (PNEC) ................................................................19
7.1.2.1 PNEC water...........................................................................................................................19
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BBP ANNEX XV ?IDENTIFICATION OF SVHC FORMAT
7.1.2.2 PNEC sediment .....................................................................................................................19
7.2 Terrestrial compartment .................................................................................................................................19
7.2.1 Toxicity test results .............................................................................................................................19
7.2.1.1 Toxicity to soil macro organisms ..........................................................................................19
7.2.1.2 Toxicity to terrestrial plants ..................................................................................................19
7.2.1.3 Toxicity to soil micro-organisms ..........................................................................................19
7.2.1.4 Toxicity to other terrestrial organisms ..................................................................................19
Toxicity to birds ....................................................................................................................19
Toxicity to other above ground organisms............................................................................19
7.2.2 Calculation of Predicted No Effect Concentration (PNEC_soil) ........................................................19
7.3 Atmospheric compartment..............................................................................................................................19
7.4 Microbiological activity in sewage treatment systems ...................................................................................19
7.4.1 Toxicity to aquatic micro-organisms...................................................................................................20
7.4.2 PNEC for sewage treatment plant .......................................................................................................20
7.5 Calculation of Predicted No Effect Concentration for secondary poisoning (PNEC_oral)............................20
7.6 Conclusion on the environmental classification and labelling .......................................................................20
8 PBT, VPVB AND EQUIVALENT LEVEL OF CONCERN ASSESSMENT ......................................................21
8.1 Comparison with criteria from annex XIII .....................................................................................................21
8.2 Assessment of substances of an equivalent level of concern..........................................................................21
8.3 Emission characterisation ...............................................................................................................................21
8.4 Conclusion of PBT and vPvB or equivalent level of concern assessment .....................................................21
INFORMATION ON USE, EXPOSURE, ALTERNATIVES AND RISKS ..............................................................22
1 INFORMATION ON EXPOSURE ........................................................................................................................22
2 INFORMATION ON ALTERNATIVES...............................................................................................................38
2.1 Alternative substances ....................................................................................................................................38
2.2 Alternative techniques ....................................................................................................................................40
3 RISK-RELATED INFORMATION .......................................................................................................................40
OTHER INFORMATION ............................................................................................................................................45
REFERENCES .............................................................................................................................................................46
TABLES
Table 1: Summary of physico- chemical properties, from EU RAR (2007) ................................................................ 9
Table 2: Concentration of BBP [礸/l] in the influent of Austrian STPs.......................................................................25
Table 3: Concentration of BBP [礸/l] in the effluent of Austrian STPs ......................................................................25
Table 4: Concentration of BBP [mg/kg dwt] in sewage sludge ........................................................................................... 27
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ANNEX XV ?IDENTIFICATION OF SVHC FORMAT BBP
Table 5: Concentration of BBP [礸/kg dwt 105癈] in biota (fish)................................................................................................... 29
Table 6: Concentration of BBP [mg/kg] articles of daily use......................................................................................30
Table 7: Concentration of BBP [mg/kg] in house dust................................................................................................31
Table 8: Concentration of BBP [ng/l] in groundwater.................................................................................................33
Table 9: Summary of exposure levels in the production of BBP (Scenario 1) ............................................................36
Table 10: Summary of exposure levels for the industrial use of BBP-containing products (Scenario 2)....................36
Table 11: Summary of exposure levels for the professional end-use of semi- and end products containing BBP
(Scenario 3)..................................................................................................................................................................37
Table 12: Internal exposure to BBP for consumers .....................................................................................................38
Table 13: Estimated daily human intake of BBP through environmental exposure ....................................................38
Table 14: Estimated daily human intake of BBP at regional levels.............................................................................39
Table 15: Combined exposure to BBP ........................................................................................................................39
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BBP ANNEX XV ?IDENTIFICATION OF SVHC FORMAT
PROPOSAL FOR IDENTIFICATION OF A SUBSTANCE AS A
CMR CAT 1 OR 2, PBT, VPVB OR A SUBSTANCE OF AN
EQUIVALENT LEVEL OF CONCERN
Substance Name: benzyl butyl phthalate
EC Number: 201-622-7
CAS number: 85-68-7
? It is proposed to identify the substance as a CMR according to Article 57 (c).
Summary of how the substance meets the CMR (Cat 1 or 2), PBT or vPvB criteria, or is
considered to be a substance of an equivalent level of concern
BBP is classified according to Directive 67/548/EEC as
Repr. Cat. 2; R 61
Repr. Cat. 3; R 62
N; R 50-53
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ANNEX XV ?IDENTIFICATION OF SVHC FORMAT BBP
Registration number(s) of the substance or of substances containing the substance:
Not available.
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BBP ANNEX XV ?IDENTIFICATION OF SVHC FORMAT
JUSTIFICATION
1 IDENTITY OF THE SUBSTANCE AND PHYSICAL AND CHEMICAL
PROPERTIES
1.1 Name and other identifiers of the substance
Benzyl butyl phthalate
Chemical Name:
Benzyl butyl phthalate
EC Name:
85-68-7
CAS Number:
Benzyl butyl phthalate
IUPAC Name:
1.2 Composition of the substance (from EU RAR (2007))
Chemical Name: Benzyl butyl phthalate
EC Number: 201-622-7
CAS Number: 85-68-7
IUPAC Name: Benzyl butyl phthalate
Molecular Formula: C19H20O4
Structural Formula:
Molecular Weight: 312,35
Typical concentration (% w/w): Degree of purity > 98.5 % (w/w)
Concentration range (% w/w): -
Identity and percentage (w/w) of < 1.0% dibenzyl phthalate (CAS No. 523-31-9)
< 0.5% benzyl benzoate (CAS No. 120-51-4)
impurities:
< 0.5% dibutyl phthalate (CAS No. 84-74-2)
< 2 ppm -clorotoluen (CAS No. 100-44-7)
< 2 ppm --diclorotoluen (CAS No. 98-87-3)
< 0.5 ppm pentaerythritol tetrakis (3-(3,5-di-tert-butyl-4-
Additives
hydoxyphenyl)propionate.
(CAS No. 6683-19-8)
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ANNEX XV ?IDENTIFICATION OF SVHC FORMAT BBP
1.3 Physico-chemical properties
Table 1: Summary of physico- chemical properties, from EU RAR (2007)
REACH ref Property IUCLID Value [enter
Annex, ? section comment/reference
or delete column]
VII, 7.1 Physical state at 20癈 and 3.1 liquid
101.3 kPa
VII, 7.2 Melting/freezing point 3.2 <-35癈 Monsanto internal
data
VII, 7.3 Boiling point 3.3 370癈 at 10.10 hPa Bayer AG MSDS
VII, 7.5 Vapour pressure 3.6 0.00112 Pa at 20癈 Hoyer and Peperle
(1957)
VII, 7.7 Water solubility 3.8 2.8 mg/l
VII, 7.8 Partition coefficient n- 3.7 Log Kow 4.84
octanol/water (log value) partition
coefficient
IX, 7.16 Dissociation constant 3.21
2 MANUFACTURE AND USES
Not relevant for this type of dossier.
3 CLASSIFICATION AND LABELLING
3.1 Classification in Annex I of Directive 67/548/EEC
BBP was inserted into Annex I of Directive 67/548/EEC with the 29. ATP ( 2004/73/EC) and is
classified as follows:
Index: Number: 607-430-00-3
Repr. Cat. 2; R 61
Repr. Cat. 3; R 62
N; R 50-53
Specific concentration limits: none
Labelling:
Symbols: T; N
R-Phrases: 61-62-50/53
S-Phrases: 53-45-60-61
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BBP ANNEX XV ?IDENTIFICATION OF SVHC FORMAT
3.2 Self classification(s)
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ANNEX XV ?IDENTIFICATION OF SVHC FORMAT BBP
4 ENVIRONMENTAL FATE PROPERTIES
4.1 Degradation
4.1.1 Stability
Corresponds to IUCLID 4.1
4.1.2 Biodegradation
4.1.2.1 Biodegradation estimation
4.1.2.2 Screening tests
4.1.2.3 Simulation tests
4.1.3 Summary and discussion of persistence
4.2 Environmental distribution
4.2.1 Adsorption/desorption
Corresponds to IUCLID 4.4.1
4.2.2 Volatilisation
Corresponds to IUCLID 4.4.2
4.2.3 Distribution modelling
4.3 Bioaccumulation
4.3.1 Aquatic bioaccumulation
4.3.1.1 Bioaccumulation estimation
4.3.1.2 Measured bioaccumulation data
4.3.2 Terrestrial bioaccumulation
4.3.3 Summary and discussion of bioaccumulation
4.4 Secondary poisoning
Assessment of the potential for secondary poisoning
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BBP ANNEX XV ?IDENTIFICATION OF SVHC FORMAT
5 HUMAN HEALTH HAZARD ASSESSMENT
5.1 Toxicokinetics (absorption, metabolism, distribution and elimination)
5.2 Acute toxicity
5.2.1 Acute toxicity: oral
5.2.2 Acute toxicity: inhalation
5.2.3 Acute toxicity: dermal
5.2.4 Acute toxicity: other routes
5.2.5 Summary and discussion of acute toxicity
C&L including weight-of-evidence considerations.
5.3 Irritation
Not relevant for this type of dossier.
5.4 Corrosivity
Not relevant for this type of dossier.
5.5 Sensitisation
Not relevant for this type of dossier.
5.6 Repeated dose toxicity
5.6.1 Repeated dose toxicity: oral
5.6.2 Repeated dose toxicity: inhalation
5.6.3 Repeated dose toxicity: dermal
5.6.4 Other relevant information
5.6.5 Summary and discussion of repeated dose toxicity:
C&L, dose-response estimation including weight-of-evidence considerations.
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ANNEX XV ?IDENTIFICATION OF SVHC FORMAT BBP
5.7 Mutagenicity
5.7.1 In vitro data
5.7.2 In vivo data
5.7.3 Human data
5.7.4 Other relevant information
5.7.5 Summary and discussion of mutagenicity
C&L, dose-response estimation including weight-of-evidence considerations.
5.8 Carcinogenicity
5.8.1 Carcinogenicity: oral
5.8.2 Carcinogenicity: inhalation
5.8.3 Carcinogenicity: dermal
5.8.4 Carcinogenicity: human data
5.8.5 Other relevant information
5.8.6 Summary and discussion of carcinogenicity
C&L, dose-response estimation including weight-of-evidence considerations.
5.9 Toxicity for reproduction
5.9.1 Effects on fertility
5.9.2 Developmental toxicity
5.9.3 Human data
5.9.4 Other relevant information
Endocrine effects of BBP
Endocrine activity has been assessed in various in vitro and in vivo studies on BBP and its most
important metabolites MBeP (mono-benzyl-phthalate) and MBuP (mono-n-butyl-phthalate) as
described in the EU RAR, 2007:
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BBP ANNEX XV ?IDENTIFICATION OF SVHC FORMAT
Estrogenicity
A potential estrogen activity of BBP and the major BBP metabolites MBuP and MBeP has been
investigated in both in vitro and in vivo studies. The in vitro studies include a recombinant yeast
screen assay, an estrogen-receptor (ER) competitive ligand binding assay, mammalian- and yeast-
based gene expression assays and an estrogen-dependent cell proliferation assay. In these assays
only a weak estrogen activity at high concentrations of BBP (10-100 M) was reported. In the same
assays the positive control E2 (17?estradiol) was approximately 104 to 106 more potent than BBP.
The metabolites MBuP and MBeP did not exhibit estrogenic activity in a recombinant yeast screen
assay. The estrogenic activity of BBP and its major metabolites were studied in standard in vivo
uterotrophic assays. In these studies BBP and MBuP did not possess the potential to promote
uterine growth in immature female rats exposed orally to BBP (up to 2,240 mg/kg bw/day) or
subcutaneous to BBP (up to 5,000 mg/kg bw/day), whereas, MBeP caused a significant reduction in
absolute and relative uterine weight at 500 and 1,000 mg/kg bw/day, which was most probably due
to systemic toxicity. Furthermore only weak estrogenic activity of BBP was concluded in a study
that investigated the expression of estrogen regulated mRNAs in the hypothalamus, preoptic area
and pituitary.
Anti-androgenicity
BBP was shown in one in vitro study to be a potent anti-androgen in yeast cells expressing the
androgen receptor. Nine in vivo studies are available which indicate an anti-androgen-like activity
of BBP or its major metabolites MBuP and MBeP in rats (Piersma et al., 2000; Gray et al., 2000;
Parks et al., 1999; Imajima et al., 1997; Shono et al., 2000; Nagao et al., 2000; Tyl et al., 2004; Ema
et al., 2002; Ema et al., 2003, all cited in EU RAR). Effects reported in the Piersma et al. (2000)
study included a reduction in testicular weight in offspring, and effects on testicular migration from
270 mg/kg bw/day and 580 mg/kg bw/day after in utero exposure to BBP from gestation day 6 to
20. In the Gray et al. (2000) study malformations in the reproductive organs in 84% of male
offspring (approximately 90 days of age) exposed to 750 mg/kg bw/day BBP from gestation day 14
through postnatal day 2 were reported. Furthermore in the Gray et al. (2000) and Parks et al. (1999)
studies a reduced AGD and testis weight in males at day 2 of age, and males with areolas at day 13
of age were reported. In the Imajima et al. (1997) study and the Shono et al. (2000) study testicular
descendent was studied, which is under androgenic control. In this study the testis were located
significantly higher in the abdominal cavity on gd 20 offspring compared to control rats exposed in
utero to MBuP from gd 15-18. Furthermore, in the Imajima et al. (1997) study, on pnd 30-40
cryptorchidism was reported in 84.6% of the exposed offspring, compared to 0% in the control
group. In the study by Ema et al. (2002) in utero exposure to 500 and 1,000 mg/kg BBP on gd 15-
17 induced a significant decrease in the AGD and a significant increase in the incidence of
undescended testis. In the study by Ema et al. (2003) in utero exposure to MBeP on gd 15-17 was
shown to induce a significant decrease in AGD and a significant increase in the incidence of
undescended testis. In the study by Nagao et al. (2000) a decrease in the weight of the testis,
epididymis, and seminal vesicle, and tubular atrophy and decreased germinal epithelium was
reported in F1 male offspring exposed to 500 mg/kg bw/day BBP during gestation and lactation and
evaluated at weaning or after puberty. Furthermore, a decrease in AGD was reported in male
offspring in the 500 mg/kg bw/day dose group, which is a sensitive indicator of anti-androgen
activity. In the Tyl et al. (2004) study a dose-related decrease in absolute and adjusted AGD was
reported in F1 and F2 male pups from 250 mg/kg bw/day. Furthermore, at 750 mg/kg bw/day in F1
and F2 offspring a significant decrease in reproductive organ weights, and a significant increase in
the percentage of males with reproductive tract malformations were reported.
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ANNEX XV ?IDENTIFICATION OF SVHC FORMAT BBP
An association between prenatal and postnatal exposure to phthalates and whether the exposure had
any influence on reproductive organ development in newborn boys was studied in two
epidemiological studies. In the study by Swan et al. (2005, cited in EU RAR) an association
between maternal exposures to BBP as well as other phthalates and AGI in boys was reported.
When comparing boys with prenatal MBeP (monobenzyl phthalate, reflecting exposure to BBP)
exposure the odds ratio for a shorter AGI was 3.8. For the other monoester phthalates the odds ratio
were 10.2 for MBuP (reflecting exposure to DBP), 4.7 for MEP (reflecting exposure to DEP), and
9.1 for MiBP (reflecting exposure to DINP) (all p-values < 0.05).
In the study by Main et al. (2005, cited in EU RAR) no association was found between phthalate
monoester levels (MEP, MMP, MBuP, MBeP, MINP and MEHP) in breast milk and
cryptorchidism in newborn boys. However, a significant association was found between intake of
milk contaminated with phthalates (MEP, MBuP, MMP and MINP) and postnatal surge of
reproductive hormones (SHBG, LH, testosterone and inhibin B) in newborn boys. As regards the
monoester metabolite of BBP, MBeP the tendencies were similar, however, they were not
statistically significant. These data support the hypothesis that prenatal phthalate exposure at
environmental levels may affect male reproductive development in humans. However, due to the
small sample size, (85 boys in Swan et al., 2005 and 130 boys in Main et al., 2005) further studies
with larger sample size have to be performed before clear conclusions can be drawn from these
studies.
The following study was published after publication of the EU RAR:
Hauser et al. (2006) reported altered semen quality in relation to urinary concentrations of phthalate
monoester and oxidative metabolites in humans. Semen from 463 male partners of subfertile
couples was investigated and dichotomized according WHO reference values for sperm
concentration and motility as well as the Tygberg Kruger Strict criteria for morphology. Results
were adjusted for age, abstinence time and smoking status. MBeP (mono-benzyl-phthalate) was
found in 94% of the samples. There was suggestive evidence of an association between the highest
MBeP quartile with low sperm concentration (Hauser et al., 2006).
5.9.5 Summary and discussion of reproductive toxicity
BBP has been assessed for potential toxic effects on fertility, reproductive organs, development, and
endocrine activity. It is found to adversely affect the reproductive organs in experimental animal
studies which may affect fertility. Furthermore, the substance is found to be a developmental
toxicant. This is reflected in the classification as Repr.Cat. 3; R 62 and Repr.Cat. 2; R 61
according to Directive 67/548/EEC.
BBP impairs the foetal development and causes malformations in rats and mice. A dose-related
significant reduction in absolute and adjusted anogenital distance index (AGI) in both F1 and F2
offspring from 250 mg/kg bw /day was observed in rats. At 750 mg/kg bw / day a significant
increase in F1 and F2 male pups with one or more nipples and/or areolae was reported. The
NOAEL for maternal toxicity was 750 mg/kg bw/day (Tyl et al., 2004, cited in EU RAR).
The results of several in vivo studies indicate an anti-androgen-like activity of BBP or its major
metabolites in rats following in utero exposure. Effects reported in the studies included a decreased
AGI, increases in male offspring with reproductive tract malformations, as well as effects on
testicular migration (EU RAR, 2007).
In studies commissioned by DG Environment of the European Commission a list of 146 substances
with endocrine disruption properties have been established (http://ec.europa.eu/environment/
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BBP ANNEX XV ?IDENTIFICATION OF SVHC FORMAT
docum/pdf/bkh_annex_13.pdf). BBP has been classified as Cat. 3 for wildlife, Cat. 1 for Humans
and Combined as Cat. 1 (Cat.1: Evidence for endocrine disruption in living organisms; Cat. 2:
Evidence of potential to cause endocrine disruption; Cat.3: No evident scientific basis). BBP is also
listed in a list of 66 potentially endocrine substances with classification of high exposure concern
(http://ec.europa.eu/ environment/docum/pdf/bkh_annex_15.pdf) (EUROPEAN COMMISSION
DG ENV, 2000).
It is stated in the draft risk reduction strategy (April 2007) that BBP may be subjected to the
authorisation system. In the OSPAR convention BBP is put on the list of substances for priority
action. In the OSPAR Convention it is stated that BBP is a potential endocrine substance.
5.10 Other effects
5.11 Derivation of DNEL(s) or other quantitative or qualitative measure for dose response
5.11.1 Overview of typical dose descriptors for all endpoints
5.11.2 Correction of dose descriptors if needed (for example route-to-route extrapolation)
5.11.3 Application of assessment factors
5.11.4 Selection/ identification of the critical DNEL(s)/ the leading health effect
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ANNEX XV ?IDENTIFICATION OF SVHC FORMAT BBP
6 HUMAN HEALTH HAZARD ASSESSMENT OF PHYSICO-CHEMICAL
PROPERTIES
Not relevant for this type of dossier.
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BBP ANNEX XV ?IDENTIFICATION OF SVHC FORMAT
7 ENVIRONMENTAL HAZARD ASSESSMENT
7.1 Aquatic compartment (including sediment)
There have been suggestions of estrogenic and anti-androgenic effects caused by BBP in fish.
Following recent development of draft testing protocols for endocrine disruption in fish, more data
has become available.
Estrogenicity
In an early study BBP was found to be weakly estrogenic (Jobling et al., 1995, cited in EU RAR).
BBP at a concentration of approximately 0.01 ?10 mg/l reduced in vitro binding of natural
estrogen, 17-estradiol, to the rainbow trout estrogen receptor by about 40-60%. Furthermore, the
EU RAR (2007) refers to a study performed by Christiansen et al. (2000) who injected rainbow
trout intraperitoneally with different compounds. BBP was found to cause significant induction of
vitellogenin in vivo, but was a weaker inducer than e.g. bisphenol A. In further injection studies
with juvenile rainbow trout, no induction of the estrogen receptor was observed at an exposure
concentration of 50 mg/kg BBP, but both 5 and 50 mg/kg significantly lowered plasma levels of
eggshell proteins (Knudsen et al., 1998 cited in EU RAR), indicating an inhibition of synthesis of
these proteins. Similarly, Knudsen and Pottinger (1998, cited in EU RAR) found that BBP would
bind to the estrogen receptor, but only at high concentrations. There was no apparent binding of
BBP to corticosteroid or testosterone receptors in that study. Work performed by Gimeno (at this
time at TNO, The Netherlands) on the possible estrogenic effects of BBP on sexual differentiation
in all-male carp did not indicate any effects of BBP (Gimeno, pers.comm. cited in EU RAR).
Results for estrogenicity indicate that BBP may be estrogenic at high concentrations.
Harries et al. (2000, cited in EU RAR) exposed fish to BBP (100 g/l) and nonylphenol (1, 10 and
100 g/l). Breeding pairs were exposed for 3 weeks during which reproductive performance was
monitored. Endpoints were number of spawnings, number of eggs and size of eggs. At the end of
the exposure period plasma vitellogenin and gonadosomatic index was determined. In addition,
secondary sexual characteristics in male were quantified (growth of tubercles and thickness of
dorsal fat pad). While nonylphenol caused dose-dependent estrogenic effects down to 10 g/l, no
effects were seen following BBP exposure.
Anti-androgenicity
The EU RAR (2007) furthermore refers to studies suggesting that BBP may be anti-androgenic.
These observations have been derived from mammalian studies (e.g. Zacharewski et al., 1998) as
well as an in vitro study conducted by Sohoni and Sumpter (1998). BBP has been found to be an as
potent anti-androgen as the model substance used for that purpose, flutamide. Unfortunately there is
no established model to ascertain anti-androgenicity in fish. The Harries et al. (2000) study was not
specifically designed to detect anti-androgenicity (e.g. through concomitant exposure to anti-
androgens). Therefore, the lack of response following BBP exposure in this study does not disprove
earlier suggestions that this phthalate may be anti-androgenic to wildlife. Recently, Ankley et al.
(2004) provided in vitro support for using fathead minnow to identify anti-androgenic effects, but it
is still necessary to establish such effects in vivo.
There is work ongoing within the OECD to establish appropriate test systems for endocrine
disrupting effects. The test systems are expected to include a study in fish that will include
endpoints relevant to estrogenic, androgenic, anti-estrogenic and anti-androgenic effects. The tests
performed with BBP referred to above have not incorporated the aspect of transfer from parent to
offspring included in the current test requirements for BBP. An agreement was reached with
17
ANNEX XV ?IDENTIFICATION OF SVHC FORMAT BBP
Industry to perform a partial life cycle study that was a combination of the two OECD
recommended "tier 2 tests" for assessing possible endocrine disruption effects of chemicals in fish.
The test is a combination of the so-called pair-breeding test in which egg production and
hatchability of eggs from a breeding pair of Fathead minnow is assessed and an enhanced early life
stage test in which exposure of the eggs from the pair breeding test is continued for sufficient time
to enable sexual differentiation of the offspring. Exposure concentrations should be 25 and 100 g/l.
After some pre-dosing trials a definite study with the pair breeding phase was attempted in March
2002. This study was aborted on day 47 because measured BBP concentrations in the exposure
vessels were always below the nominal concentrations and appeared to decline throughout the
study. In the nominal 25 g/l exposure tanks mean concentration on day 32 was 20 g/l and by day
47 the mean concentration had declined to 14 g/l (56% of nominal). In the nominal 100 g/l
exposure tanks mean concentration on day 32 was 72 g/l and by day 47 the mean concentration
had declined to 59 g/l (59% of nominal). Industry has performed a number of additional trials in
order to investigate the optimal conditions for performing a chronic fish test. The trials included
variable use of solvent, variable delivery systems and variable flow rates. These trials have
indicated that it will not be possible to obtain a stable test concentration > 80% of the nominal BBP
concentration as required according to the test guidelines. Apparently a plateau level could not be
obtained either. Very high flow rates were also tested (residence time 1-1.15 hour) without attaining
the required concentration level, although it seemed that a fairly stable level was achieved at about
50% of nominal. The industry report concluded that the reason for these problems was the
biodegradation of BBP to its primary biodegradation products (monobutyl-phthalate and
monobenzyl-phtalate) and that these metabolites were also rapidly degraded within this test system.
It should however be pointed out that other factors cannot be excluded like adsorption to the test
system and that some solubility problems as reported may also be part of the problem. The technical
difficulties described above have been reported to the Technical Meeting. However, the TM (cf.
minutes of TM II `03) "generally supported the request to industry to perform the endocrine effect
test. The TM realised that the results would not meet the ideal test requirements, but would accept
that in this particular case.
In the risk assessment report (EU-RAR, 2007) BBP is considered as a suspected endocrine
disruptor. It was concluded that further information is needed concerning reproductive toxicity and
endocrine effects in fish. A long term fish study on reproductive and endocrine effects has to be
performed and therefore the PNECaquatic (7.5 礸/l wwt) has to be seen provisional. From informal
contacts with the rapporteur (Norway) information was received that the long term fish study has
been conducted, but still needs to be reviewed in detail. In the OSPAR Convention it is stated that
BBP is a potential endocrine substance and BBP is put on the list of substances for priority action.
18
BBP ANNEX XV ?IDENTIFICATION OF SVHC FORMAT
7.1.1 Toxicity test results
7.1.1.1 Fish
Short-term toxicity to fish
Long-term toxicity to fish
7.1.1.2 Aquatic invertebrates
Short-term toxicity to aquatic invertebrates
Long-term toxicity to aquatic invertebrates
7.1.1.3 Algae and aquatic plants
7.1.1.4 Sediment organisms
7.1.1.5 Other aquatic organisms
7.1.2 Calculation of Predicted No Effect Concentration (PNEC)
7.1.2.1 PNEC water
7.1.2.2 PNEC sediment
7.2 Terrestrial compartment
7.2.1 Toxicity test results
7.2.1.1 Toxicity to soil macro organisms
7.2.1.2 Toxicity to terrestrial plants
7.2.1.3 Toxicity to soil micro-organisms
7.2.1.4 Toxicity to other terrestrial organisms
Toxicity to birds
Toxicity to other above ground organisms
7.2.2 Calculation of Predicted No Effect Concentration (PNEC_soil)
7.3 Atmospheric compartment
7.4 Microbiological activity in sewage treatment systems
19
ANNEX XV ?IDENTIFICATION OF SVHC FORMAT BBP
7.4.1 Toxicity to aquatic micro-organisms
7.4.2 PNEC for sewage treatment plant
7.5 Calculation of Predicted No Effect Concentration for secondary poisoning
(PNEC_oral)
7.6 Conclusion on the environmental classification and labelling
20
BBP ANNEX XV ?IDENTIFICATION OF SVHC FORMAT
8 PBT, VPVB AND EQUIVALENT LEVEL OF CONCERN ASSESSMENT
8.1 Comparison with criteria from annex XIII
8.2 Assessment of substances of an equivalent level of concern
Endocrine disrupting effects of BBP have been shown in various studies. These are summarised in
Sections 5.9 and 7.1.
8.3 Emission characterisation
8.4 Conclusion of PBT and vPvB or equivalent level of concern assessment
21
ANNEX XV ?IDENTIFICATION OF SVHC FORMAT BBP
INFORMATION ON USE, EXPOSURE, ALTERNATIVES AND
RISKS
1 INFORMATION ON EXPOSURE
1.1 Production volumes
As described in the EU RAR (2007) production of BBP has decreased during the last years. In the
period 1994-1997 there were 3 producers of BBP in the EU. Reported production in this period was
45,000 tonnes/annum, with approximately 9,000 tonnes/annum being exported outside the EU.
This resulted in a total use in the EU of 36,000 tonnes/annum. For the year 2004 industry has
estimated that 19,500 tonnes of BBP are used within the EU. Only the total production volume is
given and it was not further specified how much BBP is produced at the respective sites. According
to predictions from industry, BBP consumption is further decreasing during the ongoing year 2005.
However, these figures are confidential because one producer stopped production in 2005, and there
are only two producers left and no information is available on which producer stopped production.
For the year 2003 the substance flow of BBP (as raw material and in chemical products) in Sweden
is reported in the Swedish Product Register with a total amount of 643 tonnes.
1.2 Information on uses
Based on information from 1997 the substance was mainly used (more than 95%) as a plasticizer
(softener) of PVC or other polymers in the European Community. In 2004 the main use of BBP
(about 60%) is as a softener (plasticizer) in PVC products, with flooring as the largest single use
category (41% of the total use volume). BBP is also used with other polymers in e.g. sealants,
(polysulfide based, polyurethane based or acrylic-based), adhesives (based on polyacrylics and
polyvinylacetate), paints (e.g based on polyurethane and polyacrylics), inks and lacquers (based on
acrylics, nitrocellulose and vinyl resins). For 2004 it is known that about 8,000 tonnes/annum of the
total BBP production (19,500 tonnes/annum) is used in flooring and about 6,000 tonnes/annum in
sealants while the remaining 5,500 tonnes/annum are not further specified. In 1997 industry
submitted detailed figures for all the respective use patterns. The total sum in 1997 for all the use
patterns together, except for flooring and sealants, was 5,400 tonnes/annum ("miscellaneous" in
1997). The tonnage for "miscellaneous" in 2004 (5,500 tonnes) is nearly the same as in 1997 and
therefore it is assumed that the tonnages for all the separate uses in the "miscellaneous" categories
in 2004 are the same as in 1997. Consumer products such as sealants, adhesives, car care products,
and cosmetics may contain BBP. A relatively small use is in the food wrap or food packaging area,
which has diminished over recent years due to technological developments leading to no further
requirement for BBP in one of the food wrap applications (i.e. regenerated cellulose film). The use
of BBP in adhesives and cosmetics has also decreased during the recent years. Furthermore, BBP
has been reported at low concentrations in baby equipment and children toys; however, in these
products BBP probably occurs as byproducts/impurities and have not been added intentionally to
the products. A recent Swedish survey on phthalates in cosmetic products in Europe
(http://www.noharm.org/library/docs/Pretty_Nasty.pdf) confirms that BBP occurs in very few
products and only in trace amounts. Information about BBP in products is based on a Norwegian
survey on chemical products containing BBP in 1996 (SFT report 96:21, 1996, as cited in EU
RAR). The total amount of BBP corresponded to about 50 tonnes/a in Norway, split into 12 tonnes
in consumer products and 38 tonnes in products for occupational use in 1996 (SFT report 96:21,
22
BBP ANNEX XV ?IDENTIFICATION OF SVHC FORMAT
1996). The Nordic database SPIN (substances in preparations in Nordic countries,
http://www.spin2000.net/spin.html) provides data on the use of chemical substances in Denmark,
Finland, Sweden and Norway from the year 2000. Most recent data on total use show a decline of
BBP in the Nordic countries apart from Sweden. In Sweden 600 ?100 tonnes/annum were used
between 2000 and 2003, but an increase up to 820 tonnes/annum was registered for 2004. In
Norway a clear decline from 63 tonnes/annum in 2000 to 13 tonnes/annum in 2004 was registered.
The same trend is seen in Denmark, where the total number of products was 440 accounting for 881
tonnes/annum in 1998 compared to 93 tonnes/annum in 2004. Despite of the reduction in uses, the
data show that the substance exhibits a pattern of wide dispersive use (EU RAR 2007).
A number of 119 products containing BBP were reported to the Swedish Product Register for the
year 2005, of which 31 products are consumer products. The main product types are fillers, binders
in plastics, paint and adhesives. Furthermore, although the total amount of BBP imported (as raw
material and in chemical products) decreases between 1993 and 2005, the number of registered
products containing the substance increases more or less continuously from 52 (year 1993) to 159
(year 2005) (Swedish Product Register, as cited in EU RAR).
1.3 Information on exposure ?Environmental monitoring data
The main focus within this section is to present Austrian monitoring data which demonstrate the
wide distribution of BBP in various environmental compartments. These data are also compared to
other European monitoring data. For this purpose the risk assessment report (EU RAR 2007) and
new literature was used. New studies which have not been included in the risk assessment report
have been taken into account in this dossier.
Products available for consumers such as sealants, adhesives, car care products and food wrapping
material may contain BBP. BBP has also been reported at low concentrations in baby equipment
and children toys; however, in these products BBP occurs as by products/impurities and have not
been added intentionally to the products. The main routes of occupational exposure are by
inhalation and dermal contact. Ingestion is not considered to be relevant for occupational exposure.
The marketing and use of BBP and preparations containing BBP in toys and childcare articles is
prohibited through the 22nd amendment to the Directive 76/769/EEC on the marketing and use of
certain substances and preparations.
Measured concentrations of BBP in surface water, groundwater, influent and effluent of wastewater
treatment plants, sewage sludge, soil, biota and articles (e.g. toys) of daily use and house dust are
summarized in Tables 2 to 8.
As phthalates occur in plastics used in laboratories and sample collectors, contamination may
sometimes lead to false positive results. There is only little information available in older reports on
how such contamination had been avoided. More recent measurements are less affected by such
contamination problems. Data (Tables 2 to 8) presented within this dossier are of high quality and
ensure avoidance of contamination due to various precautionary measures (e.g. using glassware,
pre-treatment of glassware using solvents and heating, analysing blank values).
Mean values and median values are calculated by the so called minimum approach. More than 50%
of individual analysed values need to exceed the limit of quantification (LOQ) to calculate a median
or mean. Values below the limit of detection (LOD) were set to 0 for the statistical analyses and
values below the LOQ were set to LOQ.
23
ANNEX XV ?IDENTIFICATION OF SVHC FORMAT BBP
1.3.1. Compartments with positive findings of BBP
1.3.1.1. Measured concentrations of BBP in the influent and effluent of wastewater treatment
plants
BBP concentrations in the influent/effluent of sewage treatment plants (STPs) are presented in
Table 2 and Table 3. In the influent BBP was detected in concentrations up to 3.2 礸/l. The number
of positive findings varied between 6% and 100%. It should be noted, that the BBP concentration in
the influent depends on various factors such as the percentage of industrial discharges, weather
conditions or population equivalents.
Table 2: Concentration of BBP [礸/l] in the influent of Austrian STPs
Date No. No. of LOD LOQ Min. inf Max. inf Median Mean Ref.
measure positive inf inf inf inf
minimum minimum
d values findings
approach approach
[%] *
Nov. 0.07 ? unpublished
07 16 68.8% 0.28 0.25 - 1 n.d. 3.2 0.80 0.80 data
UBA, Band
121
2000 4 100% 0.04 0.07 0.09 0.39 0.25 0.25
Mar. UBA, Band
99 17 6% 0.2 0.4 <0.40 0.41 - - 151
Dec. UBA, Band
98 6 100% 0.2 0.4 0.55 1.2 0.96 1.00 141
all values in [礸/l]
Abbreviations: limit of quantitation, LOQ; inf., influent; Min. Minimum; Max. Maximum; limit of detection, LOD; Ref., Reference;
* measured values > LOQ; n.d. not detected
Effluent concentrations of BBP were found in concentrations up to 1.4 礸/l. The number of positive
findings varied between 0% and 37.5%. This can be partially explained by the fact that
improvements in the analytical methodology allowed to achieve lower LOQs in the more recent
measurements (LOQs may exhibit a range of values because of the differing characteristics of
background composition in different wastewater samples).
Table 3: Concentration of BBP [礸/l] in the effluent of Austrian STPs
Date No. No. of LOD LOQ Min.eff Max.eff Median Mean eff Ref.
minimum
measured positive eff
minimum approach
values findings
approach
[%] *
0.03 ? 0.13 ? unpublished
Nov.07 16 37.5% 0.15 0.56 n.d. 1.4 - - data
UBA, Band
2005 4 0% 0.03 0.068 n.d. <0.068 - - 121
UBA, Band
151
Mar.99 17 0% 0.2 0.4 <0.40 <0.40 - -
UBA, Band
Dec.98 6 0% 0.2 0.4 <0.40 <0.40 - - 141
all values in [礸/l]
Abbreviations: limit of quantitation, LOQ; Min. Minimum; Max. Maximum; eff, effluent; limit of detection, LOD; Ref., Reference;
* measured values > LOQ; n.d. not detected
Influent and effluent concentrations in sewage treatment plants are available for several countries
(EU RAR, 2007). It is assumed that none of the measurements represent specific local activities in
the EU as well as that much of the reduction of BBP in the effluent may be caused by adsorption to
activated sludge. Removal rates up to 90% have been reported from 80% of investigated STPs in
24
BBP ANNEX XV ?IDENTIFICATION OF SVHC FORMAT
the USA (US, EPA, 1982, as cited in RAR). Measured BBP influent concentrations in various
European countries range from not detected up to 10 礸/l. The absolute maximum concentration
measured in Europe is 320 g/l found in one sample from the effluent of a kindergarten. In contrast,
effluent concentrations range from not detected up to 17 礸/l in the regional STP, Goeteborg
(Pax閡s, 1996, as cited in EU RAR). In a STP, Goeteborg only the effluent and not the influent
concentration was measured. Average effluent concentrations of BBP from different types of small
industry measured in Norway (Nesg錼d et al., 1998, as cited in RAR) range from < 0.3 礸/l to 9.6
礸/l (laundries) and maximum 106 礸/l (wash hall for technical equipment). These data are
obviously linked to the still significant use of BBP in households, industry and trade.
25
ANNEX XV ?IDENTIFICATION OF SVHC FORMAT BBP
1.3.1.2. Measured concentrations of BBP in sewage sludge
BBP concentrations in the sewage sludge are presented in Table 4 BBP in sludge can become
relevant due to application to soil. Sludge concentrations in the Austrian STP were in the range of
0.15 to 0.27 mg/kg dwt. The aim of the study conducted 2001 (UBA, Band 136) was to investigate
the concentration of BBP (based on dry weight/kg) of wet sludge, dried and composted sludge
originating from the same STP. No difference between composted and wet sludge was revealed. All
sludge samples were taken at the same time, but different charges of sludge might explain the
different values. It is noted that some measurements were made on 4 samples only, and, the derived
percentage of positive findings may not be representative. It is also noted that the significant
increase of the percentage of positive findings between 2002 and 2007 may be mainly due to the
decrease of the LOQ.
Table 4: Concentration of BBP [mg/kg dwt] in sewage sludge
Ref.
sample type Date No. No. of LOD LOQ Min. Max. Median Mean
minimum minimum
measured positive
approach approach
values findings
[%] *
http://www.ec
Feb.07 4 100% 0.004 0.01 0.15 0.16 0.159 0.159 n.nl/horizontal
drained
sewage UBA, Band
sludge 161
2002 17 6% 0.1 0.2 n.d. 0.27 - -
UBA, Band
drained 136
UBA, Band
sewage
sludge 2001 17 6% 0.1 0.2 n.d. 0.27 - - 161
composted
sewage UBA, Band
sludge 136
2001 4 0% 0.1 0.2 n.d. n.d. - -
wet sewage UBA, Band
sludge 2001 4 0% 0.1 0.2 n.d. n.d. - - 136
not stabilised UBA, Band
sludge 121
2000 4 0% 0.4 0.8 n.d. <0.8 - -
all values in [mg/kg dwt]
Abbreviations: limit of quantitation, LOQ; Min. Minimum; Max. Maximum; limit of detection, LOD; Ref., Reference;
* measured values > LOQ; n.d. not detected; dwt., dry weight
In the risk assessment report 2007 (EU RAR, 2007) sludge concentrations in the Norwegian STP
were found in the range of 0.14 to 1.4 mg/kg dwt. In Norway, sludge concentration from municipal
wastewater treatment plants are in the range of < 0.14 ?1.4 mg/kg dwt (Braaten et. al, 1996). In
Germany, sludge concentrations of 0.6 ?3.5 mg/kg dwt (municipal) and in the range from not
detected up to 2.7 mg/kg dwt were found in industrial plants (Furtmann, 1996).
The fate of several chemicals was monitored in a Danish STP, S鴋olt at Silkeborg (Boutrup et al.,
1998, as cited in RAR). BBP was analysed in the influent and effluent and in sludge on a weekly
basis during week 46, 47 and 48 in 1997. BBP was found in the range of 0.6-1.7 g/l in the influent
and < 0.5 g/l in effluent. Sludge concentrations were between 100-410 g/kg dwt. It was
calculated that 52-95% were degraded in the STP. Agricultural soil amended with sludge did not
have detectable concentrations (< 50 g/kg dwt) of BBP.
26
BBP ANNEX XV ?IDENTIFICATION OF SVHC FORMAT
Applying the TGD defaults for BBP in a sewage treatment plant with biological treatment give 92%
removal with 42% directed to sludge. In EUSES calculations the TGD defaults for BBP have been
used.
The Austrian data in sewage sludge in comparison to older European data seem to support the fact
of decreasing use, but there are still well measurable concentrations of BBP found in sewage
sludge.
27
ANNEX XV ?IDENTIFICATION OF SVHC FORMAT BBP
1.3.1.3. Measured concentrations of BBP in biota
Measured concentrations of BBP in biota (fish) are presented in Table 5. In a study conducted by
the Umweltbundesamt, Austria (unpublished data) concentrations in biota in the range of not
detected ?12 礸/kg TS 105癈 were revealed. BBP was detectable in 28.6% of the samples (n=7).
Table 5: Concentration of BBP [礸/kg dwt 105癈] in biota (fish)
Date No. No. of LOD LOQ Min. Max. Median Mean Ref.
minimum minimum
measured positive
approach approach
values findings
[%] *
Mar. 08 7 28.6% 2.5 5 n.d. 12 - - unpublished data
all values in [礸/kg TS 105癈]
abbreviations: limit of quantitation, LOQ; Min. Minimum; Max. Maximum; limit of detection, LOD; Ref., Reference;
* measured values > LOQ; n.d. not detected; dwt. dry weight
There are only few European data in biota available. RIVM/RIC/CEFIC (Table 3.16, EU RAR
2007) measured concentrations of (< 1礸/kg and 5-22 礸/kg) in molluscs, fish (< 1 礸/kg and 2
礸/kg) and invertebrates (42 ?63 礸/kg). The total range of these data is between < 1 and 1,700
g/kg dwt. (EU RAR 2007), the Austrian data being well within this range. EUSES has estimated a
regional concentration in fish of 120 g/kg wwt. This estimate for biota is used in the risk
assessment.
28
BBP ANNEX XV ?IDENTIFICATION OF SVHC FORMAT
1.3.1.4. Measured concentrations of BBP in articles of daily use
Measured concentrations of BBP in articles of daily use are presented in Table 6. Available studies
(Umweltbundesamt, unpublished) revealed concentrations in articles of daily use in the range of not
detected ?25 mg/kg. The highest concentration (25 mg/kg) is found in products for children. BBP
was detectable in 4% of the tested products for children. In tools 7.7% of all analysed tools gave
positive findings. These data confirm that the use of BBP other than as polymer softener seems to
be low, however well measurable.
Table 6: Concentration of BBP [mg/kg] articles of daily use
sample Date No. No. of LOD LOQ Min. Max. Median Mean Ref.
minimum minimum
type measured positive
approach approach
values findings
[%] *
unpublished
Babydoll Feb.08 1 0% 12.5 25 n.d. - - data
unpublished
data
Toy Nov.07 5 0% 12.5 25 n.d. n.d. - -
unpublished
Tool Aug.06 13 7.7% 0.5 1 n.d. 1.4 - - data
Products
for unpublished
Children Jun.06 25 4% 1 10 n.d. 25 - - data
all values in [mg/kg]
abbreviations: limit of quantitation, LOQ; Min. Minimum; Max. Maximum; limit of detection, LOD; Ref., Reference; * measured values > LOQ;
n.d. not detected
Analysis of 17 plastic toys revealed that only PVC-toys contained phthalate esters. In only one doll
head (out of 7 PVC toys) BBP in content of 0.02% w/w could be detected (Rastogi et al, 1998, as
cited in RAR).
29
ANNEX XV ?IDENTIFICATION OF SVHC FORMAT BBP
1.3.1.5. Measured concentrations of BBP in house dust
This study has been conducted in order to describe in more detail the chemical environment of the house dust. BBP concentrations in the house
dust are presented in Table 7. The dust samples were taken in urban-, rural m閚ages in living habits of the inhabitants of Vienna. The sampling
was done by vacuum cleaners and the dust was collected in fresh dust bags. Due to the inhomogeneity of the samples, they were sieved. The
fraction <63祄 was used for analysis. BBP in 35 samples from households dust were collected. Most commonly identified was BBP in house
dust (97.1% of analyzed samples). The highest BBP concentration was found in house dust with a concentration of 710 mg/kg. Median
concentration of BBP in house dust is 31 mg/kg.
Table 7: Concentration of BBP [mg/kg] in house dust
Ref.
sample type Date No. No. of positive LOD LOQ Min. Max. Median Mean
minimum minimum
measure findings [%] *
approach approach
d values
House dust May 07 1 100% 2.5 5.1 350 - - unpublished data
House dust Mar. 07 7 100% 2.3-5,1 4.6-10 14 500 25 92.6 in press
House dust Feb. 07 1 100% 7 14 62 - - unpublished data
House dust Jul. 05 1 100% 0.14 0.28 9.4 - - unpublished data
House dust Nov. 04 2 100% n.a. n.a. 0,8 47 24 24 unpublished data
House dust 2004 23 96% 2.5 5 n.d. 710 38 140 UBA, Band 258
Summary of all
Nov.04-May 07
house dust-
35 97.1% 0.14-7 0.28-14 n.d. 710 31 110.0 -
samples:
all values in [mg/kg]
Abbreviations: limit of quantitation, LOQ; Min. Minimum; Max. Maximum; limit of detection, LOD; Ref., Reference;
* measured values > LOQ; n.d. not detected; n.a. not available
Kersten,. et al, 2003 studied the occurrence of BBP in 65 household dust samples (Hamburg, Germany). BBP was detected up to a concentration
of 700 mg/kg (95% percentile 230 mg/kg). In another study air samples from 59 apartments and 74 kindergartens were tested for the presence of
phthalates. In general the phthalates loads in the apartment and kindergarten were low. No significant correlation between air and dust
concentration was revealed. The BBP in household dust varied from 5 to 816 mg/kg (median: 29.7 mg/kg). Comparing the above concentration
with the acceptable tolerable intake (TDI), only a small average phthalate intake (less than 1 ?8% of the TDI) by indoor air can be assumed for
children. Rakkestad et al. (2007) studied the phthalate levels of different indoor environments related to particle size fractions (PM10 and PM 2.5).
The study showed that the predominant phthalate was DBP, but BBP occurred in both size fractions (PM10: Mean 10 ng/m3; PM2.5: Mean 11
30
BBP ANNEX XV ?IDENTIFICATION OF SVHC FORMAT
ng/m3). Inhalation of particulate matter contributes to the total phthalate exposure in indoor
environments. Air and dust samples were analysed for 89 chemicals, many of them were endocrine
disrupting compounds (Rudel, R. A et al 2003, as cited in RAR). In dust DEHP and BBP were the
chemicals detected at the highest concentration. The 90th percentile concentrations for these phthalates
in dust were 854 and 277 礸/g dust, respectively. It was concluded that inhalation exposure might be
important, thus high indoor air concentration corresponds to urine phthalate concentration. In addition, it
was stated that the personal air concentrations might be higher than ambient concentrations.
1.3.2. Monitoring data in other compartments with low exposure
1.3.2.1. Measured concentrations of BBP in groundwater, soil and surface water
BBP concentrations in the groundwater, soil and surface water are presented in Table 8. BBP could not
be detected in groundwater samples (n =5). The number of measured values was very low, so no strong
conclusion can be drawn. No data from groundwater are available in the risk assessment report (EU
RAR, 2007). The highest concentration (32 礸/kg dwt) was detected in the topsoil (0-5cm). The
following monitoring studies (UBA, Band 161, BE 150) detected BBP in concentrations lower than the
limit of quantitation (LOQ) of 400 ng/祃.
Table 8: Concentration of BBP [ng/l] in groundwater
Date No. No. of LOD LOQ Min Max Median Mean Ref.
minimum minimum
measured positive
approach approach
values findings
[%] *
Stadlbauer et. al,
Apr.02 5 0% 50 100 n.d. n.d. - - 2003
Concentration of BBP [礸/kg dwt] in soil
n.d http://www.ecn.nl/
Soil Feb.07 4 0% 4.0 8.0 . n.d. - - horizontal/
n.d http://www.ecn.nl/
. horizontal/
Compost Feb.07 4 0% 4.0 8.0 n.d. - -
topsoil (0- n.d
5cm) May.05 15 6.67% 2.5 5.0 . 32 - - in press
Concentration of BBP [ng/l] in surface water
UBA, Band 161
M鋜.99 34 0% 250 400 <400 <400 - - UBA, Band 150
all values in [ng/l]
Abbreviations: limit of quantitation, LOQ; Min. Minimum; Max. Maximum; limit of detection, LOD; Ref., Reference;
* measured values > LOQ; n.d. not detected
In the EU RAR (2007) it is stated that soil concentrations of BBP are in the range of < 0.0001-0.4
mg/kg dwt. The highest concentrations > 0.1 mg/kg dwt are found close to BBP emitting sites and waste
sites. A study in the Netherlands (Alcontrol/ECPI, 1999), reports only 5 detects of BBP in 34 samples
from 33 sites in the range < 0.004-0.009 mg/kg dwt. Another study from Denmark (Vikels鴈, 1999),
with a detection limit of 0.0001 mg/kg dwt, found 7 detects in 30 samples in the range of 0.0001-0.001
mg/kg dwt. In the EU RAR (2007) the regional PECsoil as estimated by EUSES is 3.02 礸/kg wet
weight (3.41 礸/kg dwt). Only a few values have been measured above this level. The number of
measurements of BBP in soil is low and scatters widely, the older studies include some quite high
values (400, 169, 100 g/kg dwt) while more recent studies indicate significant lower values. Values
above 3.02 g/kg wwt (3.41 g/kg dwt) indicate that there might be a local contamination source. The
maximum value (32 礸/kg dwt) found in top soil are approximately 10-fold higher then the PEC value
calculated by EUSES, which might indicate a local contamination.
31
ANNEX XV ?IDENTIFICATION OF SVHC FORMAT BBP
In the RAR, 2007 most of surface water samples show BBP concentrations of less than 1 礸/l. Up to
now, no monitoring data are available that may present local water concentrations. There are exceptions
from samples taken from industrial areas in Germany and marine measurements in the North Sea. River
Rhine and Emscher concentrations gave sometimes higher concentrations than 1 礸/l. In a study from
Braun et al (2001)., and Vethaak et al., 2002 values for the lower Rhine gave an average concentration
of 0.083 礸/l for 32 samples (includes non detects at sample detection level). BBP concentration in
surface waters in Nordrhein-Westfalen (1993) show BBP concentrations of less than 1 礸/l, only the
Wupper showed the highest median concentrations of 3.45 礸/l (max. 13.9 礸/l). It is stated in the RAR,
2007 that the high concentration may be attributed to industrial activities, the small run off and a high
population density in this area. EUSES estimated regional PECsurface water, which was used for the risk
assessment for the regional scale [0.17 礸/l]. In a study conducted by Fromme et al. (2002) BBP could
be measured above the determination limit in 22% of the surface water samples (up to a maximal 2.95
礸/l).
32
BBP ANNEX XV ?IDENTIFICATION OF SVHC FORMAT
1.4. Human Exposure
This chapter is based on the information given in the EU RAR (2007), additional data are
specifically mentioned.
1.4.1. General information
The human population can be exposed to BBP via the workplace, from the use of consumer
products and indirectly via the environment. BBP is present in a large number of end products some
of which are available for consumer use.
BBP alone (as such) and BBP in preparations above 0.5 % is prohibited for sale to consumers
according to the 29th amendment of Directive on Restriction on the Marketing and Use of Certain
Substances and Preparation (76/769/EC).
The vast majority of BBP use, > 90%, goes to plasticising of PVC or other polymers. The BBP
plasticized polymeric material has consumer and industrial uses such as flooring, sealants, and
paints. A relatively small but significant use is in the food wrap or food packaging area.
Furthermore, BBP has been reported at low concentrations in baby equipment and children toys.
However, in these products BBP probably occurs as by-product/impurity and has not been added
intentionally to the products (CSTEE, April, 1998, cited in EU RAR).
The marketing and use of BBP and preparations containing BBP in toys and childcare articles is
prohibited through the 22nd amendment to Directive (76/769/EEC): It shall not be used as substance
or as constituent of preparations, at concentrations of greater than 0,1 % by mass of the plasticised
material, in toys and childcare articles. Such toys and childcare articles containing BBP in a
concentration greater than the limit mentioned above shall not be placed on the market.
Because BBP is not chemically bound to the matrix it can migrate from the polymeric material and
become available for emissions to other matrices (environmental or biological). BBP can be
released from polymer based products during its use or after disposal. The rate of emission is
dependent on various factors, for example temperature and physical or mechanical handling of the
product.
BBP may be released to the environment through waste water effluents and emissions into the air at
the sites where it is produced, processed or formulated, as well as during use and after disposal.
BBP has been identified in air, water and soil. Human exposure may therefore occur through the
contact with contaminated air, water, soil, and food.
Human exposure to BBP can also be calculated from urinary excretion of the BBP metabolite
monobenzyl phthalate (MBeP).
In recent studies urinary phthalate metabolites have been measured in human reference populations.
These studies indicated that human exposure to phthalates including BBP is both higher and more
common than previously suspected (Blount et al., 2000a; CDC 2001; CDC 2003; Hoppin et al.,
2002; Koch et al., 2003; Brock et al., 2002, all cited in EU RAR). In such studies the total exposure
to BBP, from all sources, and via all exposure routes are measured. Based on the analysis of BBP
metabolites in urine of adults and children (1-2 years and 6-11 years) in USA and EU, the daily
intake of BBP was calculated to be as follows: for children 1-2 years 4.9 x 10-3 mg/kg bw/day
(geometric mean) and 0.0182 mg/kg bw/day (maximum value from 19 children), for children 6-11
years (95th percentile) 5.46 x 10-3 mg/kg bw/day, and for adults the calculated level (95th percentile)
was 3.5 x 10-3 mg/kg bw/day.
33
ANNEX XV ?IDENTIFICATION OF SVHC FORMAT BBP
1.4.2. Occupational exposure
Occupational exposure may occur during the production of BBP, in industrial use of BBP
containing products and in professional end use of semi- and end products containing BBP. The
main routes of occupational exposure are by inhalation and dermal contact. Ingestion is not
considered to be relevant for occupational exposure.
The following exposure scenarios are considered:
Scenario 1 Production of BBP.
Scenario 2 Industrial use of BBP containing products.
Scenario 3 Professional end use of semi- and end products containing BBP.
For scenario 1 the highest exposure occurs during drumming. Because of few measurements the
EASE-value of 1.0 mg/m3 is kept as a reasonable worst case value, together with the measured value
of 2.6 mg/m3 as a short term value. The highest dermal exposure is considered to be 420 mg/day.
Table 9: Summary of exposure levels in the production of BBP (Scenario 1)
Workplace operation Exposure by inhalation (mg/m3) Dermal exposure (mg/day)
Scenario 1A: Filling of road- and rail Reasonable worst case: 0.54 420 (E)
tankers
Scenario 1B: Drumming Reasonable worst case value: 1.0 (E) 420 (E)
Short term value: 2.6
Scenario 1C: Process sampling Reasonable worst case value: 1.0 (E) 420 (E)
(manually sampling)
Scenario 1D: Cleaning and Reasonable worst case value: 1.0 (E) 84 (E)
maintenance
E) Estimated by EASE
For scenario 2 the calendering process in flooring (2C1) seems to represent the highest exposure
level for inhalation. Dermal exposure may also be a problem during mixing of raw materials in
2A2. A reasonable worst case value of 3.0 mg/m3 and a typical value of 0.4 mg/m3 (Scenario 2C1)
are taken forward to RC, together with a dermal exposure of 420 mg/day from the same scenario.
Table 10: Summary of exposure levels for the industrial use of BBP-containing products (Scenario
2)
Exposure by inhalation (mg/m3)
Workplace operation Dermal exposure (mg/day)
2A1: Flooring with the plastisol Typical value: 0.035 -
spread coating process Reasonable worst case: 1.2
2A2: Processing of PVC floats Typical value: < 0.005 840 (E)
2B: Processing of sealants < 0.1 840 (E)
The exposure under scenario 2B
is less than in scenario 2A1
2C1: Flooring with the calendering Typical value: 0.4 420 (E)
process Reasonable worst case: 3.0
2C2: Processing of films with the < 0.03 -
extrusion process
E) Estimated by EASE
For scenario 3 no measured exposure data are available. For the use of polysulfide sealants for
glass insulation, dermal exposure has been estimated to 42 mg/day with the EASE model. The
exposure level will most probably be low for handling end products, but aerosol-forming activities
cannot be excluded. As the exposure levels of aerosol forming processes during industrial use may
34
BBP ANNEX XV ?IDENTIFICATION OF SVHC FORMAT
be comparable with the exposure levels of aerosol forming end uses, the same values given for
Scenario 2 is taken forward to the risk characterisation for Scenario 3.
Table 11: Summary of exposure levels for the professional end-use of semi- and endproducts
containing BBP (Scenario 3)
Inhalation (mg/m3)
Workplace operation Dermal (mg/day)
Scenario 3 (the values are taken form Less than for scenario 2C1: Less than for scenario 2C1:
scenario 2, see text above) Typical value: < 0.4 < 420 (E)
Reasonable worst case: < 3.0
3A: Use of polysulfide sealants for Negligible 0-42 (E)
glass insulation
3B: Use of polyurethane Typical value: < 0.005 << 84-840 (E)*
sealants/fillers/grouting agent
E) Estimated by EASE,
* It is assumed that the dermal exposure in 3B is much lower than the exposure estimated for Scenario 2A2. i.e. << 84-840 mg/day (E)
1.4.3. Consumer exposure
BBP is used in several products, some of which are available to consumers. BBP alone is not
available to consumers. Consumers may be exposed to BBP by intake of food that have been
wrapped in food packaging containing BBP and/or infant formula, from indoor air due to the use of
BBP in both PVC and non-PVC polymeric material found in the home, and by the use of baby
equipment and children toys. In a Norwegian Survey from 1996 BBP was found in 5 products
available to consumers (sealing compounds, plastics, adhesives, car care products and cosmetics)
accounting for about 12 tonnes/year. In 3 of the products, adhesives, plastics and sealants the
concentration of BBP was 1-5%, 5 ?30% and 1-30% (SFT report 96:21, 1996, as cited in RAR).
According to information from the Norwegian Food Control Authority BBP is no longer used in
cosmetics in Norway. In Sweden in 1995 BBP has been found in 79 products of which 12 are
available to consumers (National Chemical Inspectorate, Sweden, 1997, as cited in RAR).
To cover the consumers' exposure to BBP via the use of consumer products containing BBP, the
following scenarios are considered and include exposures through food, indoor air, and baby
equipment/children toys:
I: Food and food packaging
II: Indoor air
III: Baby equipment/children toys
35
ANNEX XV ?IDENTIFICATION OF SVHC FORMAT BBP
Table 12: Internal exposure to BBP for consumers
Exposure scenario Adults Children
Inhalation Oral Inhalation Oral
(mg/kg bw/day) (mg/kg bw/day) (mg/kg bw/day) (mg/kg bw/day)
Intake of BBP from food 0.0003 0.00083
and food packaginga
Intake of BBP from infant 0.00102
formula and food and food
packagingb
Intake of BBP from indoor 0.000083 0.000083
airc
Intake of BBP from baby 0.00095
equipment and children
toysd
a
...The estimated average intake of BBP based on total diet study was 0.008 mg/person/day, and the high level estimate was 0.02 mg/person/day
(MAFF, 1996a, as cited in RAR). For the risk assessment the MAFF (1996a) estimate of 0.02 mg/person/day, or 0.0003 mg/kg bw/day if the
weight is 70 kg is used as a worst case approach. Children are estimated to eat 3 times less than adults and weight 8 kg.
b
...The estimated average intake of BBP from infant formula at birth is 0.000187 mg/kg bw/day (MAFF, 1998, as cited in RAR). The estimated
intake of BBP from infant formula and via food for infants is 0.00102 mg/kg/day.
c
... Estimates of BBP in indoor air have been performed from 125 homes in Riverside California and is used for risk assessment (California
Environmental Protection Agency, 1992). The maximum exposure estimate from this study was 0.000083 mg/kg/day.
d
... Risk assessment is only considered for oral exposure of BBP from baby equipment and children toys. A worst case scenario of 0.00095
mg/kg/day is used because additional exposure to BBP may occur by dermal contact, and because more than one phthalate may occur in baby
equipment and children toys.
1.4.4. Humans exposed via the environment
BBP is widely distributed in the environment as a consequence of its manufacture, use and disposal.
In the EU RAR, 2007 a number of possible exposure scenarios are considered; i.a. the exposure of
humans through the consumption of contaminated fish.
Table 13: Estimated daily human intake of BBP through environmental exposure
Scenariosa Fraction of dose through wet fish Total human intake
[mg/kg bw/day]
IIIa large site 0.87 0.0189
IIIa small site 0.87 0.0295
IIIb-1 0.39 0.0007
0.59 0.0002
IIIb-2
IIIc 0.87 0.0043
IIId 0.87 0.0027
IIIe-1 0.91 0.0004
IIIe-2 0.74 0.0006
IIIf-1 0.88 0.0021
IIIf-2 0.60 0.0002
IIIg-1 0.89 0.0011
IIIg-2 0.86 0.0004
IIIh-1 0.88 0.0067
a
... Refers to the scenarios described in Section 3.1 of EU RAR, 2007.
36
BBP ANNEX XV ?IDENTIFICATION OF SVHC FORMAT
For regional BBP exposure assessment, production, processing/formulation, and distribution are
considered. In the following table the calculated daily human intake of BBP [mg/kg bw/day] from
different compartments are presented.
Table 14: Estimated daily human intake of BBP at regional levels
Compartment BBP Concentration Fraction of dose Total human intake
[g/kg] [mg/kg bw/day]
1.8 x 10-7
Air 0.0014
1.3 x 10-7
Root tissue 0.023 0.001
2.0 x 10-7
Leaves of plant 0.011 0.0015
2.4 x 10-6
Drinking water 0.086 0.019
5.2 x 10-8
Meat 0.012 0.0004
1.3 x 10-4
Fish 76.8 0.977
3.1 x 10-8
Milk 0.0038 0.00024
1.3 x 10-4
Total 1
1.4.5. Combined exposure
Due to the use of BBP in formulation and processing of products, and the diffuse emission of BBP
from these products, humans may be exposed to BBP from different sources. The combined
exposure to BBP is the sum of all the specific sources (occupational exposure, consumer exposure,
and indirect exposure via the environment), and by all routes of exposure. However, since
occupational exposure values will totally dominate the exposure levels for adults, it is not
considered relevant to make a separate calculation for combined exposure for adults including
occupational exposure. Children are potentially exposed via many products and sources, combined
exposure values have been calculated. Therefore, for combined exposure assessment two combined
exposures are evaluated:
I. Children exposure to BBP from toys, infant formula, indoor air and indirectly via the environment
(air, water and food).
II. Adult exposure to BBP as a consumer and indirectly via the environment (air, water and food).
Table 15: Combined exposure to BBP
Daily intake (g/kg bw/day)
Exposures
Child (0-2 years old) Adult
Food and food packaging 0.83 0.3
0.187a
Infant formula
Indoor air 0.083 0.032
Baby equipment and baby toys 0.95
Indirectly via the environment (local)b 29.5b 29.5b
0.13d 0.13d
Indirectly via the environment
(regionald)
18.2e 3.5f
Calculated daily intake from urinary
concentrations of BBP metabolitese, f
TOTAL (local)b 31.55b 29.83b
TOTAL (regionald), 2.18d 0.46d
18.2e 3.5f
(calculated from urinary excretion
of BBP metabolitese, f)
a
... Mean value from birth and 6 month.
b
... Worst case scenario from local exposure (scenario IIIa small site).
d
... Regional exposure as estimated by EUSES
e
... Regional exposure (maximum value) as measured by Brock et al. (2002, as cited in RAR)
f
... Regional exposure (95th percentile) as measured by Blount et al. (2000a, as cited in RAR)
37
ANNEX XV ?IDENTIFICATION OF SVHC FORMAT BBP
The following recent studies on combined intake levels have not been included in the EU RAR,
2007 as they were published at a later date:
In a retrospective human biomonitoring study 24h urine samples from the German Environmental
Specimen Bank for Human Tissues, which were collected from 634 subjects (predominantly
students, age range 20-29 years, 326 females, 308 males) in 9 years between 1988 and 2003 (each n
>or= 60) were analyzed for the concentrations of primary and/or secondary metabolites of various
phthalates, including benzyl butyl phthalate. For BBP slightly decreasing values were observed,
even though the medians of 1998 leveled off at around 0.2 礸/kg bw/d. Even though transgressions
of the exposure limit values of the EFSA and the US Environmental Protection Agency (US EPA)
occurred only in a relatively small share of the subjects, the cumulative exposure to all phthalates
resulting in possible dose-additive endocrine effects of these phthalates must be considered
(Wittassek et al., 2007).
A recent study investigated urinary phthalate metabolite concentrations in 102 German subjects
between 6 and 80 years of age and estimated a median daily intake of 0.3 礸/kg/day for BBP.
Children had higher exposures compared to adults and seem to have a more effective oxidative
metabolism of phthalates. Due to the endocrine disrupting properties as shown in animal
experiments the authors suggest that a concept of a cumulative TDI value may be more appropriate
for the consideration of the overall exposure and the potential human health risks resulting from
everyday and simultaneous exposure to several phthalates (Wittasek and Angerer, 2008).
2 INFORMATION ON ALTERNATIVES
2.1 Alternative substances
A number of possible substitutes for BBP as softener in PVC and in other uses have been identified,
of which several are listed below. It is important to stress that the availability of toxicological data
for these substances varies significantly and is often incomplete. COWI 2001 provides a
compendium of - by the time of publishing - available (eco)toxicological data for most substances
described here. None of the substances listed below is included in Annex I of Directive
67/548/EEC.
During the last years, chemical industry has partly been replacing BBP with DINP (Di-isononyl-
phthalate, CAS No. 58033-90-2) and DIDP (Di-isodecyl-phthalate, CAS No. 68515-19-1). Those
two phthalates are not classified as reproductive toxicants. However, they are potentially more
bioaccumulative, and are suspected to persist in soils and sediments. As they are structurally similar
to DEHP and are used in high production volumes for soft PVCs, a critical distribution in the
environment can be expected. The structural similarities may cause toxicological effects in humans
and environment (Umweltbundesamt Deutschland 2007). Thus, the following examples concentrate
on possible alternatives which are not phthalates.
Citrates (especially O-acetyl tributyl citrate (ATBC), CAS-No. 77-90-7) are esters of citric acid and
are used as softeners in PVC products, for printing inks and as softeners for plastic in concrete
(COWI 2001). They are being used for cling-films, and for toys for babies and toddlers. Their main
advantage is that they are biodegradable and not toxic, and can be derived from renewable primary
products. Their disadvantage is the considerably higher cost as compared to phthalates
(Windsperger et al. 2007).
Hexamoll瓺INCH (Di-(isononyl)-cyclohexan-1,2-dicarboxylate, CAS-No. 166412-78-8) is mainly
used for the production of toys, medical products, and other PVC products (Windsperger et al.
2007, Biedermann-Brem et al. 2008). Its technical properties are very similar to that of DEHP
38
BBP ANNEX XV ?IDENTIFICATION OF SVHC FORMAT
(Bis(2-ethylhexyl)phthalate). It has been approved by EFSA under corrigendum 2007/19/EG (4th
amendment to directive 2002/72/EG) for its use in plastic materials and articles intended to come
into contact with foodstuffs. As it was recently notified as a new substance, sufficient data on
toxicity and ecotoxicity should be available (WIndsperger et al. 2007, Umweltbundesamt
Deutschland 2003, Umweltbundesamt Deutschland 2007).
Adipates (particularly bis-(2-ethylhexyl)adipate (DEHA), CAS No. 103-23-1 and diisononyladipate
(DINA), CAS No. 33703-08-1 ) are diesters of aliphatic dicarboxylic acids and are produced with
varying alcohol groups. They are classified as low temperature plasticizers, and the compounds are
relatively sensitive to water (COWI 2001). They are mostly used in PVC, but also in fillers, in
paints and lacquers, adhesives, plastic in concrete, and rubber products. DEHA is mostly used in
packaging for foodstuffs, DINA mostly for floor covering and wallpapers (Umweltbundesamt
Deutschland 2007, Windsperger et al. 2007).
Phosphates (e.g. di(2-ethylhexyl)phosphate, CAS No. 298-07-7, tri(2-ethylhexyl)phosphate, CAS
No. 78-42-2) are triesters of phosphoric acid and includes triaryl and trialkylesters. This group of
plasticizers is more resistant to ignition and burning than all the other groups of ester plasticizers
and is most often used as flame-retardants in products with specific fire resistant demands. The
main uses are in PVC-products used in e.g. the hospital sector, packing, cables, profiles and floor
and wall coverings. Tri(2-ethylhexyl)phosphate was not mutagenic and was not found genotoxic in
chromosome aberration test and micronuclei assays. Slight evidence of carcinogenicity was
observed in mouse, but it has been concluded that the substance is not likely to cause cancer in
humans. No data were found on reprotoxicity, embryo toxicity and teratogenicity. There is no data
to determine reproductive toxicity or teratogenicity for Di(2-ethylhexyl)phosphate (COWI 2001).
Trimellitates (tri-2-ethylhexyl trimellitate, CAS No. 3319-31-1), pyromellitates and other
polycarboxylic acid esters are used for heat resistant plasticized PVC articles due to their
exceptional thermal properties. Trimellitates are similar to phthalates with respect to their
compatibility and plasticizing effect. They generally have a higher molecular weight and
corresponding lower vapour pressure, resulting in a lower migration potential to aqueous solutions
compared to phthalates and other plasticizer (COWI 2001).
Alkylsulphonic acid esters (o-toluene sulphonamide (OTSA), CAS No. 88-19-7) are based on
phenol, sulphate and an alkyl chain. The sulfonic esters are more resistant with respect to hydrolysis
than other ester based plasticizers (COWI 2001). They can be used for PVC exposed to severe
weather conditions or strong disinfectants and agents, as well as for toys (Umweltbundesamt
Deutschland 2003). O-toluene sulphonamide is reported as teratogenic in rats, but no detailed
descriptions of the study design is available. Only weak mutagenic activity is shown. There is
limited evidence that OTSA is carcinogenic when administered orally to rats. This has been
suggested as the cause of carcinogenicity of saccharin. The available data suggest that OTSA
impurities at the levels normally found in commercial saccharin do not contribute to the
carcinogenicity of saccharin. Based on very limited data the critical effect has been identified as
possible teratogenicity (COWI 2001).
Butane esters (2,2,4-trimethyl-1,3-pentanediole diisobutyrate (TXIB), CAS No. 6846-50-0) is
mostly used in PVC-products e.g. in the hospital sector, packaging, cables, profiles, floor and wall
coverings, printing ink and paint/lacquer (COWI 2001).
Polyesters (polyadipates) are medium viscous polymeric softeners derived from adipic acid, used
for oil and grease resistant uses of PVC, and can be used for the production of packaging foil and
floor coverings. They comply with several food law requirements (Windsperger et al. 2007).
39
ANNEX XV ?IDENTIFICATION OF SVHC FORMAT BBP
Epoxyester and epoxydised oils, of which epoxidised soybean oil (ESBO, CAS No. 8013-07-8),
which is produced by epoxidation of soybean oil is the dominant plasticizer. ESBO has a high
molecular weight and a spacious molecular structure, which makes it more resistant to migration
(COWI 2001).
Benzoates (Dipropylene glycol dibenzoate, CAS No. 27138-31-4) may be mainly used in adhesives
and fillers (COWI 2001).
Sebacates (Dioctyl sebacate (DOS), CAS No. 122-62-3) are used to add good low temperature
flexibility, and generally have the same plasticizing properties as adipates and azilates (COWI
2001).
2.2 Alternative techniques
An alternative technique is the adding of the "softener" (special monomers, like vinyl acetate and
maleic acid) in the stage of polymer production (co-polymerisation). As an example, vinyl chloride
(the monomer for PVC production) is co-polymerised with a certain amount of vinyl acetate (up to
20%). Thus, instead of being physically bound to the macromolecules by dipole-dipole interaction,
the softening monomer becomes part of the macromolecule (i.e. copolymer). Thereby the plastic
becomes permanently soft, and the softener does not migrate. These procedures have been known
for some time, due to the more specific complexity of the production process and the reduced
flexibility they have been implemented only on very limited scale (Windsperger et al. 2007).
It should be noted, that in several publications (Umweltbundesamt Deutschland 2003,
Umweltbundesamt Deutschland 2007) a complete switch from products containing phthalates to
other materials like polyethylene or polypropylene is suggested as another alternative. Obviously,
the applicability of this alternative depends on the use of the final product.
3 RISK-RELATED INFORMATION
Information concerning the risk for human health and the environment is summarized from the risk
assessment report (EU RAR, 2007).
Human health
The human health part of the risk assessment concludes that there is no risk has been identified and
that there is no need for further information and/or testing for risk reduction measures beyond those
which are already being applied. This conclusion is drawn for workers, consumers and man exposed
indirectly via the environment.
Workers
Conclusion (ii) There is at present no need for further information and/or testing and for risk
reduction measures beyond those which are being applied already.
Consumers
Conclusion (ii) There is at present no need for further information and/or testing and for risk
reduction measures beyond those which are being applied already. It should be noted that the
conclusion for "consumers" related to toys and childcare articles reflects the exposure situation at
the time of data collection for this RAR. BBP is not intentionally used in toys and childcare articles
in the EU but may be present as impurity in trace amounts. The possible situation that BBP might
40
BBP ANNEX XV ?IDENTIFICATION OF SVHC FORMAT
be used as a substitute for other phthalates in toys and childcare articles in the future has not been
taken into account.
Humans exposed via the environment
Conclusion (ii) There is at present no need for further information and/or testing and for risk
reduction measures beyond those which are being applied already. It should be noted that recent
epidemiological studies have indicated an association between maternal exposures to BBP as well
as to other phthalates and the length of the anogenital distance (AGD) in newborn boys. These data
support the hypothesis that prenatal phthalate exposure at environmental levels may affect male
reproductive development in humans. However, due to small sample size in the studies, this issue
will have to be further investigated, and new studies in the future should be taken into account in
the risk assessment of BBP.
Environment
Conclusion (i) Further information is needed concerning reproductive toxicity and endocrine
effects in fish. A long term fish study on reproductive and endocrine effects has to be performed
and therefore the PNECaquatic has to be seen provisional. In the risk assessment report (EU-RAR,
2007) it is stated that, BBP is considered as a suspected endocrine disruptor.
Conclusion (iii) A local risk for aquatic environment was concluded for the use category IIIa
flooring large and small sites and III h non polymer, confidential use at life cycle step III processing
and formulation. A local risk for the terrestrial compartment was concluded for the risk category IIa
(flooring large and small sites), IIIc (PVC coated textile) and IIh (non polymer use confidential) at
life cycle stage III (processing and formulation).
Conclusion (ii) 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 conclusion is reached
for the following life cycle steps/environmental compartments
o Production and distribution (Life cycle I and II) for all environmental compartments
o For the use categories IIIb, IIIc, IIId, IIIe IIIf and IIIg at life cycle step III (processing and
formulation) for surface water (including sediment)
For the use categories IIIb, IIId, IIIe IIIf and IIIg at life cycle step III (processing and
o
formulation) for the terrestrial compartment
For use and disposal (Life cycle IV and V) for all environmental compartments
o
For the atmosphere (all life cycle steps)
o
For STP at all production, formulation and processing sites
o
For secondary poisoning (all life cycle steps)
o
Conclusions (ii) for surface water (including sediment) and the terrestrial compartment have to be
seen as provisional until possible endocrine effects in fish have been resolved.
41
ANNEX XV ?IDENTIFICATION OF SVHC FORMAT BBP
3.1. Environmental Effects Assessment (EU RAR, 2007)
3.1.1 PNEC for the aquatic environment (including sediment)
There are valid long-term tests available representing the three trophic levels. The NOEC values
available are:
Fish: 30-day early life stage test: NOEC (weight gain) = 0.14 mg/l
(Pimephales promelas, EG&G Bionomics, 1981)
Invertebrate: 28-day NOEC (reproduction) = 0.075 mg/l
(Mysidopsis bahia Monsanto 86-7-2074)
Algae: 72-hour EC10 (growth rate) = 0.20 mg/l
(Navicula pelliculosa, Carolina Ecotox 14-01-1)
The lowest chronic NOEC (endpoint: reproduction) equal to 0.075 mg/l is that of the Mysidopsis
bahia test of Monsanto 86-7-2074. This NOEC value was used in the risk assessment to derive a
PNECaquatic. An assessment factor of 10 should be applied to the lowest of the NOEC values, when
there arethree valid chronic studies available.
PNECaquatic = 0.075 mg/l / 10 = 7.5 g/l
It is important to note, that the PNECaquatic is provisional as a fish reproduction study is
ongoing in order to investigate possible endocrine effects of BBP.
For deriving a PNECmarine an assessment factor of 100 has to be applied because long term toxicity
NOECs are available only from three freshwater or saltwater species for three trophic levels (algae,
crustacean and fish). No effect data for additional taxonomic groups (e.g. molluscs, echinoderms)
are available for BBP and lowering the assessment factor to 10 is therefore not justified.
PNECmarine=0.07.5 mg/l/100 = 0.75 g/l
PNECsediment = 263 /1150 l/kg . 0.0075 mg/kg . 1,000 = 1.72 mg/kg wwt
PNECmarine sediment = 263 /1,150 l/kg . 0.00075 mg/kg . 1,000= 0.172 mg/kg wwt
3.1.2 PNEC for microorganisms
There is only one test available regarding toxicity to microorganisms. According to Volskay and
Grady (1988) no effect was observed on respiratory activity in activated sludge at BBP's solubility
limit of 2.8 mg/l. As no effects were observed at the highest concentration tested no
PNECmicroorganisms could be derived.
3.1.3 PNEC for the terrestrial compartment
As no negative effects were seen in the acute toxicity test with earthworm (Eisenia foetida) no
PNECsoil could be derived.
PNECsoil > 1,000/1,000/1.13 = > 0.89 mg/kg wwt
When only one terrestrial study is available the TGD recommends that PNECsoil should also be
estimated according to the equilibrium partitioning method, using the PNECaquatic in the following
equation:
PNECsoil=315/1,700 x 0.0075 x 1,000 = 1.39 mg/kg wwt
3.1.4 Secondary poisoning
The PNECoral is determined to 33.3 mg/kg in food for birds and mammals. For the risk
characterisation this value is compared with the PEC's in fish and worm for the various exposure
scenarios. PECfish was determined using a BCF of 449 l/kg, while PECworm was determined using a
BCF of 831 l/kg.
42
BBP ANNEX XV ?IDENTIFICATION OF SVHC FORMAT
3.2 European data and risk characterisation (EU RAR, 2007)
In the EU RAR, 2007 it was concluded that there is a need for limiting the risks (environment); risk
reduction measures which are already being applied shall be taken into account.
Production and Distribution (Life cycle stage I and II)
Conclusion (ii)
The exposure scenarios for the production sites are based on site specific information and on default
values. The PEC/PNEC ratios for the aquatic compartment are below 1, thus a risk to the aquatic
environment is not expected. However, conclusion (ii) has to be seen as provisional until
possible endocrine effects in fish have been resolved.
Processing/Formulation (Life cycle stage III)
Conclusion (ii)
The exposure scenarios for processing of BBP are based on default parameters from the TGD or the
ESD "Plastics". PEC/PNEC ratios for the aquatic compartment are below 1 for the use categories
IIIb, IIIc, IIId, IIIe, IIIf and IIIg at life cycle stage III. Thus a risk to the aquatic environment is not
expected. However, conclusion (ii) has to be seen as provisional until possible endocrine effects
in fish have been resolved.
Conclusion (iii)
Two use categories show PEC/PNEC ratios > 1. These are the use categories IIIa (flooring large
and small sites) and IIIh (formulation of confidential use). The exposure scenario for IIIa is based
on the ESD "Plastics". The recently updated ESD "Plastics" has passed the OECD process and is
based on best available information. Further site specific data have not been obtained. The exposure
scenario for IIIh is based on information from Industry. The PEC/PNEC ratios for the aquatic
compartment are above 1, thus a risk to the aquatic environment can be expected. Flooring sites
were split into large sites with air treatment facilities in place and small sites without air treatment
(in accordance with the ESD on Plastics Additives from 2004). Industry stressed that the estimation
of plant size on the basis of BBP consumption may be misleading because BBP is usually not used
alone but in a mixture with other plasticisers. Hence, small sites with respect to BBP are not
necessarily small sites in terms of plasticiser use and industry has confirmed that. However,
information from industry has also shown that there are actually sites without treatment and hence
the worst case ESD-scenario for small sites, which do not have air treatment in place, could not be
omitted even though the sites may not be small sites in terms of the definition of the ESD with
respect to total plasticiser use. According to industry the emissions to waste water are an
overestimation, both for the large sites and for the small site scenario, but as no site specific
emission data have become available emission factors are takes from the ESD.
Conclusion (iii) is based on BBP consumption data from 2004. For 2005 there are only two
producers left and industry provided estimations of the expected use volume of BBP for all use
categories. These figures are confidential as there are only two producers left. The total BBP
volume used for flooring in 2005 has been further reduced, but the scenarios used in the risk
assessment are still relevant. In 2005 it is still valid to use the ESD emission factors for a small site
since sites without air treatment have been identified.
Use and Disposal (Life cycle stages IV and V)
Conclusion (ii)
These exposure scenarios are based on several assumptions and on default parameters. The
PEC/PNEC ratios for the aquatic compartment are below 1, thus a risk to the aquatic environment is
43
ANNEX XV ?IDENTIFICATION OF SVHC FORMAT BBP
not expected. However, conclusion (ii) has to be seen as provisional until possible endocrine effects
in fish have been resolved.
In the risk reduction strategy (April, 2007) it is stated that for the water bodies where emissions of
BBP may cause a risk, the relevant member states could establish national EQSs and national
pollution reduction measures to archive those EQS in 2015 in accordance with the frame work
directive (2000/60/EC). Recently, BBP was included into a list of potential priority substances
(refer to 2006/0129/COD Annex X).
44
BBP ANNEX XV ?IDENTIFICATION OF SVHC FORMAT
OTHER INFORMATION
Benzyl butyl phthalate (BBP) is on the 3rd priority list under Council Regulation (EEC) No 793/93
on the Control and Evaluation of the Risks of Existing Substances with Norway as Rapporteur. The
final risk assessment report was published in 2007. The risk reduction strategy was endorsed at the
13th RRS Meeting, publication in the Official Journal is foreseen for 2008.
Note that no re-evaluation was conducted of those references which are cited in this Annex XV
dossier and which were taken from the Risk Assessment Report for benzyl butyl phthalate (EU
RAR, 2007). The last full literature survey for the RAR was carried out in 2003 with subsequently
conducted targeted searches. For the present dossier no comprehensive literature survey was carried
out, but focus was given to exposure related data (especially monitoring data) and endocrine effects.
45
ANNEX XV ?IDENTIFICATION OF SVHC FORMAT BBP
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