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Administrative data

basic toxicokinetics in vitro / ex vivo
Type of information:
experimental study
1 (reliable without restriction)

Data source

Reference Type:
Human phase I in vitro liver metabolism of two bisphenolic diglycidyl ethers
Philippe Vervlieta,*, Siemon de Nysb, Radu Corneliu Ducac,d, Imke Boonene, Lode Godderisc, Marc Elskense, Kirsten L. van Landuytb, Adrian Covacia,*
Bibliographic source:
Toxicology Letters 332 (2020) 7–13
Report date:

Materials and methods

Objective of study:
Test guideline
no guideline available
Principles of method if other than guideline:
This study employed an in vitro assay optimized and used in previous studies (Mortele et al., 2018; Vervliet et al., 2018b, 2019).
GLP compliance:
not specified

Test material

Specific details on test material used for the study:

Results and discussion

Metabolite characterisation studies

Metabolites identified:
Details on metabolites:
Metabolism BADGE

BADGE was detected in the LC-QTOF-MS mostly as an NH4-adduct
(m/z 358.2013), at a retention time of 12.96 min. When selecting the
ammonium adduct for fragmentation, the same product ions can be
observed as earlier reported by Gallart-Ayala et al. Gallart-Ayala et al.
(2010) In the negative control samples where HLM were omitted, the
concentration of BADGE appeared to be relatively stable over the 3 h
exposure time, with only a small decrease from 1 to 3 h of exposure,
which can be linked to an increase of the intensity of BADGE.H2O. In
samples where HLM were present (HLM samples and negative controls
without cofactors), the signal of BADGE was around 8 times lower at
the zero-hour time point. In addition, the intensity of the signal of
BADGE decreased over time in the HLM samples. In the negative con-
trols without cofactor, BADGE was undetectable after 3 h exposure, in
the HLM samples, this was already after 1 h of exposure.
BADGE.2H2O was mainly detected as an NH4-adduct (m/z
394.2226) at a retention time of 10.05 min. Upon fragmentation, the
product ions with m/z 135.0790 and 107.0482 were observed, which
are common fragments with BADGE. The product ion with m/z
209.1172 differs in 18 amu from the fragment ion 191.1050 observed in
BADGE, confirming the hydrolysis with addition of H2O of the epoxide
ring structure. The level of identification of this biotransformation
product reached level 1 by injecting a reference standard. Schymanski
et al. (2014) BADGE.2H2O was detected in all HLM samples and ne-
gative controls without cofactor from 0 h to 3 h, but it was not present
in the method blanks and negative controls without HLM. In the ne-
gative controls without cofactor, the abundance of BADGE.2H2O was
stable from 0 h to 3 h, but in the HLM samples, the relative area de-
creases over time.
BADGE.H2O was identified in the negative control samples without
HLMs, and absent in the other sample groups. The area of BADGE.H2O
increased in linear from 0 h to reach a maximum after 3 h of exposure.
It was detected as an NH4-adduct (m/z 376.2117) at a retention time of
11.61 min. Upon fragmentation, the product ions with m/z 135.0790
and 107.0790 corresponded to those seen when fragmenting BADGE.
The presence of product ions with m/z 191.1050 and 209.1157 con-
firmed that both the epoxide ring side chain and the hydrolyzed variant
exist in this compound and resemblance of the observed fragment ions
to those reported by Gallart-Ayala et al. resulted in a level 2a identifi-
cation.(23, 24)
In the HLM samples, a chromatographic peak at 8.26 min was de-
tected with an m/z of 410.2176. This feature was not present in any of
the negative controls or method blanks. The feature was absent at the
0 h time point but showed a steady increase to a maximal relative area
after 3 h. The database search identified this feature as an
ammonium adduct of a hydroxylation biotransformation product from
BADGE.2H2O, with a molecular formula of C21H28O7 and a mass dif-
ference from the theoretical mass of 1.48 ppm. Upon fragmentation, a
fragment ion with m/z 225.1146 was observed. This differed by 16 amu
from the 209.1157 fragment observed in BADGE.2H2O, suggesting the
presence of an extra O-atom, originating from an oxidative bio-
transformation reaction. The presence of a fragment ion with m/z
207.1009 resulting from the loss of water suggested that the hydro-
xylation occurred on an aliphatic position. Also, a specific fragment ion
with a m/z value of 165.0571 was observed for this biotransformation
product for which a formula of [C9H9O3]+ could be generated pointing
out the hydroxylation occurred on the dihydroxypropyl moiety. The
fragment ion with 107 amu was shared with all other observed features
and confirmed that the hydroxylation did not occur on a phenolic po-
sition. (Vervliet et al., 2019)
Finally, the carboxylic acid BADGE.H2O.COOH, derived from the
oxidation of BADGE.2H2O could be identified in ESI negative at a re-
tention time of 8.81 min. Because it could only be detected in very low
amounts in the 3 h samples, no MS/MS could be recorded at first.
During a targeted reinjection, MS/MS spectra could be acquired. Upon
fragmentation, a loss of C3H5O3 (corresponding to the carboxylated C3-
chain) from the parent ion led to the product ion with m/z 301.1469.
Further loss of the second C3-chain led to the product ion with m/z
227.1078, characteristic for BPA. At the higher collision energy, a
secondary characteristic BPA product ion with m/z 133.0671 was ob-
served. However, the acquired MS/MS spectra did not allow for
locating the exact position of the carboxylic acid moiety.

Metabolism BFDGE

BFDGE was detected in positive ionization as an ammonium adduct
(m/z 330.1686) at a retention time of 12.52 min. Upon fragmentation,
the product ions earlier reported by Gallart-Ayala et al. could be ob-
served for the different structural isomers. (Gallart-Ayala et al., 2010)
In the negative control samples where HLM were omitted, a decrease of
the BFDGE signal could be observed over time, starting already at the
1 h time point. As observed for BADGE, the signal of BFDGE in samples
where HLM were present (HLM samples and negative controls without
cofactors) was several times lower at the 0-h time point than in the NC
samples. In addition, the signal decreased over time resulting in un-
detectable amounts of BFDGE in these samples after 1 h.
BFDGE.2H2O was identified in all samples where microsomal liver
fractions were present from starting at the 0 h time point up to 3 h.
BFDGE.2H2O was detected as a NH4-adduct at a retention time of
9.48 min. The product ion m/z 181.0846 can be assigned to a structure
where C9H12O3 has been lost from the protonated parent molecule. A
secondary characteristic product ion for BFDGE.2H2O, m/z 107.0484
could be assigned to a fragment formula [C7H7O]+. Both ions have
previously been reported by Gallart-Ayala et al., leading to a level of
identification of L2a. (Schymanski et al., 2014; Gallart-Ayala et al.,

In contrary to BADGE.2H2O, no clear trend could be observed for
BFDGE.2H2O in the HLM samples over time, possibly due to a higher
spread of the intensities in the samples. Signal intensities in the HLM
samples were comparable to negative control sample where the co-
factor was left out. In negative controls without HLM and method
blanks, BFDGE.2H2O could not be detected.
BFDGE.H2O was identified in the negative control samples without
HLM as an ammonium adduct (m/z 348.1827) with a mass error of
7.17 ppm. The area of the signal was stable from 0 to 1 h, after which it
declined. Upon fragmentation, a mix of product ions shared with
BFDGE and BFDGE.2H2O could be observed due to the two different
propyl side chains. Product ions with m/z 163.0769 and 133.0646
confirmed the presence of the epoxide side chain while the product ion
with m/z 181.0850 confirmed the presence of the side chain resulting
from the hydrolysis of the epoxide. Finally, the product ion with m/z
107.0496 is shared with BFDGE, further confirming the identity of
BFDGE.H2O to level 3.
In negative ionisation, a chromatographic peak at 7.98 min could be
detected with a m/z of 361.1294. This feature was identified by suspect
screening as the carboxylic acid biotransformation product resulting
from the oxidation of BFDGE.2H2O, with a mass difference of 0.42 ppm.
This carboxylic acid was only present in the HLM samples after 1 and
3 h of exposure, with a maximal relative area at the 3 h time point. Fragmentation of the parent ion led to two main fragment ions:
m/z 199.0758 and m/z 93.0357. Both can be linked to a bisphenol F
core structure, but neither could pinpoint the exact location of the
carboxylic acid moiety.

Any other information on results incl. tables

Table 1
Overview of identified compounds with their molecular formula, measured mass, mass deviation (expressed as ppm difference), fragment ions from MS2 and
confirmation level according to Schymanski et al. Schymanski et al. (2014).

CompoundFormulaRT (min)Mass measuredΔ ppm Fragment IonsConfirmation level
BADGEBADGEC21H24O412.96340.16791.35191.1050; 161.0948; 135.0790; 107.0482L1
 BADGE.H2OC21H26O511.61358.17841.04209.1157; 191.1050; 161.0961; 135.0790; 107.0482L2a
 BADGE.2H2OC21H28O610.05376.1888 0.57209.1172; 135.0790; 107.0482L1
 BADGE.2H2O-OHC21H28O78.26392.18411.48225.1146; 207.1009; 177.0922; 165.0571; 135.0790; 107.0482L3
 BADGE.H2O.COOH*C21H26O78.81390.16841.39301.1469; 227.1078; 133.0671L3
BFDGEBFDGEC19H20O412.52312.1352−3.05295.1305; 277.1206; 189.0896; 163.0745; 145.0644; 133.0644;
 BFDGE.H2OC19H22O511.00330.14917.17181.0850; 163.0769; 133.0646; 107.0496L3
 BFDGE.2H2OC19H24O69.48348.1571−0.64181.0846; 107.0484L2a
 BFDGE.H2O.COOH*C19H22O77.98362.13670.42199.0758; 93.0357L3


Applicant's summary and conclusion

We have applied an adapted version of our in-house human in vitro
liver metabolism assay to study the phase I metabolism of BADGE and
BFDGE. Exposure of both diglycidyl ethers to the microsomal fractions
led to the hydrolysis of both epoxides in a NADPH-independent
manner, leading to the formation of BADGE.2H2O and BFDGE.2H2O.
Incubation of both tested compounds with microsomal fractions and
cofactors led to further oxidation of the hydrolysed compounds. For
BADGE, this resulted in the formation of a hydroxylated and carboxy-
lated biotransformation product, respectively BADGE.2H2O−OH and
BADGE.H2O.COOH. For BFDGE, the carboxylated biotransformation
product BFDGE.H2O.COOH could be identified, which has never been
reported before.
Executive summary:


In this study, we could observe a significant decrease in the signal
for BADGE when adding HLM to the reaction mixture. In addition,
BADGE.2H2O was readily present in these samples, but not when no
HLM were present. These data suggest a rapid hydrolysis of BADGE to
BADGE.2H2O when exposed to microsomal fractions. This confirms
earlier findings by Bentley et al, Boogaard et al. and Climie et al.
(Boogaard et al., 2000; Bentley et al., 1989; Climie et al. (1981b) The
hydrolysis appears to be NAPDH independent as it occurred also in the
negative control samples where the cofactor NAPDH had been omitted.
Boogaard et al. stated that this hydrolysis was catalyzed by epoxide
hydrolase, an enzyme class which does not need a cofactor, which
agrees to the findings of our study. (Bentley et al., 1989; 25)
We observed the similar behaviour for the formation of
BADGE.2H2O and BFDGE.2H2O from respectively BADGE and BFDGE
which was in accordance to earlier study by Wang et al., who suggested
the hydration of these chemicals in humans given the more frequent

detection of the hydration products in human specimens (adipose,
blood, urine).(12)
In this study, the human phase I liver metabolism reactions were
studied, catalyzed by cytochrome P450 enzymes. Although most of
these reactions are oxidations, CYP450 s can catalyze an array of re-
actions including reductions, ester cleavage, dehydration among others.
(Guengerich, 2001) For both BADGE and BFDGE, only an oxidative
reaction could be observed, resulting in the formation of an hydro-
xylated or carboxylic acid biotransformation product respectively.
The absence of O-dealkylation reactions, which could lead to the
formation of BPA and BPF from respectively BADGE and BFDGE or their
metabolites, confirmed earlier results from Bentley et al. They observed
O-dealkylation only occurred when BADGE was either presented in a
high dose, or in low dose when in combination with an inhibitor for
epoxide hydrolase. (Bentley et al., 1989)
For both BADGE and BFDGE, the monohydrolysis product (.H2O)
was present in the negative control samples (without HLM) from the
start. During incubation, the concentration for BADGE.H2O rose from
0 h to reach a maximal area after 3 h of incubation, while the area of
BFDGE.H2O remained stable during the first hour of incubation and
then declined, suggests a different behaviour for these compounds. The

decrease of BADGE in the NC samples during 3 h of exposure appeared
to be linked to the steady increase of BADGE.H2O over time. In con-
trary, the area of BFDGE also declined over time, but this did not result
in an increase of BFDGE.H2O after 3 h of exposure. This suggests that
the BFDGE.H2O degrades more rapidly to BFDGE.2H2O than is the case
for the BADGE analogue.
Subsequently, after the formation of the BADGE.2H2O or
BFDGE.2H2O hydrolysis products, further oxidative biotransformations
occur. For BADGE, this resulted in the hydroxylation of BADGE.2H2O
and also the formation of the carboxylic acid BADGE.H2O.COOH, while
for BFDGE only the carboxylic acid was formed resulting from the
oxidation of BFDGE.2H2O.
The biotransformation of BADGE showed similarities to these of the
dental monomer bisphenol A glycidyl methacrylate (BisGMA) which
has been previously studied by our group. (Vervliet et al., 2019) Upon
hydrolysis of the ester bond in the dimethacrylate BisGMA, both me-
thacrylic acid moieties are removed leading to the formation of BAD-
GE.2H2O. In both studies, subsequent oxidative biotransformation
pathways have been observed leading to the hydroxylated (BADGE.2-
H2O−OH) and carboxylated (BADGE.H2O.COOH) biotransformation
products. As with BisGMA, observed MS/MS fragment ions suggested
the hydroxylation to occur on an aliphatic position and not on one of
the aromatic rings. (Vervliet et al., 2019)
Although the acquired MS/MS fragments did not help to elucidate
the exact position of the carboxylic acid in the identified in
BADGE.H2O.COOH and BFDGE.H2O.COOH, the metabolism of other
chemicals with a 1,2-propanediol moiety could help confirm the loca-
tion. Ruddick et al. have studied the metabolism of 1,2-propanediol and
observed the formation of lactic acid. (Ruddick, 1972) In addition,
Maurer et al. and Vandenheuvel et al. have studied the metabolism of
guaifenesin (3-(2-methoxyphenoxy)-1,2-propanediol), which has
structural resemblances to both chemicals in this study. They identified
beta-(2-methoxyphenoxy)lactic acid as the major urinary metabolite.
(Maurer, 1990; Vandenheuvel et al., 1972) These studies suggest that
the carboxylic acid moiety in both biotransformation products will be
located at the terminal carbon. However, in vivo studies must be carried
out in order to confirm the formation of these carboxylic acids.
BADGE.2H2O and BFDGE.2H2O have been detected in human urine,
blood plasma and adipose tissue samples. (Wang et al., 2015; Liu et al.,
2019; Rocha et al., 2018) However, as these compounds can be easily
formed through non-specific hydrolysis reactions, one can never be sure
that the detected amounts of these compounds solely derive from

(human) metabolism (Lane et al., 2015; Poustková et al., 2004; Losada
et al., 1993). For example, Losada et al. have identified the formation of
the hydrolysis products of BADGE, BADGE.H2O and BADGE.2H2O, in
different food simulants (Losada et al., 1993). In addition, the measured
hydrolysis products could also be a result from degradation during
sample preparation as was demonstrated by Liu et al., leading to a
specific water-free sample preparation to eliminate this risk (Liu et al.,
2019). The specific metabolites BADGE.2H2O−OH, BADGE.-
H2O.COOH, and BFDGE.H2O.COOH identified in this study could po-
tentially help in eliminating possible errors in human biomonitoring of
BADGE and BFDGE due to the reasons above.
Future studies could either target these specific biotransformation
products or combine them with quantification of the hydrolysis pro-
ducts and determine and monitor ratios between the different meta-
bolites to confirm human metabolism. However, this would require
reference standards of BADGE.2H2O−OH, BADGE.H2O.COOH and
BFDGE.H2O.COOH, but these are not commercially available. In any
case, in vivo studies should first qualitatively confirm the presence of
human urine.


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