Within-person variability in urinary bisphenol A concentrations:
Measurements from specimens after long-term frozen storage$
Pablo A. Nepomnaschya,1, Donna Day Bairda,?, Clarice R. Weinbergb, Jane A. Hoppina,
Matthew P. Longneckera, Allen J. Wilcoxa
aEpidemiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, USA
bBiostatistics Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, USA
a r t i c l e i n f o
Received 8 July 2008
Received in revised form
7 April 2009
Accepted 9 April 2009
Available online 22 May 2009
a b s t r a c t
Background: Bisphenol A (BPA) is an estrogenic contaminant of food and water associated with adverse
developmental effects in laboratory animals. BPA has recently been linked to morbidity in adult
humans, but studies of developmental effects in humans are methodologically more difficult. The ability
to measure BPA in urine samples after long-term storage could aid in such studies. Because the half-life
of BPA is o6h, a single measurement would be useful only if the environmental exposure is relatively
constant over weeks or months. Our aims were to evaluate the stability of BPA in specimens after 22–24
years of storage and to measure within-person temporal variability in urinary BPA.
Methods: We measured total BPA concentration by mass spectrometry in first-morning urine samples
from 60 premenopausal women. We selected from each woman’s stored daily collections three urine
samples approximately 2 and 4 weeks apart. Samples were selected from both the follicular and luteal
phases of the menstrual cycle to assess cycle effects. Temporal variability was assessed with mixed
model regression and correlations.
Results: BPA levels had an inter-quartile range from 1.1 to 3.1ng/mg creatinine, slightly higher than
levels in specimens from NHANES collected 3–11 years later. The Spearman correlation was
approximately 0.5 for samples 2 weeks apart and 0.3 for samples 4 weeks apart. Menstrual cycle
phase did not influence levels. BPA tended to increase during the three-year collection period, but not
Conclusions: The similar distribution to NHANES samples and correlation of BPA levels taken at 2-week
intervals provide indirect evidence that BPA is relatively stable during long-term freezer storage.
The correlations indicate generally stable exposures over periods of weeks. These findings suggest that
developmental effects of BPA exposure could be investigated with measurements from stored urine.
& 2009 Published by Elsevier Inc.
Bisphenol A (BPA;2,2-bis(4-hydroxyphenyl) propane) is a high
volume, industrial chemical used in the manufacture of plastics
and epoxy resins (Burridge, 2003). Leaching of BPA from polymer
products, such as food-can liners and plastic bottles, leads to
contamination of food and water, and direct exposure can occur
from sources such as dental sealants (Kang et al., 2006). BPA has
been found in urine, plasma, fetal plasma, placental tissue,
follicular fluid, and breast milk (Vandenberg et al., 2007). By the
time of the first US survey of BPA exposure (based on a subset of
NHANES urine specimens from 1988 to 1994), exposure was
nearly ubiquitous: 95% of those tested had detectable levels
(Calafat et al., 2005).
A recent analysis of NHANES data found liver dysfunction and
diabetes associated with BPA exposure in adult humans (Lang
et al., 2008), but reproductive and developmental health concerns
derive primarily from experimental studies with laboratory
animals (Richter et al., 2007; vom Saal et al., 2007). The route of
exposure appears important, with less toxicity from oral dosing
than subcutaneous dosing (Willhite et al., 2008). However, even at
low levels, BPA has been reported to interfere with endogenous
estrogens and disrupt normal estrogenic signaling. BPA disrupts
thyroid hormone action, leads to meiotic aneuploidy, and
adversely affects postnatal development (Welshons et al., 2006).
Recent studies show higher risk of uterine and breast cancer
following prenatal dosing (Newbold et al., 2007; Durando et al.,
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Contents lists available at ScienceDirect
journal homepage: www.elsevier.com/locate/envres
0013-9351/$-see front matter & 2009 Published by Elsevier Inc.
$This research was funded by the intramural program at the National Institute
of Environmental Health Sciences, National Institutes of Health, HHS. The study
was approved by the National Institute of Environmental Health Sciences,
Institutional Review Board, and participants gave informed consent.
?Corresponding author. Fax: 9195412511.
E-mail address: email@example.com (D.D. Baird).
1Current address: Faculty of Health Sciences, Simon Fraser University,
Burnaby, BC, Canada.
Environmental Research 109 (2009) 734–737
2007). Most studies of effects of BPA in humans have been limited
by small numbers or other methodological problems including
inadequate exposure assessment (Vandenberg et al., 2007).
Human studies of developmental effects, such as increased
susceptibility to hormonally dependent cancers, would be
facilitated by specimen collection during pregnancy, long-term
storage, and BPA measurement later at the time when the
developmental outcomes are assessed. However, chemical stabi-
lity over long-term storage has not been demonstrated. Urinary
BPA–glucuronide breaks down quickly, freeing the BPA (Ye et al.,
2007), but total BPA concentrations have been shown to remain
relatively constant for at least a year of freezer storage (Calafat
et al., 2005). Stability after longer storage has not been reported.
Another difficulty in exposure assessment in human studies is
that BPA is rapidly metabolized. The estimated half-life is 5–6h
(Volkel et al., 2002). Thus, exposure assessment based on single
specimens would only reflect a person’s chronic exposure if
daily exposures are fairly constant. To our knowledge, only three
studies have examined changes over time in BPA exposure within
individuals (Arakawa et al., 2004; Mahalingaiah et al, 2008;
Teitelbaum et al., 2008), and the largest was based on only 31
individuals with repeat values. All three studies assayed samples
after short-term storage. Reproducibility in these studies was
moderate suggesting that daily exposures are fairly constant over
intervals of weeks to months.
We measured urinary BPA from 60 premenopausal women
whose specimens had been in freezer storage for more than 20
years in order to evaluate by indirect assessments the long-term
chemical stability of BPA. (BPA was not measured at time of urine
collection, so direct comparison between measurements taken
from the same specimen decades apart was not possible.) We
examined the effect of year of urine collection on BPA concentra-
tions and estimated the within-woman reproducibility over
2- and 4-week intervals. We selected specimens from each
woman during her follicular and luteal phases of the menstrual
cycle in order to evaluate menstrual cycle effects on urinary BPA
2.1.Study subjects and urine sample selection
Participants in the Early Pregnancy Study were 221 volunteers who enrolled at
a time when they discontinued birth control in order to become pregnant (Wilcox
et al.,1988). Women agreed to collect daily first-morning urine samples for up to 6
months during their attempt to conceive. Specimen collection took place from
1982 to 1986. Urine was collected in BPA-free, 30-ml-wide-mouth polypropylene
jars with screw tops. Samples were stored without preservatives in the
participants’ home freezers, with weekly pickup and transport to a central storage
unit where they were kept at ?201C. Specimens were analyzed for reproductive
hormones and then transferred to long-term storage vials (first in glass and later
polypropylene) and again stored at ?201C. Thus, specimens had been thawed and
refrozen at least twice before BPA measurement.
Sixty women were selected who had adequate quantities of urine from two
ovulatory menstrual cycles. Similar to the total group of 221 participants (Wilcox
et al.,1988), most of these 60 women were white (94%) and their ages ranged from
21 to 42 years (mean ¼ 29, SD ¼ 4). Urine samples from these 60 women were
collected in 1983 (n ¼ 77), 1984 (n ¼ 46), and 1985 (n ¼ 57). Menstrual phase at
time of sample collection was determined based on day of ovulation as estimated
later from urinary estrogen and progesterone metabolite levels (Baird et al., 1991).
For each woman, three samples were selected to include both follicular and luteal
samples. The three samples are designated in chronological order as Time 1, 2, and
3; in most cases Time 2 was during the luteal phase. For most women, the selected
samples were 2 weeks apart. All samples had unique identifiers so that the
laboratory could not identify specimens from the same woman. For 20 of the 180
collection days selected, we prepared two replicate samples as blind replicates.
Thus, a total of 200 samples were analyzed. Specimens were shipped with dry ice
by overnight freight to AXYS Laboratory (BC, Canada).
2.2. Measurement of BPA and creatinine
The combination of free and conjugated BPA was measured. Deconjugation
was performed with b-glucuronidase at 371C. A 4-methylumbelliferyl glucuronide
solution was used for monitoring the deconjugation efficiency. Samples were
extracted and cleaned using a Waters Oasis HLB solid-phase extraction cartridge.
The extract was then spiked with recovery standards. Analysis of sample extracts
for bisphenol A was conducted using Waters 2690 or Waters 2795 HPLC coupled
with a triple quadrapole mass spectrometer, running the manufacturer’s MassLynx
v.4.0 software. The mass spectrometer was run at unit mass resolution in the
multiple reaction monitoring mode. Based on spiked recovery standards, a
‘‘specimen detection limit’’ was determined for each sample by converting the
area equivalents corresponding to 3 times the height of the chromatographic noise
to a concentration (in the same way as peak areas are converted to concentrations).
The ‘‘method detection limit’’ of the assay was calculated as the greater of either
the concentration of the lowest calibration standard converted to a sample
equivalent concentration, or the sample detection limit. This value was 0.18ng/ml.
Samples were analyzed in batches. The three specimens from a given woman
were analyzed in the same batch for 58 of the 60 women. For the other two, one of
their three specimens was analyzed in a separate batch. Each batch included a
procedural blank, two spiked reference samples (one low- and one high-level
concentration spike), and a reference sample in duplicate using lab stock urine for
inter- and intra-batch comparisons. Intra- and inter-assay coefficients of variation
(CV) were 14% and 17%, respectively, based on these stock urine specimens. The
intra-assay CV calculated based on our blind replicates was 28%, which included
one extremely non-concordant pair (CV for that duplicate pair ¼ 109%). When the
outlier was dropped, the CV was 22%. No blind inter-assay CV was calculated
because there were not enough replicates distributed among batches. Creatinine
was assessed by the Jaffe assay (Taussky, 1954).
2.3. Statistical analyses
We described the distribution of BPA values for the entire sample, for each of
the three years of collection (1983, 1984, 1985), and for each of the three sampling
times for each individual (Time 1, Time 2, and Time 3) using percentiles and
geometric means. For analyses, specimens with BPA levels below the specimen-
specific detection limit (SDL) were imputed by assigning a value equal to the SDL
divided by the square root of 2 (Hornung and Reed, 1990). The initial descriptive
analyses were conducted for both unadjusted and creatinine-adjusted BPA levels
(ng/ml and ng/mg creatinine, respectively), but further analyses used creatinine-
adjusted concentrations. The distribution was right-skewed, so the natural
logarithm of the measured BPA concentration was used in statistical analyses for
which a normal distribution is optimal. Pearson and Spearman correlations were
calculated between each of the three pair-wise comparisons (Times 1 and 2, Times
2 and 3, and Times 1 and 3). We examined the effect of sampling year and
estimated within- and between-woman variation, as well as the effect of
menstrual phase, using mixed model logistic regression with woman as a random
effect. We estimated reliability based on all three measurements per woman using
the intra-class correlation coefficient (ICC). ICCs and their 95% confidence intervals
(CIs) were calculated based on methods of Shrout and Fleiss (1979) by fitting a
compound symmetry structure in SAS’ mixed procedure using a ‘‘one random
BPA was detected in 91% of samples analyzed 22–24 years after
collection. The 18 (9%) specimens with non-detectable BPA levels
were fairly evenly distributed among the 3 within-woman sampling
times (7 from Time 1, 5 from Time 2, and 6 from Time 3). Their SDLs
ranged from 0.27 to 1.7ng/ml (mean of SDLs ¼ 0.82ng/ml).
None of the 60 women had undetectable levels in more than one
of her three urine samples. Table 1 shows the distribution of
creatinine-adjusted and unadjusted BPA measurements. There was
little reduction of variability with creatinine adjustment (SD of
geometric mean was 2.6 for both) (Table 1). The overall geometric
mean BPA value was 1.8ng/mg of creatinine. The distributions of
creatinine-adjusted BPA concentration increased over the three
sampling years (Table 1), consistent with a sharp rise in US BPA
production during 1980–1985 (Chemical Economics Handbook,
2000). Creatinine-adjusted BPA distributions for the three within-
participant sampling times (Time 1, Time 2, and Time 3) were all
very similar to the overall distribution (Table 1).
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P.A. Nepomnaschy et al. / Environmental Research 109 (2009) 734–737
We found significant variability in urinary BPA concentrations
both within- and between-women, but within-woman variation
was larger (within-woman variance ¼ 0.53, SE ¼ 0.07, po0.0001;
between-woman variance ¼ 0.38, SE ¼ 0.10, p ¼ 0.0002). The
increase in BPA concentration during the 3 years of urine
collection did not reach statistical significance in the mixed
model (p ¼ 0.2). There was no evidence of an association with
menstrual cycle phase (p ¼ 0.9).
Correlations between creatinine-adjusted BPA levels for the 60
women across sampling times are shown in Fig. 1. The Spearman
correlations between consecutive samples (Time 1-to-2 and Time
2-to-3) were both above 0.5. The interval from Time 1 to Time 3
was approximately twice as long, with a correlation between
those samples of 0.3 (Fig. 1). To investigate whether specimens
held in storage for the longest time would show lower correlations
between samples, we examined Spearman correlations between
samples from the same woman for the subset collected in 1983.
The correlations were similar to those for the whole group (Time
1-to-2 ¼ 0.68, Time 2-to-3 ¼ 0.47, Time 1-to-3 ¼ 0.45). The ICC,
based on data from all three time points for all 60 women was
0.43 (95% CI ¼ 0.31, 0.56).
BPA was first synthesized more than a century ago, and its
industrial use in the United States has grown exponentially over
the last several decades (Burridge, 2003). Its estrogenic effects
have been known since the 1930s (Dodds and Lawson, 1936).
Urinary concentrations in the United States were first reported in
2005 based on a subset of the 1988–1994 NHANES III participants.
The creatinine-adjusted geometric mean for the 210 women in the
NHANES III cohort was 1.1ng/mg creatinine, with a 25th-to-75th
percentile range of 0.7–3.0ng/mg creatinine (Calafat et al., 2005).
Our samples are from 3 to 11 years earlier (1983–1985) with a
slightly higher mean (1.8ng/mg creatinine) and 25th-to-75th
percentile range (1.1–3.1ng/mg creatinine). One potentially im-
portant source of BPA exposure, plastic liners in food cans, began
before both data collection periods (Tess, 1988), so this exposure
would affect both our sample and the more recent NHANES
For our study, BPA was measured by a commercial laboratory
that adapted methodology developed at the CDC (Calafat et al.,
2005). The CVs calculated from the laboratory reference urine
sample were 14% and 17% for intra- and inter-assay CVs, although
the intra-assay CV based on the blind replicate specimens was
higher (28%). We know of no published data on BPA CVs based
on replicate specimens blinded to the laboratory. CVs based on
blinded specimens can often be higher than those calculated from
laboratory reference specimens because when the reference
specimens have known concentrations, assays are re-run when
measurements differ from their known values. This correction
process cannot be followed with blind replicates.
Short-term experiments suggest that BPA is chemically stable
in frozen urine for at least a year (Calafat et al., 2005). Long-term
stability has not been directly demonstrated; this would require a
comparison of measurements taken at time of sample collection
and then again decades later. Our results indirectly support long-
term stability. The mean urinary concentrations and the distribu-
tion of BPA levels in our sample are similar to (and in fact slightly
higher than) those of the NHANES III samples from 3 to 11 years
later (Calafat et al., 2005). The BPA concentrations tended to
increase in our samples across the 3 years of urine collection
consistent with the nearly 80% rise in US production during the
early 80s (Greiner et al., 2007). Most convincing, however, are the
correlations between samples from the same woman. Measure-
ment showed Spearman correlations over 0.5 between samples
taken at 2-week intervals but a lower correlation (0.3) between
samples taken 4 weeks apart. The relatively high short-term
correlations, with a decline in correlation over time, would be
unlikely if BPA in urine degraded in random ways over years
of storage. Adding to the plausibility of long-term stability, the
correlations we observed across 2-week intervals were similar to
correlations across 2-week intervals reported for recently-
collected specimens (Teitelbaum et al., 2008). Finally, within-
woman correlations were not lower for the subset of samples
from 1983, the samples in storage the longest, again suggesting
that longer time in storage was not related to increased
BPA that is ingested is absorbed nearly completely by the
intestinal epithelium and rapidly conjugated. The half-life is less
than 6h, and nearly all ingested BPA is excreted in urine within
96h (Volkel et al., 2002). Our data are from first-morning urine
samples, so generally they reflect excretion of BPA ingested on the
previous day, mostly the previous evening. First-morning urine
samples from the same person might be expected to show more
day-to-day concordance than spot urine specimens, because
measurements will not be as affected by diurnal variability in
ingestion. Our data show a correlation of over 0.5 for samples
taken 2 weeks apart, which suggests that day-to-day exposures
are similar in the short term. However, for samples taken 4 weeks
apart, the correlation dropped to 0.3, suggesting that exposure
becomes more variable across longer time intervals.
ARTICLE IN PRESS
Total urinary BPA concentrations, geometric means and their standard deviations
with selected percentiles, based on creatinine adjusted (ng/mg creatinine) and
unadjusted values (ng/ml) from 60 women (3 specimens from each woman at
Time 1, Time 2, Time 3 taken about 2 weeks apart), Early Pregnancy Study, urine
samples collected during 1983, 1984, or 1985.
Whole data setGeo
NMean SDMin 5th25th 50th 75th 95thMax
Creatinine adjusted 180 1.79
2.59 0.17 0.32 1.05 1.77 3.06
2.59 0.24 0.42 0.95 1.70 3.55
9.86 50.00180 1.82
Subsets (creatinine adjusted)
Year of sample collection
2.77 0.20 0.27 0.75 1.57
2.35 0.20 0.44 1.12
2.47 0.17 0.49 1.23 1.87 3.55 11.81 27.07
2.77 9.40 33.78
With-woman sample collection time
2.50 0.20 0.39 1.09 1.77 3.07
2.54 0.26 0.36 1.02 1.55 3.09
2.78 0.17 0.24 0.94 2.11
Pearson = 0.52 (95%CI=0.29-0.68)
Spearman = 0.53 (95%CI=0.31-0.69)
Pearson = 0.46 (95%CI=0.23-0.64)
Spearman = 0.56 (95%CI=0.35-0.71)
Pearson = 0.26 (95%CI=0.0002-0.48)
Spearman = 0.30 (95%CI=0.04-0.51)
Fig. 1. Correlations between sample times for 60 women from the North Carolina
Early Pregnancy Study. Data are based on creatinine-adjusted concentrations.
Times shown between samples are medians (meanT1?T2¼ 16.6 days, SD ¼ 6.8;
meanT2?T3¼ 15.3 days, SD ¼ 8.5; meanT1?T3¼ 31.8 days, SD ¼ 11.2).
P.A. Nepomnaschy et al. / Environmental Research 109 (2009) 734–737
Three previous studies measured BPA from repeat samples Download full-text
from the same individual. One included 5 Japanese individuals
(Arakawa et al., 2004), another 31 US men and women
(Mahalingaiah et al., 2008), and the third 29 New York City
children (Teitelbaum et al., 2008). The latter is the only one of
these to report correlations between samples taken at various
time intervals, and they also found decreased correlations as time
between samples increased (maximum interval was 6 months).
Therefore, single measurements are unlikely to provide accurate
estimates of long-term exposure to BPA. However, our data
suggest that BPA is generally stable in freezer storage. This raises
the possibility that developmental effects in humans might
be investigated with specimens that have been collected at the
appropriate gestational age and stored for later assay. The results
provide support for further analyses to evaluate the effects of BPA
on reproductive outcomes measured in the North Carolina Early
The field manager of the North Carolina Early Pregnancy Study
was Joy Pierce, and D. Robert McConnaughey manages the study
data files. We thank David Shore and Grace Kissling for statistical
advice. An earlier version of this manuscript was reviewed by
Walter Rogan and Retha Newbold.
Arakawa, C., Fujimaki, K., Yoshinaga, J., Imai, H., Serizawa, S., Shiraishi, H., 2004.
Daily urinary excretion of bisphenol A. Environ. Health Prevent. Med. 9, 22–26.
Burridge, E., 2003. Bisphenol A: product profile. Eur. Chem. News 17, 14–17.
Baird, D.D., Weinberg, C.R., Wilcox, A.J., McConnaughey, D.R., Musey, P.I., 1991.
Using the ratio of urinary estrogen and progesterone metabolites to estimate
day of ovulation. Stat. Med. 10, 255–266.
Calafat, A.M., Kuklenyik, Z., Reidy, J.A., Caudill, S.P., Ekong, J., Needham, L.L., 2005.
Urinary concentrations of bisphenol A and 4-nonylphenol in a human
reference population. Environ. Health Perspect. 113, 391–395.
Dodds, E.C., Lawson, W., 1936. Synthetic oestrogenic agents without the
phenanthrene nucleus. Nature 137, 996.
Durando, M., Kass, L., Piva, J., Sonnenschein, C., Soto, A.M., Munoz de Toro, M., 2007.
Prenatal bisphenol A exposure induces pre-neoplastic lesions in the mammary
gland of Wistar rats. Environ. Health Perspect. 115, 80–86.
Greiner, E.O.C., Kalin, T., Nakamura, I.K., 2007. CEH Product Review: Bisphenol A.
Chemical Economics Handbook, SRI Consulting, Menlo Park, CA.
Hornung, R.W., Reed, L.D., 1990. Estimation of average concentration in the
presence of nondetectable values. Appl. Occup. Environ. Hyg. 5, 46–51.
Kang, J.H., Kondo, F., Katayama, Y., 2006. Human exposure to bisphenol A.
Toxicology 226, 79–89.
Lang, I.A., Galloway, T.S., Scarlett, A., Henley, W.E., Depledge, M., Wallace, R.B., Melzer,
D., 2008. Association of urinary bisphenol A concentration with medical
disorders and laboratory abnormalities in adults. JAMA 300, 1303–1310.
Mahalingaiah, S., Meeker, J.D., Pearson, K.R., et al., 2008. Temporal variability and
predictors of urinary bisphenal A concentrations in men and women. Environ.
Health Perspect. 116, 173–178.
Newbold, R.R., Jefferson, W.N., Padilla-Banks, E., 2007. Long-term adverse effects of
neonatal exposure to bisphenol A on the murine female reproductive tract.
Reprod. Toxicol. 24, 253–258.
Richter, C.A., Birnbaum, L.S., Farabolllini, F., et al., 2007. In vivo effects of bisphenol
A in laboratory rodent studies. Reprod. Toxicol. 24, 199–224.
Shrout, P., Fleiss, J., 1979. Intraclass correlations: uses in assessing rater reliability.
Psychol. Bull. 86, 420–428.
Taussky, H.H., 1954. A microcolorimetric determination of creatine in urine by the
Jaffe reaction. J. Biol. Chem. 208, 853–861.
Teitelbaum, S.L., Britton, J.A., Calafat, A.M., et al., 2008. Temporal variability in
urinary concentrations of phthalate metabolites, phytoestrogens and phenols
among minority children in the United States. Environ. Res. 107, 257–269.
Tess, R.W., 1988. Epoxy resin coatings. In: May, C.A. (Ed.), Epoxy Resins: Chemistry
and Technology, second ed. Marcel Dekker, New York, pp. 719–782.
Vandenberg, L.N., Hauser, R., Marcus, M., Olea, N., Welshons, W.V., 2007. Human
exposure to bisphenol A (BPA). Reprod. Toxicol. 24, 139–177.
Volkel, W., Colnot, T., Csanady, G.A., Filser, J.G., Dekant, W., 2002. Metabolism and
kinetics of bisphenol A in humans at low doses following oral administration.
Chem. Res. Toxicol. 15, 1281–1287.
vom Saal, F.S., Akingbemi, B.T., Belcher, S.M., et al., 2007. Chapel Hill bisphenol A
expert panel consensus statement: Integration of mechanisms, effects in
animals and potential to impact human health at current levels of exposure.
Reprod. Toxicol. 24, 131–138.
Welshons, W.V., Nagel, S.C., Vom Saal, F.S., 2006. Large effects from small
exposures. III. Endocrine mechanisms mediating effects of bisphenol A at
levels of human exposure. Endocrinology 147 (Suppl. 6), S56–S69.
Wilcox, A.J., Weinberg, C.R., O’Connor, J.F., Baird, D.D., Schlatterer, J.P., Canfield, R.E.,
Armstrong, E.G., Nisula, B.C.,1988. Incidence of early loss of pregnancy. N. Engl.
J. Med. 319, 189–194.
Willhite, C.C., Ball, G.L., McLellan, C.J., 2008. Derivation of a bispenol A oral
reference dose (RfD) and drinking-water equivalent concentration. J. Toxicol.
Environ. Health, B Crit. Rev. 11, 69–146.
Ye, X., Bishop, A.M., Reidy, J.A., Needham, L.L., Calafat, A.M., 2007. Temporal stability
of the conjugated species of bisphenol A, parabens, and other environmental
phenols in human urine. J. Exp. Sci. Environ. Epidemiol. 17, 567–572.
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