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1368
v o l u m e 117 | n u m b e r 9 | September 2009
•
Environmental Health Perspectives
Research
The endocrine-disrupting chemical bis-
phenol A (BPA) has recently garnered height-
ened attention because of widespread human
exposure and disruption of normal repro-
ductive development in laboratory animals
[Center for the Evaluation of Risks to Human
Reproduction (CERHR) 2008; Chapin et al.
2008; Goodman et al. 2006; European Union
2003; vom Saal and Hughes 2005]. BPA is
thought to disrupt normal cell function by
acting as an estrogen agonist (Wozniak et al.
2005) as well as an androgen antagonist (Lee
et al. 2003). In animal studies, prenatal and
neonatal exposure to BPA has been linked to
early onset of sexual maturation (Howdeshell
et al. 1999), altered development and tissue
organization of the mammary gland (Markey
et al. 2001), induction of pre neoplastic mam-
mary gland (Durando et al. 2007) and repro-
ductive tract lesions (Newbold et al. 2007),
increased prostate size (Timms et al. 2005),
and decreased sperm production (vom Saal
et al. 1998) in offspring. Most recently, expo-
sure to BPA has also been associated with
chronic disease in humans, including cardio-
vascular disease, diabetes, and serum markers
of liver disease (Lang et al. 2008).
Orally administered BPA is rapidly
metabolized by glucuronidation during first-
pass metabolism, with a biological half-life
of approximately 6 hr and nearly complete
elimination within 24 hr (Volkel et al. 2002).
However, because of continuous and wide-
spread exposure, > 92% of the 2,517 partici-
pants ≥ 6 years of age in the U.S. 2003–2004
National Health and Nutrition Examination
Survey (NHANES) had detectable concen-
trations of BPA in their urine (Calafat et al.
2008). The geometric mean (GM) urinary
BPA concentration in that study was 2.6 µg/L
(2.6 µg/g creatinine), and the 95th percentile
was 15.9 µg/L (11.2 µg/g creatinine).
An important source of human exposure is
thought to be the ingestion of food and drink
that has been in contact with epoxy resins
or polycarbonate plastics (Kang et al. 2006).
Polycarbonate is a durable, lightweight, and
heat-resistant plastic, making it popular for
use in plastic food and beverage containers.
Indeed, nearly three-fourths of the 1.9 billion
pounds of BPA used in the United States in
2003 was used for the manufacture of poly-
carbonate resin (CERHR 2008). Other com-
mon uses of BPA include the manufacture of
epoxy resins used as composites and sealants
in dentistry and in the lacquer lining of alumi-
num food and beverage cans (CERHR 2008;
European Union 2003).
Laboratory studies have demonstrated
that biologically active BPA is released from
polycarbonate bottles after simulated normal
use (Brede et al. 2003; Le et al. 2008). High
temperatures as well as acidic and alkali solu-
tions cause polymer degradation via hydroly-
sis, resulting in increased BPA migration. After
incubation for 8, 72, and 240 hr in food-sim-
ulating solvents (10% ethanol at 70°C and
corn oil at 100°C), mean BPA migration
increased with incubation time (Onn Wong
et al. 2005). After a sequence of washing and
rinsing, Le et al. (2008) found that new poly-
carbonate bottles leached 1.0 ± 0.3 µg/mL
BPA (mean ± SD) into the bottle content after
incubation at room temperature for 7 days.
Although exposure to boiling water increased
the rate of BPA migration up to 55-fold, used
bottles did not leach significantly more BPA
than new ones. However, other studies have
found that higher concentrations of BPA leach
from used polycarbonate plastic than from
new. BPA has been observed to leach from
polycarbonate animal cages after 1 week of
incubation at room temperature, with higher
levels of migration from used versus new cages
(Howdeshell et al. 2003). Similarly, after incu-
bation in 100°C water for 1 hr, the amount of
BPA leached from baby bottles subjected to
simulated use (including dishwashing, boiling,
and brushing into the bottle) exceeded the
amount that leached from new baby bottles
(Brede et al. 2003).
Recently, some polycarbonate bottle manu-
facturers voluntarily eliminated BPA from their
products (Nalgene Outdoor 2008), and several
retailers withdrew polycarbonate bottles from
Address correspondence to K.B. Michels, Obstetrics
and Gynecology Epidemiology Center, 221 Longwood
Ave., Boston, MA 02116 USA. Telephone: (617)
732-8496. Fax: (617) 732-4899. E-mail: kmichels@
rics.bwh.harvard.edu
We thank A. Bishop and T. Jia for technical assis-
tance in the urinary phenol measurements.
is project was supported by a Harvard University
Center for the Environment faculty research grant to
K.B.M. and by funds from the National Institute of
Environmental Health Sciences Biological Analysis
Core, Department of Environmental Health, Harvard
School of Public Health to K.B.M. J.L.C. was sup-
ported by the Training Program in Environmental
Epidemiology under grant T32 ES07069.
The findings and conclusions in this report are
those of the authors and do not necessarily represent
the views of the Centers for Disease Control and
Prevention.
The authors declare they have no competing
financial interests.
Received 22 January 2009; accepted 12 May 2009.
Polycarbonate Bottle Use and Urinary Bisphenol A Concentrations
Jenny L. Carwile,1 Henry T. Luu,2 Laura S. Bassett,2 Daniel A. Driscoll,2 Caterina Yuan,2 Jennifer Y. Chang,2
Xiaoyun Ye,3 Antonia M. Calafat,3 and Karin B. Michels1,4
1Department of Epidemiology, Harvard School of Public Health, and 2Harvard College, Faculty of Arts and Sciences, Harvard
University, Cambridge, Massachusetts, USA; 3Division of Laboratory Sciences, National Center for Environmental Health, Centers for
Disease Control and Prevention, Atlanta, Georgia, USA; 4Obstetrics and Gynecology Epidemiology Center, Department of Obstetrics,
Gynecology and Reproductive Biology, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts USA
Background: Bisphenol A (BPA) is a high-production-volume chemical commonly used in the
manufacture of polycarbonate plastic. Low-level concentrations of BPA in animals and possibly in
humans may cause endocrine disruption. Whether ingestion of food or beverages from polycarbonate
containers increases BPA concentrations in humans has not been studied.
oBjectives: We examined the association between use of polycarbonate beverage containers and
urinary BPA concentrations in humans.
Methods: We conducted a nonrandomized intervention of 77 Harvard College students to com-
pare urinary BPA concentrations collected after a washout phase of 1 week to those taken after an
intervention week during which most cold beverages were consumed from poly carbonate drinking
bottles. Paired t-tests were used to assess the difference in urinary BPA concentrations before and
after polycarbonate bottle use.
results: e geometric mean urinary BPA concentration at the end of the washout phase was
1.2 µg/g creatinine, increasing to 2.0 µg/g creatinine after 1 week of polycarbonate bottle use.
Urinary BPA concentrations increased by 69% after use of polycarbonate bottles (p < 0.0001).
e association was stronger among participants who reported ≥ 90% compliance (77% increase;
p < 0.0001) than among those reporting < 90% compliance (55% increase; p = 0.03), but this dif-
ference was not statistically significant (p = 0.54).
co n c l u s i o n s : One week of polycarbonate bottle use increased urinary BPA concentrations by two-
thirds. Regular consumption of cold beverages from polycarbonate bottles is associated with a sub-
stantial increase in urinary BPA concentrations irrespective of exposure to BPA from other sources.
ke y w o r d s : biomarkers, bisphenol A, endocrine disruptors, human, polycarbonate plastic. Environ
Health Perspect 117:1368–1372 (2009). doi:10.1289/ehp.0900604 available via http://dx.doi.org/
[Online 12 May 2009]
Polycarbonate bottle use and urinary BPA
Environmental Health Perspectives
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v o l u m e 117 | n u m b e r 9 | September 2009
1369
their stores altogether (Mui 2008). Canada
has imposed a ban on the use of BPA in poly-
carbonate baby bottles in order to reduce expo-
sure of infants to BPA (Health Canada 2008),
and similar legislation is being considered by
several U.S. states (Austen 2008). However,
such actions have been largely preemptive,
as no epidemiologic study has evaluated the
physio logic consequences of polycarbonate
bottle use. erefore, we studied the impact
of cold beverage consumption from poly-
carbonate bottles on meas urable urinary BPA
concentrations among a Harvard College
population. We also measured exposure to
the phenols triclosan (TCS), methyl paraben
(MePB), propyl paraben (PrPB), and benzo-
phenone-3 (BP-3), which occurs mainly
through the use of personal care products.
erefore, because exposure of these chemicals
is considered unrelated to polycarbonate bottle
use, we assessed their association with poly-
carbonate bottle use as a negative control.
Materials and Methods
Study population. We recruited Harvard
College students in April 2008 via e-mails to
freshman dormitory, upperclass house, and
student organization mailing lists. Students
were directed to a survey website, where
they provided contact information and indi-
cated their availability for the study dates.
Participant instructions and informed consent
forms were also made available. Students at
least 18 years of age who were available for the
entire study period were considered eligible
and were invited to an introductory meeting.
The 89 students who attended the meeting
returned their signed informed consent forms,
provided demographic information (age, sex,
ethnicity), and received two stainless steel
bottles. Seven participants withdrew from the
study before completing the washout phase,
and five participants withdrew after complet-
ing the washout phase but before completion
of the intervention phase. Participants who
withdrew were similar to those who completed
the study in terms of age (median, 19 years;
range, 18–22 years) but were slightly more
likely to be female (66.7%) than students who
completed the entire study. A total of 77 par-
ticipants completed the study. A $25 com-
pensation was provided only upon completion
of the study. e study was approved by the
Human Studies Institutional Review Board of
Harvard University. The involvement of the
Centers for Disease Control and Prevention
(CDC) laboratory was limited and was deter-
mined not to constitute engagement in human
subjects research.
Study design. e study began with a 7-day
washout phase designed to minimize exposure
to BPA by limiting the consumption of cold
beverages to those contained in stainless steel
bottles. Because orally administered BPA is
rapidly excreted (Volkel et al. 2002), we con-
sidered a 1-week washout period sufficient.
We provided participants with two stainless
steel bottles and advised them to drink all cold
beverages from the stainless steel bottles and
avoid drinking water from #7 poly carbonate
plastic cold water dispensers available in col-
lege dining halls. Participants donated urine
on their choice of 2 of 3 final days of the wash-
out phase. Urine donation took place between
1700 and 2000 hours on two of the days, and
between 1600 and 1900 hours on the third
day. Two poly carbonate bottles were distrib-
uted to each partici pant on the second day
of urine donation during the washout phase.
Participants were advised to begin drinking all
cold beverages from the polycarbonate bottles
(intervention week) immediately. Urine was
donated again on the participant’s choice of
2 of 3 final days of the week of polycarbonate
bottle use between 1700 and 2000 hours. On
the final day of urine donation, participants
completed a brief questionnaire in which they
estimated their percentage compliance during
the week in which they were asked to drink
cold beverages from the polycarbonate bottles.
Stainless steel bottles (27 fluid ounces, with
#5 polypropylene loop cap) were obtained
from Kleen Kanteen (763332017107; Chico,
CA). Polycarbonate bottles [Nalgene 32 fluid
ounce, Lexan narrow mouth (#53175), and
Lexan wide mouth (#53107)] were obtained
from Karst Sports (Shinnston, WV). All par-
ticipants were permitted to keep the bottles
used in the study.
Urine sample collection. Urine was col-
lected in a polypropylene container, aliquoted,
and frozen at –20°C. After study completion,
samples were defrosted at 4°C overnight and
vortexed; equal volumes of the two samples
from each phase of the study were then com-
bined and aliquoted. We shipped aliquots of
samples (blinded to those performing labora-
tory analyses) on dry ice overnight to the CDC
for measuring BPA and other urinary phenol
concentrations; samples were also taken to
N. Rifai (Children’s Hospital, Boston, MA)
for analysis of urinary creatinine.
Urinary phenol concentrations. Total uri-
nary concentrations (free plus conjugated spe-
cies) of BPA and the other four phenols were
determined using online solid-phase extraction
coupled to isotope dilution high-performance
liquid chromatography (HPLC)-tandem mass
spectrometry (MS/MS) on a system con-
structed from several HPLC Agilent 1100
modules (Agilent Technologies, Wilmington,
DE) coupled to a triple quadrupole API 4000
mass spectrometer (Applied Biosystems, Foster
City, CA) (Ye et al. 2005). First, 100 µL
urine was treated with β-glucuronidase/sul-
fatase (Helix pomatia; Sigma Chemical Co.,
St. Louis, MO) to hydrolyze conjugated spe-
cies of the phenols. The phenols were then
retained and concentrated on a C18 reversed-
phase size-exclusion solid-phase extraction col-
umn (Merck KGaA, Darmstadt, Germany),
separated from other urine matrix components
using a pair of monolithic HPLC columns
(Merck KGaA), and detected by nega tive ion-
atmospheric pressure chemical ionization-MS/
MS. The limits of detection (LODs) in a
0.1-mL urine sample were 0.4 µg/L (BPA and
BP-3), 0.2 µg/L (PrPB), 1.0 µg/L (MePB), and
2.3 µg/L (TCS). Low-concentration (~ 4 to
~ 25 µg/L) and high-concentration (~ 10 to
~ 65 µg/L) quality-control materials, prepared
with pooled human urine, were analyzed with
standard, reagent blank, and unknown samples
(Ye et al. 2005). Creatinine was measured by a
rate-blanked method using the Hitachi 917
analyzer and Roche Diagnostics reagents (both
from Roche Diagnostics, Indianapolis, IN).
Statistical analysis. Urinary phenol concen-
trations were normalized for dilution using the
formula 100 × urinary phenol concentration
(micro grams per liter) ÷ creatinine concen-
tration (milli grams per deci liter). Creatinine-
adjusted phenol concentrations (micrograms
per gram creatinine) were not normally dis-
tributed and were therefore log-transformed.
Phenol concentrations < LOD were assigned
a value equal to one-half the LOD (Hornung
1990) prior to creatinine adjustment.
We calculated GMs for creatinine-
corrected concentrations. We used paired
t-tests to examine the association between
log-transformed urinary creatinine-adjusted
phenol concentrations and drinking-container
assignment overall and within subsets defined
by percent compliance during the inter-
vention phase (≥ median and < the median).
When the participant reported compliance as
a range, we used the mean. Two sample t-tests
were used to make comparisons between the
strata defined by percent compliance.
Results
The study population included 77 subjects
who ranged in age from 18 to 23 years, with
a median of 19 years (Table 1). On the basis
Table 1. Characteristics of 77 Harvard College
students enrolled in a nonrandomized intervention
study assessing changes in urinary phenol con-
centrations associated with use of polycarbonate
drinking containers.
Characteristic No. (%)
Sex
Male 41 (53.2)
Female 36 (46.8)
Ethnicity
Caucasian 30 (39.0)
Asian 38 (49.3)
African American 5 (6.5)
Hispanic 4 (5.2)
Percent compliance [median 90 (50–100)
of proportion (range)]
Age, years [median (range)] 19 (18–23)
Carwile et al.
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v o l u m e 117 | n u m b e r 9 | September 2009
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Environmental Health Perspectives
of self-reported data, we cate gorized race/
ethnicity into four groups: Caucasian, Asian,
African American, and Hispanic. irty par-
ticipants (39.0%) were Caucasian, 38 were
of Asian descent (49.4%), 5 were African
American (6.5%), and 4 were Hispanic
(5.2%). Forty-one subjects were male (53.3%).
Protocol compliance for the week in which
participants drank from polycarbonate bottles
ranged from 50% to 100% but was generally
high, with a median of 90%.
Nine samples (11.7%) from the washout
week and three samples (3.9%) from the inter-
vention week (period in which participants
drank from polycarbonate bottles) had BPA
concentrations < LOD. BP-3 and MePB were
detected in all participants, and PrPB was
detected in all but one participant each week.
TCS was detected in 75.3% of the samples
taken at the end of the washout week and in
74.0% of the samples collected after the inter-
vention week. e GM concentration of BPA
was 1.3 µg/L (1.2 µg/g creatinine) during the
washout period and 2.1 µg/L (2.0 µg/g creati-
nine) during the intervention week (Table 2).
GM concentrations for the washout phase and
intervention week were 46.1 and 66.8 µg/g
creatinine for BP-3; 51.3 and 48.4 µg/g crea-
tinine for MePB; 8.4 and 8.8 µg/g creatinine
for PrPB; and 15.5 and 17.3 µg/g creatinine
for TCS, respectively.
Table 3 presents results from paired t-tests
comparing urinary BPA concentrations in
weeks 1 and 2. Urinary BPA concentrations
increased by 69% after polycarbonate bottle
use. We observed a larger difference between
the intervention and washout weeks in the
stratum with intervention compliance ≥ 90%
(77% increase; p < 0.0001) relative to the stra-
tum with compliance < 90% (55%; p = 0.03);
however, the strata were not significantly dif-
ferent from each other (p = 0.54). Of the other
phenols, only urinary BP-3 concentration was
associated with polycarbonate bottle use, with
relatively higher concentrations observed after
use of poly carbonate bottles (45% increase;
p = 0.001). A slightly larger change in BP-3
concentration was observed in the less
compliant stratum (64% increase; p = 0.01)
relative to the more compliant stratum (36%
increase; p = 0.04); however, this difference
was not statistically significant (p = 0.42).
Discussion
Several previous studies have demonstrated
that biologically active BPA is released from
polycarbonate bottles into the bottle content
after simulated normal use (Brede et al. 2003;
Le et al. 2008). However, to our knowledge,
the present study is the first to quantify the
corresponding increase in urinary BPA con-
centrations after use of polycarbonate drinking
bottles. Thus, this study suggests that BPA-
containing drinking vessels release sufficient
amounts of BPA into the bottle content to
significantly raise the amount of BPA excreted
in urine in humans who drink from these bot-
tles. Specifically, in this study of 77 Harvard
College students, urinary BPA concentrations
were higher when participants consumed the
majority of cold beverages from poly carbonate
bottles compared with a washout phase in
which polycarbonate bottles were avoided.
This statistically significant increase was
observed despite background BPA exposure
from other sources, which was not assessed
nor controlled in this study. is association
persisted after stratification by self-reported
compliance during the intervention week, with
a nonsignificantly larger difference between
intervention and washout phase urinary BPA
concentrations among participants reporting
higher percent compliance. Of interest, the
urinary BPA concentrations reported for this
group of students (both before and after the
intervention) were similar to those reported
for the U.S. general population (Calafat et al.
2008) and selected populations in Southeast
Asia (Kim et al. 2003; Matsumoto et al. 2003;
Ouchi and Watanabe 2002; Yang et al. 2003).
Because of BPA’s short half-life and rapid
elimination (Volkel et al. 2002), carry over of
ingested BPA between the washout phase and
intervention phase was considered unlikely. It
is possible that certain subject characteristics
may have varied between the 2 weeks, produc-
ing a period effect that was unaccounted for by
our analyses. We considered this improbable
because of the lack of variability in the routine
of under graduate students, who attended the
same classes and ate in the same campus din-
ing halls each week. Additionally, the similar-
ity of observed urinary BPA concentrations
to national levels suggests that subjects were
exposed to typical amounts of BPA from other
sources during both weeks. Moreover, fatigue
and the participants’ exposure to mass media
concerning the leaching of BPA from poly-
carbonate bottles might have induced better
compliance during the washout phase than the
intervention phase, thus leading to an under-
estimate of the impact of poly carbonate bottle
use on urinary BPA concentrations. It is also
possible that participants may have modified
their behavior during the week of polycarbon-
ate bottle use to reduce BPA exposure from
other sources. However, other sources of BPA
exposure have not been well publicized, and
any reduction in exposure to other sources of
BPA during the intervention week would have
reduced the observed effect estimate.
We used spot urine samples for conve-
nience; however, disadvantages of this method
include interperson variability in BPA con-
centration and variability in the volume of
urine (Barr et al. 2005). Two equal-volume
Table 2. GM concentrations of phenols (µg/creatinine)
after washout and intervention.
Phenol Week of study GM (95% CI)
BPA Washout 1.2 (1.0–1.4)
Intervention 2.0 (1.7–2.4)
BP-3 Washout 46.1 (30.6–69.5)
Intervention 66.8 (42.3–105.5)
MePB Washout 51.3 (37.3–70.7)
Intervention 48.4 (36.2–64.8)
PrPB Washout 8.4 (5.4–12.9)
Intervention 8.8 (5.8–13.1)
TCS Washout 15.5 (9.5–25.3)
Intervention 17.3 (10.7–28.1)
Concentrations (µg/L) < LOD were recorded as 1/2 LOD,
which is 0.2 for BPA and BP-3; 1.15 for TCS; 0.5 for MePB;
and 0.1 for PrPB.
Table 3. Percent change in urinary concentrations of phenols associated with 1-week use of polycarbonate
drinking containers.
Phenol Percent change (95% CI) p-Value p for heterogeneity
BPA
Overall 69 (40 to 102) < 0.0001
≥ 90% compliance 77 (45 to 117) < 0.0001
< 90% compliance 55 (6 to 127) 0.03 0.54
BP-3
Overall 45 (16 to 81) 0.001
≥ 90% compliance 36 (2 to 80) 0.04
< 90% compliance 64 (11 to 142) 0.01 0.42
MePB
Overall –6 (–25 to 18) 0.60
≥ 90% compliance 17 (–10 to 51) 0.24
< 90% compliance –34 (–56 to 0) 0.05 0.01
PrPB
Overall 5 (–24 to 44) 0.77
≥ 90% compliance 15 (–23 to 70) 0.49
< 90% compliance –10 (–49 to 59) 0.70 0.46
TCS
Overall 12 (–17 to 50) 0.46
≥ 90% compliance 11 (–18 to 50) 0.50
< 90% compliance 17 (–39 to 126) 0.62 0.88
Concentrations (µg/L) < LOD were recorded as 1/2 LOD, which is 0.2 for BPA and BP-3; 1.15 for TCS; 0.5 for MePB; and 0.1
for PrPB. Twenty-eight participants reported < 90% compliance over intervention week, 48 participants reported ≥ 90% com-
pliance, and compliance was missing for one participant.
Polycarbonate bottle use and urinary BPA
Environmental Health Perspectives
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v o l u m e 117 | n u m b e r 9 | September 2009
1371
samples from each week were combined to
minimize day-to-day variability. Additionally,
we collected all urine samples in the evening,
minimizing variability related to time of day
(Mahalingaiah et al. 2008). Concern regard-
ing interperson variability is also mitigated by
recent findings that a single urinary BPA con-
centration was predictive of long-term exposure
on a scale of weeks to months (Mahalingaiah
et al. 2008). Urinary BPA concentrations were
creatinine-adjusted to account for variability
in urine dilution. Overall, the results obtained
after the analysis with and without correc-
tion of the urinary dilution were fairly similar.
However, failure to control for urinary creati-
nine concentrations resulted in a greater degree
of within-person variation and, subsequently,
decreased precision, as evidenced by wider
95% CIs. For this reason, we have presented
only the creatinine-adjusted results.
To account for the possibility of a chance
finding, we also compared the impact of poly-
carbonate bottle use on several phenols not
thought to be associated with poly carbonate
bottle use. As expected, we observed no dif-
ference for MePB, PrPB, or TCS, although
urinary concentrations of BP-3 were higher
after poly carbonate bottle use. However, after
stratification by percent compliance during the
intervention week, the association for BP-3 was
stronger in the less compliant group. By con-
trast, the association between BPA and poly-
carbonate bottle use was stronger in the more
compliant group, suggesting that BPA may
leach from polycarbonate bottles. We found
BPA and BP-3 to be strongly correlated: e
Pearson correlation coefficients between BP-3
and BPA were 0.38 (p = 0.0008) and 0.43
(p = 0.0001) during the washout week and
intervention week, respectively. Although this
study was not designed to look at other sources
of BPA, or any sources of the other phenols,
we hypothesize that the strong correlation
observed between BPA and BP-3 could be the
result of a shared source or behavior. We are
not aware of the presence of BP-3—a common
sunscreen agent in personal care products—in
polycarbonate plastic, although it can also be
used as ultraviolet stabilizer in plastic surface
coatings for food packaging to prevent poly-
mer or food photo degradation (Suzuki et al.
2005). However, because sources and routes of
exposure for many of these compounds are not
yet known, it is possible that BPA and BP-3
are used in a common product that has not
yet been identified. An alternative explanation
is that students who participated in the most
outdoor physical activity drank the most fluid
from their bottles and also applied the most
sunscreen, potentially increasing both BPA and
BP-3 levels.
Our study population included a high pro-
portion of Asian and Caucasian participants,
and our participants were young. However,
there is no obvious reason why the results of
our study should not apply to other ethnici-
ties and age groups. Furthermore, the use of
polycarbonate bottles is very popular among
college students, making this an especially
relevant population to study. Although we
assessed the effect of the exclusive use of poly-
carbonate plastic bottles as beverage contain-
ers, a proportionate increase in urinary BPA
would be expected among individuals who
use polycarbonate plastic bottles in combina-
tion with other beverage containers. Children
have been found to have higher urinary BPA
concentrations than adolescents and adults
(Calafat et al. 2008), consistent with animal
evidence of reduced glucuronidation in fetuses
and neonates (Matsumoto et al. 2002). us,
because of their reduced ability to clear BPA,
we predict that children would have higher
urinary BPA concentrations due to use of
polycarbonate plastic bottles relative to the
study population.
e major strength of this study is the non-
randomized intervention design. We compared
urinary BPA concentrations within each partic-
ipant, which precluded confounding by subject
characteristics that remain constant over time.
Although within-person confounding was pos-
sible, it is unlikely that unmeasured confound-
ing could account for the large effect estimate
we observed. e large increase in mean uri-
nary BPA concentration after regular use of
polycarbonate bottles suggests that the systema-
tic BPA variation in the two study phases was
by far greater than any random variation due
to BPA ingestion from other sources.
Furthermore, we assessed the impact of
polycarbonate bottle use in a normal use
setting. The present study could be consid-
ered a conservative estimate of true use, as
students did not have access to dish washers
and were instructed to use their containers
for cold beverages only, whereas the storage of
hot liquids is common, especially in outdoor
recreation settings. Because heating is thought
to increase the amount of BPA leached from
the polycarbonate (Le et al. 2008), we would
anticipate higher urinary BPA concentrations
after ingestion of hot beverages stored in the
same bottles.
Conclusions
To our knowledge, this is the first study to
assess the impact of polycarbonate drinking
bottle use on urinary BPA concentrations.
Despite within-person variability resulting
from other sources of BPA exposure, a meas-
urable increase in urinary BPA resulted from
only 1 week of exposure to beverages con-
tained in polycarbonate bottles. Replication
of this study in other populations may help to
inform public health policy regarding the use
of BPA in polycarbonate food and beverage
containers.
Re f e R e n c e s
Austen I. 2008. Plastic-bottle scare is a boon for some. New
York Times. Available: http://www.nytimes.com/2008/04/
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