Journal of Exposure Analysis and Environmental Epidemiology (2000) 10, 321 ± 326
# 2000 Nature America, Inc. All rights reserved 1053- 4245/00/$15.00
www.nature.com/jea
Household exposures to drinking water disinfection by-products: whole
blood trihalomethane levels
LORRAINE C. BACKER,a DAVID L. ASHLEY,b
STEPHANIE M. KIESZAKa AND JOE V. WOOTENb
MICHAEL A. BONIN,b
FREDERICK L. CARDINALI,b
a
Division of Environmental Hazards and Health Effects, National Center for Environmental Health, Centers for Disease Control and Prevention,
Atlanta, Georgia
b
Division of Laboratory Sciences, National Center for Environmental Health, Centers for Disease Control and Prevention, Atlanta, Georgia
Exposure to drinking water disinfection by - products ( DBPs ) , such as trihalomethanes ( THMs ) , has been associated with bladder and colorectal cancer in
humans. Exposure to DBPs has typically been determined by examining historical water treatment records and reconstructing study participants' water
consumption histories. However, other exposure routes, such as dermal absorption and inhalation, may be important components of an individual's total
exposure to drinking water DBPs. In this study, we examined individuals' exposure to THMs through drinking, showering, or bathing in tap water. Thirty - one
adult volunteers showered with tap water for 10 min ( n = 11 ) , bathed for 10 min in a bathtub filled with tap water ( n = 10 ) , or drank 1 l of tap water during a 10 min time period ( n = 10 ) . Participants provided three 10 ml blood samples: one sample immediately before the exposure; one sample 10 min after the exposure
ended; and one sample 30 min ( for shower and tub exposure ) or 1 h ( for ingestion ) after the exposure ended. A sample of the water ( from the tap, from the
bath, or from the shower ) was collected for each participant. We analyzed water samples and whole blood for THMs ( bromoform, bromodichloromethane,
dibromochloromethane, and chloroform ) using a purge - and - trap / gas chromatography / mass spectrometry method with detection limits in the parts - per quadrillion range. The highest levels of THMs were found in the blood samples from people who took 10 - min showers, whereas the lowest levels were found in
the blood samples from people who drank 1 l of water in 10 min. The results from this study indicate that household activities such as bathing and showering are
important routes for human exposure to THMs. Journal of Exposure Analysis and Environmental Epidemiology ( 2000 ) 10, 321 ± 326.
Keywords: chlorination, disinfection, disinfection by - products, drinking water, household exposures, trihalomethanes.
Introduction
Chlorine is the most commonly used chemical for disinfecting U.S. water supplies (King and Marrett, 1996 ); however,
chlorine reacts with organic compounds in the water to
produce halogenated hydrocarbon by - products, including
trihalomethanes (THMs; e.g., chloroform, bromoform,
bromodichloromethane, and dibromochloromethane ) . Exposure to these disinfection by -products (DBPs ) has been
associated with cancer, particularly bladder cancer in
humans (Cantor et al., 1987, 1998; Zierler et al., 1988;
McGeehin et al., 1993; King and Marrett, 1996; Freedman et
al., 1997 ). Because of the human health risk associated with
exposure to THMs that results from chlorinating drinking
water, the maximum contaminant level (MCL ) for total
THMs in finished ( treated ) drinking water is 80 g /l (U.S.
EPA, 1998 ).
1. Address all correspondence to: Dr. Lorraine C. Backer, Environmental
Epidemiologist, National Center for Environmental Health, 4770 Buford
Highway NE, MS F - 46, Atlanta, GA 30341. Tel.: +1 - 770 - 488 - 7603.
Fax: +1 - 770 - 488 - 3506. E-mail: [email protected]
Received 4 February 2000; accepted 17 May 2000.
One difficulty in demonstrating the association
between exposure and health outcome is the long latency
period for cancer development and the subsequent need
to reconstruct water consumption and exposure histories
over a long period of time. For example, King and
Marrett (1996 ) found that people exposed to THM
levels 50 g/ l for 35 years or more had 1.63 times the
risk of bladder cancer compared with those exposed for
less than 10 years. McGeehin et al. (1993 ) found that
the number of years of exposure to chlorinated drinking
water was positively associated with risk for bladder
cancer. The risk for bladder cancer increased for longer
exposure durations (i.e., the odds ratio, OR, was 1.8 for
30 years of exposure) .
Another difficulty in examining the health effects
produced by DBPs is determining how to define
exposure. Investigators have used water quality indicators
such as the source water (ground water vs. surface
water ), THM concentrations in the water supply, and the
historical chlorine dose for the water supply as indicators
of exposure to DBPs. Other studies (e.g., Zierler et al.,
1988 ) used length of residence in a community using
chlorinated drinking water as the exposure indicator. But
Backer et al.
these approaches cannot assign individual exposure
levels. King and Marrett (1996 ) assessed individual
exposures using retrospectively collected data on lifetime
water consumption. The difficulties associated with using
any of these exposure assessment methods include
variability in DBP concentrations in a given water
system over time and problems with reconstructing water
consumption history. In addition, these methods may not
account for all relevant exposure routes. For example,
household water use ( e.g., showering, bathing, flushing
toilets, or using the dishwasher, washing machine, or
faucets) can result in significant indoor air concentrations of volatile organic compounds ( VOCs ), including
DBPs and other contaminants ( e.g., trichloroethylene )
( Andelman, 1985; Giardino et al., 1992; Weisel and
Chen, 1994; Wallace, 1997; Howard - Reed et al., 1999 ),
and subsequent VOC exposure through inhalation will
vary for different individuals within a household (Wilkes
et al., 1996 ) . In addition, DBPs, such as chloroform, can
be absorbed through the skin ( Jo et al., 1990a ).
Biological specimens can be used to determine the
dose of DBPs resulting from exposure to tap water by
different routes. Both blood and breath analyses should
reflect the total internal dose from all routes of exposure
( i.e., inhalation, dermal absorption, and ingestion) and
have been used to examine internal doses of VOCs in
non -occupationally exposed individuals. For example,
Ashley et al. ( 1994 ) found detectable levels of benzene,
ethylbenzene, chloroform, and other VOCs in blood
samples from non -occupationally exposed subjects selected from the Third National Health and Nutrition
Examination Survey. Weisel et al. (1992) and Jo et al.
( 1990a,b ) have utilized breath analysis to examine
exposure to chloroform in people who showered with
chlorinated tap water. In these studies, although the
amount of time between the end of the exposure and
sample collection varied among participants, breath
samples indicated that exposure to chloroform occurs
during showering. Lindstrom et al. ( 1994 ) found that
inhalation exposures to benzene ( from gasoline -contaminated water ) during actual showering were approximately two to five times higher than corresponding
bathroom exposures ( i.e., benzene concentrations ranged
from 758 to 1670 g /m3 in the shower stall and 366 to
498 g/m3 in the bathroom during and immediately after
the shower ).
To more fully examine the association between
exposure to DBPs and cancer, researchers must account
for all of the relevant household activities (e.g.,
bathing, showering, drinking water ) in estimating an
individual's lifetime dose of DBPs. In this study, we
examined whole blood levels of THMs in individuals
exposed by bathing or showering in tap water, or by
drinking tap water.
322
Household exposures to drinking water disinfection by-products
Methods
Study Design and Population
This study was conducted in Atlanta, Georgia, using a
consent form and protocol approved by the Institutional
Review Board of the Centers for Disease Control and
Prevention (CDC ) . We obtained informed consent from
31 adult volunteers ( 20 women, 11 men ) who agreed to
participate in one of the following household activities:
showering for 10 min with tap water ( n= 11 ), immersing
themselves for 10 min in a bathtub filled with tap water
(n = 10) , or drinking 1 l of water during a 10 -min time
period (n = 10) . For the showering and bathing segments,
we asked participants to collect a sample of the water
they used and measure with a thermometer the
temperature of the water they used. The water flow,
which was the same for all participants, was 7.2 l/ min.
Automatic ventilation fans were on in the bathrooms at
all times during study activities.
Study participants were also requested to provide three
10 ml blood samples associated with the tap water
exposure: one sample immediately before the exposure;
one sample 10 min after the exposure had ended (the
exposure ended when they got out of the bath, turned off
the shower, or finished drinking the water ) ; and one
sample 30 min (for shower and tub exposure) or 1 h
(for ingestion ) following the end of the exposure. Study
participants did not drink water, shower, or bathe during
the time between drawing of the second and third blood
samples. Study participants were not requested to
complete a questionnaire.
Data Collection
Blood Samples A certified phlebotomist collected blood
samples using Vacutainer1 tubes that had been processed
to remove VOC contamination (Cardinali et al., 1995 ). The
blood samples were analyzed for THM (bromoform
[CHBr3 ] , bromodichloromethane [ CHCl2Br ], dibromochloromethane [CHClBr2 ] , and chloroform [ CHCl3 ] )
levels using a headspace purge-and -trap / gas chromatography /mass spectrometry method with detection limits in
the parts -per- quadrillion range. The mass spectrometry
portion of the method had been modified from the original
VOC analysis procedure (see Ashley et al., 1992 ) to
achieve lower detection limits. To increase the sensitivity of
the analysis for THMs in blood, we operated the mass
spectrometer in selective ion recording (SIR ) mode instead
of in full scan. Extraction of VOCs from blood, trapping on
Tenax in a glass -lined steel tube, removal of water, and
concentration on a liquid nitrogen trap were done with a
Tekmar ( Cincinnati, Ohio) 3000 purge- and -trap concentrator with an attached ALS 2016 automated sampler. We
separated the analytes with a J&W (Folsom, California ) 30
Journal of Exposure Analysis and Environmental Epidemiology (2000) 10 (4)
Household exposures to drinking water disinfection by-products
Water Samples To provide a measure of VOC exposure, we
collected tap water samples at the time of exposure. The
water samples were collected in borosilicate glass vials
which contained 125 l of a phosphate buffer /sodium
thiosulfate solution. The solution was made using J.T.
Baker ( Phillipsburg, NJ ) HPLC grade water and 1.0 M
sodium dihydrogen phosphate, 1.0 M sodium hydrogen
phosphate and 0.08 M sodium thiosulfate. This solution
raised the pH of the tap water to approximately 6.5 and
neutralized any free chlorine present in the sample. We
examined residual chlorine and pH for all samples.
We analyzed the water samples for THM levels using
solid phase microextraction ( SPME ) /gas chromatography /
mass spectrometry with method detection limits in the
parts - per- trillion range. Extraction of the THMs from the
water sample was done using a Supelco ( Bellefonte, PA )
100 m carboxen/PDMS SPME fiber attached to a Varian
( Walnut Creek, CA ) 8200 automated sampler. THMs were
absorbed onto the SPME fiber at room temperature for 10
min and then desorbed into the GC inlet at 2008C for 3 min.
We separated the analytes with a Supelco 10 m VOCOL
column with a 1.20 m film thickness mounted in a
Hewlett -Packard (Avondale, PA ) Model 5890 gas chromatograph. Mass spectral analysis was done with a
Hewlett -Packard 5972 mass selective detector. The mass
selective detector was operated in the selected ion
monitoring mode with dwell times varying from 50 to 100
ms per ion for a total scan rate of 1.69 cycles / s. We also
Journal of Exposure Analysis and Environmental Epidemiology (2000) 10 (4)
determined water concentrations using isotope dilution
mass spectrometry methods.
Data Analysis We compared the mean concentrations of
THMs in the blood of people exposed to tap water, both
before and after exposure, and by the three different routes,
using Statistical Analysis System software (SAS Institute,
Cary, North Carolina) .
Results and discussion
The whole blood levels of bromodichloromethane, dibromochloromethane, and chloroform are presented in Figures
1 ±3, respectively. There were measurable levels of THMs
in all the water and whole blood samples that were analyzed.
The highest median levels of THMs were found in the blood
samples from people who took 10- min showers, whereas
the lowest median levels were found in the blood samples
from people who drank 1 l of water in 10 min. For example,
the median levels of bromodichloromethane in blood
samples from people who took a shower were 3.3 pg/ ml
(baseline ) , 19.4 pg /ml ( 10 min after exposure ended) , and
10.3 pg/ ml ( 30 min after exposure ended ). The median
levels of bromodichloromethane in blood samples from
people who took a bath were 2.3 pg /ml (baseline ), 17.0
pg /ml ( 10 min after exposure ended ), and 9.9 pg /ml (30
min after exposure ended ). For those who drank 1 l of
water, the median levels of bromodichloromethane in the
blood samples were 2.6 pg/ ml (baseline ) , 3.8 pg /ml (10
30
T=+10**
Blood Concentration (pg/ml)
m DB -624 column, with a 1.8 m film thickness mounted
in a Hewlett - Packard ( Avondale, Pennsylvania ) Model
5890 series II gas chromatograph. The effluent from the gas
chromatograph was directed through a heated interface into
the mass spectrometer ion source. Mass spectral analysis
was done with a Micromass (Beverly, Massachusetts )
Ultima high - resolution mass spectrometer that operated at
10,000 resolving power ( 5% valley definition ) in the SIR
voltage mode. Masses were calibrated vs. a mixture of
perfluorokerosene (low boiling ) with a 50/50 mixture of
toluene and benzene. The mass spectrometry analysis,
which included methyl tert - butyl ether ( MTBE ) ,was
divided into five groups: MTBE /MTBE -d10, 4.40± 6.20
min, masses: 73.065, 74.071, and 82.122 amu;
CHCl3 / 13CHCl3, 6.20 ±7.50 min, masses 82.946, 84.943,
83.949, and 85.946 amu; CHCl2Br/ 13CHCl2Br, 8.30±
10.10 min, masses 82.946, 84.943, 83.949, and 85.946
amu; CHClBr2 / 13CHClBr2, 11.10 ±12.10 min, masses
126.895, 128.892, 127.898, and 129.896 amu; and
CHBr3 / 13CHBr3, 13.00 ± 14.20 min, 172.843, 174.840,
173.846, and 175.844 amu. Peak areas were determined
using the OPUSquan software of Micromass. We determined blood concentrations of bromoform, bromodichloromethane, dibromochloromethane, and chloroform by using
isotope dilution mass spectrometry methods.
Backer et al.
T=+10**
25
20
T=+30**
T=+30**
15
10
T=0
T=0 T=+10*
T=+60
T=0
5
0
Drinking
Bathing
Showering
Figure 1. Bromodichloromethane levels ( pg / ml whole blood ) in the
blood of study participants who bathed or showered in, or drank 1
liter of, tap water and provided blood samples before the exposure
( T = 0 ) , 10 min after the exposure ended ( T = 10 ) , and 30 ( for
bathing or showering ) or 60 ( for drinking ) min after exposure
ended. The mean concentration of bromodichloromethane in tap
water was 6 g / l. For the box plots: the box extents indicate the 25th
and 75th percentiles of the column, the line inside the box marks the
value of the 50th percentile, capped bars indicate the 10th and 90th
percentiles, and circles mark the 5th and 95th percentiles. *Significantly different from baseline, P < 0.01; **Significantly different
from baseline, P < 0.001.
323
Backer et al.
Household exposures to drinking water disinfection by-products
250
T=+10**
200
T=+30*
T=+30**
150
T=+10*
T=+60*
T=0
100
T=0
T=0
50
Drinking
0
Bathing
Showering
Figure 2. Chloroform levels ( pg / ml whole blood ) in the blood of
study participants who bathed or showered in, or drank 1 liter of, tap
water and provided blood samples before the exposure ( T = 0 ) , 10
min after the exposure ended ( T = 10 ) , and 30 ( for bathing or
showering ) or 60 ( for drinking ) min after exposure ended. The mean
concentration of chloroform in tap water was 28.0 g / l. For the box
plots: the box extents indicate the 25th and 75th percentiles of the
column, the line inside the box marks the value of the 50th percentile,
capped bars indicate the 10th and 90th percentiles, and circles mark
the 5th and 95th percentiles. *Significantly different from baseline,
P < 0.01; **Significantly different from baseline, P < 0.001.
min after drinking all the water ), and 2.8 pg /ml (1 h after
drinking the water ) . We obtained similar relative findings
for dibromochloromethane and chloroform.
The highest blood levels of each THM were found in the
samples collected 10 min after exposure ended. By the
second post - exposure time (30 min for showering or
bathing; 60 min for drinking water ), the blood levels had
8
Blood Concentration (pg/ml)
T=+10**
T=+10**
6
T=+30**
T=0
T=0
T=0
Drinking
Bathing
25
Showering
Figure 3. Dibromochloromethane levels ( pg / ml whole blood ) in the
blood of study participants who bathed or showered in, or drank 1
liter of, tap water and provided blood samples before the exposure
( T = 0 ) , 10 min after the exposure ended ( T = 10 ) , and 30 ( for
bathing or showering ) or 60 ( for drinking ) min after exposure
ended. The mean concentration of dibromochloromethane in tap
water was 1.1 g / l. For the box plots: the box extents indicate the
25th and 75th percentiles of the column, the line inside the box marks
the value of the 50th percentile, capped bars indicate the 10th and
90th percentiles, and circles mark the 5th and 95th percentiles.
*Significantly different from baseline, P < 0.01; **Significantly
different from baseline, P < 0.001.
324
30
T=+60
2
0
T=+30**
T=+10*
4
decreased significantly, but were still higher than baseline
levels. Bromoform was not found above the detection limit
in any blood or water samples in this study.
We found a dramatic difference between the whole blood
levels resulting from exposure by ingestion and those
resulting from showering and bathing (a combination of
inhalation, dermal contact, and possibly ingestion ) . The
blood levels of THMs increased by an average of 16.1 pg /
ml in subjects who showered, an average of 14.7 pg /ml in
subjects who bathed, and an average of 1.2 pg /ml in
subjects who drank 1 l of water. Thus, drinking 1 l of water
increased blood levels by less than 10% of the increase
resulting from bathing or showering for 10 min. The
increases in blood THMs from showering or bathing were
significantly greater than the increases from drinking 1 l of
water ( P <0.001 for bromodichloromethane and dibromochloromethane; P= 0.017 for chloroform ).
In addition to finding the differences in blood THM
levels among the exposure groups, we found that the
increases in blood THM levels in people who showered or
bathed fell roughly into two groups; one group had a lower
range of increases in blood levels while the other group was
clustered at a higher blood level of bromodichloromethane
after showering or bathing (Figure 4 ). The mean increases
in bromodichloromethane blood levels for the two clusters
observed after participants bathed (8.2, standard deviation
[SD ] =2.97, n =5 for the lower cluster; and 21.2 pg /ml;
SD = 4.26, n = 5 for the higher cluster ) or showered (12.1
pg /ml, SD = 1.87, n =6 for the lower cluster; and 21.0 pg /
ml, SD =2.07, n = 5 for the higher cluster ) were significantly
different ( P <0.001) . The same individuals who had higher
increases of bromodichloromethane also had higher increases of dibromochloromethane and chloroform after
these exposures. The mean increases for total THMs for the
clusters were also statistically significantly different for the
groups that bathed (P=0.05 ) or showered (P < 0.01) .
Blood Concentration (pg/ml)
Blood Concentration (pg/ml)
T=+10*
20
15
10
5
0
Shower
Bath
Figure 4. Increase in bromodichloromethane levels ( pg / ml whole
blood; ppt ) in the blood of study participants 10 min after they
bathed or showered for 10 min in tap water. The mean concentration
of bromodichloromethane in tap water was 6.0 g / l.
Journal of Exposure Analysis and Environmental Epidemiology (2000) 10 (4)
Household exposures to drinking water disinfection by-products
The reason why the data fall into two groups is not clear.
The clustering could not be explained by sex (we did not
collect information about race or smoking status). It is
possible that this clustering is the result of individual
variations in the ability to metabolize THMs. For example,
brominated THMs are substrates for glutathione S -transferase (GST ) -theta -mediated glutathione conjugation reactions ( Landi et al., 1999 ). This enzyme is polymorphically
expressed in people, and individuals who have the active
enzyme would have higher blood levels of the metabolites
( and lower levels of the parent compound ) than individuals
who do not possess the active enzyme.
The observed pattern in the increase in blood THM levels
could also be associated with the fitness of individual
participants. People who inhale larger volumes of air would
inhale higher doses of volatilized THMs, and this would be
reflected in their blood THM levels; however, we would
expect these differences to be on a continuous scale rather
than falling into two groups. Evaluation of these differences
requires further experiments that include specific evaluation
of enzyme activity and personal cardiorespiratory parameters.
Of particular interest were the measurable levels of
THMs in the baseline (pre - exposure) blood samples for all
study participants. The half - life of VOCs (such as THMs )
in human blood is typically very short (less than 1 h)
( Ashley and Prah, 1997 ), suggesting that pre -exposure
levels would be very low if not undetectable. However,
there is evidence that VOCs are stored in multiple sites
within the body and that, with repeated exposure, these
compounds may bioaccumulate (Ashley and Prah, 1997 ).
Apart from exposure to heavily chlorinated water in
swimming pools or hot tubs, the most common source of
THM exposure is from household water. The detection of
THMs in the blood of people even before they participated
in the experimental exposures suggests either that there was
a recent exposure before participating in the study or that
these compounds have bioaccumulated over time from
repeated exposure to tap water.
The concentration of contaminants in drinking water
varies over time and is dependent on the characteristics of
the source water, types of treatment methods, characteristics
of the distribution system, and ways the water is used. To
provide a measure of VOC exposure, we collected samples
of the tap water used by each study participant. The analyses
of the drinking water samples are presented in Table 1.
Drinking water sources in the Atlanta area contain very little
bromide, thus bromoform was not detected in any of the
samples. Measurable levels of bromodichloromethane,
dibromochloromethane, and chloroform were found in all
of the water samples tested. The mean total THM level in
the water used for exposure in this study was 35 g /l. The
concentrations of THMs in these samples were well below
the current EPA standard for total THMs in drinking water
Journal of Exposure Analysis and Environmental Epidemiology (2000) 10 (4)
Backer et al.
Table 1. Means and ranges of trihalomethane concentrations in tap water
used by study volunteers who participated in different household activities.
THM
Mean concentration ( g / l ) ‹ SD
Shower
Bath
Drinking
Bromoform
Bromodichloromethane
< LDa
6.27 ‹ 0.686
< LD
6.22 ‹ 0.713
< LD
5.52 ‹ 0.204
Dibromochloromethane
1.20 ‹ 0.092
1.17 ‹ 0.150
1.00 ‹ 0.027
Chloroform
31.0 ‹ 3.54
31.8 ‹ 6.26
20.4 ‹ 1.97
a
Limit of detection.
(80 g/ l). In fact, these levels are below the Stage 2
proposal of 40 g/ l. Despite the fact that the water
contained relatively low levels of THMs, this exposure
resulted in significant increases in internal dose levels of
these compounds in the subjects. The determination of
detectable levels of THMs in people's blood even before
they participated in study activities is important in
considering the human health risk from exposure to THMs
and other volatile drinking water contaminants. Repeated
exposures to THMs from various household activities could
increase the body burden of THMs and potentially increase
the risk for adverse health effects.
Exposure to THMs from drinking water can occur by
inhalation, ingestion, and dermal absorption, and the tissue
distributions of THMs vary with the route of exposure. In
our study, people who drank water consumed an average of
35 g total trihalomethanes ( TTHMs ). If this dose was
absorbed entirely by the blood (assuming an average blood
volume of 5 l), we would expect to see blood levels of
approximately 7 ng/ ml TTHM. We actually found an
average of 29 pg/ ml TTHM in this group 10 min after they
finished drinking the water. Thus, 10 min after drinking 1 l
of water, most of the ingested dose is excreted or
metabolized rather than absorbed into the blood. By
contrast, exposure to volatilized THMs by inhalation and
dermal absorption resulted in a more direct distribution to
the blood and higher blood levels. (i.e, 10 min after
showering or bathing, study participants had 152 pg/ ml
TTHM or 181 pg /ml TTHM, respectively, in their blood ).
The differences in blood THM levels following different
types of household exposures would also be affected by the
water temperature at the time of exposure. Weisel and Chen
(1994) reported that calculated THM exposure levels were
50% higher when using THM concentrations in heated
water than when using THM concentrations in cold water.
In our study, THM concentrations were higher in bath or
shower water than in cold tap water ( see Table 1) , and
blood THM levels in people who showered or bathed were
significantly higher than the blood levels of those who
drank water. However, the specific temperature of the water
used for bathing or showering did not appear to have an
important impact on subsequent blood THM levels. The
325
Backer et al.
average temperature of the water used for showering was
378C ( range 34 ±438C ) and the average temperature of the
water used for bathing was 388C ( range 36 ± 448C ) .
The most consistent human health effect associated with
exposure to THMs is bladder cancer. The studies done by
Cantor et al. ( 1987, 1998) , Zierler et al. (1988 ), McGeehin
et al. (1993 ), King and Marrett (1996 ) and Freedman et al.
( 1997 ) produced strikingly similar results. However,
despite the consistency, the reported risk for bladder cancer
from lifetime exposure to high levels of THMs reported by
these studies was nearly universally less than 2.0. Exposure
was typically assessed by examining historical water
treatment plant records or by reconstructing a person's
water consumption history. In our study, we found that the
dermal and inhalation exposures associated with showering
and bathing resulted in much higher blood levels of THMs
than drinking 1 l of water. If blood THM levels are a risk
factor for subsequent human health effects, such as bladder
cancer, then water consumption may not be the only
important route of exposure. Accounting for an individual's
participation in household activities involving tap water, as
well as his tap water consumption, may allow a more
accurate individual exposure assessment. Our study has
demonstrated that public health messages indicating that an
individual can significantly reduce his or her exposure to
THMs by not drinking tap water may lead to a false sense of
security regarding the risk for adverse health outcomes
associated with THM exposure.
Acknowledgments
The authors thank Daniel Huff and Charles Dodson for their
assistance in collecting blood samples, Judy Bass and Maria
Mirabelli for their assistance in conducting the field study,
and the volunteers from National Center for Environmental
Health for their participation in this study.
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