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Children's Health
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Urinary 1-Hydroxypyrene as a Biomarker of PAH Exposure in 3-Year-Old Ukrainian Children Amy Pelka Mucha,1,2 Daniel Hryhorczuk,1,2 Andrij Serdyuk,3 Joseph
Nakonechny,4 Alexander Zvinchuk,5 Serap Erdal,2 Motria
Caudill,2 Peter Scheff,1,2 Elena Lukyanova,4 Zoreslava
Shkiryak-Nyzhnyk,6 and
Natalia Chislovska6 1Great Lakes Center for Occupational and Environmental Safety and
Health, and 2Division of Environmental and Occupational Health Sciences,
University of Illinois at Chicago, School of Public Health, Chicago, Illinois,
USA; 3Institute of Hygiene and Medical Ecology, Kiev, Ukraine; 4Institute
of Medico-Ecological Problems, Chernivtsi, Ukraine; 5University
of Illinois at Chicago Louise Hamilton Data Management Center, Kiev, Ukraine; 6Institute
of Pediatrics, Obstetrics and Gynecology, Kiev, Ukraine Abstract Urinary 1-hydroxypyrene (1-OHP) is a biomarker of polycyclic aromatic hydrocarbon (PAH) exposure. We measured urinary 1-OHP in 48 children 3 years of age in Mariupol, Ukraine, who lived near a steel mill and coking facility and compared these with 1-OHP concentrations measured in 42 children of the same age living in the capital city of Kiev, Ukraine. Children living in Mariupol had significantly higher urinary 1-OHP and creatinine-adjusted urinary 1-OHP than did children living in Kiev (adjusted: 0.69 vs. 0.34 µmol/mol creatinine, p < 0.001 ; unadjusted: 0.42 vs. 0.30 ng/mL, p = 0.002) . Combined, children in both cities exposed to environmental tobacco smoke in their homes had higher 1-OHP than did children not exposed (0.61 vs. 0.42 µmol/mol creatinine ; p = 0.04 ; p = 0.07 after adjusting for city) . In addition, no significant differences were seen with sex of the children. Our sample of children in Mariupol has the highest reported mean urinary 1-OHP concentrations in children studied to date, most likely due to their proximity to a large industrial point source of PAHs. Key words: air pollution, biomarker, children, environment, polycyclic aromatic hydrocarbons. Environ Health Perspect 114:603-609 (2006) . doi:10.1289/ehp.7898 available via http://dx.doi.org/ [Online 20 October 2005]
Address correspondence to A.P. Mucha, University of Illinois at Chicago, School of Public Health, Great Lakes Center for Occupational and Environmental Safety and Health, 2121 W. Taylor (M/C 922) , Chicago, IL 60612 USA. Telephone: (312) 413-0378. Fax: (312) 413-7369. E-mail: apmucha@uic.edu We gratefully acknowledge all the children and their families for their participation. We thank E. Delisio for his able technical assistance with mapping Mariupol. This work was supported in part by U.S. Environmental Protection Agency Cooperative Agreement CX826321-01-0 and the National Institutes of Health Fogarty International Center Grant 5 D43 TW00653. Additional in-kind support was provided by participating research institutions. The authors declare they have no competing financial interests. Received 30 December 2004 ; accepted 19 October 2005. |
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Polycyclic aromatic hydrocarbons
(PAHs) are a group of three-
and four-ring compounds that
are formed as a result of incomplete
combustion. Sources of environmental
contamination can be both industrial
and nonindustrial, with the most
common sources being cigarette
smoke, coal-fired utilities,
steel plants, vehicle exhaust,
wood-burning ovens and fireplaces,
and charcoal-grilled and smoked
food. The greatest exposures
to PAHs generally occur via cigarette
smoke, emissions from wood-burning
ovens and fireplaces, and consumption
of grilled and broiled foods
[International Agency for Research
on Cancer (IARC) 1987]. PAHs
are ubiquitous in the environment
and are found in many environmental
media, including indoor and ambient
air, soil, and diet. Children
tend to have higher PAH exposure
to air, soil, and dust than do
adults because of child-specific
behavior patterns, such as hand-to-mouth
activity and more time spent
close to and on the ground, as
well as having a higher inhalation
rate on a per unit body-weight
basis compared with adults (Committee
on Environmental Health 1999;
Landrigan et al. 1998). PAHs
have been shown to bind to the
aryl hydrocarbon receptor and
affect multiple systems (Nebert
and Atlas 1978). In addition,
they act as carcinogens in numerous
animal species and are used as
positive controls in skin painting
cancer studies. PAHs have also
been shown to be human carcinogens
in occupational settings and
have been found to be causally
associated with skin and lung
cancer. Coke oven emissions are
classified as known human carcinogens
[IARC 1987; U.S. Environmental
Protection Agency (EPA) 2003a],
of which PAHs are a major constituent.
PAHs have also been shown in
animals to cause humoral and
cellular immune toxicity (Davila
et al. 1996).
Because PAH exposure occurs
as a mixture of compounds, and
because pyrene is almost always
found in this mixture, pyrene
and its metabolite 1-hydroxypyrene
(1-OHP) are considered appropriate
surrogate markers of total PAH
exposure (Jacob and Seidel 2002).
Among the many PAH compounds,
pyrene is emitted in large amounts
and almost always found in the
presence of other PAHs, acting
as a surrogate marker for all
PAHs (Viau 2002). In the body,
pyrene is primarily metabolized
via the cytochrome P450 1A1 (CYP1A1)
enzymes and excreted in the urine
as 1-OHP (Jacob and Seidel 2002).
Therefore, 1-OHP can be assessed
relatively easily in urine samples
(Jongeneelen 1994). 1-OHP has
been found to be a good short-term
measure of exposure to PAHs.
The half-lives of 1-OHP reported
in the literature include between
6 and 35 hr (Jongeneelen et al.
1990), from 16 to 20 hr (Buchet
et al. 1992), and more recently,
9.8 hr using volunteers and facial
masks (Brzeznicki et al. 1997).
In general, urinary 1-OHP represents
the last 24 hr of cumulative
PAH exposure (Jongeneelen 1994).
1-OHP has been validated as
a biomarker of occupational exposure
to PAHs, including in coke oven
workers (Jacob and Seidel 2002;
Jongeneelen 2001; Viau 2002).
Concentrations have ranged from
0.3 to 25 µmol/mol creatinine
in coke oven workers (Jongeneelen
2001; Levin 1995). 1-OHP levels,
after environmental exposures,
are lower by one to two orders
of magnitude, depending on background
exposures and smoking habits
(Jongeneelen 2001).
Table 1
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Figure 1. Literature
summary of 1-OHP concentrations
in children.
aChuang
et al. 1999, bFiala
et al. 2001, cZhao
et al. 1990, dVyskocil
et al. 2000, evan
Wijnen et al. 1996, fSiwinska
et al. 1998, gSiwinska
et al. 1999, hNorthridge
et al. 1999, iJongeneelen
et al. 1994. |
Figure 2. Map
of Mariupol, Ukraine. |
Studies of childhood PAH exposure
and measurement of urinary 1-OHP
have almost entirely been with
lower-level PAH contamination
than in the present study. Overall,
data are much more scarce for
children’s environmental
PAH exposure than for workers’ exposure.
Studies in children have been
done in several countries, with
most identifying diet as the
most important contributor to
1-OHP (Chuang et al. 1999; van
Wijnen et al. 1996; Vyskocil
et al. 2000) and other studies
finding a role for traffic and
environmental tobacco smoke (ETS)
(Kanoh et al. 1993; Siwinska
et al. 1998). A review of 1-OHP
concentrations in children is
presented in Table 1 and displayed
in Figure 1.
Van Wijnen et al. (1996) determined
the urinary 1-OHP levels in Dutch
children living in five distinct
areas with differing levels of
PAHs in soil and ambient air,
from background traffic releases
to areas with mine tailings.
The researchers investigated
the influence of recent consumption
of food with high PAH content,
indoor and outdoor sources of
PAHs, hand-to-mouth behavior,
and play habits of children obtained
through a questionnaire on urinary
1-OHP levels. Only indoor sources
of PAHs showed a small, positive
association with 1-OHP levels.
The authors concluded that the
possible ambient environment-related
differences were potentially
too small to be detected in the
variations of the intake of PAHs
from daily diet. In Japan, Kanoh
et al. (1993) assessed urinary
1-OHP levels of school children
in two areas of Tokyo along arterial
roads and in one suburban area.
Children living in the higher
traffic areas had significantly
higher 1-OHP levels than did
the children in the less polluted
area, by a factor of 1.1-1.6
(Kanoh et al. 1993). Zhao et
al. (1992) assessed biologic
exposure of a small group of
school children in Beijing, where
ambient air has significant PAH
pollution, and 1-OHP levels were
elevated, as shown in Table 1.
Siwinska et al. (1998) found
that 1-OHP levels in children
in Poland increased because of
exposure to ETS only in the case
of mother’s smoking, but
the differences were not significant
(p > 0.05). Studies
in North Carolina children found
no statistically significant
relationship between urinary
PAH metabolites and the estimated
daily doses derived from PAH
concentrations in the relevant
environmental media because of
the great variability among individuals
(Chuang et al. 1999). In another
study of two small groups of
children recruited from a kindergarten
in a high-traffic-density area
and from a kindergarten in a
less contaminated area in Montreal,
Canada (Vyskocil et al. 2000),
no relationship was found between
absorbed pyrene doses, by ingestion
or by inhalation, and 1-OHP levels
in urine. This was attributed
to uncertainties in the estimates
of PAH uptake from food and/or
small sample size limiting statistical
power of the study. A study conducted
in a Czech city with four groups
of children recruited from polluted
(high traffic density) and nonpolluted
areas found seasonal variation
in 1-OHP and attributed variation
to differences in tobacco smoke
exposure (Fiala et al. 2001).
In this study we investigated
young children living in close
proximity to a significant environmental
point source of PAHs--a steel
mill and associated coke oven;
a map of Mariupol with PAH sources
and where the study participants
live is provided in Figure 2.
This analysis thus offered the
opportunity to investigate whether
a large environmental exposure
relates to a significant increase
in the PAH biomarker 1-OHP.
Study site description. Mariupol
is a city of approximately 530,000
in southeastern Ukraine, situated
on the Azov Sea (Figure 2). Mariupol
is considered one of the most
heavily polluted cities in Ukraine,
with multimedia contamination
in the air, water, and soil.
Mariupol’s landscape is
dominated by two major steel
plants and an associated coking
facility. These plants use older
equipment, some installed in
the 1950s, with outdated technologies
and minimal pollution control
equipment. The two steel mills
and coking facility combined
are responsible for > 99%
of air pollutants emitted from
stationary sources in the city,
two of which are located next
to a residential area. The city’s
coking facility is reported to
emit > 30 kg of benzo[a]pyrene
(BaP) annually into the atmosphere;
the steel plants emit thousands
of tons of nitrous oxides, carbon
monoxide, and particulate matter
[Ministry for Environmental Protection
and Nuclear Safety of Ukraine
(MEPNS) 1998]. Azovstal is the
name of the steel mill and coke
oven within 3 miles of the participants’ residences.
A sample of children living in
Kiev, the capital city of Ukraine
with a population of 2.6 million,
served as the comparison population.
Epidemiologic design. This
study, Environmental Pollutants
and Health Status of Children,
was conducted as part of the
Family and Children of Ukraine
study, the Ukrainian component
of the multicountry European
Longitudinal Study of Pregnancy
and Childhood (ELSPAC). ELSPAC
is a prospective and geographically
based series of population studies,
which begin in pregnancy and
follow the cohort of births until
7 years of age. The overall goal
of the larger study is to identify
risk factors for problems in
pregnancy, reproductive outcomes,
and childhood development (ELSPAC
1989).
In 1998, at the time of the
ELSPAC assessment at 3 years
of age, the parents of 884 children
from Mariupol and 637 children
from Kiev completed survey questionnaires.
Children between 2.5 and 3.5
years of age were eligible for
recruitment for participation
in the Environmental Pollutants
and Health Status of Children
study, a cross-sectional morbidity
study (n = 295 eligible; n =
244 enrolled: Mariupol, n =
171; Kiev, n = 73). Within
this subset, 48 children from
Mariupol and 42 children from
Kiev were randomly selected for
urinary measurement of 1-OHP.
The biologic exposure assessment
study coincided with the administration
of the ELSPAC questionnaire for
3-year-old children; data from
this questionnaire were included
for analysis. In addition, a
supplementary questionnaire on
immune status was also implemented.
Children participating in this
biomarker study received the
ELSPAC questionnaire for 3-year-olds,
abstracts of medical records
for children 18 months to 3 years
of age, and a supplementary immune
health questionnaire. The ELSPAC
3-year-old questionnaire collected
data on general health and medical
treatment, diet, social and language
development, and the child’s
environment. This questionnaire
was designed as a self-administered
instrument to be completed by
the mother or guardian. A trained
district pediatrician from the
local polyclinic then reviewed
the questionnaire for completeness
and inaccuracies and supplemented
unanswered questions through
an interview with the mother.
The immune questionnaire was
adopted from methods described
by Straight et al. (1994). The
immune questionnaire covers specific
immune-related diseases and symptoms
such as allergy symptoms, diagnosed
infectious disease, and antibiotic
use. This questionnaire was designed
to be administered as an interview
of the mother or guardian and
was given to the parent bringing
the child into the clinic for
the assessment.
Data on age, sex, and second-hand
smoke exposure were derived from
these questionnaires. All questionnaires
were translated and reverse translated
for accuracy and delivered by
native speakers to the children
and parent(s). Questionnaire
data could not be obtained from
one study participant from Kiev.
Collection and measurement
of urinary 1-OHP. Biomarker
collection occurred during
16-21 March 1998 in Mariupol
and 24-26 March 1998 in Kiev.
A few days before field implementation
of the study, urine sample
collection receptacles were
provided to the families
by a nurse from the health
clinics with instructions
to collect first morning
urine samples on the day
of attending the clinic.
The samples were kept at
room temperature until delivered
to the clinic. Nurses also
answered questions and provided
information on when the child
and parent were to come to
the clinic for further evaluation
and sample delivery. Biologic
samples were either received
or collected on the same
day as reporting to the clinic.
No participant objected to
providing urine samples,
although six children did
not provide enough urine
for sample analysis (n =
90).
Collected urine samples were
kept frozen at 18°C until
transported on dry ice to the
Institute of of Occupational
Medicine and Environmental Health
laboratory (Sosonowiecz, Poland)
for sample analysis. The analysis
method employed for 1-OHP detection
is a reverse-phase high-performance
liquid chromatography method
with enzymatic hydrolysis, using β-glucuronidase/arylsulfatase
(Jongeneelen et al. 1987). Creatinine,
a clearance protein that adjusts
for differences in urinary concentration,
was also measured at the same
laboratory.
Ambient air analysis. Ambient
air sampling was conducted at
one site in Mariupol, in an area
determined to be representative
of study participants’ exposure,
based on wind variability data.
Samples were collected using
37-mm quartz filters and measured
particulate-phase PAHs only.
The following PAHs were measured
in the 10 µm fraction of
particulate matter (PM10):
anthracene, fluoranthene, pyrene,
benzo[a]anthracene, chrysene,
benzo[b]fluoranthene,
benzo[k]fluoranthene,
benzo[a]pyrene, indeno[1,2,3-cd]pyrene,
dibenz[a,h]anthracene,
benzo[g,h,i]perylene,
benzo[e]pyrene, dibenz[a,c]anthracene,
perylene, dibenz[a,i]pyrene,
and coronene. Samples were collected
over a 24-hr averaging period
every 6 days starting on 31 March
1998 until 8 September 1998.
PAHs in PM10 were
measured using thin-layer chromatography
and spectral luminescence detection
according to standard Ukrainian
methods at the Ukrainian Scientific
Centre for Hygiene in Kiev (Poshyvanyk
1999).
Statistical analysis. All
statistical analyses were performed
using SPSS (SPSS Inc., Chicago,
IL, USA) and PEPI (Programs for
Epidemiology; USD Inc., Stone
Mountain, GA, USA). We assessed
distributions of 1-OHP for normality.
Because 1-OHP exhibited non-normal
distributions, exposure data
were log-transformed to better
approximate the assumed normality
of the statistical tests. We
calculated descriptive statistics,
specifically the mean, median,
SD, and geometric mean, for 1-OHP
biomarker data and age of study
participants. Means and SDs of
stratified data controlling for
resident city and second-hand
smoke exposure status were also
estimated. We assessed differences
in means with Student’s t-test,
using log-transformed data. The
result was considered statistically
significant if the p-value
was equal to or less than 0.05.
Study participants. Urine
samples for 1-OHP analysis
were collected in 42 children
from
Kiev and 48 children from Mariupol.
A description of the participants
for both cities is given in
Table 2. The percentage of males
is
slightly higher in the Mariupol
group (50% vs. 44% in Kiev).
The mean age of children from
both cities is similar (3.0
vs. 3.1 years of age). A slightly
higher percentage of children
lived with smokers in Mariupol
(46%) compared with Kiev children
(37%).
1-OHP results for Mariupol
and Kiev. Descriptive
statistics of 1-OHP of children
living in each city are presented
in Table 3. To adjust for
individual differences in
spot urine concentrations,
creatinine-adjusted 1-OHP
(1-OHP/creatinine) concentrations
are shown along with the
unadjusted values. Because
not all samples were of sufficient
quantity to test for both
1-OHP and creatinine, a subset
of samples had data for both
parameters and thus a smaller
sample size for creatinine-adjusted
1-OHP results (Mariupol, n =
32; Kiev, n = 41).
As shown in Table 3, the
mean 1-OHP for Mariupol was
significantly higher than
the Kiev mean, for both adjusted
(0.69 vs. 0.34 ng/mL; p < 0.0001)
and unadjusted (0.52 vs.
0.30 ng/mL; p =
0.002) data sets. Tests of
statistical significance
were done on log-transformed
data to meet assumptions
of normality.
1-OHP distributions, both as
raw and as log-transformed data,
are presented in Figures 3 and
4, respectively. These distributions
illustrate significant differences
in biologic exposure levels of
children living in these two
Ukrainian cities with different
PAH sources. Log-transformed
data visually present the validity
of normality assumption for the
statistical tests performed.
Effect of sex. When
both sexes have been tested,
previous studies have shown that
1-OHP tends to be higher in males
than in females (Jongeneelen
1994; Siwinska et al. 1998, 1999).
Table 4 presents 1-OHP concentrations
by sex and city. No significant
differences in 1-OHP mean concentrations
by sex were found, for adjusted
or unadjusted (and log-transformed)
data. In addition, females had
higher mean 1-OHP concentrations
than did males, although the
difference was not statistically
significant.
ETS exposure. To
examine the effect of second-hand
smoke exposure on biologic exposure
levels, we performed a stratified
analysis of 1-OHP urinary levels
and city of residence (Table
5). Even after stratifying on
exposure to second-hand smoke,
Mariupol children had mean 1-OHP
levels more than twice as high
as those of Kiev children using
the log-transformed 1-OHP data
(p = 0.004). Although
there were no statistically significant
differences in 1-OHP levels between
children exposed and unexposed
to second-hand smoke within either
city, there was a statistically
significant difference in 1-OHP
concentrations if exposed to
ETS, when using the combined
city log-transformed data (p =
0.04). In addition, we used a
regression model where association
between the independent variables
of second-hand smoke exposure
and city of residence and the
dependent variable of 1-OHP concentrations
was assessed. Although passive
smoking exposure was associated
with 1-OHP, it was not statistically
significant (p = 0.07),
as shown in Table 6. The regression
analysis also revealed that resident
city was a highly significant
variable (p < 0.001).
PAHs in ambient air. Twenty-two
particulate phase PAH samples
were collected approximately
2 weeks after biomarker data
collection. The BaP range was
6.9-18.8 ng/m3, with
a mean of 11.8 ng/m3.
Pyrene concentrations ranged
from 0.02 (half of the detection
limit) to 20.6 ng/m3,
with a mean of 7.6 ng/m3.
Mariupol children living within
3 miles of a steel mill and coke
oven have the highest mean urinary
concentrations of 1-OHP yet reported
for young children. The upper
end of the Mariupol 1-OHP distribution
overlaps with reported values
for occupationally exposed adults
and smokers (Levin 1995). There
was a statistically significant
difference between children living
in the point-source-affected
area versus those living in the
urban high-traffic environment
of Kiev, the capital city of
Ukraine. This is one of the first
studies investigating children
living in close proximity to
steel mills and coke ovens, which
are significant environmental
sources of PAHs. Most other studies
have focused primarily on children
exposed to PAHs from traffic
and/or dietary sources of PAHs
(Fiala et al. 2001; Kanoh et
al. 1993; Vyskocil et al. 2000;
Zhao et al. 1990).
Several of the earlier studies
in children have shown that diet
is the most significant contributor
to 1-OHP (Fiala et al. 2001;
Vyskocil et al. 2000), with some
acknowledging that any environmental
component was too small to clearly
assess its contribution (van
Wijnen et al. 1996). We did not
assess dietary contributions
to 1-OHP or have sufficient environmental
monitoring data to perform a
multimedia exposure analysis.
However, it seems probable that
the increased PAH exposure from
local industries, in general,
contributes significantly to
1-OHP levels in these children,
compared with those who live
without environmental PAH exposure
of this magnitude.
Only a few studies (Jongeneelen
1994; Siwinska et al. 1998) have
investigated the effect of sex
on children’s 1-OHP concentrations.
Other studies either did not
report any effects of sex or
the association could not have
been assessed because only one
sex was tested (Chuang et al.
1999; Fiala et al. 2001; Kanoh
et al. 1993; Karahalil et al.
1998; Northridge et al. 1999;
van Wijnen et al. 1996; Vyskocil
et al. 2000). In both of the
cases where an effect of sex
was seen (males had higher 1-OHP
concentrations), the association
was significant only when using
unadjusted (for creatinine) and
non-log-transformed data. Our
findings of no effect of sex
were based on log-transformed
1-OHP data, both adjusted and
unadjusted. We observed higher
1-OHP levels in females, but
the difference was not statistically
significant, using creatinine-adjusted,
unadjusted, or log-transformed
data.
ETS or second-hand smoke contains
PAHs and can thus be an important
contributor to 1-OHP levels.
Occupational studies have shown
that smokers have a significantly
higher amount of 1-OHP than do
nonsmokers (Jongeneelen 2001).
Some studies of children have
tried to account for tobacco
smoke exposure by measuring PAHs
in indoor air or via an exposure
questionnaire (Chuang et al.
1999; Fiala et al. 2001; Siwinska
et al. 1998, 1999; van Wijnen
et al. 1996). Second-hand smoke
exposure was significant only
when looking at the total group
of children, comparing mean 1-OHP
in those exposed with those unexposed,
but not within each city. Our
results did not clearly show
an effect of ETS likely because
the environmental industrial
exposure was so predominant.
Because the air quality data
were not concurrently collected
with the biomarker data in Mariupol,
because of logistical reasons,
the utility of the PAH air quality
data in interpreting biologic
exposure information was limited.
In addition to study analyses
of ambient air, Hydromet (the
Ukrainian state environmental
control organization) routinely
collected ambient air data in
both Mariupol and Kiev [Ministry
for Environmental Protection
and Nuclear Safety of Ukraine
(MEPNS) 1998]. Annual averages
for the following contaminants
in Mariupol for 1998 were sulfur
dioxide, 0.20 mg/m3;
nitrogen dioxide, 0.04 mg/m3;
BaP, 3.8 ng/m3; and “dust,” 0.20
mg/m3. For Kiev, the
1998 annual averages were SO2,
0.013 mg/m3; NO2,
0.07 mg/m3; BaP, 1.8
ng/m3; and “dust,” 0.10
mg/m3. Previous analyses
of environmental sources in Mariupol
indicate that the two steel mills
and coking facility combined
are responsible for > 99%
of air pollutants emitted from
stationary sources in the city
(MEPNS 1998). For comparison,
we compared Ukrainian Hydromet
data with U.S. EPA modeled estimates
of toxic air pollutants using
1996 air data (MEPNS 1998; U.S.
EPA 2003b). One of the contaminants
estimated was “7-PAH,” which
is composed of benz[a]anthracene,
benzo[b]fluoranthene,
benzo[k]fluoranthene,
benzo[a]pyrene, chrysene,
dibenz[a,h]anthracene,
and indeno[1,2,3-cd]pyrene.
The BaP concentration in Mariupol
alone compares with the 95th
percentile of seven PAHs from
U.S. EPA modeled estimates (0.0038 µg/m3),
indicating the high degree of
PAH contamination in the air
compared with the United States.
This study indicates that children
living next to industrial point
sources of PAHs can have very
high 1-OHP levels. Mariupol children,
who live near significant point
sources of PAH contamination,
had elevated 1-OHP concentrations
compared with other measured
Ukrainian children without such
environmental contamination.
Future research should focus
further on this highly exposed
population to better understand
their sources of PAH exposure,
including their diets. A more
detailed and multimedia exposure
analysis would identify those
exposure pathways contributing
most to total body burden and
better define exposure reduction
and risk management options.
In addition, more specific and
long-term biomarkers, such as
PAH-DNA adducts, could be employed
to link with measures of health
effects. |
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Last Updated: April 20, 2006
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