Termes les plus recherchés
[PDF](+63👁️) Télécharger High human exposure to pyrene (polycyclic aromatic hydrocarbon) in Kinshasa, a capital of the Democratic Republic of Congo. pdf
This article is from Archives of Public Health, volume 71.Abstract
Background: Data on human exposure to chemicals in Africa are scarce. A biomonitoring study was conducted in a representative sample of the population in Kinshasa (Democratic Republic of Congo) to document exposure to polycyclic aromatics hydrocarbons. Methods: 1-hydroxypyrene (1-OHP) was measured by HPLC fluorescence in spot urine samples from 220 individuals (50.5% women), aged 6–70 years living in the urban area and from 50 additional subjects from the sub-rural area of Kinshasa. Data were compiled as geometric means and selected percentiles, expressed without (μg/L) or with creatinine adjustment (μg/g cr). Multiple regression analyses were applied to factTélécharger gratuit High human exposure to pyrene (polycyclic aromatic hydrocarbon) in Kinshasa, a capital of the Democratic Republic of Congo. pdf
Tuakuila et at. Archives of Public Health 2013, 71:14
http://www.archpublichealth.conn/content/71 /I /1 4
ARCHIVES OF PUBLIC HEALTH
RESEARCH Open Access
High human exposure to pyrene (polycyclic
aromatic hydrocarbon) in Kinshasa, a capital of
the Democratic Republic of Congo
Joel Tuakuila^'^^ Martin Kabamba^ and Honore Mata^
Abstract
Background: Data on human exposure to chemicals in Africa are scarce. A biomonitoring study was conducted in
a representative sample of the population in Kinshasa (Democratic Republic of Congo) to document exposure to
polycyclic aromatics hydrocarbons.
Methods: 1-hydroxypyrene (1-OHP) was measured by HPLC fluorescence in spot urine samples from 220
individuals (50.5% women), aged 6-70 years living in the urban area and from 50 additional subjects from the
sub-rural area of Kinshasa. Data were compiled as geometric means and selected percentiles, expressed without
([jg/L) or with creatinine adjustment [\iq/q cr). Multiple regression analyses were applied to factors (creatinine,
grilled meat habits and smoking habits) influencing 1-OHP (stepwise procedure, criteria: probability F to enter
< 0.05 and probability F to remove > 0.10).
Results: According to the regression models, creatinine, grilled meat habits and smoking habits contribute to
explain 45% of the variation in population's urinary 1-OHP by the environmental exposure. Overall, living in urban
area of Kinshasa was associated with increased levels of 1-OHP in urine as compared to a population living in the
sub-rural area [GM: 1.8 |jg/L (n = 220) versus 1.4 |jg/L (n = 50), p < 0.01] as well as compared to the reference values
from databases involving American or German populations.
Conclusion: This study reveals the high pyrene (PAH) exposure of the Kinshasa population. However, more work,
with a rigorous design in the exposed population (monitoring of air concentrations and identifying other sources of
pyrene -PAH exposure), is needed to establish further documentation.
Keywords: Biomonitoring, Environmental pollution. Organic compounds. Public health, Polycyclic aromatic
hydrocarbons
Background
Polycyclic aromatic hydrocarbons (PAH) are produced
when organic materials undergo incomplete combustion.
They are composed of two or more benzene rings and
occur, depending on the type of pyrolytic process and of
source material, in various compounds, but always in the
form of a mixture. Because so many incomplete combus-
tion processes occur, PAH are ubiquitous environmental
contaminants. Exposure to PAH is associated with lung.
^ Correspondence: joeltuakuila@yahoo.fr
^Medical and Environmental Chemistry, Faculty of Sciences, University of
Kinshasa, Kinshasa, Democratic Republic of Congo
^Louvain Center for Toxicology and Applied Pharmacology (LTAP), Universite
catholique de Louvain, Avenue E. Mounier 53, box 52.02.12, 1200 Brussels,
Belgium
esophageal, gastric, colorectal, bladder, skin, prostate, and
cervical cancers in human and animal models [1].
Pyrene is present in almost all PAH mixture in relatively
high concentrations and there is a good correlation between
pyrene and other components in PAH mixture [2]. 1-OHP
(1-hydroxypyrene), a major metabolite of pyrene, has been
widely used as an indicator of internal exposure to PAH [3,4].
The main source of PAH intake is food, on the one hand
as a result of airborne PAH precipitating onto cereals, fruit
and vegetables, and on the other hand as a result of PAH
generated during the preparation of food. For example,
smoked food and food grilled on open flames display sub-
stantial levels of PAH content [5].
O© 2013 Tuakuila et a!.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative
BIoIVIGCI CGntrsI commons Attribution License (http://creativecommons.Org/licenses/by/2.0), which permits unrestricted use, distribution, and
reproduction in any medium, provided the original work is properly cited.
Tuakuila et at. Archives of Public Health 2013, 71:14
http://www.archpublichealth.conn/content/71 /I /1 4
Page 2 of 5
A very important source of PAH exposure among the
general population is tobacco smoke [6]. Smokers' intake
of pyrene in cigarette smoke is of the same order of
magnitude as intake from average food consumption [7].
It has been shown that domestic wood burning, resi-
dential charcoal burning stoves and barbecue charcoal
combustion turn out to be important sources of pollu-
tant exposure to humans [8,9].
In DRC (Democratic Republic of Congo), only 5% of the
population has access to electricity. As a result, wood en-
ergy production accounts for 85% of total energy con-
sumption and fuel wood and charcoal are by far the most
heavily consumed energy sources in DRC [10,11], used
primarily for household heating and cooking.
In this study, we provide the first data for biomonitoring
PAH in a representative sample of the Kinshasa population.
The values were compared to those reported by the refer-
ence values from American [12] or German databases [13].
Methods
Study design
In the absence of reliable population registers and in
view of the practical difficulties of conducting a truly
random sampling in the population of Kinshasa, we ap-
plied a two-stage systematic sampling approach [14]. In
the first stage, the 22 administrative entities of Kinshasa
were listed in alphabetical order and 11 out of them
were selected as follows: a first entity was drawn ran-
domly from the list and every other subsequent entity
was then included, thus ensuring a comprehensive
coverage of the entire urban area of Kinshasa. In the sec-
ond stage, we aimed to recruit about 25 healthy male
and female subjects between 6 and 70 years from each
of the 11 entities. In a mobilization campaign (mainly by
word of mouth), healthy subjects were invited to come
to the local health center to provide a urine sample.
After exclusion of 13 individuals because of possible dir-
ect occupational exposure to PAH (asphalt application,
waste incineration, aluminum smelting), 220 individuals
provided a urine sample and were included in the
present study (80% of the target number was reached).
Informed consent was obtained from each subject and
information on age, gender, place of residence and
smoking habits were recorded. With the same methods
of mobilization campaign, fifty additional subjects living
in the sub-rural area of Kinshasa were also included.
The characteristics of two areas (urban/sub-rural) se-
lected: urban area had high percentage of population
density; motorization, old second hand vehicles and car
traffic whereas sub-rural had high percentage of green
area [15]. This study was approved by the Congolese
committee of medical ethics and the study results will
be informed back to individuals sample donors with
proper explanations.
Laboratory methods
Great care was taken to avoid contamination during all
the steps of collection, transport and analysis. Spot urine
specimens were collected in metal-free polystyrene con-
tainers and stored at -20°C. The samples were then kept
frozen and transported in a cool box to be analyzed by the
Louvain centre for Toxicology and Applied Pharmacology
(Brussels, Belgium). We determined urinary 1-OHP by
HPLC (High Performance Liquid Chromatography) as de-
scribed previously [16,17] with some modifications [18].
Briefly, 2.0 mL urine was used for each sample, and the
identification and quantification of 1-OHP were based on
retention time and peak area measured using a linear re-
gression curve obtained from internal standard solutions.
The limit of quantification (LOQ) was 0.20 (ig/L. The valid
urine 1-OHP concentrations were expressed as (ig/L or
(ig/g of creatinine. The determinations of urinary cotinine
(LOQ = 50 (ig/L) were done by HPLC according to the
methods previously described [19]. Creatinine was deter-
mined (LOQ = 0.1 g/L) on a Beckman Synchron LX 20
analyser (Beckman Coulter GmbH, Krefeld, Germany) by
the Jaffe method [20]. For quality control, internal controls
and reference materials were run together with the sam-
ples on a daily basis.
Statistical analyses
Concentrations were log transformed for data analysis.
Geometric means (GM), ninety-five percent confidence
intervals (CI) and percentiles were calculated using NCSS
version 2004 (NCSS Institute Inc. 2004). The limit of
quantification (LOQ) divided by 2 was used for imput-
ation of values lower than the LOQ [21]. Differences be-
tween samples with normal distribution were examined by
the T-test and Chi-square test. Stepwise multiple linear re-
gression analyses of log-transformed data were used to es-
timate the influence independent variables (creatinine,
grilled meat habits and smoking habits) on the 1-OHP
(stepwise procedure, criteria: probability F to enter < 0.05
and probability F to remove > 0.10). A p-value lower than
0.05 was considered as statistically significant for all tests.
Results
Age of these 220 urban subjects was between 6 and
70 years and 31 years on average (standard deviation:
18). Most participants were adults (74.5%) and nearly
half (50.5%) were female. Among adults, thirty-six per-
cent were current smokers. The characteristics of sub-
rural subjects are also presented in Table 1.
Geometric mean (GM) urinary 1-OHP was 1.8 (ig/L
(95% CI: 1.6, 2.0) (Table 2). Three (1.4%) 1-OHP measure-
ments were less than the LOQ. As expected, smokers had
higher cotinine urinary levels (Cot-U) than non-smokers
[GM (95% CI): 137.3 (ig/L (115.5, 163.2) versus GM (95%
CI): 87.7 (ig/L (70.4, 104.3)].
Tuakuila et at. Archives of Public Health 2013, 71:14
http://www.archpublichealth.conn/content/71 /I /1 4
Page 3 of 5
Table 1 Demographic characteristics of the participants
Urban
Sub-rural
P
Number of subjects
220
50
Age, years^
31 ±18 [6-70]
36 ±15 [6-60]
0.55
6-14, n (%)
56 (25.4%)
12 (24.0%)
0.83
>14, n (%)
164 (74.5%)
38 (76.0%)
Sex:
Male, n (%)
109 (49.5%)
21 (42.0%)
0.93
Female, n (%)
1 1 1 (50.5%)
29 (58.0%)
Current Smokers, n (%)
79 (35.9%)
6 (12.0%)
<0.01
'Arithmetic mean ± SD [Range].
There was a statistically significant difference (p-value <
0.01) with smoking habits (0 for no/1 for yes) for 1-OHP,
Age (0 for 6-14 years/ 1 for > 14 years) and sex (0 for
female/ 1 for male) were not shown a significant difference
(Table 2),
In multivariable analyses, creatinine (continuous log-
variable), grilled meat habits (0 for non-consumers/ 1 for
consumers) and smoking habits (cotinine as continuous
log-variable) were the parameters significantly associated
with urinary excretion of 1-OHP with 0.449 as a value of
(Table 3).
Discussion
None of the measured values of Urinary 1-OHP was sig-
nificantly different among the 11 urban entities investi-
gated; indicating that our sampling strategy "unweigted
clusters" did probably not introduce a strong bias in the
representativeness of our population sample.
Urinary 1-OHP, a metabolite of PAH, has been shown to
be an indicator of both uptake of pyrene from foods and
exposure to exogenous PAH [22]. However, an important
limitation of this biomarker is that it only reflects recent ex-
posure and tends to vary widely within individuals [23-26].
The distribution of urinary 1-OHP levels of the reference
population are not Gaussian. Normalization can be
obtained when expressing experimental data as a base 10
logarithm. Our results (Table 2) showed a significant differ-
ence in 1-OHP levels between current smokers and non-
smokers (GM: 2.3 (ig/L versus 1.3 (ig/L, p < 0.01), which
may be due to the fact that tobacco smoking may influence
levels of urinary of 1-OHP [7,18,27-29].
In agreement with other studies, we found higher 1-OHP
levels in consumers of grilled meat than in non-consumers
(0 for non-consumers GM: 1.2 (ig/L versus 1 for consumers
GM: 4.0 (ig/L, p < 0.01) (Figure 1; Table 2), which is not sur-
prising since grilled meat represents an important source of
PAH exposure [7,30-32].
Table 2 Urinary concentrations of 1-OHP in the Kinshasa population (n = 220; 6-70 years)
N Urinary concentrations of 1-OHP
Min
P50
P95
Max
GM (CI 95%)
Total
Mg/L
220
0.1
1.6
6.6
26.8
1.8 (1.6-2.0)
jjg/g cr
0.1
1.2
5.8
14.8
1.3 (1.1 - 1.4)
Sex Men
Mg/L
109
0.2
1.6
6.5
26.8
1.6 (1.4- 1.9)
0.19
Mg/g cr
0.2
0.9
4.7
14.8
1 .0 (0.9 - 1 .2)
Women
Mg/L
111
0.1
1.8
7.6
16.4
1.9 (1.6-2.2)
Mg/g cr
0.1
1.3
6.5
12.1
1.5 (1.2 - 1.7)
Age 6-14 years
Mg/L
56
0.4
2.1
7.6
14.7
2.1 (1.6-2.6)
0.10
Mg/g cr
0.3
1.7
8.9
14.8
1.9 (1.4-2.5)
> 14 years
Mg/L
164
0.1
1.5
5.9
26.8
1.7 (1.5 - 1.9)
Mg/g cr
0.1
1.0
4.7
12.9
1.1 (0.9- 1.2)
Smoking habits Current smol<ers
Mg/L
79
0.1
2.0
8.2
26.8
2.3 (1.9-2.7)
<0.01
Mg/g cr
0.1
1.2
6.3
12.9
1.3 (1.0- 1.5)
Non-smol<ers
Mg/L
141
0.2
1.6
5.2
16.4
1.5 (1.3 - 1.7)
Mg/g cr
0.2
1.1
5.8
14.8
1.2 (1.0 - 1.4)
Grilled meat habits Consumers
Mg/L
65
0.5
4.1
14.1
26.8
4.0 (3.4 - 4.7)
<0.01
Mg/g cr
0.5
2.3
12.3
14.8
2.5 (2.1 - 3.1)
Non-consumers
Mg/L
155
0.1
1.3
2.8
6.5
1.2 (1.1 - 1.4)
Mg/g cr
0.1
0.8
3.2
5.5
0.9 (0.8 - 1 .0)
N sample size; P50, P95 = percentiles; Min minimum value, Max maximum value;
GM geometric mean (CI = 95% confidence Interval); ^p-value (f-test on log-transformed values).
N < Limit of quantification (0.20 \xq/l) = 3 (1.4%).
Tuakuila et at. Archives of Public Health 2013, 71:14
http://www.archpublichealth.conn/content/71 /I /1 4
Page 4 of 5
Table 3 Multiple regression analysis models of 1-OHP
levels
Independent variable
Coefficient P (95% CI)
Adjusted
Intercept
0.415 (0.253 to 0.579)
0.449
Creatinine^
0.193 (0.035 to 0.349)
Grilled meat habits^
0.505 (0.426 to 0.584)
Smoking habits ^
0.081 (0.003 to 0.157)
^Creatinine represented as continuous log-variable, '^Grilled meat represented
as 0 for Non-consumers and 1 for consumers; ^ Smoking habits: cotinine
represented as continuous log- variable, R^: explained variance (i.e. the square
of the correlation coefficient). Results are given for those variables that
correlated, and only when the regression was significant (p < 0.05).
As reported in the literature [12,33], investigations
have not shown significant differences neither for sex
groups nor for age groups (Table 2).
In Stepwise multivariable analyses, creatinine (continuous
log- variable), grilled meat habits (yes/no) and smoking
habits (continuous log-variable) were the independent pa-
rameters significantly associated with urinary unadjusted
values of 1-OHP (depend parameter) with 0.45 as a value of
(Table 3),
As in other surveys, increased 1-OHP levels were measured
in residents of urban areas compared to sub-rural settings
[GM: 1.8 (ig/L (n = 220) versus 1.4 (ig/L (n = 50), p<0.01].
The high percentage of smokers (Table 1) in the urban popu-
lation could, at least partly, explain this difference.
The mean 1- OHP level in the sub-rural and the urban
populations (smokers and non-smokers combined) ex-
ceeded the American and German levels (smokers and
non-smokers combined) [12,13]. Children from Kinshasa
were found to have much higher levels (GM [95%CI]:
2.1 (ig/L [1.6-2.6] for children 6-14 years) than American
children (GM [95%CI]: 0.09 (ig/L [0.07-0.11] for children
6-11 years; GM [95%CI]: 0.10 (ig/L [0.085-0.129] for
children 12-19 years) [34]. Inhalation of emissions from
charcoal burning or from cooking on open fires or trad-
itional stoves fueled with biomass (wood, charcoal, crop
and waste residues, ...) either outdoor or in poorly venti-
lated spaces, and consumption of this broiled, smoked,
fried or grilled food (Figure 1) are likely to contribute to
the high levels of urinary 1-OHP in Kinshasa subjects.
The present study has several limitations. First, with regard
to sample collection, selection of urinary sample donors did
not follow rigid sampling strategy (such as random sampling)
but by chance, which was practically inevitable under present
survey conditions. Second, low number of subjects and char-
acteristics selected. Third, passive smoking exposure is a
factor affecting PAH exposure; this factor did not evaluate.
Despite such limitations, however, it is prudent to conclude
that data from the present study constitutes levels generally
exceeded in the Kinshasa population. Living in urban area of
Kinshasa is associated with increased levels of 1-OHP in
urine as compared to a reference population living in a sub-
rural area of the same region. Increased levels were also
Tuakuila et at. Archives of Public Health 2013, 71:14
http://www.archpublichealth.conn/content/71 /I /1 4
Page 5 of 5
found by comparison with the reference values from data-
bases involving American or German populations.
Conclusion
This study reveals the high pyrene (PAH) exposure of
the Kinshasa population requiring the determination of
PAH concentrations in ambient air of Kinshasa and
limits values for the protection of human health.
Competing interests
The authors declare that they have no competing interests.
Authors' contributions
JT drafted the manuscript. All authors commented the draft versions. All
authors read and approved the final manuscript.
Acknowledgments
We are highly indebted to the study participants and to the staff of investigators,
as well as all the local health services and health centers of the Kinshasa Public
Health System that supported the field work. We also thank Pr Lison, Pr Hoet, Pr
Haufroid, Mr Boesmans and Mrs Lissenko for their collaboration. The financial
support of the Belgian Technical Cooperation (Cooperation Technique Belge-CTB
/Belgische Technische Cooperatie-BTC) was gratefully acknowledged.
Received: 4 April 2013 Accepted: 18 June 2013
Published: 19 June 2013
References
1 . Agency for Toxic Substances and Disease Registry ATSDR: Toxicological Profile for
Polycyclic Aromatic IHydrocarbons. Atlanta: Agency for Toxic Substances and
Disease Registry. Available from http://www.atsdr.cdc.gov/toxprofiles/tp.asp?
id=122&tid=25. Accessed 04. 05. 2013.
2. Tsai PJ, Shih TS, Chen HL, Lee WJ, Lai CH, Liou SH: Urinary 1-
hydroxypyrene as an indicator for assessing the exposures of booth
attendants of a high way toll station to polycyclic aromatic
hydrocarbons. Environ Sci Teclinol 2004, 38:56-61.
3. Jongeneelen FJ, Anzion RBM, Henderson PT: Determination of
hydroxylated metabolites of polycyclic aromatic hydrocarbons in urine.
J Chromatogr 1987, 413:227-232.
4. Hansen AM, Mathiesen L, Pedersen M, Knudsen LE: Urinary 1-
hydroxypyrene (1-HOP) in environmental and occupational studies-
a review. Int J Hyg Environ Health 2008, 21 1 :471-503.
5. International Programme on Chemical Safety (IPCS): Selected Non-
heterocyclic Polycyclic Aromatic Hydrocarbons (Environmental Health Criteria
202). Geneva: International Programme on Chemical Safety, WHO; 1998.
6. International Agency for Research on Cancer (lARC): lARC Monographs on
the Evaluation of the Carcinogenic Risk of Chemicals to Humans, Vol. 38,
Tobacco smoking. Lyon: International Agency for Research on Cancer; 1986.
7. Van Rooij JGM, Veeger MMS, Bodelier-Bade MM, Scheepers PTJ, Jongeneelen
FJ: Smoking and dietary intake of polycyclic aromatic hydrocarbons as
sources of interindividual variability in the baseline excretion of 1-
hydroxypyrene in urine. Int Arch Occup Environ Health 1994, 66:55-65.
8. Pandit G, Srivastava P, Rao A: Monitoring of indoor volatile organic
compounds and polycyclic aromatic hydrocarbons arising from
kerosene cooking fuel. Sci Total Environ 2001 , 279:1 59-1 65.
9. Molnar P, Gustafsona P, Johannessona S, Bomanb J, Barregarda L,
Sallstena G: Domestic wood burning and PM2.5 trace elements: Personal
exposures, indoor and outdoor levels. Atmos Environ 2005, 39:2643-2653.
10. Food and Agriculture Organization (FAO): Forests and energy in developing
countries. Forests and energy working paper 2007, 2:32.
11. Marien JN: Urban and peri-urban forestry in Africa: what perspectives for wood
energy? Conference on urban and peri-urban forestry «Trees connecting people:
In action together* held in Bogota (Colombia). July 28th to August 1st, 2008.
12. Centers for Disease Control and Prevention (CDC): National Health and
Nutrition Examination Survey 2003-2004. Atlanta (GA): Fourth National Report
on Human Exposure to Environmental Chemicals; 2009. http://www.cdc.
gov/exposurereport/pdf/FourthReport.pdf Accessed 20/01/2011.
13. Becker K, Schuiz C, Kaus S, Seiwert M, Seifert B: German environmental
survey 1998 (GerES III): environmental pollutants in the urine of the
German population. Int J Hyg Environ Health 2003, 206:15-24.
14. Ancelle T: Statistique Epidemiologie. lere. Paris: Maloine; 2002.
15. Tuakuila J, Lison D, Mbuyi F, Haufroid V, Hoet P: Elevated Blood Lead
Levels and sources of exposure in the Population of Kinshasa, the
capital of The Democratic Republic of Congo. J Expo Sci Environ Epidemiol
2013, 23(1):81-87.
16. Jongeneelen FJ: Biological monitoring of polycyclic aromatic
hydrocarbons. Scand J Work Environ Health 1986, 12:137-143.
17. Li X, Leng S, Guo J, Guan L, Zheng Y: An improved high performance
liquid chromatography method for determination of 1-hydroxypyrene
in urine [in Chinese]. Wei Sheng Van Jiu 2003, 32:616-617.
18. Liu AL, Lu WQ, Wang ZZ, Chen WH, Lu WH, Yuan J, et al: Elevated levels of
urinary 8-hydroxy-2-deoxyguanosine, lymphocytic micronuclei, and
serum glutathione S-transferase in workers exposed to coke oven
emissions. Environ Health Perspect 2006, 1 14:673-677.
19. Benowitz NL: Cotinine as a biomarker of environmental tobacco smoke
exposure. Epidemiol Rev 1996, 18:188-204
20. Jaffe' MZ: About the precipitation caused by pikrinic acid in normal urine
and about a new reaction of creatinine. Z P/iys/o/ Chem 1986, 10:391-400.
21 . Hornung RW, Reed LD: Estimation of average concentration in the presence
of nondetectable values. Applied Occup Environ Hygiene 1990, 5:46-51 .
22. Jongeneelen FJ: Benchmark guideline for urinary 1-hydroxypyrene as
biomarker of occupational exposure to polycyclic aromatic
hydrocarbons. Ann Occup Hyg 2001, 45:3-13.
23. Jongeneelen FJ, van Leeuwen FE, Oosterink S, Anzion RBM, van der Loop F,
Bos RP, et al: Ambient and biological monitoring of cokeoven workers:
determinants of the internal dose of polycyclic aromatic hydrocarbons.
British J Industrial Med 1 990, 47:454-461 .
24. Buckley TJ, Lioy PJ: An examination of the time course from human
dietary exposure to polycyclic aromatic hydrocarbons to urinary
elimination of 1-hydroxypyrene. Br J Ind Med 1992, 49:1 13-124
25. Boogaard PJ, van Sittert NJ: Exposure to polycyclic aromatic hydrocarbons in
petrochemical industries by measurement of urinary 1-hydroxypyrene.
Occup Environ Med 1 994 51 :250-258.
26. Viau C, Carrier A, Vyskocil A: Urinary excretion of 1-hydroxypyrene in
volunteers exposed to pyrene by the oral and dermal route.
Sci Total Environ 1995, 163:179-186.
27. Zao ZH, Quan WY, Tian DH: Experiments on the effects of several factors
on the 1-hydroxypyrene level in human urine as an indicator of exposure
to polycyclic aromatic hydrocarbons. Sci Total Environ 1992, 113:197-207.
28. Heudorf U, Angerer J: Urinary monohydroxylated phenanthrenes and
hydroxypyrene-the effects of smoking habits and changes induced by
smoking on monooxygenase-mediated metabolism. Int Arch Occup Environ
Mr/i 2001, 74(3):1 77-1 83.
29. Adonis M, Martinez V, Riquelme R, Ancic P, Gonzalez G, Tapia R, et al:
Susceptibility and exposure biomarkers in people exposed to PAHs from
diesel exhaust. Toxicol Lett 2003, 144(1):3-15.
30. Vaessen HAMG: Dietary intake of polycyclic aromatic hydrocarbons.
Toxicol Environ Chem 1988, 16:281-294
31. De Vos RH: Polycyclic aromatic hydrocarbons in Dutch total diet
samples (1984-1986). Ed Chem Toxic ] 990, 28(4):263-268.
32. Yang M, Kim S, Lee E, Cheong HK, Chang SS, Kang D, et al: Sources of
polycyclic aromatic hydrocarbon exposure in non-occupationally
exposed Koreans. Environ Mol Mutagen 2003, 42(4):250-257.
33. Chuang JC, Callahan PJ, Lyn CW, Wilson NK: Polycyclic Aromatic
Hydrocarbon exposures of children in low-income families.
J Expo Anal Environ Epidemiol 1 999, 9:85-98.
34 Huang W, Caudill SP, Grainger J, Needham LL, Jr Patterson DG: Levels of 1-
hydroxypyrene and other monohydroxy polycyclic aromatic
hydrocarbons in children: a study based on US reference range values.
Toxicol Lett 2006, 163:10-19.
doi:1 0.1 1 86/0778-7367-71-1 4
Cite this article as: Tuakuila et al.: High human exposure to pyrene
(polycyclic aromatic hydrocarbon) in Kinshasa, a capital of the
Democratic Republic of Congo. Archives of Public Health 2013 71:14.
Lire la suite
- 2.84 MB
- 15
Vous recherchez le terme ""

63

71

26