Aryl hydrocarbon receptor mediated activities in road dust from ametropolitan area, Hanoi—Vietnam: Contribution of polycyclic aromatic hydrocarbons PAHs and human risk assessment Le Huu
Trang 1Aryl hydrocarbon receptor mediated activities in road dust from a
metropolitan area, Hanoi—Vietnam: Contribution of polycyclic aromatic
hydrocarbons (PAHs) and human risk assessment
Le Huu Tuyena,b, Nguyen Minh Tuea,b, Go Suzukic, Kentaro Misakia, Pham Hung Vietb,
Shin Takahashia,d,⁎ , Shinsuke Tanabea
aCenter for Marine Environmental Studies (CMES), Ehime University, 2-5 Bunkyo-cho, Matsuyama, Japan
bResearch Centre for Environmental Technology and Sustainable Development (CETASD), Hanoi University of Science, 334 Nguyen Trai Street, Hanoi, Viet Nam
cCenter for Material Cycles and Waste Management Research, National Institute for Environmental Studies (NIES), 16-2 Onogawa, Tsukuba, Japan
dCenter of Advanced Technology for the Environment, Agricultural Faculty, Ehime University, 3-5-7 Tarumi, Matsuyama, Japan
H I G H L I G H T S
• First assessment of total AhR-mediated toxic activities in road dust using DR-CALUX
• PAHs known as carcinogens were found at high levels in Hanoi
• PAHs contributed only 0.8–76% to AhR agonist activities in road dust
• Exposure to PAHs in road dust may pose high cancer risk for Hanoi residents
a b s t r a c t
a r t i c l e i n f o
Article history:
Received 15 November 2013
Received in revised form 23 January 2014
Accepted 23 January 2014
Available online xxxx
Keywords:
Ah-receptor
Dioxins
PAHs
CALUX
Road Dust
Vietnam
Dioxin-Responsive Chemical-Activated LUciferase gene eXpression assay (DR-CALUX) was applied to assess the total toxic activity of the mixture of PAHs and related compounds as well as dioxin-related compounds in road dust from urban areas of Hanoi, Vietnam Road dust from Hanoi contained significantly higher DR-CALUX activ-ities (3 to 39, mean 20 ng CALUX-TEQ/g dw) than those from a rural site (2 to 13, mean 5 ng CALUX-TEQ/g dw) The total concentrations of 24 major PAHs (Σ24PAHs) in urban road dust (0.1 to 5.5, mean 2.5μg/g dw) were also
6 times higher than those in rural road dust (0.08 to 1.5, mean 0.4μg/g dw) Diagnostic ratios of PAHs indicated vehicular engine combustion as the major PAH emission source in both sites PAHs accounted for 0.8 to 60% (mean 10%) and 2 to 76% (mean 20%) of the measured CALUX-TEQs in road dust for Hanoi the rural site, respec-tively Benzo[b]-/benzo[k]fluoranthenes were the major TEQ contributors among PAHs, whereas DRCs
contribut-ed b0.1% to CALUX-TEQs for both rural and urban sites These results suggest TEQ contribution of other aryl hydrocarbon receptor agonists in road dust Significant PAH concentrations in urban dust indicated high muta-genic and carcinomuta-genic potencies Estimated results of incremental life time cancer risk (ILCR) indicated that Vietnamese populations, especially those in urban areas such as Hanoi, are potentially exposed to high cancer risk via both dust ingestion and dermal contact This is the first study on the exposure risk of AhR agonists, includ-ing PAHs and DRCs, in urban road dust from a developinclud-ing country usinclud-ing a combined bio-chemical analytical approach
© 2014 Elsevier B.V All rights reserved
1 Introduction
Industrialization, urbanization and high economic growth in recent
years are accompanied by degradation of environmental quality in
developing countries, where the pollution of the ambient air in large cities
has become a major concern Located in the Red River delta, Hanoi, Vietnam's capital is one of the biggest cities in Asia with over 3.4 million inhabitants in the city proper and its urban districts Hanoi urban area consists of 7 urban districts that cover 918.5 km2in a total of 3344 km2
of the Hanoi metropolitan area Among the six thickly populated Asian cities including Vietnam (Hanoi), Bandung (Indonesia), Bangkok (Thailand), Beijing (China), Chennai (India), and Manila (Philippines), Hanoi has been reported as the most polluted city by dust with the mean of atmospheric particulate matter in the range of 18–168 (PM2.5) and 33–262 μg m−3 (PM10 − 2.5) and frequently exceeded the
Science of the Total Environment xxx (2014) xxx–xxx
⁎ Corresponding author at: Center of Advanced Technology for the Environment,
Agricultural Faculty, Ehime University, 3-5-7 Tarumi, Matsuyama, Japan Tel./fax: +81
89 927 8171.
E-mail address:shint@agr.ehime-u.ac.jp (S Takahashi).
0048-9697/$ – see front matter © 2014 Elsevier B.V All rights reserved.
http://dx.doi.org/10.1016/j.scitotenv.2014.01.086
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Trang 2corresponding 24-h U.S EPA standards (65 and 150μg m− 3) (Oanh
et al., 2006) The hourly average of suspended particulate matter in
Hanoi has been reported by yet another study as 0.4–1.5 mg/m3
exceed-ing the Vietnamese standard of 0.2 mg/m3(Saksena et al., 2006)
According to the Ministry of Natural Resources and Environment, the
dust density on Hanoi streets and roads is in the range of 20–40 g/m2/
year, especially with higher values on the ring roads with figures up
to 100–400 g/m2/year whereas 10 g/m2/year is the normal average in
developed countries The traffic in Hanoi has been reported as the
most important contributor of particulate matter emission (Oanh
et al., 2006) A previous study on the traffic volume has been performed
using video camera recording in the year 2004 and the results showed
that there were around 10,000 motorbikes passed a selected point per
hour This traffic volume has reached over 18,000 motorcycles in
2005 Additionally, the number of cars and light trucks has also
increased (Yen et al., 2007) In highway, the motorcycles' density is
9100 vehicles per hour Meanwhile the corresponding values are
13,600 and 3500 vehicles per hour for the arterial and residential
areas, respectively (Oanh et al., 2012) Moreover, diesel vehicles were
reported as the highest contributors of particulate matter in Hanoi
(Oanh, 2009) Air particle pollution by vehicles has been associated
with polycyclic aromatic hydrocarbons (PAHs), a major source of which
is vehicle exhaust, and high levels of PAHs in road dust from Asian
devel-oping countries were reported (Wang et al., 2009; Boonyatumanond
et al., 2007; Lee et al., 2001) Road dust is also a sink for complex mixtures
of traffic-related pollutants (Keller and Lamprecht, 1995) and may
contain aliphatic hydrocarbons, PAHs and their derivatives, as well as
other organic substances (Bodzek et al., 1993; Yassaa et al., 2001; Lee
et al., 2001) However, contaminations by traffic-related pollutants
including PAHs in Hanoi road dust and related human health risk have
not been investigated comprehensively
PAHs are well-known for their carcinogenic, mutagenic and
terato-genic characteristics and they can cause various toxic impacts to human
and wildlife (Behnisch et al., 2001; Sjiigren et al., 1996; Poland et al.,
1982; Senft et al., 2002; Nebert et al., 2004) Their toxicities usually
involve a common mechanism such as binding to the aryl hydrocarbon
receptor (AhR), induction of AhR-related genes and subsequent
transfor-mation to toxic metabolites (Behnisch et al., 2001) AhR has been
associated with tumor-promotion and enhanced oxidative stress
(Sjiigren et al., 1996; Poland et al., 1982; Senft et al., 2002; Nebert et al.,
2004) Not only PAHs but also many of their derivatives occurring in
am-bient environment, such as methylated and oxygenated compounds,
have been reported to transactivate AhR (Trilecová et al., 2011;
Sonneveld et al., 2007; Sovadinová et al., 2006) Moreover, some other
chemicals often occur in the environment at low concentrations
com-pared with PAHs, but with a high AhR-mediated activity (e.g
dioxin-related compounds) It is important to know not only concentration levels
of organic compounds in the environment but also their toxicities to
eval-uate the integrated risk for human health effects and environmental risk
assessment Regarding this matter, reporter gene assays such as
DR-CALUX have been known as a useful method to evaluate the
AhR-mediated toxicities of contaminants in the environment (Behnisch et al.,
2003; Machala et al., 2001) Therefore, an approach that aims to establish
a causal link between chemical substances and biological effects in
envi-ronmental samples is necessary to assess the total toxic activity of the
mixture of PAHs and related compounds released from traffic-related
processes, in addition to the conventional chemical analysis of PAHs
This study analyzed road dust collected from Hanoi, a city with the
highest levels of traffic-related air pollution in East Asia (Oanh et al.,
2006) and Duong Quang as a rural reference site, to investigate the
con-tamination status by AhR agonists including not only the well-known
PAHs and dioxin-related compounds (DRCs) but also other potential
compounds The AhR-mediated toxic activities were evaluated using
Chemical-Activated LUciferase gene eXpression (CALUX) assays PAHs
and DRCs were also analyzed to determine their contribution to the
over-all toxic activities Finover-ally, US-EPA incremental lifetime cancer risk model
were applied to identify the human health risk for PAH exposure to road dust via ingestion and dermal contact
2 Material and methods
2.1 Sampling site description
In recent years, as a result of its economic growth, infrastructure in Hanoi, capital of Vietnam has seen considerable change Though urban and suburban road extension has been marginal, traffic is generally increasing, leading to higher traffic density and congestion According to the Transport Police Department of Hanoi, registered motorcycles in Hanoi are increasing at ~13.5% per year and car ownership at ~10% a year Duong Quang, a mostly agricultural commune located at approxi-mately 50 km to the east of Hanoi in My Hao district, Hung Yen province, was chosen as the reference site The population of this commune was approximately 6500, and motorbikes were the main transport vehicles
2.2 Sample collection
We collected 24 road dust samples from Hanoi urban area and 6 sam-ples from Duong Quang in January 2011 (Fig S1) Each dust sample of approximately 300 g was collected from an area of 20–50 m in length and 0.5 m in width at the side of the road using straw broom After collection, the samples were preserved at −25 °C until analysis
2.3 Sample pre-treatment and extraction
Road dust samples were air-dried, and then sieved through a 500μm stainless sieve to remove coarse particles Two grams of the sample was extracted with an acetone/hexane mixture and then toluene using a rapid solvent extractor (SE100, Mitsubishi Chemical Analytech, Japan) according to a previously reported method (Tue et al., 2010) A 0.2 g-equivalent portion of the crude extract was then concentrated, solvent-exchanged into 0.1 ml biochemical-grade dimethyl sulfoxide (DMSO) and stored at 4 °C for in vitro determination of AhR-mediated activities using DR-CALUX assay The remaining extract was used for chemical analysis of PAHs Every set of seven samples was accompanied with a procedural blank
2.4 DR-CALUX
The AhR-inducing potencies of the crude extracts were determined by the DR-CALUX assay This method assays utilize the rat hematoma cell line H4IIE (BioDetection Systems, The Netherlands) stably transfected with the firefly luciferase gene containing a multimerized dioxin response element in front of a minimal promoter All assays were performed following the BioDetection Systems' protocol described elsewhere (Suzuki et al., 2004, 2006) Briefly, 80,000 cells/well were seeded on 96-well plates After 24 h of incubation at 37 °C and 5% CO2, the cells were treated with exposure medium contained DMSO solutions (0.8% DMSO
in final wells) of either the reference standard
2,3,7,8-tetrachlorobenzo-p-dioxin (TCDD, 0 to 37.5 nM) or the samples (diluted by a factor of 1
to 1000) After another 24 h of incubation, the cells were subjected to lu-minescence measurement The AhR agonist activities were derived from the diluted samples with similar response to 1–3 pM TCDD (usually 300
to 1000 time dilution), and expressed in amounts of TCDD equivalent (CALUX-TEQ) per gram dry weight (dw) Each experiment was done in triplicate No significant effect on cell viability was observed in 3-(4,5-di-methylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay (Suzuki
et al., 2013) for these diluted samples
2.5 Chemical analysis
The extract for PAH analysis was spiked with deuterated PAH surrogate standards and cleaned-up using 1.2% deactivated alumina
L.H Tuyen et al / Science of the Total Environment xxx (2014) xxx–xxx
Trang 3chromatography (4 g, eluted with 80 ml of dichloromethane/hexane
1:1 v/v), activated silica gel chromatography (4 g, eluted with 80 ml of
dichloromethane/hexane 5:95 v/v) and gel permeation chromatography
(described inTue et al., 2010), and then finally spiked with chrysen-d12
as internal standard Naphthalene (Nap), acenaphthylene (Acy),
acenaphthene (Ace), fluorene (Flu), phenanthrene (Phe), anthracene
(Ant), fluoranthene (Fluh), pyrene (Pyr), benzo[c]phenanthrene (B[c]
Ph), cyclopenta[c,d]pyrene (CPP), benz[a]anthracene (B[a]A), chrysene
(Chy), benzo[b]-, benzo[k]-, and benzo[j]fluoranthene (B[b]F, B[k]F and
B[j]F), 7,12-dimethylbenz[a]anthracene (DMBA), benzo[e]- and benzo
[a]pyrene (B[e]P and B[a]P), 3-methylcholanthrene (MCA), indeno
[1,2,3-c,d]pyrene (I(IDP + B[g]P), dibenz[a,h]anthracene (DBA), benzo
[g,h,i]perylene (B[g]P), dibenzo[a,h]-, dibenzo[a,i]-, dibenzo[a,l]pyrene
(DB[ah]P, DB[ai]P and DB[al]P were determined using a gas
chromato-graph (Agilent 5975C Series) connected to a mass spectrometer
with electron-impact ionization DRCs such as polychlorinated and
polybrominated dibenzo-p-dioxins/dibenzofurans (PCDDs/Fs and
PBDDs/Fs) and dioxin-like PCBs (DL-PCBs) were analyzed using a
sepa-rate extract according to a method described elsewhere (Tue et al., 2010)
2.6 Cancer risk assessment
The incremental lifetime cancer risk (ILCR), adopted fromU.S EPA
(1991)and modified in a previous study (Chen and Liao, 2006; Wang
et al., 2011; Peng et al., 2011), was used to quantitatively estimate the
risk of exposure to PAHs in road dusts Eqs.(1) to (2)was applied to
eval-uate cancer risk of adults and children exposed to PAHs via ingestion and
dermal contact, respectively
ILCRsIngestion¼CS CSFIngestion ffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffi
BW=70 3 p
IRIngestion EF ED
ILCRsDermal¼CS CSFDermal ffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffi
BW=70 3 p
SA AF ABS EF ED
BW AT 106
ð2Þ
where CS is the B[a]P-equivalent concentration of PAHs in dust
(μg kg− 1, calculated using equivalency factors inTable 1), CSFIngestion
and CSFDermal, are carcinogenic slope factors of B[a]P (7.3, and
25 mg kg− 1d− 1, respectively (Knafla et al., 2006; US EPA, 1994,
2011)), BW is the body weight (average 57.7 and 16.8 kg for adults
and children, respectively (Walpole et al., 2012; Dang et al.,
2010)), AT is the average life span (70 years), EF is the exposure
fre-quency (180 days year− 1(Ferreira-Baptista and De Miguel, 2005)),
ED is the exposure duration (30 and 6 years, respectively (US EPA,
2004)), IRIngestionis the dust intake rate (50 and 100 mg day− 1for
adults and children, respectively (US EPA, 2011)), AF is the dermal
adherence factor (0.07 and 0.2 mg cm− 2h− 1for adults and children,
respectively (US EPA, 2004)), SA is the dermal surface exposure
(5700 and 2800 cm2day− 1for adults and children, respectively
(US EPA, 2004)), and ABS is the dermal adsorption fraction (0.13
(US EPA, 2004)) The total risks were the sum of risks associated
with all exposure routes
2.7 Statistical analysis
The R software packages version 2.15.2 were used to perform
statisti-cal analyses The Wilcoxon rank sum test was used to examine the
signif-icance of the difference in levels between Hanoi and Duong Quang
Pearson's correlation analysis was applied to check the relationships
between PAH concentrations and toxicity levels (log-transformed
values) A p value of b0.05 is considered as indicating statistical
significance
3 Results and discussion
3.1 CALUX-TEQs
AhR-mediated activities were detected in all the road dust samples analyzed with DR-CALUX (see examples of dose–response curves in Supplementary Fig S2) Significant higher CALUX-TEQs in road dust were found for Hanoi than for the rural site Duong Quang (3 to 39,
mean 20 ng/g dw compared with 2 to 13, mean 5 ng/g dw, p b 0.005)
(Fig 1) When compared with the results of in vitro AhR-mediated activ-ities reported in a number of studies on environmental samples, the CALUX-TEQs in Hanoi road dust were higher than those of Vietnamese settled house dust (median: 12 ng CALUX-TEQ/g dw) (Tue et al., 2012) and of flood-resuspended dust in Germany (7 ng TEQ/g dw,
Ethoxyresorufin-O-deethylase assay) (Wölz et al., 2010) The CALUX-TEQs in Duong Quang and Hanoi road dust were 14 and 56 times higher than that of a household sewage sludge compost crude extract from Japan (0.36 ng CALUX-TEQ/g dw) (Suzuki et al., 2004), suggesting that road dust in Vietnam, especially from the urban site, contained large amounts
of AhR agonists (Fig 1)
3.2 PAH concentrations
Significantly higher concentrations of Σ24PAHs were found in Hanoi road dust (0.1 to 5.5, mean 1.5μg/g dw) than in rural road dust (0.08 to 1.4, mean 0.4μg/g dw) B[b]F, B[k]F, I(IDP + B[g]P, Chy, B[a]A, and B[j]F, most potent AhR agonists among PAHs in in vitro assay, were found at three fold higher concentrations in the urban site than in the rural site whereas DBA, also known as high AhR-mediated activity response in
in vitro assay, was found in urban road dust at slightly higher level than
in rural road dust Concentrations of PAHs recommended for carcinogenic
Table 1 AhR-mediated, mutagenic and carcinogenic potencies.
Congeners AhR-mediated potency Mutagenic potency Carcinogenic potency
Relative to TCDD Relative to B[a]P Relative to B[a]P
Phe 1.3E−06 a – 0.0005
Fluh 2.3E−08 b – 0.05 Pyr 0.00033 c – 0.001 B[c]Ph 4.5E−07 b 0.05 0.023 CPP 6.53E−07 b 6.9 0.02 B[a]A 0.000143 a 0.08 0.005 Chy 0.00033 c 0.01 0.03 B[b]F + B[k]F 0.013 c 0.36 0.15 B[j]F 0.00037 b 0.26 0.05
B[a]P 0.00053 b 1 1 B[e]P 5.2E−07 c – 0.002
IDP 0.002487 a 0.31 0.1 DBA 0.0043 c 0.29 1.1
DB[ah]P 0.000071 b 1.4 1 DB[ai]P 0.00017 b 3.6 0.1 DB[al]P 4.9E−06 b 24 1 Mutagenic potencies cited from Durant et al (1996) ; Carcinogenic Potencies cited from
Larsen and Larsen (1998)
a Cited from Behnisch et al (2003)
b Cited from Machala et al (2001)
c Cited from Suzuki (2005 , unpublished).
d Cited from Marvanová et al (2008)
Trang 4screening by the European Union and the US Environmental Protection
Agency (EU- and EPA-PAHs) in Hanoi road dust were among the highest
reported for surface dust from various regions (Table 2) The B[a]P
con-centrations in Hanoi road dust were 2, 9 and 24 times higher than those
in dust from Duong Quang, Tehran—Iran and Cairo—Egypt, respectively,
and comparable to those in dust from Beijing—China (Wang et al., 2010;
Hassanien and Abdel-Latif, 2008; Saeedi et al., 2012)
3.3 Profiles and potential sources of PAHs
The proportions of PAHs in Hanoi road dust were in the order of
Fluh N Pyr N Phe N Chy N B[b]F + B[k]F N B[g]P N Ant N B[e]P N Nap N
I(IDP + B[g]P N B[a]P N B[a]A N B[j]F N Flu whilst the in rural road
dust was Phe N Fluh N Pyr N B[b]F + B[k]F N Nap N Chy N B[g]P N
B[a]P N Flu N Ant N B[a]A N B[e]P N I(IDP + B[g]P N B[j]F (Fig 2)
Such difference in the proportions of PAHs between the urban Hanoi
and rural road dusts may be due to their emission sources The compound
ratios that have the same molar mass are assumed to have similar
phys-icochemical properties Therefore, ratios in between specific PAHs could
be used to identify and characterize the emission sources The ratios of
Phe/(Phe + Ant) (mean 0.87 for both sites), B[a]A/(B[a]A + Chy) (mean 0.27 and 0.3 for urban and rural sites, respectively) and B[a] P/B[g]P (0.53 and 0.86 for urban and rural sites, respectively) indicate that a major source of PAHs in Vietnamese road dust was fuel combustion
in vehicle engines (Phe/(Phe + Ant) N 0.7,Guo, 2003), B[a]A/(B[a]A + Chy) = 0.22–0.55,Martuzevicius et al., 2011), B[a]P/B[g]P = 0.42–1.36 (Kume et al., 2007; Katsoyiannis et al., 2011) rather than petrogenic source (B[a]A/(B[a]A + Chy) b 0.2,Martuzevicius et al., 2011) The ratios
of Flu/(Flu + Pyr) (mean 0.12 and 0.28 for the urban and rural sites, respectively) suggest that these compounds were from combustion
of gasoline (b0.5,Ravindra et al., 2008) rather than diesel (N0.5, Ravindra et al., 2008), whereas the ratios of Pyr/B[a]P (5.2 and 2.6, re-spectively) and I(IDP + B[g]P/B[g]P (0.53 and 0.62 for urban and rural sites, respectively) suggest high contribution of diesel combustion (Pyr/B[a]P ≈ 10, IND/B[g]P ≈ 1,Ravindra et al., 2008) in addition to gas-oline combustion (Pyr/B[a]P ≈ 1,Ravindra et al., 2008, IND/B[g]P = 0.27–0.4,Ravindra et al., 2008) for the presence of these higher-ring PAHs in road dust In addition, the ratios of Fluh/(Fluh + Pyr) ranged from 0.44 to 0.76 (mean 0.52, urban) and 0.47 to 0.6 (mean 0.55, rural), B[a]A/(B[a]A + Chy) ranged from 0.17 to 0.58 (mean 0.3,
0 5 10 15 20 25 30 35 40
Vietnam (Urban RD) Vietnam (Rural RD) Vietnam (E-waste HD) Vietnam (Rural HD) Germany (Flood Dust) Japan (HSS Compost)
a
b
c
d
Fig 1 Concentration of CALUX-TEQ in different samples from various regions (gray bars: this study, white bars: cited from ( a,b Tue et al., 2012 , c Wölz et al., 2010 and d Suzuki et al., 2004 ), RD: road dust, HD: house dust, HSS: household sewage sludge.
Table 2
Concentrations (ranges and arithmetic means) of EPA-/EU-PAHs, their theoretical-TEQs (Theo-TEQs), mutagenic equivalents (Theo-MEQs), carcinogenic equivalents (Theo-CEQs) and AhR-mediated activity (CALUX-TEQs) in road dust from various regions (ng/g dw).
PAHs Priority list IARC classification Hanoi Beijing a Cairo b Duong Quang Tehran c
B[a]A EPA, EU 2B 55 (2.3–308) 42 2.8 19 (2.0–97) 10 Chy EPA, EU 2B 120 (8.4–535) 105 9.1 40 (5.2–142) 20 B[b]F + B[k]F EPA, EU 2B 140 (7.1–1080) 115 3.5 49 (7.0–208) 9
B[a]P EPA, EU 1 57 (3.8–271) 94 2.4 23 (3.1–99) 6
Total PAHs 1500 (127–5542) 922 700 430 (76–1400) 325
Theo-TEQs 2.1 (0.10–15) 1.6 0.10 0.70 (0.10–3.1) 0.30
ND: not detected, NA: not analyzed.
a Cited from Wang et al (2010)
b Cited from Hassanien and Abdel-Latif (2008)
c Cited from Saeedi et al (2012)
L.H Tuyen et al / Science of the Total Environment xxx (2014) xxx–xxx
Trang 5urban) and 0.18 to 0.57 (mean 0.3, rural) confirming traffic-related
or-igin of PAHs, predominantly from gasoline emissions (Fluh/(Fluh +
Pyr) = 0.4–0.6,Tsapakis and Stephanou, 2003; Ravindra et al., 2008, B
[a]A/(B[a]A + Chy) = 0.4–0.6,Ravindra et al., 2008) Interestingly,
ra-tios of B[a]P/(B[a]P + B[e]P) were 0.46 to 0.6 in average, indicating
fresh vehicle emissions (approximately 0.5,Oliveira et al., 2011)
(Table S1) The results of calculation of the I(IDP + B[g]P/(I(IDP + B
[g]P + B[g]P) and B[a]P/B[g]P, plotted inFig 3, showed that vehicular
traffic was the major contributor of PAHs in Hanoi whereas mixed
sources were the contributors in Duong Quang
3.4 Contribution of PAHs to the AhR-mediated toxicity
Toxic contributions of PAHs in the samples were evaluated by
com-parison of CALUX-TEQs measured with DR-CALUX and total theoretical
TEQs (Theo-TEQs) Theo-TEQ of a compound was calculated as the
prod-uct of its concentration and its TCDD-relative potency (REP) in CALUX
assays reported in previous studies (Behnisch et al., 2003; Machala
et al., 2001; Marvanová et al., 2008) Significantly higher Theo-TEQs
were observed in urban sites which are almost three times higher than
those in rural site (Table 3) To compare Theo-TEQs between the present
study and other reports, the PAH concentrations from previous studies
were also converted to Theo-TEQs by multiplying them with respective
REPs The highest levels of Theo-TEQs were found in Hanoi followed by
Beijing, and the Theo-TEQs in Duong Quang (rural site) were higher
than those in Tehran and Cairo (urban sites) Abundant contributor for
Theo-TEQs was B[b] + B[k]F for all regions (Table 3) As shown in
Fig 4A, Theo-TEQs in road dust accounted for 0.8 to 60% of the CALUX-TEQs (mean 9.8%) for Hanoi and 2.0 to 76% (mean 19.9%) for Duong Quang The principal contributors as potent AhR agonists were B[b]F + B[k]F (8% and 17% for urban and rural sites, respectively), I(IDP + B[g]P (0.7% and 1.2%), Pyr (0.4% for both sites), Chy (0.2 and 0.4%), and B[a]P (0.1 and 0.3%) (Table S2) Among the PAHs analyzed
in this study, B[b]F + B[k]F were also major contributors of Theo-TEQs (Fig 4B & Table S3) B[b]F + B[k]F were also major contributors
of Theo-TEQs in other regions (44 to 91 % total Theo-TEQs) except in Cairo (Egypt) where Pyr contributed equally to B[b]F + B[k]F These re-sults indicate the necessity to use effect-based bioassays in addition to chemical analysis to avoid missing non-target toxic contributors in risk assessment of human exposure to toxic chemicals in environment
As shown inFig 5, significant correlations were observed between
total PAHs and Theo-TEQs (Pearson's ρ = 0.96, p b 0.005 for both
sites) Total PAHs and CALUX-TEQs also correlated for the urban site
(ρ = 0.63, p b 0.001), suggesting that major contributors of toxic
ac-tivities may share the same sources with PAHs In contrast, no such
correlation was found in the rural site (p = −0.6), which can be
ex-plained by variable AhR-mediated potencies of different PAH conge-ners present in samples (Koppen et al., 2001)
3.5 Concentration of dioxin-related compounds and their contributions to the AhR-mediated toxicity
Concentrations of total PCDD/Fs found in the urban site ranged from
40 to 170, mean 90 pg/g dw (0.60 pg WHO-TEQ/g dw, based on toxic
0 5 10 15 20 25 30 35 40
Nap Acy Ace Flu Phe Ant Fluh Pyr
B[c]Ph CPP B[a]A Chy
B[b]F+B[k]F
B[j]F DMBA B[a]P B[e]P MCA IDP DBA B[g]P
DB[ah]PDB[ai]PDB[al]P
Hanoi Duong Quang
Fig 2 Profiles of PAHs in road dust.
0.0 0.5 1.0
B[a]P/B[g]P
Hanoi Duong Quang
0.0 0.5 1.0
B[a]P/B[g]P
Hanoi Duong Quang
Fig 3 Plot of IDP/(IDP + B[g]P) and B[a]P/B[g]P in road dust.
Trang 6equivalency factors fromVan den Berg et al., 2006, see Table S4) was
slightly higher than those in the rural site which ranged from 50 to 70,
mean 50 pg/g dw (0.30 pg WHO-TEQ/g dw), whereas concentrations of
DL-PCBs were 28 times higher (970 to 110,000, mean 17,000 pg/g dw
or 3.1 pg WHO-TEQ/g dw vs 230 to 600, mean 400 pg/g dw or 0.20 pg
WHO-TEQ/g dw) (Table S5) Concentrations of brominated dioxins
(PBDD/Fs) in urban dust ranged from 50 to 1100, mean 400 pg/g dw
(2.1 pg WHO-TEQ/g dw) were also significantly higher than those in
rural dust which ranged from nd to 260, mean 80 ng/g dw (0.50 pg
WHO-TEQ/g dw) (Table S6) No significant difference was observed
between the proportions of DRCs in the urban and rural sites (Fig S3)
Among PCDD/Fs, PCDDs were major compounds, particularly OCDD and
HpCDDs, whereas HpBDFs and OBDF were the predominant among
PBDD/Fs (Fig S4) Among DL-PCBs, CB118 had the highest concentrations
followed by CB105 In order to evaluate the contributions of individual
and total DRCs we also used REPs reported in previous studies (detail in
Table S4,Olsman et al., 2007; Behnisch et al., 2003) to calculate the theo-retical TEQ of DRCs Contributions of DRCs to CALUX-TEQs were in the range between 0.004 and 0.08% (mean 0.03%) for rural site and between 0.006 and 0.25% (mean 0.06%) for urban site Contributions of brominated dioxins (PBDD/Fs) to CALUX-TEQs were very small (b0.005%) compared
to those of PCDD/Fs and DL-PCBs in both rural and urban sites The major contributor of DRCs in rural site was 1,2,3,4,6,7,8-HpCDD (15 to 61%, mean 39%) and CB126 (9 to 23%, mean 15%), and in urban site they were CB126 (20 to 61%, mean 33%), 1,2,3,4,6,7,8-HpCDD (2 to 28%, mean 15%) and 2,3,4,7,8-PeCDF (ND to 31%, mean 12%) Considering these results on theoretical TEQs of DRCs and major PAHs, occurrence of unidentified potential AhR agonists in the dust samples can be suggested Further studies are necessary to determine other related compounds (e.g., oxygenated and methylated PAHs) which have been reported to transactivate AhR signaling pathway (Trilecová et al., 2011)
3.6 Mutagenic and carcinogenic equivalents of PAHs and their contribution
The theoretical mutagenic and carcinogenic equivalents of a PAH were calculated by multiplying the concentrations in road dust by appropriate mutagenic and carcinogenic potencies relative to B[a]P (Durant et al., 1996; Larsen and Larsen, 1998), and the total values were expressed as Theo-MEQs and Theo-CEQs, respectively The Theo-MEQs were 10 to
278 ng/g dw (mean 65 ng/g dw) in the rural site and 14 to 858 ng/g dw (mean 208 ng/g dw) in urban site (Table S7) Contributions by individual PAHs to mutagenic potencies was in the order of B[a]P (27%) N B[b]F + B [k]F (24%) N CPP (10%) N I(IDP + B[g]P (9%) N B[g]P (7%) N B[j]F (5%) N others (6%) for urban site and B[a]P (35%) N B[b]F + B[k]
F (27%) N CPP (11%) N B[g]P (9%) N I(IDP + B[g]P (8%) N B[j]F (4%) N others (17%) for rural site (Fig 4C) The Theo-CEQs in rural site ranged from 6 to 166 ng/g dw with a mean value of 40 ng/g dw whereas this value ranged from 7 to 546 ng/g dw with a mean of 117 ng/g dw for urban site (Table S8) Contributions by individual PAHs to carcinogenic potencies are in order of B[a]P (48%) N B[b]F + B[k]F (17%) N Fluh (12%) N DBA (6%) N I(IDP + B[g]P (5%) N Chy (3%) N others (5%) for urban site and B[a]P (57%) N B[b]F + B[k]F (18%) N Fluh (7%) N I(IDP + B[g]P (5%) N Chy (3%) N DBA (3%) N others (12%) for rural site (Fig 4D) Significant mutagenic and carcinogenic potencies found in this study should be considered in view of potential health risk and
Table 3
Theo-TEQs calculated from PAHs in road dust of various regions (ng/g).
PAHs Hanoi Beijing a Cairo b Duong Quang Tehran c
Phe 2.5 × 10 −4 1.4 × 10 −4 5.3 × 10 −4 7.8 × 10 −5 9.1 × 10 −5
Fluh 6.3 × 10 −6 3.6 × 10 −6 1.6 × 10 −6 1.2 × 10 −6 3.0 × 10 −7
Pyr 7.7 × 10 −2 3.2 × 10 −2 5.5 × 10 −2 1.4 × 10 −2 6.6 × 10 −3
B[c]Ph 2.0 × 10 −6 NA NA 1.9 × 10 −6 NA
CPP 2.1 × 10 −6 NA NA 7.0 × 10 −7 NA
B[a]A 8.0 × 10 −3 6.0 × 10 −3 4.0 × 10 −4 3.1 × 10 −3 1.4 × 10 −3
Chy 3.9 × 10 −2 3.5 × 10 −2 3.0 × 10 −3 1.3 × 10 −2 6.6 × 10 −3
B[b]F + B[k]F 1.8 1.5 4.6 × 10 −2 6.3 × 10 −1 1.2 × 10 −1
B[j]F 1.2 × 10 −2 NA NA 4.2 × 10 −3 NA
DMBA 4.5 × 10 −6 NA NA 6.7 × 10 −6 NA
B[a]P 3.0 × 10 −2 5.0 × 10 −2 1.3 × 10 −3 1.2 × 10 −2 3.2 × 10 −3
B[e]P 3.4 × 10 −5 NA NA 1.2 × 10 −5 NA
IDP 1.3 × 10 −1 5.0 × 10 −3 NA 4.6 × 10 −2 6.7 × 10 −2
DBA 1.2 × 10 −2 2.2 × 10 −2 NA 9.2 × 10 −3 6.5 × 10 −2
DB[ah]P 6.6 × 10 −4 NA NA 5.9 × 10 −5 NA
DB[ai]P 2.7 × 10 −4 NA NA ND NA
DB[al]P 2.2 × 10 −6 NA NA ND NA
Total 2.1 1.6 0.10 0.70 0.30
ND: not detected, NA: not analyzed.
a Cited from Wang et al (2010)
b Cited from Hassanien and Abdel-Latif (2008)
c Cited from Saeedi et al (2012)
9.8
19.9
90.2 80.1
82.0 84.4
7.6 5.6
4.8 2.8
27 35
24 27
6
17 11
10 9
7 8
9 4
5
Urban site
Rural site
Urban site
Rural site
Urban site Rural site
Urban site Rural site
48 57
18 18
5
12 7
12 3
6 5
5 3
3
Fig 4 Contribution of Theo-TEQs to CALUX-TEQs (A), individual PAHs to Theo-TEQs (B), individual PAHs to mutagenic equivalents (Theo-MEQs) (C), and individual PAHs to carcinogenic equivalents (Theo-CEQs) (D).
L.H Tuyen et al / Science of the Total Environment xxx (2014) xxx–xxx
Trang 7cancer risk will be evaluated in health risk assessment section DB[al]P
and B[b]F + B[k]F were the major mutagenic contributors in
Vietnamese road dust, similar to the results calculated for Beijing and
Greater-Cairo, whereas I(IDP + B[g]P and B[a]P were the major
muta-genic PAHs in Tehran The major carcinomuta-genic PAHs found in
Vietnamese road dust were B[a]P and B[b]F + B[k]F, whereas in Cairo
road dust they were B[a]P and Fluh, and in Tehran were B[a]P and B[g]
P Strong positive correlations were observed between pairs of
Theo-TEQs/Theo-MEQs and Theo-TEQs/Theo-CEQs (correlation coefficients
ranged from 0.95 to 0.98, p b 0.001, Fig S5) which can be explained by
the fact that PAHs with higher AhR-mediated activities also tend to
have higher mutagenic and carcinogenic potencies In summary, the
levels of AhR-mediated toxicity and carcinogenicity calculated for PAHs
in Hanoi road dust were comparable to those of a heavily air
particle-polluted region (Beijing) and significantly higher than those of Duong
Quang, Cairo and Tehran (Table 2) In contrast, mutagenic equivalent
levels in Hanoi were significantly higher than those in Beijing, Duong
Quang, Tehran and Cairo (Table 2)
3.7 Health risk assessment
To assess human health risk by exposure to PAHs, incremental life
time cancer risk (ILCR) model was used as a tool to assess human cancer
risk The ILCR model was developed to quantitatively estimate the
expo-sure risk for road dust PAHs based on U.S EPA standard model This
model could be applied to evaluate cancer risk for human who are
exposed to urban dust via two pathways — ingestion and dermal contact
with dust particles (Wang et al., 2011; Peng et al., 2011) Carcinogenic
potencies relative to B[a]P (Larsen and Larsen, 1998), carcinogenic slope
factor (CSF), and probabilistic risk assessment framework were applied
to estimate cancer risk incurred from exposure to PAHs via these two
pathways Probabilistic risk assessment for personal exposure to
carci-nogenic PAHs showed that an ILCR between 10−6and 10−4indicates
potential risk, whereas ILCR greater than 10−4suggests high potential
health risk (Liao and Chiang, 2006) The acceptable level is equal or lower than 10− 6(Chiang et al., 2009) Our estimated results suggest that children and adults in both study sites in Vietnam are exposed to high potential carcinogenic risk via both dust ingestion and dermal contact pathways Cancer risk levels via ingestion in urban sites (1.3 × 10−4and 1.5 × 10−4for children and adults, respectively) were somewhat higher than those in rural sites (4.7 × 10−5and 5.1 × 10−5for children and adults, respectively) Similarly, cancer risk levels via dermal contact in urban sites (3.3 × 10−4and 5.2 × 10−4for children and adults, respective-ly) were also somewhat higher than those in rural sites (1.2 × 10−4and 1.8 × 10−4) (Table S9,Fig 6) The result of cancer risk assessment obtained
in this study also raises the concern over the potential effect of ambient air contaminated by PAHs on the occurrence of common diseases related to urban air pollution in Hanoi urban areas, where higher rates of respira-tory and skin disease cases were observed compared with sub-urban areas (Hung, 2010), and such effect needs immediate attention
4 Conclusions
To our knowledge, this is the first report on the determination and toxicant contributors' assessment of PAHs and DRCs in road dust from Hanoi, a sub-tropical Asian metropolitan area, by DR-CALUX assay and confirmation by chemical analysis Profiles of PAHs determined by chem-ical analysis indicated that fossil fuel combustion is the major PAH source
in not only urban dust but also rural dust Particularly, it could have been released from the incomplete diesel and gasoline combustion in vehicles
An examination of toxic contribution in this study indicated that PAHs are major contributor of overall AhR-mediated activities in road dust with smaller contribution of DRCs The differences between CALUX-TEQ and Theo-TEQs in road dust samples for both sites indicated occurrence of unknown potential AhR agonists in the road dust It could be PAH deriv-atives such as oxygenated PAHs, nitrogenated PAH, or methylated PAHs Approaches in this study are very useful for determination of overall tox-icity of road dust as well as evaluation of specific chemical components in
0.1 0.2 0.5 1.0 2.0
200 500 1000 2000 5000 0.1
0.2 0.5 1.0 2.0 5.0 10.0
2
4 6 8 10 12
Total PAHs (ng/g)
200 500 1000 2000 5000 5
10 20
Total PAHs (ng/g)
Fig 5 Relationships between total PAHs and Theo-TEQs (A: rural site, Pearson's ρ = 0.96, p b 0.005; B: urban site, Pearson's ρ = 0.96, p b 0.001) and relationship between total PAHs and CALUX-TEQs (C: rural site, Pearson's ρ = −0.3, p N 0.1; D: urban site, Pearson's ρ = 0.63, p b 0.001).
Trang 8environmental samples whereas further studies are required to
deter-mine unidentified potential agonists in the contaminated road dust The
results from this study also suggests that further studies on the status of
contaminant and toxic effect assessment of PAHs and PAH derivatives in
ambient air (particulate and gas phases) in Hanoi should be carried out
Acknowledgments
This study was partly supported by Grants-in-Aid for Scientific
Research (A: 25257403) from Japan Society for the Promotion of Science
(JSPS) and the Environment Research and Technology Development Fund
(K123001 and 3K133010) from the Ministry of the Environment, Japan
The award of a JSPS postdoctoral fellowship to N.M.T (P 13072) is also
acknowledged
Appendix A Supplementary data
Supplementary data to this article can be found online athttp://dx
doi.org/10.1016/j.scitotenv.2014.01.086
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