Aryl hydrocarbon receptor mediated activities in road dust from a metropolitan area,...

Science of the Total Environment xxx (2014) xxx–xxx

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Aryl hydrocarbon receptor mediated activities in road dust from ametropolitan area, Hanoi—Vietnam: Contribution of polycyclic aromatichydrocarbons (PAHs) and human risk assessment

Le Huu Tuyen a,b, Nguyen Minh Tue a,b, Go Suzuki c, Kentaro Misaki a, Pham Hung Viet b,Shin Takahashi a,d,⁎, Shinsuke Tanabe a

a Center for Marine Environmental Studies (CMES), Ehime University, 2-5 Bunkyo-cho, Matsuyama, Japanb Research Centre for Environmental Technology and Sustainable Development (CETASD), Hanoi University of Science, 334 Nguyen Trai Street, Hanoi, Viet Namc Center for Material Cycles and Waste Management Research, National Institute for Environmental Studies (NIES), 16-2 Onogawa, Tsukuba, Japand Center 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.

⁎ Corresponding author at: Center of Advanced TecAgricultural Faculty, Ehime University, 3-5-7 Tarumi, M89 927 8171.

E-mail address: [email protected] (S. Takahashi

0048-9697/$ – see front matter © 2014 Elsevier B.V. All rihttp://dx.doi.org/10.1016/j.scitotenv.2014.01.086

Please cite this article as: Tuyen LH, et al, AryContribution of polycyclic aromatic..., Sci Tot

a b s t r a c t
a r t i c l e i n f o
Article history:Received 15 November 2013Received in revised form 23 January 2014Accepted 23 January 2014Available online xxxx

Keywords:Ah-receptorDioxinsPAHsCALUXRoad DustVietnam

Dioxin-Responsive Chemical-Activated LUciferase gene eXpression assay (DR-CALUX) was applied to assess thetotal toxic activity of the mixture of PAHs and related compounds as well as dioxin-related compounds in roaddust 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 24major PAHs (Σ24PAHs) in urban road dust (0.1 to 5.5, mean 2.5 μg/g dw)were also6 times higher than those in rural road dust (0.08 to 1.5, mean 0.4 μg/g dw). Diagnostic ratios of PAHs indicatedvehicular 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]fluorantheneswere themajor TEQ contributors among PAHs, whereasDRCs contribut-ed b0.1% to CALUX-TEQs for both rural and urban sites. These results suggest TEQ contribution of other arylhydrocarbon receptor agonists in road dust. Significant PAH concentrations in urban dust indicated high muta-genic and carcinogenic potencies. Estimated results of incremental life time cancer risk (ILCR) indicated thatVietnamese populations, especially those in urban areas such as Hanoi, are potentially exposed to high cancerrisk via both dust ingestion and dermal contact. This is thefirst study on the exposure risk of AhRagonists, includ-ing PAHs and DRCs, in urban road dust from a developing country using a combined bio-chemical analyticalapproach.

© 2014 Elsevier B.V. All rights reserved.

1. Introduction

Industrialization, urbanization and high economic growth in recentyears are accompanied by degradation of environmental quality indeveloping countries,where the pollution of the ambient air in large cities

hnology for the Environment,atsuyama, Japan. Tel./fax: +81

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l hydrocarbon receptor mediaal Environ (2014), http://dx.d

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 millioninhabitants in the city proper and its urban districts. Hanoi urban areaconsists of 7 urban districts that cover 918.5 km2 in a total of 3344 km2

of the Hanoi metropolitan area. Among the six thickly populated Asiancities 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 themean 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

ted activities in road dust from a metropolitan area, Hanoi—Vietnam:oi.org/10.1016/j.scitotenv.2014.01.086

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2 L.H. Tuyen et al. / Science of the Total Environment xxx (2014) xxx–xxx

corresponding 24-h U.S. EPA standards (65 and 150 μg m−3) (Oanhet al., 2006). The hourly average of suspended particulate matter inHanoi has been reported by yet another study as 0.4–1.5mg/m3 exceed-ing the Vietnamese standard of 0.2 mg/m3 (Saksena et al., 2006).According to the Ministry of Natural Resources and Environment, thedust 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 upto 100–400 g/m2/year whereas 10 g/m2/year is the normal average indeveloped countries. The traffic in Hanoi has been reported as themost important contributor of particulate matter emission (Oanhet al., 2006). A previous study on the traffic volume has been performedusing video camera recording in the year 2004 and the results showedthat there were around 10,000 motorbikes passed a selected point perhour. This traffic volume has reached over 18,000 motorcycles in2005. Additionally, the number of cars and light trucks has alsoincreased (Yen et al., 2007). In highway, the motorcycles' density is9100 vehicles per hour. Meanwhile the corresponding values are13,600 and 3500 vehicles per hour for the arterial and residentialareas, respectively (Oanh et al., 2012). Moreover, diesel vehicles werereported as the highest contributors of particulate matter in Hanoi(Oanh, 2009). Air particle pollution by vehicles has been associatedwith polycyclic aromatic hydrocarbons (PAHs), a major source of whichis vehicle exhaust, and high levels of PAHs in road dust from Asian devel-oping countries were reported (Wang et al., 2009; Boonyatumanondet al., 2007; Lee et al., 2001). Road dust is also a sink for complexmixturesof traffic-related pollutants (Keller and Lamprecht, 1995) and maycontain aliphatic hydrocarbons, PAHs and their derivatives, as well asother organic substances (Bodzek et al., 1993; Yassaa et al., 2001; Leeet al., 2001). However, contaminations by traffic-related pollutantsincluding PAHs in Hanoi road dust and related human health risk havenot been investigated comprehensively.

PAHs are well-known for their carcinogenic, mutagenic and terato-genic characteristics and they can cause various toxic impacts to humanand wildlife (Behnisch et al., 2001; Sjiigren et al., 1996; Poland et al.,1982; Senft et al., 2002; Nebert et al., 2004). Their toxicities usuallyinvolve a common mechanism such as binding to the aryl hydrocarbonreceptor (AhR), induction of AhR-related genes and subsequent transfor-mation to toxic metabolites (Behnisch et al., 2001). AhR has beenassociated 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 otherchemicals 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 knownot only concentration levelsof organic compounds in the environment but also their toxicities to eval-uate the integrated risk for human health effects and environmental riskassessment. 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 establisha causal link between chemical substances and biological effects in envi-ronmental samples is necessary to assess the total toxic activity of themixture of PAHs and related compounds released from traffic-relatedprocesses, in addition to the conventional chemical analysis of PAHs.

This study analyzed road dust collected from Hanoi, a city with thehighest 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-knownPAHs and dioxin-related compounds (DRCs) but also other potentialcompounds. The AhR-mediated toxic activities were evaluated usingChemical-Activated LUciferase gene eXpression (CALUX) assays. PAHsand DRCswere also analyzed to determine their contribution to the over-all toxic activities. Finally, US-EPA incremental lifetime cancer risk model

Please cite this article as: Tuyen LH, et al, Aryl hydrocarbon receptor mediaContribution of polycyclic aromatic..., Sci Total Environ (2014), http://dx.d

were applied to identify the human health risk for PAH exposure to roaddust 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 inHanoi, capital of Vietnam has seen considerable change. Though urbanand suburban road extension has been marginal, traffic is generallyincreasing, leading to higher traffic density and congestion. According tothe Transport Police Department of Hanoi, registered motorcycles inHanoi are increasing at ~13.5% per year and car ownership at ~10% ayear. Duong Quang, a mostly agricultural commune located at approxi-mately 50 km to the east of Hanoi inMyHao district, Hung Yen province,was chosen as the reference site. The population of this commune wasapproximately 6500, and motorbikes were the main transport vehicles.

2.2. Sample collection

We collected 24 road dust samples fromHanoi urban area and 6 sam-ples from Duong Quang in January 2011 (Fig. S1). Each dust sample ofapproximately 300 g was collected from an area of 20–50 m in lengthand 0.5 m in width at the side of the road using straw broom. Aftercollection, 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 500 μmstainless sieve to remove coarse particles. Two grams of the sample wasextracted with an acetone/hexane mixture and then toluene using arapid solvent extractor (SE100, Mitsubishi Chemical Analytech,Japan) according to a previously reported method (Tue et al., 2010). A0.2 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-mediatedactivities using DR-CALUX assay. The remaining extract was used forchemical analysis of PAHs. Every set of seven samples was accompaniedwith a procedural blank.

2.4. DR-CALUX

TheAhR-inducing potencies of the crude extractswere determined bythe DR-CALUX assay. This method assays utilize the rat hematoma cellline H4IIE (BioDetection Systems, The Netherlands) stably transfectedwith thefirefly luciferase gene containing amultimerizeddioxin responseelement in front of a minimal promoter. All assays were performedfollowing 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 weretreated with exposure medium contained DMSO solutions (0.8% DMSOin 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 1to 1000). After another 24 h of incubation, the cells were subjected to lu-minescence measurement. The AhR agonist activities were derived fromthe diluted samples with similar response to 1–3 pM TCDD (usually 300to 1000 time dilution), and expressed in amounts of TCDD equivalent(CALUX-TEQ) per gram dry weight (dw). Each experiment was done intriplicate. No significant effect on cell viability was observed in 3-(4,5-di-methylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay (Suzukiet al., 2013) for these diluted samples.

2.5. Chemical analysis

The extract for PAH analysis was spiked with deuterated PAHsurrogate standards and cleaned-up using 1.2% deactivated alumina



Table 1AhR-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

Nap – – –

Acy – 0.00056 –

Ace – – –

Flu – – –

Phe 1.3E−06a – 0.0005Ant – – 0.0005Fluh 2.3E−08b – 0.05Pyr 0.00033c – 0.001B[c]Ph 4.5E−07b 0.05 0.023CPP 6.53E−07b 6.9 0.02B[a]A 0.000143a 0.08 0.005Chy 0.00033c 0.01 0.03B[b]F + B[k]F 0.013c 0.36 0.15B[j]F 0.00037b 0.26 0.05DMBA 5.4E−06d – –

B[a]P 0.00053b 1 1B[e]P 5.2E−07c – 0.002MCA – – –

IDP 0.002487a 0.31 0.1DBA 0.0043c 0.29 1.1B[g]P – 0.19 0.02DB[ah]P 0.000071b 1.4 1DB[ai]P 0.00017b 3.6 0.1DB[al]P 4.9E−06b 24 1

Mutagenic potencies cited from Durant et al. (1996); Carcinogenic Potencies cited fromLarsen 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).

3L.H. Tuyen et al. / Science of the Total Environment xxx (2014) xxx–xxx

chromatography (4 g, eluted with 80 ml of dichloromethane/hexane1:1 v/v), activated silica gel chromatography (4 g, eluted with 80 ml ofdichloromethane/hexane 5:95 v/v) and gel permeation chromatography(described in Tue et al., 2010), and then finally spiked with chrysen-d12as 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 andB[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 spectrometerwith electron-impact ionization. DRCs such as polychlorinated andpolybrominated dibenzo-p-dioxins/dibenzofurans (PCDDs/Fs andPBDDs/Fs) and dioxin-like PCBs (DL-PCBs) were analyzed using a sepa-rate extract according to amethod described elsewhere (Tue et al., 2010).

2.6. Cancer risk assessment

The incremental lifetime cancer risk (ILCR), adopted from U.S. EPA(1991) and modified in a previous study (Chen and Liao, 2006; Wanget al., 2011; Peng et al., 2011), was used to quantitatively estimate therisk 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 anddermal contact, respectively.

ILCRsIngestion ¼CS� CSFIngestion �

ffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiBW=703

p� �� IRIngestion � EF� ED

BW� AT� 106 ð1Þ

ILCRsDermal ¼CS� CSFDermal �

ffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiBW=703

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 in Table 1), CSFIngestionand CSFDermal, are carcinogenic slope factors of B[a]P (7.3, and25 mg kg−1 d−1, respectively (Knafla et al., 2006; US EPA, 1994,2011)), BW is the body weight (average 57.7 and 16.8 kg for adultsand 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)), IRIngestion is the dust intake rate (50 and 100 mg day−1 foradults and children, respectively (US EPA, 2011)), AF is the dermaladherence factor (0.07 and 0.2 mg cm−2 h−1 for adults and children,respectively (US EPA, 2004)), SA is the dermal surface exposure(5700 and 2800 cm2 day−1 for 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 associatedwith all exposure routes.

2.7. Statistical analysis

The R software packages version 2.15.2 were used to perform statisti-cal analyses. TheWilcoxon 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 relationshipsbetween PAH concentrations and toxicity levels (log-transformedvalues). A p value of b0.05 is considered as indicating statisticalsignificance.


3. Results and discussion

3.1. CALUX-TEQs

AhR-mediated activities were detected in all the road dust samplesanalyzed with DR-CALUX (see examples of dose–response curves inSupplementary Fig. S2). Significant higher CALUX-TEQs in road dustwere 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, theCALUX-TEQs in Hanoi road dust were higher than those of Vietnamesesettled 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 higherthan that of a household sewage sludge compost crude extract from Japan(0.36 ng CALUX-TEQ/g dw) (Suzuki et al., 2004), suggesting that roaddust in Vietnam, especially from the urban site, contained large amountsof AhR agonists (Fig. 1).

3.2. PAH concentrations

Significantly higher concentrations of Σ24PAHs were found in Hanoiroad dust (0.1 to 5.5, mean 1.5 μg/g dw) than in rural road dust (0.08 to1.4, mean 0.4 μg/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 atthree fold higher concentrations in the urban site than in the rural sitewhereas DBA, also known as high AhR-mediated activity response inin vitro assay, was found in urban road dust at slightly higher level thanin rural road dust. Concentrations of PAHs recommended for carcinogenic



0

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Vietnam (Urban RD) Vietnam (Rural RD) Vietnam (E-waste HD) Vietnam (Rural HD) Germany (Flood Dust) Japan (HSS Compost)

CA

LU

X-T

EQ

(ng

/g)

a

bc

d

Fig. 1. Concentration of CALUX-TEQ in different samples from various regions (gray bars: this study, white bars: cited from (a,bTue et al., 2012, cWölz et al., 2010 and dSuzuki et al., 2004),RD: road dust, HD: house dust, HSS: household sewage sludge.


screening by the European Union and the US Environmental ProtectionAgency (EU- and EPA-PAHs) in Hanoi road dust were among the highestreported 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 thosein 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 ofFluh 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 roaddust 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 Hanoiand rural roaddustsmaybedue to their emission sources. The compoundratios that have the same molar mass are assumed to have similar phys-icochemical properties. Therefore, ratios in between specific PAHs couldbe used to identify and characterize the emission sources. The ratios of

Table 2Concentrations (ranges and arithmetic means) of EPA-/EU-PAHs, their theoretical-TEQs (TheoAhR-mediated activity (CALUX-TEQs) in road dust from various regions (ng/g dw).

PAHs Priority list IARC classification Hanoi

Nap EPA 2B 43 (0.30–188)Acy EPA – 11 (0.60–58)Ace EPA 3 3.6 (0.15–25)Flu EPA 3 29 (3.4–123)Phe EPA 3 190 (20–669)Ant EPA 3 68 (1.6–297)Fluh EPA 3 276 (15–1153)Pyr EPA 3 230 (12–646)B[c]Ph 2B 4.4 (ND–29)CPP EU 2A 3.2 (ND–22)B[a]A EPA, EU 2B 55 (2.3–308)Chy EPA, EU 2B 120 (8.4–535)B[b]F + B[k]F EPA, EU 2B 140 (7.1–1080B[j]F EU 2B 33 (1.5–171)DMBA – 0.80 (ND–10)B[a]P EPA, EU 1 57 (3.8–271)B[e]P 3 65 (1.9–365)MCA – 0.80 (ND–8.5)IDP EPA, EU 2B 54 (3.7–224)DBA EPA, EU 2A 2.7 (ND–26)B[g]P EPA, EU 3 97 (6.1–285)DB[ah]P EU 2B 9.2 (ND–50)DB[ai]P EU 2B 1.6 (ND–38)DB[al]P EU 2A 0.5 (ND–8.9)Total PAHs 1500 (127–554CALUX-TEQs 20 (2.6–39)Theo-TEQs 2.1 (0.10–15)Theo-MEQs 208 (14–856)Theo-CEQs 117 (6.5–546)

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).


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) indicatethat amajor source of PAHs in Vietnamese road dustwas fuel combustionin 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 petrogenicsource (B[a]A/(B[a]A+Chy) b 0.2,Martuzevicius et al., 2011). The ratiosof Flu/(Flu + Pyr) (mean 0.12 and 0.28 for the urban and rural sites,respectively) suggest that these compounds were from combustionof 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 ruralsites, 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-ringPAHs in road dust. In addition, the ratios of Fluh/(Fluh + Pyr) rangedfrom 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,

-TEQs), mutagenic equivalents (Theo-MEQs), carcinogenic equivalents (Theo-CEQs) and

Beijinga Cairob Duong Quang Tehranc

94 21.5 23 (1.2–51) 27 2.7 3.6 (0.80–8.4) 489 NA 0.6 (ND–1.1) 4139 13.6 12 (3.3–20) 8109 403.7 60 (16–133) 7017 6.9 15 (ND–70) 6155 68.2 54 (10–176) 1398 165.6 44 (7.4–147) 20NA NA 4.1 (ND–20) NANA NA 1.1 (ND–5.1) NA42 2.8 19 (2.0–97) 10105 9.1 40 (5.2–142) 20

) 115 3.5 49 (7.0–208) 9NA NA 12 (ND–59) NANA NA 1.2 (ND–2.4) NA94 2.4 23 (3.1–99) 6NA NA 23 (2.3–110) NANA NA 0.050 (ND–0.30) NA2.0 NA 18 (2.4–86) 275.0 NA 2.1 (ND–7.1) 1531 NA 23 (3.3–79) 30NA NA 0.80 (ND–2.6) NANA NA ND NANA NA ND NA

2) 922 700 430 (76–1400) 325NA NA 5 (1.9–13) NA1.6 0.10 0.70 (0.10–3.1) 0.30148 4.0 65 (9.2–279) 29129 7.0 41 (6.1–166) 29



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Nap Acy Ace Flu PheAnt

Fluh

Pyr

B[c]Ph

CPPB[a

]A Chy

B[b]F

+B[k]F

B[j]F

DMBA

B[a]P

B[e]P

MCA

IDP

DBAB[g

]P

DB[ah]P

DB[ai]P

DB[al]P

Pro

posi

tion

(%

)

Hanoi Duong Quang

Fig. 2. Profiles of PAHs in road dust.


urban) 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, indicatingfresh 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 in Fig. 3, showed that vehiculartraffic was the major contributor of PAHs in Hanoi whereas mixedsources 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 theoreticalTEQs (Theo-TEQs). Theo-TEQ of a compound was calculated as the prod-uct of its concentration and its TCDD-relative potency (REP) in CALUXassays reported in previous studies (Behnisch et al., 2003; Machalaet al., 2001; Marvanová et al., 2008). Significantly higher Theo-TEQswere observed in urban sites which are almost three times higher thanthose in rural site (Table 3). To compare Theo-TEQs between the presentstudy and other reports, the PAH concentrations from previous studieswere also converted to Theo-TEQs by multiplying them with respectiveREPs. The highest levels of Theo-TEQs were found in Hanoi followed byBeijing, and the Theo-TEQs in Duong Quang (rural site) were higherthan those in Tehran and Cairo (urban sites). Abundant contributor forTheo-TEQs was B[b] + B[k]F for all regions (Table 3). As shown in

0.0

0.5

1.0

0.0

B[a

Hanoi

Traffic Emission

Mixed Source

0.0

0.5

1.0

0.0

B[a

Hanoi

Traffic Emission

Mixed Source

IDP/(ID

P + B

[g]P)

Fig. 3. Plot of IDP/(IDP + B[g]P) a


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 DuongQuang. The principal contributors as potent AhR agonists wereB[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 and0.4%), and B[a]P (0.1 and 0.3%) (Table S2). Among the PAHs analyzedin 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 contributorsof Theo-TEQs in other regions (44 to 91 % total Theo-TEQs) except inCairo (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 tochemical analysis to avoid missing non-target toxic contributors inrisk assessment of human exposure to toxic chemicals in environment.

As shown in Fig. 5, significant correlations were observed betweentotal PAHs and Theo-TEQs (Pearson's ρ = 0.96, p b 0.005 for bothsites). 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 suchcorrelation 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 tothe AhR-mediated toxicity

Concentrations of total PCDD/Fs found in the urban site ranged from40 to 170, mean 90 pg/g dw (0.60 pg WHO-TEQ/g dw, based on toxic

0.9 1.5

]P/B[g]P

Duong Quang

Mixed Source

Coal Combustion

0.9 1.5

]P/B[g]P

Duong Quang

Mixed Source

Coal Combustion

nd B[a]P/B[g]P in road dust.



Table 3Theo-TEQs calculated from PAHs in road dust of various regions (ng/g).

PAHs Hanoi Beijinga Cairob Duong Quang Tehranc

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 NACPP 2.1 × 10−6 NA NA 7.0 × 10−7 NAB[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 NADMBA 4.5 × 10−6 NA NA 6.7 × 10−6 NAB[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 NAIDP 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 NADB[ai]P 2.7 × 10−4 NA NA ND NADB[al]P 2.2 × 10−6 NA NA ND NATotal 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).


equivalency factors from Van den Berg et al., 2006, see Table S4) wasslightly 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 ofDL-PCBs were 28 times higher (970 to 110,000, mean 17,000 pg/g dwor 3.1 pg WHO-TEQ/g dw vs 230 to 600, mean 400 pg/g dw or 0.20 pgWHO-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 inrural dust which ranged from nd to 260, mean 80 ng/g dw (0.50 pgWHO-TEQ/g dw) (Table S6). No significant difference was observedbetween the proportions of DRCs in the urban and rural sites (Fig. S3).Among PCDD/Fs, PCDDs were major compounds, particularly OCDD andHpCDDs, whereas HpBDFs and OBDF were the predominant amongPBDD/Fs (Fig. S4). AmongDL-PCBs, CB118 had the highest concentrationsfollowed by CB105. In order to evaluate the contributions of individualand total DRCs we also used REPs reported in previous studies (detail in

9.8

19.9

90.2

80.1

0% 10% 20% 30% 40% 50% 60% 70% 80% 90% 100%

Theo-TEQs Unexplained Activity

A

27

35

24

27

6

1711

10

9

7

8

9

4

5

0% 10% 20% 30% 40% 50% 60% 70% 80% 90% 100%

Urban site

Rural site

Urban site

Rural site

U

U

B[a]P B[b]F+B[k]F CPP B[g]P IDP B[j]F Others

C

Fig. 4. Contribution of Theo-TEQs to CALUX-TEQs (A), individual PAHs to Theo-TEQs (B), individequivalents (Theo-CEQs) (D).


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 therange between 0.004 and 0.08% (mean 0.03%) for rural site and between0.006 and 0.25% (mean 0.06%) for urban site. Contributions of brominateddioxins (PBDD/Fs) to CALUX-TEQs were very small (b0.005%) comparedto those of PCDD/Fs and DL-PCBs in both rural and urban sites. Themajor contributor of DRCs in rural site was 1,2,3,4,6,7,8-HpCDD (15 to61%, mean 39%) and CB126 (9 to 23%, mean 15%), and in urban sitethey 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%). Consideringthese results on theoretical TEQs of DRCs and major PAHs, occurrence ofunidentified 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 totransactivate AhR signaling pathway (Trilecová et al., 2011).

3.6.Mutagenic and carcinogenic equivalents of PAHs and their contribution

The theoreticalmutagenic and carcinogenic equivalents of a PAHwerecalculated by multiplying the concentrations in road dust by appropriatemutagenic and carcinogenic potencies relative to B[a]P (Durant et al.,1996; Larsen and Larsen, 1998), and the total values were expressed asTheo-MEQs and Theo-CEQs, respectively. The Theo-MEQs were 10 to278 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 individualPAHs tomutagenic 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 siteranged from 6 to 166 ng/g dwwith a mean value of 40 ng/g dwwhereasthis value ranged from 7 to 546 ng/g dwwith a mean of 117 ng/g dw forurban site (Table S8). Contributions by individual PAHs to carcinogenicpotencies 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%) forurban 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 inthis study should be considered in view of potential health risk and

82.0

84.4

7.6

5.6

4.8

2.8

0% 10% 20% 30% 40% 50% 60% 70% 80% 90% 100%

B[b]F+B[k]F IDP Pyr Chy B[a]P B[j]F Others

B

rban site

Rural site

rban site

Rural site

48

57

18

18

5

127

12

3

6

5

5

3

3

0% 10% 20% 30% 40% 50% 60% 70% 80% 90% 100%

B[a]P B[b]F+B[k]F Fluh DBA IDP Chy Others

D

ual PAHs tomutagenic equivalents (Theo-MEQs) (C), and individual PAHs to carcinogenic



100 200 500 1000

0.1

0.2

0.5

1.0

2.0

The

o-T

EQ

s (n

g/g)

A

200 500 1000 2000 5000

0.1

0.2

0.5

1.0

2.0

5.0

10.0

The

o-T

EQ

s (n

g/g)

B

100 200 500 1000

2

4

6

8

1012

Total PAHs (ng/g)

CA

LU

X-T

EQ

s (n

g/g)

C

200 500 1000 2000 5000

5

10

20

Total PAHs (ng/g)

Total PAHs (ng/g) Total PAHs (ng/g)

CA

LU

X-T

EQ

s (n

g/g)

D

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 andCALUX-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).


cancer risk will be evaluated in health risk assessment section. DB[al]Pand B[b]F + B[k]F were the major mutagenic contributors inVietnamese road dust, similar to the results calculated for Beijing andGreater-Cairo, whereas I(IDP + B[g]P and B[a]P were the major muta-genic PAHs in Tehran. The major carcinogenic PAHs found inVietnamese road dust were B[a]P and B[b]F + B[k]F, whereas in Cairoroad 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 coefficientsranged from 0.95 to 0.98, p b 0.001, Fig. S5) which can be explained bythe fact that PAHs with higher AhR-mediated activities also tend tohave higher mutagenic and carcinogenic potencies. In summary, thelevels of AhR-mediated toxicity and carcinogenicity calculated for PAHsin Hanoi road dust were comparable to those of a heavily air particle-polluted region (Beijing) and significantly higher than those of DuongQuang, Cairo and Tehran (Table 2). In contrast, mutagenic equivalentlevels in Hanoi were significantly higher than those in Beijing, DuongQuang, Tehran and Cairo (Table 2).

3.7. Health risk assessment

To assess human health risk by exposure to PAHs, incremental lifetime cancer risk (ILCR) model was used as a tool to assess human cancerrisk. The ILCR model was developed to quantitatively estimate the expo-sure risk for road dust PAHs based on U.S. EPA standard model. Thismodel could be applied to evaluate cancer risk for human who areexposed to urban dust via two pathways— ingestion and dermal contactwith dust particles (Wang et al., 2011; Peng et al., 2011). Carcinogenicpotencies relative to B[a]P (Larsen and Larsen, 1998), carcinogenic slopefactor (CSF), and probabilistic risk assessment framework were appliedto estimate cancer risk incurred from exposure to PAHs via these twopathways. Probabilistic risk assessment for personal exposure to carci-nogenic PAHs showed that an ILCR between 10−6 and 10−4 indicatespotential risk, whereas ILCR greater than 10−4 suggests high potential


health risk (Liao and Chiang, 2006). The acceptable level is equal orlower than 10−6 (Chiang et al., 2009). Our estimated results suggestthat children and adults in both study sites in Vietnam are exposed tohighpotential carcinogenic risk via bothdust ingestion anddermal contactpathways. Cancer risk levels via ingestion in urban sites (1.3 × 10−4 and1.5 × 10−4 for children and adults, respectively) were somewhat higherthan those in rural sites (4.7 × 10−5 and 5.1 × 10−5 for children andadults, respectively). Similarly, cancer risk levels via dermal contact inurban sites (3.3× 10−4 and 5.2×10−4 for children and adults, respective-ly) were also somewhat higher than those in rural sites (1.2 × 10−4 and1.8×10−4) (Table S9, Fig. 6). The result of cancer risk assessment obtainedin this study also raises the concern over the potential effect of ambient aircontaminated by PAHs on the occurrence of common diseases related tourban air pollution in Hanoi urban areas, where higher rates of respira-tory and skin disease cases were observed compared with sub-urbanareas (Hung, 2010), and such effect needs immediate attention.

4. Conclusions

To our knowledge, this is the first report on the determination andtoxicant contributors' assessment of PAHs and DRCs in road dust fromHanoi, a sub-tropical Asian metropolitan area, by DR-CALUX assay andconfirmation by chemical analysis. Profiles of PAHs determined by chem-ical analysis indicated that fossil fuel combustion is themajor PAH sourcein not only urban dust but also rural dust. Particularly, it could have beenreleased from the incomplete diesel and gasoline combustion in vehicles.An examination of toxic contribution in this study indicated that PAHs aremajor contributor of overall AhR-mediated activities in road dust withsmaller contribution of DRCs. The differences between CALUX-TEQ andTheo-TEQs in road dust samples for both sites indicated occurrence ofunknown 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



1.0E-06

1.0E-05

1.0E-04

1.0E-03

1.0E-02

Rural site Urban site Rural site Urban site

Can

cer

Ris

k L

evel

s

Children Adults

Ingestion Dermal

Fig. 6. Estimated values of incremental life time cancer risk.


environmental samples whereas further studies are required to deter-mine unidentified potential agonists in the contaminated road dust. Theresults from this study also suggests that further studies on the status ofcontaminant and toxic effect assessment of PAHs and PAH derivatives inambient air (particulate and gas phases) in Hanoi should be carried out.

Acknowledgments

This study was partly supported by Grants-in-Aid for ScientificResearch (A: 25257403) from Japan Society for the Promotion of Science(JSPS) and the Environment Research and TechnologyDevelopment 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 alsoacknowledged.

Appendix A. Supplementary data

Supplementary data to this article can be found online at http://dx.doi.org/10.1016/j.scitotenv.2014.01.086.

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Aryl hydrocarbon receptor mediated activities in road dust from a metropolitan area,...

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