Supporting Information

Transcription

1 Supporting Information MANUSCRIPT TITLE: Importance of Dermal Absorption of Polycyclic Aromatic Hydrocarbons Derived from Barbecue Fumes AUTHORS: Jia-Yong Lao, Shan-Yi Xie, Chen-Chou Wu, Lian-Jun Bao, Shu Tao, and Eddy Y. Zeng ADDRESS: School of Environment and Guangdong Key Laboratory of Environmental Pollution and Health, Jinan University, Guangzhou , China Laboratory of Earth Surface Processes, College of Urban and Environmental Science, Peking University, Beijing 1871, China NO. OF TEXTS: 6 NO. OF TABLES: 13 NO. OF FIGURES: 8 NO. OF PAGES: 5 S1

2 Table of Contents Text S1 Text S2 Text S3 Text S4 Barbecue questionnaire Estimation of PAHs dermal intake from barbecue fume Estimation of PAHs inhalation intake from barbecue fume Estimation of PAHs dietary intake and dermal intake from exposed clothing Text S5 Text S6 Data Analysis for Urinary OH-PAHs Sampling, Analysis Methods, and Conclusions for Indoor Experiments Table S1 Acronyms and molecular weight (MW; g mol -1 ) of polycyclic aromatic hydrocarbons Table S2 Table S3 The basic characteristic of participants in the present study Octanol-water partition coefficient (log kow, unitless), Henry s law constant (H; Pa m 3 mol -1 ), and calculated kp_g of polycyclic aromatic hydrocarbons Table S4 The proportion of particle-bound PAHs deposited in the head airways (HA), tracheobronchial region (TB), and alveolar region (AR) of the human respiratory tract, and their corresponding deposition concentrations (Cdp; ng m -3 ) Table S5 Table S6 Sensitivity data for dermal and inhalation intake of PAHs Measured PAH concentrations (ng g -1, wet weight) in barbecued foods Table S7 Wet weight (g) of barbecued foods consumed by participants in group A S2

3 Table S8 Intake amounts (ng) of low molecular-weight PAHs via dietary exposure Table 9 The ratios of excretion to intake for Nap, Flu, Phe, and Pyr via diet, dermal absorption, combined dermal and inhalation exposure, and inhalation Table S1 Measured PAH concentrations (geometric mean ± standard deviation; ng m -2 ) in cotton cloth samples of group A, B, and C after exposure Table S11 Daily intake (ng day -1 ) of PAHs via dermal absorption from exposed clothes based on the measured PAH concentrations in clothes Table S12 Measured gaseous and particulate concentrations (ng m -3 ) of polycyclic aromatic hydrocarbons (PAHs) of background, site 1 and site 2 while barbecuing indoor Table S13 Pearson correlation coefficients between net excreted amounts of OH-PAHs in urine, PAHs concentration measured in silicone wristbands and forearms wipes of group E. Figure S1 Photo showing the location of atmospheric sampling and the arrangement of the indoor barbecue event Figure S2 Net excreted amounts of OH-PAHs for combined dermal and inhalation exposure to indoor barbecue fumes (D) and for dermal absorption from the fumes (E). Net excreted amount has been corrected by the urinary initial concentration level in each participant S3

4 Figure S3 Measured concentration of PAHs in wristband samples (ng per wristband) and forearms-wipe samples (ng per m 2 of forearms surface areas) collected from twelve participants of group D (dermal and inhalation exposure) and group E (dermal absorption) Figure S4 Concentration of nine OH-PAHs in urine samples collected from seven participants, who were exposed to PAHs via dietary ingestion, dermal absorption, and inhalation, for a pre-exposure and post-exposure period. Figure S5 Concentration of nine OH-PAHs in urine samples collected from seven participants, who were exposed to PAHs via dermal absorption and inhalation, for a pre-exposure and post-exposure period. Figure S6 Concentration of nine OH-PAHs in urine samples collected from six participants, who were exposed to PAHs via dermal absorption, for a pre-exposure and post-exposure period. Figure S7 Concentrations of nine OH-PAHs in urine samples collected from six participants of group D, who were exposed to PAHs via dermal and inhalation exposure, for a pre-exposure and post-exposure period. Figure S8 Concentrations of nine OH-PAHs in urine samples collected from six participants of group D, who were exposed to PAHs via dermal and inhalation exposure, for a pre-exposure and post-exposure period. S4

5 Text S1. Barbecue Questionnaire 1. Participant identifier: 2. Group: 3. Gender: Male Female 4. Age: 5. Weight: Kg 6. Height: cm 7. Have you ever smoked a cigarette before? Yes No 8. Frequency of smoking: Every day Once a week Occasionally Never 9. Do you often breathe in secondhand smoke? Yes No 1. Have you ever eaten barbecued food? Yes No 11. Frequency of eating barbecue food? Ten times/year Seven to nine times/year Four to six times/year Once to three times/year - Never 12. What is your favorite food on the barbecue? Meats Vegetables 13. Have you ever drunk alcohol while sampling? Yes No 14. Do you usually eat fruits? Yes No 15. Do you usually exercise? Yes No 16. How often do you drink alcohol? Usually Occasionally Never 17. What is the proportion of meats to vegetables ratio in routine? > 5 % < 5 % 1:1 18. Daily water intake: 1 ml 1 15 ml 15 2 ml 2 ml All the participants are non-smokers, and never or occasionally drink alcohol in their daily life. However, all the participants did not drink alcohol during sampling. Twenty-five S5

6 percent of the participants eat BBQ food 1 3 times a year, while 4% eat BBQ food over 7 times a year. S6

7 Text S2. Estimation of PAHs Dermal Intake from Barbecue Fume Body surface area (SA) is evaluated by Stevenson formula, 1 SA.61BH.128BW.1529 (S1) where BH is the height of the participant (cm); BW is the body weight of the participant (kg) (Table S3); and SA is the body surface area of the participant (m 2 ). Dermal intake of PAHs is estimated based on the transdermal permeability coefficient (kp_g) of gaseous PAHs. The value of kp_g is calculated with the equations described by Weschler and Nazaroff, 2, 3 p_cw 2 / 3.7log Kow.722 MW k 36 1 (S2) k p_g MW kp_cw 1 1/( ) (S3) 2.6HRT k v p_cw d where kp_cw is the permeability coefficient for a PAH compound to transfer through the stratum corneum by the medium of water to get in contact with the skin (cm h -1 ); kow is the octanol-water partition coefficient of the target analyte ; MW is the molecular weight of the target analyte (g mol -1 ); kp_g is the transdermal permeability coefficient of the PAH compound in the gas phase (m h -1 ); H is the Henry s law constant (Pa m 3 mol -1 ); R is the ideal gas constant (8.314 Pa m 3 K -1 mol -1 ); T is the skin temperature (35 K); vd is the mass-transfer coefficient that describes the external transport of the PAH compound from the gas phase through the boundary layer adjacent to the skin (m h -1 ); and vd(g) is 6 m h -1 for gas-phase PAHs. In the present study, kp_d is defined as the transdermal permeability coefficient of particle-bound PAHs (m h -1 ), also estimated by eq S3, but vd(p) of particle-bound PAHs are estimated based on the model results of a previous study by Shi and Zhao 4, i.e., the deposition velocity of particle size fraction in > 3.2, ,.1-.56, and μm are 1.65 ±.29,.157 ±.7,.372 ±.96, and.63 ±.11 m h -1. S7

8 The dermal intakes of gaseous PAHs (EDdg) and particulate PAHs (EDdp) are estimated by the following equations 3 EDdg C k SA f t (S4) g p_g EDdp C k SA f t (S5) p p_d where Cg and Cp are the concentrations of gaseous and particulate PAHs, respectively (ng m - 3 ); f is the exposed dermal fraction; and t is the time for exposure (h). For Monte Carlo simulation, the body surface area is assumed to be log-normally distributed with a mean of 1.74 m 2 and standard deviation value of.11, based on the heights and weights of the participants in the present study. The exposed dermal fraction is assumed to follow uniform distribution with a minimum value of 15% and a maximum value of 3%. S8

9 Text S3. Estimation of PAHs Inhalation Intake from Barbecue Fume Particle size distribution data were used to calculated the deposition efficiency and concentrations of particulate PAHs in three main regions of the human respiratory tract, based on the International Commission on Radiological Protection (ICRP) model. 5 Three regions are the head airway (HA, including nose, mouth, pharynx, and larynx), tracheobronchial region (TB), and alveolar region (AR). The deposition efficiency in the head airway (DFHA,i) is estimated by DF 1 1 IFi ( ) (S6) HA, i 1 exp( ln D ) 1 exp( ln D ) p,i where Dp,i (μm) is the mean particle diameter in different size fractions, assumed to be 2 µm for size fraction >18µm; and IFi is the inhalable fraction, i.e., the fraction of PAHs that can be inhaled through the nose and/or mouth, which is estimated by IF.5 (1 exp(.6 )) (S7) i D p, i The deposition efficiency in the tracheobronchial region (DFTB,i) is estimated by p,i DF TB, i (exp(.234(lnd p,i 3.4) ) 63.9exp(.819(lnD p,i 1.61) )) (S8) D p,i The deposition efficiency in the alveolar region (DFAR,i) is estimated by DF AR, i (exp(.416(lnd p,i 2.84) ) 19.11exp(.482(lnD p,i 1.362) )) (S9) D p,i The deposition concentration (Cdp(j,i)) of particle-bound PAHs in the human respiratory tract is estimated by C DF C (S1) dp(j, i) j, i i where DFj,i is the deposition efficiency in each region (j; HA, TB, and AR) of the human respiratory tract for Dp,i. 6 S9

10 Inhalation intake of gas-phase PAHs (EDig) and particle-phase PAHs (EDip) are estimated by 3 EDig C IR t (S11) g EDip Cdp IR t (S12) where Cdp is the sum of particulate PAHs concentrations deposited in three regions of the respiratory tract (ng m -3 ) and IR is the participants breathing rate, chosen as 1.5 m 3 h -1. 7, 8 For Monte Carlo simulation, the breathing rate is assumed to be log-normally distributed with the mean 1.5 m 3 h -1 and standard deviation value of.5. S1

11 Text S4. Estimation of PAHs Dietary Intake and Dermal Intake from Exposed Clothes Dietary intake (EDfood) was estimated by: ED C IN (S13) food food food where Cfood is the concentration of PAHs in barbecue food (ng g -1 ); INfood is the amount of dietary ingestion (g). Dermal contact with exposed clothes contributes to dermal intake of PAHs, which is estimated by 9 ED cloth C cloth 6 1 d A F F F T n (S14) cloth skin mig contact pen contact where EDcloth is the amount of PAHs dermal intake from exposed clothing (ng day -1 ); Ccloth is the PAHs concentration in clothing (ng kg -1 ); 1-6 is the conversion factor (kg mg -1 ); dcloth is the density of clothing (mg cm -2 ), which is 2 mg cm -2 in the present study; Askin is the area of body surface covered with clothing (cm 2 ); Fmig is the fraction of PAHs migrating to the skin per day (1 day -1 ); Fcontact is fraction of skin area covered with clothing (unitless); Fpen is the penetration rate (unitless); Tcontact is the contact duration for clothing and skin (days); and n is the mean number of events per day (1 day -1 ). 9 Monte Carlo simulation is used for uncertainty analysis. Askin is assumed to follow a uniform distribution with a minimum value of 712 and a maximum value of 14. Fmig is assumed to follow a uniform distribution with a minimum value of.1 and a maximum value of.8. Fpen is assumed to follow a uniform distribution with a minimum value of.1 and a maximum value of 1. Tcontact is chosen as one day. Fcontact is chosen as 1. Direct air flow under clothes was taken into consideration in uncertainty analysis. S11

12 Text S5. Data Analysis for Urinary OH-PAHs Urinary concentrations of OH-PAHs corrected by creatinine were calculated by: 6 C Cr CCr M Cr 1 (S15) C C (S16) C urine 3 urine, Cr 1 Cr where MCr is the molecular molar mass of creatinine (g mol -1 ); CCr is the creatinine concentration in urine (μmol L -1 ); CCr is the creatinine concentration in urine (g L -1 ); Curine is the urinary OH-PAHs concentration (μg L -1 ); Curine,Cr is the urinary OH-PAHs concentration corrected by creatinine (ng g -1 ). Urinary OH-PAHs net excreted amounts (N, ng) were calculated by 3 C i Cr C Cr C i, Cr Vi 1 urine, o(urine, N (S17) where C(urine,Cr) is the mean concentration of OH-PAHs of the participant before exposure (ng g -1 ); Ci(urine,Cr) is the concentration of OH-PAHs of the participant in each collection time after exposure (ng g -1 ); Ci,Cr is the creatinine concentration in the corresponding urine (g L -1 ); Vi is the urine volume of the corresponding urine (ml). S12

13 Text S6. Sampling, Analysis Methods, and Conclusions for Indoor Experiments Target Population and Sampling Strategy. Indoor barbecue was conducted at a new office room from 14:3 to 17:3 on January 6, 218 in Guangzhou suburban areas, used charcoal as heating source. Twelve males aged 22 to 29 participated in the sampling campaign, and were divided into two groups. Group D consisted of six participants subjecting to dermal and inhalation exposures. Group E consisted of six participants with dermal absorption only, who also wore same hoods to avoid inhaling barbecue fumes. All participants were allowed to eat boiled foods only, and were served lunch and dinner with the same weight and type of food on January 6. Pre-exposure urine samples were collected three times, at approximately 15 h before barbecue, in the morning but before lunch, and immediately before the beginning of barbecue. Post-exposure samples were collected in 35 h after barbecue, i.e., sampling period for urine collection was from January 5 to January 7. The participants recorded collection time and urine sample total volume, and completed a questionnaire (Text S1). The urine samples were collected in polypropylene centrifuge tubes and stored at 8 o C until analysis. Atmospheric background sampling was conducted from 12:3 on January 4 to 17:3 on January 5 for 29 h by using Micro-Orifice Uniform Deposit Impactor (MOUDI) followed with polyurethane foam, which were described in the main text. Atmospheric samples of barbecue fumes were collected near a barbecue stove but behind the participants at site 1 and site 2 respectively (Figure S1). Participants of group D and group E wore same materials of T-shirts and shorts, and wore silicone wristbands (white color, width: 1.1 cm, diameter: 4.5 cm, average weight: g), then were mixed up one by one sitting in a circle around a stove. After exposure, both forearms of participants were wiped with gauze pads soaked in ethanol. The skin-wipe samples were collected in polytetrafluoretyhylene (PTFE) tubes S13

14 contained dichloromethane (DCM), while silicone wristband samples were collected in PTFE tubes. All these samples were stored at 2 o C and analyzed as soon as possible. Pretreatment and Extraction. Silicone wristbands were pretreated similarly as described by O Connell et al., 1 i.e., silicone wristbands were firstly rinsed with Milli-Q water and methanol, then were sonicated three times with ethyl acetate and hexane mixture (1:1 in volume), two times with ethyl acetate and methanol mixture (1:1 in volume). The solvent-cleaned wristbands were dried under stream of N2 and stored in PTFE tube. Gauze pads (7 cm 7 cm) were precleaned similarly as described by Gong et al., 11 i.e., gauze pads were sonicated three times with DCM and dried in vacuum desiccator, then wrapped in aluminum foil and sealed in lightly vacuum plastic bag. Each sample was spiked with the surrogate standards before extraction. Silicone wristband samples were Soxhlet extracted with 2 ml of hexane and acetone mixture (1:1 in volume) for 24 h. 12 Skin-wipe samples were sonicated three times with 3 ml of DCM for 3 min. Each extract of wristband and skin-wipe samples was concentrated, solventexchanged to hexane and further concentrated to 1 ml with a Zymark TurboVap 5 (Hopkinton, MA). The concentrated extract was purified and fractionated with a glass column filled with 5 cm neutral silica gel, and 1 cm anhydrous sodium sulfate from bottom to top. The fraction containing PAHs was eluted with 2 ml of hexane, and further concentrated to 5 μl in vial under a gentle stream of N2. The extract was spiked with the internal standards before instrumental analysis with GCMS. Extraction of urine samples, gaseous, and particulate samples were carried out using the same methods described in the main text. Quality Assurance and Quality Control. For atmospheric, wristband and skin-wipe samples, the recoveries of the surrogate standards, i.e., naphthalene-d8, acenaphthene-d1, S14

15 phenanthrene-d1, chrysene-d12, perylene-d12, and benzo[ghi]perylene-d12, were 69 ± 1%, 74 ± 11%, 78 ± 15%, 87 ± 1%, 84 ± 12%, and 84 ± 8%. Conclusions. Barbecue heating by charcoal could emit large amounts of PAHs, even high molecular-weight PAHs. The concentrations of PAHs on wristband samples and skinwipe samples confirmed that participants could absorb PAHs via dermal absorption from BBQ fumes, and also indicated all participants from different exposure groups were exposed to the same PAH concentrations. The urinary net excreted amounts of low molecular-weight PAHs via dermal absorption were greater than those via inhalation in the indoor BBQ event, further confirming dermal absorption was a more important pathway for intake of low molecular-weight PAHs than inhalation. The urinary net excreted amounts of OH-Flu and OH-Phy were significantly correlated with the concentrations of Flu and Pyr in wristbands respectively, based on Pearson correlation coefficients. S15

16 Table S1. Acronyms and molecular weight (MW, g mol -1 ) of polycyclic aromatic hydrocarbons Compound Acronyms MW NO. of benzene rings Naphthalene Nap Acenaphthylene Acy Acenaphthene Ace Fluorene Flu Phenanthrene Phe Anthracene Ant Fluoranthene Fla 22 3 Pyrene Pyr 22 4 Benzo[a]anthracene BaA Chrysene Chr Benzo[b]fluoranthene BbF Benzo[k]fluoranthene BkF Benzo[a]pyrene BaP Indeno[1,2,3-cd]pyrene IcdP Dibenz[a,h]anthracene DahA Benzo[ghi]perylene BghiP S16

17 Table S2. The basic characteristic of participants in the present study Participant Body weight (kg) Height (cm) Age (years) A A A A A A A B B B B B B B C C C C C C S17

18 Table S3. Octanol-water partition coefficient (log kow; unitless), Henry s law constant (H; Pa m 3 mol -1 ), and calculated kp_g of polycyclic aromatic hydrocarbons log kow a H b kp_g Nap Acy Ace Flu Phe Ant Fla Pyr BbF BkF BaP IcdP BghiP a Values of log kow are obtained from the literature. 13 b H is obtained from the literature. 14 S18

19 Table S4. The proportion of particle-bound PAHs deposited in the head airways (HA), tracheobronchial region (TB), and alveolar region (AR) of the human respiratory tract, and their corresponding deposition concentrations (Cdp; ng m -3 ) Proportion Cdp HA TB AR HA TB AR Total Acy 83% 5.2% 12% Ace 77% 5.% 17% Flu 79% 5.% 16% Phe 78% 4.8% 18% Ant 87% 3.7% 8.6% Fla 82% 4.4% 13% Pyr 84% 4.2% 12% BaA 78% 5.1% 16% Chr 74% 5.7% 2% B[b+k]F 75% 4.9% 2% BaP 6% 6.8% 33% IcdP 65% 6.3% 29% DahA a - RL b RL RL RL BghiP 79% 5.3% 16% PAH a : means data is not available. b RL is the acronym of the reporting limit at 56 pg m -3 with an air volume of 4.5 m 3 S19

20 Table S5. Sensitivity data for dermal and inhalation intake of PAHs f SA vd(p) IR Gaseous dermal intake Flu Phe Pyr Particulate dermal intake Flu Phe Pyr Total dermal intake Flu Phe Pyr Gaseous dermal and inhalation intake Flu Phe Pyr Particulate dermal and inhalation intake Flu Phe Pyr Total dermal and inhalation intake Flu Phe Pyr As inhalation intake only was affected by breathing rate, the sensitivity value of breathing rate is 1. for inhalation intake. f is the exposed dermal fraction; SA is the body surface area; vd(p) is the mass-transfer coefficient that describes the external transport of the PAH compound from the particle phase through the boundary layer adjacent to the skin (m h -1 ); IR is the participants breathing rate. S2

21 Table S6. Measured PAH concentrations (ng g -1, wet weight) in barbecued foods Coprinus comatus Beef Squid Chicken breast Chicken wing Fragrant-flowered garlic Lamb kebabs Sausage Nap Acy Ace Flu Phe Ant Fla Pyr BaA Chr B[b+k]F BaP.26 RL a <RL IcdP <RL <RL <RL <RL <RL <RL <RL <RL DahA <RL <RL <RL <RL <RL <RL <RL <RL S21

22 BghiP <RL <RL <RL <RL <RL <RL <RL <RL Total a RL is the abbreviation of reporting limit at.1 ng g -1 for 5 g food. S22

23 Table S7. Wet weight (g) of barbecued foods consumed by participants in group A A1 A2 A3 A4 A5 A6 A7 Coprinus comatus Beef Squid Chicken breast Chicken wing Fragrant-flowered garlic Lamb kebabs Sausage S23

24 Table S8. Intake amounts (ng) of low molecular-weight PAHs via dietary exposure A1 A2 A3 A4 A5 A6 A7 Nap Flu Phe Pyr S24

25 Table S9. The ratios of excretion to intake for Nap, Flu, Phe, and Pyr via diet, dermal absorption, combined dermal and inhalation exposure, and inhalation Diet Dermal absorption Dermal contact+inhalation Inhalation Nap.53±.21 a Flu.38±.24.11± ±.1 Phe.14±.9.36±.2.28±.8.16±.31 Pyr.6±.64.43±.34.35±.17.25±.5 a Data are not available. Intake values of selected PAHs are calculated values, while excretion values are measured values in urine. The ratios of excretion to intake were estimated by Monte Carlo simulation. S25

26 Table S1. Measured PAH concentrations (geometric mean ± standard deviation; ng m -2 ) in cotton cloth samples of groups A, B, and C after exposure ClothA ClothB ClothC Nap 454±14 489±21 475±128 Acy 59±16 53±12 65±13 Ace 61±16 51±17 71±2 Flu 45± ±66 46±71 Phe 249± ± ±57 Ant 28±42 284±69 252±66 Fla 528±72 519±77 445±47 Pyr 482±75 513±12 464±29 BaA 312±88 339±18 351±86 Chr 87±228 84±28 818±221 B[b]F <RL a <RL <RL B[k]F <RL <RL <RL BaP <RL <RL <RL IcdP <RL <RL <RL DahA <RL <RL <RL BghiP <RL <RL <RL a RL is the acronym of the reporting limit at 12.5 ng m -2 with a cloth area of.4 m 2. Group A: dietary, dermal, and inhalation exposure; Group B: dermal and inhalation exposure; Group C: dermal absorption. S26

27 Table S11. Daily intake (ng day -1 ) of PAHs via dermal absorption from exposed clothes based on the measured PAH concentrations in clothes. Intake Nap 121( ) a Acy 14(1.1-39) Ace 15(1.1-42) Flu 98( ) Phe 614(47,177) Ant 65( ) Fla 115(9.3-31) Pyr 117( ) BaA 84( ) Chr 198(15-559) B[b+k]F b BaP IcdP DahA BghiP Total 144( ) a Mean and the 95% confidence interval. b Data are not available. The intake amounts of PAHs from clothes were estimated based on the PAHs concentrations contained in 2 cm 2 cm cotton cloth samples. The estimated results were based on the same penetration factor for all PAHs, and more details were presented in Text S4. S27

28 Table S12. Measured gaseous and particulate concentrations (ng m -3 ) of polycyclic aromatic hydrocarbons (PAHs) of background, site 1 and site 2 while barbecuing indoor Cg Cp Background Site 1 Site 2 Background Site 1 Site 2 Nap Acy Ace Flu Phe Ant Fla Pyr BaA Chr B[b+k]F <RL a <RL <RL BaP <RL <RL <RL IcdP <RL <RL <RL DahA <RL <RL <RL <RL a BghiP <RL <RL <RL PAH a RL is the acronym of the reporting limit at 46 pg m -3 with an air volume of 5.4 m 3. S28

29 Table S13. Pearson correlation coefficients between net excreted amounts of OH-PAHs in urine, PAHs concentration measured in silicone wristbands and forearms wipes of group E. Wristbands Forearms wipes Nap Flu Phe Pyr Nap Flu Phe Pyr Urine OH-Nap.676 a OH-Flu * b OH-Phe OH-Pyr ** c Forearms wipes Nap Flu Phe Pyr a p >.5, b * p <.5, c ** p <.1. S29

30 Figure S1. Photo showing the location of atmospheric sampling and the arrangement of the indoor barbecue event S3

31 Net Excreted Amount via Urine (ng) OH-Nap OH-Flu OH-Phe OH-Pyr D E Figure S2. Net excreted amounts of OH-PAHs for combined dermal and inhalation exposure to indoor barbecue fumes (D) and for dermal absorption from the fumes (E). Net excreted amount has been corrected by the urinary initial concentration level in each participant S31

32 4 14 Concentration (ng wristband -1 ) (a) Wristbands D E Concentration (ng m -2 ) D E (b) Forearms wipes Nap Flu Phe Pyr Nap Flu Phe Pyr Figure S3. Measured concentration of PAHs in (a) wristband samples (ng per wristband) and (b) forearms-wipe samples (ng per m 2 of forearms surface areas) collected from twelve participants of group D (dermal and inhalation exposure) and group E (dermalabsorption). S32

33 5 4 A1 2-OH-Nap 5 4 A1 1-OH-Nap 5 4 A1 2-OH-Flu A1 1+9-OH-Phe Concentration (ng g -1 creatinine) A1 2-OH-Phe A2 2-OH-Nap A1 3-OH-Phe A2 1-OH-Nap A1 4-OH-Phe A2 2-OH-Flu A1 1-OH-Pyr A2 1+9-OH-Phe A2 2-OH-Phe A2 3-OH-Phe Collection time (h) A2 4-OH-Phe A2 1-OH-Pyr Figure S4-1. Concentration of nine OH-PAHs in urine samples collected from participants A1 and A2 in Group A, who were exposed to PAHs via dietary ingestion, dermal absorption, and inhalation, for a pre-exposure and post-exposure period. S33

34 8 7 A3 2-OH-Nap A3 1-OH-Nap A3 2-OH-Flu A3 1+9-OH-Phe Concentration (ng g -1 creatinine) A3 2-OH-Phe A4 2-OH-Nap A3 3-OH-Phe A4 1-OH-Nap A3 4-OH-Phe A4 2-OH-Flu A3 1-OH-Pyr A4 1+9-OH-Phe A4 2-OH-Phe 3 25 A4 3-OH-Phe 5 4 A4 4-OH-Phe 1 8 A4 1-OH-Pyr Collection time (h) Figure S4-2. Concentration of nine OH-PAHs in urine samples collected from participants A3 and A4 in Group A, who were exposed to PAHs via dietary ingestion, dermal absorption, and inhalation, for a pre-exposure and post-exposure period. S34

35 4 3 A5 2-OH-Nap 5 4 A5 1-OH-Nap 2 15 A5 2-OH-Flu 2 15 A5 1+9-OH-Phe Concentration (ng g -1 creatinine) A5 2-OH-Phe A6 2-OH-Nap A5 3-OH-Phe A6 1-OH-Nap A5 4-OH-Phe A6 2-OH-Flu A5 1-OH-Pyr A6 1+9-OH-Phe A6 2-OH-Phe A6 3-OH-Phe A6 4-OH-Phe A61-OH-Pyr Collection time (h) Figure S4-3. Concentration of nine OH-PAHs in urine samples collected from participants A5 and A6 in Group A, who were exposed to PAHs via dietary ingestion, dermal absorption, and inhalation, for a pre-exposure and post-exposure period. S35

36 Concentration (ng g -1 creatinine) 8 7 A7 2-OH-Nap A7 2-OH-Phe A7 1-OH-Nap A7 3-OH-Phe A7 2-OH-Flu A7 4-OH-Phe A7 1+9-OH-Phe A7 1-OH-Pyr Collection time (h) Figure S4-4. Concentration of nine OH-PAHs in urine samples collected from participants A7 in Group A, who were exposed to PAHs via dietary ingestion, dermal absorption, and inhalation, for a pre-exposure and post-exposure period. S36

37 B1 2-OH-Nap B1 1-OH-Nap B1 2-OH-Flu B1 1+9-OH-Phe Concentration (ng g -1 creatinine) B1 2-OH-Phe B2 2-OH-Nap B1 3-OH-Phe B2 1-OH-Nap B1 4-OH-Phe B2 2-OH-Flu B1 1-OH-Pyr B2 1+9-OH-Phe B2 2-OH-Phe B2 3-OH-Phe B2 4-OH-Phe B2 1-OH-Pyr Collection time (h) Figure S5-1. Concentration of nine OH-PAHs in urine samples collected from participants B1 and B2 in Group B, who were exposed to PAHs via dermal absorption and inhalation, for a pre-exposure and post-exposure period. S37

38 B3 2-OH-Nap B3 1-OH-Nap B3 2-OH-Flu B3 1+9-OH-Phe Concentration (ng g -1 creatinine) B3 2-OH-Phe B4 2-OH-Nap B3 3-OH-Phe B4 1-OH-Nap B3 4-OH-Phe B4 2-OH-Flu B3 1-OH-Pyr B4 1+9-OH-Phe B4 2-OH-Phe 25 2 B4 3-OH-Phe 35 3 B4 4-OH-Phe 2 15 B4 1-OH-Pyr Collection time (h) Figure S5-2. Concentration of nine OH-PAHs in urine samples collected from participants B3 and B4 in Group B, who were exposed to PAHs via dermal absorption and inhalation, for a pre-exposure and post-exposure period. S38

39 9 8 B5 2-OH-Nap 1 8 B5 1-OH-Nap 6 5 B5 2-OH-Flu 3 25 B5 1+9-OH-Phe Concentration (ng g -1 creatinine) B5 2-OH-Phe B6 2-OH-Nap B5 3-OH-Phe B6 1-OH-Nap B5 4-OH-Phe B6 2-OH-Flu B5 1-OH-Pyr B6 1+9-OH-Phe B6 2-OH-Phe B6 3-OH-Phe Collection time (h) B6 4-OH-Phe B6 1-OH-Pyr Figure S5-3. Concentration of nine OH-PAHs in urine samples collected from participants B5 and B6 in Group B, who were exposed to PAHs via dermal absorption and inhalation, for a pre-exposure and post-exposure period. S39

40 Concentration (ng g -1 creatinine) 8 14 B7 2-OH-Nap B7 1-OH-Nap B7 2-OH-Phe B7 3-OH-Phe B7 4-OH-Phe B7 2-OH-Flu B7 1+9-OH-Phe B7 1-OH-Pyr Collection time (h) Figure S5-4. Concentration of nine OH-PAHs in urine samples collected from participants B7 in Group B, who were exposed to PAHs via dermal absorption and inhalation, for a pre-exposure and post-exposure period. S4

41 C1 2-OH-Nap C1 1-OH-Nap C1 2-OH-Flu C1 1+9-OH-Phe Concentration (ng g -1 creatinine) C1 2-OH-Phe C2 2-OH-Nap 3 4 C1 3-OH-Phe 25 C1 4-OH-Phe C2 1-OH-Nap C2 2-OH-Flu C1 1-OH-Pyr C2 1+9-OH-Phe C2 2-OH-Phe 5 4 C2 3-OH-Phe 5 4 C2 4-OH-Phe 2 15 C2 1-OH-Pyr Collection time (h) Figure S6-1. Concentration of nine OH-PAHs in urine samples collected from participants C1 and C2 in Group C, who were exposed to PAHs via dermal absorption, for a pre-exposure and post-exposure period. S41

42 C3 2-OH-Nap C3 1-OH-Nap C3 2-OH-Flu C3 1+9-OH-Phe Concentration (ng g -1 creatinine) C3 2-OH-Phe C4 2-OH-Nap C3 3-OH-Phe C41-OH-Nap C3 4-OH-Phe C4 2-OH-Flu C3 1-OH-Pyr C4 1+9-OH-Phe C4 2-OH-Phe 25 2 C4 3-OH-Phe C4 4-OH-Phe C4 1-OH-Pyr Collection time (h) Figure S6-2. Concentration of nine OH-PAHs in urine samples collected from participants C3 and C4 in Group C, who were exposed to PAHs via dermal absorption, for a pre-exposure and post-exposure period. S42

43 Concentration (ng g -1 creatinine) C5 2-OH-Nap C5 2-OH-Phe C6 2-OH-Nap C6 2-OH-Phe C5 1-OH-Nap C5 3-OH-Phe C6 1-OH-Nap C6 3-OH-Phe C5 4-OH-Phe C6 2-OH-Flu C5 1-OH-Pyr C6 4-OH-Phe C6 1-OH-Pyr Collection time (h) 8 6 C5 2-OH-Flu C5 1+9-OH-Phe C6 1+9-OH-Phe Figure S6-3. Concentration of nine OH-PAHs in urine samples collected from participants C5 and C6 in Group C, who were exposed to PAHs via dermal absorption, for a pre-exposure and post-exposure period S43

44 Concentration (ng g -1 creatinine) D1 2-OH-Nap D1 2-OH-Phe D2 2-OH-Nap D2 2-OH-Phe D1 1-OH-Nap D1 3-OH-Phe D2 1-OH-Nap 25 D2 2-OH-Flu D2 3-OH-Phe Collection time (h) D1 2-OH-Flu D1 4-OH-Phe D2 4-OH-Phe D1 1+9-OH-Phe D1 1-OH-Pyr D2 1+9-OH-Phe D2 1-OH-Pyr Figure S7-1. Concentration of nine OH-PAHs in urine samples collected from participants D1 and D2 in Group D, who were exposed to PAHs via dermal and inhalation exposure, for a pre-exposure and post-exposure period. S44

45 16 12 D3 2-OH-Nap 2 15 D3 1-OH-Nap D3 2-OH-Flu D3 1+9-OH-Phe Concentration (ng g -1 creatinine) D3 2-OH-Phe D4 2-OH-Nap D3 3-OH-Phe D4 1-OH-Nap D3 4-OH-Phe D4 2-OH-Flu D3 1-OH-Pyr D4 1+9-OH-Phe D4 2-OH-Phe D4 3-OH-Phe D4 4-OH-Phe D4 1-OH-Pyr Collection time (h) Figure S7-2. Concentration of nine OH-PAHs in urine samples collected from participants D3 and D4 in Group D, who were exposed to PAHs via dermal and inhalation exposure, for a pre-exposure and post-exposure period. S45

46 4 3 D5 2-OH-Nap 8 6 D5 1-OH-Nap D5 2-OH-Flu 5 4 D5 1+9-OH-Phe Concentration (ng g -1 creatinine) D5 2-OH-Phe D6 2-OH-Nap D5 3-OH-Phe D6 1-OH-Nap D5 4-OH-Phe D6 2-OH-Flu D5 1-OH-Pyr D6 1+9-OH-Phe D6 2-OH-Phe D6 3-OH-Phe D6 4-OH-Phe D61-OH-Pyr Collection time (h) Figure S7-3. Concentration of nine OH-PAHs in urine samples collected from participants D5 and D6 in Group D, who were exposed to PAHs via dermal and inhalation exposure, for a pre-exposure and post-exposure period. S46

47 E1 2-OH-Nap E1 1-OH-Nap E1 2-OH-Flu E1 1+9-OH-Phe Concentration (ng g -1 creatinine) E1 2-OH-Phe E2 2-OH-Nap E1 3-OH-Phe E2 1-OH-Nap E1 4-OH-Phe E2 2-OH-Flu E1 1-OH-Pyr E2 1+9-OH-Phe E2 2-OH-Phe E2 3-OH-Phe Collection time (h) E2 4-OH-Phe E2 1-OH-Pyr Figure S8-1. Concentration of nine OH-PAHs in urine samples collected from participants E1 and E2 in Group E, who were exposed to PAHs via dermal exposure, for a pre-exposure and post-exposure period. S47

48 E3 2-OH-Nap E3 1-OH-Nap E3 2-OH-Flu E3 1+9-OH-Phe Concentration (ng g -1 creatinine) E3 2-OH-Phe E4 2-OH-Nap E3 3-OH-Phe E4 1-OH-Nap E3 4-OH-Phe E4 2-OH-Flu E3 1-OH-Pyr E4 1+9-OH-Phe E4 2-OH-Phe E4 3-OH-Phe 1 E4 4-OH-Phe Collection time (h) E4 1-OH-Pyr Figure S8-2. Concentration of nine OH-PAHs in urine samples collected from participants E3 and E4 in Group E, who were exposed to PAHs via dermal exposure, for a pre-exposure and post-exposure period. S48

49 5 4 E5 2-OH-Nap 1 8 E5 1-OH-Nap 12 1 E5 2-OH-Flu 25 2 E5 1+9-OH-Phe Concentration (ng g -1 creatinine) E5 2-OH-Phe E6 2-OH-Nap E5 3-OH-Phe E6 1-OH-Nap E5 4-OH-Phe E6 2-OH-Flu E5 1-OH-Pyr E6 1+9-OH-Phe E6 2-OH-Phe 4 3 E6 3-OH-Phe 4 3 E6 4-OH-Phe E6 1-OH-Pyr Collection time (h) Figure S8-3. Concentration of nine OH-PAHs in urine samples collected from participants E5 and E6 in Group E, who were exposed to PAHs via dermal exposure, for a pre-exposure and post-exposure period. S49

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