Exposure to SVOCs from Inhaled Particles: Impact of Desorption

Apr 28, 2017 - E-mail: [email protected] (Y.Z.)., *Phone: 848 445-2073. ... in the RT, encountering different cell populations with varying...
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Exposure to SVOCs from inhaled particles: the impact of desorption Cong Liu, Yinping Zhang, and Charles J. Weschler Environ. Sci. Technol., Just Accepted Manuscript • Publication Date (Web): 28 Apr 2017 Downloaded from http://pubs.acs.org on April 28, 2017

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Environmental Science & Technology

Exposure to SVOCs from inhaled particles: the impact of desorption Cong Liu1, Yinping Zhang2,4* , and Charles J. Weschler2,3,4* 1

School of Energy and Environment, Southeast University, Nanjing, Jiangsu 2010096, China Department of Building Science, Tsinghua University, Beijing 100084, China 3 Environmental and Occupational Health Sciences Institute, Rutgers University, Piscataway, NJ 08854, USA 4 Beijing Key Laboratory of Indoor Air Quality Evaluation and Control, Beijing 100084, China 2

*Corresponding emails: [email protected]; [email protected]

ABSTRACT: Inhaled semivolatile organic compounds (SVOCs) are simultaneously present in gas- and particle-phases. Particles desorb a fraction of their SVOCs moving through the human respiratory tract (RT). Quantifying such desorption is challenging, but important since gas- and particle-phase SVOCs deposit in different locations in the RT, encountering different cell populations with varying health consequences. This paper presents a mass transfer model to quantify this desorption process in the head, tracheobronchial and alveolar regions of the RT. The desorption of SVOCs from inhaled particles can be gauged using the ratio of particle residence time to the time required to achieve particle/gas equilibrium. Results indicate that the larger this ratio, the more likely particles desorb the SVOCs they carry. For particles smaller than 0.5 µm diameter and SVOCs with a particle/gas partition coefficient (unitless) of 1010, accounting for desorption reduces the estimated particle-phase SVOC concentrations in the alveolar region by more than 35%; the reduction is almost 700% for 0.05 µm diameter particles. In hypothetical scenarios representing common indoor and outdoor situations, neglecting desorption significantly overestimates the concentration of ultrafine particle associated SVOCs in the alveolar region. This model is a preliminary step towards more nuanced estimates of exposure to inhaled SVOCs. Keywords: PM2.5, Ultrafine particles, Equilibrium, Dynamic partitioning, Kinetics

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TOC art:

: Particles : Particles with SVOCs

C _without desorption − C _w ith desorption C _with desorption 0 200 % 400 % 600 % 800 %

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0

45

dp=0.05 µm

dp=0.1 µm dp=0.2 µm

log Kpart=10

dp=0.5µm 1

2 3 4 Particle residence time Gas-particle equilibration time

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NOMENCLATURE A (m2) Aout (m2) Ap (m2) Cmp (µg/m3) Cg (µg/m3) Cs (µg/m3) Csp (µg/m3, mass of particle associated SVOCs/volume of air) dp DF fi hm (m/s) Kpart (unitless) Ks (unitless) Q (m3/s) Qout (m3/s) T (s) TV (m3) V (m3) vd (m/s) Vout (m3) Vp (m3) vt (m/s) Subscripts ex H, TB and Alv out and 0 Greek and other symbols α (unitless) β (m3/µg of particles) ε

θ (unitless) ρp (µg/m3)

Surface area of a region in the respiratory tract Area of exposed surfaces in the ambient environment; i.e., where particles are deposited Surface area of one single particle Particle mass concentration Gas-phase SVOC concentration SVOC concentration in the internal wall of respiratory tract Particle-phase SVOC concentration Aerodynamic particle diameter Fraction of particle loss due to deposition to wall of respiratory tract Mass fraction of particles in size bin i in the ambient environment Mass transfer coefficient over the surface area of respiratory tract Particle/gas partition coefficient Partition coefficient between mucus on the wall of respiratory tract and air Breathing rate of a person Ventilation rate in the ambient environment Breath period Tidal volume Volume of a region in the respiratory tract Deposition rate of particles Volume of the ambient environment Volume of one single particle Mass transfer coefficient around particles Indicates concentrations calculated excluding desorption Head region, tracheobronchial region and alveolar region, respectively Concentrations in the outdoor environment and initial value, respectively Ratio of equilibration time to residence time Csp,out /(Cmp,outCg,out) Relative difference between normalized particle-phase SVOC concentration in the alveolar region ignoring desorption (Csp,Alv,ex*) and accounting for desorption (Csp,Alv*) Ratio of SVOC mass desorbed from particles to the total inhaled particle-phase SVOC mass Particle density 3

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φ (s) * 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 66 67 68 69 70 71 72 73 74 75 76 77 78 79 80 81 82 83 84 85 86 87 88

Characteristic timescale to establish SVOC/particle equilibrium Indicates a normalized parameter

INTRODUCTION When air is inhaled, semivolatile organic compounds (SVOCs) are present in both the gas-phase and sorbed to airborne particles. The distribution between these phases depends, in part, on an SVOC’s volatility or octanol/air partition coefficient and the concentration of particles1-3. This distribution is anticipated to change as inhaled air travels through the respiratory tract; particles release (desorb) a fraction of their SVOCs as gas-phase SVOCs are depleted. SVOCs are likely to penetrate deeper into the respiratory tract and to interact with cellular layers longer if they are associated with submicron particles as opposed to being in the gas-phase.4 SVOCs that deposit in different regions of the respiratory tract encounter different cell populations, are removed by different mechanisms, and have different clearance times, all of which influences their potential toxicity 5. In the case of particles containing SVOCs, health effects depend not only on the site where they are deposited 6, but also the amount of SVOCs they carry when deposited 7. Understanding the desorption of SVOCs in the respiratory tract is important to understanding the potential health impacts of inhaled SVOCs. Pankow 8 proposed that a compound such as nicotine, inhaled in tobacco smoke, can deposit in the respiratory tract (RT) by four different mechanisms: (1) gas-phase nicotine directly deposits to respiratory tract tissue; (2) nicotine desorbs from particles and then deposits on tissue; (3) particles deposit; nicotine desorbs from deposited particles and then deposits on tissue; and (4) particles deposits; nicotine diffuses directly from particles to tissue. In the past two decades, efforts have been made to examine the second of these processes – desorption of particleassociated nicotine – in a denuder 9-14. This is in some ways similar to what occurs in the human respiratory tract. However, there are two fundamental limitations with a denuder model when applied to the human respiratory tract. One concerns physical structure and functioning. Breathing is a periodic process consisting of inhalation and exhalation, with the volume of the alveolar region changing during a breath cycle. This feature has not been captured by previous models developed for denuders. The other concerns particle deposition to the wall of the human respiratory tract 15-17. This important removal process will limit the residence time of particles in the RT, and thus influence desorption. Particle deposition is not included in the denuder models in the aforementioned studies. Furthermore, in the case of nicotine and smoke particles, the system was simplified to an aqueous solution of nicotine and acid 10-11, 13. This simplification only works as a rough approximation 18, and prevents the conclusions obtained for a denuder from being extrapolated to the human respiratory tract, at least in a quantitative sense. The objectives of this study are therefore: 1) to develop an improved mass transfer model to quantitatively estimate the exposure of the human respiratory tract to particle-associated and desorbed SVOCs; 2) to examine the impact of particle size on desorption and exposure; and 3) to identify other key parameters influencing desorption and exposure. METHODOLOGY Model development

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Figure 1. Schematic of the human respiratory tract (inhalation). The black circles represent airborne particles, and the red envelopes represent particle-associated SVOCs. The thickness of the orange envelope qualitatively represents the amount of SVOC associated with the particles. In this study the respiratory tract is simplified into three regions. The upper respiratory tract is lumped as the “head region” (H). The lower respiratory tract is divided into two regions: the “tracheobronchial region” (TB, from trachea to terminal bronchioles) and the “alveolar region” (Alv, from respiratory bronchioles to alveoli). Hinds 17 reported formulas to determine deposition fractions of particles in these three regions, and several other studies have examined characteristics of pollutant deposition in the human respiratory tract by dividing the lower respiratory tract into tracheabronchial and alveolar regions 19-21. Given the scope of this preliminary study, we consider the simplification shown in Figure 1 to be reasonable. A series of mass transfer models have been developed to describe the accumulation of airborne SVOCs in the respiratory tract 22-25. The present formulation ignores mouth breathing; during inhalation, air is drawn in through the nasal airway. The model developed includes a better characterization of dynamic gas/particle mass transfer, particle deposition to the wall of the respiratory tract, and a more realistic description of the human respiratory tract. Desorption of SVOCs out of deposited particles (Pankow’s process (3) – see above) is not accounted for. The equations for the head, tracheobronchial, and alveolar regions are in the supporting information (SI, equations S1-S22). For the purpose of comparison with the present model, equations S23S32 in the SI show the governing equations for the particle-phase SVOC concentration when SVOC desorption from particles is excluded (the subscript ex in equations S23-S32 indicates concentrations when the desorption effect is excluded). The relationship between Csp,out and Cg,out is developed from the dynamic SVOC/particle interaction model 26, 27: C sp ,out = β C mp ,out C g ,out (1)

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β=

K part

1

ρ p   Vp K part      vt Ap   

117 118 119 120 121 122 123 124 125 126 127 128 129 130 131 132 133 134 135 136 137 138 139 140 141 142 143 144 145

Vout   Qout + vd ,out Aout

   + 1 

(2)

where Csp,out (µg/m3, mass of particle associated SVOCs/volume of air) is the ambient particlephase concentration, Cg,out (µg/m3) is the ambient gas-phase SVOC concentration, Qout (m3/s) is the ventilation rate in the environment, Vout (m3) is the volume of the environment, vd,out (m/s) is the deposition velocity of particles to surfaces in the environment, and Aout (m2) is the surface area where particles are deposited. Model assumptions, normalization and parameterization The following assumptions have been made to facilitate the derivation of the model and the subsequent analysis: (1). The volumes and surface areas of head and tracheobronchial regions are constant. (2). The surface concentration in the internal wall of the RT (Cs,i) is zero. (3). To a first approximation, the alveolar region can be modeled as a sphere (i.e., the relationship between surface area and volume of a sphere applies to the alveolar region -A1/2/V1/3=constant). (4). Both gas- and particle-phase concentrations in each of the three regions are uniformly distributed, although different in each region. (5). The breathing rate is a square-wave function of time 23. (6). Monodisperse particles are analyzed in this study, not polydisperse. A constant particle mass concentration (Cmp,out) of 20 µg/m3 is used for the baseline case as outlined in Table 1. (7). The impact of coagulation on particles in the respiratory tract is neglected. The influence of assumptions (2) and (6) on the results is examined in the following section. To generalize the following analysis and avoid unnecessary complication caused by large variations in typical values of Cg,out for SVOCs commonly found indoors 28, we normalized the gas- and particle-phase concentration by Cg,out as follows: C g ,i * =

C s ,i * = 146 147 148 149 150

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C g ,i C g ,out

, Csp ,i * =

Cs , i K s , i Cg ,out

Csp ,i Cg ,out

, (3)

, Csp ,out * =

Csp ,out C g ,out

= β Cmp ,out ,

where the subscript i indicates H, TB, Alv, H,ex, TB,ex, or Alv,ex, and ex indicates concentrations calculated excluding desorption. β is as defined in equation (2). Table 1 provides baseline values (sitting adult males) for the parameters used in the model. Table 1. Baseline values (sitting adult males) for parameters used in the model. Parameters H TB Alv 3 a -6 -6 V (m ) 70×10 90×10 3000×10-6 2 a A (m ) 0.03 0.4 60 6

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DF b

151 152 153 154 155 156 157 158 159 160 161 162 163 164 165 166 167 168 169 170 171 172 173

dp=0.05µm dp=0.1µm dp=0.2µm dp=0.5µm

0.037 0.021 0.026 0.10 0.24

0.068 0.027 0.0085 0.0071 0.24

0.31 0.14 0.062 0.082 0.14

hm (m/s) c Physiology TV (m3) a 750×10-6 a T (s) 5 Q (m3/s) =TV/(T/2)=300×10-6 Environment conditions Cmp,out (µg/m3) 20 -1 d Qout/Vout (h ) 0.6 -1 Aout/Vout (m ) 3 vt (m/s) e dp=0.05µm 31 dp=0.1µm 27 dp=0.2µm 21 dp=0.5µm 12 vd,out (m/s) f dp=0.05µm 6.8×10-6 dp=0.1µm 4.2×10-6 dp=0.2µm 4.0×10-6 dp=0.5µm 7.7×10-6 3 ρp (µg/m ) 1.0×1012 a 29 . The values for the alveolar region are the initial ones. The values of TV and T are set for nasal breathing while sitting; b 17 ; c 19; d 30 ; e 26, 27; f 31

RESULTS and DISCUSSION SVOC concentrations in the human respiratory tract when desorption is considered As an illustrative example of variations during the breathing cycle, Figure 2 shows SVOC concentrations in the head, tracheobronchial and alveolar regions when the desorption effect is included. The example is for particles of dp = 0.05 µm and SVOCs with log Kpart = 11 (a common value for indoor SVOCs 28, which results in Csp,out* = 2.0 based on equation 3). It can be seen that both the gas- and particle-phase SVOC concentrations reach a quasi steady-state within 30 cycles (150 s) of inhalation-exhalation. The gas- and particle-phase concentrations increase during inhalation and decrease during exhalation. In this example (log Kpart = 11), the particlephase concentration is at least one order of magnitude higher than the gas-phase one. The gasphase concentration in the head region is more than two orders of magnitude higher than that in the other two regions, indicating that gas-phase pollutants are deposited mainly in the head region. This is consistent with the literature 8, 32. The difference between the particle- and gasphase concentrations becomes more significant as particles travel deeper into the respiratory tract, reflecting the high mass transfer rate of gas-phase SVOC to the surface of the respiratory tract (hm A). Similar results, with different ratios of gas- and particle-phase concentrations, were also obtained for particles between 0.05 and 0.5µm diameter and SVOCs with Kpart between 1010 and 1012.

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3.0

Normalized concentrations (Cg* & Csp*)

2.5

a: head region

Gas-phase Particle-phase

2.0 1.5 1.0 0.5

0.04 0.02 0.00 0

10

140

150

Time (s)

174 175 3

Gas-phase Particle-phase

Normalized concentrations (Cg* & Csp*)

b: tracheobronchial region 2

1

-4 0.0002 2×10

-4

10 0.0001 0 0.0000

0

176

10

140 Time (s)

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1.0 Normalized concentrations (Cg* & Csp*)

0.8

c: alveolar region

0.6 0.4 Gas-phase Particle-phase

0.2 -5

10 1E-5 -6

10 1E-6 -7

10 1E-7

-8

10 1E-8

0

177 178 179 180 181 182 183 184 185 186 187 188 189 190 191 192 193 194

140

150

Time (s)

Figure 2. Normalized gas- and particle phase concentrations of a hypothetical SVOC in different regions of the human respiratory tract. dp =0.05µm, log Kpart=11, Csp,out*=2.0. This figure contains 30 cycles (150s) of inhalation-exhalation. The desorption effect is included.

The impact of particle size and SVOC volatility on SVOC desorption in the alveolar region Given that steady-state has been achieved by the final cycle (cycle 30) of inhalation-exhalation in Figure 2, we will use the average particle-phase SVOC concentration in this cycle to examine the desorption effect. We find that desorption impacts the particle-phase SVOC concentration in the head and TB region much less than in the alveolar region. In addition, the alveolar region is more consequential to pollutant exposures than the other two regions, as this region hosts the gas exchange with blood. Hence, the primary focus of this section is the alveolar region. Particle size A parameter, ε, is defined as the relative difference between normalized particle-phase SVOC concentration in the alveolar region ignoring desorption (Csp,Alv,ex*) and accounting for desorption (Csp,Alv*), that is: C C * − Csp,Alv * ε = sp ,Alv ,ex − 1 = sp ,Alv ,ex (4) . C C * sp,Alv

195 196 197 198 199 200

10

sp,Alv

This parameter characterizes the magnitude of the desorption effect. A higher value of ε corresponds to a larger effect. The average values of Csp,Alv* and Csp,Alv,ex* in the 30th cycles were used to calculate ε. To examine the influence of particle size on ε, a parameter, α, is next defined as the ratio of residence time to equilibration time:

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α= 201 202 203 204 205 206 207 208 209 210 211

VAlv ( Q + vd A )

ϕ

,ϕ=

V p K part

Ap vt

=

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d p K part 6vt

(5)

.

where VAlv (m3) is the volume of the alveolar region, Q (m3/s) is the breathing rate, vd (m/s) is the particle deposition velocity, A (m2) is the area of surfaces where particles are deposited, vt (m/s) is the mass transfer coefficient around particles, Ap (m2) is the surface area of a single particle, Vp (m3) is the volume of a single particle, Kpart is the particle/gas partition coefficient (dimensionless), dp (m) is the particle diameter. VAlv/(Q+vdA) (unit: “s”) represents the characteristic residence time of particles in the alveolar region. φ characterizes the timescale to establish SVOC/particle equilibrium 33. Ventilation functions as a removal mechanism only during the exhalation process. On average, considering both the inhalation and exhalation processes, it would be reasonable to use Q/2 (Q is the breathing rate, see Table 1) here. The following relationship between deposition fraction and deposition velocity can be used to determine the deposition term: Q DFAlvCmp ,out vd ,Alv AAlv = (6) , 2C mp ,Alv

212

Then equation (5) can be transformed to:  Q Q DFAlv Cmp ,out  V  +  2 2Cmp ,Alv .   α=

(7)

ϕ

213 214 215 216 217 218 219 220 221 222 223 224 225

The volume of the alveolar region changes throughout the breathing cycle. We use the initial volume of the alveolar region as V (see Table 1), and the average particle mass concentration at the quasi steady-state as Cmp,Alv. Figure 3 shows that for SVOCs with Kpart =1010, ε is higher than 35% for particles with diameters between 0.05 and 0.5 µm, with a value of 700% for 0.05 µm particles. As particle size decreases α increases, and the desorption effect (represented by ε) becomes more significant. This is because, as the residence time becomes longer than the equilibration time, particles have relatively more time to release the SVOCs they carry. Particle size impacts both the residence time (DF is a function of particle size, see Table 1) and equilibration time (φ, see equation (5), and vt, see Table 1, are functions of particle size). This means that α can be used as an indicator to evaluate the relative significance of the desorption effect for various SVOC-particle systems.

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800 dp=0.05 µm

ε (%)

600

dp=0.1 µm

400

log Kpart=10 dp=0.2 µm

200

dp=0.5µm

0 0

226 227 228 229 230 231 232 233 234 235 236 237 238 239 240 241 242 243 244

1

2

3

4

5

Particle residence time/gas-particle equilibration time, α

Figure 3. The impact of desorption in the alveolar region. The y-axis indicates the percent difference in the particle-phase SVOC concentration between including and excluding the desorption effect (equation 4). The x-axis indicates a parameter that is the ratio of particle residence time to time to achieve gas/particle equilibrium (equation 7).

SVOC volatility Figure 4 plots ε against log Kpart of SVOCs for particles between 0.05 and 0.5 µm diameter. As Kpart decreases, i.e. SVOC volatility increases, ε increases. This can also be explained by α, defined in equation (5). As Kpart gets smaller, the value of φ decreases -- less time is needed to attain SVOC/particle equilibrium, or for a given length of time, more SVOC can be exchanged between the gas- and particle-phase, resulting in an increased α and consequently increased ε. This is consistent with Figure 3. Quantitatively, when log Kpart increases tenfold (from 10 to 11 or from 11 to 12), ε decreases roughly tenfold. For example, for particles of 0.1 µm diameter, ε is 407%, 38% and 3.8% for log Kpart of 10, 11 and 12, respectively. Figure 4 also shows that for SVOCs with Kpart higher than 1012, ε will be less than 10% for particles larger than 50 nm.

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1000 dp (µm) 0.05 0.1 0.2 0.5

ε (%)

100

10

1 PCB-153 BaP

BghiP

BBzP PCB-180

BDE-99

0.1 10

245 246 247 248 249 250 251 252 253 254 255 256 257 258

11

12

log Kpart

Figure 4. Influence of an SVOC’s unitless particle/gas partition coefficient, Kpart, on the desorption effect for different particle diameters, dp. See text for an explanation based on the parameter α. The diamond markers indicate the value of log Kpart for several SVOCs commonly found indoors. These values are calculated as fom*KOA, with fom (mass fraction of organic matter) assumed to be 0.4 and KOA (octanal/air partition coefficient) values taken from reference 34.

Ratio of desorbed SVOC mass to inhaled particle-phase SVOC mass In the previous sub-sections the desorption effect was examined by comparing particle-phase SVOC concentrations accounting for and ignoring desorption. It is also of interest to examine the ratio of SVOC mass desorbed from particles to the total inhaled particle-phase SVOC mass, which can be calculated as:

 Vi vt Cmp ,Alv Ap  Csp ,i C −   dt g ,Alv ∫0 Vp ρ p  Cmp ,Alv K part ρ p   . θi = T QCsp ,out 2 T

259 260 261 262 263

(8)

where i is H, TB and Alv. T/2, instead of T, is used in the denominator of the right side of equation (8) because particles are drawn into the respiratory tract only during inhalation (not exhalation). Combining the definition of dimensionless parameters in equation (3), equation (8) can be transformed to:

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 Vi vt Cmp ,Alv Ap  Csp ,i * C * −   dt g ,Alv ∫0 Vp ρ p  Cmp ,Alv K part ρ p   θi = . T Qβ Cmp ,out 2 T

264 265 266 267 268 269 270 271 272 273 274 275 276 277

(9)

Results obtained using equation (9) indicate that, of the total SVOC mass desorbed from particles, less than 16% of the desorption occurs in the head and tracheobronchial regions. Hence, the following discussion will focus on the ratio of desorbed SVOC mass to inhaled particle-phase SVOC mass within the alveolar region, θAlv. Figure 5 shows results for particles between 0.05 and 0.5 µm diameter and SVOCs with log Kpart of 10 and 11. For particles smaller than 0.1 µm (ultrafine particles or UFP), more than 50% of the total inhaled particle-associated SVOCs with log Kpart of 10 will be desorbed before being deposited in the alveolar region; for SVOCs with log Kpart of 11, more than 20% will be desorbed. As Kpart increases, θAlv decreases. As particle size increases, θAlv decreases. The exception is the comparison between 0.05 µm and 0.1 µm particles for SVOCs with log Kpart of 10, in which case θAlv for 0.1 µm is slightly higher than θAlv for 0.05 µm. This may be due to less deposition of 0.1 µm compared to 0.05 µm particles in the head, tracheobronchial and alveolar regions, resulting in more 0.1 µm particles that can desorb SVOCs before deposition occurs. 100 log Kpart 10 11

80

θAlv (%)

60

40

20

0 0.0

278 279 280 281 282 283 284 285 286

0.1

0.2

0.3

0.4

0.5

dp (µm)

Figure 5. The percentage of SVOC mass desorbed from particles relative to the total inhaled particle-phase SVOC mass in the alveolar region.

Impact of desorption on particle-phase SVOC deposition in the alveolar region for various size ranges The relative contribution of the deposition of SVOCs associated with particles in size bin i to total deposition of particle-phase SVOCs in the alveolar region, yi, can be calculated as: 13

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287

yi = 288 289 290 291 292 293 294 295

DFAlv,i fi βi (1 + ε i ) fluxi = ∑ fluxi ∑ ( DFAlv,i fi βi (1 + ε i ) ) .

(10)

where fi is the mass fraction of particles in size bin i in the ambient environment. The derivation of fluxi is included in the supporting information (equations S33-S36). β and ε are defined in equations (2) and (4), respectively. When the desorption effect is not considered, i.e. εi = 0, the relative contribution of SVOCs associated with particles in size bin i to total deposition of particle-phase SVOCs, ys,i, can be calculated as:

ys ,i = 296 297 298 299 300 301 302 303 304 305 306 307 308 309 310 311 312 313 314 315 316 317 318 319 320 321 322 323 324 325 326 327

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DFAlv ,i fi βi ∑ ( DFAlv ,i fi βi ) .

(11)

As the desorption effect is significant only for particles smaller than 0.5 µm, we divide suspended particles into five size bins: 0-0.1 µm, 0.1-0.3 µm, 0.3-0.5 µm, 0.5-2.5 µm and 2.5-10 µm. The latter two bins are necessary to calculate the relative contribution of the first three bins to total deposition of particle-associated SVOCs. We consider three particle scenarios in the present study: an indoor case, an outdoor roadside case and an outdoor suburban case. Table S1 in the supporting information lists the values of the parameters used to calculate the contribution of particles in various sizes. Equation (11) (no desorption effect) predicts that, in the alveolar region, more than 92% of the particle-associated SVOC deposition is a consequence of deposition of fine particles (