Environmental Tobacco Smoke as a Source of ... - ACS Publications

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Environmental Tobacco Smoke as a Source of Polycyclic Aromatic Hydrocarbons in Settled Household Dust Eunha Hoh,*,† Richard N. Hunt,† Penelope J. E. Quintana,† Joy M. Zakarian,§ Dale A. Chatfield,⊥ Beth C. Wittry,† Edgar Rodriguez,† and Georg E. Matt*,‡ †

Graduate School of Public Health, San Diego State University, San Diego, CA, USA Department of Psychology, San Diego State University, San Diego, CA, USA § San Diego State University Research Foundation, San Diego, CA, USA ⊥ Department of Chemistry and Biochemistry, San Diego State University, San Diego, CA, USA ‡

S Supporting Information *

ABSTRACT: Environmental tobacco smoke is a major contributor to indoor air pollution. Dust and surfaces may remain contaminated long after active smoking has ceased (called ‘thirdhand’ smoke). Polycyclic aromatic hydrocarbons (PAHs) are known carcinogenic components of tobacco smoke found in settled house dust (SHD). We investigated whether tobacco smoke is a source of PAHs in SHD. House dust was collected from 132 homes in urban areas of Southern California. Total PAHs were significantly higher in smoker homes than nonsmoker homes (by concentration: 990 ng/g vs 756 ng/g, p = 0.025; by loading: 1650 ng/m2 vs 796 ng/m2, p = 0.012). We also found significant linear correlations between nicotine and total PAH levels in SHD (concentration, R2 = 0.105; loading, R2 = 0.385). Dust collected per square meter (g/m2) was significantly greater in smoker homes and might dilute PAH concentration in SHD inconsistently. Therefore, dust PAH loading (ng PAH/m2) is a better indicator of PAH content in SHD. House dust PAH loadings in the bedroom and living room in the same home were significantly correlated (R2 = 0.468, p < 0.001) suggesting PAHs are distributed by tobacco smoke throughout a home. In conclusion, tobacco smoke is a source of PAHs in SHD, and tobacco smoke generated PAHs are a component of thirdhand smoke.

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PAHs have been identified as class B2 probable carcinogens.12,13 In indoor environments, PAHs have been detected at high levels as a major toxic component in house dust.14−21 Contaminated house dust can get into indoor air, food, and water.22 A major uptake of contaminated house dust occurs by hand-tomouth behavior, which occurs more often in young children.23 B2 PAHs exceeded 40 μg/g, resulting in an excess cancer risk of greater than 1 × 10−4 for a high dust ingestion rate scenario in some house dust collected in the U.S. and Canada.19,21 However, the contribution of ETS to PAH content in SHD is unclear, as most studies have not demonstrated a statistically significant difference in dust PAH levels between smoker and nonsmoker homes.14,16,17,19 The lack of association between tobacco use at home and PAH levels, however, may be due to the fact that these studies were not specifically designed to evaluate the contribution of ETS to house dust PAHs. Cigarette smoking was one of many variables examined (including heating

INTRODUCTION Environmental tobacco smoke (ETS) is a mixture of sidestream smoke and mainstream smoke exhaled from smokers’ lungs. ETS contains over 4000 chemicals with more than 60 known carcinogens.1−3 ETS has been classified as a human carcinogen and an indoor air pollutant.4−6 The chemicals in ETS have a wide range of physicochemical properties, and their behaviors and properties depend on indoor environment conditions (e.g., ventilation, temperature, and humidity).7,8 Among these chemicals, semivolatile organic compounds can partition to air particles, which can settle as house dust through accumulation or adsorb to surfaces in indoor environments. These semivolatile organic compounds can then be re-emitted into the air or resuspended as air particulates and settle in another location, which is also known as the ‘grasshopper effect’.9 More importantly, if the organic compounds are persistent, house dust containing the ETS compounds acts as a reservoir even after there is no active smoking. Therefore, humans may be exposed to residual ETS compounds, called thirdhand smoke.10,11 Among the semivolatile and persistent ETS components, polycyclic aromatic hydrocarbons (PAHs) are of particular concern. Benzo(a)pyrene is a known human carcinogen and many other © 2012 American Chemical Society

Received: Revised: Accepted: Published: 4174

January 23, 2012 March 5, 2012 March 7, 2012 March 7, 2012 dx.doi.org/10.1021/es300267g | Environ. Sci. Technol. 2012, 46, 4174−4183

Environmental Science & Technology

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data point before logarithmic transformation. We examined concentrations and loadings of each PAH and total PAHs between smoker and nonsmoker homes using two-sample t-tests with unequal variances. The Type I error rate was set at α = 0.05 and comparisons between smoker and nonsmoker homes were tested in a nondirectional (two-tailed) fashion. We examined linear regression tests on house dust PAHs versus nicotine levels and the PAH levels in the living rooms versus bedrooms. Additionally, Tobit regression analysis for leftcensored data caused by nondetects was used to examine linear modes of the individual PAHs.

with coal, vehicle emission, track-in, etc.) affecting house dust PAHs. The only article to report a significant effect of ETS on PAHs in house dust was a 2004 review and meta-analysis, reporting a significant effect for urban but not rural homes.18 In this study, we aimed to determine the impact of ETS on PAHs in SHD by comparing PAH content in SHD from homes of smokers (N = 89) and nonsmokers (N = 43) in urban San Diego County, California. Seventy-three homes (43 nonsmoker homes and 30 smoker homes) had a child living in the home (average 4.8 years old, range 0.7−11.3 years). We examined the PAH concentration in SHD (ng/g) and the PAH loading in SHD (ng/m2) for comparison. Because nicotine is a specific marker of ETS in indoor environments,24,25 we examined the relationship of PAH and nicotine levels in SHD. We also examined the spatial distribution of PAHs by comparing the PAH content in SHD from living rooms and bedrooms in the same home. Other variables related to life style and home characteristics were evaluated for their association with PAH content in SHD. Lastly, we explored the relationship between exposure assessment to PAHs in SHD and possible health risks.

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RESULTS Comparison of Dust Levels of PAHs in Smoker and Nonsmoker Homes. We summarized the dust levels of 16 PAHs in the living rooms of smoker homes and nonsmoker homes in concentration (ng/g) and loading (ng/m2) separately in Table 1 and Table 2. Total PAHs (ΣPAH) loading and concentration levels in SHD were significantly higher in smoker homes than nonsmoker homes (p = 0.025; p = 0.012), but the difference was more pronounced in PAH loading (median ΣPAH: 990 ng/g vs756 ng/g; 1650 ng/m2 vs 796 ng/m2). B2 PAHs is the sum of probable carcinogenic PAHs, benzo(a)anthracene, chrysene, benzo(b&k)fluoranthene, benzo(a)pyrene, indeno(1,2,3-c,d)pyrene, and dibenz(a,h)anthracene. For loading and concentration, the median levels of B2 PAHs were higher in smoker homes (423 ng/g vs 331 ng/g, 701 ng/m2 vs 331 ng/m2), but the difference was only statistically significant for loading (p = 0.014). When comparing individual PAH congeners, all of the median PAH levels were higher in smoker homes than nonsmoker homes in both concentration and loading except acenaphthene in concentration. Phenanthrene, fluoranthene, pyrene, benz(a)anthracene, and chrysene were significantly higher in smoker homes in both concentration and surface loading comparisons. Loadings for 6 additional PAHs (acenaphthylene, fluorene, benzo(b&k) flouranthene, indeno(1,2,3-c,d) pyrene, benzo(g,h,i) perylene) were significantly higher in smoker homes than nonsmoker homes. Association of PAHs and Nicotine. Nicotine in dust serves as a unique marker ETS24,25 and had been measured previously in the same dust samples.26 To examine the contribution of tobacco use to PAH loading and concentration in SHD, we examined a linear regression model for the association between nicotine and PAHs. We included smoker and nonsmoker homes as well as living room and bedroom SHD samples, so the total SHD samples obtained were N = 208 (concentration) and N = 203 (loading). We first tested a model for ΣPAH. The nicotine concentration in SHD explained 10% of the variance of ΣPAH concentration (R2 = 0.102, p < 0.001) as indicated in part A of Figure 1, whereas the nicotine loading explained 39% of the variance of ΣPAH loading (R2 = 0.385, p < 0.001) as indicated in part B of Figure 1. We then tested a linear regression for individual PAH loading data (Figure S1 of the Supporting Information). The median R2 values of the individual PAH congener loading was 0.327 (range of R2: 0.14−0.416). Because of the nondetect samples, we examined Tobit regression models for left-censored data. All of the individual PAH loadings showed statistically significant associations with the nicotine loadings (median pseudo R2 = 0.209 (p < 0.001; range of pseudo R2: 0.053−0.309).

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EXPERIMENTAL SECTION Materials, sample extraction, instrumentation for PAH analysis, and QA/QC are described in the Supporting Information. Sample Collection. Dust samples were collected between 2005 and 2007 from homes in urban areas of San Diego County, California. Data for this study were collected as part of a larger study in which residents were eligible to participate if they were age 18 or older, spoke English, had lived in their current home for at least 6 months, and reported that everyone in their household was planning to move within the next month.26 Initially, 100 smoker homes and 50 nonsmoker homes were recruited, meeting the following conditions. Smoker homes were those in which residents had smoked indoors during at least 5 of the past 6 months, including the current and most recent month, and had smoked a minimum of 7 cigarettes per week inside the home during the week prior to collection of the dust samples. Nonsmoker homes were those where no smoker had lived and no visitors had smoked indoors during the past 6 months. All the nonsmoker homes and 30 of the smoker homes had a resident under 12 years old. The recruitment procedures and detailed demographic data are described elsewhere.26 A majority of participants were recruited through advertisements in local print and San Diego County Women, Infants, and Children Supplemental Food and Nutrition Program offices. Ethnicity was self-reported as 38% White-non Hispanic, 29% Black, 17% Hispanic, and 16% other race/ ethnicity. Interviews related to indoor smoking and secondhand smoke exposure were conducted with primary participants, and other residents when available. Dust was collected from a meter square area (or from a larger area if needed to collect approximately one-quarter of an inch of dust in a collection bottle) from the living room and from a bedroom (smoker homes only: a child’s or a nonsmoker’s, or the smoker’s bedroom in homes with no nonsmokers) using the HVS4 (CS3 Inc., Venice, FL) cyclone vacuum. Dust was transported cooled, then sieved in a 150 μm methanol washed stainless steel sieve. Dust was stored at −20 °C until analysis. Statistical Analysis. The statistical analyses were conducted with SPSS version 17.0 and Stata IC version 9. Because of the wide and skewed distribution (over several orders of magnitude), we applied logarithm transformation to each variable. Nondetect data were entered as zero, and 1.0 was added to each 4175

dx.doi.org/10.1021/es300267g | Environ. Sci. Technol. 2012, 46, 4174−4183

a

43/43 42/43 43/43 43/43 43/43 43/43 43/43 43/43 43/43 43/43 43/43 39/43 43/43 42/43 43/43

naphthalene acenaphthylene acenaphthene fluorene phenanthrene anthracene fluoranthene pyrene benz(a)anthracene chrysene benzo(b&k) flouranthene benzo(a) pyrene indeno(1,2,3-c,d)pyrene dibenz(a,h)anthracene benzo(g,h,i) perylene b B2 PAHs total PAHs

1.79 nd 1.34 5.05 24.6 1.95 11.9 19.9 4.15 7.30 24.7 nd 4.85 nd 21.4 47.7 209

Min 7.79 1.79 3.47 7.67 67.8 5.41 39.9 50.8 13.3 35.3 114 24.0 22.4 3.70 64.0 223 534

25% 10.3 3.15 5.45 10.2 94.5 9.55 75.9 79.8 19.2 45.7 145 40.8 36.5 7.10 101 331 756

Median 21.3 7.10 8.47 15.1 135 14.6 101 121 37.2 80.0 256 68.7 59.3 10.8 163 513 1040

75%

Non-Smoker Homes (n = 43) 1410 (59.2) 50.5 24.7 76.4 393 72.5 364 301 214 226 395 129 171 51.8 320 1020 2480

Max a

86/89 87/89 83/89 89/89 85/89 88/89 87/89 89/89 89/89 89/89 88/89 78/89 87/89 75/89 89/89

Dec/All nd nd nd 1.75 14.1 nd nd nd 3.60 6.70 nd nd nd nd 2.60 32.5 163

8.00 2.66 2.92 8.02 94.5 5.96 70.6 77.9 17.5 41.2 121 19.7 31.0 2.15 82.3 259 666

25% 12.6 4.33 5.15 12.1 132 13.0 115 127 31.1 75.3 185 47.8 58.6 7.79 132 423 990

Median

Smoker Homes (n = 89) Min 19.3 8.36 9.06 18.5 198 22.4 206 213 57.2 128 288 87.7 94.9 16.9 193 684 1580

75% 122 64.6 31.9 102 1160 78.5 817 626 210 380 745 282 528 127 731 1960 4390

Max

0.687 (0.784)a 0.154 0.330 0.536 0.031 0.572 0.003 0.019 0.020 0.026 0.347 0.859 0.071 0.751 0.108 0.066 0.025

P value

Adjusted for an outlier (1410 ng/g). bSum of probable carcinogens, benzo(a)anthracene, chrysene, benzo(b&k)fluoranthene, benzo(a)pyrene, indeno(1,2,3-c,d)pyrene, and dibenz(a,h)anthracene.

Dec/All

PAH (ng/g)

Table 1. PAH Concentrations (ng/g) in Settled House Dust Samples Collected from Smoker and Nonsmoker Homes and the Significance of Statistical Difference Test (p-Value); Dec/All Indicates the Number of Samples Detected above the Blank Level over the Total Number of Samples Analyzed; a Bold and Italic Font Indicates Statistical Significance

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a

42/42 41/42 42/42 42/42 42/42 42/42 42/42 42/42 42/42 42/42 42/42 38/42 42/42 41/42 42/42

Min 0.802 nd 0.577 0.619 7.72 0.269 3.17 5.03 0.773 2.46 16.7 nd 1.82 nd 4.98 22.1 47.8

6.86 1.88 2.78 6.84 50.5 4.29 27.9 31.4 8.52 21.6 70.4 18.6 14.3 2.29 49.5 173 439

25% 13.7 3.99 5.90 11.3 119 11.5 84.1 109 24.5 60.3 163 40.9 41.5 7.35 99.0 331 796

Median 23.8 10.0 13.9 26.2 332 20.5 212 275 61.4 131 443 108 107 18.0 249 902 2326

75%

Non-Smoker Homes (n = 42) Dec/All 85/88 86/88 84/88 88/88 88/88 84/88 87/88 86/88 88/88 88/88 87/88 77/88 86/88 74/88 88/88

Max 7060 (119)a 150 67.1 182 2130 321 2930 2420 826 1550 3180 1040 1380 273 2150 8250 18700 nd nd nd 0.677 10.7 nd nd nd 1.41 2.17 nd nd nd nd 4.62 9.94 74.8

Min 10.2 2.35 3.33 11.3 102 6.85 80.9 107 18.1 47.0 117 17.1 33.3 1.74 78.9 283 700

25% 17.8 7.89 7.47 18.6 226 16.7 219 198 60.2 126 369 63.6 93.4 9.47 230 701 1650

Median

Smoker Homes (n = 88) 45.2 21.7 18.9 43.9 475 45.2 393 432 118 236 736 184 222 37.7 515 1800 3550

75%

Max 1470 764 775 3800 8590 1390 8950 10000 2330 5390 8730 3080 3534 552 9560 23600 68900

P value 0.310 (0.056)a 0.031 0.384 0.049 0.014 0.106 0.002 0.008 0.005 0.006 0.042 0.444 0.019 0.534 0.021 0.014 0.012

Adjusted for an outlier (7060 ng/m2). bSum of probable carcinogens, benzo(a)anthracene, chrysene, benzo(b,k)fluoranthene, benzo(a)pyrene, indeno(1,2,3-c,d)pyrene and dibenz(a,h)anthracene.

Dec/All

PAH (ng/m )

naphthalene (ng/g) acenaphthylene acenaphthene fluorene phenanthrene anthracene fluoranthene pyrene benz(a)anthracene chrysene benzo(b&k) flouranthene benzo(a) pyrene indeno(1,2,3-c,d)pyrene dibenz(a,h)anthracene benzo(g,h,i) perylene b B2 PAHs total PAHs

2

Table 2. PAH Loadings (ng/m2) in Settled House Dust Samples Collected from Smoker and Nonsmoker Homes and the Significance of Statistical Difference Test (p-Value); Dec/All Indicates the Number of Samples Detected above the Blank Level over the Total Number of Samples Analyzed; a Bold and Italic Font Indicates Statistical Significance

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R2 = 0.268). For PAH loading, the linear regressions were improved in both cases and reached the same R2 value (R2 = 0.376). This improvement of a linear regression from concentration to loading is consistent with the improvement found in the total data set. This result suggests that carpet affects dust loading in homes inconsistently. Distribution of PAHs within Homes. The association of the ΣPAH content in SHD in smoker homes’ bedrooms and living rooms was examined using linear regression. In addition, we separately examined all homes having both living room and bedroom SHD samples and the same floor types of a living room and a bedroom to eliminate impact from different floor types between a living room and a bedroom. Both PAH concentration and loading were tested (Figure 3). In the whole data set, there were statistically significant relationships between the ΣPAH contents in SHD from living rooms and their associated bedrooms in both concentration and loading (R2 = 0.182, p < 0.001, R2 = 0.205, p < 0.001, respectively) (Figure 3). These linear relationships were improved in both concentration and loading only within the homes with a same floor type used for living room and bedroom, and the improvement was more pronounced in loading (R2 = 0.237, p < 0.001 vs R2 = 0.468, p < 0.001) (Figure 3). The results suggest that PAHs may be transported within a house and floor type may affect behaviors of SHD or PAHs in SHD.

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DISCUSSION PAHs in SHD and Contribution from ETS. This study demonstrates that SHD from smoker homes contains higher levels of PAHs than SHD from nonsmoker homes. In addition, we observed a significant association between nicotine concentration in SHD, a marker of thirdhand smoke, and levels of PAHs. In combination, these findings suggest cigarette smoking is a source of PAHs in SHD and PAHs are a component of thirdhand smoke. This finding supports previously reported evidence from a meta-analysis that showed a weak but statistically significant association of ETS and PAHs.18 Whereas ETS was discussed as a potential source of PAHs in SHD in previous studies,14,19,20 no single study has reported a statistically significant association. One possible reason is the lack of statistical power in previous research. Sample sizes of the earlier studies typically ranged from 10 to 20 (with a low percentage of smoker homes), whereas it was 132 in this study. None of the previous studies were specifically designed to test the impact of ETS. In addition, smoking behavior in the home was carefully characterized in our study and used as a criterion for subject recruitment. Another possible reason why previous studies failed to detect a significant difference between smoker and nonsmoker homes may be because PAH content in SHD was measured as concentration (weight/weight). In our study, greater differences were apparent when the PAH content was described in loading rather than concentration. PAH loading is calculated by multiplying the concentration of PAHs (ng/g) by the weight of the dust collected per surface area (g/m2). Interestingly, we found that SHD weight per square meter (i.e., dust loading) was significantly higher in smoker homes than in nonsmoker homes (p = 0.029) (Figure S2 of the Supporting Information). This result suggests that dust loading played a larger diluting factor for the concentration of PAHs in smoker homes. The higher dust loading in smoker homes raises the question of why smoker homes were dustier. Differences in the type of floor might be a contributing factor to dust loading. Yet dust

Figure 1. Linear regressions of logartithms of total PAH content and nicotine in settled house dust samples in concentration (A) and loading (B). All of the house dust samples collected from both nonsmoker and smoker homes were included and also both living rooms and bedrooms were included for this linear regression. The number of samples are N = 208 for (A) Concentration and N = 203 for (B) Loading.

Carpet vs Other Floor Types. The floor type of each home was characterized during the survey. Three-fourths (78%) of homes had wall to wall carpet and the rest had noncarpet flooring such as wood, tile, or linoleum. To minimize uncertainty of the impact of different floor types, we only chose the homes with wall to wall carpet and compared PAH content in SHD between smoker homes and nonsmoker homes again. Among the carpeted homes, 67 were smoker homes and 35 were nonsmoker homes. Results were mostly consistent with results for the total samples. For concentration, 4 PAHs (fluoranthene, pyrene, benz(a)anthracene, chrysene) were significantly higher in smoker homes than nonsmoker homes (p = 0.03). For loading, 11 PAHs were significantly higher in smoker homes than nonsmoker homes (p = 0.042). The ΣPAH and B2 PAH contents in SHD were significantly higher in smoker homes in PAH dust loading (p = 0.009; p = 0.010) but not dust concentration. We examined a linear regression of ΣPAH and nicotine content in SHD separately for carpeted homes and other floor type homes. There were statistically significant relationships between ΣPAH and nicotine content in SHD among carpeted homes and other floor type homes (Figure 2). For PAH concentration, a lower linear regression was observed in carpeted homes (carpeted homes R2 = 0.080; other floor type homes 4178



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Figure 2. Linear regressions of logartithms of total PAH content and nicotine in settled house dust samples from wall to wall carpeted homes and other floor type homes in concentration (A) and loading (B). The number of samples are as follows: (A) Carpet in concentration (N = 172), (A) Others in concentration (N = 35), (B) Carpet in loading (N = 168), and (B) Others in loading (N = 34).

they can bring more outside dust or soil into homes. Therefore, loading seems a better indicator of PAH content in SHD when evaluating contamination in indoor environments. Although PAH concentration and loadings in SHD were significantly higher in smoker homes than nonsmoker homes in our study, the difference was relatively small. The PAH emission factors for ETS are 2.1 ng −11.2 μg for individual PAH congeners in gas phase per cigarette and 1 to 412 ng for individual PAH congeners in particulate phase per cigarette.30 Therefore, total emission of PAHs from ETS per day in a smoker home is relatively small compared to other known sources of PAHs (e.g., coal tar based sealant). The emitted PAHs can settle as house dust through accumulation of the particulate PAHs partitioned from the gas phase PAHs. However, SHD is not the only compartment to accumulate PAHs. Other household materials such as carpet and furnishings can accumulate a large amount of PAHs by sorption to their surfaces.7 It is also

loading was still significantly higher in smoker homes than nonsmoker homes when we only selected homes with wall-towall carpeting. Another factor contributing to high dust loading in smoker homes might be cigarette smoking itself. Tobacco smoke contains particulate matter (PM) and most particles range in size less than 2.5 μm.27 The particulate matter in this range can grow through coagulation and may contribute to the mass of dust in the home. The existing research indicates a cigarette emits 10−14 mg of respirable particles (PM2.5).28,29 The average indoor air concentration of respirable dust in smoker homes was at least twice as high as in nonsmoker homes.17 However, it is unclear how much it would contribute to SHD, and further research is necessary. It would be interesting to learn more about behaviors of smokers and occupants of smoker homes that may affect dust loading (e.g., smoking frequency and location, cleaning frequency). For instance, smokers may go outside more often to smoke cigarettes, so 4179



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Figure 3. Relations between total PAH content in SHD collected from living rooms and those from their associated bedrooms in concentration (1) and loading (2). The linear regression was tested for all the homes (A) and was also tested for the homes with same floor type only between living room and bedroom (B). The sample sizes are N = 74 for (1A), N = 63 for (1B), N = 72 for (2A), and N = 61 for (2B). All the linear regressions are significant (p < 0.001).

Table 3. Total PAH Concentrations in SHD (μg/g) in This Study and Published Studies Investigating Homes in North America source

location

N

dust collection

urban/rural

east/west

# of smoker homes

ref 18 ref 18 ref 18 ref 18 ref 19 ref 18 ref 21 ref 18 ref 18 This study

North Carolina North Carolina North Carolina North Carolina Ottawa, Canada Ohio Texas Arizona Washington San Diego, CA

13 10 24 13 51 24 23 22 9 132

HVS3 HVS3 HVS3 no data home vacuum cleaner HVS3 HVS3 No data HVS3 HVS4

urban/rural urban/rural urban/rural unknown urban urban urban unknown urban urban

east east east east east east east west west west

1 0 5 unknown 7−8 12 1 unknown 0 89

important to consider that cigarette smoking is not only source of PAHs in indoor environments. Heating, insect repellents, construction materials, and outdoor PAH concentrations contribute to the indoor PAH levels.31 On the other hand, in our study, the difference of dust levels of nicotine in smoker homes versus nonsmoker homes was much larger (by concentration: 39.6 μg/g vs 2.9 μg/g; by loading: 58.8 μg/m2 vs 3.6 μg/m2)26 because cigarette smoking was the only source of nicotine in an indoor environment. An additional noteworthy finding in our study is that the ΣPAH concentration in SHD in our study is near the lower end of the published data in North America (Table 3). The median and geometric means of ΣPAH concentration in SHD in our study are 0.990 and 0.911 μg/g. These are lower than observed

# of PAHs median geomean 16 16 16 16 13 16 16 16 13 16

0.968 0.957 3.42 1.55 9.53 47.4 28.8 1.11 7.72 0.990

1.09 1.29 3.49 2.00 12.9 60.4 29.2 1.23 8.38 0.911

min

max

0.364 0.367 1.07 0.478 1.50 11.1 1.12 0.505 5.40 0.163

8.83 8.31 14.2 13.8 325 513 341 6.74 22.8 4.39

in homes in other U.S. states (Ohio, Texas, Washington) and in Canada but are similar to those measured in homes in Arizona (1.11 μg/g and 1.23 μg/g) and North Carolina (0.957− 3.42 μg/g and 1.09−3.49 μg/g).18,19,21 The highest ΣPAH concentration in SHD was observed in Ohio.18 The median and geomean ΣPAH concentrations were 47.4 μg/g and 60.4 μg/g, which are approximately 50 times higher than those in our study. The PAH concentration in SHD was second highest in Texas, where Mahler and colleagues reported that dust from parking lots paved with coal tar based sealcoat was a major source of PAHs in SHD.21 Use of the coal tar based sealcoat was dominant in central and eastern U.S., whereas use of asphalt-based sealcoat was dominant in western U.S. PAHs in the asphalt-based sealcoat were 1000 times lower than in coal 4180



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tar based sealcoat products.32 In Mahler et al’s study,21 the apartments were separated into those with and without coal tar based sealcoat, and the median concentrations of PAHs in SHD were 129 and 5.1 μg/g, respectively. Comparing these numbers to our study suggests that the use of the coal tar based sealcoats can result in PAH concentrations in SHD significantly higher (more than a factor of 100) than those found for smoker homes in our study. This suggests that even though cigarette smoking appears to contribute to PAHs in SHD, the incremental increase attributable to cigarette smoking is relatively small compared to that of coal tar based sealcoats. Another potential source of PAHs in SHD may be related to cold weather. In the northern U.S., house heating during the cold season is necessary. Gas based heating or frequent use of fireplaces including wood burning would be sources of PAHs in indoor environments and may increase PAHs in SHD. Therefore, our study location, San Diego, CA, may be an ideal location to test the impact of ETS to PAH content in SHD, minimizing other potential sources of PAHs. Association between Levels of PAHs and Nicotine in SHD. This is the first individual study to show a statistically significant association between levels of PAHs and nicotine in SHD (Figure 1). Because nicotine is a unique marker of ETS in indoor environments, this association provides additional evidence that ETS is a source of PAHs in SHD, accounting for 10% and 38% of variance in ΣPAH concentration and loading, respectively. The increase of R2 from 0.102 (concentration) to 0.385 (loading) supports our earlier argument that loading provides a better representation of the chemical contents in SHD than concentration. The larger R2 in loading versus concentration is observed for the homes with carpet and the homes with other floor types separately in Figure 2. The R2 difference between concentration and loading is more pronounced in the homes with carpet than the other group. Interestingly, this difference of R2 between the two groups (carpet and others) in concentration disappeared when loading of PAHs in SHD was used instead. Dust loading might be the reason. The medians of dust loading were 1.65 g/m2 in homes with carpet (N = 100) and 1.07 g/m2 in homes with other floor types (N = 29), and the difference was statistically significant (p = 0.013). The variability of dust loading was larger in homes with carpet than the others (standard deviation: 7.09 carpet vs 2.65 others) and might affect the PAH concentrations in SHD inconsistently. Carpets can accumulate more dust by track-in from outside because of the deepness of the fabric and the large surface area.22 However, the deepness of the fabric varies from carpet to carpet, and consequently, the potential accumulation of dust can vary as well. Over time, carpets degrade and themselves generate dust and particles, the degree of which varies as well. Removal of fine dust in carpets is affected by types of vacuum cleaners according to their power, presence of a HEPA filter, and frequency of vacuuming. We tested other potential variables to explain the residual unexplained variance, ∼60%, in PAH content in SHD attributable to other sources than ETS. The reported smoking rate of residents in the smoker homes was examined, but it only explained 3% in additional variance in both a total data set and smoker homes only. Seasonal effects were investigated based on the collection date (summer and winter), but there was no difference. This is not surprising because San Diego, California, has mild winters, allowing smokers to open windows and smoke outdoors regardless of the season. Frequency of fireplace use in the month before data collection was also investigated as

a potential source, but few homes had fireplaces and no statistically significant association emerged. We also tested traffic volume within a 300 and 150 m radius from each household (California Environmental Health Tracking Program: http:// www.ehib.org/page.jsp?page_key=136), but there was no significant association between traffic volume and PAH content in SHD. Recent studies show that nicotine sorbs to particles and surfaces of walls and furniture and persists in indoor environments for a long time.7,8,26,33 For instance, our recent study found that nicotine content in SHD was higher in former smoker homes compared to former nonsmoker homes when nonsmokers moved in an average of three months after the homes were vacated.26 Moreover, new nonsmoking residents were exposed to the residual nicotine from former smokers as measured by nicotine on the hands and cotinine in the urine of the new residents. These findings suggest that nicotine in SHD is composed of recently produced and aged ETS. Currently, we know very little about the stability and aging of PAHs in indoor environments. PAHs can react with oxidants (e.g., ozone, nitrate, and hydroxyl radical) in both gas- and particulate phases and produce more toxic compounds such as nitro-PAHs and oxy-PAHs.34−36 Nitro-PAHs can be 100 000 times more mutagenic and 10 times more carcinogenic compared to parent PAHs.37 These PAH derivatives have been detected in atmosphere and urban dust38,39 but have not been investigated in indoor settings or as products of indoor tobacco smoke pollution. These are important questions which require further research to protect human exposure, especially children’s exposure to toxic ETS chemicals such as PAHs via thirdhand smoke. PAH Contents in SHD in Relation to Exposure. Exposure to PAHs via SHD is more of a concern in children, especially toddlers because of their frequent hand-to-mouth behaviors, higher respiration rate, and larger surface to body ratio. In addition, their physical closeness to the floor and active behaviors (running and jumping) increase their exposure to SHD. We observed that the ΣPAHs in SHD from bedrooms were well correlated with those from their associated living rooms (Figure 3). The bedroom SHD samples were collected from a child’s bedroom (N = 22), a nonsmoker’s bedroom (N = 11), a smoker’s bedroom (N = 32), a bedroom shared by a child and a smoker (N = 7), and other rooms not the living room (N = 2) in smoker homes. The result is consistent with other research about the transport of tobacco smoke compounds within a house or apartment as well as between neighboring apartments.33 Because of PAHs’ semivolatility and persistence in the environment, PAHs may be present as thirdhand smoke in SHD or surfaces and transported via the grasshopper effect9−11 within indoor environments long after active cigarette smoke ceased. Exposure assessment to PAHs via dust ingestion depends on two factors, PAH concentration and daily dust ingestion rate. Similarly, the cancer risk assessment resulting from the nondietary ingestion depends on B2 PAH concentration in SHD and daily dust ingestion rate. In a conservative scenario, toddlers consume 50 mg of SHD daily.23 However, the actual amount of dust ingestion can depend on dustiness of their homes. In this study, dustiness varied widely from house to house; dust loading (sieved dust ≤150 μm) ranged from 0.055 g/m2 to 56.9 g/m2. The dust loading was not correlated with B2 PAH concentration in SHD (Figure S3 of the Supporting Information). Thus, the worst case is that a floor is extremely dusty and the dust PAH concentration is high. In this 4181



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study, 73 homes had a child ≤11 yr old with an average 4.78 yr old (0.65−11.25 yr old). We calculated the excess cancer risk from nondietary ingestion of the B2 PAH concentrations in SHD measured in the 73 homes during preschool years as Maertens and colleages did.19 At a “high” dust ingestion scenario (0.1 g/day), 24 homes out of the 73 homes result in excess cancer risks above “acceptable risk” level (one cancer case per million people: 1 × 10−6). At “moderate” dust ingestion scenario (0.05 g/day), 3 homes had a concentration of B2 PAHs that exceed the acceptable risk level, 10−6. At a very conservative dust ingestion rate (0.01 g/day), none of the homes exceeded the risk level. We should point out, however, that the cancer risk estimated in this study is lower than that in Maertens’ study.19 This is the case because the PAH levels in SHD in this study are at the lower range of PAH levels published in North America. This intake scenario also does not include resuspension and inhalation of fine dust by children40 as part of the risk assessment. In conclusion, we found that cigarette smoking was a significant source of PAH content in SHD in these Southern California households. To prevent the additional accumulation of PAHs in SHD caused by tobacco use, smoking cessation and indoor smoking bans are obvious initiatives. It is less obvious, however, what to do about existing PAHs in SHD. Future research is needed to understand the aging and persistence of PAHs in SHD in the presence and in the absence of continued smoking and oxidants commonly found in home indoor environments. We also have to learn more about methods for removal of PAHs that have accumulated in SHD. Studies have shown that vacuuming with HEPA filtrated vacuum cleaners provides a significant reduction of dust, thus minimizing PAH exposure from dust.22,41 While this is a promising direction, these types of vacuums may not be affordable for low-income families and can be difficult to maintain to sustain effectiveness. Because PAHs in SHD have many different sources, a comprehensive strategy to prevent the exposure to PAHs in SHD will benefit from contributions of multiple disciplines and multiple methods to reduce exposure to young children and other residents.

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sive Partnerships to Reduce Cancer Health Disparities Program (#1U54CA132384 and #1U54CA132379.) The authors thank Sarah N. Larson, M.S., R.D. and the San Diego State University Research Foundation WIC program staff for their assistance.

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(1) Jenkins, R. A.; Guerin, M. R.; Tomkins, B. A. The Chemistry of Environmental Tobacco Smoke: Composition and Measurement; Lewis Publishers: Boca Raton, FL, 2000; pp 49−75. (2) Tobacco Smoking; IARC monographs on the evaluation of the carcinogenic risk of chemicals to humans, 38; IARC: Lyon, France, 1986. (3) The Changing Cigarette: Chemical Studies and Bioassays; NCI monographs on risks associated with smoking cigarettes with low tar machine-measured yields of tar and nicotine 13; U.S. Department of Health and Human Services, National Institutes of Health, National Cancer Institute: Bethesda, MD, 2001;http://cancercontrol.cancer. gov/tcrb/monographs/13/m13_5.pdf (4) Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency; SmokingandTobacco Control Monograph 10; NIH Publication 99− 4645;U.S. Department of Health and Human Services, National Institutes of Health, National Cancer Institute: Bethesda, MD, 1999; http://cancercontrol.cancer.gov/tcrb/monographs/10/m10_ complete.pdf (5) Hackshaw, A. K.; Law, M. R.; Wald, N. J. The accumulated evidence on lung cancer and environmental tobacco smoke. Brit. Med. J. 1997, 315, 980−988. (6) Proposed Identification of Environemntal Tobacco Smoke as a Toxic Air Contaminant, Part A: Exposure Assessment. Sacramento, CAL EPA Air Resources Board, Office of Environmental Health Hazard Assessment: Sacramento, CA, 2005; http://www.arb.ca.gov/regact/ ets2006/app3parta.pdf (7) Van Loy, M. D.; Riley, W. J.; Daisey, R. M.; Nazaroff, W. W. Dynamic behavior of semivolatile organic compounds in indoor air. 2. Nicotine and phenanthrene with carpert and wallboard. Environ. Sci. Technol. 2001, 35, 560−567. (8) Singer, B. C; Hodgson, A. T.; Guevarra, K. S.; Hawley, E. L; Nazaroff, W. W. Gas-phase organics in environmental tobacco smoke: 1. Effects of smoking rate, ventilation, and furnishing level on emission factors. Environ. Sci. Technol. 2002, 36, 846−853. (9) Lioy, P. J. Empolying dynamical and chemical processes for contaminant mixtures outdoors to the indoor environment: The implications for total human exposure analysis and prevention. J. Expo. Sci. Env. Epid. 2006, 16, 207−224. (10) Winickoff, J. P.; Friebely, J.; Tanski, S. E.; Sherrod, C.; Matt, G. E.; Hovell, M. F.; McMillen, R. C. Beliefs about the health effects of “Thirdhand” smoke and home smoking bans. Pediatrics 2009, 123, e74−e79. (11) Matt, G. E.; Quintana, J. E.; Destaillats, H.; Gundel, L. A.; Sleiman, M.; Singer, B. C.; Jacob, P. III; Benowitz, N.; Winickoff, J. P.; Virender, R.; Talbot, P.; Schick, S.; Samet, J.; Wang, Y.; Hang, B; Martins-Green, M.; Pankow, J. F.; Hovell, M. F. Thirdhand tobacco smoke: Emergence evidence and arguments for a multidisciplinary research agenda. Environ. Health Persp. 2011, 119, 1218−1226. (12) Tobacco Smoke and Involuntary Smoking: IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans; 83. IARC: Lyon, France. (13) U.S. Environmental Protection Agency: Integrated Risk Information System. http://www.epa.gov/NCEA/iris/. (14) Chuang, J. C.; Callahan, P. J.; Menton, R. G.; Gordon, S. M. Monitoring methods for polycylic aromatic hydrocarbons and their distribution in house dust and track-in soil. Environ. Sci. Technol. 1995, 29, 494−500. (15) Mukerjee, S.; Ellenson, W. D.; Lewis, R. G.; Stevens, R. K.; Somerville, M. C.; Shadwick, D. S.; Willis, R. D. An environmental scoping study in the Lower Rio Grande Valley of Texas: III Residential

ASSOCIATED CONTENT

S Supporting Information *

Information regarding materials, sample extraction, instrumentation for PAH analysis, QA/QC, linear regression of individual PAHs and nicotine in SHD in loading, histograms of dust loading in homes by smoking status, and B2 PAH concentration in SHD vs dust loading. This material is available free of charge via the Internet at http://pubs.acs.org.

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REFERENCES

AUTHOR INFORMATION

Corresponding Author

*E-mail: [email protected], phone: 619-594-4671 fax: 619594-6112 (E.H.); e-mail: [email protected], phone: 619-594-0503, fax: 619-594-1332 (G.E.M.). Notes

The authors declare no competing financial interest.

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ACKNOWLEDGMENTS This research was supported by funds from the California Tobacco-Related Disease Research Program of the University of California (Grant 13RT-0161H). Parts of this study were also supported by the National Cancer Institute, Comprehen4182



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microenvironmental monitoring for air, house dust, and soil. Environ. Int. 1997, 23, 657−673. (16) Chuang, J. C.; Callahan, P. J.; Lui, C. W.; Wilson, N. K. Polycyclic aromatic hydrocarbon exposures of children in low-income families. J. Expo. Sci. Env. Epid. 1999, 9, 85−98. (17) Fromme, H.; Lahrz, T.; Piloty, M.; Gebhardt, H.; Oddoy, A.; Rüden, H. Polycyclic aromatic hydrocarbons inside and outside of apartments in an urban area. Sci. Total Environ. 2004, 326, 143−149. (18) Maertens, R. M.; Bailey, J.; White, P. A. The mutagenic hazards of settled house dust: A review. Mutat. Res. 2004, 567, 401−425. (19) Maertens, R. M.; Yang, X.; Zhu, J.; Gagne, R.; Douglas, G. R.; White, P. A. Mutagenic and carcinogenic hazards of settled house dust I: Polycyclic aromatic hydrocarbon content and excess lifetime cancer risk from preschool exposure. Environ. Sci. Technol. 2008, 42, 1747− 1753. (20) Mannino, M. R.; Orecchio, S. Polycyclic aromatic hydrocarbons (PAHs) in indoor dust matter of Palermo (Italy) area: Extraction, GCMS analysis, distribution and sources. Atmos. Environ. 2008, 42, 1801− 1817. (21) Mahler, B. J.; Van Metre, P. C.; Wilson, J. T.; Musgrove, M. Coal-tar-based parking lot sealcoat: An unrecognized source of PAH to settled souse dust. Environ. Sci. Technol. 2010, 44, 894−900. (22) Roberts, J. W; et al. Monitoring and reducing exposure of infants to pollutants in house dust. In Reviews of Environmental Contamination and Toxicology, Vol 201; Whitacre, D. M., Ed.; Springer: New York, 2009; pp 1−39. (23) Highlights of the Child-Specific Exposure Factors Handbook (Final Report); EPA/600/R-08/135; EPA, National Center for Environmental Assessment, Office of Research and Development: Washington, DC, 2009; http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid= 200445#Download (24) Whitehead, T.; Metayer, C.; Ward, M. H.; Nishioka, M. G.; Gunier, R.; Colt, J. S.; Reynolds, P.; Selvin, S.; Buffler, P.; Rappaport, S. M. Is house-dust nicotine a good surrogate for household smoking? Am. J. Epidemiol. 2009, 169, 1113−1123. (25) Daisey, J. M.; Mahanama, K. R. R.; Hodgson, A. T. Toxic volatile organic compounds in simulated environmental tobacco smoke: Emission factors for exposure assessment. J. Expo. Anal. Environ. Epidemiol. 1998, 8, 313−334. (26) Matt, G. E.; Quintana, P. J. E.; Zakarian, J. M.; Fortmann, A. L.; Chatfield, D. A.; Hoh, E.; Uribe, A. M.; Hovell, M. F. When smokers move out and nonsmokers move in: Residential thirdhand smoke pollution and exposure. Tob. Control. 2011, 20, e1. (27) Nazaroff, W. W.; Hung, W. Y.; Sasse, A. G. B. M.; Gadgil, A. J. Predicting regional lung deposition of environmental tobacco smoke particles. Aerosol. Sci. Tech. 1993, 19, 243−254. (28) Nelson, P. R.; Conrad, F. W.; Kelly, S. P. Comparison of environmental tobacco smoke to aged and diluted sidestream smoke. J. Aerosol Sci. 1998, 29 (Suppl 1), S281−S282. (29) Martin, P.; Heavner, D. L.; Nelson, P. R.; Maiolo, K. C.; Risner, C. H.; Simmons, P. S.; Morgan, W. T.; Ogden, M. W. Environmental tobacco smoke (ETS): A market cigarette study. Environ Int. 1997, 23, 75−90. (30) Gundel, L. A.; Mahanama, K. R. R.; Daisey., J. M. Semivolatile and particulate polycyclic aromatic hydrocarbons in environmental tobacco smoke: Cleanup, speciation and emission factors. Environ. Sci. Technol. 1995, 29, 1607−1614. (31) Ohura, T.; Amagai, T.; Fusata, M.; Matsushita, H. Polycyclic aromatic hydrocarbons in indoor and outdoor environments and factors affecting their concentrations. Environ. Sci. Technol. 2004, 38, 77−83. (32) Van Metre, P. C.; Mahler, B. J.; Wilson, J. T. PAHs Underfoot: Contaminated dust from coal-tar sealcoated pavement is widespread in the United States. Environ. Sci. Technol. 2009, 43, 20−25. (33) Matt, G. E.; Quintana, P. J. E.; Hovell, M. F.; Bernert, J. T.; Song, S.; Novianti, N.; Juarez, T.; Floro, J.; Gehrman, C.; Garcia, M.; Larson, S. Households contaminated by environmental tobacco smoke: Sources of infant exposures. Tob. Control 2004, 13, 29−37.

(34) Barbas, J. T.; Sigman, M. E.; Dabestani, R. Photochemical oxidation of phenanthrene sorbed on silica gel. Environ. Sci. Technol. 1996, 30, 1776−1780. (35) Allen, J. O.; Dookeran, N. M.; Tafhizadeh, K.; Lafleur, A. L.; Smith, K. A.; Sarofirm, A. F. Measurement of oxygenated polycyclic aromatic hydrocarbons associated with a size-segregated urban aerosol. Environ. Sci. Technol. 1997, 31, 2064−2070. (36) Gross, S.; Bertram, A. K. Reactive uptake of NO3, N2O5, NO2, HNO3, and O3 on three types of polycyclic aromatic hydrocarbon surfaces. J. Phys. Chem. 2008, 112, 3104−3113. (37) Durrant, J. L.; Busby, W. F.; Lafleur, A. L.; Penman, B. W.; Crespi, C. L. Human cell mutagenicity of oxygenated, nitrated and unsubstituted polycylic aromatic hydrocarbons associated with urban aerosols. Mutat. Res-Gen. Tox. 1996, 371, 123−157. (38) Bamford, H. A.; Baker, J. E. Nitro-polycyclic aromatic hydrocarbon concentrations and sources in urban and suburban atmospheres of the Mid-Atlantic region. Atmos. Environ. 2008, 37, 2077−2091. (39) Albinet, A.; Leoz-Garziadia, E; Budzinski, H; Villenave, E. Simultaneous analysis of oxygenated and nitrated polycyclic aromatic hydrocarbons on standard reference material 1649a (urban dust) and on natural ambient air samples by gas chromatography-mass spectrometry with negative ion chemical ionization. J. Chromatogr. A. 2006, 1121, 106−113. (40) Raja, S.; Xu, Y.; Ferro, A. R.; Jaques, P. A.; Hopke, P. K. Resuspension of indoor aeroallergens and relationship to lung inflammation in asthmatic children. Environ. Int. 2010, 36, 8−14. (41) Yu, C. H.; Yiin, L.; Fan, Z.; Rhoads, G. G. Evaluation of HEPA vacuum cleaning and dry steam cleaning in reducing levels of polycyclic aromatic hydrocarbons and house dust mite allergens in carpets. J. Environ. Monit. 2009, 11, 205−211.

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