Environ. Sci. Technol. 2005, 39, 5592-5599
Prediction of Personal Exposure to PM2.5 and Carcinogenic Polycyclic Aromatic Hydrocarbons by Their Concentrations in Residential Microenvironments T A K E S H I O H U R A , * ,† T A K A H I R O N O D A , † TAKASHI AMAGAI,† AND MASAHIRO FUSAYA‡ Institute for Environmental Sciences, University of Shizuoka, 52-1 Yada, Shizuoka 422-8526, Japan, and Shizuoka Institute of Environment and Hygiene, 4-27-2 Kita-ando, Shizuoka 420-8637, Japan
We measured exposure to fine particles (PM2.5) and polycyclic aromatic hydrocarbons (PAHs), including carcinogenic PAHs, in multiple locations for a diverse population of participants who resided in Shizuoka, Japan. In summer and winter 2002 we surveyed personal concentrations, those of four primary indoor microenvironmentssliving room, bedroom, kitchen (summer only), and workplacesand those outside the subjects’ houses. Concentrations of PM2.5 and PAHs tended to be higher during winter. Median PM2.5 concentration was highest in living room samples during winter but in personal samples during summer. The median PAH concentrations normalized to the cancer potency equivalence factor of benzo[a]pyrene (BaP-TEQ) was highest in the bedroom during winter but outdoors in summer. Personal exposure level profiles differed markedly between smokers and nonsmokers. Personal exposures to BaP ([BaP]P) and BaP-TEQ ([BaPTEQ]P) in nonsmokers were strongly correlated. Personal exposures of nonsmokers, as calculated from the corresponding time-weighted indoor and outdoor concentrations, were consistent with measured levels of BaP but not PM2.5. Personal exposure of nonsmokers to BaP, as calculated from the time-weighted living room, bedroom, and either workplace or outdoor concentrations, accounted for 92-107% of the measured levels of BaP-TEQ.
Introduction Polycyclic aromatic hydrocarbons (PAHs) associated with particles are ubiquitous environmental pollutants produced by incomplete combustion of organic substances (1-3). Anthropogenic sources of PAHs include the combustion of materials such as coal, oil, gas, and wood for energy supply (4-6). In particular, industrial plants such as coke and aluminum production, residential heating, and power generation account for the majority of human-produced PAH sources (1, 3, 5, 7, 8). Indoor emission sources of PAHs include smoking, cooking, heating, and furniture (9-11). In addition to these local sources, regional effects such as long-range * Corresponding author phone: +81 54 264 5789; fax: +81 54 264 5798; e-mail:
[email protected]. † University of Shizuoka. ‡ Shizuoka Institute of Environment and Hygiene. 5592
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ENVIRONMENTAL SCIENCE & TECHNOLOGY / VOL. 39, NO. 15, 2005
transport and the volatilization of previously deposited PAHs from surfaces can be important factors in urban ambient PAH concentrations (12). Past research has shown that concentrations of low-molecular-weight (usually 3-ring) PAHs typically are higher indoors than outdoors, whereas those of high-molecular-weight (4-ring and larger) PAHs are somewhat higher outdoors than indoors (11). This trend is due to differences in the corresponding emission sources. Some PAHs, including chrysene, benz[a]anthracene, and benzo[a]pyrene (BaP), all of which have >4 rings, are procarcinogens (13, 14). A previous study showed that these carcinogenic PAHs were associated with fine particles (PM2.5) and that the contribution of BaP to the total carcinogenic PAH was in the range of 51-64% (15). In addition, fine particles (PM2.5) themselves are of great health concern because, when inhaled, they can be deposited more deeply in the lungs than coarse particles (16). Therefore, the combination of toxic chemicals with fine particles can have an especially deleterious effect on human health and can predispose people to respiratory disease. Several studies have shown a relationship between PM2.5 and human health, up to and including mortality and morbidity (16, 17). In air pollution epidemiology, exposure assessment traditionally is based on fixed-site measurements in ambient air (18, 19). In particular, surveys of indoor microenvironments have been carried out to evaluate human exposure, because most people spend most of their daily lives inside (11, 15). However, the air pollutant levels obtained from these indoor measurements may not accurately reflect the personal exposure levels because, depending upon their activities, people spend different amounts of time in different indoor microenvironments. Lachenmyer and Hidy have urged the necessity of complete characterization of indoor microenvironments with prevailing activity patterns, because there is some evidence of seasonal factors in the observations of indoor, outdoor, and personal exposure levels of PM2.5 (20). Models are available for the prediction of personal exposure to respirable particles in light of the indoor and/or outdoor levels. However, we previously found no significant correlation between PM2.5 and associated BaP concentrations (15). Therefore, the prediction model reported for particles could be not adapted to particle-associated PAHs. Here, we report the winter and summer concentrations of PM2.5 and 21 particle-associated PAHs (including carcinogens) measured concurrently in outdoor, residential indoor (living room, kitchen, and bedroom), and workplace environments, as well as in the subjects themselves. On the basis of these data, we constructed a model for estimating personal exposure in light of PM2.5 and PAH levels in the indoor microenvironments and outdoors.
Materials and Methods Materials. The target compounds for this survey were 21 3to 7-ring PAHs. The PAH standard reagents (Wako Chemicals, Osaka, Japan) were of the highest purity available and were dissolved in acetonitrile. Dichloromethane for extraction was residual pesticide analysis grade (Wako Chemicals), dimethyl sulfoxide (DMSO) for sample preparation was fluorometric analysis grade (Dojindo Chemical Corp., Kumamoto, Japan), and methanol and distilled water for the mobile phase were HPLC grade (Wako Chemicals). The compounds monitored were as follows, and their abbreviations and cancer potency equivalence factors (21) are given in parentheses: fluoranthene (Fluor, 0), pyrene (Py, 0), 1-methylpyrene (1MP, 0), triphenylene (Trp, 0), p-terphenyl (pTer, 0), chrysene (Chry, 0.01), benz[a]anthracene (BaA, 0.1), perylene (Pery, 0), benzo10.1021/es050571x CCC: $30.25
2005 American Chemical Society Published on Web 06/24/2005
[e]pyrene (BeP, 0), benzo[b]fluoranthene (BbF, 0.1), benzo[k]fluoranthene (BkF, 0.1), benzo[j]fluoranthene (BjF, 0.1), benzo[a]pyrene (BaP, 1), indeno[1,2,3-cd]pyrene (IP, 0.1), benzo[ghi]perylene (BghiP, 0), dibenz[a,c]anthracene (DBacA, 0), dibenz[a,h]anthracene (DBahA, 0), benzo[b]chrysene (BbC, 0), picene (Pi, 0), coronene (Cor, 0), and dibenzo[a,e]pyrene (DBaeP, 1). Sampling. Fractionated particles in personal, indoor, and outdoor air were monitored for adults living in Shizuoka Prefecture, Japan. Surveys were completed in winter (21 February to 13 March) and summer (9 to 27 September) 2002. A total of 55 subjects (21 subjects in both seasons, and 13 summer only) were recruited for the study and were eligible for monitoring of respirable particles and associated PAHs. There were 35 men (63% of the study population) and 20 women (37%), aged 24-61 years (mean age 42 years). The integrated indoor areas measured were the living room (L), bedroom (B), kitchen (K, measured during summer only), and workplace (W). Indoor and outdoor air samples of 24 h duration were collected simultaneously with personal sampling. The outdoor sampler was placed away from exhaust ducts and lighting and heating sources for the house. Sampling Apparatus. Personal exposure to fine particles (particle diameter
