Indoor levels of polycyclic aromatic hydrocarbons in homes with or without wood burning for heating

The aim of this study was to investigate the impact of domestic wood burning on indoor levels of polycyclic aromatic hydrocarbons (PAHs). Indoor and outdoor concentrations of 27 PAHs were measured during wintertime in homes with (n= 13) or without (n 0) wood-burning appliances and at an ambient site in a Swedish residential area where wood burning for space heating is common. Twenty-four hour indoor levels of anthracene, benzo(ghi)fluoranthene, cyclopenta(cd)pyrene, benz(a)anthracene, chrysene/triphenylene, benzo(a)pyrene (BaP), indeno(1,2,3-cd)pyrene, benzo(ghi)perylene, and coronene were significantly (about 3- to 5-fold) higher in homes with, compared with homes without, wood-burning appliances. The outdoor levels of PAHs were generally higher than the indoor levelsfor all PAHs exceptforthe methylated phenanthrenes. The total PAH cancer potency (sum of BaP equivalents) was significantly higher (about 4 times) in the wood-burning homes compared with the reference homes, with BaP being the largest contributor, while phenanthrene made the largest contribution to the total PAH concentration in indoor and outdoor air. The median indoor BaP level in the wood-burning homes (0.52 ng/m3) was 5 times higher than the Swedish health-based guideline of 0.1 ng/m3, which was also exceeded outdoors on all days (median 0.37 ng/m3).     

Polycyclic aromatic hydrocarbons in indoor and outdoor environments and factors affecting their concentrations

A highly sensitive analytical method for the simultaneous determination of 39 gaseous and particulate polycyclic aromatic hydrocarbons (PAHs) was used to determine the PAH composition of indoor and outdoor air in Shimizu, Japan. In both indoor and outdoor air, gaseous PAH concentrations were higher in summer than in winter, whereas particulate PAH concentrations were higher in winter than in summer. Correlation analysis indicated that indoor PAH compositions, especially the gaseous PAH composition, differed significantly from outdoor PAH compositions. Gaseous PAH concentrations indoors were significantly affected by insect repellents and heating sources. Particulate PAH concentrations indoors were significantly affected by cigarette smoking, the age and type (wood) of the house, and outdoor PAH concentrations. Inhalation risk associated with carcinogenic PAHs was estimated by using toxic equivalency factors based on the potency of benzo[a]pyrene (BaP). The carcinogenicity of the indoor PAH mixture was dominated by naphthalene followed by BaP and dibenz[a,h]anthracene.     

Polycyclic aromatic hydrocarbons in the indoor and outdoor air of three cities in the U.S

The indoor and outdoor concentrations of 30 polycyclic aromatic hydrocarbons (PAHs) were measured in 55 nonsmoking residences in three urban areas during June 1999-May 2000. The data represent the subset of samples collected within the Relationship of Indoor, Outdoor, and Personal Air study (RIOPA). The study collected samples from homes in Los Angeles, CA, Houston, TX, and Elizabeth, NJ. In the outdoor samples, the total PAH concentrations (sigmaPAH) were 4.2-64 ng m(-3) in Los Angeles, 10-160 ng m(-3) in Houston, and 12-110 ng m(-3) in Elizabeth. In the indoor samples, the concentrations of sigmaPAH were 16-220 ng m(-3) in Los Angeles, 21-310 ng m(-3) in Houston, and 22-350 ng m(-3) in Elizabeth. The PAH profiles of low molecular weight PAHs (3-4 rings) in the outdoor samples from the three cities were not significantly different. In contrast, the profiles of 5-7-ring PAHs in thesethree citieswere significantlydifferent, which suggested different dominant PAH sources. The signatures of 5-7-ring PAHs in the indoor samples in each city were similar to the outdoor profiles, which suggested that indoor concentrations of 5-7-ring PAHs were dominated by outdoor sources. Indoor-to-outdoor ratios of the PAH concentrations showed that indoor sources had a significant effect on indoor concentrations of 3-ring PAHs and a smaller effect on 4-ring PAHs and that outdoor sources dominated the indoor concentrations of 5-7-ring PAHs.     

Prediction of personal exposure to PM2.5 and carcinogenic polycyclic aromatic hydrocarbons by their concentrations in residential microenvironments

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 microenvironments-living room, bedroom, kitchen (summer only), and workplace--and 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 ([BaP-TEQ]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.     

Indoor and outdoor polycyclic aromatic hydrocarbons in residences surrounding a Söderberg aluminum smelter in Canada

Ambient air in 18 residences surrounding an aluminum smelter were sampled to study the relationship between indoor and outdoor polycyclic aromatic hydrocarbons (PAHs). Objectives of the study were to quantify the indoor distribution of PAHs, indoor/outdoor (I/O) concentration ratios, and the relationship among PAH compounds. Correlation coefficients inside residences suggested an indoor source of 2-3 ring PAHs and an external source of 4-6 ring PAHs. The I/O ratios of 4-6 ring PAHs for homes without any substantial indoor sources were below unity, indicating that the presence of these PAHs was attributable to the aluminum smelter. Least squares linear regression of the coupled measurements without indoor sources of 5-6 ring PAHs resulted in average infiltration efficiencies (P(PAH)) of 0.49, 0.20, and 0.47 for benzo[a]pyrene, benzo[k]fluoranthene, and benzo[g,h,i]perylene, respectively. These P(PAH) values suggest that simultaneous measurements of indoor and outdoor concentrations of PAHs > 4 rings predominantly associated with the fine fraction of particulate matter could provide useful estimates of particle infiltration efficiency. Overall, study results indicate that when an industrial facility is the main source of outdoor 4-6 ring PAHs, the contribution of facility emissions may greatly exceed indoor sources in nonsmoking residences.     

Chlordanes in the indoor and outdoor air of three U.S. cities

Indoor and outdoor concentrations of six chlordane components (trans-chlordane, cis-chlordane, trans-nonachlor, cis-nonachlor, oxychlordane, and MC5) were measured at 157 residences, all of which were inhabited by nonsmoking individuals, in three urban areas during June 1999-May 2000. The analyses were conducted on a subset of 48 h integrated samples collected in Los Angeles County, CA, Houston, TX, and Elizabeth, NJ within the Relationship of Indoor, Outdoor, and Personal Air (RIOPA) study. Both particle-bound (PM2.5; quartz fiber filter) and vapor-phase (PUF sorbant) chlordane concentrations were separately measured by GC/EI MS after solvent extraction. The outdoor (gas + particle) total chlordane (trans-chlordane + cis-chlordane + trans-nonachlor + cis-nonachlor) concentrations ranged from 0.036 to 4.27 ng m(-3) in Los Angeles County, from 0.008 to 11.00 ng m(-3) in Elizabeth, and from 0.062 to 1.77 ng m(-3) in Houston. The corresponding indoor total chlordane concentrations ranged from 0.037 to 112.0 ng m(-3) in Los Angeles County, from 0.260 to 31.80 ng m(-3) in Elizabeth, and from 0.410 to 38.90 ng m(-3) in Houston study homes. Geometric mean concentrations were higher in indoor air than outdoor air (1.98 vs 0.58 ng m(-3) in CA; 1.30 vs 0.17 ng m(-3) in NJ; 4.18 vs 0.28 ng m(-3) in TX), which suggests there are significant indoor sources of chlordane species in a subset of homes in each of the three cities. Calculated source strengths relate to home age, with the highest apparent indoor source strengths occurring in unattached single-family homes built during the period from 1945 to 1959. Principle indoor sources of chlordanes likely include volatilization from residues of indoor application of chlordanes and infiltration from subsurface and foundation application of chlordane-containing termiticides during home construction.     

Microbial and chemical assessment of regions within New Orleans, LA impacted by Hurricane Katrina

The city of New Orleans, LA was severely impacted by flooding and wind damage following landfall of Hurricane Katrina in August 2005. The city's drinking water infrastructure was severely compromised and massive amounts of sediment were redeposited throughout the flooded region. Thousands of homes were water-damaged resulting in the rapid growth of mold. In September and October 2005 a convenience sample of selected homes, tap water, surface water, and sediment within New Orleans was assessed for mold contamination, microbial contamination, and heavy metal concentrations. At selected sites, indoor mold spore concentrations were compared to outdoor concentrations. The purpose of this study was to conduct a baseline environmental assessment in an effort to identify public health threats caused by wind and flood damage. Surface waters contained high concentrations of bacterial indicators whereas no bacteria were detected in tap water, even from taps containing no chlorine residual. Sediment samples contained concentrations of lead and arsenic similarto pre-Katrina concentrations. Outdoor total spore (sp) concentrations ranged from >6500 to 84 713 sp/m(3). Indoor concentrations ranged from 6142 to 735 123 sp/m(3). For the 13 locations with matched indoor/ outdoor samples, the mean indoor/outdoor spore ratio was 4.11 (ranging from 0.27 to >11.44). Inside 5 of the 13 homes, total spore counts/m(3) exceeded 100 000, with measurements in the moldiest home exceeding 700 000 sp/ m(3). In conclusion, surface waters had high concentrations of bacterial contamination but no bacterial indicators were present in tap water. Sediment samples did not have appreciable increases in lead or arsenic. Flooded homes, however, contained substantial concentrations of mold which could present a public health exposure route to individuals repopulating and restoring the City of New Orleans.     

Use of personal-indoor-outdoor sulfur concentrations to estimate the infiltration factor and outdoor exposure factor for individual homes and persons

A study of personal, indoor, and outdoor exposure to PM2.5 and associated elements has been carried out for 37 residents of the Research Triangle Park area in North Carolina. Participants were selected from persons expected to be at elevated risk from exposure to particles, and included 29 persons with hypertension and 8 cardiac patients with implanted defibrillators. Participants were monitored for 7 consecutive days in each of four seasons. One goal of the study was to estimate the contribution of outdoor PM2.5 to indoor concentrations. This depends on the infiltration factor Finf, the fraction of outdoor PM2.5 remaining airborne after penetrating indoors. After confirming with our measurements the findings of previous studies that sulfur has few indoor sources, we estimated an average Finf for each house based on indoor/outdoor sulfur ratios. These estimates ranged from 0.26 to 0.87, with a median value of 0.55. Since these estimates apply only to particles of size similar to that of sulfur particles (0.06-0.5 microm diameter), and since larger particles (0.5-2.5 microm) have lower penetration rates and higher deposition rates, these estimates are likely to be higher than the true infiltration factors for PM2.5 as a whole. In summer when air conditioners were in use, the sulfur-based infiltration factor was at its lowest (averaging 0.50) for most homes, whereas the average Finf for the other three seasons was 0.62-0.63. Using the daily estimated infiltration factor for each house, we calculated the contribution of outdoor PM2.5 to indoor air concentrations. The indoor-generated contributions to indoor PM2.5 had a wider range (0-33 microg/m3) than the outdoor contributions (5-22 microg/m3). However, outdoor contributions exceeded the indoor-generated contributions in 27 of 36 homes. A second goal of the study was to determine the contribution of outdoor particles to personal exposure. This is determined by the "outdoor exposure factor" Fpex, the fraction of outdoor PM2.5 contributing to personal exposure. As with Finf, we estimated Fpex by the personal/outdoor sulfur ratios. The estimates ranged from 0.33 to 0.77 with a median value of 0.53. Outdoor air particles were less important for personal exposures than for indoor concentrations, with the median outdoor contribution to personal exposure just 49%. We regressed the outdoor contributions to personal exposures on measured outdoor PM2.5 at the central site. The regressions had R2 values ranging from 0.19 to 0.88 (median = 0.73). These values provide an indication of the extent of misclassification error in epidemiological estimates of the effect of outdoor particles on health.     

Indoor air is a significant source of tri-decabrominated diphenyl ethers to outdoor air via ventilation systems

Ventilation of indoor air has been hypothesized to be a source of PBDEs to outdoors. To study this, tri-decabrominated diphenyl ethers were analyzed in outgoing air samples collected inside ventilation systems just before exiting 33 buildings and compared to indoor air samples from microenvironments in each building collected simultaneously. Median ∑(10)PBDE (BDE- 28, -47, -99, -153, -183, -197, -206, -207, -208, -209) concentrations in air from apartment, office and day care center buildings were 93, 3700, and 660 pg/m(3) for outgoing air, and 92, 4700, and 1200 pg/m(3) for indoor air, respectively. BDE-209 was the major congener found. No statistically significant differences were seen for individual PBDE concentrations in matched indoor and outgoing air samples, indicating that outgoing air PBDE concentrations are equivalent to indoor air concentrations. PBDE concentrations in indoor and outgoing air were higher than published outdoor air values suggesting ventilation as a conduit of PBDEs, including BDE-209, from indoors to outdoors. BDE-209 and sum of BDE-28, -47, -99, and -153 emissions from indoor air to outdoors were roughly estimated to represent close to 90% of total emissions to outdoor air for Sweden, indicating that contaminated indoor air is an important source of PBDE contamination to outdoor air.     

Origin, occurrence, and source emission rate of acrolein in residential indoor air

Acrolein, a volatile, unsaturated aldehyde, is a known respiratory toxicant and one of the 188 most hazardous air pollutants identified by the U.S. EPA. A newly developed analytical method was used to determine residential indoor air concentrations of acrolein and other volatile aldehydes in nine homes located in three California counties (Los Angeles, Placer, Yolo). Average indoor air concentrations of acrolein were an order of magnitude higher than outdoor concentrations at the same time. All homes showed similar diurnal patterns in indoor air concentrations, with acrolein levels in evening samples up to 2.5 times higherthan morning samples. These increases were strongly correlated with temperature and cooking events, and homes with frequent, regular cooking activity had the highest baseline (morning) acrolein levels. High acrolein concentrations were also found in newly built, uninhabited homes and in emissions from lumber commonly used in home construction, suggesting indoor contributions from off-gassing and/or secondary formation. The results provide strong evidence that human exposure to acrolein is dominated by indoor air with little contribution from ambient outdoor air.     

Tollbooth workers and mobile source-related hazardous air pollutants: how protective is the indoor environment?

Tollbooth workers are potentially exposed to high levels of mobile source-related air pollutants due to the proximity and intensity of the source. To evaluate this worker hazard, we measured the concentration of air toxins including volatile organic compounds (VOCs) and particle-bound polycyclic aromatic hydrocarbons (PAHs) inside and outside a Baltimore Harbor Tunnel tollbooth during the summer of 2001. Mean outdoor benzene and 1,3-butadiene concentrations varied by shift with the morning (10.7 and 19.8 microg/m3) exceeding afternoon (7.2 and 14.9 microg/m3) and the lowest levels observed during the night (3.7 and 4.9 microg/m3, respectively) when traffic volume was the lowest. In comparison, considerable protection was provided to workers bythe indoor environment where lower concentrations of 1,3-butadiene and benzene were observed for all three shifts (2.9 and 6.7, 0.9 and 3.2, and 0.9 and 2.4 microg/m3, respectively). The greatest protection offered by the tollbooth was observed during the afternoon shift (5-8-fold reduction in indoor concentration), whereas the morning and night shifts experienced similar protection (2-4-fold reduction). Chlorinated hydrocarbons were observed at higher concentrations within the tollbooth, indicating the presence of indoor sources and the opportunity for exposure mitigation. Levels of PAHs were similarly reduced from outdoors (50 ng/m3) to indoors (15.4 ng/m3). The protective nature of the tollbooth highlighted in this study is likely due to the positive pressure control ventilation system that was present at this specific facility, which represents 55% of tollbooths in Maryland. This study provides an estimate of tollbooth workers potential exposures to various mobile source-related pollutants and highlights the protective nature of tollbooths equipped with positive pressure control ventilation systems.     

Evaluating differences between measured personal exposures to volatile organic compounds and concentrations in outdoor and indoor air

Accurate estimation of human exposures to volatile organic compounds (VOCs) is a key element of strategies designed to protect public health from the adverse effects of hazardous air pollutants. The focus here is on examining the capability of three different exposure metrics (outdoor community concentrations, indoor residential concentrations, and a simple time-weighted model) to estimate observed personal exposures to 14 VOCs. The analysis is based on 2-day average concentrations of individual VOCs measured concurrently in outdoor (O) air in three urban neighborhoods, indoor (I) air in participant's residences, and personal (P) air near the breathing zone of 71 healthy, nonsmoking adults. A median of four matched P-I-O samples was collected for each study participant in Minneapolis/St. Paul over three seasons (spring, summer, and fall) in 1999 using charcoal-based passive air samplers (3M model 3500 organic vapor monitors). Results show a clear pattern for the 14 VOCs, with P > I > O concentrations. Intra-individual variability typically spanned at least an order of magnitude, and inter-individual variability spanned 2 or more orders of magnitude for each of the 14 VOCs. Although both O and I concentrations generally underestimated personal exposures, I concentrations provided a substantially better estimate of measured P concentrations. Mean squared error (MSE) as well as correlation measures were used to assess estimator performance at the subject-specific level, and hierarchical, mixed effects models were used to estimate the bias and variance components of MSE by tertile of personal exposure. Bias and variance both tended to increase in the upper third of the P exposure distribution for O versus P and I versus P. A simple time-weighted model incorporating measured concentrations in both outdoor community air and indoor residential air provided no improvement over I concentration alone for the estimation of P exposure.     

Perfluorinated sulfonamides in indoor and outdoor air and indoor dust: occurrence, partitioning, and human exposure

Perfluorinated alkyl sulfonamides (PFASs) which are used in a variety of consumer products for surface protection were investigated through a comprehensive survey of indoor air, house dust, and outdoor air in the city of Ottawa, Canada. This study revealed new information regarding the occurrence and indoor air source strength of several PFASs including N-methylperfluorooctane sulfonamidoethanol (MeFOSE), N-ethylperfluorooctane sulfonamidoethanol (EtFOSE), N-ethylperfluorooctane sulfonamide (EtFOSA), and N-methylperfluorooctane sulfonamidethylacrylate (MeFOSEA). Passive air samplers consisting of polyurethane foam disks were calibrated and used to conduct the indoor and outdoor survey. Indoor air concentrations for MeFOSE and EtFOSE (1490 and 740 pg m(-3), respectively) were about 10-20 times greater than outdoor concentrations, establishing indoor air as an important source to the outside environment. EtFOSA and MeFOSEA concentrations were lower in indoor air (40 and 29 pg m(-3) respectively) and below detection in outdoor air samples. For indoor dust, highest concentrations were recorded for MeFOSE and EtFOSE with geometric mean concentrations of 110 and 120 ng g(-1), while concentrations for EtFOSA and MeFOSEA were below detection and 7.9 ng g(-1) respectively. MeFOSE and EtFOSE concentrations in house dust followed levels in indoor air. However, resolution of the coupled air and dust data (for the same homes) was not successful using existing KoA-based models for surface-air exchange. The partitioning to house dust was greatly underpredicted. The difficulties with existing models may be due to the high activity coefficient of PFASs in octanol and/or a situation where the dust is greatly oversaturated with respect to the air due to components of the dust being contaminated with PFASs. A human exposure assessment based on median air and dust concentrations revealed that human exposure through inhalation (100% absorption assumed) and dust ingestion were approximately 40 and approximately 20 ng d(-1), respectively. However, for children the dust ingestion pathway was dominant and accounted for approximately 44 ng d(-1).     

Spatial distribution of polybrominated diphenyl ethers in southern Ontario as measured in indoor and outdoor window organic films

Organic films were collected from indoor and outdoor window surfaces, along an urban-rural transect extending northward from Toronto, Ontario, Canada, and analyzed for 41 polybrominated diphenyl ether congeners (PBDE). For exterior films, urban sigmaPBDE concentrations were approximately 10x greater than rural concentrations, indicating an urban-rural gradient and greater PBDE sources in urban areas. Urban films ranged from 2.5 to 14.5 ng/m2 (mean = 9.0 ng/ m2), excluding the regional "hotspot" Electronics Recycling Facility, compared to 1.1 and 0.56 ng/m2 at the Suburban and Rural sites. Interior urban films (mean = 34.4 ng/m2) were 3 times greater than rural films (10.3 ng/m2) and were representative of variations in building characteristics. Indoor films were 1.5-20 times greater than outdoor films, consistent with indoor sources of PBDEs and enhanced degradation in outdoor films. Congener profiles were dominated by BDE-209 (51.1%), consistent with deca-BDE as the main source mixture, followed by congeners from the penta-BDE mixture (BDE-99:13.6% and -47:9.4%) and some octa-BDE (BDE-183:1.5%). Congener patterns suggest a degradative loss of lower brominated compounds in outdoor films versus indoor films. Gas-phase air concentrations were back-calculated from film concentrations using the film-air partition coefficient (K(FA)). Mean calculated air concentrations were 4.8 pg/m3 for outdoor and 42.1 pg/m3 for indoor urban sites, indicating that urban indoor air is a source of PBDEs to urban outdoor air and the outdoor regional environment.     

Determination of the sources of indoor PM2.5 in Amsterdam and Helsinki

Daily PM2.5 samples were repeatedly collected (1-8 times) in the homes of elderly nonsmoking individuals with coronary heart disease in Amsterdam, The Netherlands (33 individuals) and Helsinki, Finland (44 individuals). Sources of indoor PM2.5 were evaluated using a two-way multilinear engine model. Because the indoor elemental data lacked a traffic marker, separation of traffic related PM was attempted by combining the indoor data with fixed site outdoor data that also contained NO. Six outdoor sources, including long-range transport (LRT), urban mixture, oil combustion, traffic, sea-salt, and soil were identified, and three indoor sources were resolved: resuspension, potassium-rich and copper-rich sources. The average contribution of the indoor factors was 6% (1.1 microg m(-3)) and 22% (2.4 microg m(-3)) in Amsterdam and Helsinki, respectively. The highest longitudinal correlations between source-specific outdoor and indoor PM2.5 concentrations were found for LRT and urban mixture; the median R was above 0.6 for most sources. The longitudinal correlations were lower in Helsinki than in Amsterdam. Indoor-generated PM2.5 was not related to ambient concentrations. We conclude that using outdoor and indoor data together improved the source apportionment of indoor PM2.5. The results support the use of fixed site outdoor measurements in epidemiological time-series studies on outdoor air pollution.     

Calibration of a passive sampler for both gaseous and particulate phase polycyclic aromatic hydrocarbons

A novel passive air sampler was designed and tested that individually collects the gaseous and particulate phase polycyclic aromatic hydrocarbons (PAHs) in air. The sampler was calibrated against a conventional active sampler in an indoor environment. A PUF (polyurethane foam) disk and a piece of GFF (glass fiber filter) were installed in a sampling shelter for collecting gaseous and particulate phase PAHs, respectively. The passive samplers were deployed in seven indoor locations for 86 days. Six times during this period, 24-h conventional active sampling was conducted for calibration at an average interval of 17-days. Principle component analysis showed that the measured congener profile compositions were totally different between the gaseous and particulate phase PAHs, but similar between the passive and the active samples. This suggested that gaseous and particulate phase PAHs were primarily trapped by the PUF disk and GFF, respectively. Linear relationships between the passively and the actively measured and log-transformed concentrations were derived for calibration of both gaseous and particulate phase PAHs. The uptake rates of the sampler were 0.10 +/- 0.014 m3/d and 0.007 +/- 0.001 m3/d for gaseous and particulate phase PAHs, respectively. The rates were significantly lower than those reported in the literature using similar PUF samplers, mainly because of the special design with limited air circulation.     

Comparison of personal, indoor, and outdoor exposures to hazardous air pollutants in three urban communities

Two-day average concentrations of 15 individual volatile organic compounds (VOCs) were measured concurrently in (a) ambient air in three urban neighborhoods, (b) air inside residences of participants, and (c) personal air near the breathing zone of 71 healthy, nonsmoking adults. The outdoor (O), indoor (I), and personal (P) samples were collected in the Minneapolis/St. Paul metropolitan area over three seasons (spring, summer, and fall) in 1999 using charcoal-based passive air samplers (3M model 3500 organic vapor monitors). A hierarchical, mixed-effects statistical model was used to estimate the mutually adjusted effects of monitor location, community, and season while accounting for within-subject and within-time-index (monitoring period) correlation. Outdoor VOC concentrations were relatively low compared to many other urban areas, and only minor seasonal differences were observed. A consistent pattern of P > I > O was observed across both communities and seasons for 13 of 15 individual VOCs (exceptions were carbon tetrachloride and chloroform). Results indicate that ambient VOC measurements at central monitoring sites can seriously underestimate actual exposures for urban residents, even when the outdoor measurements are taken in their own neighborhoods.     

Sources, emissions, and fate of polybrominated diphenyl ethers and polychlorinated biphenyls indoors in Toronto, Canada

Indoor air concentrations of polybrominated diphenyl ethers (PBDEs) and polychlorinated biphenyls (PCBs) measured in 20 locations in Toronto ranged 0.008-16 ng·m(-3) (median 0.071 ng·m(-3)) and 0.8-130.5 ng·m(-3) (median 8.5 ng·m(-3)), respectively. PBDE and PCB air concentrations in homes tended to be lower than that in offices. Principal component analysis of congener profiles suggested that electrical equipment was the main source of PBDEs in locations with higher concentrations, whereas PUF furniture and carpets were likely sources to locations with lower concentrations. PCB profiles in indoor air were similar to Aroclors 1248, 1232, and 1242 and some exterior building sealant profiles. Individual PBDE and PCB congener concentrations in air were positively correlated with colocated dust concentrations, but total PBDE and total PCB concentrations in these two media were not correlated. Equilibrium partitioning between air and dust was further examined using log-transformed dust/air concentration ratios for which lower brominated PBDEs and all PCBs were correlated with K(OA). This was not the case for higher brominated BDEs for which the measured ratios fell below those based on K(OA) suggesting the air-dust partitioning process could be kinetically limited. Total emissions of PBDEs and PCBs to one intensively studied office were estimated at 87-550 ng·h(-1) and 280-5870 ng·h(-1), respectively, using the Multimedia Indoor Model of Zhang et al. Depending on the air exchange rate, up to 90% of total losses from the office could be to outdoors by means of ventilation. These results support the hypotheses that dominant sources of PBDEs differ according to location and that indoor concentrations and hence emissions contribute to outdoor concentrations due to higher indoor than outdoor concentrations along with estimates of losses via ventilation.     

Preliminary assessment of U.K. human dietary and inhalation exposure to polybrominated diphenyl ethers

This study reports concentrations of BDEs 47, 99, 100, 153, and 154 in outdoor air [median sigmaPBDE (sum of BDEs 47, 99, 100, 153, and 154) = 18 pg m(-3)] in air from a range of office and home indoor microenvironments (median sigmaPBDE = 762 pg m(-3)) and vegan and omnivorous duplicate diet samples (median sigmaPBDE = 154 and 181 pg g(-1) dryweightforvegan and omnivorous diets, respectively). Median daily human exposure to sigmaPBDE via inhalation is 6.9 ng/person and 90.5 ng/person via diet but the relative significance of these pathways may vary considerably between individuals. Median concentrations in indoor air were higher in workplace (sigmaPBDE = 1082 pg m(-3)) than in domestic (sigmaPBDE = 128 pg m(-3)) microenvironments, and substantial differences in concentrations in air from different rooms in the same office building were found. When data from the only mechanically ventilated room was excluded, a significant positive correlation (p < 0.001) was observed between PBDE concentrations and both the number of electrical appliances and polyurethane foam-containing chairs. Concentrations of sigmaPBDE and BDEs 47 and 99 were significantly higher (p < 0.1) in omnivorous diet samples than in vegan diet samples, implying that while plant-based foods contribute appreciably, higher exposure occurs via ingestion of animal-based comestibles.     

Environmental tobacco smoke as a source of polycyclic aromatic hydrocarbons in settled household dust

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/m(2) vs 796 ng/m(2), p = 0.012). We also found significant linear correlations between nicotine and total PAH levels in SHD (concentration, R(2) = 0.105; loading, R(2) = 0.385). Dust collected per square meter (g/m(2)) was significantly greater in smoker homes and might dilute PAH concentration in SHD inconsistently. Therefore, dust PAH loading (ng PAH/m(2)) 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 (R(2) = 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.