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Mutagenic and Carcinogenic Hazards of Settled House Dust I: Polycyclic Aromatic Hydrocarbon Content and Excess Lifetime Cancer Risk from Preschool Exposure

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Safe Environments Programme, Healthy Environments and Consumer Safety Branch, Health Canada, Tunney’s Pasture 0803A, Ottawa, Ontario, Canada, K1A 0K9

*Corresponding author e-mail: [email protected].

§Deceased April 2006.

Cite this: Environ. Sci. Technol. 2008, 42, 5, 1747–1753

Publication Date (Web):January 23, 2008

https://doi.org/10.1021/es702449c

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Abstract

Settled house dust (SHD) may be a significant source of children’s indoor exposure to hazardous substances including polycyclic aromatic hydrocarbons (PAHs). In this study, organic extracts of sieved vacuum cleaner dust from 51 homes were examined for the presence of 13 PAHs via GC/MS. PAHs were found in all samples with levels of total PAHs ranging between 1.5 and 325 µg g⁻¹. The PAH concentrations in the SHD were correlated with information contained in corresponding household questionnaires. Analyses showed levels of PAHs to be negatively associated with noncombustion activities such as vacuum cleaning frequency. A risk assessment was conducted to evaluate the excess lifetime cancer risks posed to preschool aged children who ingested PAHs in SHD. The assessment revealed that exposure to PAHs at levels found in 90% of the homes (<40 µg g⁻¹) would result in excess cancer risks that are considered acceptable (i.e., 1–100 × 10⁻⁶). However, exposure to higher levels of PAHs found in five homes yielded risks that could be higher than 1 × 10⁻⁴.

Synopsis

Assessments of house dust PAH (polycyclic aromatic hydrocarbon) contamination reveals that levels in some homes could yield unacceptable increases in excess cancer risk

Introduction

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Previous studies have noted that concentrations of chemical contaminants may be higher in indoor air than in outdoor air (1). Indoors, many contaminants adsorb to particulate matter, which is initially suspended in air and later settles out as dust. Research suggests that settled house dust (SHD) may be a significant source for indoor exposures to many pollutants (2). Previous studies have revealed the presence of numerous chemical contaminants in SHD including pesticides, smoke residues, PCBs, flame retardants, plasticizers, heavy metals, and asbestos (3-8). With Canadians spending as much as 70% of their time at home and up to 90% of their time indoors (9), the health risks posed by exposure to contaminants indoors are of significant concern.

Polycyclic aromatic hydrocarbons (PAHs) have also been detected in SHD (for a review, see Maertens et al. (10)), and many of these compounds are known mutagens or animal carcinogens (11). There exists a high potential for human exposure to PAHs because of the ubiquity of their sources in both indoor and outdoor environments. As products of incomplete combustion, indoor sources of PAHs include cooking (12, 13), heating (14), smoking (15), wood burning (16), candle burning (17), and incense burning (12, 18). Outdoor sources include vehicle exhaust (19), forest fires, volcanoes, and industrial processes such as aluminum smelting and coke production (20).

Exposure to PAHs in SHD are of particular concern for children who tend to crawl on the floor and place objects in their mouths that have been in direct contact with dusty floors (21). A small number of studies have assessed children’s exposure to PAHs in SHD as compared to other matrices (22-24). These assessments show that dietary ingestion of PAHs in food is often the primary exposure pathway for children. However, they also show that nondietary ingestion of carcinogenic PAHs in dust and soil is significant and is a more important exposure route than inhalation of PAHs in air. Exposure assessments indicate that toddlers playing on the floor and exhibiting hand-to-mouth behavior can ingest more than 2.5 times more PAHs than adults (25). Furthermore, since a child’s body weight is only about one-fifth that of an average adult, a child’s intake of PAHs in dust, in milligrams per kilogram of body weight per day, is likely to be far greater than that for an adult. In addition, early developmental stages of organ, immune, and nervous systems in children are thought to contribute to an enhanced contaminant sensitivity (26). Consequently, the adverse health risks for children exposed to PAHs in SHD are believed to be considerably greater than those for adults.

In Canada, PAHs are priority substances for assessment under the Canadian Environmental Protection Act (CEPA), and a number have been declared toxic under this Act (20). However, to our knowledge, there are no published studies that have evaluated PAH concentrations in SHD from Canadian homes. The objectives of this study, which includes a companion publication, are (i) to quantify levels of PAHs in SHD collected from homes in Ottawa, Canada, (ii) analyze relationships between these levels and various attributes of the households (e.g., home location, presence of smokers, percent carpet covering), and (iii) estimate the carcinogenic risks associated with preschool children’s nondietary ingestion of PAHs in SHD.

Experimental Section

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Study Design and Dust Sample Collection

Vacuum cleaner bags were collected between November 2002 and March 2003 from 75 homes located in Ottawa, the capital city of Canada. A two-stage stratified sampling process was used to randomly select homes that were representative of both urban and suburban locations within the city. A description of the sampling design is provided elsewhere (27). The bags were removed from the vacuum cleaner, placed in zip-seal plastic bags (Fisher Scientific, Ottawa, Canada), and transported to the laboratory where they were stored at −20 °C.

All participants answered a detailed questionnaire that was designed to collect information on the house and any activities that might affect chemical loading. The majority of household occupants classified their home as being located in a quiet residential area (61%). Fewer homes were located in a main residential area (29%), and an even lower number were located in a main commercial (6%) or rural area (4%). Most of the households were characterized as nonsmoking households (85%). Only 15% contained occupants who smoked, and the median number of cigarettes smoked per day was eight. The primary heating source in most of the homes was natural gas (83%); oil and electric heat were less common (11% and 4%, respectively), and one home did not describe the heating source.

Sample Preparation

Prior to sieving, the vacuum cleaner bags were thawed overnight in a fume hood. The dust was removed from the bags using large forceps and placed into a USA Standard Testing Sieve, ASTM E-11 specification, with a 150 µm opening. The dust was shaken through the sieve using an AS200 Digit Analytical Sieve Shaker (Retsch GmbH & Co. KG, Haan, Germany). The shaker was run at 80% (amplitude = 20 mm) for 10 min. Any visible hairs were removed from the collection pan using tweezers, a paintbrush, or both. The sieved dust (<150 µm) was then resieved on the shaker for an additional 3 min. The sieved dust was transferred to a glass jar, and the weight of the sieved dust was recorded. The jars were sealed with Teflon tape and stored at −20 °C until analysis. Of the 75 dust samples that were collected, 51 samples contained sufficient dust for chemical analyses.

Extraction and Sample Cleanup Procedures

Approximately 0.3 g of each of the 51 dust samples were extracted with dichloromethane (DCM) and hexane (1:1) using an ASE 200 Accelerated Solvent Extractor (ASE) (Dionex, Oakville, ON, Canada). The ASE settings were 175 °C and 1500 PSI, with a preheat time of 7 min, a heat time of 5 min, and a static extract time of 10 min. The extracts were collected in vials containing 5 g of anhydrous sodium sulfate.

Extracts were filtered through 0.45 µm Whatman Teflon syringe filters, reduced to 0.5 mL under nitrogen at 30 °C, and brought up to 2 mL in DCM. Gel permeation chromatography (GPC), using a Waters Autopurification system with tandem Waters Envirogel GPC columns (19 × 300 mm and 19 × 150 mm, styrene/divinylbenzene) (Waters, Mississauga, ON, Canada) was used to remove high molecular weight compounds. The GPC was performed and calibrated according to EPA Method 3640a (28).

Gas Chromatography–Mass Spectrometry

A solvent exchange to hexane was performed, and the dust extracts were analyzed for 13 PAHs including acenaphthylene, fluorene, phenanthrene, anthracene, pyrene, benz[a]anthracene, benzo[a]pyrene, benzo[b]fluoranthene, benzo[k]fluoranthene, chrysene, indeno[1,2,3-c,d]pyrene, dibenz[a,h]anthracene, and benzo[g,h,i]perylene via gas chromatography/mass spectrometry (GC/MS). Analyses were conducted using a Hewlett-Packard 5890 gas chromatograph (GC) fitted with an HP-5MS capillary column (30 m × 0.25 mm × 0.25 µm film thickness) (J&W Scientific, Folsom, CA) and equipped with a HP5972 mass selective (MS) detector (Agilent Technologies, Palo Alto, CA). The initial GC temperature was held at 50 °C for 2 min, then ramped 8 °C min⁻¹ to 300 °C, and held at 300 °C for 12 min. The injection port temperature was 270 °C, and the detector temperature was 280 °C. One microliter volumes were injected in splitless mode. The purge time was 2 min. The MS was operated in the selected ion monitoring mode. The masses monitored included the molecular ions and their associated characteristic fragment ions. A calibration standard consisting of a standard solution of 13 PAHs (EPA 525 PAH Mix A, Supelco, PA) and two deuterated PAHs (acenaphthene d₁₀and benzo[a]pyrene d₁₂) were run with each batch of samples. Prior to GC/MS analyses, each sample was spiked with two deuterated standards (acenaphthene-d₁₀ and benzo[a]pyrene-d₁₂) that permit the normalization of GC/MS peak area. Identification of the PAHs was based on their retention time relative to the calibration standard solution. Quantification of the PAHs, based on the internal standards, was conducted using MSD Productivity ChemStation (29).

QA/QC

A recovery efficiency study was conducted (N = 4) using 15 µg of the EPA 525 PAH Mix A, and recovery efficiencies ranged between 57 and 76%. All PAH concentration values were corrected for the recoveries. Empty cells were included as blanks with each batch of samples that was processed. No detectable amounts of PAHs were found in any of the blanks. Six randomly selected dust samples (10% of the samples) were subjected to duplicate analysis. The average relative percent difference (RPD) for the PAHs ranged from 3.4% to 9.5%. The method detection limit (MDL) in this study was defined as the instrument detection limit (IDL), which was calculated from repeats of low concentration standards, divided by the recoveries (MDL = IDL/recovery). The MDLs, recovery efficiencies and average RPD in duplicates are summarized in Table 1.

Table 1. Monitored Ions and Fragments, Method Detection Limits (MDL), Recovery Efficiencies, and Relative Percent Difference in Duplicates (RPD) for the Quantification of 13 PAHs in SHD Extracts by GC/MS

PAH	mass to charge ratio of monitored ions and fragments	IDL (ng µL⁻¹)	recovery efficiency (%)	corrected MDL (µg g⁻¹)^a	av RPD^b
acenaphthylene	152, 151, 76	0.0017	57.1	0.011	5.5
fluorene	166, 164, 82	0.0025	65.8	0.014	6.7
phenanthrene	178, 176, 89	0.0022	70.1	0.011	6.9
anthracene	178, 176, 89	0.0019	62.7	0.011	9.5
pyrene	202, 101, 100	0.0025	74.7	0.012	3.7
benz[a]anthracene	228, 114, 101	0.0041	72.4	0.021	5.1
chrysene	228, 114, 101	0.0052	75.7	0.025	3.8
benzo[b]fluoranthene	252, 126, 113	0.0039	72.1	0.019	4.5
benzo[k]fluoranthene	252, 126, 113	0.0072	74.3	0.035	5.5
benzo[a]pyrene	252, 126, 113	0.0080	57.1	0.051	4.5
indeno[1,2,3-c,d]pyrene	276, 138, 137	0.0074	68.1	0.040	3.4
dibenz[a,h]anthracene	276, 138, 137	0.0105	70.6	0.054	4.0
benzo[g,h,i]perylene	278, 139, 138	0.0063	69.7	0.033	3.6

Corrected MDL = IDL (ng µL⁻¹) × 1000 (final volume, µL)/1000 (ng μg⁻¹)/0.275 (sample mass, g)/recovery efficiency.

RPD = absolute difference between the duplicate divided by their average value times 100%.

Cancer Risk Assessment of PAHs in Settled House Dust

The following equation was used to estimate the excess lifetime cancer risks associated with nondietary ingestion of PAHs in SHD during preschool years (30)

for B2 PAHs 1 through n, where C = concentration (µg g⁻¹) of each carcinogenic PAH in the SHD samples. The PAHs included in this assessment were benzo[a]anthracene (BaA), benzo[a]pyrene (BaP), benzo[b]fluoranthene (BbF), benzo[k]fluoranthene (BkF), chrysene (CHRY), dibenz[a,h]anthracene (DBahA), and indeno[1,2,3-c,d]pyrene (I123cdP). All of these PAHs are categorized as probable human carcinogens (B2) on the basis of U.S. EPA classifications (31). PEF = Potency equivalency factor. These factors are applied to the individual PAH concentrations to express the potency of each PAH in terms of benzo[a]pyrene. The PEFs were BaA = 0.1, BbF = 0.1, BkF = 0.1, CHRY = 0.001, I123cdP = 0.1, DBahA = 5. All PEFs were taken from Collins et al. (32), except for DbahA, which was taken from Nisbet and Lagoy (33). IR = Daily ingestion rate of dust (g day⁻¹). Three ingestion rates were considered: 0.01, 0.05, and 0.1 g day⁻¹. Investigators estimate that children ingest between 0.05 and 0.1 g of dust per day depending on the season and the amount of time spent indoors (34). Both 0.05 and 0.1 g day⁻¹ are considered to be conservative estimates, erring on the side of greater exposure. On the basis of studies with tracer elements, other researchers have suggested that children likely ingest closer to 0.04 g day⁻¹ of soil and dust combined (35). Dust is estimated to account for only a quarter of this value (35, 36). Consequently, a lower ingestion rate of 0.01 g day⁻¹ was also used. EF = exposure factor. The average proportion of a seventy year lifetime that preschoolchildren are exposed to dust via nondietary ingestion. Seven hours per day was considered an average exposure rate based on the fact that preschool-aged children spend approximately 19–20 h day⁻¹ indoors (37, 38) and sleep for approximately 12–13 h day⁻¹ (38, 39). It was assumed that preschool-aged children would be exposed from birth up to the fifth birthday. BW = average body weight (kg). A standard value of 13 kg was used (40). SF = slope factor ((mg kg⁻¹ day⁻¹)⁻¹). This is the estimate of the probability of a response occurring per unit intake of the PAH over a lifetime. For these analyses, an oral slope factor for benzo[a]pyrene of 7.3 (mg kg⁻¹ d⁻¹)⁻¹was used (31). Slope factors represent the upper-bound estimate of risk per unit dose for an average population (41). AF = adjustment factor. This factor accounts for exposures taking place during early life stages when children are more susceptible to the effects of chemical toxins (26). For exposure to carcinogens with a mutagenic mode of action, the U.S. EPA recommends an adjustment factor of 10 for children less than 2 years of age and an adjustment factor of 3 for children between 2 and 15 years of age (42). Therefore, a composite adjustment factor of 5.8 was used for this risk assessment where exposures occur from birth to 5 years of age.

Data Analyses

All descriptive statistics (e.g., minimum, maximum, mean), ordinary least-squares linear regression, and Pearson correlations were performed using the SAS System, version 8.2, for Windows (43). PAH concentration data, as well as the data for two variables contained in the homeowner survey (vacuum frequency and number of people living in the house), were log transformed to equalize the variance across the range of observations. The Shapiro−Wilk statistic and inspection of normal probability plots were used to assess normality of residuals. Significant outliers were identified by calculation of the studentized deleted residual (44). In those cases where PAH values were below the detection limit, a value of one-half the detection limit was substituted into the data set for statistical analyses.

Results and Discussion

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Levels of Polycyclic Aromatic Hydrocarbons (PAHs)

The dust extracts were evaluated for the presence of 13 targeted PAHs (Table 2). The individual concentrations of the 13 PAHs spanned between 2 and 3 orders of magnitude both for a single PAH and between different PAHs. Acenaphthylene was detected in the lowest concentrations, while benzo[b]fluoranthene was detected in the highest. With a molecular weight of 152.2 and a vapor pressure of 0.378 Pa (45), acenaphthylene is more readily volatilized and generally found only at low levels in dust samples (23, 46-48). In contrast, benzo[b]fluoranthene is heavier and less volatile and has previously been detected in the highest concentrations in dust samples (47, 49). Although PAHs with a higher number of rings generally have lower volatilities, there were no consistent trends in concentration of the PAHs based on the number of rings.

Table 2. Minimum, Maximum, and Mean Values of 13 PAHs Measured in the Extracts of Settled House Dust Collected from Homes in Ottawa, ON^a

PAH	MDL^b(µg g⁻¹)	no. of samples below MDL	minimum (µg g⁻¹)	maximum (µg g⁻¹)	median (µg g⁻¹)	arithmetic mean (µg g⁻¹)	SEM^c	geometric mean (µg g⁻¹)
acenaphthylene	0.011	30	0.005	0.171	0.005	0.039	0.007	0.015
fluorene	0.013	7	0.007	1.37	0.093	0.170	0.032	0.084
phenanthrene	0.012	0	0.149	21.0	1.48	2.78	0.558	1.53
anthracene	0.011	2	0.006	6.62	0.196	0.485	0.136	0.222
pyrene	0.012	0	0.207	46.0	1.46	4.36	1.15	1.91
benz[a]anthracene	0.021	0	0.105	32.1	0.696	2.38	0.707	0.956
chrysene	0.025	0	0.150	35.1	1.19	3.29	0.858	1.46
benzo[b]fluoranthene	0.019	0	0.160	54.0	1.66	4.87	1.31	2.01
benzo[k]fluoranthene	0.034	0	0.049	19.0	0.532	1.60	0.442	0.674
benzo[a]pyrene	0.051	0	0.040	38.8	0.803	2.91	0.899	0.963
indeno[1,2,3-c,d]pyrene	0.039	0	0.100	33.5	0.911	3.07	0.819	1.29
dibenz[a,h]anthracene	0.054	0	0.022	6.27	0.185	0.549	0.148	0.250
benzo[g,h,i]perylene	0.034	0	0.118	31.4	0.793	2.79	0.764	1.13
total PAHs^d			1.50	325	9.53	29.3	7.78	12.9
B2 PAHs^e			0.656	219	6.06	18.7	5.17	7.68

Values are corrected for recovery efficiencies.

Method detection limit. Samples below the MDL were assigned a value of one half of the MDL.

Standard error of the arithmetic mean.

Sum of the 13 targeted PAHs.

Sum of the PAHs classified as probable human carcinogens by the U.S. EPA (31).

The sum of the 13 PAHs, referred to hereafter as total PAHs, ranged between 1.5 and 325 µg g⁻¹, with a geometric mean of 12.9 µg g⁻¹. These values are similar to the findings of a previous review in which the total PAHs for samples collected from urban, rural, and suburban homes ranged between 0.4–544 µg g⁻¹ with a geometric mean of 4.5 µg g⁻¹ (10). The distribution of the total PAHs in the samples was positively skewed (skewness = 4.00).

The sum of the seven PAHs classified as probable human carcinogens by the U.S. EPA (2003), referred to hereafter as the B2 PAHs, accounted for approximately 60% of the total PAHs. Similar results were observed in other studies where the concentrations of the B2 PAHs, were shown to be approximately one-half of the total PAH concentrations (24, 50).

The house with the lowest total PAH concentration (1.5 µg g⁻¹) was a newly constructed home whose owners moved in shortly before the sampling took place. The house with the highest total PAH level (325 µg g⁻¹) was an 18-year-old residence whose only distinguishing feature was that it was 90% carpeted. Lewis et al. (1994) noted that contaminants have the potential to accumulate in carpet dust (21), and therefore, a high percentage of carpeting in this home may have resulted in high PAH levels.

The German Federal Environmental Agency’s Commission for Indoor Air Quality has established the only current guideline for PAHs in house dust. It states that exposure to concentrations above 10 µg of benzo[a]pyrene per gram of household dust should be minimized to prevent adverse health effects (51). In the present study, three samples (11% of total) contained concentrations of benzo[a]pyrene that were above 10 µg g⁻¹ (ppm), with maximum values reaching 39 µg g⁻¹. Although there are currently no Canadian guidelines for PAH contaminants in SHD, guidelines for PAHs in residential soils, a comparable particulate matrix, do exist. The 2003 Canadian Environmental Quality Guideline for benzo[a]pyrene in residential soil is 0.7 µg g⁻¹ (ppm) (52). More than half of the SHD samples examined in this study contained concentrations above this value. The Environmental Quality Guideline for benzo[b]fluoranthene in residential soils is 1 µg g⁻¹. The geometric mean value for benzo[b]fluoranthene in SHD was 2 µg g⁻¹, and the maximum value was 54 µg g⁻¹. Similarly, other PAHs were also observed to exceed Canadian Environmental Quality Guidelines for residential soils.

Empirical Relationships Between Dust PAH Content and Household Attributes

Empirical relationships between dust PAH content and the attributes of the homes from which the dust was collected (see Table 1, Supporting Information) were investigated. Previous studies have shown that PAH concentrations in the indoor environment are related to PAH source activities such as smoking (15, 24), cooking (13), fireplace and woodstove use (53, 54), and urban location (10). However, in the present analyses, no significant relationships were observed between dust PAH concentrations and the PAH sources identified in the homeowner survey. This was unexpected because an earlier review by our group, based on 132 observations from 18 publications (10), showed that both cigarette smoking and an urban home location were weakly but significantly related to PAH contamination of dust. The absence of empirical relationships in the present study may be the result of a relatively small sample size.

Relationships were also evaluated between PAH concentrations and other survey variables (i.e., not combustion related). Weak, but significant, negative relationships (r = −0.29 to −0.32, p < 0.05) were found between the concentrations of PAHs with four rings or more and the frequency of vacuuming. This finding suggests that the cleaning habits of the inhabitants in some way reduces the PAH concentration of the dust. It is possible that homeowners who vacuum more frequently do so because their homes are noticeably dustier. Dustier homes may contain more diluted PAH concentrations. Alternatively, vacuum frequency may be an indicator of general cleanliness, and “cleaner” residents may engage in activities that reduce the likelihood of PAH contamination in the indoor area (e.g., removal of shoes, more ventilation during PAH generating events).

Cancer Risk Assessment of PAHs in Settled House Dust

To assess the potential consequences associated with exposure to carcinogenic PAHs, a risk assessment was conducted using the concentration data for PAHs classified as probable human carcinogens (B2) by the U.S. EPA (31). Specifically, the risk assessment evaluated the excess lifetime cancer risk resulting from nondietary ingestion of carcinogenic PAHs in SHD during preschool years.

Figure 1 shows the levels of excess cancer risk plotted against the concentration of B2 PAHs found in each house dust sample. Risk curves are shown for low, medium, and high dust ingestion scenarios. The results indicate that exposure to carcinogenic PAHs at levels found in 90% of the sampled households (i.e., <40 µg g⁻¹) results in excess cancer risks that are generally between 1 × 10⁻⁶ and 1 × 10⁻⁴. Five of the house dust samples contained levels of carcinogenic PAHs that were higher than 40 µg g⁻¹. Examination of the household survey results for these homes did not reveal any distinguishing characteristics that could account for the higher PAH levels.

Figure 1. Excess cancer risks resulting from nondietary ingestion of B2 PAHs in SHD during preschool years. Three ingestion rates (IR) are considered. Arrow denotes the 90th percentile of the B2 PAH concentrations.

To interpret the outcome of the risk assessment, the results can be evaluated against “acceptable risk” levels. One cancer case per million people is commonly used as a baseline level of acceptable risk. However, depending on exposure scenarios, agencies assessing risk frequently build upon this level and adopt ranges of acceptable risk. When the risk assessment outcomes of the present study are compared to the Canadian maximum acceptable level of risk (i.e., 1 × 10⁻⁵) (55), the interpretation varies substantially according to ingestion rate. If the lowest ingestion rate is considered, only 5 homes (10%) contain PAH levels that result in unacceptable risk. If the middle ingestion rate is considered, 21 homes (41%) contain levels of carcinogenic PAHs (>8 µg g⁻¹) resulting in unacceptable risk. Similarly, at the highest ingestion rate, 34 homes (67%) contain levels of carcinogenic PAHs (>4.2 µg g⁻¹) resulting in unacceptable risk.

These results can be compared to a previously conducted assessment by Roberts et al. which also evaluated the lifetime cancer risks associated with the ingestion of PAHs in SHD (2). The exact number, type, and proportion of individual PAHs that made up the total PAH concentration in the Roberts et al. study are unknown; however, general comparisons can still be made with houses in the present study that had similar levels of total carcinogenic PAHs. The results in Table 3 show that the risk values calculated in the Roberts et al. study are consistently higher (approximately six times higher) than in the present study. The higher values may be partially accounted for by the use of a higher slope factor (i.e., 11.3 instead of 7.3).

Table 3. Comparisons of Levels of Excess Cancer Risk Resulting from the Nondietary Ingestion of PAHs in Settled House Dust

	ingestion rate = 0.05 g day⁻¹		ingestion rate = 0.1 g day⁻¹
PAH concentration	Roberts et al.^a	this study	roberts et al.^a	this study
0.97 µg g⁻¹	7.8 × 10⁻⁶	1.6 × 10⁻⁶	1.6 × 10⁻⁵	3.2 × 10⁻⁶
4.2 µg g⁻¹	3.4 × 10⁻⁵	5.1 × 10⁻⁶	6.8 × 10⁻⁵	1.0 × 10⁻⁵
21 µg g⁻¹	1.7 × 10⁻⁴	2.6 × 10⁻⁵	3.4 × 10⁻⁴	5.1 × 10⁻⁵

Values taken from ref 2.

The BaP slope factor employed for the risk assessment calculations in this study represents the risk of gastric cancer following dietary ingestion (56). Therefore, it is also useful to compare the excess lifetime risk values calculated in the present study with incidence and mortality rates of gastric cancer in Canada (Table 4).

Table 4. Comparison of Gastric Cancer Incidence and Mortality in Canada with Calculated Risk Estimates

statistic	per 100 000
new cases of stomach cancer in Canada (2001 raw values)^a	12.8

age-adjusted incidence of stomach cancer in Canada (2001)^a	16.8

age-adjusted mortality from stomach cancer in Canada (2002)^a	11.0

excess risk at 50th percentile PAH concentration for 0.01 g day⁻¹ingestion	0.1

excess risk at 50th percentile PAH concentration for 0.05 g day⁻¹ingestion	0.7

excess risk at 50th percentile PAH concentration for 0.10 g day⁻¹ingestion	1.3

excess risk at maximum PAH concentration for 0.01 g day⁻¹ingestion	5.5

excess risk at maximum PAH concentration for 0.05 g day⁻¹ingestion	27.4

excess risk at maximum PAH concentration for 0.10 g day⁻¹ingestion	54.9

Cancer statistics from Canadian Cancer Society/National Cancer Institute of Canada (57). Values are totals that include both sexes. Values for total new cases is incidence per 100 000 adults 20 years or older. Population statistics from Statistics Canada (58).

The data show that exposures to SHD in houses where the PAH concentration is at the 50th percentile will result in essentially a negligible risk. However, the risk associated with the highest ingestion rate and the most contaminated sample is more than 3-fold greater than the age-adjusted incidence. Therefore, although excess risk of this magnitude would be relatively infrequent, concern is certainly justified.

As with all risk assessments, the calculation of risk involves a number of assumptions and uncertainties that have the potential to influence the outcome of the assessment. Future estimates of risk would benefit from more accurate, age-specific estimates of dust ingestion rates, including in relation to dust loading. In addition, since human exposure to compounds such as PAHs occurs in mixtures, additional information on the cumulative (geno)toxicity of compounds in real mixtures would provide a more accurate indication of actual risk.

This work, which characterized the PAH contamination of SHD, is part of a larger effort investigating the contamination, mutagenic activity and carcinogenic risk of SHD collected from homes in Ottawa, Canada. Specifically, this portion of the study assessed the levels of 13 priority PAHs, investigated empirical relationships between household attributes and PAH levels, and calculated the excess cancer risk posed by the detected carcinogenic PAHs to preschool children. Not surprisingly, the distribution of total PAH concentration was heavily skewed, and most (e.g., 90%) SHD samples contained less than 40 µg g⁻¹. Moreover, the geometric mean PAH concentration (12.9 µg g⁻¹) was in the same range as those described in other house dust studies (10). Empirical analyses failed to detect relationships between PAH concentration and combustion activity, and the source(s) of the detected PAHs remain unclear.

It should be noted that this study only investigated PAH contamination and excess risk posed by seven carcinogenic PAHs, and toxicity data is lacking on PAHs with higher molecular weights (i.e., larger than BaP). It is likely that SHD, a highly complex environmental matrix, contains dozens, perhaps even hundreds, of chemical contaminants that can contribute to the risk of adverse health effects. It would prove interesting to use a nontargeted approach to investigate the toxicological activity of chemical fractions derived from SHD. Moreover, a strategy such as effect-directed fractionation (59) could be employed to track and eventually identify toxic substances in highly complex environmental matrices such as SHD. In our companion paper (60), we use a nontargeted, bioassay-based approach to investigate the mutagenic activity of SHD extracts.

Supporting Information

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Table containing additional details regarding the topics included in the Health Canada Indoor Air Study of November 2002−March 2003. Survey questions were abbreviated and include only those relevant to settled house dust. This material is available free of charge via the Internet at http://pubs.acs.org.

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Author Information

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Corresponding Author
- Paul A. White - Safe Environments Programme, Healthy Environments and Consumer Safety Branch, Health Canada, Tunney’s Pasture 0803A, Ottawa, Ontario, Canada, K1A 0K9
Authors
- Rebecca M. Maertens - Safe Environments Programme, Healthy Environments and Consumer Safety Branch, Health Canada, Tunney’s Pasture 0803A, Ottawa, Ontario, Canada, K1A 0K9
- Xiaofeng Yang - Safe Environments Programme, Healthy Environments and Consumer Safety Branch, Health Canada, Tunney’s Pasture 0803A, Ottawa, Ontario, Canada, K1A 0K9
- Jiping Zhu - Safe Environments Programme, Healthy Environments and Consumer Safety Branch, Health Canada, Tunney’s Pasture 0803A, Ottawa, Ontario, Canada, K1A 0K9
- Rémi W. Gagne - Safe Environments Programme, Healthy Environments and Consumer Safety Branch, Health Canada, Tunney’s Pasture 0803A, Ottawa, Ontario, Canada, K1A 0K9
- George R. Douglas - Safe Environments Programme, Healthy Environments and Consumer Safety Branch, Health Canada, Tunney’s Pasture 0803A, Ottawa, Ontario, Canada, K1A 0K9

Acknowledgment

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Funding for this work was provided under the Canadian Regulatory Strategy for Biotechnology and the Canadian Environmental Protection Act. We are grateful to Jennifer Bailey for technical assistance in dust preparation, Ron Newhook and Leonora Marro for questionnaire design and house selection, and Peter Bothwell, Ed Sieradzinski, and Yong-lai Feng for field work. We would also like to thank Guosheng Chen and Rocio Aranda-Rodriguez for valuable comments and criticisms.

References

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The risk to human health posed by contaminated soil in a residential area depends on the potential extent of exposure to soil and on the toxic properties of the contaminants. A detailed soil exposure analysis is presented for young children, older children, and adults living in a house surrounded by contaminated soil. From this analysis, a lifetime exposure model is derived and used to assess chronic health risks.
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Regulatory toxicology and pharmacology : RTP (1989), 10 (2), 123-37 ISSN:0273-2300.
Sixty-four children aged 1-4 years were evaluated for the extent to which they ingest soil. The study followed the soil tracer methodology of S. Binder, D. Sokal, and D. Maughan (1986, Arch. Environ. Health, 41, 341-345). However, the present study included a number of modifications from the Binder et al. study. The principal new features were (1) increasing the tracer elements from three to eight; (2) using a mass-balance approach so that the contribution of food and medicine ingestion would be considered; (3) extending the period of observation from 3 days to 8 days; and (4) validating the methodology by having adult volunteers ingest known amounts of soil in a mass-balance validation study. The principal findings reveal the following. (1) The adult study confirmed the validity of the tracer methodology to estimate soil ingestion. (2) Of the eight tracers employed in the adult study, only Al, Si, and Y provided sufficient recovery data that was directly acceptably stable and reliable. (3) If food ingestion determinations were taken into consideration, the median estimates of soil ingestion from the eight tracers ranged from a low of 9 mg/day (Y) to a high of 96 mg/day (V); the median values of Al, Si, and Y, the three most reliable tracers, ranged from 9 mg/day to 40 mg/day. (4) One child had soil ingestion values ranging from 5 to 8 g/day, depending on the tracer. (5) If food ingestion had not been considered, the estimates of soil ingestion would have increased about two- to sixfold, depending on the tracer with Ti and Y being most affected by food intake. (6) Since soil and dust samples did not significantly differ in their levels of tracer elements, no reliable differentiation between the contribution of ingestion of dust and soil could be made. (7) These findings are generally consistent with the previously reported findings of Binder et al. (1986) and P. Clausing, B. Brunekreff, and J.H. van Wijnen (1987, Int. Arch. Occup. Med., 59, 73) if these latter studies are corrected for ingestion of tracers in food and medicine. The findings also account for the apparent discrepancy between the estimates from Al and Si and estimates based on Ti in previous studies. Thus the elevated estimates of soil ingestion by Ti were substantially reduced when food ingestion is considered.
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PAHs form during the incomplete combustion of org. substances and hence they are distributed ubiquitously in the environment. PAHs in the diet are the main source of exposure in man. In 1997 a new source of potential PAH exposure was discovered: very high levels of polycyclic arom. hydrocarbons (PAHs) and benzo-a-pyrene (BaP) were detected in household dust from former American Forces housing in Frankfurt am Main, Germany, built in 1955/1956. This contamination was caused by a parquet glue contg. coal tar, the use of which was formerly std. building practice in Germany. Because the inhabitants of these flats were very concerned about the effects on their health, they were offered the opportunity to take part in biomonitoring examns. to assess individual internal PAH exposure. Participants and methods: 1213 inhabitants from 511 flats/houses took part in the investigation; this corresponds to 12.7% of the total inhabitants of the former US housing estates in Frankfurt am Main. Spot urine samples were collected and frozen until anal. for 1-, 2-, 3- and 4-hydroxyphenanthrene and 1-hydroxypyrene, which was carried out using a very sensitive and practical high performance liq. chromatog. method with fluorescence detection, approved by the Deutsche Forschungsgemeinschaft. Results: The level of internal exposure to PAHs in study participants living in homes where parquet glue contg. PAHs had been used did not differ from the levels found in particpants in whose homes PAH-contg. parquet glue was not used. This was true for the whole group as well as subgroups divided according to age and smoking behavior. Internal exposure was not influenced by different levels of external exposure (BaP in parquet glue and in household dust). Spearman rank correlations between the level of BaP in parquet glue and in household dust were low and insignificant. Conclusion: An increase in internal PAH exposure due to high levels of PAHs in parquet glue and household dust could not be detected. This confirms earlier results with small collectives, where only low and insignificant trends were found towards higher internal PAH exposure caused by contaminated homes. Therefore, the ad-hoc working group of the Commission for Indoor Air Quality of the German Federal Environmental Agency stated that a definitive threshold limit value cannot be defined for PAH contamination in parquet glue and household dust. For reasons of disease prevention, however, BaP contamination in household dust exceeding 10 mg/kg should be minimized.
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Figure 1. Excess cancer risks resulting from nondietary ingestion of B2 PAHs in SHD during preschool years. Three ingestion rates (IR) are considered. Arrow denotes the 90th percentile of the B2 PAH concentrations.
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  Investigations of indoor air pollution by different heating systems in private homes are described. A total of 16 homes, 7 with coal burning, 1 with open fireplace (wood burning), and 8 with central heating were studied. CO, CO2, and sedimented dust concns. were measured in indoor air, and total suspended particulates, heavy metals, and of polycyclic arom. hydrocarbons were measured in indoor and outdoor air. Measurements were made during winter (heating period) and summer (non-heating period). Generally, higher indoor air pollution, (CO, sedimented dust, and some heavy metals) was obsd. in homes with coal burning and open fireplace vs. homes with central heating. In one case, high indoor air pollution was obsd. in a home with central heating. This apartment was on the ground floor of a block of flats and the basement central heating system had a malfunctioning exhaust system.
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15. 15
  Mitra, S.; Ray, B. Patterns and sources of polycyclic aromatic hydrocarbons and their derivatives in indoor air Atmos. Environ. 1995, 29, 3345– 3356
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  Patterns and sources of polycyclic aromatic hydrocarbons and their derivatives in indoor air
  Mitra, Somenath; Ray, Bonnie
  Atmospheric Environment (1995), 29 (22), 3345-56CODEN: AENVEQ; ISSN:1352-2310. (Elsevier)
  Select polycyclic arom. hydrocarbons (PAHs), their derivs., and nicotine were measured in eight homes in Columbus, Ohio, during the winter of 1986/1987 (Chuang et al. 1988). These homes had different indoor PAH sources, namely, environmental tobacco smoke, gas cooking/heating, and elec. cooking stoves. We use a combination of correlation anal., factor anal. and multiple regression to identify and apportion the different sources of PAHs. We find that, of all the sources, environmental tobacco smoke appears to have the greatest impact on the total indoor PAH concns. In smokers' homes, more than 87% of the total PAH is due to this source. Background sources are the largest contributor to PAHs in nonsmokers' homes. We also study the source apportionment of total extractable org. material (EOM) measured in the homes. In smokers' homes, EOM can be attributed mainly to environmental tobacco smoke (49%) and background sources (42%).
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16. 16
  Rogge, W. F.; Hildemann, L. M.; Mazurek, M. A.; Cass, G. R. Sources of fine organic aerosol. Pine, oak, and synthetic log combustion in residential fireplaces Environ. Sci. Technol. 1998, 32, 13– 22
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  Lau, C.; Fiedler, H.; Hutzinger, O.; Schwind, K. H.; Hosseinpour, J. Levels of selected organic compounds in materials for candle production and human exposure to candle emissions Chemosphere 1997, 34, 1623– 1630
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  Lung, S. C.; Hu, S. Generation rates and emission factors of particulate matter and particle-bound polycyclic aromatic hydrocarbons of incense sticks Chemosphere 2003, 50, 673– 679
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  Dubowsky, S. D.; Wallace, L. A.; Buckley, T. J. The contribution of traffic to indoor concentrations of polycyclic aromatic hydrocarbons J. Exposure Anal. Environ. Epidemiol. 1999, 9, 312– 321
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  The contribution of traffic to indoor concentrations of polycyclic aromatic hydrocarbons
  Dubowsky, Sara D.; Wallace, Lance A.; Buckley, Timothy J.
  Journal of Exposure Analysis and Environmental Epidemiology (1999), 9 (4), 312-321CODEN: JEAEE9; ISSN:1053-4245. (Stockton Press)
  A photoelec. aerosol sensor (PAS) was used to measure real-time indoor concns. of polycyclic arom. hydrocarbons (PAHs) at three residences. Semi-quant. measurements of total indoor particle-bound PAH and temp. were collected continuously every minute for approx. 2 wk at each location. The purpose of this study was to examine the effect of traffic on indoor concns. of PAHs. This was accomplished by collecting indoor measurements at an urban, semi-urban, and suburban residential location with varying levels of, and proximity to, traffic. Since the homes were occupied, the effects of cooking, the dominant indoor source, were also examd. among the three nonsmoking households. The results indicate that traffic was the main outdoor source of PAH concns. measured indoors for all locations. In fact, a significant (p<0.001) traffic-related trend in weekday PAH concn. was detected with a geometric mean concn. at the urban location (31 ng/m3) nearly two times that at the semi-urban location (19 ng/m3) and over three times larger than the suburban location (8.0 ng/m3), once adjusted for indoor sources. Hourly av. concn. profiles also revealed weekday rush hour peaks of PAHs at all locations. No pronounced peaks and significantly lower concns. (10, 10, and 4.9 ng/m3) were seen during the weekends for all locations i.e., the urban, semi-urban and suburban locations, resp. Indoor sources including frying/sauteing, broiling, and candle-burning were characterized by peak concn., duration of PAH elevation, and potential dose. This anal. suggests that cooking, and esp. frying/sauteing, may be an important source of indoor PAH concns.
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20. 20
  Polycyclic Aromatic Hydrocarbons; Priority Substances List Assessment Report; Environment Canada, Health Canada: Ottawa, Canada, 1994.
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  Lewis, R. G.; Fortmann, R. C.; Camann, D. Evaluation of methods for monitoring the exposure of small children to pesticides in the residential environment Arch. Environ. Contam. Toxicol. 1994, 26, 37– 46
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22. 22
  Wilson, N. K.; Chuang, J.; Lyu, C.; Menton, R. G.; Morgan, M. K. Aggregate exposures of nine preschool children to persistent organic pollutants at day care and at home J. Exposure Anal. Environ. Epidemiol. 2003, 13, 187– 202
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  22
  Aggregate exposures of nine preschool children to persistent organic pollutants at day care and at home
  Wilson, Nancy K.; Chuang, Jane C.; Lyu, Christopher; Menton, Ronald; Morgan, Marsha K.
  Journal of Exposure Analysis and Environmental Epidemiology (2003), 13 (3), 187-202CODEN: JEAEE9; ISSN:1053-4245. (Nature Publishing Group)
  In the summer of 1997, we measured the aggregate exposures of nine preschool children, aged 2-5 yr, to a suite of org. pesticides and other persistent org. pollutants that are commonly found in the home and school environment. The children attended either of two child day care centers in the Raleigh-Durham-Chapel Hill area of North Carolina and were in day care at least 25 h/wk. Over a 48-h period, we sampled indoor and outdoor air, play area soil and floor dust, as well as duplicate diets, hand surface wipes, and urine for each child at day care and at home. Our target analytes were several polycyclic arom. hydrocarbons (PAH), organochlorine pesticides, and polychlorinated biphenyls (PCB); two organophosphate pesticides (chlorpyrifos and diazinon), the lawn herbicide 2,4-dichlorophenoxyacetic acid (2,4-D), three phenols (pentachlorophenol (PCP), nonyl phenols, and bisphenol-A), 3,5,6-trichloro-2-pyridinol (TCP), and two phthalate esters (benzylbutyl and di-Bu phthalate). In urine, our target analytes were hydroxy-PAH, TCP, 2,4-D, and PCP. To allow estn. of each child's aggregate exposures over the 48-h sampling period, we also used time-activity diaries, which were filled out by each child's teacher at day care and the parent or other primary caregiver at home. In addn., we collected detailed household information that related to potential sources of exposure, such as pesticide use or smoking habits, through questionnaires and field observation. We found that the indoor exposures were greater than those outdoors, that exposures at day care and at home were of similar magnitudes, and that diet contributed greatly to the exposures. The children's potential aggregate doses, calcd. from our data, were generally well below established ref. doses (RfDs) for those compds. for which RfDs are available.
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23. 23
  Wilson, N. K.; Chuang, J. C.; Lyu, C. Levels of persistent organic pollutants in several child day care centers J. Exposure Anal. Environ. Epidemiol. 2001, 11, 449– 458
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  23
  Levels of persistent organic pollutants in several child day care centers
  Wilson, Nancy K.; Chuang, Jane C.; Lyu, Christopher
  Journal of Exposure Analysis and Environmental Epidemiology (2001), 11 (6), 449-458CODEN: JEAEE9; ISSN:1053-4245. (Nature Publishing Group)
  Concns. of a suite of persistent org. chems. were measured in multiple media in 10, child day care centers in central North Carolina. Five centers served mainly children from low-income families, as defined by the federal Women, Infants, and Children Assistance Program, and 5 served mainly children from middle-income families. Targeted chems. were chosen due to their probable carcinogenicity, acute or chronic toxicity, or hypothesized potential for endocrine system disruption. Targeted compds. included polycyclic arom. hydrocarbons (PAH), pentachloro- and nonyl-phenol, bisphenol-A, di-Bu and butylbenzyl phthalate, polychlorinated biphenyls (PCB), organochlorine pesticides, diazinon and chlorpyrifos, and 2,4-D. Sampled media were indoor and outdoor air, food and beverages, indoor dust, and outdoor play area soil. Target compd. concns. were detd. using a combination of extn. and anal. methods, depending on the media. Anal. was predominantly by gas chromatog.-mass spectrometry (GC-MS) or gas chromatog. with electron capture detection (GC-ECD). Targeted pollutant concns. were low and well below levels generally considered of concern as possible health hazards. Potential exposure to target compds. was estd. from concns. in the various media, children's daily time-activity schedules at day care, and best currently available ests. of inhalation rates (8.3 m3/day) and soil ingestion rates (100 mg/day) of children, ages 3-5. Potential exposure to target compds. differed depending on compd. class and sampled media. Potential exposure through dietary ingestion was greater than that through inhalation, which was greater than that through non-dietary ingestion, for all PAH, phenols, and organophosphate and organochlorine pesticides. Potential exposure through dietary ingestion was greater than that through non-dietary ingestion, which was greater than that through inhalation, for those PAH which are probable human carcinogens (B2 PAH), the phthalate esters, and 2,4D. For PCB, exposure through inhalation was greater than that through non-dietary ingestion; exposure through dietary ingestion was smallest. Differences in targeted compd. levels between centers which served mainly low-income clients and those which served mainly middle-income clients were small and depended on the compd. class and the medium.
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24. 24
  Chuang, J. C.; Callahan, P. J.; Lyu, C. W.; Wilson, N. K. Polycyclic aromatic hydrocarbon exposures of children in low-income families J. Exposure Anal. Environ. Epidemiol. 1999, 9, 85– 98
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  24
  Polycyclic aromatic hydrocarbon exposures of children in low-income families
  Chuang J C; Callahan P J; Lyu C W; Wilson N K
  Journal of exposure analysis and environmental epidemiology (1999), 9 (2), 85-98 ISSN:1053-4245.
  Children in low-income families may have high exposures to polycyclic aromatic hydrocarbons (PAH). Such exposures could result from household proximity to heavy traffic or industrial sources, environmental tobacco smoke, contaminated house dust or soil, among others. The objectives of this study were: to establish methods for measuring total PAH exposure of children in low-income families, to estimate the PAH exposures of these children, and to estimate the relative importance of the environmental pathways for PAH exposure. Analytical methods to determine PAH in air, dust, soil, and food and to determine hydroxy-PAH in urine samples were evaluated and validated. A two-home pilot study was conducted in downtown Durham, North Carolina (NC) during February 1994. One smoker's and one nonsmoker's household, which had preschool children and income at or below the official U.S. poverty level, participated. A nine-home winter and a nine-home summer study were conducted in Durham and the NC Piedmont area during February 1995 and August 1995, respectively. A summer study in four smokers' homes was also conducted. In each of these studies, multimedia samples were collected and analyzed for PAH or hydroxy-PAH. Summary statistics, Pearson correlations, and analysis of variance were performed on the combined data from these four field studies. An effective screening method was established for recruiting low-income families. The field protocol involved measurements of three homes in 2-day periods. This protocol should be suitable for large-scale studies. The results showed that indoor PAH levels were generally higher than outdoor PAH levels. Higher indoor PAH levels were observed in the smokers' homes compared to nonsmokers' homes. Higher outdoor PAH levels were found in inner city as opposed to rural areas. The relative concentration trend for PAH in dust and soil was: house dust > entryway dust > pathway soil. The PAH concentrations in adults' food samples were generally higher than those in children's food samples. Children's potential daily doses of PAH were higher than those of adults in the same household, when intakes were normalized to body weights. Inhalation is an important pathway for children's exposure to total PAH because of the high levels of naphthalene present in both indoor and outdoor air. Dietary ingestion and nondietary ingestion pathways became more important for children's exposure to the B2 PAH (ranked as probable human carcinogens, B2 by the U.S. EPA's Integrated Risk System), most of which are of low volatility. The analysis of variance results showed that inner city participants had higher total exposure to B2 PAH than did rural participants.
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25. 25
  Roberts, J. W.; Budd, W. T.; Ruby, M. G.; Bond, A. E.; Lewis, R. G.; Wiener, W.; Camann, D. Development and field testing of a high volume sampler for pesticides and toxics in dust J. Exposure Anal. Environ. Epidemiol. 1991, 1, 143– 155
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  Development and field testing of a high volume sampler for pesticides and toxics in dust
  Roberts, John W.; Budd, William T.; Ruby, Michael G.; Bond, Andrew E.; Lewis, Robert G.; Wiener, Russell W.; Camann, David E.
  Journal of Exposure Analysis and Environmental Epidemiology (1991), 1 (2), 143-55CODEN: JEAEE9; ISSN:1053-4245.
  A high-vol. surface sampler is described which samples dust for pesticides and toxic chems. in nonoccupational exposure studies. The sampler is a high-powered vacuum cleaner equipped with a nozzle that can be adjusted to a specific static pressure and specific air flow within the nozzle, a cyclone to sep. the larger particles from the air stream, a high efficiency quartz fiber filter for particles, and a polyurethane foam plug absorber for semivolatile org. compds. The sampler collects fine dust on either a plush or level loop carpet. The field test involved 9 homes in Jacksonville, Florida, to det. dust loading on the surface and the concn. of pesticides in the dust. Gas chromatog. with electron-capture detection and gas chromatog./mass spectrometry were used to det. the pesticides.
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  Collins, J. F.; Brown, J. P.; Alexeeff, G. V.; Salmon, A. G. Potency equivalency factors for some polycyclic aromatic hydrocarbons and polycyclic aromatic hydrocarbon derivatives Regul. Toxicol. Pharmacol. 1998, 28, 45– 54
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  Potency equivalency factors for some polycyclic aromatic hydrocarbons and polycyclic aromatic hydrocarbon derivatives
  Collins, J. F.; Brown, J. P.; Alexeeff, G. V.; Salmon, A. G.
  Regulatory Toxicology and Pharmacology (1998), 28 (1), 45-54CODEN: RTOPDW; ISSN:0273-2300. (Academic Press)
  Potency equivalency factors (PEFs) for cancer induction relative to benzo[a]pyrene have been derived for 21 polycyclic arom. hydrocarbons (PAHs) and PAH derivs. based on a data preference scheme. PEFs have been derived only for PAHs with demonstrated carcinogenicity in bioassays. Cancer potency values and inhalation unit risks are presented for four addnl. carcinogenic PAHs based on expedited risk assessments conducted for California's Proposition 65. A much larger no. of PAHs and PAH derivs. are considered mutagenic or genotoxic and may have limited evidence for carcinogenicity, but these compds. are not considered in this evaluation. New cancer bioassay data and possibly structure-activity anal. may indicate that addnl. PAHs are carcinogenic. Thus, addnl. PAHs may be identified as potential human carcinogens when such data become available. However, until that time the PEFs proposed for use in risk assessment were estd. only for PAHs currently classified as carcinogens. (c) 1998 Academic Press.
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  Nisbet, I. C.; LaGoy, P. K. Toxic equivalency factors (TEFs) for polycyclic aromatic hydrocarbons (PAHs) Regul. Toxicol. Pharmacol. 1992, 16, 290– 300
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  Toxic equivalency factors (TEFs) for polycyclic aromatic hydrocarbons (PAHs)
  Nisbet, Ian C. T.; LaGoy, Peter K.
  Regulatory Toxicology and Pharmacology (1992), 16 (3), 290-300CODEN: RTOPDW; ISSN:0273-2300.
  The toxicity criteria are not available for all the polycyclic arom. hydrocarbons (PAHs). In the past, EPA has assessed risks posed by mixts. of PAHs by assuming that all carcinogenic PAHs are as potent as benzo[a]pyrene (B[a]P), one of the most potent PAHs. The available information on the toxicity of the PAHs suggests that most are considerably less potent than B[a]P and therefore, the EPA approach is likely to overestimate risks. Several approaches have been developed to allow the relative potency of the different PAHs to be considered in a site-specific risk assessment. This paper evaluates these approaches and presents a modified version that more accurately reflects the state of knowledge on the relative potency of these compds.
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  Assessment of health risk from exposure to contaminated soil
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  The risk to human health posed by contaminated soil in a residential area depends on the potential extent of exposure to soil and on the toxic properties of the contaminants. A detailed soil exposure analysis is presented for young children, older children, and adults living in a house surrounded by contaminated soil. From this analysis, a lifetime exposure model is derived and used to assess chronic health risks.
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  Calabrese, E. J.; Barnes, R.; Stanek III, E. J.; Pastides, H.; Gilbert, C. E.; Veneman, P.; Wang, X.; Lasztity, A.; Kostecki, P. T. How much soil do young children ingest: An epidemiologic study Regul. Toxicol. Pharmacol. 1989, 10, 123– 137
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  How much soil do young children ingest: an epidemiologic study
  Calabrese E J; Barnes R; Stanek E J 3rd; Pastides H; Gilbert C E; Veneman P; Wang X R; Lasztity A; Kostecki P T
  Regulatory toxicology and pharmacology : RTP (1989), 10 (2), 123-37 ISSN:0273-2300.
  Sixty-four children aged 1-4 years were evaluated for the extent to which they ingest soil. The study followed the soil tracer methodology of S. Binder, D. Sokal, and D. Maughan (1986, Arch. Environ. Health, 41, 341-345). However, the present study included a number of modifications from the Binder et al. study. The principal new features were (1) increasing the tracer elements from three to eight; (2) using a mass-balance approach so that the contribution of food and medicine ingestion would be considered; (3) extending the period of observation from 3 days to 8 days; and (4) validating the methodology by having adult volunteers ingest known amounts of soil in a mass-balance validation study. The principal findings reveal the following. (1) The adult study confirmed the validity of the tracer methodology to estimate soil ingestion. (2) Of the eight tracers employed in the adult study, only Al, Si, and Y provided sufficient recovery data that was directly acceptably stable and reliable. (3) If food ingestion determinations were taken into consideration, the median estimates of soil ingestion from the eight tracers ranged from a low of 9 mg/day (Y) to a high of 96 mg/day (V); the median values of Al, Si, and Y, the three most reliable tracers, ranged from 9 mg/day to 40 mg/day. (4) One child had soil ingestion values ranging from 5 to 8 g/day, depending on the tracer. (5) If food ingestion had not been considered, the estimates of soil ingestion would have increased about two- to sixfold, depending on the tracer with Ti and Y being most affected by food intake. (6) Since soil and dust samples did not significantly differ in their levels of tracer elements, no reliable differentiation between the contribution of ingestion of dust and soil could be made. (7) These findings are generally consistent with the previously reported findings of Binder et al. (1986) and P. Clausing, B. Brunekreff, and J.H. van Wijnen (1987, Int. Arch. Occup. Med., 59, 73) if these latter studies are corrected for ingestion of tracers in food and medicine. The findings also account for the apparent discrepancy between the estimates from Al and Si and estimates based on Ti in previous studies. Thus the elevated estimates of soil ingestion by Ti were substantially reduced when food ingestion is considered.
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  Calabrese, E. J.
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  Iglowstein, I.; Jenni, O. G.; Molinari, L.; Largo, R. H. Sleep duration from infancy to adolescence: reference values and generational trends Pediatrics 2003, 111, 302– 307
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  Chuang, J. C.; Chou, Y. L.; Nishioka, M.; Andrews, K.; Pollard, M.; Menton, R. Field Evaluation of Screening Techniques for Polycyclic Aromatic Hydrocarbons, 2,4-Diphenoxyacetic Acid, and Pentachlorophenol in Air, House Dust, Soil, and Total Diet;
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  Internal exposure to PAHs of children and adults living in homes with parquet flooring containing high levels of PAHs in the parquet glue
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Table containing additional details regarding the topics included in the Health Canada Indoor Air Study of November 2002−March 2003. Survey questions were abbreviated and include only those relevant to settled house dust. This material is available free of charge via the Internet at http://pubs.acs.org.
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Mutagenic and Carcinogenic Hazards of Settled House Dust I: Polycyclic Aromatic Hydrocarbon Content and Excess Lifetime Cancer Risk from Preschool Exposure

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Abstract

Synopsis

Introduction

Experimental Section

Study Design and Dust Sample Collection

Sample Preparation

Extraction and Sample Cleanup Procedures

Gas Chromatography–Mass Spectrometry

QA/QC

Cancer Risk Assessment of PAHs in Settled House Dust

Data Analyses

Results and Discussion

Levels of Polycyclic Aromatic Hydrocarbons (PAHs)

Empirical Relationships Between Dust PAH Content and Household Attributes

Cancer Risk Assessment of PAHs in Settled House Dust

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