olycyclic or polynuclear aromatic hydrocarbons (PAHs) are a group of V compounds composed of two or more fused aromatic rings. EPA has identified 16 unsubstituted PAHs as priority pollutants. Some of these PAHs
are
considered to be possible
probable human carcinogens, and hence their distribution in the environment and possible exposure to humans have been the focus of much attention (1, 2). The eight PAHs that are typically considered
CHARLES A. MENZIE BONNIE B. POTOCKI Menzie-Cura & Associates Chelmsford, MA 01824
JOSEPH SANTODONATO New York State Electric & Gas Binghamton, NY 13902
Downloaded via TULANE UNIV on January 9, 2019 at 11:33:18 (UTC). See https://pubs.acs.org/sharingguidelines for options on how to legitimately share published articles.
or
as
are:
possible or probable carcinogens benzo[a]anthracene, chrysene,
benzo[h]fluoranthene, benzo[A]fluoranthene, benzo[a]pyrene, indeno[l,2,3,c-d]pyrene, dibenzo-
[a,h]anthracene and benzo[g,h,i]perylene (1, 2). PAHs are introduced into the environment via natural and anthropogenic combustion processes. Volcanic eruptions and forest and prairie fires are among the major sources of naturally produced
dition, the potential doses of
carcinogenic PAHs are estimated for humans engaged in everyday activities exclusive of occupational settings. The potential doses are estimated as the amounts of PAHs ingested with food, water, soil, or air. We do not consider the potential dose via dermal contact in this paper, but it may be important in some situations. The potential dose is the amount
of
a
chemical that could be ab-
sorbed if the chemical
were
100%
bioavailable. However, exposure to a substance via different pathways
We compiled concentrations of carcinogenic PAHs for water, air, sediment, soil, and food from literature and available monitoring data. For air, sediments, and soil we obtained raw data from national monitoring programs and site investigations for which “background” soil concentrations were reported. We estimated total carcinogenic PAH concentrations from published or raw data provided on the individual compounds. Data reported only as total PAH concentrations were excluded. We reviewed data with regard to the detection limits used in the studies. These detection limits are media specific. Only data generated using appropriate detection limits are used in this paper. Potential doses were calculated for an exposure population comprised of males in the 19 to 50 age group. We expect exposures to women to be somewhat less because they don’t consume as much food on average. For children, absolute doses via food will also probably be less, but
EXPOSURE TO CARCINOGENIC PAHs. However, anthropogenic activities have dramatically increased the quantity of PAHs in the environ-
ment, with the majority emitted from fossil fuel combustion sources such as automobiles, coking plants, asphalt production, and manufacturing facilities that use fossil fuels (2-4). PAHs have been detected in soil, air, sediments, and water (2, 5) and studied in connection with sites where fossil fuels and waste residuals were used or produced. PAHs also occur in various consumer products and food (6). Because PAHs are ubiquitous, humans are exposed to these chemicals as part of everyday living. This review focuses on the subgroup of PAH compounds considered to be possible or probable human carcinogens and examines their concentrations in the environment. In ad1278
Environ. Sci. Technol., Vol. 26, No. 7, 1992
and media does not yield comparable absorbed doses because of differential absorption and matrix effects. In general, chemicals administered to the lung as fine particulates, in aerosol form, or orally via drinking water are expected to be more bioavailable than chemicals administered in solid matrices such as food or soil; bioavailability from soil is expected to be less than from food. Further, the carcinogenic potencies of chemicals may differ depending on route of exposure. Although the importance of pathway and media is recognized, it is difficult to quantify the relationship between potential, applied, and absorbed doses for everyday exposures. Despite these limitations, estimates of potential dose provide insights into relative contributions of sources.
or incidental ingestion of soils will probably be higher because of children’s play activities. The Total Human Environmental
doses from dermal contact
Exposure Study (THEES)
con-
ducted in 1986-87 examined human exposure to benzofajpyrene (BaP) via inhalation and food pathways for 13 households in Phillipsburg, NJ (7, 8). These data provide an important check on the estimates presented here.
PAHs in the Environment Food. Based on a review of the literature (6, 9-11), the general range of carcinogenic PAHs in major U.S, food groups was estimated (Table 1); most of the data are from the 1970s. Food groups were selected to correspond with information available on the dietary habits of the U.S.
0013-936X/92/0926-1278$03.00/0
©
1992 American Chemical Society
population. The ranges shown in the table are averages of many “low” and “high” values reported for food items within each food group. Food groups that tend to have the highest levels of PAHs in-
clude charcoal-broiled
or
smoked
meats, leafy vegetables, grains, and fats and oils. For these food groups,
concentrations of carcinogenic PAHs are typically in the tens of micrograms per kilogram (ppb). The presence of PAHs on leafy vegetables and grains is believed to be caused by atmospheric deposition. Estimates of concentrations in food are uncertain because of limited data, the likelihood that concentrations in vegetable and grain products reflect local conditions in the growing area, and the age of the data (most were collected in the 1970s). The extreme values are greater than those reported in Table 1. We have attempted to capture the range in the central tendency of all the data by separately averaging the low values and high values reported by various studies. Thus, the data should be viewed as an approximate range of concentrations that, on average, may be in the various food groups. The THEES conducted in 1987-88 found that the concentrations of one PAH, BaP, in 58 prepared meals averaged 0.15 pg/kg with a range of 0.005 to 1.17 pg/kg (8). If these values are adjusted for total carcinogenic PAHs [i.e., assuming that BaP is 0.1-0.3 of the total), then this range is similar to that estimated for various food groups. Water. Concentrations of carcinogenic PAHs in water are provided in Table 2 for natural and drinking water supplies. Data are available for raw and treated water within 24 U.S. counties from 1978-81 and for 10 water supplies in the eastern United States. A limited amount of data are available for other surface and groundwater sources. Surface water concentrations of carcinogenic PAHs ranged from 0.1 to 829.6 ng/L. Frequently, surface water concentrations were found between 2 ng/L and 50 ng/L, As anticipated, surface water concentrations were higher than drinking water or groundwater concentrations because of the presence of suspended solids on which many of the PAHs are adsorbed. Groundwater is naturally filtered as it flows through various soil matrices, and PAHs adsorb well to organic soil. Groundwater concentrations reported in the studies ranged from 0.2 ng/L to Environ. Sci. Technol., Vol. 26, No. 7, 1992
1279
TABLE
26 12 12
35 26 12
6, 9 6. 9 9
8
12
6.9
0,10 9
0.10 36
9
carcinogenic PAHs in ambient air range from about 1 ng/m3 to hundreds of ng/m3 (Table 2). The median value for carcinogenic PAHs estimated from the NPN is 2.6 ng/ m3, and 72% of the estimated values are less than 10 ng/m3. The bulk of the higher values falls between 12 and 70 ng/m3. The median value from the NPN data (2.6 ng/m3) was similar to those from other published data (5,7 ng/m3) and for that estimated for the New Jersey data set (4,4 ng/m3). Indoor air levels of carcinogenic PAHs reflect ambient outdoor air as
6, 9, 10, 12
well
1
Concentrations of carcinogenic PAH in food items
Food
Noncharcoal broiled Charcoal broiled or smoked Beef Pork Poultry
Frankfurters/sausage
Average minimum reported values (tig/kg)
Average maximum reported values (Ffl/kg)
0.11
0.69
Reference 10
Fish
Fish/shellfish Smoked fish/shellfish
Vegetables Tomatoes Green leafy vegetables Potatoes/other
1,06 19
1.06 46
11
21
6, 9 6, 9 6, 9, 10
Grains
0.60
9
6, 9, 10
Fruits
0.50
2.40
6, 10
Beverages Nonalcoholic Alcoholic Fluid milk
Other Fats & oils Cheese
2 0.01
27 0.08 0.09
6, 9 6 10
3.40 1.70
66 1.70
6, 9, 10 9, 10
0.04
6.9 ng/L and are probably lower in
many ambient groundwaters.
Treated water (drinking-water) concentrations were distributed over 0,1 ng/L to 61.6 ng/L. Most drinking-water values fell between 1 and 10 ng/L. In the THEES performed in
Phillipsburg, NJ (8), BaP was not detected in drinking water at a detection limit of 0.1 ng/L. The PAH concentration in water can increase as a result of passage through coated distribution pipes (5). An effort was made to obtain cur-
carcinogenic PAH concentrations in drinking water for Chicago, Los Angeles, Detroit, and New Orleans. However, the public water supply departments for these cities stated they do not monitor for PAHs in drinking water. EPA, the American Water Works Association, and the Water Pollution Control Federation were also contacted, but these had no recent data for PAH levels in rent data
on
water or drinking water. Air. We examined air data from published literature gathered during the 1970s [12, 13) and 1980s [14-25, 42, 43) for carcinogenic
raw
PAHs (Table 2). Concentrations varied throughout the country. In the Great Lakes region, levels ranged from 0.2 to 3.0 ng/m3 [13, 14). A similar level of carcinogenic PAHs, 3.5 ng/m3, was observed in a subur1280
Environ. Sci. Technol., Vol. 26, No. 7, 1992
area of Las Vegas, NV (15). In a rural area of Minnesota, total carcinogenic levels in air of 5,7 ng/m3 have been reported (16). Highly urbanized cities have shown levels of
ban
15 ng/m3 and 50 ng/m3 (15, 17, 42).
Data on BaP collected as part of the National Particulate Network (NPN) Program (18) were obtained from the EPA Aerometric Information Retrieval System. The BaP data were generated through analysis of total suspended particulate filter samples collected from 65 sites located in rural and urban areas. These data may underestimate the amount
of BaP because
some
of the
chemical may be lost from the filter as air is drawn through it. We estimated the mean annual concentration of BaP for each of these sites for the period of record. Because other studies (Table 2) indicated that BaP comprises between 5% and 30% of carcinogenic PAHs in outdoor air, we selected a value of 10% (i.e., we multiplied by 10) to estimate carcinogenic PAHs in air from the NPN data for BaP. During the THEES in New Jersey (3), outdoor PM10 measurements revealed a mean BaP concentration of 0.9 ng/m3, which was at approximately the 70th percentile based on our examination of the NPN data. The resultant estimates of total
as
indoor
sources.
Approxi-
mately 50% of outdoor particulate concentration of BaP has been estimated to penetrate indoors (3). Concentrations can be spatially and temporally variable within homes (20, 42). Levels in a typical clean office environment were about 1.5 ng/m3 in one study (19). Median indoor air levels of carcinogenic PAHs in homes appear to be on the order of 8 ng/m3 with a range of less than 1 ng/m3 and maximum values in the 30-80 ng/m3 range. Carcinogenic PAHs in air can be locally elevated as part of everyday activities such as residential wood and coal burning, mainstream and sidestream tobacco smoke, and certain traffic conditions. These activities contribute to temporal variations in indoor and outdoor air. Carcinogenic PAHs can be emitted into homes from improperly operated stoves and fireplaces (21). For example, in a Wisconsin study of seven homes, carcinogenic PAH concentrations ranged up to 100 times higher when wood stoves were in operation; indoor air levels 1.7-12.6 ng/m3 (22). Tobacco smoke can be a major source of carcinogenic PAHs. Mainstream smoke from unfiltered cigarettes may contain 0.1-0.25 gg/cigarette of carcinogenic PAHs (23). Indoor air levels associated with sidestream tobacco smoke have been reported in the range of 329 ng/m3 (Table 2), and tobacco smoke is recognized as an important contributor to indoor air levels were
(8, 23, 43).
Certain traffic conditions can result in comparatively high levels of carcinogenic PAHs in air. For example, average concentrations of 58 and 253 ng/m3 were observed for two studies of the Baltimore Harbor tunnel (24). Soil. Data on carcinogenic PAHs in “ambient” soils were obtained from a review of the literature and
TABLE 2
Carcinogenic PAH concentrations in environmental media Media
Number of slte&'studies
Water Surface water* Groundwater Drinking water
25 10 10
Air Outdoor Published studies NPN data based on TSP New Jersey data based on TSP Columbus, OH“ Indoor Clean office Homes (Ohio) Homes (New Jersey) Homes with tobacco smoke Rooms with tobacco smoke Rooms with wood stoves Room with kerosene heater Room without kerosene heater
28 85 27 12 1
9 10 4
7 1 1
Soil Forest Rural Urban Road dust
16
8 15 7
Median concentration
Range concentration
ng/L
ng/L 8.0
2.8
0.1-830 0.2-6.9 0.1-62
ng/m3
ng/m3
1.2
5.7
2.6“ 4.4a 13.0
Reference
0.2-65 1.0-146.0“ 2-9“
5, 12, 14 5, 12 5, 12
2, 13-17, 24 18 25
2-75
42
0.6-29 1,0-80a 7-29 3-23
42
1.5
19
8 9a
13.0
3.8 15.0 1.6
2~13
mg/kg (dry wt.) 0.05 0.07 1.10 137.0
mg/kg (dry wt.)
7 42 23 22
43 43
0.01-1.3 0.01-1.01 0.06-5.8
8-336
2, 2, 2, 2,
26-32 26-32 26-32
26-32
Sediment 1.4 Published studies* 65 0.1 NOAA status and trends data 148 “Total carcinogenic PAH was estimated by multiplying reported BaP concentration by 10 (see text). 6
0.003-232 0.002-13.21
2
33
Biased toward locations where sediments or water were contaminated. “Associated with the indoor air monitoring program for Ohio.
from our analysis of site investigation reports that present data for “background samples” (2, 9, 2632)-, measurements are from the late 1970s and the 1980s (Table 2). Most of the latter data were taken from reports assembled as part of programs conducted by the Gas Research Institute and the Electric Power Research Institute. Carcinogenic PAHs are found in all surface soils. Typical concentrations in forest soil range from 5 gg/kg to 100 gg/kg. These concentrations indicate nonanthropogenic
well as anthropogenic sources of PAHs. Plant synthesis, forest and prairie fires, and volcanic activity contribute to natural background PAH levels. Elevated PAH concentrations in forest soils near major highways and industries may be attributed to air pollution. Soils in some forests exhibit carcinogenic PAH concentrations on the order of 1000 gg/kg. Substantial amounts of PAHs are transferred to forest soil via vegetative litterfall because the compounds adsorb from air onto organic matter such as broad-leaf and needle surfaces (30). Rural soils typically contain caras
cinogenic PAHs. At the Rothamsted Experimental Station in southeastern England, regional atmospheric fallout is considered the principal source of carcinogenic PAHs to the rural soils {29). It has become apparent that in the 20th century, PAH agricultural soil concentrations have increased in industrialized areas (27). The representative span for agricultural soils is 10-100 gg/kg. The highest concentration of carcinogenic PAHs reported for agricultural soils is about 1000 gg/kg, similar to forest soils. As anticipated, metropolitan areas have higher soil concentrations of carcinogenic PAHs than do forest and agricultural soils because of the proximity of urban areas to sources of fossil fuel combustion. The majority of urban soil concentrations fall in the 600-3000 gg/kg range. Higher values near areas of heavy transportation or industrialization are probable. In our view values on the order of 1000-3000 gg/kg (1-3 ppm) are in the upper range of typical urban background. The highest ambient concentrations of carcinogenic PAHs in soils have been reported for road dust, which
contain levels of 8000-336,000 gg/kg (8-336 ppm). We suspect that the high “urban” values reported in the literature (200 ppm) are probably mostly road dust. Sediment. Data on carcinogenic PAHs in sediments were obtained from a review of the literature (2) and our analysis of the National Oceanic and Atmospheric Administration (NOAA) Status and Trends data obtained during the 1980s for coastal sediments (33) (Table 2). Published values varied widely and ranged from 0.003 mg/kg for a coral reef area to 232 mg/kg for a polluted area in Boston Harbor. We calculated the concentrations of carcinogenic PAHs for 612 sediment samples in which carcinogenic PAHs were detected from approximately 200 coastal and estuarine sites distributed throughout the Atlantic, Pacific, and Gulf coasts. The frequency distribution of these data indicated a median value of 0.1 mg/kg (ppm) and a maximum value of 13.2 mg/kg. can
Potential dose Estimates of potential dose were developed for a “reference man” beEnviron. Sci. Technol., Vol. 26, No. 7, 1992
1281
tween 19 and 50 years of age. The
estimates are presented on a total body basis and are in units of micrograms per day. From food. Statistics available from the U.S. Department of Agriculture (34, 35} were used to determine an average diet for U.S. males and to estimate components of a vegetarian diet and a heavy meat diet comprising products with high PAH levels. Potential dietary intakes of carcinogenic PAHs in food are illustrated in Figure 1. Each bar is designated “low” or “high,” which relates to the general range of PAH concentrations in each food group. For the average American
FIGURE
1
Potential doses of carcinogenic PAHs from food for three U.S. diet types 14
12
10
I
I
WH Grains
and
5
1
pg/day, with unprocessed
grains and cooked meats the greatest sources of the compounds. A who consumes a heavy meat person diet has the highest estimated carcinogenic PAH potential dose, on the
order of 6 to 9 pg/day. Charcoalbroiled or smoked meat and fish are major additional sources of carcino-
genic PAHs. Our estimates of the potential dose of carcinogenic PAHs via the diet are similar to those reported by others (10, 36, 37, 44). However, there are a number of sources of uncertainty in the estimates, including variations among groups in caloric intake and methods of food handling and preparation. In an ideal situation, PAH analysis of prepared meals would be used to characterize the actual carcinogenic PAH potential dose via the diet for a defined population as was done for BaP in the THEES (8). In that study, the estimated mean daily ingestion of BaP in food was approximately 0.1 pg/ day with a range of 0.002 to 1.1 pg/ day. If these numbers are adjusted for total carcinogenic PAHs, they are similar to the lower range of estimates derived for this paper. A vegetarian diet can offer an elevated PAH intake compared with the average diet if it comprises leafy vegetables (lettuce and spinach) and unrefined grains. It has been suggested (6, 9, 10) that unrefined plant foodstuffs may be the principal source of ingested PAHs rather than smoked products; our analysis appears to support this suggestion. Atmospheric deposition is considered the primary pathway for PAH contamination of vegetables (38). Broad leafy vegetables contain more PAHs than plants with narrow leaves, which indicates a correlation between plant surface area and 1282
Environ. Sci. Technol., Vol. 26, No. 7, 1992
L_J
Vegetables
B
Beverages
i
H
High
Fruits
CD
High
a
0
High
X < CL
diet, the intake of carcinogenic
PAHs is estimated to be between
Meats/fish
Low
m
i
Average
Low
Low
Vegetarian
Heavy meat
Type of diet
adsorption of atmospheric PAHs. We do not know if the reported data consider washing of the vegetables or how much PAH may remain following washing. Grains contribute a large part of PAH intake to the average diet (58). However, refining or processing harvested grain may reduce the carcinogenic PAH content within the grain before consumption. Others (10) have also concluded that although cereal groups might not have the highest concentration of carcinogenic PAHs, they are a major component by weight of the total diet. From air. To estimate the potential dose of carcinogenic PAHs by inhalation, we made calculations
for nonsmokers as well as for individuals who smoke a pack of cigarettes per day (Figure 2). The potential doses of carcinogenic PAHs via inhalation of ambient air were estimated using the standard EPA assumption that an individual's respiration rate is 20 m3/day (39). This rate was multiplied by 148 ng/m3 (the maximum value estimated for either indoor or outdoor air), 8 ng/m3 (median for indoor air of homes), and 1 ng/m3 (typical minimum value for indoor and outdoor air). These values span the range of reported indoor air levels including exposure to secondary tobacco smoke (3-29 ng/m3) and emissions from woodstoves (1.7-12.6 pg/m3). Thus, the selected values provide a reasonable range for exposure to PAHs in air. The estimated potential doses range between about
0.02 pg/day and 3 pg/day for inhalation. The median value was 0.16 pg/ day. Because people in the United States spend more than 70% of their
time indoors, and employed adults average less than 45 min/day outdoors, inhalation of indoor air is likely to be an important route of exposure (20). For an individual who smokes a pack of unfiltered cigarettes a day, the potential dose of carcinogenic PAHs due to mainstream smoke is estimated to be an additional 2 to 5 pg/day. Thus, tobacco smoking can significantly contribute to the potential dose via inhalation, A chain smoker might smoke three packs per day; for unfiltered cigarettes this could result in a potential dose of 6 to 15 pg/day. From water. Assuming an average drinking-water consumption rate of 2 L/day (39), the potential
dose of carcinogenic PAHs via drinking water [Figure 2) ranges between 0.0002 pg/day and 0.12 pg/ day based on the concentration range given in Table 2. The median value was 0.006 pg/day. From incidental ingestion of soil. Incidental ingestion of soil by adult males was estimated to be on the order of a few milligrams a day; we used 50 mg/day of soil based on LaGoy (40), but recognize that this estimate is uncertain and likely to be conservative. Soil ingestion rates on the order of 50 mg/day are more typical for small children (41). Potential dose of carcinogenic PAHs via incidental soil ingestion
tered cigarettes may have a potential dose twice that of nonsmokers. These estimates of potential dose do not include occupational exposures or doses associated with use of consumer products such as cosmetics applied to the skin or various asphaltic materials applied to roofs or driveways. Use of these products will increase an individual’s potential dermal or inhalation dose of PAH compounds.
FIGURE 2
Potential doses of carcinogenic PAHs from various media® 10
Mainstream Ambient air tobacco smoke0 *
°
Drinking water
Incidental ingestion of soil
Ranges and median or middle values are depicted. One pack of unfiltered cigarettes.
Charles A. Menzie is principal and founder of Menzie-Cura, Inc., an environmental consulting firm in Chelmsford, MA. Previously, he was a manager
TABLE 3
Comparison of p otential doses of carcinogenic PAHs Maximum values
Median values
Percent of total
Intake (ng/day)
Source of PAHs
Intake (Mg/day)
Percent of total
Nonsmokers 3 0.05 0.006 0.06 3.12
Food Air Water Soil Total
Mainstream smoke
Total
12
2.70 0.124 0.4 15.22
79 18 1
2
100
Smokers (nonfittered cigarettes) 2-5 6-15 (1
All other sources
96.2 1.6 0.2 1.9 100.00
of environmental services at EG&G Environmental Consultants. He has an M.A. degree from City College of New York and a Ph.D. in environmental science from City University of New York.
3
(3 packs/day) 15
5-S
21-30
pack/day)
at 50 mg/day is shown in Figure 2, The estimates are based on maximum, median, and minimum concentrations of carcinogenic PAHs from Table 2 for urban and rural soils. For urban populations, the
potential dose of carcinogenic
PAHs ranged from 0.003 to 0.3 pg/ day. The median value was 0.06 pg/ day. If some of the soil that is incidentally ingested is road dust tracked into homes, then the potential doses would be higher.
Comparison of ambient sources Food may be the main source of carcinogenic PAHs for nonsmokers and is generally one to two orders of magnitude higher than any other source (Table 3]. In certain cases where urban air contains the highest ambient concentrations of PAHs, air is a major contributing source. The THEES (8) also com-
pared the importance of the ingestion and inhalation routes for BaP. The study indicated that the range and magnitude of dietary exposures were much greater than for inhalation; nevertheless, there were ample individual cases where inhalation of BaP was the predominant exposure
Bonnie B. Potocki holds a B.S. degree from the University of Connecticut and is an M.S. degree candidate in environmental toxicology at Northeastern University.
route.
Drinking water and ambient soils are minor sources of these compounds. The importance of soil as a
depends on the assumptions made concerning incidental ingestion. We have assumed that an adult source
would incidentally ingest 50 mg/ day of soil. The total potential dose of carcinogenic PAHs for adult males who nonsmokers is estimated to be a median 3 pg/day and a maximum 15 pg/day. Mainstream tobacco smoke is a substantial additional potential dose. Smokers of nonfilare
Joseph Santodonato has an M.S. degree
from the State University of New York at Buffalo and a Ph.D. in environmental science from SUNY-Syracuse. He is a certified industrial hygienist specializing in chemical toxicology and risk assessment and a senior compliance specialist for New York State Electric & Gas Corp. Environ. Sci. Tech not, Vol. 26, No. 7, 1992
1283
Summary Carcinogenic PAH compounds are introduced into the environment by natural and anthropogenic sources and are present in food, air, water, and soil. Food and air appear to be the major sources of these compounds for humans engaged in everyday activities. Collectively they yield doses of between 1 and 15 pg/day. For individuals who smoke one or more packs of unfiltered cigarettes a day, there may be an additional dose of between 2 and 15 pg/day. These estimates of potential dose can serve as rough benchmarks against which other of PAHs can be compared. sources
(9)
References
C10^
Evaluation and Estimation of Potential Carcinogenic Risks of Polynuclear Aromatic Hydrocarbons; Carcinogen Assessment Group, Office of Health and Environmental Assessment. Office of Research and Development. U.S. Environmental Protection Agency: Washington, DC, 1985. Gas Research Institute. Management of Manufactured Gas Plant Sites: Risk Assessment; Gas Research Institute: Chicago, IL, 1987; Vol. Ill, GRI-87/
(1)
(2)
0260.3.
Locating and Estimating Air Emis-
(3)
(4)
(5) (6)
j8)
(11)
sions From Sources of Polycyclic Organic Matter; Office of Air Quality Planning and Standards. U.S. Environmental Protection Agency: Research Triangle Park, NC, 1987. Sources and Emissions of Polycyclic Organic Matter; Pollutant Assessment Branch. Office of Air Quality Planning and Standards. U.S. Environmental Protection Agency: Research Triangle Park, NC, 1983. Basu, D. K.; Saxena, J. Chemosphere 1987, 16, 2595-612. Bjorseth, A. Handbook of Polycyclic Aromatic Hydrocarbons; Marcel Dekker: New York, 1983. Lioy, P. L. et al. Arch. Environ. Health 1988, 43, 304-12. Waldman, J. M. et al. /. Exp. Anal. Environ. Epid. 1991, 1, 193-225. Crosby, N. T. et al. Analyst 1981, 106, 135-45. Dennis, M. J. et al. Food Chem. Toxicol. 1983, 21, 569-74.
Toxicological Profile for Polycyclic
Aromatic Hydrocarbons (Draft); Agency for Toxic Substances and Disease Registry. U.S. Public Health Service; Atlanta, GA, 1989. (12) Ambient Water Quality Criteria for Polynuclear Aromatic Hydrocarbons; Office of Water. U.S. Environmental Protection Agency: Washington, DC,
gjifilar eabcH^
vironmental Management Project;
U.S. Environmental Protection Agency Region VIII. Environmental Services Division. Air & Toxics Division. Air Toxic Branch: Denver, CO, 1989,
Environmental Protection Agency. Air Toxic Clearinghouse. Aerometric Information Retrieval System Quick Look Report, National Particulate Network, Benzo[a]pyrene/ Total Suspended Particulate Data
(18) U.S.
(19) (20)
(21)
Fax: 614-447-3671
Telex: 440159 ACSP Ul or 892582 ACSPUBS
1284
Environ. Sci. Technol., Vol. 26, No. 7, 1992
1986. (27) Edwards, N. /. Environ. Qual. 1983, 12, 427-41. (28) Gas Research
Institute/Electric Power
Research Institute Database for PAHs
(29) (30) (31)
(32)
in Freshwater Sediment and Soil from Site Investigations; Chicago, IL (unpublished). Jones, K. C. et al. Environ. Sci. Technol. 1989, 23, 95-101. Matzner, E. Water, Air Soil Pollut. 1984, 21, 425-34. Pucknat, A. W. Characteristics of PNA in the environment. Health impacts of polynuclear aromatic hydrocarbons; Noyes Data Corporation: Park Ridge, NJ, 1981; pp. 78-122. Smith, M. A. Tentative Guidelines for Acceptable Concentrations of Contaminants in Soils; Issued by CDEP, England, 1981; ICRCL 47/81. A Summary of Selected Data on Chemical Contaminants in Sediments Collected During 1984, 1985, 1986, and 1987; National Status & Trends Program for Marine Environmental Quality. National Oceanic and Atmo-
MD, 1988. (34) Pao, E. M. et al. Home Economics Research Report No. 44; U.S. Department of Agriculture: Washington, DC,
Call Toll Free (within the U.S.): 1 -800-333-9511 Outside the U.S., Call: 614-447-3776
Cable Address: JIECHEM Or Mail your order to: American Chemical Society Department L0011 Columbus, OH 43268-0011
Edison Institute: Annapolis, MD,
Testing Report for 1989-1990; Department of Transportation: Las Vegas, NV. (16) Hennepin County Preoperational Incinerator Siting Report from 19871989; Radian Corporation, Minnesota Pollution Control Agency: St. Paul, MN, 1989. (17) Data Summary Report on the Air Toxics Monitoring Program for the Denver Metropolitan Area Integrated En-
Each month, INDUSTRIAL &
ENGINEERING CHEMISTRY RESEARCH delivers peer-reviewed, primary research on the fundamental and theoretical aspects of chemical engineering,..process design and development...and.product R&D. Be Prepared—Subscribe Today!
dards for Groundwater and Soil”; prepared by Dames & Moore Co.; Electric
(33)
PUBLISHED MONTHLY Editor: Donald R. Paul Univ. of Texas, Austin
Quality information that gives you the leading edge
102. (24) Benner, B.; Gordon, G.; Wise, S. A. Environ. Sci. Technol. 1989, 23, 1269-78. (25) Harkov, R. et al. Environ. Sci. Technol. 1984, 18, 287-91. (26) “How Clean is Clean? Clean-up Stan-
1980. (13) Eisenreich, S. Environ. Sci. Technol. 1981, 15, 30-38. (14) Baker, J.; Eisenreich, S. Environ. Sci. Technol. 1990, 24, 342-52. (15) Preliminary Clark County, Nevada
Special Monitoring and Emission
IND^ScERING.
Cooper, C. S.; Grover, P. L., Eds.; Springer Verlag: New York; pp. 63-
(22)
1986-1989. Wilson, N. K. et al. Environ. Sci. Technol. 1989, 23, 1112-16. Lioy, P. J.; Panitz, E. New Jersey Medicine 1988, 85, 921-26. McCrillis, R.; Burnet, P. “Effects of Operating Variables on Emissions from Wood Stoves”; Proceedings of 1988 EPA/APCA International Symposium Measurement of Toxic and Related Air Pollutants; Research Triangle Park, NC. Daisey, J. Environ. Int. 1989, 15, 43542.
(23) Hoffman, D.; Hecht, S. S. In Chemical Carcinogenesis and Mutagenesis I;
spheric Administration: Rockville,
1982. (35) Nationwide Food Consumption Sur-
of Food Intakes by Individuals, Men 19-50 years, 1 Day, 1985; United States Department of Agriculture. Human Nutrition Information Service. Nutrition Monitoring Division; United States Department of Agriculture: Washington, DC, 1986; Report No. 86-1. (36) Vaessen, H. A. et al. Toxicol. Environ. vey: Continuing Survey
Chem. 1988, 16, 281-94. (37) Speer, K; Montag, A. Oelen. Fat Sci. Technol. 1988, 90, 163-67. (38) Jones, K. C.; Grimmer, J.; Johnston,
A. E. Science of the Total Environ-
ment 1989, 78, 117-30. (39) Exposure Factors Handbook; U.S. En-
vironmental Protection
Agency:
Washington, DC, 1989; EPA/600/889/043.
(40) LaGoy, P. Risk Analysis 1987, 7, 35559. (41) Thompson, K. M.; Burmaster, D. E. Risk Analysis 1991, 11, 339-42. (42) Chuang, J. C. et al. Pilot Study of Sam-
pling and Analysis for Polynuclear Aromatic Compounds in Indoor Air; Washington, DC, December 1986; EPA/600/4-86/03 6, NTIS PB87129524.
J. L. et al. Environ. Sci. Technol. 1991, 25, 1732-38. (44) Santodonato, J. et al. /. Environ. Path. Toxicol. 1981, 54, 1-364.
(43)
Mumford,
