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PUBLIC HEALTH ASSESSMENT

Air Addendum

AMOCO-SUGAR CREEK
(a/k/a AMOCO-SUGAR CREEK)
SUGAR CREEK, JACKSON COUNTY, MISSOURI

A. FIGURES

Site Location Map
Figure 1. Site Location Map

Intro Map
Figure 2. Intro Map

Norledge Area Air Sampling Locations - 1999
Figure 3. Norledge Area Air Sampling Locations - 1999

B. TABLES

Table 1.

Off-site Air Benzene Levels* Amoco - Sugar Creek, Missouri
Sampling Date Benzene Levels at Home 1 (g/m3) Benzene Levels at Home 2 (g/m3) Benzene Levels at Home 3 (g/m3) Benzene Levels at Home 4 (g/m3) Benzene Levels at Home 5 (g/m3) Benzene Levels at Home 6 (g/m3) Benzene Levels at Home 7 (g/m3) Benzene Outdoor Levels (g/m3)
June 1999 33 - 57 48 - 70 1.3 - 1.9 2.8 - 4.1 0.58 - 0.99 1.6 - 4.2 12 - 18 0.31 - 0.86
July 1999 0.81 - 2.3 NA NA 2.1 - 2.5 NA 1.3 - 2.2 NA 0.40 - 2.4

* Source: Environmental Protection Agency. 1999. Indoor air report provided by Leland Grooms, EPA: analysis request report for activity: ELG01, description: basement sampling. EPA Region 7: Kansas City, Kansas.

ATSDR Benzene comparison values for the air media:
0.1 g/m3 or 0.03 ppb = Cancer Risk Evaluation Guide
13 g/m3 or 4 ppb = Intermediate Environmental Media Evaluation Guide
160 g/m3 or 50 ppb = Acute Environmental Media Evaluation Guide

g/m3 micrograms per cubic meter of air
NA not applicable (only three of the seven homes were re-sampled in July 1999)
ppb parts per billion

Table 2.

Off-site Air Sampling Results for June and July 1999* Amoco - Sugar Creek, Missouri
Compound Indoor Concentration Range (g/m3) Max. Conc. Sampling LocationOutdoor Concentration Range (g/m3) Comparison Value (g/m3)
Acetone ND - 1,700 Home 1 9.4 - 75 31,000
(13,000 ppb)
Chronic EMEG
Acrylonitrile ND - 1.9 Home 2 ND - 1.3 0.01 CREG
2 RfC
Allyl chloride ND - 1.1 Home 1 ND 1 RfC
Benzene 0.58 - 70 Home 2 0.31 - 2.4 0.1 CREG
13
(4 ppb)
IEMEG
Bromomethane ND - 1.4 Home 1 ND 5.1 RBC (n)
Bromodichloromethane ND - 0.25 Home 4 ND 0.1 RBC (c)
Butanal ND - 42 Home 3 ND - 28 None  
1-Butanol ND - 3.6 J Home 1 ND - 3.3 J 370 RBC (n)
2-Butanol ND - 0.56 Home 4 ND - 0.24 J None  
2-Butanone ND - 26 Home 2 0.81 - 11 1,000 RfC
Carbon disulfide ND - 7.3 Home 3 ND - 3.2 930
(300 ppb)
Chronic EMEG
700 RfC
Carbon tetrachloride 0.59 - 0.85 Home 3 0.59 - 0.83 0.07 CREG
310
(50 ppb)
IEMEG
Chloroethane ND - 0.27 Home 4 ND 10,000 RfC
Chloroform ND - 7.1 Home 3 ND - 0.21 0.04 CREG
98
(20 ppb)
Chronic EMEG
240
(50 ppb)
IEMEG
Chloromethane 0.88 - 6.8 Home 7 ND - 1.2 103
(50 ppb)
Chronic EMEG
410
(200 ppb)
IEMEG
Decane ND - 20 Home 4 ND - 0.54 2,100
(600 ppb)
Chronic EMEGb
1,2-Dichlorobenzene ND - 0.29 Home 1 ND - 0.43 33 RBC (n)
1,3-Dichlorobenzene ND - 0.23 Home 1 ND 3.3 - 320 RBC (n)
1,2-Dichloroethane ND - 0.46 Home 4 ND 0.04 CREG
810
(200 ppb)
Chronic EMEG
Ethyl benzene ND - 46 Home 1 ND - 1.5 870
(200 ppb)
IEMEG
1,000 RfC
Heptanal ND - 63 J Home 2 ND - 13 None  
Heptane ND - 29 Home 1 ND 2,100
(600 ppb)
Chronic EMEG
Hexane ND - 58 Home 2 ND - 2.6 2,100
(600 ppb)
Chronic EMEG
2-Hexanone ND - 2.4 Home 2 ND - 1.2 J None  
Isopropylbenzene ND - 3.0 Home 1 ND None  
Methylene Chloride ND - 83 Home 3 1.3 - 14 3 CREG
1,000
(300 ppb)
IEMEG
1,000
(300 ppb)
Chronic EMEG
4-Methyl-2-pentanone
(Methyl Isobutyl Ketone)
ND - 4.3 Home 2 ND - 0.61 J 205,000
(50,000 ppb)
TLV
2-Methyl-2-propanol
(tert-butyl alcohol)
ND - 32 Home 1 ND - 0.43 303,000
(100,000 ppb)
TLV
Nonane ND - 12 J Home 1 ND - 0.56 J 2,100
(600 ppb)
Chronic EMEG
Octane ND - 11 Home 2 ND - 0.26 2,100
(600 ppb)
Chronic EMEG
Pentanal (n-Valeraldehyde) ND - 20 Home 4 0.82 - 18 176,000
(50,000 ppb)
TLV
Pentane 0.24 - 160 Home 2 0.52 - 3.8 1,770,000
(600,000 ppb)
TLV
2-Pentanone
(Methyl Propyl Ketone)
ND - 11 Home 1 ND - 3.7 J 705,000
(200,000 ppb)
TLV
3-Pentanone
(Diethyl Ketone)
ND - 1.9 Home 1 ND - 0.40 705,000
(200,000 ppb)
TLV
Propanal
(Propionaldehyde)
ND - 82 J Home 2 1.7 - 59 240**
(100 ppb)
 
1-Propanol
(n-Propyl Alcohol)
ND - 4.3 Home 3 ND - 0.93 Only slightly more toxic than isopropyl alcohol. (See isopropyl alcohol.)
2-Propanol
(Isopropyl Alcohol)
ND - 50 Home 2 ND - 5.1 Used in after shave & rubbing alcohol. Not significantly toxic below 980,000 ug/m3 (400,000 ppb).
Styrene ND - 7 Home 2 ND 255
(60 ppb)
Chronic EMEG
1,000 RfC
Tetrachloroethylene ND - 11 Home 4 ND - 0.43 2 CREG
270
(40 ppb)
Chronic EMEG
Toluene 0.97 - 380 Home 1 0.97 - 9.9 3,800
(1,000 ppb)
Chronic EMEG
1,2,4-Trichlorobenzene ND - 1.0 Home 1 ND 210 RBC (n)
1,1,1-Trichloroethane 0.35 - 19 Home 7 0.55 - 3.6 3,800
(700 ppb)
IEMEG
Trichloroethylene ND - 3.4 Home 2 ND 0.6 CREG
540
(100 ppb)
IEMEG
1,1,2-Trichlorotrifluoroethane ND - 0.76 Home 1 ND - 190 7,670,000
(1,000,000 ppb)
TLV
1,2,4-Trimethylbenzene ND - 64 Home 1 ND - 3.2 123,000
(25,000 ppb)
TLV
1,3,5-Trimethylbenzene ND - 17 Home 7 17ND - 0.6 123,000
(25,000 ppb)
TLV
Xylenes - ortho ND - 52 Home 1 ND - 1.9 434,000
(100,000 ppb) (o-, m-, p- isomers)
TLV
Xylene, m and/or p ND - 180 Home 1 ND - 4.7 430
(100 ppb)
Chronic EMEG

* Source: Environmental Protection Agency. 1999. Indoor air report provided by Leland Grooms, EPA: analysis request report for activity: ELG01,description: basement sampling. EPA Region 7: Kansas City, Kansas.

Only those compounds detected in at least one of the sampling rounds are included in the table (that is, VOCs not detected in any round of sampling were not included in the table).

The units for the comparison values are in g/m3 unless otherwise specified.

Based on different risk assessments from different EPA sources, EPA Region III has calculated several different RBCs for 1,3-dichlorobenzene in air during the last 2 years or so. All of them incorporated substantial margins of safety and represented safe levels of chronic, lifetime exposure. Considering the scarcity of relevant health effects data available for this compound, the lower estimates most likely reflect differences in methodology, and not new evidence of greater toxicity. The available human and animal data do not suggest that 1,3-dichlorobenzene at low levels poses any threat to human health.

The chronic EMEG for n-Hexane can be used as a conservative surrogate for higher homologues of n-Hexane for which there are no chemical-specific comparison values (e.g., pentane, heptane, octane, nonane, and decane), because the toxicity of straight-chain alkanes tends to decrease with increasing chain length.

** There are no comparison values for propanal (propionaldehyde). However, rats tolerated inhalation of 90,000 ppb of propionaldehyde, for 20 days, 6 hr/day, with no obvious pathology. Also, ATSDR has not listed any toxic effects levels for the related aldehyde acrolein (2-propenal) below 100 ppb, and acrolein is much more toxic than is propanal. Therefore, the 100 ppb level can be safely assumed to be a highly conservative no-effect level for propanal.

CREG Cancer risk evaluation guide
EMEG Environmental media evaluation guide
IEMEG Intermediate environmental media evaluation guide
J Estimated concentration
ND Not detected
ppb Parts per billion
RBC(n) Risk based concentration - noncancer
RfC Reference concentration
RMEG Reference dose media evaluation guide
TLV Threshold limit value
g/m3 micrograms per cubic meter of air

Table 3.

Off-site Indoor Air Sampling Results for October 1999* Amoco - Sugar Creek, Missouri
CompoundSample 002
Conc. (ppb)
Sample 003
Conc. (ppb)
Sample 004
Conc. (ppb)
Sample 005**
Conc. (ppb)
Sample Concentration at Basement Drain on 10/15/99 (ppb) Comparison Value
(ppb)
Benzene ND 2.0 1.4 1.6 1.1 0.03
(0.1 g/m3)
CREG
4 IEMEG
Chloroform ND 1.1 ND 1.4 ND 0.008
(0.04 g/m3)
CREG
20 Chronic EMEG
50 IEMEG
1,2-Dichlorobenzene ND 1.8 ND ND ND 5.5
(33 ug/m3)
RBC (n)
1,3-Dichlorobenzene ND 5.8 4.6 6.6 1.1 0.55 - 53
(3.3 - 320 ug/m3)
RBC (n)
1,4-Dichlorobenzene ND 1.4 ND ND ND 200 IEMEG
100 Chronic EMEG
Dichlorodifluoromethane ND 2.1 2.3 1.7 1.6 1,000,000
(4,950,000 ug/m3)
TLV
Ethyl benzene ND 3.9 2.9 3.5 2.1 200 IEMEG
Methylene Chloride ND 1.4 ND ND 1.0 0.9
(3 g/m3)
CREG
300 IEMEG
300 Chronic EMEG
Styrene ND 10.5 9.6 13.1 1.6 60 Chronic EMEG
1,1,2,2-Tetrachloroethane ND 2.0 ND ND ND 1,000
(6,900 ug/m3)
TLV
Tetrachloroethylene ND ND ND ND 1.0 0.3
(2 g/m3)
CREG
40 Chronic EMEG
Toluene ND 20.8 13.7 16.7 8.6 1,000 Chronic EMEG
1,1,1-Trichloroethane ND 1.4 2.2 1.1 ND 700 IEMEG
1,1,2-Trichloroethane ND 2.0 2.0 ND ND 10,000
(55,000 ug/m3)
TLV
Trichloroethylene ND ND ND ND 1.0 0.12
(0.6 g/m3)
CREG
100 IEMEG
Trichlorofluoromethane ND 2.8 3.5 2.2 1.6 1,000,000 STEL
1,1,2-Trichloro-1,2,2-trifluoroethane ND ND ND ND 1.0 1,000,000 TLV
1,2,4-Trimethylbenzene ND 9.8 5.9 5.9 3.7 25,000 TLV
1,3,5-Trimethylbenzene ND 1.34 7.6 9.4 1.6 25,000 TLV
Xylenes - ortho ND 4.1 2.2 2.5 2.2 100,000 (o-, m-, p- isomers) TLV
Xylene, m and/or p ND 19.7 10.5 11.4 9.9 100 Chronic EMEG

* Sources: Agency for Toxic Substances and Disease Registry. 1999. October 21 fax sent by Denise Jordan-Izaguirre, ATSDR, to Danielle Langmann, ATSDR, concerning air sampling results (sample number: B85745, laboratory report: 99IH3502). Atlanta: US Department of Health and Human Services.

Ecology and Environment, Inc. 1999. October 16 fax sent by Bill Mehnert, Ecology and Environment, Inc., to Bob Aston, EPA, that includes draft air sampling data from an October 15 to October 17, 1999, sampling event. Kansas City, Kansas.

Only those compounds detected in at least one of the sampling rounds are included in the table (that is, VOCs not detected in any round of sampling were not included in the table).

Sample 002: Collected in the living room 10/15/99 - 10/16/99

Sample 003: Collected in the basement 10/15/99 - 10/16/99

Sample 004: Collected in the living room 10/16/99 - 10/17/99

** Sample 005: Collected in the basement 10/16/99 - 10/17/99

The units for the comparison values are in ppb unless otherwise specified.

Using different risk assessments from different EPA sources, EPA Region III has calculated several different RBCs for 1,3-dichlorobenzene in air during the last 2 years or so. All of them incorporated substantial margins of safety and represented safe levels of chronic, lifetime exposure. Considering the scarcity of relevant health effects data available for this compound, the lower estimates most likely reflect differences in methodology, and not new evidence of greater toxicity. The available human and animal data do not suggest that 1,3-dichlorobenzene at low levels poses any threat to human health.

CREG Cancer risk evaluation guide
EMEG Environmental media evaluation guide
IEMEG Intermediate environmental media evaluation guide Table 3 (page 4 of 4).
J Estimated concentration
ND Not detected
ppb Parts per billion
RBC(n) Risk based concentration - noncancer
RfC Reference concentration
RMEG Reference dose media evaluation guide
STEL Short term exposure limit
TLV Threshold limit value
g/m3 micrograms per cubic meter of air

C. COMPARISON VALUES

ATSDR comparison values are media-specific concentrations considered safe under default conditions of exposure. They are used as screening values in the preliminary identification of site-specific "contaminants of concern." The latter term should not be misinterpreted as an implication of "hazard." As ATSDR uses the phrase, a "contaminant of concern" is a chemical substance detected at the site in question and selected by the health assessor for further evaluation of potential health effects. Generally, a chemical is selected as a "contaminant of concern" because its maximum concentration in air, water, or soil at the site exceeds one of ATSDR's comparison values.

It must however be emphasized that comparison values are not thresholds of toxicity. Although concentrations at or below the relevant comparison value can reasonably be considered safe, it does not automatically follow that any environmental concentration exceeding a comparison value would be expected to produce adverse health effects. The principal purpose behind protective health-based standards and guidelines is to enable health professionals to recognize and to resolve potential public health hazards before they become actual public health consequences. For that reason, ATSDR's comparison values are typically designed to be 1 to 3 orders of magnitude (or 10 to 1,000 times) lower than the corresponding no-effect levels (or lowest-effect levels) on which they are based. The probability that such effects will actually occur depends not on environmental concentrations alone. Rather, the probability depends on a unique combination of site-specific conditions and individual lifestyle and genetic factors that affect the route, magnitude, and duration of actual exposure.

Listed and described below are the various comparison values that ATSDR uses to select chemicals for further evaluation, as well as other non-ATSDR values that are sometimes used to put environmental concentrations into a meaningful frame of reference.

CREG = Cancer Risk Evaluation Guide
MRL = Minimal Risk Level
EMEG = Environmental Media Evaluation Guide
IEMEG = Intermediate Environmental Media Evaluation Guide
RMEG = Reference Dose Media Evaluation Guide
RfD = Reference Dose
RfC = Reference Concentration
RBC = Risk-Based Concentration
MCL = Maximum Contaminant Level

Cancer Risk Evaluation Guides (CREGs) are estimated contaminant concentrations expected to cause no more than one excess cancer in a million persons exposed over a lifetime. CREGs are calculated from EPA's cancer slope factors, or cancer potency factors, using default values for exposure rates. It should be noted, however, that neither CREGs nor cancer slope factors can be used to make realistic predictions of cancer risk. The true cancer risk is always unknown and could be as low as zero.

Minimal Risk Levels (MRLs) are estimates of daily human exposure to a chemical (doses expressed in mg/kg/day) that are unlikely to be associated with any appreciable risk of deleterious noncancer effects over a specified duration of exposure. MRLs are calculated using data from human and animal studies and are reported for acute (<14 days), intermediate (15-364 days), and chronic (>365 days) exposures. MRLs are published in ATSDR toxicological profiles for specific chemicals.

Environmental Media Evaluation Guides (EMEGs) are concentrations derived from ATSDR minimal risk levels by factoring in default body weights and ingestion rates.

Intermediate Environmental Media Evaluation Guides (IEMEGs) are calculated from ATSDR minimal risk levels; they factor in body weight and ingestion rates for intermediate exposures (those occurring for more than 14 days and less than 1 year).

Reference Dose Media Evaluation Guide (RMEG) is the concentration of a contaminant in air, water or soil that corresponds to EPA's RfD for that contaminant when default values for body weight and intake rates are taken into account.

Reference Dose (RfD) is an estimate of the daily exposure to a contaminant unlikely to cause noncarcinogenic adverse health effects. Like ATSDR's MRL, EPA's RfD is a dose expressed in mg/kg/day.

Reference Concentrations (RfC) is a concentration of a substance in air that EPA considers unlikely to cause noncancer adverse health effects over a lifetime of chronic exposure.

Risk-Based Concentrations (RBCs) are media-specific concentrations derived by Region III of the Environmental Protection Agency from RfD's, RfC's, or EPA's cancer slope factors. They represent concentrations of a contaminant in tap water, ambient air, fish, or soil (industrial or residential) considered unlikely to cause adverse health effects over a lifetime of chronic exposure. RBCs are based either on cancer ("c") or noncancer ("n") effects.

Maximum Contaminant Levels (MCLs) represent contaminant concentrations in drinking water that EPA deems protective of public health (considering the availability and economics of water treatment technology) over a lifetime (70 years) at an exposure rate of 2 liters of water per day.

Threshold Limit Values (TLVs) are time-weighted average concentrations for a normal 8-hour workday and a 40-hour workweek, to which nearly all workers may be repeatedly exposed, day after day, without adverse effect.

D. METHODOLOGY OF EVALUATING CHEMICALS OF CONCERN

ATSDR addresses the question of whether exposure to contaminants at the maximum concentrations detected would result in adverse health effects. While the relative toxicity of a chemical is important, the human body's response to a chemical exposure is determined by several additional factors, among which are

  • the concentration (how much) of the chemical to which the person was exposed,
  • the amount of time the person was exposed (how long),
  • the way the person was exposed (through breathing, eating, drinking, or direct contact with something containing the chemical), and
  • Lifestyle factors (for example, occupation and personal habits) have a major impact on the likelihood, magnitude, and duration of exposure. Individual characteristics such as age, sex, nutritional status, overall health, and genetic constitution affect how the human body absorbs, distributes, metabolizes, and eliminates a contaminant. A unique combination of all these factors will determine the individual's physiologic response to a chemical contaminant and any adverse health effects the individual could suffer as a result of the chemical exposure.

ATSDR evaluates contaminants detected in environmental media at a site and determines whether an exposure to them has public health significance. ATSDR begins this evaluation by gathering reports that contain relevant environmental data for the site. These data are reviewed to determine whether contaminant levels are above health-based comparison values. Health-based comparison values are estimates of the daily human exposure to a substance that are not likely to result in adverse health effects over a specified duration of exposure. These values are developed for specific media (such as air and water) and for specific durations of exposure (such as acute and chronic).

Health-based comparison values represent conservative levels of safety and not thresholds of toxicity. Thus, although concentrations at or below a comparison value may reasonably be considered safe, concentrations above a comparison value will not necessarily be harmful. Comparison values are intentionally designed to be much lower, usually by orders of magnitude, than the corresponding no-effect levels (or lowest-effect levels) determined in laboratory studies to ensure that even the most sensitive populations (such as children or the elderly) are protected.

To determine whether people are being exposed to contaminants or whether they were exposed in the past or will be exposed in the future, ATSDR examines the path between a contaminant and a person or group of people who could be exposed. Completed exposure pathways have five required elements. ATSDR evaluates each possible pathway at a site to determine whether all five factors exist and whether people are being exposed, were exposed, or could in the future be exposed. The following five factors or elements must exist for a person to be exposed to a contaminant:

  1. A source of contamination,
  2. transport through an environmental medium,
  3. a point of exposure,
  4. a route of human exposure, and
  5. an exposed population.

ATSDR classifies exposure pathways in one of the following three categories.

  • Completed Exposure Pathway. ATSDR calls a pathway "complete" if it is certain that people are exposed (or were exposed or will be exposed) to contaminated media. Completed pathways require that the five elements exist and indicate that exposure to the contaminant has occurred, is occurring, or will occur.
  • Potential Exposure Pathway. Potential pathways are those in which at least one of the five elements is missing, but could exist. Potential pathways indicate that exposure to a contaminant could have occurred, could be occurring, or could occur in the future.
  • Eliminated Exposure Pathway. In an eliminated exposure pathway, at least one of the five elements is missing and will never be present. From a human health perspective, pathways can be eliminated from further consideration if ATSDR is able to show that 1) an environmental medium is not contaminated, or that 2) no one is exposed to contaminated media.

E. SUPPORTING TOXICOLOGICAL INFORMATION

The information in this appendix provides an in-depth review of the eight chemicals that exceeded health-based comparison values in air in the Norledge area (Sections 1 and 2). A discussion on the combined effect of these contaminants is covered in Section 3. In Section 4 ATSDR describes for the selected chemicals of concern the various cancer classifications of the National Toxicology Program (NTP), the International Agency for Research on Cancer (IARC), the Environmental Protection Agency (EPA), and the American Conference of Governmental Industrial Hygienists (ACGIH).

1 Benzene

1.1 General Benzene Information

Benzene (benzol or coal tar naphtha) is a known human carcinogen, and is classified as such by the National Toxicology Program (NTP), the International Agency for Research on Cancer (IARC), the Environmental Protection Agency (EPA), and the American Conference of Governmental Industrial Hygienists (ACGIH).

Benzene is a common solvent isolated from coal tar and crude oil. Although it is naturally released into the atmosphere as an emission of volcanos, forest fires, and even many plants, the primary sources of benzene exposure for the general population are tobacco smoke (50%), automobile service stations, vehicle exhaust and industrial emissions (20%), and vapors from benzene-containing household products such as glues, paints, furniture wax, and some detergents (ATSDR 1997a). Environmental exposure to benzene has been reviewed by the EPA (Wallace 1996). More than 99% of personal exposure to benzene is through the air, averages about 15 g/m3 (4.7 ppb) and ranges from 7 to 29 g/m3 (2 to 9 ppb). These values reflect the results of EPA's Total Exposure Assessment Methodology (TEAM), a study conducted between 1980 and 1987 using personal air quality monitors to measure direct personal exposures in about 800 persons around the United States. This sample was designed to be representative of the non-occupational exposure of 800,000 people in these areas.

Due partly to the domestic use of household products and due partly to home insulation, indoor air concentrations (on the order of 10 g/m3 or 3.1 ppb) typically exceed outdoor air concentrations, which average 6 g/m3 (1.9 ppb) and range from 2 to 19 g/m3 (0.6 to 5.9 ppb). (Note: air concentrations of benzene can be converted from g/m3 to ppb by dividing by 3.2, or from ppb to g/m3 by multiplying by 3.2.) Levels in the city are generally higher than those in rural areas. Average rural background levels of benzene in air historically range from 0.1 to 17 ppb (IARC 1982). More current figures for the range of average rural background levels in the U.S. are not available. Still, 1986 statewide average levels at about 20 sites throughout California fluctuated between 1.6 and 2.2 ppb until 1993 and 1994 when they dropped to about 1.25 ppb, probably as a result of various actions taken to reduce automobile emissions (Wallace 1996). Average levels were higher in winter and lower in summer.

In smokers, the benzene in mainstream cigarette smoke overwhelms all other sources combined. The average smoker could be exposed to 10 times as much benzene as is the average non-smoker (Wallace 1996). For non-smokers, most benzene exposure is ultimately derived from automobile exhaust and gasoline vapor emissions (Egeghy et al 2000). No significant effect on personal exposure has been detected in persons living close to major fixed sources of benzene, such as oil refineries, storage tanks, and chemical plants (Wallace 1996).

1.2 Evaluation of Site-Specific Benzene Exposures

Benzene was detected in indoor air above health-based comparison values during the June, July, and October 1999 sampling events (see Tables 1 and 3, Appendix B). The highest levels, 57 and 70 g/m3, were detected in basements in June 1999; however, one of these homes was re-sampled in July 1999 and the highest level of benzene detected at that time was only 2.3 g/m3 (Table 1, Appendix B).

The median of the indoor air values for samples collected in June and July 1999 was 0.77 ppb (or 2.45 g/m3) benzene. Therefore, average chronic exposures in the Norledge area, like those across the country, are in the low ppb range. Although nationwide background levels, like those in the Norledge area, can often exceed ATSDR's cancer-based screening value for benzene (0.1 g/m3 or 0.03 ppb), no adverse health effects, including cancer, would be expected (see clarification in the following text).

Benzene detected in two Norledge area homes ranged from 33 to 70 g/m3. The concentrations detected in these two homes, as well as the maximum level detected in a third home (18 g/m3) during the June 1999 round of sampling, exceeded ATSDR's intermediate environmental media evaluation guide (IEMEG) of 4 ppb or 13 g/m3. This health-based comparison value represents a concentration of benzene in air that is not likely to result in adverse health effects for exposures lasting from 2 weeks to a year. This particular intermediate EMEG is based on a behavioral effect, i.e., a facilitated aversion response observed in male Kunming mice exposed to 780 ppb (2,496 ug/m3) benzene for 2 hours a day, 6 days a week, for 30 days (Li et al 1992). To avoid an electrical shock, mice exposed to 780 ppb benzene found their way to a safe area at the end of a "Y" maze more quickly, on average, than did untreated control mice. The intermediate EMEG based on this observed effect includes a safety factor of 90. The maximum concentration of benzene detected in indoor air of Norledge area homes (70 g/m3 or 22 ppb) exceeded this comparison value by only 6% of the incorporated safety factor. ATSDR considers that no adverse health effects would be expected at such levels.

The lowest human effect levels reported in ATSDR's recently updated ATSDR Toxicological Profile for Benzene; that is, 690 ppb for leukopenia (Xia et al 1995) and 300 ppb for leukemia (Ott et al 1978), are 31 and 13 times higher, respectively, than the highest level of benzene detected in indoor air in the Norledge area. These values (690 ppb and 300 ppb) represent the lowest measured concentrations in a range of industrial hygiene measurements in each facility in the two studies, which were 690 to 140,000 ppb and 300 to 35,000 ppb, respectively. Use of the lowest measured concentration as an indicator of exposure in the facilities is conservative and will likely underestimate actual exposures. Assuming a normal dose-response relationship in which lower doses are less toxic than higher ones and consistent with the epidemiological and toxicological literature (Paustenbach et al 1992; Rinsky et al 1987; Wong 1995), any adverse effects caused by benzene would be expected to occur in workers exposed to the higher, rather than the lower, end of those exposure ranges. In an update of the Ott study, it was noted that "workers who died of leukemia had the potential for unquantified, but potentially high, exposures to benzene" (Bond et al 1986).

ATSDR's benzene CREG is based primarily on studies of U.S. workers (the Pliofilm cohort) exposed to high levels of benzene (up to hundreds of ppm or hundreds of thousands of ppb) during rubber manufacture, mostly during the 1940s. Like all CREGs, it is based on an EPA-estimated cancer slope factor which is in turn based on the assumption that the dose-response relationship is constant with dose; that is, that the proportion of effects seen at high doses will be the same in the low-dose range where the effects are unmeasurable.

Available studies indicate no detectable excess of leukemia below cumulative exposures of 40 ppm-years (Rinsky et al 1987). This would be numerically, if not biologically, equivalent to about 190 ppb, 24 hours a day, over a 70-year lifetime. However, this apparent threshold is most likely an underestimate because it is based on underestimated exposures and the inclusion of all leukemias, not just AML. When only AML is considered, the estimated threshold was found to be at least 200 ppm-years (numerically equivalent to 950 ppb, 24 hours a day, over a 70-year lifetime), based on the original set of exposure estimates, and higher still using later, more accurate exposure estimates (Paustenbach et al 1992; Wong 1995). (The notation "ppm-year" represents a numerical attempt to integrate the levels and durations of exposure observed in occupational studies as a product of the two. A worker exposed to 2 ppm for 20 years and one exposed to 20 ppm for 2 years both received the "same" cumulative exposure that is, expressed in ppm-years. The distinction is made between numerical and biological equivalence because, although an aspirin a day for 70 years would be numerically equivalent to 70 aspirin a day for 1 year, the two dose rates would produce very different biological effects. Although the first dose regimen might protect one from cardiovascular disease the second would be lethal.)

For the reasons discussed in this section, none of the estimated benzene exposures in the Norledge area would be expected to produce any adverse health effects of either a cancerous or non-cancerous nature.

2 Evaluation of Site-Specific Exposures: Other Chemicals

Other than benzene, no indoor air contaminant was detected at levels in excess of any of ATSDR's non-cancer comparison values. CREGs were exceeded by the maximum detected concentrations of seven other compounds listed in Tables 2 and 3 (Appendix B). The highest levels of chloroform (7.1 g/m3), methylene chloride (83 g/m3), tetrachloroethylene (11 g/m3), trichloroethylene (3.4 g/m3), carbon tetrachloride (0.85 ug/m3), 1,2-dichloroethane (0.46 ug/m3), and 1,1,1-trichloroethane (19 ug/m3) detected in indoor air exceeded ATSDR's CREGs of 0.04, 3.0, 2.0, 0.6, 0.07, 0.04, and 0.6 ug/m3, respectively. None of these contaminants, however, pose a current cancer hazard to Sugar Creek residents (see following text).

2.1 Methylene Chloride

The CREG for methylene chloride is based on inhalation studies in mice exposed 6-hours a day, 5 days a week, for life (104 weeks) to 2,000,000 ppb or 7,000,000 g/m3 methylene chloride. Several, more-relevant, epidemiological studies have detected no excess risk of cancer deaths in workers exposed to methylene chloride at levels up to 475,000 ppb or 1,650,000 g/m3 (ATSDR 1998). Therefore, chronic exposures to methylene chloride at the levels detected in Norledge area homes would not be expected to result in cancer.

2.2 Tetrachloroethylene (PCE)

ATSDR's CREG for tetrachloroethylene or PCE, a non-genotoxic animal carcinogen, was originally based on cancer risk assessment which EPA withdrew some 12 years ago; a more up-to-date assessment is not available (IRIS 1999). In the chronic bioassays on which this risk assessment was based (NTP 1986; ATSDR 1997c), doses of 100,000-200,000 ppb PCE administered by inhalation produced liver cancer in mice (but not in rats); at 200,000-400,000 ppb, it also caused a statistically insignificant increase in kidney tumors in male (but not female) rats (ATSDR 1997c). The PCE-related tumors produced in these studies required doses in excess of anything humans might reasonably be expected to encounter and appear to have involved species-specific mechanisms likely in humans to be either inoperative or much less pronounced (Green 1990). PCE has also been extensively studied in dry cleaning workers whose exposure typically exceeds that of Sugar Creek residents by several orders of magnitude (ATSDR 1997c). None of the epidemiological data suggests that the levels of PCE detected in Norledge area homes represent a realistic cancer hazard.

2.3 Trichloroethylene (TCE)

ATSDR's CREG for trichloroethylene or TCE (another largely non-genotoxic animal carcinogen) was also originally based on a cancer risk assessment which EPA withdrew a decade ago and still has "under review" (IRIS 1999). EPA's original cancer risk assessment for TCE was based on lung tumors seen in mice (but not rats) at high doses (e.g., 150, 300, and 600 ppm in 3 different strains of mice), but not at lower doses (ATSDR 1989). When administered orally, TCE also induces liver tumors in mice (but not rats) and kidney tumors in male rats (but not mice or female rats). As in the case of PCE, these tumors appear to be dependent on both extremely high doses and on high-threshold, species-specific mechanisms of action that are weak or non-existent in humans (Green 1990). In yet another similarity with PCE, numerous occupational studies of inhalation exposure to TCE in workers have yielded generally negative results for cancer (ATSDR 1997d). Therefore, chronic exposure to the levels detected in Norledge area homes would not be expected to result in cancer.

2.4 Chloroform

Concentrations of chloroform in indoor air at Sugar Creek (non-detect to 7.1 g/m3) are below ATSDR's chronic inhalation MRL of 20 ppb (98 g/m3). Therefore, air exposures are not expected to result in any non-cancer adverse health effects. Because "chloroform is not likely to be carcinogenic to humans by any route of exposure under exposure conditions that do not cause cytotoxicity and cell regeneration" (EPA 2001), comparison values that are protective of non-cancer adverse health effects would also protect against cancer. Therefore, because the ATSDR MRL was not exceeded, there is accordingly no basis for expecting that the levels detected in indoor air in Norledge area homes would represent a cancer hazard.

2.5 Carbon Tetrachloride

Carbon tetrachloride is a potent hepatotoxin, nephrotoxin, and central nervous system (CNS) depressant at high doses and is a liver carcinogen in animals. But no adverse effects have been observed in humans repeatedly exposed to 10 ppm, which is 74,000 times the maximum levels detected indoors in the Norledge area (NIOSH 1981), nor do any existing data suggest a cause-and-effect relationship between carbon tetrachloride exposure and cancer in humans. Like the chloroform CREG, the CREG for carbon tetrachloride is based on an inhalation cancer risk estimate which EPA derived from oral dose-response data on liver tumors in rodents. Therefore, indoor air exposures to the levels of carbon tetrachloride detected in the Norledge area would not be expected to result in cancerous or non-cancerous adverse health effects in exposed residents.

2.6 Acrylonitrile

In the most reliable of the epidemiological studies on acrylonitrile, cancer incidence did not increase significantly in 1,345 male textile workers relative to unexposed workers followed over a period of 32 years (O'Berg 1980; O'Berg et al 1985). Using his original results, O'Berg (1980) concluded that an association with lung cancer might exist, but that any possible association was weaker in O'Berg's follow-up study (O'Berg et al 1985). Also, in another well-designed epidemiological study, no association with lung cancer was detected in 1,774 male workers with known acrylonitrile exposure and 32 years of follow up (Collins et al 1989). EPA's cancer risk assessment for acrylonitrile (and, hence, ATSDR's CREG) was based on the statistically insignificant excess incidence of respiratory cancer seen in the O'Berg (1980) study after adjusting for smoking (IRIS 1999). Given the weakness of this potential association in the original study and its decline or absence in subsequent studies of workers with significant occupational exposure, ATSDR considers that the lower levels of indoor air exposure in the Norledge area do not pose any realistic cancer risk to exposed residents.

2.7 1,2-Dichloroethane

As in the case of carbon tetrachloride, EPA's inhalation cancer risk estimate for 1,2-dichloroethane was extrapolated from an old, positive, oral bioassay in rats gavaged daily with over a 100,000 times the maximum estimated doses in the Norledge area. In the study on which ATSDR based its chronic inhalation minimal risk level for 1,2-dichloroethane (Cheever et al 1990; ATSDR 2001), no increased carcinogenic (or non-carcinogenic) effects were seen in rats chronically exposed for 2 years to 50,000 ppb 1,2-dichloroethane; that is, over 400,000 times the maximum exposures in the Norledge area. Therefore, indoor air exposures to the levels of 1,2-dichloroethane detected in the Norledge area would not be expected to result in cancer or any other adverse health effects.

In conclusion, at the maximum levels detected in indoor air in the Norledge area, neither benzene nor any of the other seven compounds which exceeded ATSDR's CREGs pose a carcinogenic hazard to residents under site-specific conditions of exposure.

3 Evaluation of Site-Specific Exposures: Mixtures

Because the individual contaminants detected at the site are present at levels below those that might be expected to result in adverse health effects, ATSDR considers that the combined effect of all these contaminants is not likely to be of public health concern.

This conclusion is based on studies suggesting that a mixture does not produce noncarcinogenic adverse health effects in dosed animals when the components of that mixture are present at levels below their respective no-observed-adverse-effect levels (NOAELs); that is, at concentrations which would have produced no adverse effects in animals treated separately with the individual chemicals (Feron et al. 1993; Jonker et al. 1990; Jonker et al. 1993a; Jonker et al. 1993b; Groten et al. 1991). In two of these experiments (Jonker et al. 1993a; Jonker et al. 1993b) all of the component chemicals affected the same target organ, but through different mechanisms. In two others (Jonker et al. 1990; Groten et al. 1991), the chemicals had different target organs and exhibited different modes of action, as do most chemicals in typical environmental mixtures. Subsequent experiments have shown similar results (Feron et al. 1995; Groten et al. 1997).

Especially relevant is a recent study by Wade et al. (2002) in which animals were exposed for 70 days to a mixture of 16 different organochlorines (including dioxin, polychlorinated biphenyls, DDT and several other pesticides) and two metals (lead and cadmium). Each substance was present at the minimum risk level (MRL) or tolerable daily intake (TDI), or, for dioxin, at the no-observed-effect level (NOEL) used to calculate the TDI. No adverse health effects were observed.

United States regulatory agencies assume, for conservative public health policy, that carcinogens exhibit no threshold other than zero dose (the "zero-threshold assumption"). But because of biological safeguards, such as compensatory mechanisms and repair processes, carcinogens exhibit practical thresholds in the laboratory, as do non-carcinogens (SOT 1981; Williams and Weisburger 1991, page 152-5; Cunningham et al. 1994; Pitot and Dragan 1996, page 254-5; Waddel 2003). It is likely that the principle described in the previous paragraphs will be applicable to carcinogens as well as to noncarcinogens; animal evidence supports this principle. When Hasegawa et al. (1994) administered 10 carcinogenic heterocyclic amines in combination to rats at 1/100 of the doses known to be carcinogenic individually, the effects did not differ significantly from controls. These doses were 100 times lower than established cancer effect levels. Environmental levels of exposure that humans encounter are typically much lower by many orders of magnitude. These results suggest that mixed exposures to carcinogens below all known adverse effects levels are unlikely to pose any demonstrable carcinogenic risk to exposed humans.

The above research findings support the conclusion that because the individual contaminants detected at this site were present at levels well below those that might be expected to produce cancerous or noncancerous adverse health effects, the combined effect of all these contaminants is also unlikely to be of public health concern.

4 Cancer Classifications

For the eight chemicals exceeding their respective CREG comparison values ATSDR provides the cancer classifications of NTP, IARC, EPA, and ACGIH in the following table. The differences between the classifications for individual substances reflects differences in the parent organization's definitions and methodologies.

Table E-1:

Cancer Classifications for Air Chemicals
Chemical NTP IARC EPA ACGIH
Benzene Known to be a carcinogen 1 - Carcinogenic to humans A - Known human carcinogen A1 - Confirmed human carcinogen
Methylene Chloride Reasonably anticipated to be a carcinogen 2B - Possibly carcinogenic to humans B2 - Probable human carcinogen A3 - Confirmed animal carcinogen
PCE Reasonably anticipated to be a carcinogen 2A - Probably carcinogenic to humans Not available at this time A3 - Confirmed animal carcinogen
TCE Not listed by NTPa 2A - Probably carcinogenic to humans Under review A5 - Not suspected as a human carcinogen
Chloroform Reasonably anticipated to be a carcinogen 2B - Possibly carcinogenic to humans B2 - Probable human carcinogen A3 - Confirmed animal carcinogen
Carbon Tetrachloride Reasonably anticipated to be a carcinogen 2B - Possibly carcinogenic to humans B2 - Probable human carcinogen A3 - Confirmed animal carcinogen
Acrylonitrile Reasonably anticipated to be a carcinogen 2B - Possibly carcinogenic to humans B1 - Probable human carcinogen A2 - Suspected human carcinogen
1,2-Dichloroethane Reasonably anticipated to be a carcinogen 2B - Possibly carcinogenic to humans B2 - Probable human carcinogen A4 - Not classifiable as a human carcinogen

a If NTP approves committee recommendations, the 9th Report on Carcinogens will list TCE as "Reasonably Anticipated to be a Human Carcinogen".

EPA classifies a substance as a "probable" (B1 or B2) human carcinogen on the basis of what that agency considers to be "sufficient" evidence of carcinogenicity in animal studies and either "limited" (B1) or "inadequate" (B2) evidence in humans. EPA classifies a substance as a "possible" (C) human carcinogen if the animal evidence is "limited" and no human data are available.

IARC classifies a substance as a "probable" (2A) human carcinogen if the animal evidence is judged to be "sufficient" and the available human evidence is "limited." That agency classifies a substance as a "possible" (2B) human carcinogen if the animal evidence is less than sufficient and/or human data are "limited."

NT's classification of a substance as "reasonably anticipated to be a carcinogen" indicates only that under some set of exposure conditions the substance does cause cancer in one or more species of laboratory animal.

The ACGIH classification "suspected human carcinogen" (A2) is reserved for substances for which either the human data are accepted as adequate in quality but are conflicting or insufficient to classify the agent as a confirmed human carcinogen, or the agent is carcinogenic in experimental animals at dose(s), by route(s) of exposure, at site(s), of histological types(s), or by mechanism(s) considered relevant to worker exposure (ACGIH 1998).

The ACGIH classification "confirmed animal carcinogen" with unknown relevance to humans (A3) indicates that an agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histological types(s), or by mechanism(s) that might not considered relevant to worker exposures. Additionally, ACGIH's A3 designation indicates that 1) available epidemiologic studies do not confirm an increased risk of cancer in exposed humans, and 2) available evidence suggests that the agent is not likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure (ACGIH 1998).

ACGIH designates as "not classifiable as a human carcinogen" (A4), agents which cause concern that they could be carcinogenic for humans but which because of a lack of data cannot be conclusively assessed. In vitro animal studies do not provide indications of carcinogenicity sufficient to classify the agent into one of the other categories (ACGIH 1998). ACGIH classifies as "not suspected as a human carcinogen" (A5) any agent which is not suspected to be a human carcinogen on the basis of properly controlled epidemiological studies in humans. These studies have sufficiently long follow up, reliable exposure histories, sufficiently high dose, and adequate statistical power to conclude that either exposure to the agent does not convey a significant risk of cancer to humans, or that the evidence suggesting a lack of carcinogenicity in experimental animals is supported by mechanistic data (ACGIH 1998).

References:

[ACGIH] American Conference of Governmental Industrial Hygienists. 1998. 1995-1996 threshold limit values for chemical substances and physical agents and biological exposure indices. Cincinnati, OH.

[ATSDR] Agency for Toxic Substances and Disease Registry. 1989. Toxicological profile for trichloroethylene. Atlanta: US Department of Health and Human Services.

[ATSDR] Agency for Toxic Substances and Disease Registry. 1997a. Toxicological profile for benzene (update). Atlanta: US Department of Health and Human Services.

[ATSDR] Agency for Toxic Substances and Disease Registry. 1997b. Toxicological profile for chloroform (update). Atlanta: US Department of Health and Human Services.

[ATSDR] Agency for Toxic Substances and Disease Registry. 1997c. Toxicological profile for tetrachloroethylene (update). Atlanta: US Department of Health and Human Services.

[ATSDR] Agency for Toxic Substances and Disease Registry. 1997d. Toxicological profile for trichloroethylene (update). Atlanta: US Department of Health and Human Services.

[ATSDR] Agency for Toxic Substances and Disease Registry. 1998. Toxicological profile for methylene chloride (update). Atlanta: US Department of Health and Human Services.

[ATSDR] Agency for Toxic Substances and Disease Registry. 2001. Toxicological profile for 1,2-dichloroethane (update). Atlanta: US Department of Health and Human Services.

Bond GG, McLaren EA, Baldwin CL et al. 1986. An update of mortality among chemical workers exposed to benzene. Br J Ind Med 43:685-691.

Cheever KL, Cholakis JM, el-Hawari AM, et al. 1990. Ethylene dichloride: the influence of disulfiram or ethanol on oncogenicity, metabolism, and DNA covalent binding in rats. Fundam Appl Toxicol 14:243-261.

Collins JJ, Page LC, Caporossi JC et al. 1989. Mortality patterns among employees exposed to acrylonitrile. J Occup Med 31:368-371.

Cunningham ML, Elwell MR, Matthews HB. 1994. Relationship of carcinogenicity and cellular proliferation induced by mutagenic noncarcinogens vs carcinogens. Fundam Appl Toxicol 23:363-9.

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[EPA] Environmental Protection Agency. 1986. Guidelines for carcinogenic risk assessment. Fed Reg 51:33997-8.

[EPA] Environmental Protection Agency. 2001. Toxicological review of chloroform in support of summary information on IRIS. Available online at http://www.epa.gov/iris/.

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Groten JP, Sinkeldam EJ, Luten JB, Van Bladern PJ. 1991. Interaction of dietary calcium, potassium, magnesium, manganese, copper, iron, zinc, and selenium with the accumulation and oral toxicity of cadmium in rats. Food Chem Toxicol 4:249-58.

Hasegawa R, Miyata E, Futakuchi M, Hagiwara A, Nagao M, Sugimura T. 1994. Synergistic enhancement of hepatic foci development by combined treatment of rats with 10 heterocyclic amines at low doses. Carcinogenesis 15:1037-41.

[IARC] International Agency for Research on Cancer. 1982. Benzene, in IARC Monographs, Volume 29, Some industrial chemicals and dyestuffs. Lyons, France. p. 99-106.

[IRIS] Integrated Risk Information System. 1999. Cincinnati, OH: US Environmental Protection Agency, Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office. (This on-line government database contains information documenting EPA's RfD's, RfCs, and carcinogenicity assessments for lifetime exposure. For the purposes of this public health assessment, ATSDR consulted the chemical-specific files for PCE, TCE, chloroform, and acrylamide.)

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Larson JL, Wolf DC, Butterworth BE. 1994. Induced cyto toxicity and cell proliferation in the hepatocarcinogenicity of chloroform in female B6C3F1 mice: comparison of administration by gavage in corn oil vs ad libitim in drinking water. Fundam Appl Toxicol 22:90-102.

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