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PETITIONED PUBLIC HEALTH ASSESSMENT

AMOCO OIL COMPANY
(a/k/a AMOCO OIL COMPANY - SUGAR CREEK (FINDS) SS#0716)
SUGAR CREEK, JACKSON COUNTY, MISSOURI


APPENDIX A: FIGURES

Amoco Oil Company Site Location Map
Figure 1. Amoco Oil Company Site Location Map

Demographic Statistics
Figure 2. Demographic Statistics

Norledge Area Groundwater Sampling Location Map - 1997
Figure 3. Norledge Area Groundwater Sampling Location Map - 1997

Off-site Groundwater and Soil Sampling Location Map - 1998
Figure 4. Off-site Groundwater and Soil Sampling Location Map - 1998

Soil Gas Sampling Location Map - 1995
Figure 5. Soil Gas Sampling Location Map - 1995

Air Sampling Location Map
Figure 6. Air Sampling Location Map


APPENDIX B: TABLES

Table 1.

Off-site Exposure Pathway Elements
Pathway Name Exposure Pathway Elements Time Frame
Source Media Point of Exposure Route of Exposure Exposed Population
Completed Exposure Pathways
Air (indoor) Amoco; other sources in the home (e.g., paint cans) Indoor Air Residential homes in the Norledge area Inhalation People who reside or work in homes in the Norledge area Past;
Current;
Future
Potential Exposure Pathways
Groundwater Amoco Private Wells Norledge area Ingestion;
Inhalation;
Dermal
People who may install and use private wells Future
Soil Amoco Subsurface Soil Norledge area Dermal Residents and workers who disturb subsurface soil Current;
Future
Eliminated Exposure Pathways
Groundwater Amoco Private Wells None None None Past;
Current
Soil Gas Amoco Soil Gas None None None Past;
Current;
Future


Table 2.

Off-site Groundwater Sampling Results for the Norledge Area
Compound Concentration Range (µg/L) Comparison Value (ppb) Date of Max. Conc.
Acetone ND - 160 20,000 IEMEG (child) 3/27/96
70,000 IEMEG (adult)
Acenaphthene ND - 2 J 6,000 IEMEG (child) 2/28/96
60,000 IEMEG (adult)
Benzene ND - 2,560 1 CREG 7/6/98
5 MCL
Bis(2-ethylhexyl)phthalate ND - 88 3 CREG 3/28/96
6 MCL
N-butylbenzene ND - 140 61 RBC(n) 3/28/96
Sec-butylbenzene ND - 230 61 RBC(n) 3/28/96
Tert-butylbenzene ND - 3 J 61 RBC(n) 3/28/96
Butylbenzyl phthalate ND - 2 J 2,000 RMEG (child) 3/28/96
7,000 RMEG (adult)
2-Chlorophenol ND - 2 J 50 RMEG (child) 3/28/96
200 RMEG (adult)
4-Chloro-3-methylphenol ND - 5 J 3,000 Florida 3/28/96
2,4-Dimethylphenol ND - 66 200 RMEG (child) 3/27/96
700 RMEG (adult)
Ethyl benzene ND - 2,720 1,000 RMEG (child) 5/22/97
4,000 RMEG (adult)
700 MCL
Isophorone ND - 12 JD 2,000 Chronic EMEG (child) 3/27/96
7,000 Chronic EMEG (adult)
40 CREG
Isopropylbenzene
(Cumene)
ND - 770 1,000 RMEG (child) 3/28/96
4-Isopropyltoluene
(p-Cymene)
ND - 150 A natural plant volatile (100 ppm in fresh, ripe mangos) 3/28/96
Methyl tert butyl ether ND - 6,160 3,000 IEMEG (child) 4/15/98
10,000 IEMEG (adult)
Methylene chloride ND - 6 2,000 Chronic EMEG (child) 3/26/96
7,000 Chronic EMEG (adult)
5 CREG
4-Methyl-2-pentanone
(Methyl Isobutyl Ketone)
ND - 67 140 RBC(n) 3/26/96
2-Methylnaphthalene ND - 46 700a Chronic EMEG (child) 3/27/96
2,000a Chronic EMEG (adult)
Naphthalene ND - 569 200 IEMEG (child) 3/29/96
700 IEMEG (adult)
Phenol ND - 4 J 6,000 RMEG (child) 3/27/96
20,000 RMEG (adult)
N-propylbenzene ND - 1,081 61 RBC(n) 3/29/96
Pyrene ND - 2 J 300 RMEG (child) 3/28/96
1,000 RMEG (adult)
Toluene ND - 1,920 200 IEMEG (child) 12/15/98
700 IEMEG (adult)
1,000 MCL
1,2,3-Trichlorobenzene ND - 2 J 100b RMEG (child) 3/28/96
400b RMEG (adult)
1,2,4-Trichlorobenzene ND - 2 J 100 RMEG (child) 3/28/96
400 RMEG (adult)
1,2,4-Trimethylbenzene (Pseudocumene) ND - 2,200 D 12 RBC(n) 3/27/96
1,3,5-Trimethylbenzene
(Mesitylene)
ND - 802 12 RBC(n) 3/27/96
O-xylene ND - 1,400 D 12,000 RBC(n) 3/27/96
M,P-xylene ND - 4,700 D 2,000c IEMEG (child) 3/27/96
7,000c IEMEG (adult)
10,000c MCL
Xylenes (o, m, p) ND - 9,010 2,000 IEMEG (child) 12/15/98
7,000 IEMEG (adult)
10,000 MCL
GRO ND - 112,000 None 4/15/99
DRO ND - 206,000 J None 5/22/97

Sources: Amoco Oil Company, 1997; EnviroRemedy International, Inc., 1996; Hydro-LOGIC, Inc., 1998a; Hydro-LOGIC, Inc., 1998b; Hydro-LOGIC, Inc., 1999; Pace Analytical, 1998c; Pace Analytical, 1999a; Pace Analytical, 1999b; Southwest Laboratories of Oklahoma, Inc., 1999; ThermoRetec, 1999; TriTechnics Corporation, 1996.

a Comparison value is for 1-methylnaphthalene.
b Comparison value is for 1,2,4-trichlorobenzene.
c Comparison value is for total xylenes.

Table Acronyms and Abbreviations:

CREG = Cancer Risk Evaluation Guide
Conc. = Concentration
D = Surrogates or matrix diluted out when sample run at secondary dilution
DRO = Diesel Range Organics
EMEG = Environmental Media Evaluation Guide
GRO = Gasoline Range Organics
IEMEG = Intermediate Environmental Media Evaluation Guide
J = Estimated concentration
Max. = Maximum
MCL = Maximum Contaminant Level
ND = Non-detect
µg/L = micrograms per Liter (equivalent to ppb)
ppb = parts per billion (equivalent to µg/L)
ppm = parts per million
RBC(n) = Risk Based Concentration (noncancer)
RMEG = Reference Dose Media Evaluation Guide


Table 3.

Off-site Private Well Sampling Results
Compound Concentration (µg/L) Comparison Value (ppb)
Benzene 617 1 CREG
5 MCL
Toluene 720 200 IEMEG (child)
700 IEMEG (adult)
1,000 MCL
Ethyl benzene 982 1,000 RMEG (child)
4,000 RMEG (adult)
700 MCL
Xylenes (o, m, p) 378 2,000 IEMEG (child)
7,000 IEMEG (adult)
10,000 MCL
GRO 15,000 None
DRO 4,070 None

Source: Hydro-LOGIC, Inc., 1998a.
Date Sampled: July 3, 1998.

Table Acronyms and Abbreviations:

CREG = Cancer Risk Evaluation Guide
DRO = Diesel Range Organics
GRO = Gasoline Range Organics
IEMEG = Intermediate Environmental Media Evaluation Guide
MCL = Maximum Contaminant Level
g/L = micrograms per Liter (equivalent to ppb)
ppb = parts per billion (equivalent to g/L)
RMEG = Reference Dose Media Evaluation Guide


Table 4.

Off-site Soil Sampling Results
Compound Concentration Range (mg/kg) Comparison Value (ppm) Depth of Max. Conc. (ft)
Benzene ND - 177 20 CREG 12-14
Toluene ND - 186 1,000 IEMEG (child) 12-14
10,000 IEMEG (adult)
Ethyl benzene ND - 220 5,000 RMEG (child) 16-18
70,000 RMEG (adult)
Xylenes (o, m, p) ND - 808 10,000 IEMEG (child) 12-14
100,000 IEMEG (adult)
2-Methyl naphthalene 1.272 4,000 Chronic EMEG (child)a Unknown
50,000 Chronic EMEG (adult)a
Methyl tert butyl ether ND - 0.005 20,000 IEMEG (child) 45-47
200,000 IEMEG (adult)
Naphthalene 4.0; 6.384 1,000 IEMEG (child) Unknown
10,000 IEMEG (adult)
GRO ND - 11,400 None 12-14
DRO ND - 2,720 None 16-18
TPH 33.1 - 127 None 7.5

Sources: Amoco, 1998; Analytical Report, 1999; EnviroRemedy International, Inc., 1996; Hydro-LOGIC, Inc., 1998a; Hydro-LOGIC, Inc., 1998b; Hydro-LOGIC, Inc., 1999; Southwest Laboratories of Oklahoma, Inc., 1999; ThermoRetec, 1999.

Dates Sampled: July 6 to July 9, 1998; December 15, 1998; December 23, 1998; January 22, 1999; April 15, 1999.

a Comparison value is for 1-Methyl naphthalene.

Table Acronyms and Abbreviations:

Conc. = Concentration
CREG = Cancer Risk Evaluation Guide
DRO = Diesel Range Organics
ft = foot
GRO = Gasoline Range Organics
IEMEG = Intermediate Environmental Media Evaluation Guide
mg/kg = milligrams per kilogram (equivalent to ppm)
ppm = parts per million (equivalent to mg/kg)
RMEG = Reference Dose Media Evaluation Guide
TPH = Total Petroleum Hydrocarbons


Table 5.

Off-site Soil Gas Sampling Results
Compound Concentration Rangea (g/m3) Location of Max. Conc. Comparison Value (g/m3)b
Benzene ND - 33,173 G-19 0.1 CREG
13 (4 ppb) IEMEG
160 (50 ppb) Acute EMEG
Toluene ND - 31,540 WGS-3 3,800 (1,000 ppb) Chronic EMEG
11,000 (3,000 ppb) Acute EMEG
400 RfC
Ethyl benzene ND - 28,684 G-24 870 (200 ppb) IEMEG
1,000 RfC
Xylenes ND - 21,062 G-11 430 (100 ppb) Chronic EMEG
Total BTEX ND - 77,400 G-19 None

Source: TriTechnics Corporation, 1995b.
Date Sampled: March 1995.

a The concentrations of contaminants in soil gas do not generally reflect concentrations in the breathing zone. The measurements are obtained by mechanically evacuating volatiles from the soil.
b The units for the comparison values are in µg/m3, unless otherwise specified.

Table Acronyms and Abbreviations:

BTEX = Benzene, toluene, ethyl benzene, and xylene
CREG = Cancer Risk Evaluation Guide
EMEG = Environmental Media Evaluation Guide
IEMEG = Intermediate Environmental Media Evaluation Guide
Max. Conc. = Maximum concentration
ND = not detected
ppb = parts per billion
RfC = Reference Concentration
RMEG = Reference Dose Media Evaluation Guide
µ g/m3 = micrograms of hydrocarbon compound per cubic meter of air


Table 6.

Off-site Air Sampling Results (June 1998)
Compound Indoor Concentration Range (µg/m3) Control Indoor Concentration Range (µg/m3) Comparison Value (µg/m3)a
Acetone ND - 30 ND 31,000
(13,000 ppb)
Chronic EMEG
Acetonitrile ND - 10 ND 52 RBC(n)
Benzene ND - 62 6.1 - 120 0.1 CREG
13
(4 ppb)
IEMEG
160
(50 ppb)
Acute EMEG
2-Butanone ND - 5 ND 1,000 RfC
Chloroform ND - 7.9 ND 0.04 CREG
98
(20 ppb)
Chronic EMEG
240
(50 ppb)
IEMEG
490
(100 ppb)
Acute EMEG
Chloromethane ND - 1.6 ND 103
(50 ppb)
Chronic EMEG
410
(200 ppb)
IEMEG
1,030
(500 ppb)
Acute EMEG
1,4-Dichlorobenzene ND - 3,400 73 601
(100 ppb)
Chronic EMEG
1,200
(200 ppb)
IEMEG
4,800
(800 ppb)
Acute EMEG
Dichlorodifluoromethane ND - 5.5 5.5 180 RBC(n)
Ethyl benzene ND - 66 10 - 78 870
(200 ppb)
IEMEG
1,000 RfC
Methylene Chloride ND - 4.6 6.7 3 CREG
104
(30 ppb)
IEMEG
1,400
(400 ppb)
Acute EMEG
N-Pentane ND - 8 ND > 600b Chronic EMEG
Propene ND - 10 ND > 30c RfC
Tetrachloroethene ND 11 2 CREG
270
(40 ppb)
Chronic EMEG
1,400
(200 ppb)
Acute EMEG
Toluene ND - 460 38 - 420 3,800
(1,000 ppb)
Chronic EMEG
11,000
(3,000 ppb)
Acute EMEG
1,1,1-Trichloroethane ND - 19 9.4 3,800
(700 ppb)
IEMEG
10,900
(2,000 ppb)
Acute EMEG
Trichloroethene ND 4.5 0.6 CREG
540
(100 ppb)
IEMEG
10,700
(2,000 ppb)
Acute EMEG
Trichlorofluoromethane ND - 6.3 7.4 730 RBC(n)
1,2,4-Trimethylbenzene ND - 100 25 123,000
(25,000 ppb)
TLV
1,3,5-Trimethylbenzene ND - 90 17 123,000
(25,000 ppb)
TLV
Xylenes ND - 230 39 - 280 430
(100 ppb)
Chronic EMEG

Source: ThermoRetec, 1998.
Dates Sampled: June 16 to June 19, 1998.

a The units for the comparison values are in µg/m3 unless otherwise specified.
b The chronic EMEG for n-Hexane is provided, which is more toxic than pentane.
c The RfC for propylene oxide is provided, which is the active metabolite of propene.

Table Acronyms and Abbreviations:

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
µ g/m3 = micrograms per cubic meter of air


Table 7.

Off-site Air Sampling Results (November 1998 & October 1999)
Compound Concentration Rangea (ppbv) Comparison Value (ppb)b
Benzene ND - 5 0.03
(0.1 µg/m3)
CREG
4 IEMEG
50 Acute EMEG
Toluene ND - 6.9 1,000 Chronic EMEG
3,000 Acute EMEG
Ethyl benzene ND - 1.1 200 IEMEG
Xylenes (M & P) ND - 3.5 100c Chronic EMEG
Xylenes (O) ND - 0.95 2,000
(7,300 µg/m3)
RBC(n)
Chloromethane ND - 2.5 50 Chronic EMEG
200 IEMEG
500 Acute EMEG
1,4-Dichlorobenzene ND - 16 100 Chronic EMEG
200 IEMEG
800 Acute EMEG
Dichlorodifluoromethane ND - 0.83 40
(180 µg/m3)
RBC(n)
Styrene ND - 0.72 60 Chronic EMEG
Trichlorofluoromethane ND - 2.1 130
(730 µg/m3)
RBC(n)
1,2,4-Trimethylbenzene ND - 1.4 25,000 TLV

Source: Pace Analytical, 1998a; Pace Analytical, 1998b; ThermoRetec, 2000.
Date Sampled: November 16, 1998, and October 21-22, 1999.

a Only those contaminants detected are presented in the table.
b The units for the comparison values are in ppb unless otherwise specified.
c Comparison value is for total xylenes.

Table Acronyms and Abbreviations:

CREG = Cancer Risk Evaluation Guide
EMEG = Environmental Media Evaluation Guide
IEMEG = Intermediate Environmental Media Evaluation Guide
ND = not detected
ppb = parts per billion
ppbv = parts per billion volume
RBC(n) = Risk Based Concentration - noncancer
RfC = Reference Concentration
RMEG = Reference Dose Media Evaluation Guide
TLV = Threshold Limit Value
µ g/m3 = micrograms of hydrocarbon compound per cubic meter of air


APPENDIX C: COMPARISON VALUES

ATSDR comparison values are media-specific concentrations that are considered to be 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.

However, it must be emphasized that comparison values are not thresholds of toxicity. Although concentrations at, or below, the relevant comparison value may reasonably be considered safe, it does not automatically follow that any environmental concentration that exceeds a comparison value would be expected to produce adverse health effects. The principle purpose behind protective health-based standards and guidelines is to enable health professionals to recognize and 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 does not depends on environmental concentrations alone, but 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 Guides
MRL = Minimal Risk Level
EMEG = Environmental Media Evaluation Guides
IEMEG = Intermediate Environmental Media Evaluation Guide
RMEG = Reference Dose Media Evaluation Guide
RfD = Reference Dose
RfC = Reference Dose 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. However, neither CREGs nor cancer slope factors can be used to make realistic predictions of cancer risk. The true risk is always unknown and may be as low as zero.

Minimal Risk Levels (MRL) 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 that are calculated from ATSDR minimal risk levels by factoring in default body weights and ingestion rates.

Intermediate Environmental Media Evaluation Guides (IEMEG) 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 (RBC) 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) that are 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.


APPENDIX D: METHODOLOGY OF EVALUATING CHEMICALS OF CONCERN

The Agency for Toxic Substances and Disease Registry (ATSDR) has determined levels of chemicals that can reasonably (and conservatively) be regarded as harmless, based on the scientific data the agency has collected in its toxicological profiles. The resulting comparison values and health guidelines, which include ample safety factors (also known as an uncertainty factor) to ensure protection of sensitive populations, are used to screen contaminant concentrations at a site and to select substances (referred to as "chemicals of concern") that warrant closer scrutiny. A "chemical of concern" is defined by ATSDR as any chemical that is detected in air, water, or soil at concentrations exceeding one or more of ATSDR's comparison values. (Refer to Appendix C for a more complete description of ATSDR's comparison values, health guidelines, and other values ATSDR uses to screen site contaminants.)

It is important to understand that comparison values are not thresholds of toxicity. Although concentrations at, or below, the relevant comparison value may reasonably be considered safe, it does not necessarily follow that any concentration that exceeds a comparison value would be expected to produce adverse health effects. Indeed, the principle purpose behind protective health-based standards and guidelines is to enable health professionals to recognize and resolve potential public health problems before that potential is realized. For that reason, ATSDR's comparison values are typically designed to be 1 to 3 orders of magnitude lower than the corresponding no-effect levels (or lowest-effect levels) on which they are based.

When screening individual contaminants, ATSDR staff compare the highest single concentration of a contaminant detected at the site with the lowest comparison value available for the most sensitive of the potentially exposed individuals (usually children or pica children). Typically the cancer risk evaluation guide (CREG) or chronic environmental media evaluation guide (EMEG) is used. This "worst-case" approach introduces a high degree of conservatism into the analysis and often results in the selection of many contaminants as "chemicals of concern" that will not, upon closer scrutiny, be judged to pose any hazard to human health. In the interest of public health, it is prudent to use a screen that identifies many "harmless" contaminants, as opposed to one that may overlook even a single potential hazard to public health. The reader should keep in mind the conservativeness of this approach when interpreting ATSDR's analysis of the potential health implications of site-specific exposures.

As ATSDR's most conservative comparison value, the CREG, requires special mention. ATSDR's CREG is a media-specific contaminant concentration derived from the chronic (essentially, lifetime) dose of that substance which, according to an Environmental Protection Agency (EPA) estimate, corresponds to a 1-in-1,000,000 cancer risk level. Note, this does not mean that exposures equivalent to the CREG are expected to cause 1 excess cancer case in 1,000,000 (1x10-6) persons exposed over a lifetime. Nor does it mean that every person in a population of one million has a 1-in-1,000,000 risk of developing cancer from the specified exposure. Although commonly interpreted in this way, EPA estimates of cancer "risk" are estimates of population risk only and cannot be applied meaningfully to any individual. EPA explicitly stated in it's 1986 Cancer Risk Assessment Guidelines that "The true risks are unknown and may be as low as zero" (EPA, 1986).

Reference:

EPA, 1986. Environmental Protection Agency. Guidelines for Carcinogenic Risk Assessment. Fed. Reg., 51: 33997-33998, September 24, 1986.


APPENDIX E: BENZENE

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 recently been reviewed by the Environmental Protection Agency (EPA) (Wallace, 1996). More than 99% of personal exposure to benzene is through the air, averages about 15 µg/m3 (4.7 ppb) and ranges from 7 to 29 µg/m3 (2 to 9 ppb). These values reflect the results of EPA's Total Exposure Assessment Methodology (TEAM), a study conducted between 1980 through 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 partly to home insulation, indoor air concentrations (on the order of 10 µg/m3 or 3.1 ppb) typically exceed outdoor air concentrations, which average 6 µg/m3 (1.9 ppb) and range from 2 to 19 µg/m3 (0.6 to 5.9 ppb). (Note: air concentrations of benzene may be converted from µg/m3 to ppb by dividing by 3.2, or from ppb to µg/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. However, since 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 may 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. 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).

The lowest human effect levels reported in ATSDR's recently updated ATSDR Toxicological Profile for Benzene, i.e., 690 ppb for leukopenia (Xia et al.,1995) and 300 ppb for leukemia (Ott et al., 1978), are 36 and 16 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 "the workers who died of leukemia had the potential for unquantified, but potentially high, exposures to benzene" (Bond et al., 1986).

ATSDR's benzene cancer risk evaluation guide (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 that, in turn, is based on the assumption that the dose-response relationship is constant with dose (i.e., that the proportion of effects seen at high doses will be the same in the low-dose range where effects are unmeasurable). This is the zero-threshold policy assumption that forms the basis of virtually all quantitative cancer risk estimates in the United States. This zero-threshold assumption allows risk assessors to extrapolate from high-dose animal data into the realm of very low environmental doses. Because no health effects data exist at such low levels of exposure, the resulting quantitative cancer risk estimates are hypothetical. As stated in EPA's 1986 Guidelines on Cancer Risk Assessment, "the true risk is unknown and may be as low as zero" (EPA, 1986).

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, i.e., 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. The first dose regimen might protect one from cardiovascular disease, while the second would be lethal.)

No unequivocally adverse health effects have been observed in animals or humans chronically exposed to 1,000 ppb (1 ppm) or less of benzene in air. The benzene levels measured in the homes were 1 to 3 orders of magnitude below this level. The air data indicate that the residents are not constantly exposed to the highest levels of benzene that were found in their homes, but to benzene levels that fluctuate within their homes. Therefore, none of the benzene exposures in the Norledge area would be expected to produce any adverse health effects of either a cancerous or non-cancerous nature. Nevertheless, ATSDR considers it prudent public health policy to reduce or eliminate, wherever possible, excess exposure to substances which at higher concentrations can be toxic.

References:

ATSDR, 1997a. Agency for Toxic Substances and Disease Registry. Toxicological Profile for Benzene (Update), Atlanta, Georgia. September 1997.

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. 1986.

EPA, 1986. Environmental Protection Agency. Guidelines for Carcinogenic Risk Assessment. Fed. Reg., 51: 33997-33998, September 24, 1986.

IARC, 1982. International Agency for Research on Cancer. "Benzene." pp. 99-106 in IARC Monographs, Volume 29, Some Industrial Chemicals and Dyestuffs, Lyons, France, 1982.

Lamm, S.H., Walters, A..S., Wilson, R., Byrd, D.M., and Grunwald, H., 1989. "Consistencies and Inconsistencies underlying the Quantitative Assessment of Leukemia Risk from Benzene Exposure," Environmental Health Perspectives 82: 289-297. 1989.

Ott M.G., Towsend J.C., Fishbeck W.A., et al., 1978. "Mortality among workers occupationally exposed to benzene," Arch Environ Health 33: 3-10. 1978.

Paustenbach, D.J., Price, P.S., Ollison, W., Jernigan, J.D., Bass, R.D., and Peterson, H.D., 1992. Reevaluation of benzene exposure for the Pliofilm (rubberworker) cohort (1936-1976). J. Toxicol. Environ Health 36; 177-231. 1992.

Paxton, M.B., 1996. "Leukemia Risk Associated with Benzene Exposure in the Pliofilm Cohort," Environmental Health Perspectives 104 (Suppl 6): 1431-1436. 1996.

Raabe, Gerhard and Wong, Otto, 1996. "Leukemia Mortality by Cell Type in Petroleum Workers with Potential Exposure to Benzene," Environmental Health Perspectives 104 (Suppl 6): 1381-1392. 1996.

Rinsky, R.A., Smith, A.B., Hornung, R., Filloon, T., Young, R., Okun, A., and Landrigan, P., 1987. Benzene and Leukemia: An epidemiological risk assessment. N. Eng. J. Med. 316: 1044-50. 1987.

Wallace, Lance, 1996. "Environmental Exposure to Benzene: An Update," Environmental Health Perspectives 104 (Suppl 6): 1129-1136. 1996.

Wong, Otto, 1995. "Risk of Acute Myeloid Leukemia and Multiple Myeloma in Workers Exposed to Benzene," Occupational and Environmental Medicine 52: 380-384. 1995.

Xia Z-L, Xi-Peng J, Pei-Lian L, et al., 1995. "Ascertainment corrected prevalence rate (ACPR) of leukopenia in workers exposed to benzene in small-scale industries calculated with capture-recapture methods," Biomed Environ Sci. m8: 30-34. 1995.

Yin, Song-Nian, Hayes, Richard B, Linet, Martha S., Li, Gui-Lan, Dosemeci, Mustafa, Travis, Lois B, Zhang, Zhi-Nan, Li, De-Gao, Chow, Wong-Ho, Wacholder, Sholom, Blott, William J, and the Benzene Study Group, 1996. "An expanded cohort study of cancer among benzene-exposed workers in China", Environmental Health Perspectives 104 (Suppl 6): 1339-1341. 1996


APPENDIX F: HEALTH ENDPOINTS

Brain Cancer:

The cause of most brain cancer remains largely unknown. It is important to differentiate between primary brain tumors and metastatic tumors that originate from another primary site (e.g., lung). About 25% of people who die of cancer have brain metastases. Primary brain tumors in children are associated with certain underlying diseases, including neurofibromatosis, tuberous sclerosis, and von Hippel-Lindau angiomatosis. Family clusters of central nervous system (CNS) tumors have been reported. High-dose ionizing radiation may cause brain cancer in humans and certain alkylating agents, especially nitrosamides, are effective neurocarcinogens in laboratory animals; in humans, however, the data are mixed and inconclusive (Inskip, et al., 1995).

Leukemia:

The only contaminant of concern identified so far at Amoco/Sugar Creek is benzene, and the only specific cancer consistently seen in excess among benzene-exposed workers is acute myelogenous leukemia (AML). However, benzene-induced AML exhibits a relatively high threshold; it is only seen in workers who have experienced prolonged, high-level exposure, i.e., >200 ppm-years (Wong, 1995). The known risk factors for leukemia include radiation, benzene, alkylating drugs, myelodysplastic syndromes, and hereditary syndromes such as Franconi's aplasia and Down's syndrome (Casciato & Lowitz, 1988).

Lymphoma:

Viral etiology and immunodeficiency states are strongly associated with the development of lymphomas. To date, however, no exposures to chemicals in the environment are known to cause lymphomas in humans. Notwithstanding some suggestive early studies, the weight of evidence for a link between non-Hodgkin's lymphoma and organochlorines is weak and inconsistent. The histologic diagnoses for reported lymphoma is unknown (Merck, 1992a).

Alzheimer's:

The etiology of Alzheimer's disease remains unknown in spite of intensive research efforts. Recent studies of genetic linkage in familial Alzheimer's disease have focused on the genes for amyloid precursor protein (APP) and apolipoprotein E (Drouet et al., 2000). Several risk factors of Alzheimer's disease have been revealed by epidemiological studies, including age, family history, head trauma, thyroid dysfunctions, and aluminum (Al) (Chang & Dyer, 1995). Although genetic and other biological factors are important in Alzheimer's disease, environmental factors could also contribute to its development. The most studied of these are aluminum, zinc, foodborne poisons, and viruses.

Multiple Sclerosis:

Multiple sclerosis (MS) is an autoimmune disease of unknown etiology. It is generally believed that the inflammation and demyelination observed in MS are caused by microbe-activated T-cells which cross the blood-brain barrier and cross-react with myelin proteins. MS appears to be the result of a complex interaction between multiple genetic susceptibility factors and various environmental triggers, including viral infections. Interestingly, incidence increases with latitude away from the equator (e.g., from Queensland to Tasmania, Australia), and risk is reduced by migration from a high MS prevalence area to a low prevalence area before (but not after) puberty (Merck 1992b). This pattern is not consistent with industrial emissions as a causative agent. In any case, because natural, non-specific triggers are ubiquitous in the environment, the availability of man-made triggers would probably not be a limiting or determining factor in the incidence of MS.

References:

Casciato, Dennis A. and Lowitz, Barry B., 1988. Manual of Oncology. Third Edition, Little, Brown and Company, New York, N.Y. 1988.

Chang, LW and Dyer RS, 1995. Handbook of Neurotoxicology. Marcel Dekker, Inc., New York, NY, pp. 123-7.

Drouet B, Pincon-Raymond M, Chambaz J, Pillot T, 2000. "Molecular basis of Alzheimer's disease". Cell Mol Life Sci 57(5):705-15.

Inskip, Peter D., Linet, Martha S., and Heineman, Ellen F., 1995. "Etiology of brain tumors in adults", Epidemiologic Reviews 17(2): 382-414. 1995.

Merck, 1992a. The Merck Manual of Diagnosis and Therapy, Vol. I, General Medicine, pp. 1075-82.

Merck, 1992b. The Merck Manual of Diagnosis and Therapy, Vol. I, General Medicine, pp. 1287-89.

Wong, Otto, 1995. "Risk of Acute Myeloid Leukemia and Multiple Myeloma in Workers Exposed to Benzene," Occupational and Environmental Medicine 52: 380-384. 1995.


APPENDIX G: CHEMICAL MIXTURES

Since the individual contaminants detected at this site have consistently been present well below levels 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 either. This conclusion is based on studies which suggest that a mixture produces no adverse health effects in dosed animals when the components of that mixture are present at levels below their respective no-observed-adverse-effect levels (NOAEL), i.e., at concentrations that would have produced no adverse effects in animals treated separately with those component chemicals (Feron et al., 1993; Jonker at el., 1990; Jonker at el., 1993; Groton at el., 1991). In two of these experiments, all of the component chemicals affected the same target organ, albeit through different mechanisms. In two others, the chemicals had different target organs and exhibited different modes of action, as do most chemicals in typical environmental mixtures.

Considering that ATSDR comparison values are typically 10-1000 times lower than their corresponding NOAELs, it is reasonable to expect that environmental contaminants will not produce any combined effects, even if their individual concentrations exceed their respective EMEGs by a significant fraction of the associated safety factor (which ATSDR refers to as a composite "uncertainty factor"). However, in the Norledge area, with the sole exception of benzene, all of the air contaminants detected so far have been present at levels below ATSDR's EMEGs, making interactive effects extremely unlikely. It should be noted, however, that allergic reactions and psychogenic responses to nuisance gasses are not dose-related, and that health-based comparison values are not (and cannot be) designed to prevent responses in hypersensitive individuals.

The same principles described above for the interaction of non-carcinogens may apply to carcinogens, as well. Due to the prevalence of the regulatory assumption of zero-threshold for chemical carcinogens, one does not usually discuss the latter in terms of their NOAELs. Nevertheless, it seems almost certain, based on empirical evidence and established pharmacological principles, that thresholds of effect will exist for carcinogens, as well as for non-carcinogens (Williams and Weisburger, 1991). Available data suggest that even some genotoxic carcinogens (and not just nongenotoxic carcinogens like dioxin and arsenic) do exhibit thresholds, and often at rather high dose levels, relative to typical, environmentally relevant, human exposures (SOT, 1981; Cunningham, 1994). A significant number of thyroid tumors and neoplastic liver nodules were seen in rats exposed for 102 weeks (roughly equivalent to a rat's lifespan) to a mixture of 40 different carcinogenic compounds that targeted different organs (including, liver, thyroid, skin, and urinary bladder) at 1/50 of the doses at which each of the individual chemicals would have produce tumors in 50% of the exposed animals (Takayama et al., 1989). Adopting the regulatory assumption of linearity (solely for the purpose of dose perspective, since the true risk in humans would be unknown and could be as low as zero) the chronically administered dose of each one of these 40 carcinogens was, equivalent to an estimated "risk" of 1/50 X 0.50 = 10-2, i.e., a risk level 10,000 times higher than that (10-6) on which ATSDR's CREGs are usually based. However, 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 (Hasegawa et al., 1994). These doses were 100 times lower than established cancer effect levels, not the NOAELs (which were unknown). ATSDR's CREGs, and the environmental levels of exposure that humans encounter, are typically much lower, still, by many orders of magnitude. These results suggest that mixed exposures to carcinogens at levels that exceed their respective CREGs, but are well below all known effects levels, will not pose any realistic carcinogenic risk.

The aforementioned research findings, in combination with the fact that ATSDR's comparison values are typically 10-1000 times lower than the corresponding NOAELs, suggest that environmental contaminants should not be expected to produce combined effects, even if their individual concentrations exceed their respective EMEGs by a significant fraction of the associated safety factor (also known as an uncertainty factor). Considering how much lower CREGs and environmental exposures usually are, compared to the doses used by Hasegawa et al (1994), a similar argument is probably applicable to carcinogens, as well.

References:

Cunningham, M.L., Elwell, M.R., and Matthews, H.B, 1994. Relationship of carcinogenicity and cellular proliferation induced by mutagenic noncarcinogens vs carcinogens. Fundamental and Applied Toxicology, 23: 363-369.

Feron VJ, Jonker D, Groten JP, Horbach GJMJ, Cassee FR, Schoen ED, Opdam JJG., 1993. Combination technology: From challenge to reality. Toxicology Tribune 1993; 14: 1-3.

Groton 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 and Chemical Toxicology 1991; 4: 249-258.

Hasegawa, R, Miyata, E, Futakuchi, M, Hagiwara, A, Nagao, M, Sugimura, T and Ito, N, 1994. Synergistic enhancement of hepatic foci development by combined treatment of rats with 10 heterocyclic amines at low doses. Carcinogenesis 15: 1037-1041.

Jonker D, Woustern RA, Van Bladern PJ, Til HP, Feron VJ., 1990. Four week oral toxicity study of a combination of eight chemicals in rats: comparison with the toxicity of the individual compounds: Food and Chemical Toxicology 1990; 28: 623-631.

Jonker D, Jones MA, Van Bladern PJ, Woustern RA, Til HP, Feron VJ., 1993. Acute 24 hour toxicity of a combination of four nephrotoxicants in rats compared with the toxicity of the individual compounds: Food and Chemical Toxicology 1993; 31: 45-52.

SOT, 1981. Society of Toxicology. Re-evaluation of the ED01 Study. Fundamental and Applied Toxicology 1:27-128.

Takayama, S, Hasagawa, H and Ohgaki, O, 1989. Combination effects of forty carcinogens administered at low doses to male rats. Jpn. J. Cancer Res. 80: 732-736.

Williams, Gary M., and Weisburger, John H, 1991. "Chemical Carcinogenesis". pp.153-154 in Chapter 5 of: Casarett and Doull's TOXICOLOGY: The Basic Science of Poisons. (Mary O Amdur, John Doull, and Curtis Klaassen, Editors.) Pergamon Press pp 127-200.


APPENDIX H: GLOSSARY OF TERMS

Absorption:
The process of taking in, as when a sponge takes up water. Chemicals can be absorbed through the skin into the bloodstream and then transported to other organs. Chemicals can also be absorbed into the bloodstream after breathing or swallowing.


Acute:
Occurring over a short time, usually a few minutes or hours. For purposes of health assessment, ATSDR defines acute exposures as those lasting up to two weeks. An acute exposure can result in short- or long-term health effects.


Ambient:
Surrounding. For example, ambient air is usually outdoor air (as opposed to indoor air).


Carcinogen:
Any substance that may produce cancer.


Chronic:
Occurring over a long period of time (more than 1 year).


Comparison Values:
Estimated contaminant concentrations in specific media that are not likely to cause adverse health effects, given a standard daily ingestion rate and standard body weight. The comparison values are calculated from the scientific literature available on exposure and health effects.


Concentration:
The amount of one substance dissolved or contained in a given amount of another. For example, sea water contains a higher concentration of salt than fresh water.


Contaminant:
Any substance or material that enters a system (e.g., the environment, human body, food, etc.) where it is not normally found.


Dermal:
Referring to the skin. Dermal absorption means absorption through the skin.


Dose:
The amount of substance that actually enters the body over a specified period of time. Dose is expressed in terms of unit weight of chemical per unit body weight per unit of time, e.g., mg/kg/day.


Epidemiology:
The study of the occurrence of disease in human populations and the factors associated with the frequency and distribution of that disease.


Exposure:
Contact with a chemical by swallowing, breathing, or direct contact (such as through the skin or eyes). Exposure may be short term (acute) or long term (chronic).


Hazard:
A possible source of danger or harm (i.e., in this context, adverse health effects).


Health Outcome Data:
Information on the prevalence of death, disease or other health-related factors in the community. Such information may be derived from local, state, and national databases, medical records, tumor and disease registries, and health studies.


Indeterminate Public Health Hazard:
A formal conclusion category that ATSDR reserves for sites at which, due to the unavailability of critical information, no determination can be made regarding the existence or non-existence of a potential threat to health in the community.


Ingestion:
Swallowing (such as eating or drinking). Chemicals can get in or on food, drink, utensils, cigarettes, or hands, from which they can be ingested. After ingestion, chemicals can be absorbed into the blood and distributed throughout the body.


Inhalation:
Breathing. Exposure may occur from inhaling contaminants, because the contaminants can be deposited in the lungs, taken into the blood, or both.


Media (Environmental):
Soil, water, air, plants, animals, or any other parts of the environment that can contain contaminants.


Petitioned Public Health Assessment:
A public health assessment conducted at the request of a member of the public. When a petition is received, a team of environmental and health scientists is assigned to gather information to ascertain, using standard public health criteria, whether there is a reasonable basis for conducting a public health assessment. Once ATSDR confirms that a public health assessment is needed, the petitioned health assessment process is essentially the same as the public health assessment process.


Public Health Action:
As used in ATSDR public health advisories, public health assessments, and health consultations, this term refers to activities designed to prevent exposures and/or to mitigate or prevent adverse health effects in populations living near hazardous waste sites or releases. These actions may include eliminating immediate exposures (e.g., by providing an alternative water supply), monitoring indicators of exposure in bodily fluids (e.g., blood and urine) to better assess exposure, and providing health education for health care providers and community members.


Public Health Hazard:
A formal conclusion category that ATSDR reserves for sites at which chronic, long-term exposure (>1 year) to potentially hazardous contaminants may cause illness in the community.


Route of Exposure:
The way in which a person may contact a chemical substance. The primary routes of exposure are ingestion (as in eating or drinking), inhalation (as in breathing), and dermal or skin contact (as in bathing).


Toxicological Profile:
An ATSDR reference document that identifies and reviews key, peer-reviewed literature describing the properties of a hazardous substances, the levels of significant exposure to that substance, and the associated acute, subacute (intermediate), and chronic health effects in laboratory animals and humans, where known. Toxicological Profiles also describe the experimental and/or epidemiological bases of ATSDR's existing comparison values for the substance, and identify knowledge gaps and research needs.

APPENDIX I: CANCER CLASSIFICATIONS

For the five chemicals exceeding their respective cancer risk evaluation guide (CREG) comparison values, ATSDR describes 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) in the table below. The differences between the classifications for individual substances reflects differences in the parent organization's definitions and methodologies.

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
Tetrachloroethene Reasonably anticipated to be a carcinogen 2A - Probably carcinogenic to humans Not available at this time A3 - Confirmed animal carcinogen
Trichloroethene 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

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

Cancer classifications are useful for determining which regulatory practices are, by policy, most appropriately applied to a given substance. However, they were not designed for, and cannot be used in, the prediction of human cancer incidence rates under various conditions of exposure. Even substances classified by EPA, IARC, NTP, or ACGIH as "known" human carcinogens are known to cause cancer in humans only under the conditions specified in the studies on which those classifications are based. With rare exceptions, a substance is classified by these agencies as a "known" human carcinogen only if there is "sufficient" evidence of carcinogenicity in humans.

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".

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

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 may not be 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 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 exposure to the agent does not convey a significant risk of cancer to humans; or, the evidence suggesting a lack of carcinogenicity in experimental animals is supported by mechanistic data (ACGIH, 1998).

More so than those of EPA, IARC, and NTP, ACGIH's cancer classifications address the issue of human relevance, i.e., the likelihood that a substance demonstrated to be carcinogenic in animal studies will also be carcinogenic to humans under realistic conditions of worker exposure (8 hours a day, 40 hours a week). As a result, they are more informative and provide more perspective on the "possible" and "probable" human carcinogens identified by EPA, IARC, and NTP. Thus, ACGIH's cancer categories complement, rather than contradict, those of other agencies.


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