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Table 4.

EAFB Groundwater Plume Characteristics
Operable Unit Site Depth of Plume (ft bgs) Contaminant Range of Concentrationsa (ppb)
1 16 8-37 BTEX 1-10,000
1,2 DCA 1-100
1,2-C DCE 1-10,000
MTBE 1-1,000
PCE 1-10
17 11-46 BTEX 1-1,000
1,2 DCA 1-10
1,2-C DCE 1-10
MTBE 1-100
PCE 1-10
20 11 BTEX 1-10,000
41 28-30 1,2-C DCE 1
45 13-30 1,2 DCA 1
55 30 BTEX 1-10
1,2 DCA 1
2 15 54 MTBE 1-10
223 44 Benzene 1-100
1,2 DCA 1-10
EDB 0.1-1
5 50-55 BTEX 1-100
TCE 1-100
71 53-56 Benzene 1-10
1,2 DCA 1
76 50 TCE 1-10
86 43 TCE 1-100
4 133 27-130 1,4-Dioxane 1-100
NDMA 0.002-0.01
PCE 1-10
Perchlorate 4-10
TCE 1-10,000
162 65-206 NDMA 0.001-0.1
PCE 1-1,000
Perchlorate 1-10
TCE 1-100
177 42-124 NDMA 0.002-0.05
PCE 1-1,000
Perchlorate 4-100
TCE 1-1,000
461 31-111 TCE 100-1,000
5 188 120-123 TCE 10-500
194 122-125 TCE 10
199 124-126 Perchlorate 1,000
201 127-129 Perchlorate 10-5,000
240 90-95 CCl4 1-25
286 124-126 Perchlorate 10-5,000
6 206 5-18 TCE 5-500
207 5-18 BTEX 10-20,000
5-18 TCE 5-45,000
211 5-18 TCE 5-1,000
8 25 18-42 NDMA 2,000-5,000,000
TCE 5-50,000
8 297 65 Benzene 1-10,000
1,2 DCA 0.5-1,000
31 29 JP-4 Estimated at 100-20,000
JP-8 Estimated at 400-80,000
61 10 TCE 5
17-34 1,2 DCA 1
TCE 5-2,500
34 TCE 5

Source: JT3/CH2MHill 2002

a Concentrations represent approximate ranges only.

bgs below ground surface
BTEX benzene/toluene/ethylbenzene/xylene
CCl4 carbon tetrachloride
1,2 DCA 1,2-dichloroethane
1,2-C DCE cis-1,2-dichloroethene
EDB ethylene dibromide
ft feet
JP-4 jet fuel #4
JP-8 jet fuel #8
MTBE methyl-tert-butyl ether
NDMA N-nitrosodimethylamine
PCE tetrachloroethylene
ppb parts per billion
TCE trichloroethylene

Table 5:

Summary of Dioxin Air Sampling Data from Site 16 and Site 18.
Sampling Event Range of Concentrationsa Detected (pg/m3) Comparison Value (pg/m3) Comparison Value Source
Site 16
June 9-11, 1997 0.001-0.064 0.042 RBC
June 11-12, 1997 0.008-0.026 0.042 RBC
November 1997 ND (0.047-0.138)b 0.042 RBC
April 2001 0.023c 0.042 RBC
Site 18
April 2001 ND (0.256-0.375)c 0.042 RBC

Sources: AFFTC 2001; Weston 1998a, 1998b

aConcentrations are total dioxins and furans, calculated using half the detection limit for all non-detects.
b Reported as all non-detect; values in parentheses are total dioxins, calculated using half the detection limit.
c Reported concentration is modeled for 600 meters downwind.

pg/m3 picograms per cubic meter
RBC risk-based concentration


Location Map of Edwards Air Force Base
Figure 1. Location Map of Edwards Air Force Base

Map of Operable Units at Edwards Air Force
Figure 2. Map of Operable Units at Edwards Air Force

Demographic Statistics
Figure 3. Demographic Statistics

ATSDR's Exposure Evaluation Process
Figure 4. ATSDR's Exposure Evaluation Process

ATSDR Public Health Hazard Categories
Figure 5. ATSDR Public Health Hazard Categories

Contaminant Plumes and On-base Supply Wells
Figure 6. Contaminant Plumes and On-base Supply Wells

Contaminant Plumes and On-base Supply Wells
Figure 7. Contaminant Plumes and On-base Supply Wells

Location of Site 426, Edwards Air Force Base
Figure 8. Location of Site 426, Edwards Air Force Base

Location of Site 16 and 18, Edwards Air Force Base
Figure 9. Location of Site 16 and 18, Edwards Air Force Base

Windrose (1992-1997) for Site 16 and Site 18, Edwards Air Force Base
Figure 10. Windrose (1992-1997) for Site 16 and Site 18, Edwards Air Force Base


Overview of ATSDR's Methodology for Evaluating Potential Public Health Hazards

An exposure dose is the amount of a chemical a person is exposed to over time.To evaluate exposures on Edwards Air Force Base (EAFB), ATSDR evaluated available data to determine whether contaminants were above ATSDR's comparison values. For those that were, ATSDR derived exposure doses and compared them against health-based guidelines. ATSDR also reviewed relevant toxicologic and epidemiologic data to obtain information about the toxicity of contaminants of interest. Exposure to a certain chemical does not always result in harmful health effects. The type and severity of health effects expected to occur depend on the exposure concentration, the toxicity of the chemical, the frequency and duration of exposure, and the multiplicity of exposures.

Comparing Data to ATSDR's Comparison Values

Comparison values are derived using conservative exposure assumptions. Comparison values reflect concentrations that are much lower than those that have been observed to cause adverse health effects. Thus, comparison values are protective of public health in essentially all exposure situations. As a result, concentrations detected at or below ATSDR's comparison values are not considered to warrant health concern. While 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. It cannot be emphasized strongly enough that comparison values are not thresholds of toxicity. The likelihood that adverse health outcomes will actually occur depends on site-specific conditions and individual lifestyle and genetic factors that affect the route, magnitude, and duration of actual exposure, and not an environmental concentration alone.

For this public health assessment, ATSDR evaluated data that were collected from drinking water wells (groundwater), potential chemical warfare materiel (CWM) areas (soil and soil gas), dual extraction systems at Site 16 and Site 18 (air), and Piute Ponds (surface water, sediment, and waterfowl) to determine whether people were exposed to contaminant concentrations that exceeded ATSDR's comparison values. The majority of detected contaminants fell at or below comparison values and were not evaluated further. Contaminants that were above comparison values were deemed worthy of further evaluation, prompting ATSDR to estimate exposure doses using site-specific exposure assumptions.

Deriving Exposure Doses

ATSDR derived exposure doses for those contaminants that were detected above ATSDR's comparison values or did not have comparison values. Exposure doses are expressed in milligrams per kilogram per day (mg/kg/day). When estimating exposure doses, health assessors evaluate chemical concentrations to which people could be exposed, together with the length of time and the frequency of exposure. Collectively, these factors influence an individual's physiological response to chemical exposure and potential outcomes. Where possible, ATSDR used site-specific information about the frequency and duration of exposures. In cases where site-specific information was not available, ATSDR applied several conservative exposure assumptions to estimate exposures for on-base and off-base residents and recreational users.

The following equation was used to estimate exposure to contaminants in drinking water:

Estimated exposure dose equals C times IR times EF times ED divided by BW times AT

C: Maximum concentration in parts per million (ppm)
IR: Ingestion rate: 2 liters per daya
EF: Exposure frequency, or number of exposure events per year of exposure: 365 days/year
ED: Exposure duration, or the time span over which exposure occurs: adult = 30 years; child = 6 years
BW: Body weight: adult = 70 kg; child = 16 kg
AT: Averaging time, or the period over which cumulative exposures are averaged (6 years or 30 years × 365 days/year for noncancer effects; 70 years × 365 days/year for cancer effects)

a The ingestion rate is a standard assumption for a primary source of drinking water (ATSDR 2002).

The following equation was used to estimate exposure to contaminants in waterfowl:

Estimated exposure dose equals C times IR times EF times ED divided by BW times AT

C: Estimated maximum concentration in waterfowl (ppm) (maximum concentration [ppm] in surface water × bioconcentration factor [BCF])
IR: Ingestion rate: adult = 181 grams per day (0.181 kg/day)b
EF: Exposure frequency, or number of exposure events per year of exposure: 7.5 days/year c
ED: Exposure duration, or the duration over which exposure occurs: adult = 30 years; child = 6 years
BW: Body weight: adult = 70 kg; child = 16 kg
AT: Averaging time, or the period over which cumulative exposures are averaged (6 years or 30 years × 365 days/year for noncancer effects; 70 years × 365 days/year for cancer effects)

b The ingestion rate represents measured average eating event intake in a Health Canada-sponsored study of waterfowl hunters (Duchesne et al. 2001).

c The exposure frequency represents measured average waterfowl eating events in a Health Canada-sponsored study of waterfowl hunters(Duchesne et al. 2001).

Using Exposure Doses to Evaluate Potential Health Hazards

ATSDR analyzes the weight of evidence of available toxicologic, medical, and epidemiologic data to determine whether exposures might be associated with harmful health effects (noncancer and cancer). As part of this process, ATSDR examines relevant health effects data to determine whether estimated doses are likely to result in harmful health effects. As a first step in evaluatingnoncancer effects, ATSDR compares estimated exposure doses to conservative health guideline values, including ATSDR's minimal risk levels (MRLs) and EPA's reference doses (RfDs). The MRLs and RfDs are estimates of daily human exposure to a substance that are unlikely to result in noncancer effects over a specified duration. Estimated exposure doses that are less than these values are not considered to be of health concern. To maximize human health protection, MRLs and RfDs have built in uncertainty or safety factors, making these values considerably lower than levels at which health effects have been observed. The result is that even if an exposure dose is higher than the MRL or RfD, it does not necessarily follow that harmful health effects will occur.

For carcinogens, ATSDR also calculates a theoretical increase of cancer cases in a population (for example, 1 in 1,000,000 or 10-6) using EPA's cancer slope factors (CSFs), which represent the relative potency of carcinogens. This is accomplished by multiplying the calculated exposure dose by a chemical-specific CSF. Because they are derived using mathematical models which apply a number of uncertainties and conservative assumptions, risk estimates generated by using CSFs tend to be overestimated.

If health guideline values are exceeded, ATSDR examines the health effects levels discussed in the scientific literature and more fully reviews exposure potential. ATSDR reviews available human studies as well as experimental animal studies. This information is used to describe the disease-causing potential of a particular chemical and to compare site-specific dose estimates with doses shown in applicable studies to result in illness (known as the margin of exposure). For cancer effects, ATSDR compares an estimated lifetime exposure dose to available cancer effects levels (CELs), which are doses that produce significant increases in the incidence of cancer or tumors, and reviews genotoxicity studies to understand further the extent to which a chemical might be associated with cancer outcomes. This process enables ATSDR to weigh the available evidence in light of uncertainties and offer perspective on the plausibility of harmful health outcomes under site-specific conditions.

Sources for Health-Based Guidelines

By Congressional mandate, ATSDR prepares toxicological profiles for hazardous substances found at contaminated sites. These toxicological profiles were used to evaluate potential health effects from contamination at EAFB. ATSDR's toxicological profiles are available on the Internet at or by contacting the National Technical Information Service at 1-800-553-6847. EPA also develops health effects guidelines, and in some cases, ATSDR relied on EPA's guidelines to evaluate potential health effects. These guidelines are found in EPA's Integrated Risk Information System (IRIS)--a database of human health effects that could result from exposure to various substances found in the environment. IRIS is available on the Internet at For more information about IRIS, please call EPA's IRIS hotline at1-301-345-2870 or e-mail at

Evaluation of Health Hazards Associated with Contamination at EAFB

ATSDR evaluated data that were collected from drinking water wells on- and off-base, potential chemical warfare materiel (CWM) areas, and ambient air near dual extraction systems at Site 16 and Site 18. For each of these areas, contaminant concentrations were compared to comparison values. Many of the contaminants were detected below their corresponding comparison values. For pathways in which chemicals were detected above comparison values and background levels, exposure doses were calculated. For most of the chemicals, the calculated exposure doses were less than their respective health guidelines (i.e., MRLs and RfDs) and were not expected to cause an increase in cancer outcomes. After evaluating the available toxicologic data for those chemicals where the exposure doses exceeded health guidelines, ATSDR concludes that none of the chemicals were detected at levels of health concern in any of the evaluated areas. See Section 3 of the PHA and Appendices D and E for more information on the exposure pathways and chemicals for which exposure doses were calculated at EAFB.


ATSDR (Agency for Toxic Substances and Disease Registry) 2002. Public Health Assessment Guidance Manual (Update). U.S. Department of Health and Human Services. June 2002.

Duchesne J-F, Gauvin D, Lévesque B, Gingras S, and Dewailly É. 2001. Health Risks Related to Waterfowl and Fish Consumption in Duck Hunters from the St. Lawrence River, Quebec, Canada. Centre Hospitalier Universitaire de Québec (CHUQ)--Centre Hospitalier de l'Universitéé Laval (CHUL) Research Center, Public Health Research Unit.


Edwards Air Force Base (EAFB) drinking water supply well sampling data identified arsenic in one water supply well: N-2 at North Base, which operated from 1964 to 1995. Arsenic is a chemical contaminant and a naturally occurring chemical that is frequently found in high doses in the EAFB area because of leaching from bedrock. Arsenic concentrations fluctuated dramatically over the years, from below detection levels to 81 parts per billion (ppb) in a reading taken in October 1992. To evaluate the likelihood, if any, that arsenic in this well could be associated with adverse health effects, ATSDR derived exposure doses and evaluated the weight of evidence for arsenic toxicity. Deriving exposure doses requires evaluation of contaminant concentrations and length of exposures. Together, these factors help influence an individual's physiological response to chemical contaminant exposure and potential outcomes.

For drinking water at EAFB, it is difficult to determine complete site-specific exposure information because of the way the water distribution system is configured. Well water across the base was and is often mixed from different supply wells before being distributed. This means that arsenic-contaminated water would have been diluted through mixing with non-contaminated water before being ingested by community water supply users. ATSDR was not able to gather enough information about past mixing practices to determine the actual concentrations of arsenic that would have been ingested when the well was operational. In the absence of complete site-specific exposure information, ATSDR applied several conservative exposure assumptions to define exposures as protectively as possible for the EAFB community well users.

ATSDR derived exposure doses using the following assumptions about a person's use of community supply well water as drinking water:

  1. ATSDR estimates that an adult drinks 2 liters and a child drinks 1 liter of water a day and that all drinking water comes from the contaminated well (though, as stated above, this was unlikely to be the case).

  2. The exposure frequency, or number of exposure events per year, was assumed to be 365 days per year, based on a 7-days-a-week exposure over 52 weeks per year.

  3. The duration of exposure is assumed to have occurred over a 30-year period for adults. This value is the 90% upper-bound limit for residency at a single residence (EPA 1997) and is the full length of time the contaminated well was operating. This estimate most likely overestimates the actual duration of exposure, which is likely less than 30 years because of assignment transfers and other factors. For a child, ATSDR used a 6 year exposure duration.

ATSDR compared the estimated doses to standard toxicity values, including ATSDR's minimal risk levels (MRLs) and EPA's reference doses (RfDs). The chronic MRLs and RfDs are estimates of daily human exposure to a substance that are unlikely to result in adverse noncancer effects over a specified duration. To be very protective of human health, MRLs and RfDs have built in "uncertainty" or "safety" factors that make them much lower than levels at which health effects have been observed. Therefore, if an exposure dose is higher than the MRL or RfD, it does not necessarily follow that adverse health effects will occur. ATSDR also compared doses to the cancer effect level (CEL). The CEL is the dose at which tumors, or cancer effects, are seen in laboratory or epidemiology studies.

For noncancer effects, ATSDR found that 30-year exposures to the maximum detected concentration of arsenic (81 ppb) would result in a dose of 0.001 mg/kg/day for adults, and 0.008 mg/kg/day for children. These doses are above the MRL and RfD (0.0003 mg/kg/day). For cancer effects, ATSDR found that estimated exposures over 30 years would result in a dose below the CEL (0.014 mg/kg/day), which is based on an epidemiology study of people exposed to arsenic for over 45 years. Even though the estimated doses for an adult or child exceed the MRL and RfD for arsenic, we do not expect that a person drinking water from this well will experience health effects. First, ATSDR assumed that a person was exposed for an extended period of time to the highest level of arsenic measured in the community supply well. This provides a very conservative estimate of potential exposure because we know from sampling data that there were commonly much lower levels of arsenic in the drinking water supply well than the maximum value. In addition, people probably did not drink water exclusively from this well for the full estimated length of time (because of water supply mixing, as discussed above). Finally, as noted, the MRL and RfD are set much lower than levels at which health effects have been observed.

ATSDR also reviewed available scientific literature on arsenic to evaluate whether adverse health effects would be likely to occur at the reported concentrations or at the estimated doses. Several epidemiologic investigations suggest an association between arsenic (inorganic) and a wide variety of adverse health effects in humans, but at doses higher than those resulting from drinking the maximum arsenic concentrations detected in the EAFB supply well. Symptoms of chronic oral exposure appear to be skin problems (e.g., hyperkeratosis, hyperpigmentation), neurological effects, cardiovascular problems, and gastrointestinal irritations (e.g., vomiting, abdominal pain). Health effects from prolonged (e.g., 45 years) exposure of arsenic have been detected at doses of 0.014 milligrams contaminant per kilogram body weight per day (mg/kg/day) and higher (ATSDR 1998). The estimated exposure doses for a person drinking community supplied well water at EAFB for a 30 year period is about 10 times lower than this dose.

ATSDR looked at potential cancer threats posed by arsenic at the measured concentrations. EPA has classified arsenic as a human carcinogen based on data provided by epidemiologic studies. The bases for classifying arsenic as a human carcinogen are results of multiple epidemiologic studies. One of the most cited reports is a Taiwanese study in which the lowest exposure levels associated with the onset of cancer (skin) were observed in people drinking water containing 170 to 800 ppb arsenic for a 45-year exposure period (ATSDR 1998). People at EAFB, however, could have been intermittently exposed to arsenic at a maximum concentration 10 times lower than this for 30 years, at most.

Furthermore, various studies indicate that at low-level exposures, arsenic compounds are detoxified (or metabolized)--that is, changed into less harmful forms--and then excreted in the urine. At higher levels of exposures, our bodies' capacity to detoxify arsenic may be exceeded. Certain studies suggest that the dose at which this happens is somewhere between 0.25 and 0.5 mg/kg/day, which is much higher than the dose level estimated here (ATSDR 1998). When our body's capacity to detoxify is exceeded, blood levels of arsenic increase and adverse health effects may occur. This appears to be true for cancer and noncancer effects. At lower doses, scientists continue to study the relevance between metabolism and toxicity.

At EPA's request, a special subcommittee of the National Research Council (NRC) reviewed the arsenic toxicity data base and evaluated the scientific basis of EPA's risk assessment for arsenic in drinking water (NRC 1999). They concluded:

  1. Sufficient evidence exists from human epidemiologic studies (Taiwan, Chile, and Argentina) that chronic ingestion of water containing several hundred parts per billion of arsenic causes skin, bladder, and lung cancer. Only very little information is available to address cancer risk at lower concentrations (as seen at EAFB). The subcommittee has therefore recommended further evaluation of the dose-response relationship between arsenic and cancer at lower doses.

  2. Noncancer effects (skin, cardiovascular, and neurologic effects) were observed at chronic exposures of 0.01 mg/kg/day and higher (which is above the dose at EAFB). No developmental or reproductive effects were demonstrated in humans, although arsenic passes through the placenta. In addition to characterizing the dose-response relationship at low doses, the subcommittee recommends further study on skin effects, cardiovascular and cerebrovascular diseases, diabetes mellitus, and reproductive effects.

  3. More information is needed on the mode of action by which arsenic causes adverse effects and cancer. For example, current information suggests that arsenic causes cancer by "inducing chromosomal abnormalities without interacting directly with DNA." If this is true, the dose-response curve would show sublinear characteristics in the low-dose range.

There is sufficient evidence to suggest that arsenic causes adverse health effects, including cancer, but at levels much higher than those measured in the EAFB community supply well. While scientists are still uncertain about the health effects, if any, of long-term, low-level exposure to arsenic in drinking water, enough evidence exists to suggest that arsenic is tolerated by humans at low doses. Given this information, ATSDR does not believe that arsenic at the levels measured in the one drinking water supply well at EAFB are high enough to cause adverse health effects or cancer.


ATSDR (Agency for Toxic Substances and Disease Registry) 1998. Toxicological Profile for Arsenic (Update). U.S. Department of Health and Human Services. August 1998.

EPA 1997. Exposure Factors Handbook. National Center for Environmental Assessment. EPA/600/P-95/00Fa. August 1997.

NRC (National Research Council) 1999. Arsenic in Drinking Water. National Academy Press.


Dioxins/Furans--An Overview

What Are Dioxins/Furans?

Polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzo-p-furans (PCDFs) are two related classes of chlorinated organic compounds with similar structures. A PCDD molecule has 8 different positions that can be occupied by a chlorine atom, while a PCDF molecule has 10 positions. The possibility of different locations for chlorine atoms in the structure of the molecule allows for 75 individual variations or "congeners" of PCDDs, and 135 of PCDFs. The only difference between these congeners is the specific number and location of the chlorine atoms in each. Different congeners that share the same number of chlorine atoms, but at different locations, are referred to as isomers. Groups of isomers that contain 1, 2, 3, 4, 5, 6, 7, or 8 chlorine atoms are called mono-, di-, tri-, tetra-, penta-, hexa-, hepta-and octa-chlorinated dioxins/furans, respectively (ATSDR 1998).

Figure 1. Core Structures of Dioxins and Furans

The relative toxicity or potency of various PCDDs and PCDFs is strongly influenced by the number and position of the chlorine atoms in the molecule. The most toxic dioxin, and the most extensively studied, is 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD or TCDD). More highly chlorinated (i.e., penta- through octa-) PCDDs/PCDFs that also have chlorine atoms at the 2, 3, 7 and 8 positions (among others) are often described as "dioxin-like compounds" in recognition of the possibility for their toxicities to be similar to that of 2,3,7,8-TCDD (ATSDR 1998).

What Are Sources of Dioxin Contamination and Exposure?

PCDDs and PCDFs are not produced deliberately; they are unwanted byproducts that can, under special conditions, be formed during combustion and certain industrial processes. Dioxins are formed as a contaminant during the manufacture of certain chlorinated organic chemicals. However, due to significant refinements in the manufacturing process, emissions from the chemical industry are no longer a major source of dioxins nationwide. Today, in the U.S., older medical and municipal incinerators are among the major remaining sources of dioxins still being released into the environment (ATSDR 1998). At EAFB, the combustion processes used to destroy other contaminants in soil and groundwater form dioxins that are released to the air.

Estimates of average daily background exposures in the U.S. general population are 0.3 to 0.6 picograms TCDD per kilogram per day (pg/kg/day) and about 1 pg/kg/day of "dioxin-like" PCDDs and PCDFs (ATSDR 1998, EPA 1994a). Over 90% of that exposure comes from eating meat, fish, and dairy products contaminated with residues that first entered the food chain many years ago (ATSDR 1998). Dioxins are very stable, highly lipophilic ("fat loving") compounds that, depending on the congener, may also be relatively resistant to metabolism or degradation. As a result, dioxins have a strong tendency to bioaccumulate in fat, bind strongly to soils and sediments high in organic content, and persist in the environment for many years. Nevertheless, average concentrations of dioxins in biological and environmental samples have been declining since the 1970s and continue to do so (EPA 2000b, 2000d). Due to the existence of natural sources, however, dioxins will never disappear completely from the environment.

Before analytical techniques were sensitive enough to demonstrate otherwise, it was commonly thought that dioxins were produced exclusively as a byproduct of industrial activities. It is now known, however, that dioxins pre-date not only the industrial revolution but the human race itself; they have recently been detected in 30 million-year-old clay deposits (Hayward at el. 1999). Dioxins are produced by natural, as well as anthropogenic,combustion processes, including forest fires. They are generated in very small amounts during the combustion of almost any organic material (Rigo et al., 1998; Wikstrom et al. 2001).

Potential Adverse Health Effects of Dioxins

Some natural substances, like botulinum toxin, are more toxic than dioxin, but TCDD produces adverse health effects in laboratory animals at lower concentrations than any other human-made chemical. Less than one millionth of a gram per kilogram of body weight (or 1 microgram per kilogram [µg/kg]) can slowly kill a guinea pig or initiate the development of cancer in rats. However, even these tiny doses are up to a million times higher than those that typically occur outside the laboratory, today. Average background doses in the U.S. and Europe are in the range of 1 trillionth of a gram per kilogram of body weight per day (0.000000000001 grams/kg/day or 1 pg/kg/day). During the Vietnam War, the herbicide Agent Orange was contaminated with parts per million of dioxin (TCDD). Today, concentrations of dioxin in highly contaminated soil are measured in the low parts per billion (ppb); in food, dioxins occur in parts per trillion (ppt); in water, in parts per quadrillion (ppq); and in air, in parts per quintillion (ppqt). Each of these units of measure is 1,000 times smaller than the previous one. For perspective, there are about 28 grams in one ounce. (In subsequent sections, doses will generally be converted to pg/kg/day to facilitate comparison to an average human background exposure of 1 pg/kg/day.)

Animal Effects

Relatively little is known about the adverse health effects of non-TCDD dioxins, but the most toxic congener, 2,3,7,8-TCDD, is one of the most extensively studied of all known environmental toxins. Wherever sufficiently high doses of TCDD have been administered, a variety of effects have been observed in almost every animal species tested. Observed effects in animals include death, weight loss, liver toxicity, immune suppression, reproductive impairments, birth defects, and cancer (ATSDR, 1998). The doses of dioxin required to produce these adverse health effects in animals vary enormously with species, as well as with strain, sex, tissue, and duration of exposure. For example, reported LD50 values for TCDD--an LD50 is the dose of a substance required to kill 50% of the exposed test animals--vary from 0.6 µg/kg (600,000 pg/kg/day) in male Hartley guinea pigs to 5,051 ug/kg (5,000,000,000 pg/kg) in Syrian hamsters. This represents more than an 8,000-fold difference between two species of rodent that are much more closely related to one another than either is to humans (ATSDR 1998).

Virtually all known chronic, intermediate, and acute effects levels for TCDD range upward from 100 to 1,000 and to 100,000 pg/kg/day, respectively. For non-TCDD dioxins, known effect levels in animals exceed a million pg/kg/day or 1 µg/kg/day (ATSDR 1998) In absolute terms, these effect levels are among the lowest recorded for any human-made toxic substance, which accounts for dioxin's reputation as "the most toxic human-made substance known." However, relative to the current potential for environmental exposure in humans, these levels are actually quite high.

ATSDR's chronic Minimum Risk Levels (MRLs) are estimates of daily doses that would not be associated with any detrimental effects over a lifetime of exposure. Most are based on animal effects and the application of conservative safety factors. For example, ATSDR's chronic MRL for TCDD of 1 pg/kg/day, which approximates average background exposures in the U.S., is based on less serious effects on social behavior in monkey offspring and an additional safety factor of 90 (ATSDR 1998).

Human Effects

Humans appear to be 10 to 100 times less sensitive to the effects of dioxin than are laboratory rats and mice (Kimbrough 1992, Aylward et al. 1998). It is generally assumed by regulatory agencies that sufficiently high dioxin exposures would produce most, if not all, of the adverse health effects in humans that have been seen in laboratory animals. The validity of this assumption, however, has not been confirmed by the highest human exposures recorded to date, and, due to the elimination of most major sources of dioxin emissions, it is extremely unlikely that even higher exposures will ever occur in the future. More than 100 epidemiological studies have looked at the potential effects of dioxin and dioxin-contaminated herbicides in humans, including exposed workers in the chemical industry, soldiers exposed to Agent Orange in Vietnam, and persons accidentally exposed to TCDD in Seveso, Italy and in Times Beach, Missouri (Institute of Medicine 1994). A weight of evidence review of all of these studies indicates that chloracne is the only adverse health effect for which there is unequivocal evidence of a causal link with dioxin exposure in humans (Gotts 1993, DeVito et al. 1995). Although not life-threatening, chloracne is a serious, potentially disfiguring skin eruption associated with unusually high exposures to dioxin, especially those that occurred prior to the 1980s as a result of occupational or environmental accidents. No human fatality directly attributable to dioxin exposure has ever been recorded.

The International Agency for Research on Cancer (IARC) recently reclassified TCDD from a "possible" human carcinogen to a "known" human carcinogen (IARC 1997). That classification, which ordinarily requires "sufficient" evidence in humans, was based in this case on "limited" evidence in humans, "sufficient" evidence in animals, and "supporting information" interpreted as suggesting a common mechanism of action for TCDD in various species, including humans. Actually, the mechanism by which TCDD and other dioxins induce adverse effects is still largely unknown (EPA 1989, 2000c). The assumption of a common mechanism based on binding to a common cellular macromolecule (the Ah-receptor) is the first among several assumptions and inferences of uncertain scientific validity that serve as the logical foundation of the interim toxicity equivalency factor (TEF) approach discussed in the next section of this appendix. (EPA 1989, 2000b, 2000c).

EPA has recently announced its own intention to re-classify TCDD as "carcinogenic to humans" and other dioxin-like compounds as "likely" human carcinogens (EPA 2000b). EPA bases its re-characterization of TCDD as "carcinogenic to humans" on extrapolations from animal data, hypotheses concerning the role of the Ah receptor in dioxin's mode of action, and purportedly equivalent "body burdens" (on a TEQ basis) in animal and human populations with cancer (EPA 2000c). At the same time, however, EPA acknowledges that the data from epidemiological studies of cancer in exposed humans "do not confirm a causal relationship between exposure to dioxin and increased cancer incidence" (EPA 2000c).

Although some data are suggestive of an association between dioxins and cancer in humans, the studies do not support firm conclusions. Even the best studies of the most heavily exposed occupational populations have provided only inconsistent and inconclusive evidence that TCDD might cause cancer in humans (Zober et al. 1990, Manz et al. 1991, Fingerhut et al. 1991, Steenland et al. 1999). Generally, the observed excess risks for all cancers, combined, and specific types of cancer, alone, were relatively small--standard mortality ratios were generally less than 2.0--and were seen only in the most highly exposed groups with estimated 2,3,7,8-TCDD exposures 100 to 1,000 times those seen in the general population. Simultaneously, affected individuals tended to have exposure to other carcinogenic substances in addition to TCDD. In the absence of controls for such confounding exposures, the observed cancer excesses could not be attributed directly to TCDD with any confidence. In one of the largest and best-conducted of these occupational studies, observed increases in lung cancer and all cancers combined (42% and 15%, respectively) became statistically insignificant when attempts were made to control for smoking (Fingerhut et al. 1991).

The highest short-term TCDD exposures ever recorded--mean exposures were over 3 million pg/kg--occurred in 1976 in Seveso, Italy, where children were exposed to more TCDD in a single day than an average U.S. citizen would be exposed to in a lifetime (Gough 1994). The highest blood level of TCDD ever recorded (56,000 ppt) was measured in a female child at Seveso just days after the accident. Yet, with the exception of chloracne, follow-up studies of the Seveso cohort have firmly established no consistent or unusual pattern, either for the frequency or type of outcome, attributable to TCDD exposure (Bertazzi and Domenico 1994). Ten to fifteen years after the 1976 accident, there was an increase in some types of cancer, a deficit in others, and an overall decrease in expected cancer rates, especially among those with the highest exposure (Bertazzi et al. 1989, Bertazzi et al. 1997). Thus, if dioxin is a human carcinogen, it must be a weak one at doses realistically achievable outside the laboratory.

A number of studies have reported measured differences in various developmental outcomes (e.g., hormone and enzyme levels of thyroxin, liver enzymes, vitamin K, neurological endpoints, white blood cell counts, and other immunological markers) in the breast-fed infants of mothers whose milk contained elevated levels of dioxins (Koppe et al. 1991, Pluim et al. 1993, Pluim et al. 1994b, Koopman-Esseboom et al. 1994, Huisman et al. 1995, Weisglas-Kuperus et al. 1995). However, the detected differences generally involve subtle and inconsistent biochemical changes that were well within the range of normal variation and are of no known clinical significance. (A caveat common to virtually all such studies is that any hypothetical risks that may be associated with the consumption of dioxin- or PCB-contaminated breast milk are minor compared to the well-established medical benefits associated with breast-feeding) (EPA, 2000c).

The TEF/TEQ Concept

The overlapping nature of some of the effects produced in animals by some congeners of PCDDs and PCDFs makes it highly desirable to include all such "dioxin-like" compounds in risk assessments for dioxin-contaminated sites. However, the relative lack of relevant toxicologic data on non-TCDD congeners made such a task virtually impossible. In the early 1980s, however, regulatory agencies temporarily solved this dilemma by developing the "Toxicity Equivalency Factor (TEF) approach," and recommending its adoption as an "interim science policy position for use in assessing risks associated with CDD/CDF mixtures, until more definitive scientific data are available" (EPA 1989).


TEFs are order of magnitude (factor of ten) estimates of the relative toxicity of dioxin-like compounds. In the TEF approach, the measured concentrations of all 2,3,7,8-PCDDs and 2,3,7,8-PCDFs are converted to "equivalent" concentrations of TCDD by multiplying the concentration of each congener in the mixture by its TEF, thereby expressing each individual concentration in terms of hypothetical "toxicity equivalents" or TEQs. The individual TEQ values are then added together, to yield a single TEQ value for all of the PCDDs and PCDFs detected at the site (EPA, 1989; ATSDR, 1998).

TEQ equals 'sum'(PCDD sub i X TEF sub i) plus 'sum' (PCDF sub i X TEF sub i

The TEFs used to calculate the TEQs were developed by EPA and the international community in 1989 and revised in 1998 by the World Health Organization (WHO), parent organization of IARC (EPA, 1989; Van den Berg et al., 1998). Alternative sets of TEFs do exist. Some states (California, for example) have developed their own versions, but all are strongly influenced by the International TEFs. The 1998 International TEFs (I-TEFs) are listed in the following table. All dioxin concentrations evaluated at EAFB were derived using the TEF approach.

International Toxic Equivalent Factors (I-TEFs) for TCDDs and TCDFs
Dioxin Group TEF Furan Group TEF
Tetrachlorodibenzo-p-dioxin (TCDD)
other TCDDs
Tetrachlorodibenzofuran (TCDF)
other TCDFs
Pentachlorodibenzo-p-dioxin (PeCDD)
other PeCDDs
Pentachlorodibenzofuran (PeCDF)
other PeCDFs
Hexachlorodibenzo-p-dioxin (HxCDD)
other HxCDDs
Hexachlorodibenzofuran (HxCDF)
2,3,7,8-HxCDF a
other HxCDFs
Heptachlorodibenzo-p-dioxin (HpCDD)
other HpCDDs
Heptachlorodibenzofuran (HpCDF)
other HpCDFs
Octachlorodibenzo-p-dioxin (OCDD)
0.0001 Octachlorodibenzofuran (OCDF)

a any isomer that contains chlorine in the 2,3,7,8-positions

Use of TEFs

The TEF method was originally developed as a means of arriving at approximations of the toxicity of mixtures of dioxin-like compounds that could then be incorporated into risk assessments. Risk assessments provide regulatory officials with a systematic basis for making risk management decisions and numerically ranking contaminated sites for cleanup. EPA considers the TEF method to be an interim approach only, one which will be replaced as soon as research yields a more accurate, practical alternative (EPA 1989).

ATSDR uses total TEQs for screening purposes only. It is currently ATSDR's policy to use TCDD-specific comparison values, expressed in TEQs, to screen all dioxin-like compounds. However, as with evaluations of all chemical contaminants, if the concentration exceeds a comparison value, further evaluation must follow, utilizing "the best medical and toxicologic information available" (ATSDR 1992). TEQs, alone, lack the information needed for the determination of probable public health implications of exposures to dioxin-like compounds. Congener-specific data are needed to properly employ chemical-specific information summarized in ATSDR's Toxicological Profiles for PCDDs and PCDFs (ATSDR 1994, 1997, 1998).

Unfortunately, the term "toxicity equivalent" has been taken literally in many places and the TEF approach is now widely used by many people outside the regulatory establishment in ways for which it was never intended. EPA has indicated repeatedly that toxicity equivalency factors are not meant to be used precisely, even in a regulatory context (EPA 1989, 1994a). It goes without saying that they cannot be used to accurately predict adverse health effects in humans.

Limitations of TEFs

The TEF approach was adopted by EPA as an interim science policy measure designed to facilitate risk management decisions (EPA 1989). From the beginning, scientific and regulatory communities around the world cited the shortcomings in the science base supporting the TEF concept, and the latter has always been subject to revision as new experimental data became available (EPA 1989). Some of the inconsistencies in the TEF method are summarized below.

TEFs are not precise measures of relative toxicity, and they were not designed for the prediction of adverse health effects (EPA 1989, 1994a). EPA considers the TEQ approach to be "a useful, but uncertain, procedure." The TEQs based on those TEFs, though useful as screening devices, cannot, therefore, be used in the Public Health Assessment process in place of actual, congener-specific data.

TEFs are order of magnitude estimates of average, relative toxicity based on highly variable data sets. TEFs are derived, by consensus, from limited experimental results that typically range over 1-to-2 orders of magnitude. These data usually come from in vitro studies and/or short-term animal studies of Ah receptor binding or P450 enzyme induction which do not represent true measures of whole-body toxicity (EPA 1989, 1994a).

Although TEFs are defined and used as constants, the numerical value of an experimentally determined TEF will, in fact, vary significantly with a number of parameters, including: dose, duration of exposure, species, sex, strain, target tissue, and biological endpoint (DeVito and Birnbaum 1995, Safe 1990, EPA 1994b). In some cases, TCDD can even have opposite effects in different species (EPA 1994b).

TEFs can be expected to become increasingly imprecise as the conditions under which they are applied become further removed from the conditions under which they were derived. (Putzrath 1996). TEFs are generally derived from relatively high-dose data obtained in vitro or from short-term rodent assays, but they are most often applied in the context of low-level environmental exposures in humans.

TEFs do not take into account many important biological factors. The health implications of exposure to a mixture of dioxin-like compounds will depend on, among other things, the bioavailability of specific congeners and the potential for antagonistic interactions between them. TEFs, however, do not account for either (EPA 1989, 1994a).

Finally, the assumption that all adverse effects of dioxin and dioxin-like compounds share a common mechanism is just that--an assumption. Whether or not it is actually true, this assumption is critical to the TEF approach because it provides the theoretical basis for the simplifying inference that TEQs are additive. However, except for the chain of events leading to the induction of certain enzymes, which is not necessarily an adverse effect, clear evidence for such an assumption is still lacking (EPA 1994c). The available data indicate that binding to the Ah receptor is not sufficient in itself to result in toxicity (EPA 1994c). The actual mechanism of action is still unknown for virtually all dioxin-induced adverse effects.

References and Documents Reviewed

ATSDR (Agency for Toxic Substances and Disease Registry) 1992. ATSDR Public Health Assessment Guidance Manual. U.S. Department of Health and Human Services. Lewis Publishers, Chelsea, Michigan.

ATSDR 1994. Toxicological Profile for Chlorodibenzofurans. U.S. Department of Health and Human Services. May 1994.

ATSDR 1997. Toxicological Profile for Polychlorinated Biphenyls (Update). U.S. Department of Health and Human Services. September 1994.

ATSDR 1998. Toxicological Profile for Chlorinated Dibenzo-p-Dioxins (Update). U.S. Department of Health and Human Services. December 1998.

Aylward et al. 1996. Relative Susceptibility of Animals and Humans to the Cancer Hazard Posed by 2,3,7,8-Tetrachlorodibenzo-p-Dioxin Using Internal Measures of Dose. Environ Sci Technol 30:3534-3543.

Bertazzi PA, Zocchetti C, Pesatori A, Guercilena S, Sanarico M, and Radice L. 1989. Ten-Year Mortality Study of the Population Involved in the Seveso Incident in 1976. Am J Epidemiol 129:1187-1200.

Bertazzi PA and di Domenico A. 1994. Chemical, Environmental, and Health Aspects of the Seveso, Italy, Accident. In: Dioxins and Health (Arnold Schecter, ed.), Plenum Press, New York, NY, 1994.

Bertazzi PA, Zocchetti C, Guercilena S, et al. 1997. Dioxin Exposure and Cancer Risk: A 15-Year Mortality Study After the "Seveso Accident." Epidemiology 8:646-652.

DeVito et al. 1995. Comparisons of Estimated Human Body Burdens of Dioxin-Like Chemicals and TCDD Body Burdens in Experimentally Exposed Animals. Environ Health Perspect 103(9):820-829.

DeVito and Birnbaum 1995. The Importance of Pharmacokinetics in Determining the Relative Potency of 2,3,7,8-Tetrachloro-Dibenzo-p-Dioxin and 2,3,7,8-Tetrachlorodibenzofuran. Fundam Appl Toxicol 24:145-148.

EPA (U.S. Environmental Protection Agency) 1989. Interim Procedures for Estimating Risks Associated with Exposure to Mixtures of Chlorinated Dibenzo-p-Dioxins and Dibenzofurans (CDDs and CDFs) and 1989 Update. Risk Assessment Forum, Washington, DC.

EPA 1994a. Health Assessment Document for 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) and Related Compounds, Volume III (External Review Draft). EPA/600/BP-92/001c. August 1994.

EPA 1994b. Health Assessment Document for 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) and Related Compounds, Volume II (External Review Draft). EPA/600/BP-92/001b. June 1994.

EPA 1994c. Health Assessment Document for 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) and Related Compounds, Volume I (External Review Draft). EPA/600/BP-92/001a. June 1994.

EPA 1998. Inventory of Sources of Dioxin in the United States (External Review Draft). EPA/600/P-98/002Aa. April 1998.

EPA 2000a. Information Sheet 1. Dioxin: Summary of the Dioxin Reassessment Science. June 12, 2000.

EPA 2000b. Information Sheet 2. Dioxin: Scientific Highlights from Draft Reassessment (2000). June 12, 2000.

EPA 2000c. Exposure and Human Health Reassessment of 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) and Related Compounds. Part II: Health Assessment for 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) and Related Compounds (External Review Draft). EPA/600/P-00/001Ae. May 2000.

EPA 2000d. Exposure and Human Health Reassessment of 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) and Related Compounds. Part III: Integrated Summary and Risk Characterization for 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) and Related Compounds (External Review Draft). EPA/600/P-00/001Ag. June 2000.

Fingerhut MA, Halperin WE, Marlow DA, et al. 1991. Cancer Mortality in Workers Exposed to 2,3,7,8-Tetrachlorodibenzo-p-Dioxin. New England Journal of Medicine 324:212-218.

Gotts RE. 1993. Toxic Risks: Science, Regulation, and Perception. In: Dioxins and Agent Orange. Ronald E. Gotts, M.D., Ph.D., National Medical Advisory Service, Bethesda, Maryland. Lewis Publishers, 1993.

Gough M. 1994. Dioxin: Perceptions, Estimates, and Measures. In: Phantom Risk: Scientific Inference and the Law (Kenneth R Foster, David Bernstein, and Peter Huber, eds.), The MIT Press, Cambridge, Massachusetts, 1994.

Hayward et al. 1999. Elevated TCDD in Chicken Eggs and Farm-Raised Catfish Fed a Diet with Ball Clay from a Southern United States Mine. Environ Res 81:248-256.

Huisman M et al. 1995. Perinatal Exposure to Polychlorinated Biphenyls and Dioxins and Its Effect on Neonatal Neurological Development. Early Hum Dev 41:111-127.

IARC (International Agency for Research on Cancer) 1997. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Volume 69: Polychlorinated Dibenzo-para-Dioxins and Polychlorinated Dibenzofurans. World Health Organization, Lyon, France.

Institutes of Medicine 1994. Veterans and Agent Orange: Health Effects of Herbicides Used in Vietnam. National Academy Press, Washington, DC.

Kimbrough 1992. Tolerable Daily Intake of 2,3,7,8-Tetrachlorodibenzo-p-Dioxin: Recent Data on Mechanism and Animal Carcinogenicity. Toxic Substances Journal 12:295-306.

Koopman-Esseboom C. et al. 1994. Effects of Dioxins and Polychlorinated Biphenyls on Thyroid Hormone Status of Pregnant Women and Their Infants. Pediatr Res 36:468-473.

Koppe JG et al. 1991. Breast Milk, Dioxins, and the Possible Effects on the Health of Newborn Infants. Sci Total Environ 106:33-41.

Manz A et al. 1991. Cancer Mortality in Chemical Plant Contaminated with Dioxin. Lancet 338:959-964.

Pluim et al. 1993. Effects of Pre- and Postnatal Exposure to Chlorinated Dioxins and Furans on Human Neonatal Thyroid Hormone Concentrations. Environ Health Perspect 101:504-508.

Pluim et al. 1994a. Dioxin and Vitamin K Status of the Newborn. J Environ Sci Health A29(4):793-802.

Pluim et al. 1994b. Clinical Laboratory Manifestation of Exposure to Background Levels of Dioxins in the Perinatal Period. Acta Pediatr 83:583-587.

Putzrath RM. 1996. Estimating Relative Potency for Receptor-Mediated Toxicity: Re-evaluating the Toxicity Equivalence Factor (TEF) Model. Regul Toxicol Pharmacol 25:68-78.

Rigo HG and Chandler AJ. 1998. Is There a Strong Dioxin: Chlorine Link in Commercial Scale Systems? Chemosphere 37:2031-2046.

Safe S. 1990. Polychlorinated Biphenyls (PCBs), Dibenzo-p-Dioxins (PCDDs), Dibenzofurans (PCDFs), and Related Compounds: Environmental and Mechanistic Considerations Which Support the Development of Toxic Equivalency Factors (TEFs). CRC Crit Rev Toxicol 21:51-88.

Steenland K et al. 1999. Cancer, Heart Disease, and Diabetes in Workers Exposed to 2,3,7,8-Tetrachlorodibenzo-p-Dioxin. J Nat Cancer Inst 91:779-786.

Van den Berg M, Birnbaum L, Bosveld ATC, et al. 1998. Toxic Equivalency Factors (TEFs) for PCBs, PCDDs, PCDFs for Humans and Wildlife. Environ Health Perspect 106:775-791.

Weisglas-Kuperus et al. 1995. Immunological Effects of Background Prenatal and Postnatal Exposure to Dioxins and Polychlorinated Biphenyls in Dutch Infants. Pediatr Res 38:404-410.

Wikstrom E and Marklund S. 2001. The Influence of Level and Chlorine Source on the Formation of Mono- to Octa-Chlorinated Dibenzo-p-Dioxins, Dibenzofurans and Coplanar Polychlorinated Biphenyls During Combustion of an Artificial Municipal Waste. Chemosphere 43(2):227-234.

Zober et al. 1990. Thirty-Four-Year Mortality Follow-up of BASF Employees Exposed to 2,3,7,8-TCDD After the 1953 Accident. Int Arch Occup Environ Health 62:139-157.


How a chemical enters a person's blood after the chemical has been swallowed, has come into contact with the skin, or has been breathed in.

Adverse Health Effect:
A change in body function or the structures of cells that can lead to disease or health problems.

The Agency for Toxic Substances and Disease Registry. ATSDR is a federal health agency in Atlanta, Georgia that deals with hazardous substance and waste site issues. ATSDR gives people information about harmful chemicals in their environment and tells people how to protect themselves from coming into contact with chemicals.

Background Level:
An average or expected amount of a chemical in a specific environment. Or, amounts of chemicals that occur naturally in a specific environment.

Used in public health, things that humans would eat - including animals, fish and plants.

See Community Assistance Panel.

A group of diseases which occur when cells in the body become abnormal and grow, or multiply, out of control

Any substance shown to cause tumors or cancer in experimental studies.

See Comprehensive Environmental Response, Compensation, and Liability Act.

Chronic Exposure:
A contact with a substance or chemical that happens over a long period of time. ATSDR considers exposures of more than one year to be chronic.

Completed Exposure Pathway:
See Exposure Pathway.

Comparison Value (CVs):
Concentrations or the amount of substances in air, water, food, and soil that are unlikely, upon exposure, to cause adverse health effects. Comparison values are used by health assessors to select which substances and environmental media (air, water, food and soil) need additional evaluation while health concerns or effects are investigated.

Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA):
CERCLA was put into place in 1980. It is also known as Superfund. This act concerns releases of hazardous substances into the environment, and the cleanup of these substances and hazardous waste sites. ATSDR was created by this act and is responsible for looking into the health issues related to hazardous waste sites.

A belief or worry that chemicals in the environment might cause harm to people.

How much or the amount of a substance present in a certain amount of soil, water, air, or food.

See Environmental Contaminant.

Dermal Contact:
A chemical getting onto your skin. (see Route of Exposure).

The amount of a substance to which a person may be exposed, usually on a daily basis. Dose is often explained as "amount of substance(s) per body weight per day".

Dose / Response:
The relationship between the amount of exposure (dose) and the change in body function or health that result.

The amount of time (days, months, years) that a person is exposed to a chemical.

Environmental Contaminant:
A substance (chemical) that gets into a system (person, animal, or the environment) in amounts higher than that found in Background Level, or what would be expected.

Environmental Media:
Usually refers to the air, water, and soil in which chemical of interest are found. Sometimes refers to the plants and animals that are eaten by humans. Environmental Media is the second part of an Exposure Pathway.

U.S. Environmental Protection Agency (EPA):
The federal agency that develops and enforces environmental laws to protect the environment and the public's health.

Coming into contact with a chemical substance.(For the three ways people can come in contact with substances, see Route of Exposure.)

Exposure Assessment:
The process of finding the ways people come in contact with chemicals, how often and how long they come in contact with chemicals, and the amounts of chemicals with which they come in contact.

Exposure Pathway:
A description of the way that a chemical moves from its source (where it began) to where and how people can come into contact with (or get exposed to) the chemical.

ATSDR defines an exposure pathway as having 5 parts:
  1. Source of Contamination,

  2. Environmental Media and Transport Mechanism,

  3. Point of Exposure,

  4. Route of Exposure; and,

  5. Receptor Population.

When all 5 parts of an exposure pathway are present, it is called a Completed Exposure Pathway. Each of these 5 terms is defined in this Glossary.

How often a person is exposed to a chemical over time; for example, every day, once a week, twice a month.

Hazardous Waste:
Substances that have been released or thrown away into the environment and, under certain conditions, could be harmful to people who come into contact with them.

Health Effect:
ATSDR deals only with Adverse Health Effects (see definition in this Glossary).

Indeterminate Public Health Hazard:
The category is used in Public Health Assessment documents for sites where important information is lacking (missing or has not yet been gathered) about site-related chemical exposures.

Swallowing something, as in eating or drinking. It is a way a chemical can enter your body (See Route of Exposure).

Breathing. It is a way a chemical can enter your body (See Route of Exposure).

Minimal Risk Level. An estimate of daily human exposure - by a specified route and length of time -- to a dose of chemical that is likely to be without a measurable risk of adverse, noncancerous effects. An MRL should not be used as a predictor of adverse health effects.

The National Priorities List. (Which is part of Superfund.) A list kept by the U.S. Environmental Protection Agency (EPA) of the most serious, uncontrolled or abandoned hazardous waste sites in the country. An NPL site needs to be cleaned up or is being looked at to see if people can be exposed to chemicals from the site.

No Apparent Public Health Hazard:
The category is used in ATSDR's Public Health Assessment documents for sites where exposure to site-related chemicals may have occurred in the past or is still occurring but the exposures are not at levels expected to cause adverse health effects.

No Public Health Hazard:
The category is used in ATSDR's Public Health Assessment documents for sites where there is evidence of an absence of exposure to site-related chemicals.

Public Health Assessment. A report or document that looks at chemicals at a hazardous waste site and tells if people could be harmed from coming into contact with those chemicals. The PHA also tells if possible further public health actions are needed.

A line or column of air or water containing chemicals moving from the source to areas further away. A plume can be a column or clouds of smoke from a chimney or contaminated underground water sources or contaminated surface water (such as lakes, ponds and streams).

Point of Exposure:
The place where someone can come into contact with a contaminated environmental medium (air, water, food or soil). For examples: the area of a playground that has contaminated dirt, a contaminated spring used for drinking water, the location where fruits or vegetables are grown in contaminated soil, or the backyard area where someone might breathe contaminated air.

A group of people living in a certain area; or the number of people in a certain area.

Public Health Assessment(s):
See PHA.

Public Health Hazard:
The category is used in PHAs for sites that have certain physical features or evidence of chronic, site-related chemical exposure that could result in adverse health effects.

Public Health Hazard Criteria:
PHA categories given to a site which tell whether people could be harmed by conditions present at the site. Each are defined in the Glossary. The categories are:
  1. Urgent Public Health Hazard

  2. Public Health Hazard

  3. Indeterminate Public Health Hazard

  4. No Apparent Public Health Hazard

  5. No Public Health Hazard

Receptor Population:
People who live or work in the path of one or more chemicals, and who could come into contact with them (See Exposure Pathway).

Reference Dose (RfD):
An estimate, with safety factors (see safety factor) built in, of the daily, life-time exposure of human populations to a possible hazard that is not likely to cause harm to the person.

Route of Exposure:
The way a chemical can get into a person's body. There are three exposure routes:
- breathing (also called inhalation),
- eating or drinking (also called ingestion), and
- or getting something on the skin (also called dermal contact).

Safety Factor:
Also called Uncertainty Factor. When scientists don't have enough information to decide if an exposure will cause harm to people, they use "safety factors" and formulas in place of the information that is not known. These factors and formulas can help determine the amount of a chemical that is not likely to cause harm to people.

The Superfund Amendments and Reauthorization Act in 1986 amended CERCLA and expanded the health-related responsibilities of ATSDR. CERCLA and SARA direct ATSDR to look into the health effects from chemical exposures at hazardous waste sites.

Sample Size:
The number of people that are needed for a health study.

A small number of people chosen from a larger population (See Population).

Source (of Contamination):
The place where a chemical comes from, such as a landfill, pond, creek, incinerator, tank, or drum. Contaminant source is the first part of an Exposure Pathway.

Special Populations:
People who may be more sensitive to chemical exposures because of certain factors such as age, a disease they already have, occupation, sex, or certain behaviors (like cigarette smoking). Children, pregnant women, and older people are often considered special populations.

A branch of the math process of collecting, looking at, and summarizing data or information.

Superfund Site:
See NPL.

A way to collect information or data from a group of people (population). Surveys can be done by phone, mail, or in person. ATSDR cannot do surveys of more than nine people without approval from the U.S. Department of Health and Human Services.

Synergistic effect:
A health effect from an exposure to more than one chemical, where one of the chemicals worsens the effect of another chemical. The combined effect of the chemicals acting together are greater than the effects of the chemicals acting by themselves.

Harmful. Any substance or chemical can be toxic at a certain dose (amount). The dose is what determines the potential harm of a chemical and whether it would cause someone to get sick.

The study of the harmful effects of chemicals on humans or animals.

Abnormal growth of tissue or cells that have formed a lump or mass.

Uncertainty Factor:
See Safety Factor.

Urgent Public Health Hazard:
This category is used in ATSDR's Public Health Assessment documents for sites that have certain physical features or evidence of short-term (less than 1 year), site-related chemical exposure that could result in adverse health effects and require quick intervention to stop people from being exposed.


ATSDR received the following comments during the public comment period (February 11 to March 23, 2003) for the Edwards Air Force Base Public Health Assessment (February 2003). For comments that questioned the validity of statements made in the Public Health Assessment, ATSDR verified or corrected the statements.

  1. Comment: The demographics maps are too small, rendering them illegible. Please increase their size.
  2. Response: ATSDR uses standard, approved, demographic maps for all of its Public Health Assessments. The intent of the demographic maps is to provide an overview of potentially exposed populations, not to provide comprehensive census information about populations in the larger vicinity of the study area. For the EAFB Public Health Assessment, the maps show population density on base, and population density trends to the north, south, east, and west of the base.

  3. Comment: Suggest deleting the Groundwater Flow direction arrows on the map and in the Legend to eliminate potential misinterpretation that water from the lake bed flows off the base.
  4. Response: ATSDR has modified Figure 7 to more clearly delineate groundwater flow patterns at EAFB. In the vicinity of North Base, groundwater (not surface water) does flow off-base. Groundwater on the eastern and western portions of the base flows towards the lake bed.

  5. Comment: The address for Ed Walker, California Toxic Substances Control, is incorrect. His current address is: 8800 Cal Center Drive, Sacramento, CA 95826-3200.
  6. Response: ATSDR has updated the document, as requested.

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