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A release of a hazardous substance does not always result in human exposure, and humanexposure does not always result in adverse health effects.

This section of the public health assessment evaluates the estimated exposure doses forcontaminants of concern for completed and potential exposure pathways for potentially affectedpopulations. In these evaluations, ATSDR considered the frequency and duration of the estimatedexposures; for cases in which a population is affected by more than one exposure pathway, wealso considered the combinations of contaminants and exposure routes. This section also presentsthe potential health effects from each contaminant of concern in a completed exposure pathway.

We considered characteristics of the exposed populations--such as age, sex, nutritional status,genetics, lifestyle, and health status--that influence how a person absorbs, distributes,metabolizes, and excretes contaminants; and, where appropriate, these characteristics areincluded in the contaminant-specific discussions.

Special Considerations of Women and Children

Women and children can sometimes be affected differently from the general population bycontaminants in the environment. Both tend to be smaller than the average person, which meansthey can be affected by smaller quantities of contaminants. The effect of hormonal variations,pregnancy, and lactation can change the way a woman's body responds to some substances. Pastexposures experienced by its mother, as well as exposure during pregnancy and lactation, canexpose a fetus or infant to chemicals through the placenta or in the mother's milk. Depending onthe stage of pregnancy, the nature of the chemical involved, and the dose of that chemical, fetalexposure can result in problems like miscarriage, stillbirth, and birth defects.

ATSDR's Child Health Initiative recognizes that developing young people, whether fetuses,infants, or children, have unique vulnerabilities. Children are not small adults; a child's exposurecan differ from an adult's exposure in many ways. A child drinks more fluids, eats more food,and breathes more air per kilogram of body weight than an adult, and furthermore has a largerskin surface area in proportion to body volume. A child's behavior and lifestyle also influenceexposure. Children crawl on floors, put things in their mouths, play close to the ground, andspend more time outdoors. These behaviors may result in longer exposure durations and higherintake rates.

Children's metabolic pathways, especially in the first months after birth, are less developed thanthose of adults. In some cases, children are better able than adults to deal with environmentaltoxins, but in others, they are less able and more vulnerable. Some chemicals that are not toxinsfor adults are highly toxic to infants.

Children grow and develop rapidly in the first months and years of life. Some organ systems,especially the nervous and respiratory systems, can experience permanent damage if exposed tohigh concentrations of certain contaminants during this period. Also, young children have lessability to avoid hazards, because they lack knowledge and depend on adults for decisions thatmay affect children but not adults.

This public health assessment assesses risks to children exhibiting pica behavior (a craving forunnatural food like soil). Information on the incidence of soil pica behavior is limited. A studydescribed in an EPA document [110] showed that the incidence of soil pica behavior wasapproximately 16% among children from a rural black community in Mississippi. However, thisbehavior was described as a cultural practice among the community surveyed, so that communitymay not represent the general population. In five other studies, only one child out of more than600 ingested an amount of soil significantly greater than the range in other children. Althoughthese studies did not include data for all populations and represented short-term ingestion only, itcan be assumed that the incidence rate of soil pica behavior in the general population is low.

There is little information on the amount of soil ingested (measured in milligrams per day, ormg/day) by children with soil pica behavior [110]. Ingestion rates between 1,000 and 10,000mg/day have been used to estimate exposure doses for pica children. In the PGDP public healthassessment, ATSDR assumed a soil ingestion rate of 2,000 mg/day for approximately 290 daysper year to represent pica behavior in children aged 1 to 3 years old. ATSDR believes that this isa health protective assumption and likely overestimated soil consumption.

In the following discussions, we will indicate whether women and children were, are, or may beexposed to contaminants of concern and discuss the possible health concerns related to theseexposures.

Identifying Potentially Affected Groups

Table 22 summarizes the completed and potential exposure pathways. This table presents theexposure pathways, exposure routes, affected population, and duration of exposure for eachcontaminant in a potential or completed exposure pathway. Contaminants that are only present inpotential exposure pathways are in italics. Note that exposure durations for metals in thegroundwater exposure pathway are assumed to be chronic (i.e., lasting 1 year or more): it isdifficult to identify the specific numbers of years of exposure for the metals, because there havenot been sufficient metals analyses in most residential wells to determine long-term trends inconcentration. Additionally, the metals have different rates of groundwater transport relative totrichloroethylene (TCE) and other volatile organic compounds.

Populations that may be exposed to specific contaminants via multiple exposure pathways musthave their pathway-specific exposure doses summed to represent a total dose. However, most ofthe contaminants listed in Table 22 are not present in multiple exposure pathways. Of the 17contaminants listed, only arsenic, radioactive materials, thallium, uranium, and vanadium havemultiple pathways of exposure to the same population. The only population that could have beenexposed to these contaminants via more than one exposure pathway were pica children livingwithin the groundwater plume areas before 1988. Less than 1% of children exhibit pica behavior[110], and it is unknown if any pica children were present in those areas. Table 22 listsradioactive materials together, because radiation doses from each isotope were summed toinclude a total dose to potentially exposed populations. Uranium, as a chemical toxin, is listedseparately.

Table 23 gives an estimate of the number of people potentially exposed through each exposurepathway. Figure 8 shows the locations of those potential exposures. The number of personspotentially exposed was determined using 1990 Census data and the exposure areas from Figure8. The 1990 Census information is appropriate to use since 1990 is close to the time when peoplestopped using contaminated well water. Comparing 1990 Census data with 1980 Census data,however, shows that the number of people potentially exposed decreased by about 10 between1980 and 1990. This means that the 1990 Census data may underestimate the number of peoplepotentially exposed. (The people who left the area were most likely less than 65 years old,including a few less than 6 years old.) Also, about 25 of these people have lived in this area sincethe plant began operation in 1952. (Refer to Appendix A.) Note that Table 23 does not includethe surface water and biota exposure pathway: most people potentially exposed through thatexposure pathway would be hunters and fishers visiting the Western Kentucky WildlifeManagement Area (WKWMA) and would not live near the site. (The census would not includethese individuals, so we do not know the number or ages of hunters and fishers.)

It is important to remember that an exposed person would not necessarily experience adversehealth effects. Tables 22 and 23 describe the potentially affected populations; they do notdescribe potential health effects. The discussion of potential health effects for each contaminantare based on calculated exposure doses for PGDP and documented health effects from humanand animal studies. These discussions are in the health implications section of this report.

Table 22.

Summary of completed and potential exposure pathways for each contaminant
(Potential contaminants, exposure pathways, and populations are in italics)
Contaminant Exposure pathway(s) Exposure Route(s) Potentially Affected Population(s) Duration of Potential Exposure
Antimony Soil Ingestion and dermal contact Children with pica behavior1 Past, present, and future: 1 to 2 years2
Arsenic Groundwater



Ingestion and dermal contact

Adults and children routinely drinking water from well RW-2943

Children with pica behavior

Past only: chronic exposure4

Past, present, and future: 1 to 2 years2

Cadmium Groundwater Ingestion Adults and children routinely drinking water from northeast and northwest plume areas Past: unknown exposure4
Chromium (tri- and hexavalent) Groundwater Ingestion Adults and children routinely drinking water from northeast and northwest plume areas Past: chronic exposure4
Hydrogen Fluoride Air Inhalation
Acute (11/17/60)

Chronic (1956)

Adults and children living < 500 meters (1,640 feet) southeast of PGDP fence

Adults and children living along northern fence boundary

Past and potential future: < 4 hours; accidental releases

Past; maximum annual releases

Lead Groundwater Ingestion Adults and children routinely drinking water from wells RW-113 and RW-297 Past and potential current: chronic exposure4
Manganese Soil Ingestion and dermal contact Children with pica behavior Past, present, and future: 1 to 2 years2
Nitrate (Nitrite) Groundwater Ingestion Children routinely drinking water from wells RW-002, RW-030, and RW-294 Past: chronic exposure4
Pentachloro-phenol Groundwater Ingestion Unknown Unknown
Polychlorinated biphenyls (PCBs) Food (biota) Ingestion Children and adults who eat significant quantities of fish caught in Little Bayou Creek Past, present, and potential future
Radioactive Materials5 Air


Surface water




Residents living < 500 meters (1,640 feet) north of PGDP fence

Residents living less than 4 kilometers (2.5 miles) southeast of PGDP fence

Workers and visitors in WKWMA

Past: 9 years (1954-1963)

Past: 1960 accident


Thallium Groundwater

Surface water

Ingestion Unknown

Visitors to WKWMA


Past, current, future

Trichloro-ethylene Groundwater Ingestion, inhalation Adults and children routinely drinking water from wells RW-002, RW-017, and RW-113 Past: 5 to 15 years chronic exposure (1973-1988)
Uranium Air Inhalation Residents living less than 4 kilometers (2.5 miles) southeast of PGDP fence Past: 1960 accident
Potential future
Vanadium Groundwater



Ingestion and dermal contact

Adults and children routinely drinking water from northeast and northwest plume areas

Children with pica behavior

Past: chronic exposure4

Past, present, and future: 1 to 2 years2

Vinyl chloride Groundwater Ingestion and inhalation Adults and children routinely drinking water from northeast and northwest plume areas Past and potential future: unknown duration
Zinc Groundwater Ingestion Only children routinely drinking from well RW-113 Past: chronic exposure4
1 Less than 1% of children aged 1 to 3 exhibit pica behavior.
2 Pica behavior may last for only 1 to 2 years for each child.
3 "RW-#" indicates a residential well and well number.
4 Chronic exposure is exposure for 1 year or more. There have not been sufficient metals analyses in most residential wells to determine long-term trends in concentration. Lead contamination may come from lead solder in plumbing, not PGDP releases.
5 This category includes uranium 234, 235, and 238; neptunium 237; plutonium 239; thorium 230; and other radioactive substances.

Table 23.

Estimated number of persons potentially exposed per exposure pathway based on 1990 Census data and potential exposure pathways
Population Description Soil/Sediment Exposure pathway Air Exposure pathway Groundwater Exposure pathway
Children under 610-147-92-3
Women 15 to 44 years16-2012-152-3
People over 6512-148-93
Total 18 and older67-7249-5211-12
Total under 1823-2818-224-5
American Indian000
Source: [25]

Areas of Contamination and Potential Human Exposure
Figure 8. Areas of Contamination and Potential Human Exposure (jpg)
Areas of Contamination and Potential Human Exposure
Figure 8. Areas of Contamination and Potential Human Exposure (pdf)

Specific Substances


Potential exposures to antimony in off-site soil are not a public health hazard.

Antimony is a metal that occurs naturally at low levels in the earth's crust. It is used inindustry--mixed with other metals to form alloys or produced as antimony oxide. The alloys areused in lead storage batteries, solder, sheet and pipe metal, bearings, castings, ammunition, andpewter. The oxide is added to cloth and plastic to make them more fire-resistant [111].

Off-site soil concentrations of antimony ranged from 1 to 50 milligrams of antimony perkilogram of soil (mg/kg) [5]. Concentrations of antimony were not uniformly distributedthroughout off-site areas. Instead, they were log-normally distributed, meaning that a fewsamples had high concentrations while most had low concentrations. In fact, most off-site soilconcentrations were below 5 mg/kg [44]. The highest concentration was found 2.5 miles (4kilometers) northwest of PGDP, at a location where wells were installed. (That sample may notbe representative of surface soil samples, and the higher concentrations may not be a potentialsource of exposure to humans.) The maximum concentration is well above the reported range ofantimony in soil for the eastern United States (less than 1 to 8.8 mg/kg [85]); it is also higherthan the background concentration reported for the PGDP area (0.21 mg/kg [112]).

ATSDR scientists used conservative assumptions to estimate exposure doses for exposure toantimony in off-site soil. The highest estimated exposure dose was 0.001 milligrams of antimonyper kilogram of body weight per day (mg/kg/day) for a child who exhibits pica behavior (seeTable 15A). The absorption and toxicity of antimony depend on the physical and chemical stateof the specific compound inhaled or ingested. Both gastrointestinal and pulmonary absorption,although generally low, are a function of compound solubility.

ATSDR has not developed a health guideline for ingestion of antimony, because availablescientific studies are lacking for this route of exposure [111]. EPA has developed a healthguideline, called a reference dose (RfD), for chronic oral exposure to antimony, which is 0.0004mg/kg/day. The reference dose is based on a lowest-observed-adverse-effect level (LOAEL) inrats, which had shortened lifespans and changes in blood glucose levels after ingesting 0.35mg/kg/day of antimony in drinking water [113]. EPA derived the RfD by dividing the LOAELfor rats by an uncertainty factor of 1,000, because humans may be more sensitive than rats, somehumans may be more sensitive than others, and there was no experimental level for rats where noadverse effects were seen. Other studies in which rodents were exposed orally have reportedeffects on lifespan, glucose levels, and cholesterol metabolism [111].

Acute exposure to antimony by humans who ingested antimony-contaminated lemonade (at anestimated dose of 0.5 mg/kg for a 70-kilogram adult who ingested 300 milliliters of lemonade)resulted in burning stomach pains, nausea, and vomiting [111,113]. Most exposed peoplerecovered from this acute exposure within a few hours to several days [111,113]. One review ofsoil ingestion studies proposed an acute toxicity screening dose of 0.528 mg/kg/day for antimonyexposure via soil for young children who exhibit pica behavior [87].

Although ATSDR's estimated exposure doses slightly exceeded EPA's health guideline, thedoses were considerably lower than the lowest levels reported to cause adverse health effects inanimals and humans [111,113]. They were also lower than the acute toxicity screening levelproposed for antimony [87]. Furthermore, we most likely overestimated actual doses, since weused extremely conservative assumptions to estimate dose.

EPA's antimony health guideline is based on a drinking water study in rats. Antimony in soil isgenerally in a less soluble form than when it is in water. Consequently, people would absorb lessantimony from soil than from water. Even with conservative assumptions about exposure andrate of absorption from soil, exposure to antimony in off-site soils near PGDP is not expected toresult in adverse health effects.


Exposures to arsenic in groundwater and potential exposures in off-site soil are not a publichealth hazard. Arsenic was also evaluated in surface water and was not identified as acontaminant of concern for that exposure pathway.

Arsenic is a naturally occurring element in our environment but additional arsenic often gets intothe environment during copper and lead smelting, wood treating, and pesticide applications. It isin our environment in both the organic form (combined with carbon and hydrogen) and theinorganic form (combined with other elements, like oxygen, chlorine, or sulfur) [114]. Arsenicwas found in two residential wells at a maximum concentration of 10 micrograms per liter ofwater (or 10 g/L). These wells were used for an unknown period of time in the past, possibly upto 35 years. ATSDR's estimated doses, which assumes daily chronic exposure, for pastgroundwater exposure to adults (0.003 mg/kg/day) and children (0.007 mg/kg/day) exceededhealth guidelines for arsenic (as shown in Table 6).

Inorganic forms of arsenic predominate in groundwater (and soils) and are generally more toxicthan organic forms [115]. When humans and other animals are exposed to inorganic arsenic, theirbodies change it to the much less toxic methylated organic form, which is readily excreted fromthe body. This methylation process is effective as long as the dose of inorganic arsenic remainsbelow 0.2 to 1 mg/day [114]. In other words, people can tolerate a certain level of arsenic withoutadverse effects. At higher levels, the body's capacity to detoxify arsenic can be exceeded orsaturated. When this happens, blood levels increase and adverse effects can occur. ATSDR'sestimated doses for groundwater and soil exposure pathways are lower than the levels needed tosaturate detoxification mechanisms in the body.

Saturation of the body's detoxification mechanism may explain why non-cancer and cancereffects of arsenic appear to have a threshold, or minimum effective dose. In addition, a growingbody of scientific evidence suggests that cancer may result from mechanisms other than directattack on genetic material, which suggests that carcinogenicity from arsenic exposure has athreshold [114].

The lowest doses of arsenic shown to cause human toxicity from chronic ingestion--namely skinand gastrointestinal effects--range from 0.014 to 0.05 mg/kg/day. These doses were estimatedfrom a study of Taiwanese people who drank arsenic-contaminated water for 45 years [116,117].EPA derived a health guideline of 0.0003 mg/kg/day based on skin effects (e.g.,hyperpigmentation and keratosis) and a cancer slope factor of 1.5 (mg/kg/day)-1 for skin cancerbased on the Taiwanese study [113].

This study has limitations that one must consider when using it to evaluate public health hazardfor PGDP residents. First, it reported an association between arsenic in drinking water and skincancer, but failed to account for potential confounding factors, including exposure to other non-water sources of arsenic, genetic susceptibility, and poor nutritional status of the exposedpopulation. Therefore, arsenic exposure may have been underestimated in the study, possiblyleading to overestimation of the number of new cancer cases predicted for incremental increasein exposure dose. Second, the cancer slope factor for arsenic is based on the conservativeassumption that no threshold exists for cancer. As discussed previously, arsenic carcinogenicityappears to have a threshold.

The amount of arsenic absorbed from the gastrointestinal tract or skin can vary widely; it dependslargely on the water solubility of the arsenic compounds (either organic or inorganic) present inthe environment. It is often assumed that most arsenic in drinking water and soil is inorganic[118,114]. Studies of the bioavailability of arsenic from drinking water indicate that water-soluble forms of inorganic arsenic are almost completely absorbed (e.g., at least 95%) from thegastrointestinal tract, while less-soluble compounds are absorbed to a lesser extent (e.g., up to30%) [115]. ATSDR scientists do not have specific information about the types of arseniccompounds (and their solubility) present in groundwater and soils off site of PGDP; therefore, we assumed for exposure dose calculations that all arsenic was water-soluble and 100% absorbed.

Despite these conservative assumptions, the estimated groundwater doses were lower than levelsshown to cause adverse effects in the Taiwanese study and considerably lower than levelsrequired to saturate detoxification mechanisms in the body.

Arsenic was detected in off-site soil in the WKWMA, southwest of the PGDP security fence. Themaximum off-site concentration was 38 milligrams of arsenic per kilogram of soil. The normalrange of soil concentrations in the eastern United States is less than 0.1 to 73 mg/kg [114], andbackground for the Paducah area is reported as 12 mg/kg [112]. ATSDR's estimated dose forpast and current exposure to children who exhibit pica behavior (for the resident exposurescenario) was 0.002 milligrams of arsenic per kilogram of body weight per day, which exceededthe health guideline for chronic ingestion of arsenic. However, our estimated dose was lowerthan the provisional acute toxicity screening dose (0.005 mg/kg/day) for acute effects (e.g., throatirritation, nausea, and vomiting) in young children who exhibit pica behavior [87].

Studies indicate that arsenic in soils is absorbed from the gastrointestinal tract of humans to alimited extent (e.g., less than 50%) following ingestion. This is thought to be primarily becausesoils contain arsenic in less-soluble forms [115]. More-soluble arsenic compounds may be 60%to 70% absorbed through the gastrointestinal tract [119], but less-soluble forms are absorbed toabout half that degree [115]. Dermal absorption of arsenic in soils is minimal compared toingestion. According to studies of monkeys and humans, arsenic absorption from the skin rangesfrom 3.2% to 4.5% [115,120,93]. For ingestion of and dermal contact with soil, we made theconservative assumption that 80% of arsenic was absorbed for either route of exposure. Thisassumption resulted in a dose estimate that most likely overestimated actual doses.

To estimate soil exposure doses, ATSDR scientists used conservative assumptions that would overestimate exposure levels expected at the site. Conservative assumptions were used to be protective and to account for the uncertainty regarding actual exposure levels to off-site populations. Actual levels of exposure would be expected to be lower. Exposure to arsenic in off-site soil near PGDP is not expected to result in adverse human health effects, even to sensitive subpopulations exposed to the maximum soil concentration.


Cadmium was detected in one off-site groundwater well (on Tennessee Valley Authorityproperty). Ingestion of water from this well is unlikely, because the well is a monitoring well onindustrial property. The analytical results for cadmium in residential wells were reported asnon-detects, but the detection limits were above ATSDR comparison values. However, exposuresestimated using the detection limits do not pose a public health hazard.

Cadmium is an element that occurs naturally in the earth's crust. All soils and rocks, includingcoal and mineral fertilizers, contain some cadmium. Pure cadmium is a soft, silver-white metal. Itis often found as part of small particles in air. It does not have a distinct taste or smell; therefore,it is not possible to taste or smell cadmium in water or air. In the United States most cadmium isextracted during the production of other metals such as zinc, lead, and copper. It has many usesin industry and consumer products, mainly batteries, pigments, metal coatings, and plastics.

Food and cigarette smoke are the largest potential sources of cadmium exposure for members ofthe general population. Average cadmium levels in U.S. foods range from 2 to 40 parts ofcadmium per billion parts of food (ppb). Average cadmium levels in cigarettes range from 1,000to 3,000 ppb. The level of cadmium in most drinking water supplies is less than 1 ppb. Thecurrent average dietary intake of cadmium in adult Americans is about 0.0004 mg/kg/day;smokers receive an additional amount--about 0.0004 mg/kg/day--from cigarettes [121].

Numerous studies indicate that the kidney is the main target organ of cadmium toxicity followingextended oral exposure to cadmium, with effects similar to those seen following inhalationexposure [121]. Elevated incidences of kidney effects (tubular proteinuria) have been found innumerous epidemiologic studies conducted on residents of cadmium-polluted areas in Japan[122,123], Belgium [124,125], and China [126].

ATSDR has derived a minimal risk level (MRL) of 0.0002 mg/kg/day for a chronic oral exposureto cadmium. The oral MRL is based on a lifetime accumulated threshold of 2,000 milligrams ofcadmium from dietary sources. The threshold is associated with kidney effects (proteinuria, orprotein in the urine) seen in residents of cadmium-polluted areas of Japan.

EPA has calculated oral chronic RfDs for cadmium of 0.001 and 0.0005 mg/kg/day for ingestionfrom food and water, respectively. The critical effect is significant proteinuria in humanschronically exposed to cadmium, using a no-observed-adverse-effect level (NOAEL) of 200milligrams per gram (mg/g) wet weight in the renal cortex and a kinetic model assuming 2.5% or5% absorption from food or water, respectively, and 0.01% per day excretion [121].

A relevant consideration is whether the proteinuria caused by cadmium exposure should beconsidered an adverse effect. By itself, the increased excretion of low-molecular-weight proteinshas no adverse effect on health. However, several studies have indicated that increased excretionof calcium also occurs with cadmium-induced kidney damage. This can lead to an adverse effect(osteoporosis), particularly in postmenopausal women.

Hypothetically, children who drink groundwater with cadmium at the concentration detected inone well would have estimated exposure doses that could result in adverse health effects. This isunlikely, however, since the well was never used as a residential source and is located on anindustrial property.

There is a high degree of uncertainty surrounding the actual exposure doses for cadmium ingroundwater, given that samples from residential wells were below the detection limit. Even ifwe assume that cadmium was present at that detection limit in these residential wells, cadmiumwould not pose a public health hazard.

Chromium, Hexavalent

Exposures to hexavalent chromium in off-site groundwater are not a public health hazard.

Chromium is a naturally occurring element found in rocks, animals, plants, soil, and volcanicgases. Chromium occurs in the environment in several forms depending on the valence state ofthe chromium metal--e.g., trivalent (III) chromium or hexavalent (VI) chromium. Chromium inthe environment (e.g., soil, water) and the body is more commonly trivalent than hexavalent[127]. Trivalent chromium is an essential nutrient in the human diet. It helps us regulate how ourbodies use insulin. Hexavalent chromium is considerably more toxic to humans than trivalentchromium. Hexavalent chromium is used in chrome plating, dye manufacturing, leather tanning,and wood preservation, and was used as a corrosion inhibitor in the cooling towers at PGDP.Because the measured groundwater analyses are not specific as to valence, we calculatedexposure doses assuming that measured concentrations are present as the more toxic hexavalentform.

Concentrations of chromium in the water from off-site groundwater monitoring wells rangedfrom 40 to 270 g/L, which exceeded the comparison value of 30 g/L for hexavalent chromium.However, none of these samples were taken from residential drinking water wells. The maximumconcentration of chromium in residential wells was 20 g/L, which is lower than the comparisonvalue. Because not all residential wells were tested, ATSDR scientists assumed that maximumlevels in off-site wells near untested residential wells represented possible human exposurelevels. The estimated doses for ingestion of chromium in residential wells, assuming exposure tomaximum concentrations in nearby off-site wells, were 0.008 mg/kg/day for an adult and 0.021mg/kg/day for a child. These doses exceeded health guidelines for hexavalent chromium. If themaximum concentration measured in residential wells was used, the estimated doses would be0.0006 mg/kg/day for an adult and 0.002 mg/kg/day for a child. (This equates to 0.04 mg/day fora 70-kilogram adult and 0.03 mg/day for a 13-kilogram child.) Therefore, we considered a rangeof possible exposure doses (shown below) whose lower bound was maximum measuredconcentrations in residential wells and whose upper bound was maximum concentrations in non-residential wells.

Person Lower-Bound to Upper-Bound Estimated Dose
Child0.002 mg/kg/day (or 0.03 mg/day) to 0.021 mg/kg/day (or 0.27 mg/day)
Adult0.0006 mg/kg/day (or 0.04 mg/day) to 0.008 mg/kg/day (or 0.56 mg/day)

ATSDR has not established a health guideline for ingestion of chromium, because the availabledata are insufficient or too contradictory to establish minimum levels of effect (e.g., LOAELs).Because chromium is an essential nutrient in the body, the National Research Council hasestablished a range of "estimated safe and adequate daily dietary intakes" (ESADDIs) forchromium. The range is 50 to 200 micrograms of chromium per day (or 0.05 to 0.2 mg/day)[128]. The upper end of this range, 200 g/day, has been adopted by ATSDR as an interimguideline for oral exposure to chromium VI and chromium III compounds [127]. This guidelineis equivalent to an exposure dose of 0.003 mg/kg/day for a 70-kilogram adult, and 0.02mg/kg/day for a 13-kilogram child. This interim guideline is similar to the health guidelineestablished by EPA for chronic ingestion of chromium VI. EPA's reference dose for chronic oralexposure, based on animal studies, is 0.003 mg/kg/day [113].

The estimated groundwater doses were slightly above ATSDR's interim guideline for "safe andadequate" intakes. As previously stated, these estimates are very conservative, because they werecalculated assuming exposure to maximum concentrations in wells near residential wells, ratherthan the residential wells themselves, and because they assumed that all chromium was present inthe (more toxic) hexavalent form. Exposure doses based on maximum concentrations measuredin residential wells are within the "safe and adequate" intake range. Therefore, ATSDR scientistsconclude that ingestion of chromium in off-site groundwater (drinking water) wells is notexpected to result in adverse human health effects.

Hydrogen Fluoride

Historically, chronic (long-term) exposures to hydrogen fluoride (HF) happened as a result ofreleases during normal process operations; acute (short-term) HF exposures happened as aresult of accidents or controlled releases. (See Appendix F for details on HF releases).

To estimate doses from long-term exposure to HF, we used a correlation between annualuranium hexafluoride releases and HF concentrations at the site perimeter. We calculatedexposure doses for potentially affected residents living north of PGDP (based on prevailing winddirections). Long-term HF exposures are not a public health hazard at PGDP.

We estimated acute HF exposure doses using accident records and air dispersion modeling. Themost serious accident (November 17,1960) created potential exposures to the southeast ofBuilding C-333. If a sensitive person was exposed to HF at the level modeled for that accident,we expect, that person would experience adverse health effects; however, due to uncertainties(e.g., quantities released, modeling, locations of individuals at time of accidents), it cannot bedetermined if that accident posed a public health hazard to an individual. Other accidentalreleases involved smaller quantities and probably did not affect the off-site population.

HF is a colorless fuming gas or liquid that is made up of a hydrogen ion and a fluoride ion. HF isused as a catalyst, as a fluorinating agent, in making fluorine and aluminum fluoride, as anadditive in rocket fuel, and for the refining of uranium.

HF is an irritant. It is very soluble in water. It dissolves easily in any water in the air or othermedia (including skin, the upper respiratory tract, eyes, plants, and soil). When HF is dissolved inwater, it is called hydrofluoric acid. Hydrofluoric acid is dangerous to humans, because it canburn the skin and eyes. At first, exposure to hydrofluoric acid may not look like a chemical burn.Skin may only appear red, and may not be painful at first. Damage to the skin can occur overseveral hours or days, and deep, painful wounds can develop. When not treated properly, seriousskin damage and tissue loss can occur. In the worst cases, people who get a large amount ofhydrofluoric acid on their skin can die when the fluoride affects the lungs and/or heart.

Breathing in a large amount of HF can harm the lungs and heart and cause death. The humanhealth effects for breathing moderate amounts of HF for several months are not well known, butrats that breathed HF for several months suffered kidney damage and nervous system changes,such as learning problems. If you breathe HF or fluoride-containing dust for several years,changes in your bones (called skeletal fluorosis) can occur.

Studies have been conducted to determine if fluoride causes cancer in people who live in areaswith fluoridated water or naturally high levels of fluoride in drinking water, or people who maybe exposed to fluorides at work. The studies have not found an association between fluoride andcancer in people.

ATSDR's provisional screening value for intermediate exposure (15 to 364 days) is 0.010milligrams per cubic meter (mg/m3), or 12 ppb, for air and 0.06 mg/kg/day for oral exposure.Concentrations below these values are not expected to cause adverse health effects. The 12 ppbcomparison value for air is more than 100 times lower than exposures that caused mild irritationof the nasal passages in human volunteers exposed for 10 days [61]. The highest average level(time-weighted average) allowed by the Occupational Safety and Health Administration (OSHA)for HF in air for a 40-hour work week made up of 8-hour work days is 2.5 mg/m3 (3 parts permillion, or 3,000 ppb). The 12 ppb provisional screening value for air concentrations of HF ismore than 250 times lower than OSHA's occupational level.

Air releases of HF have occurred at the PGDP site. Because there is a strong correlation betweenuranium releases and ambient air concentrations of HF at this site, ATSDR assumed that thelargest annual HF release coincided with the highest annual uranium release, which was in 1956.We used the estimated HF air concentration for 1956 to evaluate the health impacts of chronicexposure to HF under normal operating conditions. All of the estimated annual average HFconcentrations at the "one north monitoring station" (approximately 1 mile, or 1.6 kilometers,from the site perimeter) were below ATSDR's provisional screening value (see Appendix F,Figure F-2). The highest estimated annual average HF concentration in air (28 ppb for 1956) wasat the "perimeter north monitoring station." As such, the perimeter north monitoring stationrepresents the point of maximum off-site exposure; however, no one lives at this location. Theclosest residence is about 1,500 meters (almost a mile) from the source, about 500 meters (1,640feet) from the perimeter north monitoring station. The concentration of HF at the nearestresidence was estimated at approximately 22 ppb. The annual average concentrations for 1955and 1956 are about two times greater than annual average concentrations for other years. If actualexposures to HF occurred at 22 ppb, then mild adverse health effects may have resulted. Becauseour assumptions were so conservative, though, we believe that people were exposed to loweraverage air concentrations and no adverse health effects would have resulted. Additionally, itshould be noted that the exposure assumptions and modeling used to estimate historical air levelswere very conservative and most likely overestimated air concentrations. Past, current, andfuture long-term exposure to HF released during the normal operations of the facility does notpose a public health hazard.

ATSDR used the November 17, 1960 accident data to estimate an acute exposure dose to HF.The estimated maximum acute off-site air concentration for HF was 2.0 to 4.5 parts per million(ppm) for 2 to 4 hours. These concentrations are close to the level of acceptable occupationalstandards--but occupational standards are not meant to protect sensitive populations (e.g.,children and the elderly). If sensitive people were exposed at these levels, they may haveexperienced adverse health effects (e.g., irritation of the eyes, nose, and throat). Because of theuncertainty associated with historical events (e.g., amounts of material released, modeling,location of off-site individuals during accidents), past exposure to estimated maximum airconcentrations poses an indeterminate public health hazard.


Past exposure to lead in three residential drinking water wells may have increased the likelihoodof neurological effects in young children, and thus posed a public health hazard. Currentexposure may still be occurring if the source of the lead was from pipes and plumbing asopposed to groundwater.

Lead is a naturally occurring element found in the earth's crust [84]. It is used in a variety ofproducts and industrial processes, which can release it into the environment. Lead can beintroduced to soil through exhaust from leaded gas fumes from vehicles, spillage of leaded paintor paint chips, or application of a variety of leaded products. Ingesting and inhaling contaminatedsoils exposes people to lead. Lead in soil can contaminate groundwater and surface water undercertain environmental conditions. Pollution or use of lead solder in water delivery and householdplumbing systems can increase levels of lead in drinking water.

Lead was detected in groundwater near the site. Samples from 12 residential wells near PGDPhad concentrations of lead ranging from 10 to 110 g/L [44]. Due to the locations of the wellswith the highest levels, lead did not appear to be related to PGDP. The lead concentration was 10g/L in nine of the residential wells, 100 g/L in one well, and 110 g/L in one well. There wasone reading of 290 g/L in another residential well, but that reading could not be replicated; withthe high reading included, concentrations in this single well averaged 103 g/L. Other off-sitemonitoring wells north of Ogden Landing Road near the North-South Diversion Ditch andsouthwest of the site near the inactive landfill had concentrations ranging from 10 g/L to 210g/L. The highest concentrations were near the drainage ditch north of the site. Most of the off-site wells were sampled for lead only once. The background concentration of lead in groundwaterfor the PGDP area is 10 g/L [112].

It has long been known that lead exposure can have harmful effects. Young children and fetuseshave been the main focus of health effects research, since they are the most sensitive individuals;however, adults exposed to lead can also experience adverse health effects [129]. Infants andchildren receive higher doses from any given level of environmental lead than do adults, becausethey have a greater absorption capacity for lead than adults,. Therefore, age is an importantdeterminant of exposure dose for a given concentration of lead in drinking water (as shown inTable 24 below).

Table 24.

Estimated lead doses in adults and infants from various water concentrations
Lead concentration in water Estimated dose range in milligrams per kilogram per day
Adults Infants
15 micrograms per liter0.00050.002
40 micrograms per liter0.0010.04
60 micrograms per liter0.0020.006
100 micrograms per liter0.0030.01
290 micrograms per liter0.010.02

ATSDR reviewed 122 studies of human and animal exposures to various doses of lead. Ingeneral, exposure doses below 0.001 mg/kg/day do not harm humans or animals. Exposure dosesbetween 0.001 and 0.01 mg/kg/day produce minor changes in blood cells. Harmful effects inanimals are seen when doses reach and exceed 0.01 mg/kg/day [84].

For humans, there is a correlation between the levels of lead in blood and the harmful effects thatmay be seen. (This is illustrated in Figure 9, below.) Blood levels of lead can be elevated bysustained exposure to contaminated soil, food, air, or drinking water. Neurological effects are themost important health effects from exposure in childhood or during gestation (i.e., in the uterus).Changes in blood cells serve as indicators of exposure. The Centers for Disease Control andPrevention considers a child to have an elevated blood lead level if the amount of lead in his orher blood is 10 micrograms per deciliter (g/dL) or higher [130].

The relationship between blood lead level and lead concentration in environmental media isdetermined by several factors, including the chemical and physical form of lead, the lead particlesize, and the age of the person exposed [129]. Scientists at ATSDR and EPA have developed amodel for estimating blood lead in children based on the lead bioavailability generally observedat hazardous waste sites. This model is called the Integrated Exposure Uptake Biokinetic(IEUBK) Model for Lead in Children [131]. ATSDR scientists estimated blood levels forchildren drinking water from residential wells near PGDP using this model. We also estimatedblood lead levels using EPA's slope factors for lead [84,113]. Adult blood lead concentration isless affected by lead concentration in environmental media. To estimate adult blood lead levelsfrom environmental media, we used EPA's slope factors only [84].

The most contaminated residential wells near PGDP have been closed, and residents that relied on them are now using alternate water sources. (This is assuming that the source of the lead was the groundwater and not the residential piping and plumbing.) To estimate past blood levels for exposure to water from the residential wells, we made the conservative assumption that people were simultaneously exposed to lead in several environmental media (water, air, soil, and food). This is a valid assumption, because lead was detected in various off-site media: although levels were below environmental comparison (screening) values, all media would contribute to the body burden of lead.

We assumed that children were exposed tolead at a concentration of 0.1 micrograms percubic meter (g/m3) in air, 200 microgramsper gram (g/g) of soil and dust, and from2.4 to 3.4 micrograms per day(g/day)--depending on age--in the diet[131]. We assumed exposure to childrenbecause they are particularly sensitive to theadverse effects of lead [84,129]. Adults,including pregnant women, were not and arenot likely to have elevated blood lead levelsif they were exposed to the mean residentialwell water concentrations.

Whether we estimated blood lead levelsfrom the model, or from slope factors, wefound that children drinking water fromwells with lead concentrations less than 60g/L were not likely to experience adversehealth effects from exposure. Water from thethree wells containing approximately 100g/L could have raised blood levels abovethe action level of 10 g/dL in childrenunder 4 years old while the wells were inuse. Therefore, we conclude that blood levelsin the past may have been sufficient to havemarginal effects on hearing, intelligencequotient (IQ), and growth in young childrenusing these wells (as illustrated in Figure 9).

Effects of lead on children and adults--Lowest observed adverse affect levels
Figure 9. Effects of Lead on Children and Adults--Lowest Observed Adverse Affect Levels

After exposure ends, blood lead level and thelikelihood of harmful effects, declines withtime (at a half-life of 25 days) [129].However, some of the lead in blood can be taken up by the bones and remain there for decades[129]. Bone lead can be a source of blood lead under conditions that might cause bonedesorption, such as pregnancy, poor diet, or older age [129]. We recommend that residents whoare concerned about lead in their drinking water have their wells tested.


Manganese was detected in off-site soil at levels ranging from 34 to 4,020 mg/kg (ppm). Theresidential exposure scenario had an estimated exposure dose for a child with pica behavior (achild who exhibits an abnormal appetite for soil) that exceeded ATSDR's screening value. Theestimated exposure doses for an adult and normal child were below ATSDR's screening value.Based on conservative exposure assumptions, ATSDR believes that manganese exposure dosesfrom off-site soil is not a public health hazard.

Manganese is a naturally occurring substance found in many types of rock. Pure manganese is asilver-colored metal, somewhat like iron in its physical and chemical properties. Manganese doesnot occur in the environment as pure metal. Rather, it occurs combined with other chemicals,such as oxygen, sulfur, and chlorine.

Rocks containing high levels of manganese compounds are mined and used to producemanganese metal, which is mixed with iron to make various types of steel. Some manganesecompounds are used in batteries, ceramics, pesticides, and fertilizers; and in dietary supplements.

Ingesting a small amount of manganese each day is important in maintaining your health. Theamount of manganese in a normal human diet (about 2 to 9 mg/day) seems to be enough to meeta person's daily need; however, no cases of illness from eating too little manganese have beenreported in humans. In animals, eating too little manganese can interfere with normal growth,bone formation, and reproduction.

Too much manganese can cause serious illness. Although there are some differences betweendifferent kinds of manganese, most manganese compounds seem to cause the same effects.Manganese miners or steel workers inhaling high levels of manganese dust may have mental andemotional disturbances, and body movements may become slow and clumsy. This combinationof symptoms is a disease called manganism. Workers usually do not develop symptoms unlessthey have been exposed for many months or years at high levels. Manganism occurs because toomuch manganese permanently injures a part of the brain that helps control body movements. It isnot certain whether eating or drinking too much manganese can cause manganism [132].

There is little evidence to suggest that cancer is a major concern for people exposed tomanganese. EPA does not classify manganese as a human carcinogen.

The most significant exposure to manganese for the general population is from food, with anaverage ingestion rate of 3.8 mg/day. Other estimates of daily intake for adults range from 2.0 to8.8 milligrams. Even though gastrointestinal absorption of manganese is low (3% to 5%), oralexposure is also the primary source of absorbed manganese [132].

Manganese intake among individuals varies greatly, depending upon dietary habits. For example,an average cup of tea may contain 0.4 and 1.3 milligrams of manganese [132]. Thus, someonewho drinks three cups of tea per day might receive up to 4 mg/day from this source alone,doubling his or her the average intake.

The Food and Nutrition Board of the National Research Council estimated the adequate and safeintake of manganese for adults at 2.5 to 5 mg/day [132]. It is possible that a significantproportion of Americans, especially women, are not consuming sufficient manganese, althoughno cases of manganese deficiency have been documented in humans. However, infants may beingesting more than the estimated safe and adequate dose for their age group (which is 0.7 to 1.0mg/day), due to high manganese levels in prepared infant foods and formulas [132].

ATSDR has derived a provisional MRL of 0.07 mg/kg/day for a chronic oral exposure (365 daysor more) to manganese in soil. EPA has derived a chronic oral RfD of 0.14 mg/kg/day formanganese in the diet [133]. This value is equal to the average daily intake of manganese in thediet (10 mg/day) that is considered adequate and safe. The RfD was derived assuming an averagebody weight of 70 kilograms. An uncertainty factor was not employed, because (1) theinformation used to determine the RfD was taken from many large populations, (2) humans exertan efficient homeostatic control over manganese such that body burdens are kept constantthrough variations in diet, (3) there are no sub-populations that are believed to be more sensitiveto manganese at this level, and (4) manganese is an essential element, required for normal humangrowth and maintenance of health.

When assessing exposure to manganese from drinking water or soil, EPA recommends, oneshould use a modifying factor (an uncertainty factor based on professional judgement) of 3, basedon some evidence that infants younger than 28 days have a higher uptake of manganese inliquids, excrete less absorbed manganese, and, as neonates, pass the absorbed manganese moreeasily through the blood-brain barrier. The resulting chronic oral RfD for manganese in water andsoil would be 0.05 mg/kg/day. The estimated exposure dose for a pica child is 0.1 mg/kg/day(assuming ingestion of 2 grams of soil per day for 290 days per year). However, if one assumesthat manganese in soil behaves similarly to manganese in food (i.e., that its bioavailability issimilar), then a comparison value at or near 0.14 mg/kg/day would be deemed more appropriate,and the estimated exposure dose for a pica child would not exceed this value.

Nitrates and Nitrites

Exposures to nitrate from PGDP sources are not a public health hazard.

Nitrate and nitrite are naturally occurring compounds, part of the nitrogen cycle. Because nitriteis easily oxidized into nitrate, nitrate is the form that is typically found in groundwater andsurface water. Nitrate is the primary source of nitrogen for plants. Wastes containing organicnitrogen are decomposed in soil or water by bacteria to form ammonia. Ammonia is thenoxidized to nitrite and nitrate. Agricultural and residential use of nitrogen-based fertilizers,nitrogenous wastes from livestock and poultry production, and urban sewage treatment systemshave increased levels of nitrate in soil and water. Certain plants (cauliflower, spinach, collardgreens, broccoli, carrots, and other root vegetables) have a naturally higher nitrate content thanother plant foods and can account for a large percentage of nitrate in the diet. Nitrate and nitritecompounds are also used for color enhancement and preservation of processed meat products.Nitrate is used in foods to prevent botulism, a life-threatening food-borne illness.

Nitrate-containing compounds are water soluble, which means that they can be carried in water.Thus, nitrate can enter drinking water supplies through surface water runoff, home sewagesystems, agricultural fields, and groundwater recharge.

In agricultural areas, a seasonal pattern of increased nitrate levels in drinking water has beenseen. This increase occurs most often in spring, when fertilizers are applied and nitrate istransported through storm runoff or groundwater recharge. The most common route of exposureoccurs through drinking contaminated water, eating vegetables with naturally high levels ofnitrate, and eating foods preserved with nitrate.

Nitrate was detected in off-site groundwater (in RW-002) once used for residential purposes at amaximum concentration of 29.2 milligrams per liter (mg/L) as total nitrate (NO3). ATSDRbelieves that no one (not even infants or children) would have experienced adverse health effectsfrom exposure through drinking water, even if they consumed nitrate-impacted drinking water atthe maximum concentration detected. Nitrate is not now present in residential wells, and it is notexpected to impact residential wells in the future. It should be noted that nitrate was detected insurface water at a maximum concentration of 84.6 mg/L as NO3. If people consumed thecontaminated surface water at the maximum detected level on a regular basis for an extendedperiod of time, they might experience adverse health effects. However, this exposure scenario isvery unlikely.

ATSDR has developed Reference Dose Media Evaluation Guides (RMEGs) for chronic (1 yearor more) oral exposure to nitrate in water. Media concentrations less than the RMEG are unlikelyto pose a health threat. The chronic RMEGs for a child are 20 mg/L for nitrate-nitrogen (NO3-N)and 90 mg/L for NO3; for adults, the chronic RMEGs are 60 mg/L for NO3-N and 270 mg/L forNO3. The RMEG for nitrate is not protective of infants, so ATSDR recommends using EPA'sMaximum Contaminant Level Goal, or MCLG (10 mg/L for NO3-N) as a guideline to evaluatepotential infant exposure.

RMEGs are media-specific chemical comparison values derived from EPA's RfDs. RfDs arehealth-based guidelines for non-cancer effects. An RfD is an estimate of the amount of achemical that a person can be exposed to, on a daily basis, that is not anticipated to cause adversehealth effects over a person's lifetime. MCLGs, which EPA sets after reviewing health effectsstudies, are the maximum levels of contaminants in drinking water at which no known oranticipated adverse effect on the health of persons would occur, and that allow an adequatemargin of safety. MCLGs are non-enforceable public health goals. When determining an MCLG,EPA considers the risk that sensitive sub-populations (infants, children, the elderly, and thosewith compromised immune systems) will experience various adverse health effects. Forchemicals that can cause adverse non-cancer health effects, MCLGs are based on RfDs.

EPA requires that the amount of nitrate (as NO3-N) in public drinking water supplies not exceed10 mg/L. (This regulation does not cover private wells.) If the results of a water analysis arereported as NO3 (total nitrate) instead of NO3-N, the equivalent value would be 45 mg/L.

Nitrate can affect the blood's ability to carry oxygen. Nitrate's acute toxicity is due to itsbiological conversion to nitrite, which oxidizes ferrous iron in the hemoglobin to producemethemoglobin. The presence of methemoglobin interferes with the oxygen transport system inthe blood. Methemoglobinemia (blue-baby syndrome) is caused by high levels of nitrite (orindirectly by nitrate) in blood. Infants are more sensitive to nitrate for several reasons. Infantsconsume more water relative to their body weight than adults, and the hemoglobin in an infant'sblood (called fetal hemoglobin) is more easily changed into methemoglobin than an adult'shemoglobin. Also, an infant's digestive system is less acidic, which enhances the conversion ofnitrate to nitrite. The two most common symptoms related to the consumption of watercontaining high levels of nitrate are methemoglobinemia and acute diarrhea. Fatalities frommethemoglobinemia occur infrequently, and are most common in rural areas. Illness and deathcaused by methemoglobinemia are not always recognized, so methemoglobinemia's occurrencemay be under-reported.

Families with infants should use an alternate water supply if their well is known to containelevated levels of nitrate. When preparing infant formula, families should use nitrate-free water.If a private well is used, it should be inspected for proper construction and tested for nitrate andbacteria levels. Foods containing nitrate, as well as sausage preserved with nitrate and nitrite,have caused symptomatic methemoglobinemia in children.

Nitrates can react with other substances to form N-nitroso compounds. Some of these N-nitrosocompounds have caused cancer in animals. However, the mechanism for this is not well defined.Human and experimental animal studies have failed to provide conclusive evidence thatingestion of nitrate or nitrite causes cancer.

Based on the information presented above, nitrate concentrations detected in off-site groundwaterare not expected to cause an adverse public health effect in adults, infants, or children.


Pentachlorophenol was not detected in any off-site drinking water wells, but the detection limitin residential wells (approximately 50 g/L) was five times higher than ATSDR's comparisonvalue (10 g/L). Even if concentrations are assumed to be 50 g/L, the resulting exposures arenot a public health hazard.

Pentachlorophenol is a man-made substance that was used widely as a pesticide, herbicide, andwood preserver [134]. Pentachlorophenol by itself is slightly water soluble. However, technical-grade pentachlorophenol that is used as a pesticide or wood preserver typically contains othercontaminants, such as chlorinated dibenzodioxins, that are not as soluble. One of thesechlorinated dibenzodioxins, octochlorodibenzodioxin (OCDD), is 189 million times less solublein water than pentachlorophenol [134,135]. Environmental contamination at most industrial sitescontains technical-grade as opposed to pure-grade pentachlorophenol. When waste technical-grade pentachlorophenol seeps into the soil and migrates downward toward the groundwater,OCDD comes out of solution and remains in the surface soils. This has apparently occurred atPGDP, because OCDD and other chlorinated dibenzodioxins are present at low levels in the top3 feet of soil on site, but are not detected in samples taken at depths greater than 3 feet [44]. Inorder for pentachlorophenol in soil to reach groundwater under PGDP, it must travel through 30to 100 feet of silt and clay; by then, it is essentially free of less-soluble dioxin contaminants,which have sorbed to soils. Therefore, pentachlorophenol in groundwater is essentially the sameas pure-grade pentachlorophenol.

Pentachlorophenol was detected in one off-site monitoring well, at a maximum concentration of 8 g/L. It was not detected in any off-site residential wells; however, the well sampling could not detect pentachlorophenol at concentrations below 50 g/L, which is higher than the comparison value used to select contaminants of concern. ATSDR scientists used this detection limit to estimate exposure doses of 0.005 mg/kg/day for a child and 0.001 mg/kg/day for an adult.

ATSDR has developed a health guideline (0.001 mg/kg/day) for intermediate-duration oralexposure to pentachlorophenol. This guideline is based on observations of increased serum levelsof liver enzymes in rats, which is considered suggestive of liver toxicity [134]. When rats weregiven food contaminated with either technical-grade or pure pentachlorophenol, those receiving 1to 25 mg/kg/day of technical-grade product showed signs of liver injury. ATSDR based its healthguideline on the lowest dose (1.2 mg/kg/day) of technical-grade pentachlorophenol shown tocause liver injury, because it is likely that most hazardous waste sites contain technical-grade asopposed to pure pentachlorophenol. We applied an uncertainty factor of 1,000 to this lowestdose, because humans may be more sensitive to pentachlorophenol than rats, because somehumans are more sensitive than others, and because the animal study involved intermediate-duration (rather than chronic) exposure. The only effect caused by the pure pentachlorophenol inthis study was an increased liver concentration of an enzyme needed to eliminatepentachlorophenol in the rat's urine. This effect was observed at doses above 5 mg/kg/day.

It is more likely that people near PGDP were exposed to pure, rather than technical-grade,pentachlorophenol. To evaluate health effects from exposure to pure pentachlorophenol indrinking water, we could derive a tentative, site-specific oral health guideline for chronicduration based on the highest dose (5 mg/kg/day) that failed to cause liver injury in rats. If, asabove, we divided by an uncertainty factor of 1,000 to account for differences in sensitivity andexposure duration, this tentative health guideline would be 0.005 mg/kg/day. ATSDR's estimatedexposure doses are equal to or lower than this health guideline. Exposure to pentachlorophenol ingroundwater at the detection limit concentrations is not expected to result in adverse healtheffects.

EPA classifies pentachlorophenol as a probable human carcinogen (a cancer-causing substance).The classification is based on studies of rats that developed liver cancer and hemangiosarcoma(blood vessel tumors) after being exposed to technical-grade pentachlorophenol andpentachlorophenol containing lower levels of dioxins than technical-grade. The doses required toproduce cancers in these studies were at least 3,000 times higher than the maximum dosesATSDR estimated for ingestion of drinking water from the residence near PGDP [113]. Thetypes of liver tumor observed in these rats are also associated with dioxin exposure; thehemangiosarcomas are not.

From this information, EPA derived a cancer slope factor of 0.12 mg/kg/day based on all tumorscombined [113]. However, there is no clear evidence from high occupational exposures thatpentachlorophenol causes cancer in humans [134]. Therefore, there is even less likelihood thatlower environmental exposures could produce these effects. There is also no evidence of humanangiosarcomas among people exposed to pentachlorophenol [134]. Even if we assume thatcancer is a possibility for humans, and we consider maximum estimated exposure doses to beequal to the residential well detection limit, cancer effects are not likely for people who may haveingested pentachlorophenol-contaminated water in the past.

ATSDR scientists conclude that past ingestion of pentachlorophenol in off-site groundwater(drinking water) is not expected to cause adverse human health effects.

Polychlorinated Biphenyls

Exposure to polychlorinated biphenyls (PCBs) through consumption of biota (fish and deer) fromthe WKWMA is not a public health hazard.

PCBs are a group of man-made chlorinated organic compounds that contain hundreds ofindividual chemicals, called congeners, with varying toxicities. PCBs can be liquids or solids;they are oily, colorless to light yellow, tasteless, and odorless. They are difficult to burn and aregood insulators. These properties once made them useful for a variety of purposes: coolants andlubricators in transformers, capacitors, and other electrical equipment; additives in paint, plastics,newspaper print, and dyes; extenders in pesticides; and heat transfer and hydraulic fluids. Duringthe 1970s, scientists found PCBs in ambient air, soil, water, and sediment, even though there areno known natural sources of PCBs in the environment. EPA banned the production of PCBs in1978. Traces of PCBs can still be found in the tissues of wildlife, domestic animals, andpeople--PCBs have chemical and physical properties that make them persistent in theenvironment and readily accumulate in the fatty tissues of organisms. Overall, levels of PCBs inthe environment have been declining since 1978 [95,136].

Although PCBs are no longer made in the United States, people can still be exposed to them.Transformers are useful for several decades, and many older transformers (and capacitors) stillcontain PCBs. Old electrical appliances may release PCBs when they get hot and contaminateinside air. Discarded capacitors and transformers can also release PCBs into the environmentfrom landfills. Heavy electrical power consumers, such as PGDP, are also sources ofenvironmental PCBs.

PCBs are poorly soluble in water and tend to adsorb onto sediments in lakes and streams. PCBspresent in sediment may enter the aquatic food chain and smaller fish, which in turn, becomePCB sources for larger fish. Birds and land predators, such as man, may be exposed to PCBswhen they eat contaminated biota. At each step in the "food chain," PCBs that have accumulatedin the animals' fatty tissues can appear in greater concentration, or "bioconcentrate," in thespecies that eat them. PCBs were found in fish sampled from several locations in Little BayouCreek, and to a much lesser extent in fish sampled from Big Bayou Creek. PCB levels in deertissue were extremely low and do not pose any threat. More recent (1997) samples from deerhave been below the detection limit in multiple tissues (muscle, liver, fat, and mammary).

The Commonwealth of Kentucky has issued a health advisory regarding consumption of specificspecies of fish from Little Bayou Creek. The PGDP 1989 Environmental Report indicated thattotal PCB concentrations in fish from Little Bayou Creek averaged approximately 5 microgramsof PCB per gram of fillet (g/g); see Table 17A(2). The highest average total PCB concentrations(17.95 g/g) were reported in sunfish collected from Outfall #11, which is part of the LittleBayou Creek area. The total PCB concentrations in fish tissue from Outfall #11, based onsamples from three sunfish, were more than three times greater than average total PCBconcentrations from the Little Bayou Creek area. The Outfall #11 data is limited, and seems notto be representative of the Little Bayou Creek area. Also, Outfall #11 is fenced and posted withwarning signs. Accordingly, we did not use Outfall #11 data when we calculated the average totalPCB concentration for the Little Bayou Creek area. Total PCB concentrations in fish from BigBayou Creek were approximately five times lower (average approximately 1 g/g) than fish fromLittle Bayou Creek.

Fish tissue samples collected in Big Bayou Creek and Little Bayou Creek in 1993 and 1994indicated that concentrations had decreased since 1989: they were about 10 times lower than the1989 reported values. Additionally, total PCB levels in fish tissue from Big Bayou Creek (0.143g/g) were about four times lower than concentrations detected in fish tissue from Little BayouCreek (0.553 g/g). Background samples, collected from Hinds Creek, did not contain detectablelevels of PCBs. In 1993, 40% of the fish sampled from Big Bayou Creek did not containdetectable levels of PCBs. In 1994, that number was 20% (fewer fish were sampled in 1994,which may account for the difference between years). Also, in 1993 and 1994, several fish fromLittle Bayou Creek did not have detectable levels of PCBs.

In 1997, the Kentucky Division of Waste Management collected 20 sunfish from Little BayouCreek and analyzed them for levels of PCBs in fillets. The average concentration of total PCBs(0.561 g/g) in fish tissue from Little Bayou Creek was similar to the 1993-1994 results. Two ofthe twenty fish sampled did not have detectable levels of PCBs in fillets. Fish tissue results werenot available for Big Bayou Creek in 1997.

ATSDR evaluated whether adults and children eating fish from either Big Bayou Creek or theLittle Bayou Creek system could obtain PCB doses that would cause adverse health effects.ATSDR assumed that subsistence and recreational anglers got 20% of their total fish intake fromthe creeks for 30 years. The estimated exposure dose for children (assumed to be the children ofsubsistence/recreational anglers) was based on a 6-year exposure duration. The consumption ratefor recreational anglers was 8 grams per day (g/day), which equates to 20 meals per year at 150grams (5.3 ounces) per meal. For subsistence anglers, the consumption rate was 60 g/day; thatequates to 150 meals per year at 150 grams (5.3 ounces) per meal. A recreational angler's childwas assumed to consume 3 g/day, which equates to 20 meals per year at 50 grams (1.8 ounces)per meal. A subsistence angler's child was assumed to consume 8 g/day--equal to 150 meals peryear at 50 grams (1.8 ounces) per meal. If a fish tissue sample was below the detection limit, weused the detection limit as the measured value for total averaged values. This is a conservativeapproach that could overestimate the exposure dose.

ATSDR believes that people are more likely to fish in the (less-contaminated) Big Bayou Creekarea than in Little Bayou Creek. This is because of the posted fish advisories and more limitedaccess to Little Bayou Creek. Additionally, Big Bayou Creek provides a better habitat for fishthat people typically eat.

Ingestion or inhalation of PCBs at high exposure doses has been shown to cause skin irritations,such as chloracne and rashes, in animals and humans [95,113]. The doses required to producesuch effects are quite high: daily, occupational exposure doses ranging from 0.07 and 0.14mg/kg/day failed to produce adverse health effects in workers [95]. Reports of developmentaleffects from lower exposures are controversial and have not been verified [95].

Generally, humans appear to be less sensitive than other animals to the toxic effects of PCBs. Inlaboratory animals, PCBs have been shown to produce skin effects (similar to those seen inpeople exposed at high doses) as well as effects on the thyroid, immune system, liver, toenails,and eyelids. Of the laboratory animals tested (i.e., rabbits, minks, mice, rats, ferrets, andmonkeys), the rhesus monkey appears to be the most sensitive [113]. PCBs have been shown toimpair the monkey's immune system (in addition to producing skin, fingernail, and toenaileffects), at doses as low as 0.005 mg/kg/day. This dose is almost 28 times lower than the doseshown not to harm people. ATSDR and EPA have developed a health guideline of 0.00002mg/kg/day, based on adverse effects in monkeys [95,113].

Several human studies have reported that low level environmental PCB exposure during in uteroor neonatal development can effect the child's neurologic system [137,138], immunologic system[139,140], or development [141,142,143]. However, study limitations have been reported,including: unmeasured exposure concentrations, possible exposure to other neurotoxic chemicals(e.g., dioxins, mercury, lead, organochlorine pesticides), and inadequate control for confoundingfactors (e.g., birth weight and maternal smoking, alcohol, and drug use). Therefore, these studiessuggest, but do not prove, an association between prenatal or neonatal exposures to PCBs andneurologic, immunologic and developmental effects in young children. Because of theselimitations, it cannot be equivocally determined whether low level environmental PCB exposuresaffect prenatal or neonatal development.

Rats are the only laboratory species shown to develop cancer after ingesting PCBs [95,113]. Theanimals were administered doses of PCBs that were considerably higher than environmentaldoses. For example, the doses given rats in one study were equivalent to human doses of 0.35 to3.0 mg/kg/day. In order to use animal data to predict whether humans are likely to developcancer, we often must assume that the relationship between PCB dose (administered) and cancerdevelopment is the same at high and low doses. We must also assume that there is no dose atwhich there is not a risk for cancer development. Many scientists believe that these assumptionsare valid for substances that cause cancer by directly attacking (i.e., mutating) genetic material inall living cells. But the assumption is much less likely to hold for substances that cause cancerwithout directly attacking genetic material. PCBs are considered by many scientists to inducetumors (in rats) primarily through mechanisms that do not involve genetic mutation [113].

To evaluate the potential for cancer in humans using data from animal studies, scientists mustmake assumptions about the ways humans resemble or differ from the animal "models." EPA'sstandard methodology uses a "scaling factor" to account for differences in the size of the testanimals (e.g., body weight, lung surface area) compared to humans, and a cancer slope factor topredict the likelihood of cancer developing per unit dose (measured in mg/kg/day) [144].

One approach, called physiologically based pharmacokinetic (PBPK) modeling, incorporatesinformation about how a substance and its degradation products are chemically modified anddistributed throughout the body following exposure. When PBPK models were used to comparehow different animal species handle PCBs and their metabolites, many inconsistencies werefound, making cross-species predictions highly uncertain [95].

These considerations may explain why there are no scientific reports of cancer in any animalspecies other than rats, not even in the sensitive rhesus monkeys, following exposure to PCBs.Also, PBPK modeling may explain the lack of conclusive reports of cancer in multiple studies ofworkers occupationally exposed to PCBs [95,113].

A recent study of more than 7,000 capacitor workers reported exposures to PCB airconcentrations as high as 1,500 g/m3. Workers in this study were employed for at least 3months, and their health status was followed for an average of more than 30 years. Using thereported exposure levels, ATSDR estimated lifetime exposure doses of 0.0004 to 0.009mg/kg/day for these workers. Using standard EPA methods to predict the likelihood of cancer atthese doses, one would have expected to see additional cancers among the 1,687 workers whoreceived the highest PCB exposures. However, the study found no excess cancers of the liver orany other organ [136]. The estimated occupational exposure doses that failed to producedetectable increases in liver cancer were more than 5 to 185 times higher than the lifetimeexposure doses estimated for subsistence and recreational fishers who could have ingested fishfrom waters near PGDP or been exposed to PCBs in off-site soils.

Therefore, ATSDR scientists conclude that exposure to PCBs from ingestion of deer and fishfrom Big Bayou and Little Bayou Creeks is not expected to result in adverse health effects.

Radioactive Materials (Radiation Exposures)

Radioactive materials, both naturally occurring and man-made, have been detected in all mediaat PGDP. The cumulative radiation dose from potential chronic exposure to those media is not apublic health hazard. Potential acute exposures from an accident in 1960 are an indeterminatehealth hazard.

Radioactive material's concentrations and total annual quantities were reported for each medium(e.g., soil) by DOE (and formerly by the U.S. Energy Research and Development Administrationor the U.S. Atomic Energy Commission). For media in which the materials' off-siteconcentrations were not reported, ATSDR estimated the concentrations by using computermodels. The predominant radioactive materials at PGDP are, and were in the past, uranium 234,uranium 235, uranium 238, and technetium 99. These contaminants were screened in all media.Other radioactive contaminants (e.g., thorium 230, plutonium 239, neptunium 237) wereanalyzed in some media and estimated in some cases; however, these other radioactivecontaminants contributed approximately 10% or less to the exposures doses.

Table 25 lists the maximum estimated annual committed effective doses for children and adultsin different media. Note that the potential exposure doses occurred at different times and indifferent places: realistically, the total doses from each exposure pathway should not be addedtogether. Current exposure doses are much less than those estimated for the first 10 years of plantoperations.

The potential health effects from each radioactive material per route of exposure were reviewed.Also, the potential health effects from estimated radiation doses from all routes of exposure wereconsidered, as were organ doses. The estimated radiation exposure dose from all media for anyyear of plant operation does not exceed 500 millirems (mrem), or 5 millisieverts (mSv), exceptfor a potential acute exposure in 1960. The International Commission on Radiological Protection(ICRP) recommends, for annual committed effective dose to the general population, a limit of100 mrem (1 mSv) above background [145]. Before 1990, the ICRP recommendation was 500mrem (5 mSv) per year. Although the ICRP recommendations were lowered for chronic exposureover a 70-year life span, no adverse health effects have been seen at the estimated chronicexposure doses for PGDP, and no apparent increased cancer risk would be expected [145,147].

Table 25.

Maximum estimated annual committed effective doses for radiation exposure near PGDP
Exposure pathway Route of Exposure Maximum Estimated Annual Committed Effective Dose for Children Maximum Estimated Annual Committed Effective Dose for Adults
Groundwater1 Ingestion 7 mrem
(0.07 mSv)
7 mrem
(0.07 mSv)
Surface water2 Ingestion 2.0 mrem
(0.02 mSv)
0.8 mrem
(0.01 mSv)
Soil/sediment3 Ingestion 9 mrem (pica child)
(0.09 mSv)
0.6 mrem (workers)
(0.01 mSv)
Food/biota4 Ingestion 0.4 mrem
(0.00 mSv)
0.7 mrem
(0.01 mSv)
Air5 Inhalation (chronic)

Inhalation (acute)

340 mrem
(3.4 mSv)

500 to 1,500 mrem
(5 to 15 mSv)

340 mrem
(3.4 mSv)

500 to 1,500 mrem
(5 to 15 mSv)

1 The maximum concentration of technetium 99 used in the calculation was detected in 1988, before the first well was taken out of service.
2 The maximum concentrations used in the calculation were detected in 1959 and 1960.
3 Most of these samples were collected and analyzed in the 1990s.
4 Most of these samples were collected and analyzed in the 1990s.
5 The concentrations used in this model were estimated for 1956.
Key: mrem = millirems; mSv = millisieverts

ATSDR concludes that past or current chronic exposure to radioactive materials in off-site mediafrom normal plant operations is not expected to result in adverse human health effects.

For potential acute exposure, there are many uncertainties involved in determining estimateddoses, including quantities released, the duration of the release, and the exact location ofindividuals at the time of the accident. Epidemiological worker studies of chronic exposures touranium dust suggest, but do not confirm, evidence of adverse health effects, primarily malignantand non-malignant lung diseases. However, these workers were chronically exposed to higherlevels of insoluble uranium than estimated exposure doses calculated for past accidents. Animalstudies on rats investigated acute exposures to uranyl nitrate (a more-soluble form) and reportedan increased frequency of lung tumors and osteosarcomas. However, the doses in these studieswere substantially higher than the estimated exposure doses from the 1960 accident and theexperiment did not provide enough information for confident extrapolation of risk coefficients tohumans [146]. Because of the uncertainties in the release quantities and whether the airborneexposure pathway was complete during this accident, ATSDR scientists concluded that the 1960accident posed an indeterminate health hazard. If an individual was exposed to the maximumestimated exposure and using EPA's cancer risk coefficients [147], we would predict a moderateincreased cancer risk.

For more information on uranium, refer to the discussion for that element (below).


Exposure to thallium in off-site surface water and groundwater is not a public health hazard.

Thallium is an element that occurs naturally in the environment. Certain industrial processes(e.g., cement manufacturers, coal-burning power plants, and smelters) release thallium to theenvironment [148]. Environmental thallium is found chemically combined with other substancessuch as oxygen, sulfur, and halogens. Most of the chemical compounds are soluble in water. Thegeneral public is exposed to low levels of thallium through eating, smoking tobacco, andbreathing second-hand tobacco smoke. The average person takes in about 2 micrograms ofthallium per gram of food daily. Once ingested, thallium distributes throughout the human body;it can cross the placenta in pregnant women and be distributed to the developing fetus.

Thallium was detected in surface water near PGDP. The maximum thallium concentration insurface water was 5,260 g/L in Big Bayou Creek near the inactive southwest landfill [44].Using this maximum concentration, we estimated that incidental ingestion of water from BigBayou Creek would result in an exposure dose of 0.001 mg/kg/day for adults and 0.002mg/kg/day for children 1 to 6 years old.

Thallium was not found in drinking water wells, but the lowest level of analytical detection was10 g/L--higher than EPA's drinking water standard of 2 g/L [148]. Therefore, we used thedetection limit of 10 g/L to estimate exposure doses. This gave us doses of 0.0003 mg/kg/dayfor an adult and 0.001 mg/kg/day for a child, assuming that these residential wells were the solesource of drinking water.

ATSDR has no health guideline for ingestion of thallium. EPA has RfDs for several thalliumcompounds. Each RfD covers a particular compound and is based on animal studies for thatcompound. For example, the RfD for thallium sulfate is based on a failure to observe harmfuleffects in rats that were administered as much as 0.25 mg/kg/day of thallium by gavage (stomachtube). EPA divided this number by an uncertainty factor of 3,000 to account for humans beingmore sensitive than rats to thallium, for some humans being more sensitive than others, and for alack of chronic toxicity data; this gave EPA an RfD of 0.00008 mg/kg/day [113].

The thallium dose that did not cause toxicity to rats (i.e., 0.25 mg/kg/day) was 200 times higherthan the maximum exposure dose that ATSDR estimated for surface water or groundwateringestion, despite the fact that we used very conservative assumptions to estimate dose. If morerealistic exposure assumptions were used, our estimated doses would be even lower. Forexample, our surface water dose is based on the assumption that a child ingests half a liter ofmaximally contaminated water a month for 6 years and an adult ingests this amount for 30 years.It is probably not very likely that a young child, who is under constant care by an adult, wouldconsume these quantities of surface water at this maximum concentration. Likewise, it is unlikelythat an adult would ingest a half liter of maximally contaminated surface water once a month for30 years. Lastly, our groundwater doses are not based on measured concentrations in drinkingwater, but on levels of analytical detection. The actual levels in these wells were lower than thedetection limit.

Therefore, ATSDR scientists conclude that ingestion of thallium in surface water from BigBayou Creek or from drinking water wells located near PGDP is not expected to result in adversehuman health effects.


Past exposure to TCE at levels found in well RW-002 was a public health hazard for children,because it increased the likelihood of neurological effects such as speech and hearing deficits.No public health hazard currently exists, because this residential well is no longer in use and theexposure pathway is incomplete.

TCE is a nonflammable, oily, colorless liquid that has a sweet odor and a sweet, burning taste.Years ago, TCE was used as an anaesthetic. It is now used as a solvent to remove grease frommetal parts and to make other chemicals. It is heavier than water and has low solubility (up toone part TCE per thousand parts of water at room temperature) [149]. These qualities make TCEa troublesome contaminant at hazardous waste sites.When present in groundwater, TCE tends tosettle into a layer at the bottom of the aquifer and then continuously dissolves into thegroundwater. This may result in high levels of TCE in the aquifer for years after the originalrelease of contamination has ended. This has happened at PGDP and is the reason why there wasTCE contamination in private well water.

TCE contamination of groundwater beneath the PGDP facility and in nearby private wells wasdiscovered in August 1988. TCE was detected at concentrations above ATSDR's comparisonvalue in four off-site residential wells. Maximum levels of TCE, ranging from 20 to 43 g/L,were found in three of the wells (RW-004, RW-017, RW-113); a maximum level of 960 g/Lwas found in a fourth well (RW-002). As a result of this sampling, the Department of Energy(DOE) immediately provided bottled water to residents with contaminated well water--until theycould be supplied with municipal water--and completely discontinued private well use.

Groundwater sampling was not conducted before 1988. Sampling conducted after 1988, whenthe wells were no longer used for drinking, revealed higher levels of TCE than were first detectedin 1988. This finding was not unexpected, considering the results of groundwater modeling ofcontaminant movement from sources on site. Modeling results indicate that levels of TCE before1988 were likely to have been lower than levels detected in 1988. ATSDR scientists cannotdetermine with certainty whether TCE was present in private wells, or at what levels, before1988. At most, residents used water from the most contaminated well (RW-002) for 5 to 15years. If these wells are used in the future, or if new wells are drilled into the plumes, theresidents could be exposed to much higher concentrations of TCE than in 1988.

There are several reports of an increased occurrence of nervous system and developmentaleffects, and cancer, from ingestion and inhalation of TCE by animals and humans [149,150,151].Human health studies suggest an increased incidence of cancer of various types (e.g., bladder,lymphoma, kidney, respiratory tract, cervix, skin, liver, and stomach) from exposure to TCE;however, no studies provide clear, unequivocal evidence that exposure is linked to increasedcancer risk in humans [149,150,151]. The available studies suffer from inadequatecharacterization of exposure, small numbers of subjects, and the fact that subjects were likelyexposed to other potentially carcinogenic chemicals. There is, however, sufficient evidence thatTCE exposure results in cancer development in animals, although animal studies may not berelevant for evaluating health hazard to humans [149,151].

In 1989, EPA withdrew its cancer assessment for TCE, which was based primarily on animalstudies conducted in 1990 and earlier, because more recent pharmacokinetic and mechanisticdata for TCE became available [113,152]. An updated approach to TCE cancer assessment usingexisting animal data and state-of-the-science papers has been proposed [152]. The approach,though high-dose animal studies support it, does not appear entirely relevant for evaluating healthhazard from human environmental exposure. There are several reasons for this. First, cancer inanimals appears to result from species-specific mechanisms that are not entirely relevant tohumans [149,151]. Second, the animals used in these studies were exposed to very high doses ofTCE, several orders of magnitude higher than estimated for PGDP residents, and the overalldeath rate in the animal studies was high. The surviving animals were not likely to have been ingood health and, therefore, would have been more susceptible to adverse effects from TCEexposure (like infections and illnesses) than healthy animals. Third, the overall findings fromanimal studies are inconsistent: some studies report an increased incidence of cancer, while anequal number do not report an increase at similar levels of exposure [149]. Fourth, the studies didnot evaluate the effect of exposure to stabilizers and impurities in TCE; these things may also becarcinogenic. For these reasons, ATSDR scientists decided to focus on non-cancer effects ofTCE.

ATSDR derived a health guideline of 0.1 ppm for intermediate-duration (15 to 364 days)exposure to TCE by inhalation. This guideline, equivalent to 0.15 mg/kg/day, is based onneurological and cardiac effects (e.g., decreased wakefulness and decreased post-exposure heartrate) in rats. The lowest dose that produced these effects was 50 ppm in air, which is equivalentto 77 mg/kg/day. The estimated dose for PGDP residents (using the maximum concentrationfrom a drinking water well) was similar to the ATSDR health guideline and more than two ordersof magnitude lower than the lowest effect level observed in animals.

ATSDR derived a health guideline of 0.2 mg/kg/day for ingestion of TCE based on an acute-duration (less than 14 days) study showing developmental and behavioral changes in mouse pupsadministered 50 mg/kg/day of TCE [153]. In this study, the TCE was dissolved in oil andadministered by stomach tube (gavage) [149]. The findings of this study are not entirely relevantfor evaluating health hazard for PGDP residents exposed to TCE in well water for severalreasons. First, gavage doses in the animal study were administered as one large dose per day,while PGDP residents were likely to have been exposed to TCE in drinking water several times aday. (The body handles a single large dose much differently than it does a series of smallerdoses.) Second, the total dose entering the body is higher and maintained for a longer time whenTCE is dissolved in oil than when it is dissolved in water. Lastly, exposure to TCE in the animalstudy lasted less than 14 days, while maximum exposures to PGDP residents (from the RW-002well) may have occurred over a period of 5 to 15 years. Despite these limitations, the findings aresupported by other animal and human studies.

ATSDR's TCE Sub-Registry reports an excessive number of children aged 9 years old oryounger with speech and hearing deficits [154]. Although the exposure levels of these childrenwere not well characterized, the findings support the types of outcome seen in animals. Severalstudies of workers and community residents suggest a possible association between exposure toTCE (and other chemicals) and developmental outcomes [150,155,156,157]. However, none ofthe studies provide conclusive evidence for a causal relationship, largely because informationabout TCE exposure was incomplete and exposure to other chemicals was likely [149,151].

Collectively, the scientific data indicate that the developing nervous system in young animals andhumans may be sensitive to the toxic effects of TCE [149]. It is not clear whether past exposuresto TCE by PGDP residents with contaminated wells were sufficient to result in similar outcomes.In order to be protective of the most sensitive individuals, ATSDR concludes that past exposureto contaminated water from well RW-002 may have resulted in neurological effects in childrenchronically using this water prior to 1989.


Short-term (1-hour average) off-site uranium air concentrations were modeled for the timeperiod corresponding to the 1960 accidental release. Estimated levels were above ATSDR'sintermediate comparison values and occupational standards at the nearest residence (southeastof Building C-333). If people were exposed to the estimated air concentrations, they could haveexperienced adverse health effects. However, the accident occurred at 4:00 a.m. in mid-November, when people were most likely indoors and asleep. Because of uncertainties (e.g.,quantities released, locations of individuals at the time of the accident) it cannot be determined ifthis accident posed a public health hazard.

Long-term exposure to airborne uranium also occurred during the years 1954 to 1963, as aresult of elevated operational emissions. Because the prevailing winds were from the south andsouthwest, the primary exposed population was residents living north and northeast of thefacility. This population may also have some exposure to uranium via soil and/or groundwaterexposure pathways. Even if chronic exposure to air, soil, and groundwater occurredsimultaneously, adverse health effects are not expected.

Under current, normal operating conditions, uranium air concentrations are not a public healthhazard.

Uranium is a radioactive metal, which is naturally present in rocks, soil, groundwater, surfacewater, air, plants, and animals in small amounts. It contributes to a natural level of radiation inour environment, called background radiation. The amount of uranium in drinking water in theUnited States is generally less than 1 picocurie per liter (or approximately 1.5 g/L) [158].

Natural uranium, enriched uranium, and depleted uranium are mixtures of primarily threeuranium isotopes (U-238, U-235, and U-234; chemically similar but with a different number ofneutrons). Natural uranium is, by weight, more than 99% U-238, 0.72% U-235, and 0.005% U-234. Enriched uranium is more than 0.72% U-235 by weight, and depleted uranium is less than0.72% U-235 by weight. All three isotopes are radioactive but have different specific activities,that is, radioactivity per gram of material. U-238 has the lowest specific activity; U-234 has thehighest.

Uranium can harm people in two ways, as a chemical toxin and as a radioactive substance. (Thatis, its chemical and radioactive properties can both be harmful, and these two things areconsidered separately.) Because natural uranium produces very little radioactivity, the chemicaleffects of uranium are generally more harmful than the radioactive effects. However, moreradioactive mixtures (like enriched uranium) can harm the kidney more than natural uranium dueto the combined effects of chemical and radioactive properties.

The kidney is the primary target organ for the chemical effects of ingested and inhaled uranium.The extent of toxicity is determined primarily by exposure route, type of uranium compound, andsolubility of that compound. Ingested uranium compounds are generally less toxic to the kidneysthan inhaled uranium compounds, partly because uranium is poorly absorbed from the intestinaltract. Highly soluble uranium compounds are generally more toxic to the kidneys than less-soluble compounds via ingestion, because the more-soluble compounds are more readilyabsorbed (that is, they pose a greater potential dose to the kidney). Absorption of uranium is low(less than 5%) by all exposure routes (inhalation, ingestion, and dermal).

Studies using laboratory animals provide most of the evidence for kidney toxicity. ATSDR hasestablished intermediate (15 to 364 days) exposure health guidelines for inhalation of bothsoluble and insoluble uranium compounds. The guideline for insoluble uranium is 8 x 10-3mg/m3. This guideline is based on structural changes (lesions) in kidneys of dogs exposed touranium dioxide dust 6 hours a day, 6 days a week, for 5 weeks [159]. The health guideline forinhalation of soluble uranium is 4 x 10-4 mg/m3, based on kidney lesions in dogs exposed touranium chloride in air 6 hours a day, 6 days a week, for 1 year [160]. Neither study providedinformation about the size of the uranium particles used, so ATSDR based its guideline on theconservative assumption that uranium particles were 2 microns or less in diameter.

The estimated 1-hour average off-site air concentration of uranium during the accident(approximately 4.3 ppm at the nearest residence) exceeded the intermediate-exposure health-based guideline for inhalation. On-site air concentrations would have been even higher, though itis uncertain whether on-site personnel were exposed to elevated air concentrations. ATSDR hasnot derived health-based guidelines for acute exposure. The estimated off-site air concentrationexceeded the occupational standards for soluble and insoluble uranium compounds. If peoplewere actually exposed to the estimated air concentrations, then a public health hazard existed.ATSDR does not believe that exposures occurred at this level, since the accident occurred at 4:00a.m. in mid-November over a period of 4 hours.

Discussions with residents and site officials have not indicated any reports of acute symptomsassociated with this accident (for either uranium or HF). Because of the lack of exposureinformation and considering that concentrations were derived from air dispersion modeling, weconclude that an indeterminate health hazard existed for uranium air concentrations in the past.


Exposure to vanadium from off-site groundwater and/or soil is not a public health hazard.

Vanadium is a naturally occurring element in the earth's crust, fuel oil, and coal. Vanadium ismostly used as an alloying agent in steel production, although small amounts are also used inrubber, plastics, and ceramics [161]. Vanadium is a metallic element that occurs in six oxidationstates and numerous inorganic compounds. Vanadium's toxicity depends on its physical andchemical state, particularly on its valence state and solubility. Vanadium is poorly absorbedthrough the gut, but more readily absorbed through the lungs.

Vanadium was detected at a maximum concentration of 20 g/L in one off-site residential(drinking water) well. Although this concentration is lower than ATSDR's comparison value of30 g/L, we selected vanadium as a contaminant of concern because maximum concentrationsdetected in off-site monitoring wells located near residential wells were as high as 210 g/L.ATSDR scientists used the maximum groundwater concentration (210 g/L) to estimateexposure (ingestion) doses of 0.006 mg/kg/day for adults and 0.02 mg/kg/day for children. If wehad used the concentrations measured in residential wells, the estimated doses would have beenan order of magnitude lower--0.0006 mg/kg/day for adults and 0.002 mg/kg/day for children.

ATSDR's intermediate screening value for ingestion of vanadium is 0.003 mg/kg/day based on astudy where rats were administered vanadium in their drinking water for 3 months [161]. In thisstudy, the treated rats showed mild changes to the kidneys at a minimum dose of 0.6 mg/kg/day,while no adverse effects were seen at the lower dose of 0.3 mg/kg/day. The lower dose wasconsidered the NOAEL, and is the basis for ATSDR's health guideline. The NOAEL for rats (0.3mg/kg/day) was divided by an uncertainty factor of 100, because humans are presumed to bemore sensitive than rats to vanadium and because some humans are more sensitive than others.The uncertainty factors may be overly conservative: scientific information suggests that humansare actually less sensitive than rats to ingested vanadium. Human volunteers who swallowed amaximum dose of 1.3 mg/kg/day of vanadium for 45 to 68 days showed no effects when testedfor injury to their liver, blood cells, or kidneys [161]. An adult would have to drink more than4,500 liters a day of water contaminated at the highest level in the residential well to take in theamount of vanadium that did not cause adverse effects in the human volunteers. A child wouldhave to take in 650 liters a day to take in this amount.

Vanadium was detected in off-site soil at levels ranging from 0.01 to 300 mg/kg (ppm). Theaverage vanadium content of soils in the United States is 200 mg/kg; vanadium seems to be mostabundant in the western United States. Using the 67th percentile concentration to calculate anexposure dose, we found only one exposure scenario had an estimated exposure dose (0.006mg/kg/day for a pica child) that exceeded ATSDR's screening value for intermediate (15 to 364days) oral exposure. ATSDR's screening value (0.003 mg/kg/day) is based on a drinking waterstudy in rats. Water, though, tends to contain more-soluble forms of vanadium than do weatheredsoils. Consequently, less vanadium would be absorbed from soil than from water. The estimatedexposure dose for pica children is approximately 200 times less than the dose given to humanvolunteers mentioned above. Based on the conservative exposure assumptions, vanadium's poorabsorption from the gut, and the implication that humans are less sensitive to ingested vanadiumthan rats, ATSDR does not expect adverse health effects to result from ingestion of vanadium insoil.

Therefore, ATSDR concludes that ingestion of vanadium in off-site drinking water wells and/orsoil is not expected to result in adverse human health effects for past, current, or future exposureto children or adults.

Vinyl Chloride

Potential past exposure to vinyl chloride in residential drinking water is an indeterminate publichealth hazard. It is not known whether anyone was exposed or at what levels due to inadequatedetection limits. No public health hazard currently exists, because no one is using theseresidential wells.

Vinyl chloride is a man-made substance used in the production of polyvinyl chloride (PVC) andother plastic products. It is one of the substances generated when TCE breaks down ingroundwater. As TCE degrades in groundwater, the resulting vinyl chloride concentration mayincrease downgradient, depending on a number of factors, including the chemical characteristicsof the soil through which the contaminated groundwater travels and the distance traveled [162].

Vinyl chloride has not been detected in residential wells but was found in two samples from onemonitoring well used to test for off-site groundwater contamination in the PGDP area. Themaximum concentration of vinyl chloride in this well was 110 g/L. The test well was locatednear four residential wells that were not found to contain vinyl chloride; however, the lowerlimits of analytical detection for these well samples were higher than EPA's MaximumContaminant Level (MCL) of 2 g/L for public drinking water supplies. In addition, very fewresidential well water samples (12 in all) were analyzed for vinyl chloride.

Well Range of Sample Detection Limits
RW-0021-500 g/L (four samples)
RW-0042-10 g/L (four samples)
RW-0174-10 g/L (three samples)
RW-11310 g/L (one sample)

The detection limit for RW-002 was 500 g/L on October 24, 1989, but the detection limit forthis well was 1 g/L on August 14, 1990. Therefore, vinyl chloride was probably not a problemwhen RW-002 was being used; however, there is some uncertainty due to variations in the TCEplume concentrations from seasonal factors. The lowest detection limits for wells RW-017 andRW-113 were 4 and 10 g/L, respectively. Both values are above the MCL.

ATSDR's estimated ingestion doses, assuming exposure to the maximum concentration found inthe test well, were 0.006 mg/kg/day for an adult and 0.02 mg/kg/day for a child.

ATSDR has developed a health guideline of 0.00002 mg/kg/day for chronic ingestion of vinylchloride. This is based on a study of rats that developed liver toxicity from exposure to vinylchloride (in PVC) in their diet. The lowest dose at which adverse liver effects wereobserved--the LOAEL--was 0.018 mg/kg/day. An uncertainty factor of 1,000 was applied to theLOAEL, because humans may be more sensitive than rats to vinyl chloride, some humans aremore sensitive than others, and there was no dose level tested at which adverse effects were notobserved [163]. ATSDR's estimated doses, based on maximum test well concentrations, werehigher than the health guideline and similar to the LOAEL (for children).

However, we are not certain whether people drank water from wells potentially contaminatedwith vinyl chloride. Therefore, the health hazard from past exposure to vinyl chloride cannot bedetermined. These wells are not currently being used. If we make the assumption that peoplewere exposed to vinyl chloride at maximum "detection limit" concentrations, then we concludethat people may experience adverse health effects. ATSDR scientists recommend that detectionlimits for degradation products of TCE, such as vinyl chloride, in groundwater analyses are lowenough to determine whether concentrations exceed health-based guidelines.

Given the lack of accurate concentration measurements for vinyl chloride in residential wells andexposure information, we conclude that past exposure is an indeterminate health hazard.


Past exposure to zinc from one residential well near PGDP was not a public health hazard. Nopublic health hazard currently exists, because this well is no longer being used.

Zinc is a naturally occurring element that is commonly used in industrial processes [164]. It isfound in man-made products, such as metal alloys, dry cell batteries, metal beverage containers,and zinc-coated pipes. Zinc is also used in many over-the-counter medicines, sunblocks, anddeodorants, and is also present in leafy vegetables, meat, poultry and fish.

Zinc was detected one time in one residential well, at a concentration of 5,090 g/L. ATSDR'sestimated ingestion doses, assuming exposure at this concentration, were 0.15 mg/kg/day for anadult and 0.50 mg/kg/day for a child.

Zinc is an essential element in the human diet [164]. Zinc deficiencies can produce loss ofappetite, growth retardation, skin changes, slow healing of wounds, and depressed mentalfunction in children [164]. The individual response to deficiency varies depending on age; theamount of meat, dairy products, and fibrous vegetables in the diet; and (for women) whether oneis pregnant or nursing infants. The average American dietary intake is 15 mg/day for men and 12mg/day for women [128]. If women are nursing infants less than 6 months old, they need toconsume 19 mg/day. Elderly people generally consume lower amounts of zinc (7 to 10 mg/day),but healthier, more active elderly people consume closer to average levels. If a person's diet islow in zinc-containing foods, they may need to consume 36 to 45 mg/day to prevent deficiencies[164].

Long-term ingestion of excessive amounts of zinc can be related to toxicity, including decreasedhigh-density (good) cholesterol levels, impaired immune function, and anemia [113]. Theseeffects have been observed at estimated total dietary intakes of 1 mg/kg/day (which is equivalentto 60 mg/day for a 60-kg woman and 70 mg/day for a 70-kg man) and are the basis for EPA'shealth guideline of 0.3 mg/kg/day.

ATSDR's estimated exposure dose from the well water for a 13-kilogram child (0.392mg/kg/day) exceeded the health guideline (0.3 mg/kg/day), but was lower than the lowest levelshown to cause adverse health effects and lower than the recommended dietary intake for adults.Also, the estimated exposure dose for a child would decrease as the child developed into an adult(the estimated adult dose was 0.15 mg/kg/day), so the child dose does not represent a chronicexposure dose over a lifetime.

Therefore, ATSDR scientists do not expect adverse health effects to result from past exposure tozinc in drinking water from this residential well near PGDP.



For people living near PGDP, complete and potential exposure pathways have been identified fordifferent contaminants. However, the levels of exposure are low, and the potentially exposedpopulation for each exposure pathway is very small relative to the county-wide health outcomedata available. A health outcome data review compares the frequency of specific diseases withina particular area to the frequency in an outside population or standard. While this type of analysiscan provide information about whether a population has experienced higher than expected ratesof selected diseases, there are important limitations to the analysis and to its application for avery small population.

First, data are collected regularly only for select and limited health outcomes. Cancer registriescollect data on the incidence of cancers, vital statistics bureaus collect data on mortality, andbirth defect registries collect data on birth outcomes. The incidence of asthma was a communityconcern, but there is no database that would allow a comparison of the rate of asthma cases withan outside population or standard.

A second limitation of the data used for comparisons is that they are usually collected,assembled, and analyzed at the county or state level. The populations of concern near PGDP areextremely small--for each exposure pathway, only a few households are included. Expanding thestudy area to include everyone in the county as the potentially exposed group would dilute apossible association by including a large number of persons who were not exposed. In addition,with a small group of households, very few specific diseases occur over time. When there are fewevents occurring in a small population, it is difficult to get a good estimate of how many excesscases a group experienced.

Recognizing these limitations, we are limited in this report to using standard health outcome dataanalysis methods. (We do recognize that other options may be available for future studies.)Representatives of ATSDR and Boston University identified and reviewed data on cancerincidence for McCracken and Ballard Counties in Kentucky [165] and Massac County in Illinois[166], although there were no completed exposure pathways identified for people in Illinois.Statistics from cancer registries are discussed below. Data from the cancer registries are publiclyavailable on the Internet and in written reports.

ATSDR representatives reviewed a report, "Report of an Environmental Health Survey ofIndividuals Exposed to Contaminated Groundwater From the DOE Paducah Gaseous DiffusionPlant", which was conducted in 1989 by the University of Cincinnati Medical Center at therequest of Martin Marietta Energy Systems, Inc.[167]. The foundation evaluated residents in theaffected area who were initially asked to stop using their well water. This report is discussedbelow.

ATSDR representatives also reviewed information collected in January 2000 by Tri StateConsulting of Independence, Kentucky. The consulting firm nurses interviewed 77 individualsliving within one and one-half mile radius of PGDP. The results of their report include self-reported symptoms and adverse health effects among those individuals.

Statistics From Cancer Registries

ATSDR and Boston University representatives evaluated data using age-adjusted rates for ninegeneral types of cancer from 1991 through 1998. (Age-adjusted rates were used since it is widelyrecognized that the overall risk of getting cancer increases with age.) The types of cancerincluded brain/central nervous system, bladder, female breast, Hodgkin's lymphoma, kidney,leukemia, liver, lung, and non-Hodgkin's lymphoma. These data are limited, since they are notlinked to exposure and are recorded for counties and area development districts. The potentialaffected population (between 15 and 90 persons) is relatively small compared to the countypopulations (approximately 63,000 in McCracken County, 8,000 in Ballard County, and 15,000in Massac County). The only type of cancer that may warrant further statistical review would bebladder cancer in Ballard County; however, we found no association between bladder cancer inBallard County and exposure to environmental contamination from this site.

Environmental Health Survey of Individuals Exposed to Contaminated Groundwater [167]

In this survey, researchers from the University of Cincinnati examined 16 individuals (6 exposedto elevated concentrations of trichloroethylene, or TCE, and 10 non-exposed). Three of theexposed subjects were exposed to concentrations well above EPA's drinking water standard forTCE. The other three were exposed to levels at or very close to the standard. The evaluationincluded (1) an environmental and medical questionnaire; (2) a physical examination; (3) acomplete blood count and fecal hemocult; (4) hepatic, renal, and hemopoietic parameters; (5)hair and fingernail samples collected for technetium 99 measurements; and (6) serumpolychlorinated biphenyl levels. (Polychlorinated biphenyls, or PCBs, had been detected innearby surface water and sediment.)

The researchers found no evidence of clinically manifested medical problems associated withexposure. Although the exposed group measured consistently higher than the non-exposed groupon renal, hemopoietic, and hepatic tests, the results were not statistically significant. The meanvalue for both groups was within normal range. The study consisted of self-selected, geneticallyrelated subjects, which may have biased the survey. The sample size was also too small to allowstatistically significant comparisons between individuals with higher or lower exposures.Researchers did not look for TCE in the blood, because the biological half-life of TCE is veryshort and the study was performed too long after exposures to have detected TCE.

The recommendations made by the researchers were as follows: (1) provide medical surveillance, on an annual basis, to anyone exposed to drinking water that exceeded EPA's drinking water standard; (2) continue monitoring wells in the affected area and provide non-contaminated water supplies; (3) determine the extent and movement of contamination in the groundwater; and (4) remediate the sources of contamination. ATSDR scientists support these recommendations. DOE has continued to monitor wells in the affected area and have provided municipal water. The extent of the contamination has been determined and continues to be monitored. Movement of the groundwater plumes in the Regional Gravel Aquifer to the northwest and northeast of the site has been modeled. Although the sources of contamination have not been remediated, interim actions have been taken to reduce the movement of the plumes or the concentrations in the plumes. The sources of the contamination will eventually be remediated. DOE provided medical surveillance, on an annual basis, to people exposed to drinking water that exceeded EPA's drinking water standard and who voluntarily participated in the surveillance program; however, after a couple of years, the volunteers discontinued their participation [168].


ATSDR and Boston University representatives used various methods to gather communityconcerns at this site. ATSDR used direct mail to solicit concerns from about 1,700 communitymembers. ATSDR received about 500 responses to this mailing. ATSDR also held five publicavailability meetings in Paducah and Heath, Kentucky, to gather concerns. Staff from ATSDRand Boston University also gathered concerns by participating in public meetings sponsored byDOE, by attending several Site Specific Advisory Board meetings, and through telephoneconversations and informal meetings with members of the public.

Each individual concern may not be listed, since many concerns were very similar. For moredetailed information about these concerns, refer to Appendix B. Community concerns regardingPGDP have been divided into three categories: exposures, health, and procedures.

Exposure Concerns


  1. A resident is concerned about possible inhalation exposures due to past air releases of radioactive and non-radioactive contaminants.
  2. In the past, people living along the site's northern fence boundary could have beenexposed to airborne hydrogen fluoride and radioactive materials (primarily uranium andtechnetium 99). These exposures would have happened between 1954 and 1963. Also,people less than 2.5 miles (4 kilometers) southeast of the site may have been exposed touranium and hydrogen fluoride during an accident on November 17, 1960. It is unlikely,though, that anyone was exposed during that accident: it happened at 4 a.m., and thetemperature was freezing. Please see this report's air exposure pathways section forfurther information about exposure via air exposure pathways. For more about potentialadverse health effects from such exposure, please refer to the public health implicationssection.

  3. A resident asked, "Why is there so much smoke from the plant, especially when low clouds are over the area?"
  4. The "smoke" or "clouds" seen over the Paducah Gaseous Diffusion Plant are steam orwater vapor released during the operations of the cooling towers. Different weatherconditions, with related wind and temperature variations, affect the behavior of these"clouds." On an overcast day or when the earth is cooler than the atmosphere, they maynot rise--they appear as "low clouds." Visible releases also come from the C-310 stackand the coal-burning plant, but they are not as noticeable off site.

  5. A resident stated that the C-310 stack vented uranium. This individual is concerned that emissions are not controlled and may be released to the environment.
  6. We believe that the incident this resident is referring to occurred in October 1989. At thattime there was a release of uranium into the environment from the C-310 purge stack.Approximately 205 grams (a little less than pound) were released into the atmosphere.The release resulted from a malfunction of the primary and secondary trap system that isused to keep uranium from escaping into the environment. The problem that led to thisaccident has been fixed. Refer to the air exposure pathway section for more information.

  7. A resident commented, "The air we breathe is absolutely unbelievable. The odors and pollution are really bad."
  8. Odors are a common concern, but they do not necessarily mean that there is a healthhazard. For some contaminants, the concentration needed to produce an odor can be quitesmall--not high enough to produce a health hazard. Refer to the air exposure pathwaydiscussion for more information about airborne contaminants in the PGDP area.

  9. A resident asked, "With the TVA fly ash fallout, will this shorten my life by ten years?"
  10. We do not have information about airborne releases from the Tennessee Valley Authority(TVA) Shawnee Steam Plant. However, the plant's permit(s) from the Kentucky Divisionof Air Quality restrict emissions from its stacks. Every year, coal-burning plants shouldbe reporting levels of particulates, sulfur dioxide, nitrogen oxides, etc., that they release.For more information, you may want to contact the Kentucky Department forEnvironmental Protection, Division of Air Quality. The state offices are in Frankfurt, butthere is also a Paducah regional office: 4500 Clarks River Road, Paducah, Kentucky. Forinformation about the release of airborne contaminants from PGDP, refer to the airexposure pathway section and the public health implications section.

  11. A resident asked, "What do current and past air and water quality monitoring of the region surrounding these sites and the rivers indicate about radiation levels and pollution from other potentially harmful chemicals?"
  12. This public health assessment presents information on the present and past levels ofcontamination arranged by medium (air, water, soil, etc.). There are no current exposuresto contaminants from PGDP at levels that present a health hazard. There were pastexposures that could have been of health concern to some people living near the site.Please refer to the public health implications section for descriptions of the potentiallyaffected areas and for discussions of potential health effects by substance.


  1. A member of the public stated that the public needs to know numbers/names of heavy metals, chemicals, radioactive substances, cubic yards of contaminated soil, etc., that are in and around the plants.
  2. This public health assessment has listed the contaminants of concern at the site. We havealso summarized the contaminants' concentrations in various media (air, water, soil, andfood). One of the techniques used at the site for soil sampling is designed to spot-check alarge area (approximately 3,000 acres, or 1,200 hectares) concentrating on areas mostlikely to have some contamination. This type of sampling is not all inclusive, and cannotbe used to determine how many cubic yards of contaminated soils are in and aroundPGDP. More extensive sampling is done to characterize a site that has been identified asbeing contaminated and will be cleaned up. For each project, the volume of contaminatedsoil is estimated before the project begins--but even then, estimates are frequently in error.

  3. A resident stated that they were worried about radionuclides in the soil and water. They eat a lot of food from their garden.
  4. There are no past or current off-site exposures to radioactive contaminants at levels thatwould be harmful to a person's health with the exception of the accidental release whichoccurred November 17, 1960. The concentrations of radionuclides in soil and sediment,surface water, groundwater, and food and biota are discussed under each exposurepathway. The potential for any health effect is discussed for all radioactive contaminants(radiation exposure) in the public health implications section. ATSDR is recommendingcontinued monitoring of groundwater, surface water, and biota, and development of aspatially and statistically consistent soil sampling program.

Surface Water and Sediment

  1. A member of the public is concerned about possible exposure to contaminated surface water and sediments in ditches and streams and about contamination when Big Bayou and Little Bayou Creeks overflow into people's fields and yards.
  2. A member of the public is concerned about toxic waste being dumped in LittleBayou Creek and being put in the landfill. "When we complained about the smell,they said it was chicken manure and in another case they said the smell was causedby bovine manure."

    The creeks receive effluent from the plant. They are currently being monitored forcontamination by DOE and the Commonwealth of Kentucky. PGDP has permits todischarge the effluent into the creeks as long as the concentrations of the variouschemicals are kept below certain levels. In this public health assessment, we determinedthat certain contaminants were released to the surface water at their highestconcentrations in 1959, 1960, and 1962. These highest levels were used in the publichealth implications section to determine past potential exposures. Estimated exposureswould not have been a health hazard to humans based on the exposure scenarios we used.(Refer to the surface water exposure pathway section for more details.)

    The solid waste management units (landfills) are permitted by the Commonwealth ofKentucky (Division of Waste Management). If you have concerns about what is permittedfor these landfills, or about the management of the landfills, the state should be able to provide you with this information.

    We looked at the effects of the landfills on the groundwater, surface water, soils, andsediments. There is an inactive sanitary landfill outside the security fence to the southwestof the site that is affecting Big Bayou Creek and the groundwater in the immediate area.DOE is aware of the problem and continues to monitor the soils and sediment, and thesurface water and groundwater. Several things could cause the smell referred to in thecomment; however, without more details, we cannot comment. Although the smell maybe a nuisance, it may not indicate a hazardous situation.

    During a flood, when the creeks overflow into people's fields, it is possible thatcontaminated sediment can spread; however, the concentrations of the contaminantsshould be less than the concentrations in the creek sediment. This has been confirmed byresults from sampling the creek banks. When the dose estimates were calculated foroccasional exposure, the concentrations in the sediment were used. For incidentalingestion of soil or sediment, the contaminant concentrations do not present a healthhazard.


  1. A resident stated that they have a pond around their house that they use, and they drink water from a private drinking well.
  2. Please refer to the previous pathway sections on groundwater and surface water.

    If you are concerned about your drinking water well, and you are within DOE's WaterPolicy area (between the site and the Ohio River, and between Metropolis Lake Road andBethel Church Road), you can contact DOE or their contractor (Bechtel Jacobs Company)to have your water tested. You can also contact the Kentucky Department forEnvironmental Protection, Division of Water. We have listed telephone numbers andcontacts for several agencies at the end of this comment section.

  3. A resident asked if there is contaminated groundwater west of the plant.
  4. Groundwater contamination has been detected northwest of the site and southwest of thesite near an inactive landfill. This individual seemed to be concerned about residentialwells directly west of the site on or near Bethel Church Road. We have no indication thatresidential wells west of the plant are affected by groundwater contamination from the site.

  5. A resident stated, "I am very concerned about the contaminated drinking water. I am of the belief that groundwater has been monitored closely in the past and strongly hope that it will continue to be."
  6. DOE has indicated that the groundwater in the potentially impacted areas will continue to be monitored closely.

  7. A citizen stated that they were told that residential well water would be checked in a 6-mile radius of the plant 3 or 4 years ago, and they are still waiting for their well to be tested.
  8. Please refer to the groundwater exposure pathway section. If you are located in the DOEWater Policy area, contact DOE or their contractor, Bechtel Jacobs Company, to get yourwater tested. You can also contact the Kentucky Department for EnvironmentalProtection, Division of Water or Division of Waste Management. Refer to the list at the end of this section.

  9. A citizen asked, "Why is the well water not checked around here [Kevil] for anything that could be dangerous to our health? Everything travels in all directions, not just east [referring to the groundwater plume]."
  10. The groundwater gradients do not flow from the site toward Kevil. The aquifer wheremost residential wells are located is the Regional Gravel Aquifer. Although there arethree groundwater plumes--one to the northwest of the site, one to the west-southwest,and one to the northeast--the groundwater gradients for this aquifer flow to the north-northeast, toward the Ohio River. If you are concerned about your water quality, youshould contact the Purchase County Health Department or the West McCracken WaterDistrict. A list of agencies can be found at the end of this section.

  11. A citizen commented, "I am concerned about the size and location of the plume. I also want to know if the plume is to the river or on the other side of the river." This citizen is worried about wells on the other side of Metropolis being contaminated and wants to know if Metropolis wells were monitored.
  12. Bechtel Jacobs Company (and previously Lockheed Martin Environmental Services) hasa groundwater monitoring program that includes surveillance of over 200 monitoringwells, TVA wells, and residential wells. The purpose of this surveillance is to detect, asearly as possible, groundwater contamination resulting from the movement of thegroundwater plume or from past or present land disposal of wastes. Based on the resultsof this program, it appears that the northwest plume may surface in Big Bayou Creek nearthe TVA plant or in the Ohio River. We believe that the northwest and northeast plumesrecharge to the Ohio River, but the trichloroethylene (TCE) and technetium 99 (Tc-99)concentrations are so low that they are difficult to detect.

    Sampling on the other side of the river did not detect any contaminants characteristic ofPGDP operations. The water in Metropolis is provided by the city. People outside the citylimits receive water from the Fort Massaic Water District. The water for this company isdrawn from Eddyville, Illinois, which is 25 miles (40 kilometers) north of the city of Joppa.

  13. A resident commented, "We have a private well that we use 'daily,' and we fear that we could very well be drinking contaminated water."
  14. A resident wondered how safe his/her drinking water really is.

    Refer to the groundwater exposure pathway section for the areas potentially affected bythe site. DOE has provided an alternative water source for anyone in the area of the plantwhose well has been affected by contamination from PGDP. Any resident who isconcerned about his/her own private well can request that his/her well be tested by theKentucky Department for Environmental Protection, Division of Water. We have listed anumber and a contact person at the end of the comment section.

  15. A citizen was concerned that he may still be drinking contaminated groundwater. DOE tested his wells some years ago, but he did not know the results. He wondered why all the homes around him have been supplied with city water, while his has not.
  16. In this case, the resident was not the land owner. The test results from the residential wellhad been supplied to the land owner, who chose not to sign the DOE Water Policyagreement with DOE (which would have restricted him from drilling additional wells).The land owner owns a lot of land in the area and did not want to be restricted fromdrilling additional wells on his property. Therefore, this residence was not put onmunicipal water. The well in question was not contaminated with TCE or Tc-99, and isnot very close to the northwest plume. The tenant was assured that the test results were negative.

  17. Several citizens asked, "What are the potential health effects from drinking contaminated water or breathing air following radioactive releases from PGDP and documented groundwater contamination?"
  18. A description of possible health effects is given in the public health implications section.

  19. A resident commented, "We are on well water, which was fine when we had it thoroughly tested thirty years ago by the health department. Since all the problems at the plant, I have had it tested numerous times and they said it was high in salt content. How did the salt get there after all these years? The only time it happened was after they drilled test wells about 1 mile east of my house. I am sure they are putting something in those wells that made my water salty, as well as smells."
  20. We do not have enough information to specifically address this concern. Please contactthe Reidland office of the Kentucky Department for Environmental Protection, Divisionof Water; the local representative of the Kentucky Division of Waste Management; or theWest McCracken Water District Office. Phone numbers and contact persons are listed atthe end of this section.

  21. One citizen asked, "What steps have been undertaken to protect existingunderground aquifers and groundwater from additional contamination? How arecurrent contamination problems being handled? Is this program adequate?"
  22. DOE is operating extraction and treatment systems to remove TCE from the northwestand northeast plumes. The northwest treatment system also removes Tc-99. The systemsdo not appear to be preventing the advancement of the plumes, although they may haveslowed the plumes down and kept contaminant concentrations from increasing off site.DOE currently has a board of technical experts looking at alternative projects toremediate the groundwater; proposals for such projects have been presented to the public.

    DOE is limiting the drilling of monitoring wells into the McNairy Aquifer to make it lesslikely that a conduit to this deeper water supply will appear. They also are looking atremediating the sources of the contaminants on site. They are continuing to monitorresidential wells that could be in the path of the plumes.


  1. Several citizens were concerned about adverse health effects from consumption of contaminated fish and game from the West Kentucky Wildlife Management Area.
  2. A subsistence fisherman/hunter was concerned about health effects of eatinganimals he catches. He catches and eats crappies, bluegill, some largemouth bass(but not from KOW), and buffalo carp. His wife eats raccoon once or twice a year,and also rabbit. He eats squirrel once a year. He used to eat soft shell turtles, but hecannot find them anymore. He eats about 6 to 7 pounds of fish a month. He fishes inBarkley Lake (another fish and wildlife area nearby), KOW at this site, andsometimes the pond to the right of the main gate at PGDP.

    Another citizen said that she had been on the site to fish from time to time. Shefished for several different kinds of fish at various places. She made at least onemeal a month from the fish she caught. She has fished in the game reserve; the lakenorth of the game reserve; lakes near Martin Marietta (PGDP); north in BarkleyCounty; Noah Lake, when it was not drained to be cleaned; the West Paducah CoonHunters Club; and near the TVA plant. She has eaten crappie, bluegill (mostcommon), bass, buffalo, and carp. Also, she has cooked turtle once. If the fish is too fatty she will not clean or eat it.

    Another citizen said she did not hunt but would eat what was given to her. Thisincluded rabbit, groundhog, squirrel, possum, raccoon, and turtle. Her concernswere:

    • She knew about the signs that posted mercury warnings for bass, but did not understand why some fish were posted while others were not.

    • She also knew of people who fished to make ends meet (elderly women onMedicare whose medicine was so expensive they fished in order to eat). If she did not eat the fish she caught, she gave it to someone else.

    There is no evidence that occasionally eating the fish or game caught in the WKWMAwill make you sick. In our calculations, we assumed that someone could be eating 20% ofthe fish and meat in their diet from animals caught there. The PCB levels in deer are verylow and do not pose a health threat. Still, people should not eat fish from Big Bayou andLittle Bayou Creeks as their main source of protein.

    It is important that people limit their intake of fish (2 fish meals/month) caught in theWKWMA ponds or Little Bayou Creek where warning signs are posted. These signs listthe types of fish because these fish have been found to contain chemicals that can harmyou if you eat them in large amounts. (Because different fish have different food sourcesthey ingest and retain different concentrations of contaminants.) Especially young women(who are, or can get, pregnant) and children should not eat the fish that are listed on thewarning signs. However, occasionally eating other fish from this area will not causeharm, because they do not contain enough chemicals to make you sick. Also, if you eatturtles, you should only eat them occasionally and should remove the fat before eating them.

  3. A citizen was concerned that some of the fish in the ponds and creeks are deformed (especially catfish and bluegill).
  4. We advise that you do not eat any fish that appears to be deformed. Please report anydeformed fish, deer, or other animals to the local Kentucky Fish and Wildliferepresentative who lives at the site. It is impossible to say, based on the information thatwe currently have, what may have caused the deformities. However, it is important thatthe Kentucky Department of Fish and Wildlife Resources be made aware of the type andfrequency of these occurrences.

  5. One resident stated, "We have a garden and grow most of our food here next to the plant. I'm concerned what contaminants we may be exposed to from our food."
  6. Fruits and vegetables in the area have been tested for arsenic, barium, cadmium,chromium, lead, manganese, nickel, vanadium, zinc, technetium 99, uranium 234,uranium 235, uranium 238, and plutonium 239. None of the potential exposure doses(based on maximum sample results) were at levels of health concern. No data wereavailable for fluoride in vegetables, so we used the results from broadleaf grass samples,assuming that green leafy vegetables had the same levels. Based on this assumption,fluoride would not be expected to cause harm to humans. For more details, refer to the discussion for the food and biota exposure pathway.

  7. One person asked, "Why was deer found with plutonium in the muscle?"
  8. Due to the past atmospheric testing of atomic bombs around the world, there is a lowlevel of plutonium in the environment. PGDP has also released "small" amounts ofplutonium since the 1970s, when PGDP reprocessed uranium that had been used in areactor. Plutonium in the environment can be ingested by animals, including deer.Normally, animals absorb very little plutonium into the bloodstream; most of thatabsorbed material goes to the bone. However, as with other bone-seeking elements (e.g.,calcium, strontium), a small amount of plutonium may end up in muscle tissue. Theamount of plutonium reported in the deer was not enough to harm anyone who may haveeaten it. Refer to the food and biota exposure pathway section for more information.

  9. One person asked, "To what extent are animals (including fish, game, and cattle) affected by radionuclide levels in the water and in the regional plants?"
  10. Even with the levels we used in this public health assessment (usually maximumconcentrations), there should be no adverse effects on animals in the area fromradionuclides.

  11. One of the farmers stated, "Cattle look older than they should. In 1994, a calf was born dead with a deformed jaw. Coffee Animal Clinic in LaCenter, Kentuckyexamined the calf; then the Plant took the calf. Presently he has 40 head of cattleincluding calves. In 60 years, there was only one deformity."
  12. Without more information, we cannot determine the cause of the calf's deformity or death.

Waste Materials

  1. Several citizens stated, "We are especially concerned about current and future exposures to radioactive and [other] contaminants that could be released from the 100s and 1,000s of barrels of waste stored on site. Those barrels cannot last forever. What can be safely done with their contents? Another thing that bothers me is the transportation of hazardous waste to and from the plant and what we would beexposed to in case of an accident."
  2. If you are concerned about the depleted uranium cylinders and not barreled waste, beaware that we addressed such concerns in the "other" exposure pathway section for thedepleted uranium cylinders. Please refer to that section.

    If your concern is about other hazardous waste stored on site that is not currentlyimpacting the off-site environment, you will need to contact the Kentucky Division ofHazardous Waste Management, DOE, or the U.S. Enrichment Corporation (USEC). Ifyou have more specific information about this waste, you may contact our office withyour concerns.

    The transportation of hazardous waste is strictly regulated. Hazardous waste shipmentscan be inspected by regulators prior to shipment, during transport, or on arrival at theirdestination. If there are any violations, the shipper is responsible and receives stiff finesfrom the U.S. Department of Transportation and/or the state regulatory agency. Thehazards involved in transporting the depleted uranium cylinders are discussed in thesection on "other" exposure pathways.

  3. One commenter was concerned about the level of dioxin.
  4. We looked at monitoring data in several media for several forms of dioxin. Dioxins arenot in off-site groundwater, surface water, or soils. Some dioxin is showing up in a few ofthe sediment samples, but not at locations where there would be a completed exposurepathway. No data was reviewed for dioxin in biota such as fish.

Health Concerns

  1. Several citizens were concerned about potential health problems related to waste materials stored at the site and off-site releases. Several citizens were specifically concerned about possible cancer clusters appearing in these areas: Bradford Road area, Ogden Landing/Metropolis Road/Woodville Road area, neighborhood of House Road and Ragland Community, Ballard County, and LaCenter, Kentucky.
  2. For details on the first part of this concern, please refer to the public health implicationssection. Only a small population, located close to the site, was exposed to contaminantsof concern in the past. With the current plant operations and the access restrictions toLittle Bayou Creek and the outfalls, no exposures are occurring that would cause harm to anyone off site.

    For many of the areas named above, we do not see completed exposure pathways forcontaminants from PGDP. The areas for which cancer statistics are gathered are too largeto let us pinpoint any specific neighborhood. Please refer to the exposure pathways andhealth outcome data evaluation sections of this report.

  3. One citizen asked, "How were residents downstream of PGDP affected?"
  4. Residents downstream on the Ohio River from PGDP should not have been adverselyaffected by PGDP.

  5. One resident stated, "I am very concerned about past, present, and future exposures and health outcomes (cancer and non-cancer) for my neighbors, children, and grandchildren."
  6. The public health implications section describes the potential populations that could havebeen affected by contaminants and discusses the possibilities of adverse affects and typesof potential effects by substance. ATSDR's Child Health Initiative recognizes thatvulnerabilities are inherent in the developing young child, infant, or fetus. Some of thecontaminants discussed in the public health implications section are of special concern tochildren and developing fetuses. If you have further concerns, do not hesitate to contactCarol Connell with ATSDR at (404) 639-6060.

  7. One person asked, "What health impacts may have been initiated by PGDPoperations during the period 1944 through the present? How were workers affected? How were workers' families affected?"
  8. One citizen asked, "What are the potential health effects on children whose parentshave worked at PGDP or who have been exposed to contaminated air and watersupplies?"

    This public health assessment addresses the first part of the first concern. For exposuresto off-site air and water releases, please refer to the appropriate exposure pathwaysections. For children whose parents work at PGDP, their exposure would be fromcontaminants brought home by the workers or to exposures prior to their birth. A separatestudy is being conducted to examine the exposures of workers at PGDP. If you want toknow more about the worker study, contact your union representative, the DOE publicdocument room at the Bechtel Jacobs facilities in Kevil, Kentucky, or NIOSH. (Refer to the contact list at the end of this section.)

  9. One person asked, "What percentage of birth defects and mental retardation occurring within the region may be considered related to radiation exposure from contaminated air and water supplies?"
  10. None. Off-site exposures to radioactive materials has been very low, nowhere near thelevel that would be required to cause birth defects and mental retardation. You may wantto read the substance-specific health implications information concerning potentialchemical effects.

Procedural Concerns

  1. One commenter stated, "My only request would be that if any releases areencountered that would affect the nearby community, immediate notice be given viaTV and radio."
  2. This comment is acknowledged. Your request has been forwarded to DOE; however, thecurrent operation of the plant is under USEC, with the U.S. Nuclear RegulatoryCommission having regulatory jurisdiction.

  3. One commenter stated that the sirens are not loud enough to be heard inside the house when the TV is on.
  4. This information is acknowledged and has been passed along to DOE.

  5. "When a release was made, in the past, they used pounds or kilograms. One pound does not sound bad, but when spread in the atmosphere, one pound is a lot. Why not use cubic feet of ____________ released?"
  6. Air releases are usually reported in terms of total releases for the year (in pounds orkilograms) because of the reporting requirements for site-specific air quality permits. Todetermine a contaminant's health impacts, one must either know or calculateconcentrations of that contaminant (micrograms per cubic meter of air). This tells onehow much chemical is measured in a given amount of air that a person may be breathing.This is called a unit of measurement. An adult breathes in approximately 20 cubic meters(5,200 gallons) of air into his or her lungs every day. However, no matter what units areused to measure the chemical, you can always ask for it to be explained in the form that is easiest for you to understand.

  7. To what extent are local health departments participating in the monitoring of air and water quality for the region surrounding these sites and the rivers? If they are not, how can citizens pressure them to become more involved with this issue?
  8. The Purchase District Health Department is the local health department agency forBallard and McCracken Counties (among others) in Kentucky. Although they are closelyfollowing the situation at the site, they do not normally get involved with environmentalmonitoring. The environment around the site is currently being monitored by theKentucky Department for Environmental Protection (water, air, and waste management),the Kentucky Department for Public Health (Radiation Control Program), and DOE.Formerly, the University of Kentucky Federal Facilities Oversight Unit (FFOU)performed local monitoring. Sampling independent of DOE has been done by the state forbiota, water, soils/sediment, and radioactive contaminants in air. A five-year report waspublished by the FFOU covering the years from 1991 through 1996 [80]. Citizens maycorrespond directly with the different agencies to find out the extent of their involvementat the site. Addresses and phone numbers for these agencies are listed at the end of thissection.

  9. One commenter stated, "We have no say in what is buried in the landfill they are building. This is not right."
  10. For questions concerning landfill permitting and what is allowed to be buried in thelandfills, please contact the Kentucky Division of Waste Management, Hazardous WasteManagement Branch.

  11. Citizens are confused about the relationships between DOE, Lockheed Martin Energy Systems (currently Bechtel Jacobs Company), the U.S. Nuclear Regulatory Commission, the Kentucky Federal Facilities Oversight Unit, the Kentucky Cabinet of Health Services, ATSDR, EPA, etc.
  12. Please refer to the background section of this public health assessment for the history of these agencies' involvement with PGDP.

    Although USEC now runs the operating plant, DOE's current mission at the site [169] includes:

    1. Demonstration of the innovative environmental cleanup program specific toPGDP.

    2. Safe management of the site infrastructure, including decontamination anddecommissioning of facilities no longer in use.

    3. Operation of a waste management program that includes storage of low-level,mixed transuranic waste; management of waste generated by the environmentalrestoration programs (not just from PGDP); and shipment of some waste to otherstorage, treatment, and disposal facilities.

    4. Management of the depleted UF6 cylinders.

    5. Operation of the environmental restoration program, which involves cleanup ofhistoric contamination.

    Bechtel Jacobs Company is currently the prime contractor for DOE at PGDP. Theyperform or subcontract most of these services. The U.S. Nuclear Regulatory Commissionregulates the plant operations under a license issued to the USEC. The Federal FacilitiesOversight Unit was part of the University of Kentucky's Water Resources ResearchInstitute; it was charged with helping the Kentucky Natural Resources and EnvironmentalProtection Cabinet and the Cabinet for Health Services with the environmentalmonitoring of the federal facilities activities in the Commonwealth. The FFOU no longer exists. For more information, refer to the summary and background sections of this document.

Management of Wildlife

  1. This citizen is concerned about the management of the wildlife in the game reserve. He/she thinks that someone should keep a closer watch on the wildlife.
  2. Another citizen said that he never observed live or dead fish in the creeks. In 1993or 1994, over 20 deer were found dead near Spring Bayou Church. The plant wastold of the dead deer and investigated, but no one knows the results.

    Several people mentioned that deer in the area looked "old" and sickly.

    DOE does some monitoring of wildlife in the area. The FFOU did some independentmonitoring of the wildlife; now the Kentucky Department for Environmental Protectioncarries out such monitoring. We used data from DOE and state agencies in our evaluationof the wildlife. Information can be found in DOE's Annual Environmental Reports andthe FFOU five-year report. However, concerns should be brought to the attention of the state agencies and the local fish and wildlife manager.

    The incident involving deer was mentioned by several people in the area; however, therewas no information in the documents we reviewed. Without more information orsampling results from the dead deer, we cannot explain what happened. There could beseveral other reasons for such an incident (e.g., viruses, bacteria). Both the KentuckyDepartment for Environmental Protection and the Kentucky Department for PublicHealth have state veterinarians with expertise in this area.

  3. A local farmer noticed that there are no grasshoppers, frogs, or snakes on the farm. Also, there are few birds and other insects. The reduction in the these animal and insect populations happened about 3 or 4 years ago.
  4. It is difficult to say exactly what is behind this reduction in the number of animals. We donot see any reason to think that contaminants from the site may be at fault; however, ouranalysis of the data was intended to see if there are any reasons for human healthconcerns. You may want to contact one of the agencies listed at the end of this section.

  5. One person stated, "I appreciate your concerns, however, our complaints have fallen on deaf ears." (This person did not specify an agency.)
  6. Several citizens said that there is a lack of trust in the reports from PGDP, thatDOE says that it is making headway on the problems but they don't see it, and thatDOE and its contractors are insensitive to the concerns of the citizens affected bythe site and the workers exposed on site.

    These comments are acknowledged.

Agencies That May Be Contacted for Other Concerns
Concern Individual Agency Telephone #
Questions about PGDP cleanup; also, fishing, hunting, etc. Tuss Taylor
Todd Mullins
John Maybrier

Janet Miller (local contact)

Kentucky Department for Environmental Protection
Division of Waste Management
14 Reilly Road
Frankfurt, KY 40601

Kentucky Department for Environmental Protection
Division of Waste Management
MS 103, P.O. Box 1410
Paducah, KY 42001

(502) 564-6716

(270) 441-5279

Questions about surface water or groundwater contamination from PGDP Marjorie Williams
(Paducah Office)
Kentucky Department for Environmental Protection
Division of Water
4500 Clarks River Road
Reidland, KY 42003
(207) 898-8468
Questions about radioactive contaminants and monitoring around PGDP John Volpe, Manager
Steve Hampson
Kentucky Dept. for Public Health
Radiological Health and Toxic Agents Branch
Radiation Control Program
Frankfort, KY 40621-0001
(502) 564-3700
(John Volpe)

(502) 564-8390
(Steve Hampson)

Questions concerning DOE environmental activities at PGDP Gregory Cook,
Public Affairs Manager
Bechtel-Jacobs Company
761 Veterans Avenue
Kevil, KY 42053
(270) 441-5023
Questions about cancer statistics and cancer cluster investigations Thomas Tucker, Associate Director Kentucky Cancer Registry
2365 Harrisburg Road
Suite A230
Lexington, KY 40504
(859) 219-0773
Questions about water quality that affects public health (e.g., lead) Charles Seay, Environmental Officer Purchase District Health Dept.
320 North 7th Street
Mayfield, KY 42006
(502) 247-1490
General questions about water quality and other water problems William Tanner,
Water Superintendent
West McCracken Water District
8020 Ogden Landing Road
West Paducah, KY 42086
(270) 442-3337
Questions about livestock, agricultural products, etc. Doug Wilson,
Agriculture Officer
University of Kentucky
Cooperative Extension Service
2705 Oliver Church Road
Paducah, KY 42001
(270) 554-9520
Questions related to PGDP occupational problems David Fuller PACE (Paper, Allied-Industrial, Chemical, and Energy Workers Union); formerly OCAW
P.O. Box 494
Paducah, KY 42002
(270) 442-3668
Questions concerning medical surveillance for former Gaseous Diffusion Plant workers at DOE facilities (Paducah, Portsmouth, Oak Ridge) Sylvia Kieding PACE (Paper, Allied-Industrial, Chemical, and Energy Workers Union)/formerly OCAW
2490 South Garfield Street
Denver, CO 80210
(303) 759-2604
Questions about the local economy and the city's role in the PGDP cleanup efforts James Zumwalt,
City Manager
Paducah City Hall
P.O. Box 2267
Paducah, KY 42002-2267
(270) 444-8503
Questions about local development (traffic and new housing patterns) Van Newberry, Engineer McCracken County Planning Office
3700 Coleman Road
Paducah, KY 42001
(270) 442-9163
Questions about impact of PGDP on local economy Kristin Reese Greater Paducah Economic Council
P.O. Box 1155
Paducah, KY 42002
(270) 575-6633

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