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Exposure to, or contact with, chemical contaminants drives the ATSDR public health assessmentprocess. The release or disposal of chemical contaminants into the environment does not alwaysresult in exposure or contact. Chemicals have the potential to cause adverse health effects only ifpeople actually come into contact with them. People may be exposed to chemicals by breathing,eating, or drinking a substance containing the contaminant or by skin (dermal) contact with asubstance containing the contaminant.

When people are exposed to chemicals, the exposure does not always result in adverse healtheffects. The type and severity of health effects that may occur in an individual from contact withcontaminants depend on the toxicologic properties of the contaminants; how much of thecontaminant to which the individual is exposed; how often and/or how long exposure is allowedto occur; the manner in which the contaminant enters or contacts the body (breathing, eating,drinking, or skin/eye contact); and the number of contaminants to which an individual is exposed(combinations of contaminants). Once exposure occurs, characteristics such as age, sex,nutritional status, genetics, life style, and health status of the exposed individual influence howthe individual absorbs, distributes, metabolizes, and excretes the contaminant. These factors andcharacteristics influence whether exposure to a contaminant could or would result in adversehealth effects.

To assess the potential health risks associated with contaminants at this site, we comparedcontaminant concentrations to health assessment comparison (HAC) values. HAC values aremedia-specific contaminant concentrations that are used to screen contaminants for furtherevaluation. Non-cancer HAC values are called environmental media evaluation guides (EMEGs)or reference dose media evaluation guides (RMEGs) and are respectively based on ATSDR'sminimal risk levels (MRLs) or EPA's reference doses (RfDs). MRLs and RfDs are estimates ofa daily human exposure to a contaminant that is unlikely to cause adverse non-cancer healtheffects. Cancer risk evaluation guides (CREGs) are based on EPA's chemical-specific cancerslope factors and an estimated excess lifetime cancer risk of one-in-one-million persons exposedfor a lifetime. We used standard assumptions to calculate appropriate HAC values [11].

In some instances, we compare contaminant concentrations in water to EPA's maximumcontaminant levels (MCLs). MCLs are chemical specific maximum concentrations allowed inwater delivered to the users of a public water system; they are considered protective of publichealth over a lifetime (70 years) of exposure at an ingestion rate of two liters per day. Thesetting of MCLs may also be influenced by available technology and economic feasibility.Although MCLs only apply to public water supply systems, we often use them to help assess thepublic health implications of contaminants found in water from other sources.

While exceeding a HAC value does not necessarily mean that a contaminant represents a publichealth threat, it does suggest that the contaminant warrants further consideration. The publichealth significance of contaminants that exceed HAC values may be assessed by reviewing andintegrating relevant toxicological information with plausible exposure scenarios. Estimatedexposures may be compared to reported "No Observable" and "Lowest Observable" AdverseEffects Levels (NOAELs and LOAELs) and to known effect levels in humans, when available.

Environmental Contamination

Data included in our evaluation of the Perryton Water Well Number 2 site included groundwatersampling in 1989 and 1990, groundwater and soil samples collected during the EPA's ExpandedSite Inspection (ESI) in June 1996, and additional sampling of Water Well Number 2 by EPA'scontractor in April 1999. The data packages were reviewed and validated by EPA Region 6. Inevaluating the public health significance of these data, we relied on the information provided inthe referenced documents and assumed that adequate Quality Assurance/Quality Controlmeasures were followed with regard to chain-of-custody, laboratory procedures, and datareporting. The analyses and conclusions in this public health assessment are valid only if thereferenced information is valid and complete.

    Groundwater Contamination

In June 1996, during the Expanded Site Investigation, 20 groundwater samples were collected totry to determine the extent of the contaminated groundwater plume [3]. Seventeen of thesamples were collected from Well Numbers 1 and 3 through 11 and the remaining sevengroundwater samples were collected from Well Number 2. Groundwater samples collected fromWell Number 1 and Wells Number 3 through 11 did not contain carbon tetrachloride or othercontaminants at concentrations exceeding health assessment comparison values. Groundwatersamples collected from Well Number 2 contained concentrations of carbon tetrachlorideexceeding health assessment comparison values. Concentrations ranged from 35.8 to 50.3 g/L[3]. Chloroform, a possible degradation product of carbon tetrachloride, was measured insamples from Well Number 2, at concentrations below health assessment comparison values. Lead (60.9 g/L) and copper (1,380 g/L) were measured at concentrations above EPA's actionlevels during the June 1996 sampling event; however, subsequent sampling indicated that thesedetections were artifacts of the well equipment and not contaminants of the aquifer [12].

EPA's contractor resampled Well Number 2 in April of 1999. During this sampling event100,000 gallons of water were pumped from Well Number 2 in order to accurately determine theconcentration of contaminants in the groundwater plume associated with Well Number 2 [12]. Atrazine (5.47 g/L), carbon tetrachloride (42.5 g/L), and nitrate (17,900 g/L) were detected in Well Number 2 at concentrations above their respective comparison values (Table 2).

    Soil Contamination

In June 1996 a contractor for EPA collected 48 soil samples to characterize surface and nearsurface soil conditions at the site. Sampling locations are shown in Figure 2. Forty-two sampleswere collected at various depths from 13 soil borings at the site (SB01 to SB12 and SB19). Three surface soil samples (SB13, SB14, SB15) were collected at 0.5 - 2 feet below groundsurface from drainage areas associated with the Perryton Equity Exchange and the City ofPerryton maintenance yard. One background sample (SB-16) was collected at zero to six inchesbelow ground surface from a vacant lot at the corner of Colgate and Amherst approximately1,000 feet west of Well Number 2 [3].

Soil samples were analyzed for volatile organic compounds. Carbon tetrachloride was notreported in the soil samples; however, methylene chloride and chloroform, which are possibledegradation products of carbon tetrachloride, were measured at low concentrations in soilsamples [3]. The maximum detected concentrations of these volatile organic compounds werebelow health assessment comparison values.

Pathways Analysis

We evaluated the possible pathways for exposure to contamination at Perryton Water WellNumber 2 site. We examined these possible exposure pathways to determine whether people inthe community can be exposed to (or come into contact with) contaminants from the site. Exposure pathways consist of five elements; 1) a source of contamination, 2) transport throughan environmental medium, 3) a point of exposure, 4) a plausible manner (route) for thecontaminant to get into the body, and 5) an identifiable, potentially exposed population. Exposure pathways can be complete, potential, or eliminated. For a person to be exposed to acontaminant, the exposure pathway must be complete. An exposure pathway is consideredcompleted when all five elements in the pathway are present and exposure has occurred, isoccurring, or will plausibly occur in the future. A potential pathway is missing at least one of thefive elements but may possibly be complete in the future as more data become available or siteconditions change. Eliminated pathways are missing one or more of the five elements and willnever be complete.

Based on available information, past exposure to contaminants in groundwater has occurred. The exposed population includes residents of Perryton who received their water from the northern water system. The main contaminant of concern to which people would have been exposed is carbon tetrachloride. There are no data to assess past possible exposures to atrazine or nitrates. At the time that the well was taken out of service approximately 912 people were connected to the northern water system (Table 1).

Table 1.

Exposure Pathway Evaluation-Perryton Water Well Number 2 National Priorities List Site

Carbon tetrachloride,
Atrazine??, and

Unknown source, possibly grain elevator Groundwater from Perryton Water Well Number 2 Residences using water from Well Number 2 Ingestion Inhalation Dermal contact

~ 912 users of Perryton water system north of the railroad tracks prior to 1989

Past There is sufficient evidence indicating that approximately 900 residents used water from the northern distribution system. Prior to 1989, when Well Number 2 was removed from the system, these people were exposed to contaminated groundwater.
Carbon tetrachloride,
Atrazine, and
Future Future use of water from Well Number 2 prior to treatment and blending could pose a public health hazard.

Public Health Implications

    Evaluation of the Groundwater Exposure Pathway

Summary: Carbon tetrachloride, atrazine, and nitrate were detected in water from Well Number2 at concentrations above each of their respective health assessment comparison values. ATSDRhas concluded that under current conditions the presence of these contaminants in thegroundwater does not present a public health hazard because there is no evidence that peopleare currently using the contaminated water. Prior to 1989, when people were using the water,as many as 912 people may have been exposed to one or more of these contaminants. Because ofa general lack of historical information we could not determine with any degree of certainty thepotential hazards associated with these possible past exposures. Thus, we have concluded thatpast exposure to contaminants in the groundwater represents an indeterminate public healthhazard. Future use of this water prior to treatment and blending could present a public health hazard.

Below we have provided a brief discussion of each of the three contaminants of concern. Thesediscussions include a general description of their uses, how they react in the environment, andthe general toxicological effects that have been associated with them. These descriptions arefollowed by a site specific discussion of the public health implications of possible past, present, and future exposures.

    Carbon Tetrachloride

Carbon tetrachloride has been measured in water samples from Well Number 2 from 1989 to thepresent time. The highest concentration (50.3 g/L) was measured in June 1996. Carbontetrachloride does not occur naturally. In the past it was used in the production of refrigerationfluid and propellants for aerosol cans; it also was used as a cleaning fluid, a degreasing agent,and a spot remover. Carbon tetrachloride was used in fire extinguishers and as a pesticidefumigant to kill insects in grain. Because of its harmful effects, most of these uses were bannedin the 1960s; its use as a pesticide was banned in 1986. Today carbon tetrachloride is only usedin some industrial applications [2].

When carbon tetrachloride leaks onto the ground, only a small amount of it sticks to soilparticles; the rest evaporates into the air or moves into the groundwater. In groundwater carbontetrachloride may persist for months before it breaks down into other chemicals (eg. chloroform).

Carbon tetrachloride tends to volatilize (move into the air) from tap water used for showering,bathing, cooking, and other household uses inside a home [13]. Thus, people whose tap water iscontaminated with carbon tetrachloride can be exposed to it through ingestion, inhalation, ordermal contact (absorption through the skin).

Exposure to high concentrations of carbon tetrachloride can cause liver, kidney, and centralnervous system damage. If exposure is low and then stops, the liver and kidneys can repair thedamaged cells and function normally again. The liver is especially sensitive to carbontetrachloride. In people an acute (one time) exposure to 90,000 micrograms-carbon tetrachlorideper kg-body weight (g/kg) has caused slight fatty infiltration of the liver. A single dose of110,000 g/kg has resulted in the degeneration of hepatocytes (liver cells). An acute dose of670,000 g/kg has been reported to cause severe liver necrosis. Carbon tetrachloride also hasbeen known to cause swelling of the proximal convoluted tubules of the kidney in humans afterthe administrations of a single dose of 180,000 g/kg. These concentrations are much higherthan those people drinking water from Water Well Number 2 might have been exposed to.

If exposure is very high (4,800,000 g/kg), the nervous system can be affected and people mayexperience narcosis (feel intoxicated). Single doses as low as 300,000 g/kg have causeddrowsiness in people. People also could experience headaches, dizziness, sleepiness, and nauseaand vomiting. Many of the neurological effects subside if exposure is stopped, but in severecases, coma and even death can occur. There have been no studies in people on carbontetrachloride's effects on reproduction or development, but studies in rats showed no adverse effects.

ATSDR has established an acute oral Minimal Risk Level (MRL) of 20 g/kg/day. The MRLwas derived from a study in which rats were orally dosed with 0; 5,000; 10,000; 20,000; or40,000 g-carbon tetrachloride per kilogram body weight per day (g/kg/day) for 10 consecutivedays. Progressive, dose-related liver injury was observed with centrilobular vacuolardegeneration being barely detectable in all six animals receiving 5,000 g/kg/day (this effect wasnot observed in any of the six control animals). The effects became more severe as the dose wasincreased with hepatocellular necrosis becoming evident at 10,000 g/kg/day [14]. ATSDRestablished the MRL by dividing the Lowest Observable Adverse Effects Level (LOAEL) by anuncertainty factor of 300 (3 for the conversion to a NOAEL, 10 for animal to humanextrapolation, and 10 to account for human variability).

In addition to the acute oral MRL, ATSDR also has established an intermediate oral MRL of 7g/kg/day. This MRL was derived from a study in which rats were given (by corn oil gavage) 0;1,000; 10,000; or 33,000 g/kg/day, five days per week for 12 weeks [15]. Slightly elevatedblood levels of sorbitol dehydrogenase and centrilobular vacuolization of the liver were observedin animals receiving 10,000 g/kg/day, but not in those receiving 1,000 g/kg/day. The MRLwas calculated by dividing the identified No Observable Adverse Effects Level (NOAEL) of 1mg/kg/day corrected for a seven day per week exposure, by an uncertainty factor of 100 (10 foranimal to human extrapolation and 10 to account for human variability).

The Department of Health and Human Services has determined that carbon tetrachloride mayreasonably be anticipated to be a carcinogen. Based on sufficient animal information, the U.S.Environmental Protection Agency (EPA) has classified carbon tetrachloride as a probable humancarcinogen. Animals exposed to carbon tetrachloride over a long time developed liver cancer.We do not know if breathing carbon tetrachloride causes cancer in animals. We also do not knowif breathing or ingesting it will cause cancer in people.


In April 1996, atrazine was measured in water from Water Well Number 2 at a concentration of5.47 g/L. Atrazine is a widely used herbicide for control of broadleaf and grassy weeds. Thiswhite crystalline solid was estimated to be the most heavily used herbicide in the United Statesbetween 1987 and 1989. Atrazine may be released to the environment in wastewater frommanufacturing facilities and through its use as a herbicide. It was extensively used for corn andsoybeans in mid-western states and in Texas. Other uses included control of broadleaf andgrassy weeds in sorghum, rangeland, and grass crops. Effective in 1993, the use of atrazine fornon-crop vegetation control was eliminated, and use was restricted by a requirement for a bufferzone between application sites and surface water [16].

When atrazine is released to the environment, microbial activity and chemicals in soil and watermay cause atrazine to breakdown, particularly in alkaline conditions. Sunlight and evaporationdo not reduce atrazine concentrations. Atrazine may bind to some soils, but it generally tends toleach into groundwater. Atrazine is not likely to be taken up in the tissues of plants or animals. It can be removed from water with granular activated charcoal.

For a pesticide, atrazine is considered to be slightly to moderately toxic to humans. It can beabsorbed orally, through inhalation, or through the skin. Most of the toxicological informationthat is available for atrazine comes from animal studies. Symptoms of exposure to high levels ofatrazine can include abdominal pain, diarrhea, vomiting, eye irritation, irritation of the mucousmembranes, and skin reactions. At very high doses, rats have shown excitation followed bydepression, slowed breathing, in-coordination, muscle spasms, and hypothermia. After ingestinga large dose, rats exhibited muscular weakness, hypo-activity, breathing difficulty, prostration,convulsions, and death. In animals, chronic exposure to lower levels of atrazine (5,000 to 25,000g/kg/day) has resulted in growth retardation, decreased food intake, respiratory distress,paralysis of the limbs, death, structural and chemical changes in the brain, heart, liver, lungs,kidney, ovaries, and endocrine organs. These concentrations are 1,000 to 5,000 times higherthan the highest concentration of atrazine measured in Well Number 2.

The Environmental Protection Agency (EPA) has established a chronic oral reference dose (RfD)for atrazine of 35 g/kg/day. This RfD is based on an animal study in which rats fed 25,000 g-atrazine/kg-Body Weight/day for two years exhibited a decreased body weight gain. The RfDwas derived by dividing the identified NOAEL of 3,500 g/kg/day by an uncertainty factor of100 (10 for interspecies extrapolation and 10 for intraspecies variability).

There is inadequate evidence in humans for the carcinogenicity of atrazine. There is limitedevidence in experimental animals for an increased risk of tumors associated with hormonalfactors [17]. The International Agency for Research on Cancer (IARC) has listed atrazine as a2B carcinogen (possibly carcinogenic in humans) [17].


Nitrate nitrogen was measured in water samples collected from Perryton Water Well Number 2in April of 1999. Primary sources of organic nitrates include human sewage and livestockmanure, especially from feedlots. The major environmental releases of inorganic sources ofnitrates are due to the use of fertilizers. These are primarily potassium nitrate and ammoniumnitrate. Potassium nitrates are used mainly as fertilizers (85%), with the remainder in heattransfer salts, glass and ceramics, and in matches and fireworks. Ammonium nitrates are used asfertilizers (84%) and in explosives and blasting agents (16%) [18].

Due to its high solubility and weak retention by soil, nitrates are very mobile in soil and have ahigh potential to migrate to groundwater. Nitrates and nitrites are very soluble in water. Mostnitrogenous materials in natural waters tend to be converted to nitrate, so all sources of combinednitrogen, particularly organic nitrogen and ammonia, should be considered as potential nitratesources. Because it does not volatilize, nitrate/nitrite is likely to remain in water until consumedby plants or other organisms. Ammonium nitrate will be taken up by bacteria. Nitrate is morepersistent in water than the ammonium ion. Nitrate degradation is fastest in anaerobic conditions.

The toxicity of nitrates is due to its conversion to nitrites by bacteria in the gastrointestinalsystem. Chronic ingestion of more than 5,000 g/kg/day is considered unacceptable. Commonfindings associated with nitrate poisoning include unconsciousness, dizziness, fatigue, shortnessof breath, nausea, vomiting, hypotension, and headache. Effects of chronic exposure to highlevels of nitrate/nitrite include diuresis, increased starchy deposits and hemorrhaging of the spleen.

Two epidemiological studies have investigated effects of nitrate exposure on birth defects, butthe results are internally inconsistent or inconclusive. Dorsch et al. (1984) found a statisticallysignificant increase in risk of birth defects in children of women consuming groundwater (whichcontained 5,000-15,000 g/L of nitrate) compared with women consuming rainwater (whichcontained <5,000 g/L nitrate) [19]. These authors emphasized that their results are limited by anumber of factors, and stated that "it would be premature to interpret our case-control findingsexclusively in terms of water nitrate exposure." Arbuckle et al. (1988) reported a nonstatisticallysignificant increase in the odds ratio for birth defects in children of women exposed to well-water(26,000 g/L nitrate, equivalent to 0.2 mg nitrate-nitrogen/kg/day) compared with rain water(100 g/L nitrate, equivalent to 0.8 g nitrate-nitrogen/kg/day) [20]. However, decreased oddsratios (also not statistically significant) were noted for exposure to nitrate in spring water (17,000 g/L, equivalent to 130 g nitrate-nitrogen/kg/day) or public water (26,000 g/L).

Exposure to nitrate can cause methemoglobinemia in infants. Methemoglobinemia is a seriousillness that occurs when the body converts nitrate to nitrite. Nitrite oxidizes the Fe(+2) of iron inhemoglobin to the Fe(+3) state. This compound (methemoglobin) does not bind oxygen,resulting in a reduced ability of the child to transport oxygen from the lungs to the tissues. Thiscan be an acute condition which causes the child's health to deteriorate rapidly over a period ofdays. Symptoms include shortness of breath, blueness of the skin and lips, weakness, rapidpulse, and tachypnea. There is at least one study indicating that older children are much lesssusceptible to nitrate-induced methemoglobinemia than are infants [21].

EPA has developed a reference dose for nitrate based on the early clinical signs ofmethemoglobinemia in infants ingesting water containing varying concentrations of nitrate-nitrogen. The RfD is based on the observed NOAEL of 1,600 g nitrate-nitrogen/kg/day (10,000g nitrate-nitrogen/L x 0.64 L/day divided by 4 kg BW). An uncertainty factor of unity (1) wasemployed because available data defined the NOAEL for the critical effect in the most sensitivehuman population. A range of 1,800-3,200 g/kg/day was given for the LOAEL and was basedon water concentrations ranging from 11,000-20,000 g nitrate-nitrogen/L.

Nitrate is a normal component of the human diet. A typical daily intake by an adult in the UnitedStates is about 75,000 g/day (about 200-300 g nitrate- nitrogen/kg/day) [22]. Of this, over85% comes from the natural nitrate content of vegetables such as beets, celery, lettuce andspinach. Daily intakes of nitrate by vegetarians may exceed 250,000 g/day (800 g nitrate-nitrogen/kg/day) [22]. The contribution from drinking water is usually quite small (about 2-3%of the total) [22], but could reach 85,000 g/day (290 g nitrate-nitrogen/kg/day) if watercontaining 10,000 g nitrate-nitrogen/L was consumed. Thus, some adults consuming high levelsof vegetables along with water containing high levels of nitrate (up to 10,000 gnitrate-nitrogen/L) could receive total doses of nitrate approaching the RfD.

There is inadequate evidence to state whether or not nitrates or nitrites have the potential to causecancer from lifetime exposures in drinking water.

    Discussion of Public Health Implications

Since at present, people are not using the groundwater from Well Number 2, current exposure tothe contaminants in the water (carbon tetrachloride, atrazine, nitrate) is not an issue and thecontaminants do not present a public health hazard.

In the past, when people were using water from Well Number 2, they may have been exposed toone or more of the above contaminants; however, because of the lack of historical data, we couldnot reliably reconstruct possible past exposures. Depending upon the nature of the contaminant,exposures could have occurred through ingestion (drinking water), inhalation (volatilizationduring showering and cooking), or dermal contact (washing, bathing, showering). Since waterfrom Well Number 2 was blended with water from Well Number 1 prior to distribution, it wouldbe reasonable to assume that the actual concentrations that residents could have been exposed tomay have been low.

Future use of water from Well Number 2 could present a public health hazard if it is notproperly treated and blended prior to use. Depending on site/residence-specific exposureassumptions (duration of exposure, frequency of exposure, and routes of exposure), chronic(long-term) exposure to carbon tetrachloride, at the concentrations measured in this water, couldresult an estimated low to moderate increased lifetime risk for the development of cancer. Inaddition, since infants are particularly susceptible to nitrates in water, an infant exposed tonitrates at the concentrations measured in water from Well Number 2 could receive an averagedaily dose above the NOAEL and well within the range in which adverse effects(methemoglobinemia) have been observed in human infants.


Child Health Initiative

ATSDR's Child Health Initiative recognizes that the unique vulnerabilities of infants andchildren demand special emphasis in communities faced with contamination of their water, soil,air, or food. Children are at greater risk than adults from certain kinds of exposures to hazardoussubstances emitted from waste sites and emergency events. They are more likely to be exposedbecause they play outdoors and they often bring food into contaminated areas. They are shorterthan adults, which means they breathe dust, soil, and heavy vapors close to the ground. Childrenare also smaller, resulting in higher doses of chemical exposure per body weight. Thedeveloping body systems of children can sustain permanent damage if toxic exposures occurduring critical growth stages. Most important, children depend completely on adults for riskidentification and management decisions, housing decision, and access to medical care.

ATSDR evaluated the likelihood for children living in the vicinity of the Perryton Water WellNumber 2 site to be exposed to carbon tetrachloride and other contaminants at levels of healthconcern. Children currently are not exposed to contaminants in groundwater from Well Number2. The City of Perryton public water supply wells were tested by the TNRCC in June 1999 andcontaminants were not found. Carbon tetrachloride contamination was not detected in soils inthe vicinity of the site and since the well is on the City maintenance yard, site access by childrenis not likely.

Currently, children are not being exposed to the contaminated groundwater from Well Number 2. In the past children may have been exposed to contaminants in the groundwater although datawere insufficient to evaluate possible past exposures. Future use of water from Well Number 2prior to treatment and blending could pose a health hazard to infants.

Health Outcome Data

Health outcome data (HOD) record certain health conditions that occur in populations. Thesedata can provide information on the general health of communities living near a hazardous wastesite. It also can provide information on patterns of specified health conditions. One example ofhealth outcome databases are tumor registries and vital statistics. Information from localhospitals and other health care providers also may be used to investigate patterns of disease in aspecific population. Births on or after January 1, 1998 in Ochiltree County and in all of PublicHealth Region 1 have been included in the Texas Birth Defects Registry and these data will beready for analysis in 2001 [23].

Community Health Concerns

To collect community health concerns related to the Perryton Water Well Number 2 site, wecontacted several different agencies and individuals including the Texas Department of HealthRegion 1, the Texas Natural Resource Conservation Commission and the U.S. EPA Region 6. Inaddition to state agencies, we contacted the City Manager of the City of Perryton, the Director ofPublic Works, and the Water Superintendent. TDH received community health concerns fromcitizens who attended EPA's public meeting in Perryton in August 1999. We received the following health concerns:

  1. Would carbon tetrachloride remain in the water lines even after the well containingcontaminated water was capped off?

    No, once the well was disconnected from the city water lines and the water lines wereflushed with water from an uncontaminated source, carbon tetrachloride or other wellcontaminants would not remain in the water lines.

  2. Could aplastic anemia be related to the carbon tetrachloride in Well Number 2?

    No. Aplastic anemia is not a health problem that has been associated with exposure tocarbon tetrachloride. Neither oral exposure nor inhalation exposure to carbontetrachloride have been reported to have direct effects on the blood of humans or animals [2].

  3. Could the following cancers be attributable to the contamination in Well Number 2:leukemia, liver cancer, brain cancer, and breast cancer?

    It is not possible for us to determine the cause of any individual's cancer and althoughcarbon tetrachloride has been shown to cause liver tumors in laboratory animals we donot know for sure whether it causes cancer in people. Based on the animal studies,carbon tetrachloride is considered to be a probable human carcinogen. If exposure tocarbon tetrachloride were to cause cancer in people, the risk of getting cancer from theexposure would depend upon how much people were exposed to and how often theexposures occurred. We were able to review a 1994 report on the incidence of cancer inOchiltree County. The report, which was prepared by the Texas Cancer RegistryDivision indicated that there was no significant excess of cancer incidence for any of the above-stated cancers for the years 1986 to 1992 [24].

  4. Could birth defects be possible from drinking the carbon tetrachloride in water from Well Number 2?

    Although there have been no studies in people on the effect of carbon tetrachloride ondevelopment, studies on animals have not shown that exposures to carbon tetrachlorideresult in birth defects [2].

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