PUBLIC HEALTH ASSESSMENT
CITY OF PERRYTON WELL NO. 2
(a/k/a PERRYTON WATER WELL NUMBER 2)
PERRYTON, OCHILTREE COUNTY, TEXAS
ENVIRONMENTAL CONTAMINATION / PATHWAYS ANALYSIS /
PUBLIC HEALTH IMPLICATIONS
Exposure to, or contact with, chemical contaminants drives the ATSDR public health assessment process. The release or disposal of chemical contaminants into the environment does not always result in exposure or contact. Chemicals have the potential to cause adverse health effects only if people 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 a substance containing the contaminant.
When people are exposed to chemicals, the exposure does not always result in adverse health effects. The type and severity of health effects that may occur in an individual from contact with contaminants depend on the toxicologic properties of the contaminants; how much of the contaminant to which the individual is exposed; how often and/or how long exposure is allowed to 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 how the individual absorbs, distributes, metabolizes, and excretes the contaminant. These factors and characteristics influence whether exposure to a contaminant could or would result in adverse health effects.
To assess the potential health risks associated with contaminants at this site, we compared contaminant concentrations to health assessment comparison (HAC) values. HAC values are media-specific contaminant concentrations that are used to screen contaminants for further evaluation. Non-cancer HAC values are called environmental media evaluation guides (EMEGs) or reference dose media evaluation guides (RMEGs) and are respectively based on ATSDR's minimal risk levels (MRLs) or EPA's reference doses (RfDs). MRLs and RfDs are estimates of a daily human exposure to a contaminant that is unlikely to cause adverse non-cancer health effects. Cancer risk evaluation guides (CREGs) are based on EPA's chemical-specific cancer slope factors and an estimated excess lifetime cancer risk of one-in-one-million persons exposed for a lifetime. We used standard assumptions to calculate appropriate HAC values [11].
In some instances, we compare contaminant concentrations in water to EPA's maximum contaminant levels (MCLs). MCLs are chemical specific maximum concentrations allowed in water delivered to the users of a public water system; they are considered protective of public health over a lifetime (70 years) of exposure at an ingestion rate of two liters per day. The setting 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 the public health implications of contaminants found in water from other sources.
While exceeding a HAC value does not necessarily mean that a contaminant represents a public health threat, it does suggest that the contaminant warrants further consideration. The public health significance of contaminants that exceed HAC values may be assessed by reviewing and integrating relevant toxicological information with plausible exposure scenarios. Estimated exposures may be compared to reported "No Observable" and "Lowest Observable" Adverse Effects Levels (NOAELs and LOAELs) and to known effect levels in humans, when available.
Data included in our evaluation of the Perryton Water Well Number 2 site included groundwater sampling in 1989 and 1990, groundwater and soil samples collected during the EPA's Expanded Site Inspection (ESI) in June 1996, and additional sampling of Water Well Number 2 by EPA's contractor in April 1999. The data packages were reviewed and validated by EPA Region 6. In evaluating the public health significance of these data, we relied on the information provided in the referenced documents and assumed that adequate Quality Assurance/Quality Control measures were followed with regard to chain-of-custody, laboratory procedures, and data reporting. The analyses and conclusions in this public health assessment are valid only if the referenced information is valid and complete.
In June 1996, during the Expanded Site Investigation, 20 groundwater samples were collected to try to determine the extent of the contaminated groundwater plume [3]. Seventeen of the samples were collected from Well Numbers 1 and 3 through 11 and the remaining seven groundwater samples were collected from Well Number 2. Groundwater samples collected from Well Number 1 and Wells Number 3 through 11 did not contain carbon tetrachloride or other contaminants at concentrations exceeding health assessment comparison values. Groundwater samples collected from Well Number 2 contained concentrations of carbon tetrachloride exceeding health assessment comparison values. Concentrations ranged from 35.8 to 50.3 µg/L [3]. Chloroform, a possible degradation product of carbon tetrachloride, was measured in samples from Well Number 2, at concentrations below health assessment comparison values. Lead (60.9 µg/L) and copper (1,380 µg/L) were measured at concentrations above EPA's action levels during the June 1996 sampling event; however, subsequent sampling indicated that these detections 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 event 100,000 gallons of water were pumped from Well Number 2 in order to accurately determine the concentration of contaminants in the groundwater plume associated with Well Number 2 [12]. Atrazine (5.47 µg/L), carbon tetrachloride (42.5 µg/L), and nitrate (17,900 µg/L) were detected in Well Number 2 at concentrations above their respective comparison values (Table 2).
In June 1996 a contractor for EPA collected 48 soil samples to characterize surface and near surface soil conditions at the site. Sampling locations are shown in Figure 2. Forty-two samples were 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 ground surface from drainage areas associated with the Perryton Equity Exchange and the City of Perryton maintenance yard. One background sample (SB-16) was collected at zero to six inches below ground surface from a vacant lot at the corner of Colgate and Amherst approximately 1,000 feet west of Well Number 2 [3].
Soil samples were analyzed for volatile organic compounds. Carbon tetrachloride was not reported in the soil samples; however, methylene chloride and chloroform, which are possible degradation products of carbon tetrachloride, were measured at low concentrations in soil samples [3]. The maximum detected concentrations of these volatile organic compounds were below health assessment comparison values.
We evaluated the possible pathways for exposure to contamination at Perryton Water Well Number 2 site. We examined these possible exposure pathways to determine whether people in the 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 through an environmental medium, 3) a point of exposure, 4) a plausible manner (route) for the contaminant 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 a contaminant, the exposure pathway must be complete. An exposure pathway is considered completed when all five elements in the pathway are present and exposure has occurred, is occurring, or will plausibly occur in the future. A potential pathway is missing at least one of the five elements but may possibly be complete in the future as more data become available or site conditions change. Eliminated pathways are missing one or more of the five elements and will never 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 | ||||||||
| PATHWAY NAME |
CONTAMINANTS OF CONCERN | EXPOSURE PATHWAYS ELEMENTS | TIME | COMMENTS | ||||
| SOURCE | ENVIRONMENTAL MEDIA |
POINT
OF EXPOSURE |
ROUTE OF |
EXPOSED POPULATION |
||||
| Groundwater |
Carbon tetrachloride, |
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 Nitrates |
Future | Future use of water from Well Number 2 prior to treatment and blending could pose a public health hazard. | ||||||
Summary: Carbon tetrachloride, atrazine, and nitrate were detected in water from Well Number 2 at concentrations above each of their respective health assessment comparison values. ATSDR has concluded that under current conditions the presence of these contaminants in the groundwater does not present a public health hazard because there is no evidence that people are 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 of a general lack of historical information we could not determine with any degree of certainty the potential hazards associated with these possible past exposures. Thus, we have concluded that past exposure to contaminants in the groundwater represents an indeterminate public health hazard. 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. These discussions include a general description of their uses, how they react in the environment, and the general toxicological effects that have been associated with them. These descriptions are followed 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 the present time. The highest concentration (50.3 µg/L) was measured in June 1996. Carbon tetrachloride does not occur naturally. In the past it was used in the production of refrigeration fluid 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 pesticide fumigant to kill insects in grain. Because of its harmful effects, most of these uses were banned in the 1960s; its use as a pesticide was banned in 1986. Today carbon tetrachloride is only used in some industrial applications [2].
When carbon tetrachloride leaks onto the ground, only a small amount of it sticks to soil particles; the rest evaporates into the air or moves into the groundwater. In groundwater carbon tetrachloride 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 is contaminated with carbon tetrachloride can be exposed to it through ingestion, inhalation, or dermal contact (absorption through the skin).
Exposure to high concentrations of carbon tetrachloride can cause liver, kidney, and central nervous system damage. If exposure is low and then stops, the liver and kidneys can repair the damaged cells and function normally again. The liver is especially sensitive to carbon tetrachloride. In people an acute (one time) exposure to 90,000 micrograms-carbon tetrachloride per kg-body weight (µg/kg) has caused slight fatty infiltration of the liver. A single dose of 110,000 µg/kg has resulted in the degeneration of hepatocytes (liver cells). An acute dose of 670,000 µg/kg has been reported to cause severe liver necrosis. Carbon tetrachloride also has been known to cause swelling of the proximal convoluted tubules of the kidney in humans after the administrations of a single dose of 180,000 µg/kg. These concentrations are much higher than those people drinking water from Water Well Number 2 might have been exposed to.
If exposure is very high (4,800,000 µg/kg), the nervous system can be affected and people may experience narcosis (feel intoxicated). Single doses as low as 300,000 µg/kg have caused drowsiness in people. People also could experience headaches, dizziness, sleepiness, and nausea and vomiting. Many of the neurological effects subside if exposure is stopped, but in severe cases, coma and even death can occur. There have been no studies in people on carbon tetrachloride'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 µg/kg/day. The MRL was derived from a study in which rats were orally dosed with 0; 5,000; 10,000; 20,000; or 40,000 µg-carbon tetrachloride per kilogram body weight per day (µg/kg/day) for 10 consecutive days. Progressive, dose-related liver injury was observed with centrilobular vacuolar degeneration being barely detectable in all six animals receiving 5,000 µg/kg/day (this effect was not observed in any of the six control animals). The effects became more severe as the dose was increased with hepatocellular necrosis becoming evident at 10,000 µg/kg/day [14]. ATSDR established the MRL by dividing the Lowest Observable Adverse Effects Level (LOAEL) by an uncertainty factor of 300 (3 for the conversion to a NOAEL, 10 for animal to human extrapolation, and 10 to account for human variability).
In addition to the acute oral MRL, ATSDR also has established an intermediate oral MRL of 7 µg/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 µg/kg/day, five days per week for 12 weeks [15]. Slightly elevated blood levels of sorbitol dehydrogenase and centrilobular vacuolization of the liver were observed in animals receiving 10,000 µg/kg/day, but not in those receiving 1,000 µg/kg/day. The MRL was calculated by dividing the identified No Observable Adverse Effects Level (NOAEL) of 1 mg/kg/day corrected for a seven day per week exposure, by an uncertainty factor of 100 (10 for animal to human extrapolation and 10 to account for human variability).
The Department of Health and Human Services has determined that carbon tetrachloride may reasonably 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 human carcinogen. 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 know if breathing or ingesting it will cause cancer in people.
Atrazine
In April 1996, atrazine was measured in water from Water Well Number 2 at a concentration of 5.47 µg/L. Atrazine is a widely used herbicide for control of broadleaf and grassy weeds. This white crystalline solid was estimated to be the most heavily used herbicide in the United States between 1987 and 1989. Atrazine may be released to the environment in wastewater from manufacturing facilities and through its use as a herbicide. It was extensively used for corn and soybeans in mid-western states and in Texas. Other uses included control of broadleaf and grassy weeds in sorghum, rangeland, and grass crops. Effective in 1993, the use of atrazine for non-crop vegetation control was eliminated, and use was restricted by a requirement for a buffer zone between application sites and surface water [16].
When atrazine is released to the environment, microbial activity and chemicals in soil and water may cause atrazine to breakdown, particularly in alkaline conditions. Sunlight and evaporation do not reduce atrazine concentrations. Atrazine may bind to some soils, but it generally tends to leach 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 be absorbed orally, through inhalation, or through the skin. Most of the toxicological information that is available for atrazine comes from animal studies. Symptoms of exposure to high levels of atrazine can include abdominal pain, diarrhea, vomiting, eye irritation, irritation of the mucous membranes, and skin reactions. At very high doses, rats have shown excitation followed by depression, slowed breathing, in-coordination, muscle spasms, and hypothermia. After ingesting a 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 25,000 µg/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 higher than 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 µg/kg/day. This RfD is based on an animal study in which rats fed 25,000 µg-atrazine/kg-Body Weight/day for two years exhibited a decreased body weight gain. The RfD was derived by dividing the identified NOAEL of 3,500 µg/kg/day by an uncertainty factor of 100 (10 for interspecies extrapolation and 10 for intraspecies variability).
There is inadequate evidence in humans for the carcinogenicity of atrazine. There is limited evidence in experimental animals for an increased risk of tumors associated with hormonal factors [17]. The International Agency for Research on Cancer (IARC) has listed atrazine as a 2B carcinogen (possibly carcinogenic in humans) [17].
Nitrates
Nitrate nitrogen was measured in water samples collected from Perryton Water Well Number 2 in April of 1999. Primary sources of organic nitrates include human sewage and livestock manure, especially from feedlots. The major environmental releases of inorganic sources of nitrates are due to the use of fertilizers. These are primarily potassium nitrate and ammonium nitrate. Potassium nitrates are used mainly as fertilizers (85%), with the remainder in heat transfer salts, glass and ceramics, and in matches and fireworks. Ammonium nitrates are used as fertilizers (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 a high potential to migrate to groundwater. Nitrates and nitrites are very soluble in water. Most nitrogenous materials in natural waters tend to be converted to nitrate, so all sources of combined nitrogen, particularly organic nitrogen and ammonia, should be considered as potential nitrate sources. Because it does not volatilize, nitrate/nitrite is likely to remain in water until consumed by plants or other organisms. Ammonium nitrate will be taken up by bacteria. Nitrate is more persistent 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 gastrointestinal system. Chronic ingestion of more than 5,000 µg/kg/day is considered unacceptable. Common findings associated with nitrate poisoning include unconsciousness, dizziness, fatigue, shortness of breath, nausea, vomiting, hypotension, and headache. Effects of chronic exposure to high levels 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, but the results are internally inconsistent or inconclusive. Dorsch et al. (1984) found a statistically significant increase in risk of birth defects in children of women consuming groundwater (which contained 5,000-15,000 µg/L of nitrate) compared with women consuming rainwater (which contained <5,000 µg/L nitrate) [19]. These authors emphasized that their results are limited by a number of factors, and stated that "it would be premature to interpret our case-control findings exclusively in terms of water nitrate exposure." Arbuckle et al. (1988) reported a nonstatistically significant increase in the odds ratio for birth defects in children of women exposed to well-water (26,000 µg/L nitrate, equivalent to 0.2 mg nitrate-nitrogen/kg/day) compared with rain water (100 µg/L nitrate, equivalent to 0.8 µg nitrate-nitrogen/kg/day) [20]. However, decreased odds ratios (also not statistically significant) were noted for exposure to nitrate in spring water (17,000 µg/L, equivalent to 130 µg nitrate-nitrogen/kg/day) or public water (26,000 µg/L).
Exposure to nitrate can cause methemoglobinemia in infants. Methemoglobinemia is a serious illness that occurs when the body converts nitrate to nitrite. Nitrite oxidizes the Fe(+2) of iron in hemoglobin 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. This can be an acute condition which causes the child's health to deteriorate rapidly over a period of days. Symptoms include shortness of breath, blueness of the skin and lips, weakness, rapid pulse, and tachypnea. There is at least one study indicating that older children are much less susceptible to nitrate-induced methemoglobinemia than are infants [21].
EPA has developed a reference dose for nitrate based on the early clinical signs of methemoglobinemia in infants ingesting water containing varying concentrations of nitrate-nitrogen. The RfD is based on the observed NOAEL of 1,600 µg nitrate-nitrogen/kg/day (10,000 µg nitrate-nitrogen/L x 0.64 L/day divided by 4 kg BW). An uncertainty factor of unity (1) was employed because available data defined the NOAEL for the critical effect in the most sensitive human population. A range of 1,800-3,200 µg/kg/day was given for the LOAEL and was based on water concentrations ranging from 11,000-20,000 µg nitrate-nitrogen/L.
Nitrate is a normal component of the human diet. A typical daily intake by an adult in the United States is about 75,000 µg/day (about 200-300 µg nitrate- nitrogen/kg/day) [22]. Of this, over 85% comes from the natural nitrate content of vegetables such as beets, celery, lettuce and spinach. Daily intakes of nitrate by vegetarians may exceed 250,000 µg/day (800 µg 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 µg/day (290 µg nitrate-nitrogen/kg/day) if water containing 10,000 µg nitrate-nitrogen/L was consumed. Thus, some adults consuming high levels of vegetables along with water containing high levels of nitrate (up to 10,000 µg nitrate-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 cause cancer from lifetime exposures in drinking water.
Since at present, people are not using the groundwater from Well Number 2, current exposure to the contaminants in the water (carbon tetrachloride, atrazine, nitrate) is not an issue and the contaminants do not present a public health hazard.
In the past, when people were using water from Well Number 2, they may have been exposed to one or more of the above contaminants; however, because of the lack of historical data, we could not reliably reconstruct possible past exposures. Depending upon the nature of the contaminant, exposures could have occurred through ingestion (drinking water), inhalation (volatilization during showering and cooking), or dermal contact (washing, bathing, showering). Since water from Well Number 2 was blended with water from Well Number 1 prior to distribution, it would be reasonable to assume that the actual concentrations that residents could have been exposed to may have been low.
Future use of water from Well Number 2 could present a public health hazard if it is not
properly treated and blended prior to use. Depending on site/residence-specific exposure
assumptions (duration of exposure, frequency of exposure, and routes of exposure), chronic
(long-term) exposure to carbon tetrachloride, at the concentrations measured in this water, could
result an estimated low to moderate increased lifetime risk for the development of cancer. In
addition, since infants are particularly susceptible to nitrates in water, an infant exposed to
nitrates at the concentrations measured in water from Well Number 2 could receive an average
daily dose above the NOAEL and well within the range in which adverse effects
(methemoglobinemia) have been observed in human infants.
CHILD HEALTH INITIATIVE/HEALTH OUTCOME DATA/
COMMUNITY HEALTH CONCERNS
ATSDR's Child Health Initiative recognizes that the unique vulnerabilities of infants and children 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 hazardous substances emitted from waste sites and emergency events. They are more likely to be exposed because they play outdoors and they often bring food into contaminated areas. They are shorter than adults, which means they breathe dust, soil, and heavy vapors close to the ground. Children are also smaller, resulting in higher doses of chemical exposure per body weight. The developing body systems of children can sustain permanent damage if toxic exposures occur during critical growth stages. Most important, children depend completely on adults for risk identification and management decisions, housing decision, and access to medical care.
ATSDR evaluated the likelihood for children living in the vicinity of the Perryton Water Well Number 2 site to be exposed to carbon tetrachloride and other contaminants at levels of health concern. Children currently are not exposed to contaminants in groundwater from Well Number 2. The City of Perryton public water supply wells were tested by the TNRCC in June 1999 and contaminants were not found. Carbon tetrachloride contamination was not detected in soils in the vicinity of the site and since the well is on the City maintenance yard, site access by children is 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 data were insufficient to evaluate possible past exposures. Future use of water from Well Number 2 prior to treatment and blending could pose a health hazard to infants.
Health outcome data (HOD) record certain health conditions that occur in populations. These data can provide information on the general health of communities living near a hazardous waste site. It also can provide information on patterns of specified health conditions. One example of health outcome databases are tumor registries and vital statistics. Information from local hospitals and other health care providers also may be used to investigate patterns of disease in a specific population. Births on or after January 1, 1998 in Ochiltree County and in all of Public Health Region 1 have been included in the Texas Birth Defects Registry and these data will be ready for analysis in 2001 [23].
To collect community health concerns related to the Perryton Water Well Number 2 site, we contacted several different agencies and individuals including the Texas Department of Health Region 1, the Texas Natural Resource Conservation Commission and the U.S. EPA Region 6. In addition to state agencies, we contacted the City Manager of the City of Perryton, the Director of Public Works, and the Water Superintendent. TDH received community health concerns from citizens who attended EPA's public meeting in Perryton in August 1999. We received the following health concerns:
No, once the well was disconnected from the city water lines and the water lines were flushed with water from an uncontaminated source, carbon tetrachloride or other well contaminants would not remain in the water lines.
No. Aplastic anemia is not a health problem that has been associated with exposure to carbon tetrachloride. Neither oral exposure nor inhalation exposure to carbon tetrachloride have been reported to have direct effects on the blood of humans or animals [2].
It is not possible for us to determine the cause of any individual's cancer and although carbon tetrachloride has been shown to cause liver tumors in laboratory animals we do not 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 to carbon tetrachloride were to cause cancer in people, the risk of getting cancer from the exposure would depend upon how much people were exposed to and how often the exposures occurred. We were able to review a 1994 report on the incidence of cancer in Ochiltree County. The report, which was prepared by the Texas Cancer Registry Division indicated that there was no significant excess of cancer incidence for any of the above-stated cancers for the years 1986 to 1992 [24].
Although there have been no studies in people on the effect of carbon tetrachloride on development, studies on animals have not shown that exposures to carbon tetrachloride result in birth defects [2].
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