PUBLIC HEALTH ASSESSMENT
STATE ROAD 114 GROUNDWATER PLUME
LEVELLAND, HOCKLEY COUNTY, TEXAS
PREPARERS OF THE REPORT
Susan L. Prosperie, M.S., R.S.
Health Assessor
Environmental Epidemiology and Toxicology Division
John F. Villanacci, Ph.D.
Director
Environmental Epidemiology and Toxicology Division
Dixie Davis
Health Assessment Technician
Environmental Epidemiology and Toxicology Division
ATSDR Regional Representative
George Pettigrew
Senior Regional Representative
ATSDR - Region 6
This State Road 114 Groundwater Plume Public Health Assessment was prepared by the Texas Department of Health under a cooperative agreement with the Agency for Toxic Substances and Disease Registry (ATSDR). It is in accordance with approved methodology and procedures existing at the time the public health assessment was initiated.
Alan W. Yarbrough
Technical Project Officer, SPS, SSAB, DHAC, ATSDR
The Division of Health Assessment and Consultation, ATSDR, has reviewed this public health Assessment and concurs with its findings.
Lisa C. Hayes
for Chief, State Programs Section, SSAB, DHAC, ATSDR
APPENDIX A - Acronyms and Abbreviations
|
ATSDR |
Agency for Toxic Substances and Disease Registry |
| CERCLA |
Comprehensive Environmental Response, Compensation and Liability Act of 1980 |
| CLHA | Child Longer-term Health Advisory |
| CREG | Carcinogenic Risk Evaluation Guide |
| EMEG | Environmental Media Evaluation Guide |
| EPA | U.S. Environmental Protection Agency |
| ESI | Expanded Site Investigation |
|
HAC |
Health Assessment Comparison Value |
| HOD | Health Outcome Data |
| kg | Kilogram |
| LOAEL | Low Observable Adverse Effects Level |
| LTHA | Lifetime Health Advisory |
| MCL | Maximum Contaminant Level |
| MCLG | Maximum Contaminant Level Goal |
| µg/L | Micrograms per Liter equals ppb or Parts per Billion |
| mg/kg | Milligrams per Kilogram |
| MRL | Minimal Risk Level |
| na | Not Applicable |
| ND | Not Detected |
| NOAEL | No Observable Adverse Effects Level |
| NPL | National Priorities List |
| PHA | Public Health Assessment |
| ppb | Parts per Billion |
| RfD | Reference Dose |
| RMEG | Reference Dose-based Media Evaluation Guide |
| SARA | 1986 Superfund Amendments and Reauthorization Act |
| TDH | Texas Department of Health |
| TWC | Texas Water Commission |
| TNRCC | Texas Natural Resource Conservation Commission |
Figure 1. State Road 114 Groundwater Plume Site Location and Demographics Map
Figure 2. Approximate Location of Contaminated Groundwater Plume and Water Wells as of March 2000
Figure 3. Soil Sampling Locations at former Motor Fuels Corp Property (1997)
Table 2. State Road 114 Groundwater Plume - Contaminants Exceeding Health Assessment Comparison Values - Well Water Sampling January-March, 2000 [18]
| Contaminant |
Range of Concentrations Measured (µg/L) |
Health Assessment Comparison Values (µg/L) | ||
| Private/Individual Water Wells | Business Water Wells | Municipal Water Wells | ||
| Volatile Organic Compounds | ||||
| Benzene 1,2-Dichloroethane Disinfection By-products |
ND ND-23
|
ND-680 ND-69
|
ND ND
|
1 CREG A; 5 MCL 0.4 CREG B2; 2000/7000 intEMEG; 700 CLHA; 5 MCL 100 MCL Total Trihalomethanes |
| Metals | ||||
| Arsenic Lead Manganese Vanadium |
7-11 ND ND-1,450 28-50 |
70 ND ND-13,500 ND-30 |
ND 37 22-1,390 30-40 |
30/10 chronic EMEG; 0.02 CREG A; 50 MCL B2; 15 EPA Action Level 500/2000 RMEG 30/100 intermediate EMEG |
APPENDIX D - Evaluation of Groundwater Contaminants
1,2-Dichloroethane
Long term exposure to low doses of 1,2-dichloroethane has caused kidney disease and multiple tumor types in animals. Based on sufficient animal studies but inadequate human studies, 1,2-dichloroethane has been classified as a probable (Group B2) human carcinogen [20]. The concentration of 1,2-dichloroethane in water from both residential and business wells exceeded the CREG value for this contaminant. The highest measured concentration in the residential wells was 23 µg/L, while the highest measured concentration in the business wells was 69 µg/L.
Based on these data (assuming the levels do not increase) and on EPA's cancer slope factor for 1,2-dichloroethane, we estimate that chronic ingestion (30 years) of two (2) liters of this water each day (350 days per year) would not result in any apparent increased lifetime risk for the development of cancer. In some of the residences the theoretical excess lifetime risk for developing cancer could have been higher since people also could have been exposed through inhalation and dermal contact. The actual magnitude of this increase would depend upon the actual concentrations in the air and water as well as the length of time over which the exposures occurred. Using a worst case scenario, exposure to this contaminant through all pathways combined would result in a low increased lifetime risk for developing cancer. TNRCC has installed individual treatment systems on each of the residential wells in which contaminants were found above the MCL.
Arsenic
A large number of epidemiologic studies and case reports provide evidence that ingestion of arsenic increases the risk of developing cancer. The most common effect is an increased risk of multiple skin cancers. Some of the skin cancers develop from hyperkeratotic warts or corns characteristic of chronic arsenic exposure. Multiple basal cell carcinomas also may occur, usually from cells not associated with hyperkeratinization. In most cases, skin cancer develops only after prolonged exposure; however, several studies have reported skin cancer in people exposed for less than one year. Liver, bladder, kidney, and lung cancer also have been associated with oral exposure to arsenic [21], but these associations are less well established and currently not suitable for inclusion in risk estimates.
Based on epidemiological studies, the EPA has classified arsenic as a Group A "known human" carcinogen. This classification is based on consistent evidence of increased risk of lung cancer in workers exposed to airborne arsenic-contaminated dust [22] and on the clear dose-dependent relationship between ingested arsenic and skin cancer [23, 24].
Arsenic was detected above its carcinogenic risk evaluation guide both in residential wells and in one of the business wells. Based the current data (assuming the levels do not increase) and on EPA's cancer slope factor for arsenic, we estimate that chronic ingestion (30 years) of two (2) liters of this water each day (350 days per year) could result in a theoretical low to moderate increased lifetime risk for the development of cancer.
There is some evidence that the body may detoxify arsenic suggesting that the dose-response curve for arsenic may be non-linear at low doses. Since EPA derived the cancer slope factor for arsenic using a model that assumes that the dose-response curve is linear at low doses, the slope factor based on the linear model may over estimate cancer risks at low doses. The EPA has concluded that although the current slope factor might over estimate low dose risk, data are too limited to permit a quantitative adjustment of the slope factor [25].
Manganese
Excess exposure to manganese can be harmful to human health. A combination of symptoms resulting in a disease known as manganism has been observed in mining and steel workers after long-term exposure to high levels of manganese dust in the air. These symptoms include weakness, abnormal gait, ataxia, muscular hypotonicity, and a fixed facial expression. Manganism occurs when too much manganese adversely affects the brain. Although some of the symptoms of manganism can be treated, the damage that occurs to the brain is permanent [26].
It is not known whether eating or drinking too much manganese can cause manganism. There is one study indicating a statistically significant difference in neurologic test scores between people from an area with high levels of manganese in well water compared with people from another area with low levels of manganese in well water. The concentration of manganese in the water from the high concentration area ranged from 1,600 to 2,300 µg/L; however, because of other limitations this study could not be used to determine a quantitative dose response relationship for the toxicity of manganese in humans [27].
Manganese is an essential dietary nutrient; the World Health Organization (WHO) has estimated the average dietary intake of manganese to range from approximately 2,000 to 8,800 µg/day. The Food and Nutrition Board of the National Research Council has established "estimated safe and adequate daily dietary intake levels" for this nutrient that range from 300 µg per day for infants to 5,000 µg/day for adults. The WHO had concluded that 8,000 to 9,000 µg/day is "perfectly safe" for adults [26]. Based on estimates of what is considered safe the EPA has established a RfD for manganese of 0.14 mg/kg/day which equates to approximately 10,000 µg/day for adults and 2,100 µg/day for a 15 kg child. Using the most recent data, we conclude that drinking two liters of water each day from the potable water wells likely would not result in excess manganese exposure.
Vanadium
There are very few studies regarding adverse effects in humans after oral exposure to vanadium. Human volunteers given 0.47 to 1.3 mg-vanadium per kilogram body weight as ammonium vanadyl tartrate for 45 to 68 days had intestinal cramping and diarrhea. It could not be determined whether this effect was caused by the vanadium [28]. The same volunteers showed no hematological abnormalities (as measured by white blood cell count, differential count, platelets, and reticulocytes), hepatic effects (no changes in oxaloacetic transferase, cholesterol, triglyceride, or phospholipid levels), or renal effects (normal blood urea nitrogen levels and no changes in urinalysis for albumin or hemoglobin). A no observable adverse effect level (NOAEL) of 1.3 mg-vanadium/kg-body weight for hepatic, hematologic, and renal effects was identified. No documentation of human health effects from ingestion of drinking water were located and no other significant health effects from oral exposure to vanadium have been found in humans [29].
The Agency for Toxic Substances and Disease Registry (ATSDR) has developed an intermediate-duration oral Minimal Risk Level (MRLi) for vanadium of 0.003 mg-vanadium/kg-body weight/day (mg/kg/day). The MRLi is based on a study in which rats were given selected concentrations (1, 5, 10, or 50 mg/L) of vanadium (as sodium metavanadate) for three months [30]. Serum cholesterol and glucose levels, liver function, organ weights, weight gain, and water consumption were unaffected at all exposure levels; however, the treated animals did show mild histological changes in kidneys, lungs, and spleen that became progressively more severe with increased dosages. ATSDR identified a No Observable Adverse Effects Level (NOAEL) of 5 mg/L (0.3 mg/kg/day). The MRLi of 0.003 mg/kg/day was derived by dividing the NOAEL by an uncertainty factor of 100 (10 for extrapolation from animals to humans and 10 to account for human variability).
The maximum concentration of vanadium found in the groundwater was found in water from a residential well (50 µg/L). Although a child using this water, theoretically, slightly could exceed the MRL, the estimated dose would be over 400 times lower than the NOAEL (1.3 mg/kg/day) for actual effects observed in humans exposed to vanadium in drinking water for 45 to 60 days.
Benzene
Eating or drinking benzene contaminated food or water can cause gastrointestinal irritation, dizziness, anemia, and suppression of the immune system. Based on an increased incidence of lymphoma and leukemia in people, EPA has classified benzene as a known human carcinogen. EPA used cancer risk data from human epidemiological studies of workers exposed by inhalation to derive risk factors associated with oral exposure to benzene. EPA has set the MCL of benzene in drinking water at 5 µg/L [31]. The Farmers Co-op well contained a benzene level of 680 µg/L; however, water from this well was used for non-potable purposes in a restroom. Water from this well currently is treated prior to use.
