KITSAP COUNTY - BAINBRIDGE ISLAND DUMP
BAINBRIDGE, KITSAP COUNTY, WASHINGTON
After evaluating all of the sampling data, DOH concluded that no health threat exists for people exposed for 1-5 years to any of the contaminants detected in the domestic wells to date. Although a very low chronic (long-term) health risk exists from exposure to the maximum concentration of individual contaminants (vinyl chloride in one well and arsenic in one well), there is no apparent public health hazard. ATSDR uses the "no apparent public health hazard" category for sites where human exposure to contaminated media is occurring or has occurred in the past, but the exposure is below a level of health hazard.
The Kitsap County Department of Public Works will continue sampling domestic supply wells quarterly through at least the end of 1998. DOH is working closely with the Bremerton-Kitsap County Health District and Ecology, and will continue to evaluate the sample results to determine future recommendations.
Contaminants exceeding a screening value which were further evaluated:
The following contaminants detected in individual domestic wells exceeded an ATSDR health-based screening value and were thus further evaluated in the health consultation:
- Vinyl chloride
In addition, 1,2,4-Trimethylbenzene (pseudocumene) and chloroethane (ethyl chloride) were detected, but have no published oral MRL's, RfD's, and/or slope factors against which estimated doses may be compared.
1,2,4-Trimethylbenzene is commonly found in paint thinner and is of low general toxicity. This compound is a general anesthetic at high concentrations, and at very high concentrations can cause central nervous system depression. Concentrations of 1,2,4-Trimethylbenzene found in the two drinking water samples were very low (0.2 µg/l and 0.1 µg/l), and due to their low toxicity would not be expected to cause adverse health effects.
Chloroethane was detected in one well (0.1 µg/l and 0.2 µg/l). Inhalation studies provide the only data in which to quantify cancer or non-cancer health effects for chloroethane. However, the estimated dose as a result of exposure to the maximum detected concentration of chloroethane in drinking water is well below the LOAEL and NOAEL for this compound, indicating that non-cancer health effects are not expected to occur. These health effects levels were derived from animal inhalation studies. A carcinogenicity assessment is currently under review by the EPA, thus a cancer risk cannot be derived.
Arsenic concentrations since 1996 have ranged from non-detect to 26.2 µg/l. The maximum arsenic detections, ranging from 10.7 µg/l (10/96) to 26.2 µg/l (9/96) were from well BOW31A, a private drinking water well located approximately 1,000 feet south of the landfill. This well has not been tested for inorganics since October 1996.
Arsenic is a naturally occurring element in the earth's crust and is widely distributed in the environment. Arsenic has been found naturally at higher levels in groundwater in some western Washington locations. All humans are exposed to low levels of arsenic present in the environment. Both organic and inorganic forms of arsenic exist. Inorganic arsenic is generally more toxic than organic arsenic. Inorganic arsenic compounds are used to preserve wood and to make insecticides and weed killers. At high levels, arsenic can damage nerves, the stomach, intestines, and skin. Exposure to lower levels (300 to 30,000 ppb in food or water) can cause nausea, vomiting, diarrhea, decreased production of red and white blood cells, abnormal heart rhythm, blood vessel damage, and a painful sensation in the hands and feet. Perhaps the single most characteristic effect of long-term oral exposure to inorganic arsenic is a pattern of skin changes. This includes a darkening of the skin and the appearance of small "corns" or "warts" on the palms, soles, and torso. A small number of the corns may ultimately develop into skin cancer. EPA classifies arsenic as a known (class A) human carcinogen. Ingesting inorganic arsenic increases the risk of skin cancer and tumors of the bladder, kidney, liver, and lungs.
The estimated increased cancer risk due to chronic exposure to the maximum arsenic concentration is approximately four to five additional cancers per 10,000 persons exposed as an adult, and approximately six to seven additional cancers per 10,000 persons exposed as a child through adulthood (low increased cancer risk).
The MRL and RfD are based on a NOAEL of 0.0008 mg/kg/day observed in a large Taiwanese population chronically exposed to arsenic primarily from drinking water. The critical effects were keratoses and hyperpigmentation of the skin with possible vascular complications.
Although the estimated doses for a child exposed through adulthood and for an exposed adult at the site were just over the chronic oral MRL, they were below the LOAEL established for each systemic effect studied in another study (Tseng, 1977, Cebrian, 1983, Southwick, 1983). Several epidemiological studies of moderately-sized populations (20-200 people) exposed to arsenic in drinking water have detected no dermal or other effects at average chronic doses in the range of the estimated child and adult exposure doses for this well. As a result, the estimated doses for both the child exposed through adulthood and adult exposure scenarios were below levels expected to cause adverse non-cancer health effects.
Lead concentrations since 1996 have ranged from non-detect to 67 µg/l. The two maximum lead concentrations (67 µg/l and 25.6 µg/l, total and dissolved, respectively) were from well BOW64, a Group A public water system, located approximately 1,500 feet northeast of the landfill. This system serves approximately 45 students at a school and 1 residence. For all domestic wells sampled, these were the only 2 lead detections above the 15 µg/l federal action level. When this well was re-sampled the following month, lead concentrations were 1-2 µg/l, well below EPA's 15 µg/l action level.
Lead is a naturally occurring metal found in small amounts in the earth's crust. Most of it comes from human activities such as mining, manufacturing, the burning of fossil fuels, batteries, pipes, ammunition, and paint. Everyone has some lead in their bodies as a result of exposure to natural and anthropogenic (man-made) sources.
The non-cancer effects of lead are well known. At high doses, lead is toxic to the brain and can cause encephalopathy. Lower doses cause peripheral nervous system toxicity, kidney damage, blood disorders, and hearing impairment. The most sensitive toxic effect of lead poisoning is believed to be impaired development of the central nervous system in children. This effect has been measured by observing changes in the behavior of children, including performance in school. These changes have been measured at very low lead levels in the blood. The CDC has established a blood lead level of concern of 10 micrograms of lead per deciliter of blood (µg/dl). Children who have a blood lead level that exceeded this value are considered at risk and should have their exposure reduced. Fetal exposure from the mother to high levels of lead can cause premature birth and low birth weight.
Lead is classified by the EPA as a B2 (probable human) carcinogen. This classification was based on sufficient evidence of cancer in animals and inadequate evidence in humans. Several studies have demonstrated that high doses of lead in laboratory animals can cause kidney tumors. Quantitative carcinogenic analysis of lead in drinking water was not possible due to the lack of adequate studies from which to derive a cancer potency factor. The developmental effects of lead in children are recognized as the most sensitive toxic endpoint of lead exposure. As the non-cancer endpoint is the most sensitive indicator of exposure, the lack of cancer data is not significant in determining risk.
Long-term exposure to the maximum lead concentration detected in drinking water (67 µg/l) is not expected to increase blood lead levels in children above CDC's 10 µg/dl level of concern. EPA's Integrated Exposure Uptake Biokinetic Model (IEUBK-Version 0.99D), which incorporates a background blood lead level of approximately 4 µg/dl and assumes some lead exposure from soil, dust, air, and diet, indicates that blood lead levels in children between 1 and 6 years of age (those most susceptible) would not exceed 9 µg/dl at this level of exposure.
Manganese concentrations since 1996 have ranged from non-detect to 589 µg/l. The maximum manganese detection (589 µg/l) was from well BOW12, a private well located approximately 600 feet east of the landfill.
Manganese is a widely distributed element that is essential for normal physiologic functioning in all animal species. Several health effects in humans have been associated with both deficiencies and excess intakes of manganese. Although there are many reports of toxicity to humans exposed to manganese by inhalation, much less is known about oral intakes resulting in toxicity. Only one limited study in primates by the oral route of exposure is available. While manganese is clearly an essential element, it has also been demonstrated to be the causative agent in a syndrome of neurologic and psychiatric disorders that has been described in manganese miners. Other documented symptoms resulting from exposure to high doses of manganese include lethargy, increased muscle tonus, tremor and mental disturbances. The most severe symptoms were observed in elderly people, while children appeared to be unaffected. One case study suggests that for individuals with impaired liver function, intakes of manganese that would otherwise be safe may present a problem. In contrast to inhaled manganese, ingested manganese has rarely been associated with toxicity.
A study by Kondakis et al. (1989) raises some concern for possible adverse health effects (mild neurological signs) associated with a lifetime consumption of drinking water containing about 2,000 µg/L of manganese. A report by Kawamura et al. (1941) is the only epidemiologic study describing toxicologic responses in humans consuming large amounts of manganese dissolved in drinking water. In this study, the concentration of manganese at the time of exposure was estimated to be as high as 28,000 µg Mn/l. Another case study of manganese intoxication involved a 62-year-old male. The oral intake of manganese was estimated to be approximately equivalent to 40 mg Mn/day. These concentrations are well above the maximum concentration detected.
There is no human carcinogenicity data and inadequate animal carcinogenicity data for manganese. As a result, quantitative carcinogenic analysis of manganese in drinking water was not possible due to the lack of adequate studies from which to derive a cancer potency factor.
Although both the child through adulthood and adult exposure dose estimates were slightly above the chronic oral RfD, exposures were below levels demonstrated to cause toxic effect in the 1989 study described above (i.e, below the less serious LOAEL). Further, the study had substantial limitations and did not prove that chronic oral intake of manganese can lead to neurological changes in humans.
Vinyl chloride concentrations since 1996 have ranged from non-detect to 0.77 µg/l. Vinyl chloride has been detected at low levels in 12 of the 21 domestic wells sampled (through 6/98). The maximum concentration was 0.77 µg/l at well BOW37 in October 1996. This well is located approximately 800 feet northeast of the landfill. Vinyl chloride concentrations in this well over the subsequent 6 sampling rounds (April 1997-June 1998) dropped to 0.3-0.5 µg/l, and is currently 0.4 µg/l (6/98).
Vinyl chloride is a colorless gas at normal temperatures. All vinyl chloride is manufactured or results from the breakdown of manufactured substances, such as trichloroethylene, trichloroethane, and tetrachloroethylene (commonly used cleaning and degreasing compounds). Most of the vinyl chloride produced in the United States is used to make polyvinyl chloride (PVC). PVC is used to make a variety of plastic products including pipes, wire, cable coatings and packaging materials. Other uses include furniture and automobile upholstery, wall coverings, housewares, and automotive parts.
Breathing high levels (>1,000 ppm) of vinyl chloride can cause dizziness and sleepiness. Animal studies have demonstrated that exposure to extremely high levels of vinyl chloride can damage the liver, lungs, and kidneys. Other animal studies suggest that long-term inhalation exposure to vinyl chloride may damage the sperm and testes and cause high blood pressure during pregnancy. Studies using pregnant animals show that breathing high levels (2-500 ppm) of vinyl chloride may harm their unborn offspring. Animal studies also show that vinyl chloride may cause increased numbers of miscarriages early in pregnancy. It may also cause decreased weight and delayed skeletal development in fetuses. The effects of drinking high levels of vinyl chloride are unknown. The MRL was derived from a LOAEL value of 0.018 mg/kg/day for an increased incidence of areas of cellular alteration in the livers of rats.
Results from several studies suggest that breathing air or drinking water containing low levels of vinyl chloride may increase the risk of developing cancer. Hepatic angiosarcomas in Sprague-Dawley rats were observed at doses approximately 3,000 times greater than doses estimated for persons chronically exposed to the highest vinyl chloride detection in well BOW37. Studies of workers who have been exposed to vinyl chloride over many years also indicate increased incidences of angiosarcoma of the liver. Brain, lung, and some blood cancers may also be attributed to chronic inhalation exposure to vinyl chloride. Studies of long-term exposure in rats indicate that increases in liver and mammary gland cancer may occur at very low levels of exposure in the air (5-250 ppm). The Department of Health and Human Services, International Agency for Research on Cancer, and EPA have determined that vinyl chloride is a human carcinogen.
EPA is currently reassessing vinyl chloride's carcinogenicity, and has thus removed the oral slope factor. However, for this health consultation, the former oral slope factor of 1.9 was used to estimate the excess cancer risk due to exposure to this compound. The estimated increased cancer risk, assuming chronic exposure to the maximum concentration of vinyl chloride in drinking water from well BOW37, is approximately 6 additional cancers per 100,000 persons exposed from childhood through adulthood, and approximately 4 additional cancers per 100,000 persons exposed as an adult (very low increased cancer risk).(1) The estimated doses for both the child through adult and adult exposure scenarios are below the less serious LOAEL for oral exposure, indicating that exposure to the maximum detected concentration of vinyl chloride is not expected to result in adverse non-cancer health effects.
Child Health and Developmental Effects
Various epidemiological studies have reported an association between exposure to inorganic arsenic and increased risk of adverse developmental effects (congenital malformations, low birth weight, spontaneous abortions), both by the inhalation and oral routes of exposure. In these studies, however, other chemicals may have contributed to the observed effects. Animal studies, however, do support the view that arsenic is a developmental toxicant, causing a reduced birth weight, a variety of fetal malformations (skeletal and soft tissue), and increased fetal mortality. These data suggest that although inorganic arsenic is a developmental toxicant, the developing fetus is not especially susceptible, and teratogenicity or fetotoxicity are unlikely to be of concern except at doses that are also toxic to the pregnant female (i.e., doses several orders of magnitude greater than the doses estimated from exposure to arsenic from well BOW31A).
Although developmental effects resulting from the ingestion of arsenic in drinking water have not been extensively investigated, there is no convincing evidence that ingestion of arsenic, at least at the levels encountered in drinking water wells near the Bainbridge Island Landfill site, causes developmental toxicity in children.
As indicated above, the most sensitive toxic effect of lead poisoning is believed to be impaired development of the central nervous system in children. It appears that some of the adverse health effects, particularly changes in the levels of certain blood enzymes and in aspects of children's neurobehavioral development, may occur at blood lead levels so low as to be essentially without a threshold.
It is recognized that neonates (from birth to 6 weeks) may be at increased risk of toxicity resulting from exposure to manganese because of a higher level of uptake from the GI tract and a decreased ability to excrete absorbed manganese. However, very little information exists on the developmental effects of manganese. The incidence of neurological disorders and the incidences of birth defects and stillbirths were elevated in a small population of people living on an island where there were rich manganese deposits. However, the lack of exposure data, the small sample sizes, and the absence of a suitable control group precludes associating these effects to manganese. The route of exposure was assumed to be primarily oral, but inhalation exposure was not ruled out. No studies were located regarding developmental effects in animals after oral exposure to manganese.
No human or animal studies were located regarding developmental or reproductive effects following oral exposure to vinyl chloride. However, some data suggests that fetuses, infants, and young children may be particularly susceptible to the toxic effects of vinyl chloride. Vinyl chloride can cross the placenta and enter the blood of fetuses. Developmental effects have been observed as a result of parental exposures to vinyl chloride in the air. A statistically significant increase in birth defects was observed in three cities in which facilities using vinyl chloride were located when compared to statewide and county wide averages. The greatest increases were malformations of the central nervous system, upper digestive tract, genital organs, and in the incidence of club foot.
Results of animal inhalation studies indicate that vinyl chloride produces developmental effects at concentrations that are also toxic to maternal animals. Maternal toxicity was evidenced by decreased food consumption, decreased body weight, and increased mortality. Delayed ossification was noted in fetuses at 500 ppm. Vinyl chloride exposed rats throughout gestation showed an increased incidence of hemorrhages, increased edema, decreased hemoglobin and leukocytes and decreased organ weights. However, doses at which developmental effects were observed were several orders of magnitude higher than estimated doses resulting from exposure to vinyl chloride from well BOW37.
1. A review of Health District records indicate that BOW37 was initially drilled as a private well in 1976. County Assessor records indicate that homes were built and connected to the water supply in 1983, 1986, and the mid 1990s. As a result, estimated exposures, and thus risk, would be even less than this since a 30-year exposure duration was assumed for this health consultation.