This case underscores the potential hazards of consuming groundwater from private wells. It emphasizes the need to test drinking water for a wide range of potential contaminants. Specifically, it documents the potential for significant residential exposure to naturally occurring uranium in well water. The case also highlights the special sensitivity of young children to environmental exposures in the home—a reflection of the large amount of time young children spend in their homes, their developmental immaturity, and the large volume of water they consume relative to their body mass.
Uranium is a commonly occurring radioactive mineral. It is found naturally in geologic formations such as the Brookfield Gneiss. In the formation of metamorphic rock, uranium is distributed very unevenly. It typically deposits in areas of low pressure and irregular cracks. Therefore, concentrations can vary significantly within a small area. The level of uranium that appears in drinking water depends on the flow of water through complicated fracture networks within the rock, as well as on the pH, calcium content and other characteristics of groundwater. For these reasons, concentrations of uranium in closely adjoining wells may be quite different, as was seen in this case. This pattern of significant local variability in concentrations of uranium has been observed in various locations across North America (Natural Resources Canada 2005
). Given the unpredictability of uranium concentrations in at-risk areas, testing of well water for the presence of uranium at the time of drilling a new well or the sale or transfer of a property with an existing well is a reasonable measure (ATSDR 1999
Uranium can enter the body via inhalation as well as through consumption of contaminated food or water (Mao et al. 1995
). Dermal absorption is seen principally in the instance of military veterans who have been exposed to munitions containing depleted uranium and suffered puncture wounds (Bleise et al. 2003
). Ingested uranium is absorbed from the digestive tract and appears initially in the blood, bound to red blood cells. Most is excreted via urine and feces, and experimental studies in humans have shown that about two-thirds of an injected dose of uranium is excreted within the first 24 hr and 75% within 5 days (Taylor and Taylor 1997
). Retained uranium accumulates initially in the kidneys and liver and then in the skeleton (Li et al. 2005
). Approximately 50–60% of stored uranium in the human body is found in the skeleton (Fisenne and Welford 1986
). The biological half-life of uranium in the skeleton is approximately 300 days. The amount of uranium present in skeletal tissue is proportional to cumulative absorption (Hursh and Spoor 1973
Uranium has the potential to be both chemically and radiologically toxic, but of principal concern in the context of ground-water exposure are the chemical toxic effects of uranium on the kidneys. The most extensive data on the human toxicity of uranium come from studies conducted on workers occupationally exposed in the nuclear industries (Thun et al. 1985
); these studies demonstrated increased excretion of beta-2-microglobulin with increasing duration of exposure to uranium. Investigations of Gulf War veterans exposed to depleted uranium did not find clinically significant abnormalities in renal function, but did demonstrate that mean concentrations of microalbumin were significantly elevated in the group exposed to high levels of uranium (Harley et al. 1999
; Squibb et al. 2005
). There is also evidence that uranium may cause toxic effects in bone (Kurttio et al. 2005
The pathophysiologic consequences of the proximal tubular injury associated with exposure to uranium include decreased ability to reabsorb water and small molecules, as is evidenced by the presence of elevated levels of the low-molecular-weight protein beta-2-microglobulin in the urine (Kurttio et al. 2002
; Mao et al. 1995
; Zamora et al. 1998
;). Another marker for proximal tubule damage—increased fractional excretion of calcium and phosphate—has been observed to increase in dose-related manner after chronic ingestion of water containing uranium; this change has been observed in the absence of any increase in urinary beta-2-microglobulin to creatinine ratio (Kurttio et al. 2002
). There appears to be no clear threshold for these pathophysiologic changes, and they typically become evident before any histopathologic evidence of injury is manifest (Kurttio et al. 2002
). The severity of the tubular injury caused by uranium exposure has been shown in rat experiments involving relatively high-dose exposures to range from mild proximal tubular dysfunction to tubular necrosis (Haley 1982
Although specific studies on the nephrotoxic effects of uranium in children have not been conducted, it is reasonable to assume that children would be at increased risk for adverse effects from exposure compared with adults. Children consume more water and food per kilogram of body weight than do adults () (Ershow and Cantor 1989
; National Research Council 1993
). Thus children will ingest proportionately greater quantities of any contaminants that are present in the water or food that they consume. For example, the 3-year-old girl in this case series who manifested elevated urinary excretion of beta-2-microglobulin was reported to derive a major portion of her nutritional intake from infant formula that was prepared by mixing powdered formula with contaminated well water.
Terminal differentiation and maturation of the kidneys and other organ systems occur postnatally, and these developing organs are especially vulnerable to the effects of toxic chemical exposures (National Research Council 1993
). Recent studies suggest that chronic uranium exposure is associated with increases in blood pressure (Kurttio et al. 2006
). The long-term significance of these changes is unclear. However, children’s long future life expectancy further places them at increased risk of delayed adverse health effects that may develop years or decades after exposure in early life to uranium or other chemical contaminants in drinking water.
Because of its radioactivity, concern has arisen about the possible carcinogenicity of uranium. However, the levels of uranium that have been observed to induce nephrotoxicity are much lower than those that increase risk of cancer, and uranium intake from contaminated water has not been associated with increased risk of human cancer (Auvinen et al. 2002
; Boice et al. 2003
; Kim et al. 2004
; Kurttio et al. 2002
). A recent study that examined a cluster of childhood leukemia cases in Fallon, Nevada, found that the town had levels of uranium above or greatly above the maximum contaminant level. However, the children in Fallon with leukemia did not have a higher exposure to uranium than children without leukemia (Seiler 2004
Although levels of arsenic, radium, and radon were elevated in the index family’s water supply, none of these substances are known to have nephrotoxic effects.
In summary, this case series demonstrates the potential for significant residential exposure to naturally occurring uranium in groundwater. It underscores the hazards of consuming groundwater from untested private wells (U.S. EPA 2006
). It confirms previous epidemiologic studies showing that chronic, low-level exposure to uranium in drinking water may result in mild injury to the proximal renal tubule (Kurttio et al. 2002
). It highlights the special sensitivity of young children to environmental exposures (National Research Council 1993
). Public health organizations should take the unique exposures and the special vulnerability of children into consideration when setting standards for uranium and other chemical contaminants in drinking water.