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PUBLIC HEALTH ASSESSMENT

ROCKY MOUNTAIN ARSENAL
ADAMS COUNTY, COLORADO


APPENDIX A:

ATSDR PUBLIC HEALTH HAZARD CONCLUSION CATEGORIES
CategoryDefinitionCriteria
A. Urgent public health hazard This category is used for sites that pose an urgent public health hazard asthe result of short-term exposures to hazardous substances.
  • evidence exists that exposures have occurred, are occurring, or are likely to occur in the future AND
  • estimated exposures are to a substance(s) at concentrations in the environment that, upon short-termexposures, can cause adverse health effects to any segment of the receptor population AND/OR
  • community-specific health outcome data indicate that the site has had an adverse impact on human health thatrequires rapid intervention AND/OR
  • physical hazards at the site pose an imminent risk of physical injury.
  • B. Public health hazardThis category is used for sites that pose a public health hazard as theresult of long-term exposures to hazardous substances.
  • evidence exists that exposures have occurred, are occurring, or are likely to occur in the future AND
  • estimated exposures are to a substance(s) at concentrations in the environment that, upon long-termexposures, can cause adverse health effects to any segment of the receptor population AND/OR
  • community-specific health outcome data indicate that the site has had an adverse impact on human health that requires intervention.
  • C. Indeterminate public health hazardThis category is used for sites with incomplete information.
  • limited available data do not indicate that humans are being or have been exposed to levels of contaminationthat would be expected to cause adverse health effects; data or information are not available for allenvironmental media to which humans may be exposed AND
  • there are insufficient or no community-specific health outcome data to indicate that the site has had an adverse impact on human health.
  • D. No apparent public health hazardThis category is used for sites where human exposure to contaminatedmedia is occurring or has occurred in the past, but the exposure is belowa level of health hazard.
  • exposures do not exceed an ATSDR chronic MRL or other comparable value AND
  • data are available for all environmental media to which humans are being exposed AND
  • there are no community-specific health outcome data to indicate that the site has had an adverse impact on human health.
  • E. No public health hazardThis category is used for sites that do not pose a public health hazard.
  • no evidence of current or past human exposure to contaminated media AND
  • future exposures to contaminated media are not likely to occur AND
  • there are no community-specific health outcome data to indicate that
    the site has had an adverse impact on human health.
  • APPENDIX B: DISCUSSION OF TOXICOLOGIC EVALUATION
    FOR TABLES 13 AND 14

    TABLE 13 - Alluvial/Unknown Aquifer Contaminants

    Specifically created for individual well owners, this appendix contains an evaluation of every chemicalfound in drinking water wells at a concentration detected above ATSDR's comparison values. Out ofthe hundreds of drinking and domestic wells currently in use and monitored regularly for RMA andnon-RMA contaminants, 23 wells have been identified that produce water containing nitrate or lead atlevels of public health concern (see Table 19). Local health officials have notified the users ofcontaminated wells of the possible health effects that might occur from continued use. The availableevidence indicates that Rocky Mountain Arsenal is not the source of those contaminants. The lead inthe water could be from several sources such as naturally occurring lead in the groundwater or leadcontamination in plumbing. The nitrate could be traced to many sources such as agriculturalfertilizers, animal wastes, or private on-site sewage disposal systems. There are also some wells inwhich RMA contaminants are detected, but the levels of contamination are not of public healthconcern. Private drinking water wells to the north and northwest will continue to be monitored forboth RMA and non-RMA sourced contaminants, and when a well is sampled, the results will becommunicated to the well users. An evaluation of contaminants listed previously in Tables 13 and 14 follows.

    Wells judged to contain contaminants at levels of public health concern are identified by well numberand specific contaminant and recommended actions are discussed in the Recommendations section ofthis Assessment. The section contains evaluations of private wells with a single contaminant andprivate wells with multiple contaminants. The concentrations listed below represented the most recentdetections of contaminants for drinking water wells in the Alluvial/Unknown Aquifer based onRMAED database runs of April 26, 1994 and May 4, 1994; CDPHE database queries of January 5,1994 and May 9, 1994; and Tri-County Health Department database queries of December 20, 1993through May 11, 1994. While the maximum concentrations are being evaluated in this assessment, the present concentrations in the wells may be somewhat higher or lower.

    Note: The first time a chemical appears in this appendix a detailed explanation is provided for howthe chemical concentration was evaluated for potential health effects. Thereafter, shortenedtoxicological discussions appear for that particular chemical.

    PRIVATE WELLS WITH ONLY ONE CONTAMINANT

    Arsenic

    Unspeciated arsenic has been detected in the well water from three wells: 565A, 583A, and 940A.Under the provisions of the Offpost ROD, these three wells qualify for connection to a replacementwater source and thus, the use of these wells may not continue.

    Well 565A, with an arsenic concentration of 5.69 ppb, is used for both drinking and domesticpurposes, whereas well 583A with a concentration of 14.0 ppb and well 940A with a concentration of8.29 ppb are used mainly for domestic purposes. The Maximum Contaminant Level (MCL) forarsenic in drinking water is 50 ppb.

      Drinking Water Well - 565A

    Three people use well 565A for drinking water. A daily dose estimate for water containing 5.69 ppbof arsenic is 0.00016 mg/kg/day for adults and 0.00057 mg/kg/day for children. Arsenic is verypoorly absorbed through the skin and is not a volatile compound (ATSDR, 1993e). Therefore,ingestion of arsenic is the most significant route from exposure to well water. For the U.S. populationin general, the main route of arsenic exposure is ingestion of arsenic-containing food and water(ATSDR, 1990a). The natural background concentration of arsenic (unspeciated) is less than 2.5 ppb in groundwater near RMA.

    ATSDR has established a chronic oral MRL of 0.0003 mg/kg/day for inorganic arsenic, the more toxicform of arsenic. The EPA has established a chronic oral RfD of 0.0003 mg/kg/day for inorganicarsenic. A study of 17,000 individuals exposed to arsenic-contaminated drinking water in Taiwandetermined 0.0005 mg/kg/day as the no-effect level via ingestion (ATSDR, 1993e). In humans,studies have shown that oral doses below 0.001 mg/kg/day are not likely to result in non-canceroushealth effects (ATSDR, 1993e). Because the type of arsenic in this well water is unspeciated and theestimated daily dose for children is just slightly above the MRL, RfD, and no-effect levels, ingestionof the amount of arsenic in the well water from this well is not expected to result in non-canceroushealth effects in adults or children.

    The EPA has classified inorganic arsenic as a known (Class A) human carcinogen via ingestion,because studies have reported development of skin cancers in people chronically exposed to 0.009-0.01 mg/kg/day of arsenic in drinking water (ATSDR, 1993e and ATSDR, 1990a). Some studies haveindicated that long-term ingestion of 0.02 mg/kg/day or higher of arsenic may increase the risk of development of internal tumors in the liver, kidney, bladder, and lung (ATSDR, 1993e, ATSDR,1990a, and TOMES, 1994). Based on the CSF for arsenic, ingestion of the amount of arsenic in thewell water from this well is not expected to result in a significant increase in cancer risk.

      Domestic Water Wells - 940A & 583A

    The levels of arsenic detected in the well water of wells 940A and 583A are 8.29 and 14.0 ppb,respectively. Water from those wells is used mainly for domestic uses (cooking, washing, andbathing). Two people use well 940A, and five people use well 583A.

    A daily dose estimate for water containing 8.29 ppb (well 940A) would be 0.00024 mg/kg/day foradults and 0.00083 mg/kg/day for children. Based on 14.0 ppb (well 583A), a daily dose estimatewould be 0.00040 mg/kg/day for adults and 0.0014 mg/kg/day for children. Ingestion of the amountof arsenic in those wells would not be expected to result in non-cancerous health effects in adults orchildren, even if those wells were used for drinking water. In addition, use of those wells is notexpected to result in a significant increase in cancer risk.

    Atrazine

      Domestic Water Well 373D

    Well number 373D was detected with 4.53 ppb of atrazine. Since the residents served by this wellreceive bottled water, the well is used primarily for domestic purposes. Estimates indicate that 5% ofthe water used is ingested incidentally. According to Table 13, five people use this well. The MCLfor atrazine in drinking water is 3 ppb. Under the provisions of the Offpost ROD, this well qualify forconnection to a replacement water source and thus, the use of this well may not continue.

    Atrazine exposure could occur through ingestion and inhalation of water from the well and fromdermal contact with the water (TOMES, 1994). A daily dose estimate for water containing 4.53 ppbof atrazine is 0.00013 mg/kg/day for adults and 0.00045 mg/kg/day for children. The acceptable dailyingestion intake recommended by the World Health Organization is 0.0215 mg/kg/day (TOMES,1994). EPA has established 0.035 mg/kg/day as the chronic ingestion RfD for atrazine (IRIS, 1994). Therefore, ingestion of, inhalation of, and dermal contact with this level of atrazine are not likely toresult in non-cancerous health effects in adults and children, even if this well water were used fordrinking.

    The EPA has concluded that data from toxicological studies have not indicated that exposure toatrazine through ingestion and inhalation of, or dermal contact with it, causes carcinogenic healtheffects in people (TOMES, 1994).

    Atrazine is currently undergoing review by the EPA, as are other triazines. The potential healtheffects from widespread use of triazine pesticides, including atrazine, is being re-evaluated. If newhealth guidelines are established for atrazine, that value will be used to re-evaluate the concentration ofatrazine in the water from this well.

    Lead

      Domestic Water Wells - 372A, 550A, 602A, & 603A

    Lead has been detected in the well water from four wells: 372A, 550A, 602A, 603A. All four wellsare used mainly for domestic purposes such as cooking, washing, and bathing, since bottled water issupplied to the people using these wells. Under the provisions of the Offpost ROD, all of these wells,except well 550A, qualify for connection to a replacement water source and thus, the use of three ofthese wells may not continue.

    Lead is very poorly absorbed through the skin and does not readily vaporize from water. Therefore,ingestion is a more significant route of exposure than the dermal or inhalation route (ATSDR, 1993e). One resident uses well 372A, 16 use 550A, one uses 602A, and four use 603A. The EPA ActionLevel for lead in drinking water is 15 ppb.

    The source of lead could be from several sources, such as lead contamination in the groundwater orplumbing (lead piping, lead-based solder, and water faucets containing lead). Tea and coffee madewith tap water containing lead may have an increased lead concentration due to evaporation of thewater, particularly if the coffee or tea sits on a hot plate. The natural background levels of lead in thegroundwater near RMA ranges from less than 18.6 ppb to less than 37.2 ppb. The followingconcentrations have been detected above the EPA Action Level of 15 ppb in the wells listed above: 97.0 ppb, in 372A; 65.5 ppb in 550A; 77.1 ppb in 602A; and 65.2 ppb in 603A.

    Most non-cancerous health effects that have been observed in people are based on blood lead levels. Blood lead levels, measured in micrograms per deciliter (µg/dL), are a measure of the amount of leadabsorbed by the body, not the amount of lead detected in water or some other medium (ATSDR,1991). Therefore, daily dose estimates are not included here, because they are not useful in evaluatingthe potential health effects from lead exposure.

    The health effects of lead are not immediately apparent. Once in the blood, lead is distributed to thesoft tissue (kidneys, bone marrow, liver, and brain) and mineralizing tissue (bones and teeth). Bonesand teeth contain about 95% of the total body burden of lead (ATSDR, 1992A; ATSDR, 1993f). It isthe total body burden of lead that is related to the risk of adverse health effects. Because the bodyaccumulates lead over a lifetime and releases it slowly, even small doses of lead over time can causelead poisoning. Further, relatively low blood lead levels can cause adverse health effects, some ofwhich, like decreased IQ or mild behavioral disorders, may not produce noticeable signs or symptoms(CDC, 1991). Those health effects can occur when blood lead levels are < 10 µg/dL in children. Exposure to high levels of lead can badly damage the brain, red blood cells, and kidneys of adults (40- 100 µg/dL) and children (35 - 50 µg/dL). Acute effects of exposure to high lead levels are nausea,vomiting, and headache. Lead exposure in adults may increase blood pressure when blood lead levelsare as low as 7 µg/dL. High levels of blood lead (40 µg/dL) may affect sperm or damage other parts ofthe male reproductive system making it difficult for a couple to have children (ATSDR, 1992a;ATSDR 1993f).

    Unborn babies (fetuses) and children are especially sensitive to the effects of lead. And, when womenare pregnant, lead stored in their bone marrow can enter their blood stream increasing the amount oflead reaching the fetus, resulting in premature birth, low birth weight, and decreased mental ability. Ininfants and young children, lead exposure has been shown to decrease intelligence (IQ) scores, slowtheir growth, and cause hearing problems in cases with blood lead levels less than or equal to 10µg/dL. These effects can persist as children get older and interfere with successful performance inschool (CDC, 1991). Because lead is ubiquitous in the environment, many children have elevatedblood lead levels approaching those believed to cause non-cancerous health effects (ATSDR, 1993fand ATSDR, 1992a). Consumption of drinking water containing 50 ppb of lead would correspond to arise of 10 µg/dL in the blood lead levels of children. But since these are estimates, the increases inblood lead levels may be slightly lower or higher.

    Showering and bathing with the well water from these wells is not expected to result in non-canceroushealth effects. However, because the lead levels in the well water from these wells fluctuated aboveand below the action level of 15 ppb and some of these lead levels are somewhat high, two aspects oflead exposure are of concern. One is exposure, even once, to extremely high levels of lead. Thesecond is intermittent exposure over an extended period of time, e.g., more than a year. Under theseexposure conditions, people can absorb enough lead, even at moderate levels, to raise their bodyburden of lead to levels that might pose health problems. People swallowing lead contaminated waterat the lead levels detected in the wells listed above would not be expected have acute health effects,such as nausea and vomiting, but they could absorb enough lead to cause long-term adverse healtheffects (ATSDR, 1992a). Therefore, based on the lead levels detected in these wells, use of thesewells for drinking (including infant formula) and/or cooking may result in non-cancerous healtheffects in children, infants, pregnant women and their fetuses, and other adults. Because well 550Aapparently does not qualify for a connection to replacement under the provisions of the OffpostROD and because the well also not qualify for continuation on the program for interim supplybottled water, a future pathway of human exposure to elevated levels of lead in drinking watermay be created. This well has not been sampled for lead since 1991 and it is not known if thepresent lead level in this well is at a level of health concern.

    Please see the "More Information on Lead" section below for ways to reduce and stop exposure to leadin drinking water. If you are concerned about your blood lead levels either because of the lead levelsin your drinking water or other possible lead exposure sources, there is a simple medical test availableto screen for blood lead levels. People who are concerned about their exposure to lead should see theirdoctor for more information.

    Certain subgroups of the population may be more susceptible to the harmful effects of lead exposure,besides preschool age children (< 6 years old), pregnant women and their fetuses, and the elderly. Other susceptible people may include those with genetic diseases affecting heme synthesis (acomponent of the blood), nutritional deficiencies (especially iron and calcium), and neurological orkidney dysfunction. Smoking cigarettes and drinking alcohol also may increase the risk of non-cancerous health effects (ATSDR, 1993f).

    Case reports have implicated lead as a potential renal carcinogen in people (ATSDR, 1993f). EPA hasconcluded that human data is inadequate to determine if lead exposure could cause cancerous healtheffects in people. However, using animal studies, EPA has classified lead as a probable (B2) humancarcinogen; although there are sufficient animal studies, there are inadequate human studies that showit causes cancer. Health guidelines for determining possible cancer effects in people exposed to leadhave not been established; therefore, cancerous health effects cannot be evaluated.

    More Information on Lead

    Sources of Lead Exposure

    The major sources of lead released to water are lead plumbing and plumbing solder in houses, schools,and public buildings (ATSDR, 1993f and ATSDR, 1992a). It has been used in the production of sometypes of batteries in industrial settings, and in the production of ammunition and some kinds of metalproducts (such as sheet lead, solder, and pipes). For older wells, the most common use of lead hasbeen in the construction of such wells and associated piping. Some chemicals containing lead, such astetraethyl lead and tetramethyl lead, were commonly used as gasoline additives. The use of these lead-containing chemicals in gasoline have been greatly decreased, because these additives are being phasedout. The amount of lead added to paints and ceramic products, roofing, caulking, ammunition,gasoline additives, and solder has been reduced in recent years because of lead's harmful effects inpeople and animals. Currently, workers may be exposed to lead in a variety of occupations includingsmelting and refining industries, steel welding and occurring operations, battery manufacturing plants,gasoline stations, and radiator repair shops (ATSDR, 1993f).

    You can also be exposed to lead and lead compounds from breathing air and eating soil and foods thatcontain lead. Breathing air with dust that contains lead or swallowing lead-containing soils that mightbe found near areas with heavy automobile traffic are also sources of exposure.

    Adults may also be exposed to lead through occupational exposure which may occur throughplumbing work where lead-base solder and brass fixtures are used. Other sources of occupational leadexposure may be from automobile or mechanical repair operations, battery or radiator reclamation,electronics work, welding, lead-based paints, and lead-containing sheet metal work. Certain hobbiesmay also contribute to your lead exposure such as ceramics, artisan painting, stained glass, and furniture refinishing.

    Children may be exposed to lead by swallowing non-food items such as chips of lead-containing paint. Children who put toys, other items, or their hands in their mouths may also swallow lead if lead-containing dust and dirt are on these.

    EPA Recommendations

    The EPA Office of Drinking Water has established 15 ppb as an action level for lead in drinking water(EPA, 1991). For children and adults drinking 1-14 ppb of lead, no action is necessary. For childrenand pregnant women, private well water with lead at 15 ppb or greater should stop drinking the waterand/or using it for cooking. Adults drinking well water with 15 to 50 ppb should try to reduce theirexposure. For adults drinking well water greater than 50 ppb, they should stop drinking the water andstop using it for cooking.

    Additional Health Information

    Lead toxicity greatly depends on the route of exposure. Lead must be absorbed into the body toproduce toxic effects, and the degree of absorption varies according to the route of exposure. Exposure by inhalation results in the greatest amount of absorption. Once deposited in the lowerrespiratory tract, lead is almost completely absorbed into the body. Absorption from contaminatedsources that are ingested appears to be low; however, gastrointestinal absorption depends on age. Absorption following oral exposure in children is approximately 50% compared with 15% in adults(ATSDR, 1993f), partially accounting for the increased sensitivity of children. In general, the skinacts as a barrier to lead absorption. Dermal absorption of inorganic lead compounds is much lesssignificant than absorption by inhalation (which would be most significant in the workplace) oringestion routes of exposure (ATSDR, 1993f). However, organic lead (tetraethyl lead) may beabsorbed through the skin. Regardless of the route of exposure, once lead is absorbed into the body, the biologic effects are similar.

    The interplay of lead metabolism and the physiologic status of the exposed person, especiallynutritional well-being, figure prominently in the level of lead exposure required to produce effects andindications of toxicity. A number of nutritional factors suppress lead absorption and toxicity inhumans (ATSDR, 1988c). Iron, calcium, and zinc status are inversely related to lead absorption. Generally, defects in nutrition enhance lead absorption/retention, and therefore, toxicity risk.

    Many small exposures to lead can result in chronic toxicity because lead tends to accumulate in bodytissues, especially bone. It is the total body burden of lead that is related to toxicity. Duringpregnancy or in the presence of chronic disease, lead stored in bone tissue can be released and increaseconcentrations of lead in the blood (ATSDR, 1993f).

    The most sensitive target of lead poisoning is the nervous system. The effects in children werediscussed earlier. However, central nervous system effects in adults include subtle behavioral changes,fatigue, and impaired concentration. Peripheral nervous system damage is observed, primarily inadults, as a peripheral neuropathy with mild slowing of nerve conduction velocity. Those effectsPeripheral neuropathies have been observed at blood lead concentrations of 40 µg/dL (ATSDR, 1992a).

    Lead has profound noncancerous effects on human reproduction. Men with blood levels greater than50 µg/dL from occupational exposure had adverse reproductive effects including decreasedprostate/seminal vesicle function, lowered semen volumes, and lower function maturity of sperm(ATSDR, 1992a). An increased likelihood of miscarriage has been associated with occupational leadexposure in pregnant women: Nordstrom et al. (1979) found an increased frequency of miscarriagesin women living near or working at a lead smelter.

    The fetus has no metabolic or anatomic barrier to lead. Lead absorbed by pregnant women cantransfer to the fetus via the placenta; therefore, exposure of pregnant women to lead is unsafe for thefetus. Uptake may occur during the entire pregnancy, including during development of the fetalnervous system and other target organs of lead toxicity. Developmental consequences of prenatalexposure to lead include premature birth, decreased birth weight, and neurobehavioral deficits(ATSDR, 1988c).

    Exposure to lead could result in non-cancerous hematologic effects. The threshold blood level for adecrease in hemoglobin is estimated to be 50 µg/dL for adults and 40 µg/dL for children (ATSDR,1993f). Lead can induce two types of anemia. Hemolytic anemia has been associated with acute,high-concentration lead poisoning. Chronic lead poisoning induced anemia by interfering witherythropoiesis and by diminishing red blood cell survival (ATSDR, 1992a). Anemia is not an earlyeffect of lead poisoning; it is evident only after prolonged periods of significantly elevated blood leadconcentrations.

    Occupational and general population studies provide strong evidence that a statistically significantassociation exists between blood lead levels and hypertension (ATSDR, 1993f). The association ismost evident in men 40-59 years old and is seen with blood lead levels as low as 7 µg/dL. A meanincrease in systolic blood pressure of 1.0 to 2.0 mm Hg appears to result from every doubling in bloodlead levels in men 40-59 years old; the increase is somewhat less in adult women.

    Ways to Reduce Lead Exposure

    Short-term remedies you can take individually to reduce the lead concentrations in your drinking waterand thus your exposure to lead are included below. You cannot see, taste, or smell lead in yourdrinking water, so it is important to perform these precautionary steps, especially if there is a concernabout lead in your drinking water.

    If the source of lead is the plumbing:
    Let the water run from the tap for 30 seconds to two minutes before using it for drinking and cooking. The longer water stays in water pipes, the more lead it may contain. Water that has been in the pipesfor more than four hours should be flushed for three to five minutes, for example, first thing in themorning and when you arrive home in the evening. A good indication of when to stop flushing thecold water tap is when the water becomes noticeably colder. Use cold water for cooking or makinginfant formula because water from the hot water tap dissolves lead more quickly, which will causelead concentrations to be higher in hot water.

    If the source of lead is the groundwater or aquifer:
    If a water sampling test for lead indicates that your tap water contains lead in excess of 15 ppb evenafter flushing, then you may want to consider taking the following additional measures. You maychose to use bottled water instead of tap water for drinking or cooking purposes, or you may chose touse a water purification system. Purification systems range in size and cost from the water pitcherfiltration systems to purification systems for the entire household.

    Nitrate

    By April 1994 nitrate was detected in the well water from 12 wells: 331A, 332B, 332D, 456A, 541A,547A, 739A, 969A, 973A, 981A, 1276A, and 1305A. The most likely sources of nitrates detected inthose wells would be nearby farms, stockyards, and septic sewer systems north of RMA. Aspreviously noted, the concentration of nitrate in these Offpost wells varies over time and the level ofnitrate contamination has been decreasing with time. By June 1996 no drinking water well in thisarea contained nitrate at levels greater than the 10,000 ppb MCL. In addition, all of these wells,except well 547A, qualify for connection to a replacement water supply and use of these wells may notcontinue.

    Most of these wells are each used by 3 people. However, wells 332B, 332D, 456A, and 1305A areeach used by 2 people, and four people use well 981A. Well 1276A is used by 6 people.

      Drinking Water Wells - 456A, 739A, 973A, & 1276A

    Because the residents of houses served by these wells are not on the bottled water program, the wellsare being used for both domestic and drinking water purposes. Of those wells the maximumconcentration of nitrate detected was 24,000 ppb in well 1276A. If nitrate levels had remained atthe pre-1994 levels, the following health conditions would apply.

    A daily dose estimate for water containing 24,000 ppb nitrate is 0.69 mg/kg/day for adults and 2.40mg/kg/day for children. Nitrate exposure could occur through ingestion of and dermal contact withwater containing nitrate (ATSDR, 1991; IRIS, 1994; and TOMES, 1994). Chronic ingestion of morethan 5 mg/kg/day is considered unacceptable for adults and children (TOMES, 1994). EPA hasestablished a chronic RfD of 1.6 mg/kg/day for ingestion of nitrates (IRIS, 1994 and ATSDR, 1991). Although the estimated dose for children is slightly higher than the RfD, non-cancerous health effectsare not expected in adults and children who ingest this well water.

    Neither level (5.0 or 1.6 mg/kg/day) is acceptable for infants under 6 months of age, because infantsare more susceptible to nitrate exposure than older persons (TOMES, 1994). For example, ingestionof nitrate ranging from 1 mg/kg/day to 15.5 mg/kg/day in 111 infants less than 6 months old wasassociated with increased methemoglobin levels (i.e., the mean methemoglobin level was measured tobe 1.6 percent, with the highest level being 5.3 percent), although none of the children had the typicalsymptoms of methemoglobinemia (Winton, Tardiff, and McCabe, 1971). Nitrates in well water usedto prepare infant feeding formula have been implicated as causing significant (but unspecified) illnessin children at 90,000 ppb (Comly, 1987). Therefore, using these wells at pre-1994 nitrate levels formaking infant formula might result in non-cancerous health effects in infants, especially those undersix months of age. This would also include the fetuses of pregnant women.

    In pregnant women, the level of methemoglobin increases from the normal (0.5% to 2.5% of totalhemoglobin) to a maximum of 10.5% at the 30th week of pregnancy and subsequently declines tonormal after delivery. Thus, pregnant women could be more sensitive to the induction of clinicalmethemoglobinemia by nitrites or nitrates at or near the 30th week of pregnancy (ATSDR, 1991, p. 5). For pregnant women, using these wells at pre-1994 nitrate levels for drinking or cooking might resultin non-cancerous health effects.

    The EPA has concluded that data from toxicological studies do not indicate that ingestion andinhalation of or dermal contact with nitrate or nitrite cause carcinogenic health effects in people(ATSDR, 1991, p. 8 and TOMES, 1994).

    Inhalation of nitrates is expected to be negligible from nitrate-contaminated water. Although nitratesmay be absorbed through the skin, dermal exposure cannot be assessed because little information wasfound pertaining to this route of exposure (ATSDR, 1991, p. 3 and TOMES, 1994). People who areconcerned about their exposure to nitrates should see their doctors for more information.

      Domestic Water Wells - 331A, 332B, 332D, 541A, 547A, 969A, 981A, & 1305A

    These wells are being used mainly for domestic purposes, because bottled water is supplied to theresidences with these wells. All of these wells, except well 547A, qualify for connection to areplacement water supply and use of these wells may not continue. If nitrate levels had remained atthe pre-1994 levels, the use of these wells for drinking (including infant formula) and/or cooking mayresult in non-cancerous health effects in infants and pregnant women and their fetuses.

    More Information on Nitrates/Nitrites

    Nitrate, a non-RMA sourced contaminant commonly found in rural farming areas, has been detected inmost Offpost Study Area private wells (see Tables 5A, 5B, 13, 14, and 17), generally north of RMA. The most likely source of nitrates in those wells would be, not from RMA, but from the farms,stockyards, and septic sewer systems north of RMA (ATSDR, 1991, p. 2). Two principal sources cancause elevation of the concentrations of nitrates in drinking water: 1) nitrogenous waste matter fromhumans or from dairy cattle or other livestock or poultry and 2) nitrogenous fertilizers, especiallythose used in irrigated farming. The nitrates used in nitrogen-based fertilizers (including such materialas anhydrous ammonia, which can be converted in the soil to nitrates) can seep into the groundwaterand contaminate it (Goldsmith, 1991, p. 148). Shallow, rural domestic wells (wells less than 100 feetdeep) are most likely to be contaminated with nitrates, especially in areas where nitrogen-basedfertilizers are in widespread use. During spring melt or drought conditions, both domestic wells andpublic water systems using surface water, or wells that are shallow, may have increased nitrateconcentrations (ATSDR, 1991, p. 2).

    In humans, ingested nitrate is rapidly absorbed from the proximal small bowel and distributedthroughout the body. Nitrate enters the large bowel from the blood and is rapidly converted to highlyreactive nitrite, in part by fecal microorganisms. Nitrates are rapidly converted in the liver todenitrated metabolites and inorganic nitrites, which are then excreted in the urine. Approximately60% to 70% of an ingested nitrate dose is excreted in urine within the first 24 hours. About 25% isexcreted in saliva through an active blood-nitrate transport system and could be reabsorbed. Half-livesof parent nitrate compounds are usually less than 1 hour; half-lives of metabolites range from 1 hour to8 hours (ATSDR, 1991, p. 6).

    While vegetables seldom are a source of acute toxicity, they account for more than 70% of the nitratesin a typical human diet. Cauliflower, spinach, collard greens, broccoli, and root vegetables such asbeets and carrots have naturally greater nitrate contents than other plant foods. The remainder of thenitrate in a typical diet comes from drinking water (approximately 21%) and from meat and meatproducts (approximately 6%) in which sodium nitrate is used as a preservative and color-enhancer(ATSDR, 1991, p. 2).

    Excess exposure to nitrates can produce methemoglobinemia, a disease in which oxygen is notproperly transported in the blood, resulting in an intermittent bluish discoloration. Throbbingheadache, nausea, vomiting, diarrhea, and irregular heartbeat are common symptoms of nitrateexposure. Other symptoms range from mild dizziness and lethargy to coma and convulsions. However, nitrate concentrations that produce methemoglobinemia and those symptoms are unknown(ATSDR, 1991, pp. 7 and TOMES, 1994). Symptomatic methemoglobinemia has occurred inchildren who have eaten sausage heavily treated with nitrates and nitrites. For infants, the majorsource of nitrate exposure is nitrate-contaminated drinking water used to dilute formula (ATSDR, 1991, p. 2).

    The conventional approach of boiling water to destroy microorganisms is not a safe practice whennitrate contamination is suspected; evaporation actually increases the nitrate concentration. Increasednitrate levels have been associated with increased levels of coliform bacteria. Water treatmenttechnologies (ion exchange resins or reverse osmosis) used to remove nitrate from water are notadequate to remove other associated contaminants, especially coliform bacteria. Private wells shouldbe tested annually for nitrate concentration (ATSDR, 1991, p. 14).

    PRIVATE WELLS WITH MULTIPLE CONTAMINANTS

    In this section, 14 wells affected by multiple contaminants are discussed. Six wells in that group(338A, 373D, 594A, 608A, 614A, and 967A) do not contain nitrate. The sampling completed byApril 1994 indicated that eight of the 14 wells contained levels of lead and nitrate that mayindividually result in non-cancerous health effects. When both lead and nitrate are present in a well,the potential for additive effects exists. Our evaluation determined that no interaction of the two isexpected to occur, because the concentrations of lead required to add to the effects that nitrate maycause are not high enough. Therefore, additional non-cancerous health effects are not expected fromsimultaneous exposure to the levels of nitrate and lead detected in those wells.

    Evaluating multiple chemical exposure is difficult, but we have attempted to evaluate exposure tomultiple chemicals when similar mechanisms of action (biological and chemical) and/or healthoutcomes are known to occur. It is rare that this information is known; therefore, evaluation of multiple exposures is complex.

    Wells 338A, 594A, 608A, 614A, and 967A contain multiple contaminants (refer to Table 13). All ofthese wells, except well 967A, qualify for connection to a replacement water source and use of thesewells may not continue. Evaluation of those individual contaminants indicates that no adverse healtheffects are expected from the use of those wells, even if they are used for drinking and other domesticpurposes. And, a discussion of the chemicals detected in those wells is evaluated elsewhere in thissection. Therefore, further discussion of those wells does not appear in this section.

    Any well judged, in the absence of bottled water or connection to a replacement water source, tocontain chemical concentrations of public health concern will be identified by well number andspecific contaminant. Recommended actions for such wells will then be subsequently discussed in theRecommendations section of this Assessment.

    Well 540A

    Well 540A was detected to have chloroform (8.34 ppb), PCE (2.16 ppb), lead (92.6 ppb), and nitrate(26,000 ppb). Since users of the well receive bottled water, the water from this well is used fordomestic purposes only. Estimates indicate that 5% of the water used from the well might be ingested. According to Table 13, 72 people (residents of a trailer court) use this well. The MCL for chloroform,PCE, and nitrate in drinking water are 100, 5, and 10,000 ppb, respectively. The EPA Action Levelfor lead in drinking water is 15 ppb.

    Chloroform has been detected in this well. Ingestion or inhalation of water containing chloroform, ordermal contact with such water could result in exposure. Inhalation is considered to be just assignificant as ingestion (ATSDR, 1993h). A daily dose estimate for water containing 8.34 ppb ofchloroform is 0.00024 mg/kg/day for adults and 0.00083 mg/kg/day for children. ATSDR's chronic,oral MRL for chloroform is 0.01 mg/kg/day (ATSDR, 1993h), and EPA's chronic oral RfD forchloroform is 0.01 mg/kg/day (IRIS, 1994). Ingestion and inhalation of and dermal contact with thisconcentration of chloroform are not likely to result in non-cancerous health effects in adults or children, even if this well were used for drinking.

    According to the EPA, ingested or inhaled chloroform is a B2 (probable) human carcinogen. B2 carcinogens are those substances judged by the EPA to have sufficient animal studies, but inadequateor no human studies to show that a substance causes cancer. Ingestion and inhalation of the level ofchloroform detected in this well would not pose a significant increase in cancer risk, even if this wellwere used for drinking and if this level were chronically inhaled. Evidence associating dermalexposure to chloroform with cancer in people has not been established (ATSDR, 1993h and IRIS, 1994).

    Although no adverse health effects are expected from exposure to chloroform in this well, individualsconcerned about their exposure to chloroform can dramatically reduce, through the following actions,indoor air exposure to and ingestion of VOCs, such as chloroform, present in well water used fordrinking, cooking, showering, and other such household activities:

    • Minimize the use of hot water, using warm or cool water rather than hot whenever possible. Hot water causes compounds such as chloroform to vaporize more rapidly.
    • Ventilate any area in which hot water is being used (e.g., laundry room, dishwashing areas).
    • Use a coarse spray rather than a fine spray setting on shower heads.
    • Use a slower flow rate shower head.
    • Limit showering and bathing to less than 15 minutes.
    • Ventilate bathroom before, during, and after showering or bathing (Otto, 1990, p. 73).
    • Use commercial laundries for washing clothes whenever possible. Otherwise, close off and ventilate the area between the laundry area and living area during and after use.
    • Use alternative water supplies for all purposes (drinking, bathing, laundering, etc.) to the extent possible.
    • Avoid contaminated water for home humidifiers or vaporizers.
    • Install a point-of-entry water treatment system.
    • Hook up to the existing municipal water system.

    Tetrachloroethylene (TCLEE or PCE) was detected at 2.16 ppb in this well. Ingestion or inhalationof water containing PCE or dermal contact with it could result in PCE exposure. A daily doseestimate for water with this amount of PCE would be 0.000062 mg/kg/day for adults and 0.00022mg/kg/day for children. ATSDR's intermediate, oral MRL is 0.1 mg/kg/day (ATSDR, 1993g), andEPA's chronic, oral RfD is 0.01 mg/kg/day (IRIS, 1994). Ingestion and inhalation of and dermalcontact with 2.76 ppb of PCE in this well are not likely to cause non-cancerous health effects in adults or children, even if this well were used for drinking.

    According to the EPA, PCE via ingestion and inhalation is a B2-C carcinogen; it is being consideredfor placement into either the B2 or the C cancer group. The EPA considers B2 carcinogens probablehuman carcinogens; while animal studies indicate that they cause cancer, there are not adequate humanstudies to confirm that finding. C Carcinogens are those substances for which no human studies, andonly limited animal studies, exist to indicate that they cause cancer. The level of PCE detected in thiswell (even if used for drinking) would not result in a significant increase in cancer risk. There is noestablished evidence associating dermal exposure to PCE with cancer in people (ATSDR, 1993g and IRIS, 1994).

    Lead has been found at a concentration of 92.6 ppb. Bottled water is supplied to the residents who usethis well, therefore, this well is being used mainly for household activities such as showering, cooking,and bathing. Using this well for showering and bathing is not expected to result in non-canceroushealth effects. This well qualifies for replacement to an alternative source of water.

    Nitrate Prior to April 1994, nitrate was detected in this well at a maximum concentration of 26,000ppb. Although this well is mainly used for domestic purposes, nitrate exposure could occur throughingestion of and dermal contact with water from this well (ATSDR, 1991; IRIS, 1994; and TOMES,1994). A daily dose estimate for water containing 26,000 ppb nitrate is 0.74 mg/kg/day for adults and2.60 mg/kg/day for children. Ingestion of the level of nitrate detected in this well is not expected toresult in non-cancerous health effects in adults and children, even if this well is used for drinking. However, using this well at pre-1994 nitrate levels for drinking (including infant formula) and cookingmay result in non-cancerous health effects in infants and pregnant women and their fetuses.

    Well 551A

    Lead was detected in well 551A at a concentration of 100.0 ppb and nitrate at a concentration of12,000 ppb. The residence served by this well receives bottled water, so this well is mainly used fordomestic purposes. Five residents use this well. This well qualifies for connection to a replacementwater supply and use of the well may not continue. The EPA Action Level for lead in drinking wateris 15 ppb. The MCL for nitrate in drinking water is 10,000 ppb.

    Lead has been found at a concentration of 100.0 ppb. Bottled water is supplied to the residents whouse this well, therefore, this well is being used mainly for household activities such as showering,cooking, and bathing. Using this well for showering and bathing is not expected to result in non-cancerous health effects. However, cooking with and/or drinking water from this well (includingusing the water to make infant formula) might result in non-cancerous health effects in children,infants, pregnant women and their fetuses, and other adults given the lead level in this well water andthe possibility for additional lead exposure that might occur from the environment and workplace.

    Nitrate has been detected in this well at a concentration of 12,000 ppb. Although this well is mainlyused for domestic purposes, nitrate exposure could occur through ingestion of and dermal contact withwater from this well (ATSDR, 1991; IRIS, 1994; and TOMES, 1994). A daily dose estimate for watercontaining 12,000 ppb nitrate is 0.34 mg/kg/day for adults and 1.2 mg/kg/day for children. Ingestionof the level of nitrate detected in this well is not expected to result in non-cancerous health effects inadults and children, even if this well is used for drinking. However, using this well water at pre-1994nitrate levels for drinking (including infant formula) or cooking may result in non-cancerous healtheffects in infants and pregnant women and their fetuses.

    Well 578A

    Well 578A was found to have PCE at 1.03 ppb, lead at 119.0 ppb, and nitrate at 14,000 ppb. The residence served by this well is provided with bottled water, so this well is mostly used for domesticpurposes. Five people use well 578A. This well qualifies for connection to a replacement watersource and use may not continue. The MCL for PCE and nitrate in drinking water are 5 and 10,000ppb, respectively. The EPA Action Level for lead in drinking water is 15 ppb.

    PCE was detected in this well at a concentration of 1.03 ppb. Ingestion and inhalation of watercontaining PCE or dermal contact with such water could result in exposure to PCE. A daily doseestimate for water with this amount of PCE would be 0.000029 mg/kg/day for adults and 0.0001mg/kg/day for children. Ingestion and inhalation of, and dermal contact with this amount of PCE arenot likely to result in non-cancerous health effects in adults or children, even if this well were used fordrinking. The level of PCE detected in this well (even if used for drinking) would not result in asignificant increase in cancer risk.

    Lead has been found at a concentration of 119.0 ppb. Bottled water is supplied to the residents whouse this well, therefore, this well is being used mainly for household activities such as showering,cooking, and bathing. Using this well for showering and bathing is not expected to result in non-cancerous health effects. However, cooking with and/or drinking water from this well (includingusing the water to make infant formula) might result in non-cancerous health effects in children,infants, pregnant women and their fetuses, and other adults given the lead level in this well water andthe possibility for additional lead exposure that might occur from the environment and workplace.

    Nitrate has been detected in this well at a concentration of 14,000 ppb. Although this well is mainlyused for domestic purposes, nitrate exposure could occur through ingestion of and dermal contact withwater from this well (ATSDR, 1991; IRIS, 1994; and TOMES, 1994). A daily dose estimate for watercontaining 14,000 ppb nitrate is 0.40 mg/kg/day for adults and 1.4 mg/kg/day for children. Ingestionof the level of nitrate detected in this well is not expected to result in non-cancerous health effects inadults and children, even if this well is used for drinking. However, using this well water at pre-1994nitrate levels for drinking (including infant formula) or cooking may result in non-cancerous healtheffects in infants and pregnant women and their fetuses.

    Well 579A

    Well 579A was found to have PCE at 1.43 ppb, lead at 98.8 ppb, and nitrate at 14,000 ppb. Residentsat this well have not been provided bottled water, so it is presumed that the well water is used for bothdrinking and domestic purposes. Three people use this well. This well qualifies for connection to areplacement water supply and the use of this well may not continue. The MCL for PCE in drinkingwater is 5 ppb and for nitrate is 10,000 ppb. The EPA Action Level for lead in drinking water is 15 ppb.

    PCE was detected in this well at a concentration of 1.43 ppb. Ingestion and inhalation of watercontaining PCE or dermal contact with such water could result in exposure to PCE. A daily doseestimate for water with this amount of PCE would be 0.000041 mg/kg/day for adults and 0.00014mg/kg/day for children. Ingestion and inhalation of, and dermal contact with this amount of PCE arenot likely to result in non-cancerous health effects in adults or children, even if this well were used fordrinking. The level of PCE detected in this well (even if used for drinking) would not result in a significant increase in cancer risk.

    Lead has been found at a concentration of 98.8 ppb in well number 579A. Bottled water is notsupplied to the residents who use this well, therefore, it is presumed that this well is being used fordrinking and other household activities such as showering, cooking, and bathing. Using this well forshowering and bathing is not expected to result in non-cancerous health effects. However, cookingwith and/or drinking water from this well (including using the water to make infant formula) mightresult in non-cancerous health effects in children, infants, pregnant women and their fetuses, and otheradults given the lead level in this well water and the possibility for additional lead exposure that mightoccur from the environment and workplace.

    Nitrate has been detected in well 579A. Since bottled water is not provided, it is presumed that thiswell is used for drinking water and domestic purposes. Nitrate exposure could occur through ingestionof and dermal contact with water from this well. A daily dose estimate for water containing 14,000ppb nitrate is 0.40 mg/kg/day for adults and 1.4 mg/kg/day for children. Ingestion of the level of nitrate detected in this well is not expected to result in non-cancerous healtheffects in adults and children. However, using this well at pre-1994 nitrate levels for drinking(including infant formula) or cooking may result in non-cancerous health effects in infants andpregnant women and their fetuses.

    Well 613A

    Well 613A was found to have PCE at 1.25 ppb, atrazine at 5.81 ppb, and nitrate at 11,000 ppb. Sincebottled water has been provided to these residents, well water is used primarily for domestic purposes. It is estimated that ingestion could take place 5% of the time. Two residents use this well. This wellqualifies for connection to a replacement water source and the use of this well may not continue. TheMCL for PCE, atrazine, and nitrate in drinking water are 5, 3, and 10,000 ppb, respectively. The EPAAction Level for lead in drinking water is 15 ppb.

    PCE was detected in this well. Ingestion and inhalation of water containing PCE or dermal contactwith such water could result in PCE exposure. A daily dose estimate for water containing 1.25 ppb ofPCE would be 0.000036 mg/kg/day for adults and 0.00013 mg/kg/day for children. Ingestion andinhalation of and dermal contact with this amount of PCE are not likely to result in non-canceroushealth effects in adults or children, even if this well were used for drinking. The level of PCE detectedin this well (even if used for drinking) would not result in a significant increase in cancer risk.

    Atrazine has been detected in well water from well 613A. Atrazine exposure could occur throughingestion and inhalation of and dermal contact with water containing atrazine (TOMES, 1994). Adaily dose estimate for water containing 5.81 ppb of atrazine is 0.00017 mg/kg/day for adults and0.00058 mg/kg/day for children. Ingestion of, inhalation of, and dermal contact with atrazine in thiswell are not likely to result in non-cancerous health effects in adults and children, even if this wellwere used for a drinking water supply.

    Nitrate has been detected in well 613A. Since bottled water is not provided, it is presumed that thiswell is used for drinking water and domestic purposes. Nitrate exposure could occur through ingestionof and dermal contact with water from this well. A daily dose estimate for water containing 11,000ppb nitrate is 0.31 mg/kg/day for adults and 1.1 mg/kg/day for children. Ingestion of the level ofnitrate detected in this well is not expected to result in non-cancerous health effects in adults andchildren. However, using this well at pre-1994 nitrate levels for drinking (including infant formula)and cooking may result in non-cancerous health effects in infants and pregnant women and theirfetuses.

    Well 616A

    Well 616A was found to have chloroform at 8.33 ppb, PCE at 1.26 ppb, arsenic at 10.9 ppb, andnitrate at 16,000 ppb. This residence is provided with bottled water, so this well is used mainly fordomestic purposes. Ingestion of the well water is estimated to take place 5% of the time. Six residentsuse this well. This well qualifies for a replacement water source and the use of this well may notcontinue. The MCL for chloroform, PCE, arsenic, and nitrate in drinking water are 100, 5, 50, and10,000 ppb, respectively.

    Chloroform was detected in this well. A daily dose estimate for water containing 8.33 ppb ofchloroform is 0.00024 mg/kg/day for adults and 0.00083 mg/kg/day for children. Ingestion andinhalation of and dermal contact of this concentration of chloroform in this well are not likely to resultin non-cancerous health effects in adults or children, even if this well were used for drinking. Ingestion and inhalation of the level of chloroform detected in this well would not pose a significantincrease in cancer risk, even if this well were used for drinking and if this level were chronically inhaled.

    PCE was detected in this well at a concentration of 1.26 ppb in well 616A. Ingestion and inhalation ofwater containing PCE or dermal contact with such water could result in PCE exposure. A daily doseestimate for water with 1.26 ppb of PCE is 0.000036 mg/kg/day for adults and 0.00013 mg/kg/day forchildren. Ingestion and inhalation of and dermal contact with this amount of PCE are not likely toresult in non-cancerous health effects in adults or children, even if this well were used for drinking. The level of PCE detected in this well (even if used for drinking) would not result in a significantincrease in cancer risk.

    Arsenic has been detected in well 616A at a concentration of 10.9 ppb. Ingestion is the mostsignificant route of exposure from arsenic in this well. A daily dose estimate for water containing thisamount of arsenic is 0.00031 mg/kg/day for adults and 0.0011 mg/kg/day for children. Ingestion ofthe amount of arsenic detected in this well would not be expected to result in non-cancerous healtheffects in adults or children, even if this well were used for drinking water. In addition, use of thiswell is not expected to result in a significant increase in cancer risk.

    Nitrate has been detected in this well. Although this well is used mainly for domestic purposes, nitrateexposure could occur through ingestion of and dermal contact with water from this well. A daily doseestimate for water containing 16,000 ppb nitrate is 0.46 mg/kg/day for adults and 1.6 mg/kg/day forchildren. Ingestion of the level of nitrate detected in this well is not expected to result in non-cancerous health effects in adults and children, even if this well were used for drinking. However,using this well at pre-1994 nitrate levels for drinking (including infant formula) and cooking mayresult in non-cancerous health effects in infants and pregnant women and their fetuses.

    TABLE 14 - Arapahoe Aquifer Contaminants

    There are no private wells in Table 14 that contain more than one contaminant. Therefore, themaximum concentration detected for each chemical will be evaluated, and any well judged to containchemical concentrations of public health concern will be identified by well number and specificcontaminant. Recommended actions for such wells will then be subsequently discussed in theRecommendations section of this Assessment.

    Arsenic

      Drinking Water Wells - 549A, 601A, 864A, 1354A, & 1380A

    Those wells are used for both drinking water and domestic purposes. The maximum concentrationdetected was measured in well 601A at a concentration of 14.4 ppb; the MCL for arsenic in drinkingwater is 50 ppb. Each of those wells are used by three people. Based on 14.4 ppb, a daily doseestimate would be 0.00041 mg/kg/day for adults and 0.0014 mg/kg/day for children. Ingestion of theamount of arsenic detected in well 601A or the other wells listed here would not result in non-cancerous health effects in adults or children. In addition, use of well 601A or the other wells listed inhere is not expected to result in a significant increase in cancer risk. All of the listed well, exceptwells 864A and 1354A, qualify for connection to a replacement water source and the use of these well may not continue.

      Domestic Water Well - 595A

    The level of arsenic detected in this well 595A was 9.59 ppb. The residents using this well areprovided with bottled water, so this well water is used mainly for domestic purposes. The well is usedby three people. A daily dose estimate for water containing this amount of arsenic is 0.00027mg/kg/day for adults and 0.00096 mg/kg/day for children. Ingestion of the amount of arsenic detectedin this well would not be expected to result in non-cancerous health effects in adults or children, evenif this well were used for drinking water. In addition, use of this well is not expected to result in asignificant increase in cancer risk. This well qualifies for connection to a replacement water sourceand the use of this well may not continue.

    Lead

    Lead has been found in well 931A at 18.6 ppb; the EPA Action Level for lead in drinking water is 15ppb. This well is used for both drinking and domestic purposes (cooking, washing, and bathing) sincebottled water is not provided. Using this well for showering and bathing is not expected to result innon-cancerous health effects. However, cooking with and/or drinking water from this well (includingusing the water to make infant formula) might result in non-cancerous health effects in children,infants, and pregnant women and their fetuses, given the lead level in this well water and thepossibility for additional lead exposure that might occur from the environment and workplace. Threepeople use this well. This well qualifies for connection to a replacement water source and the use ofthis well may not continue.

    APPENDIX C: ADDITIONAL INFORMATION RELATING TO
    COMMUNITY HEALTH CONCERNS

    More Information About Lupus

    Types of Lupus
    There are two main types of lupus: systemic lupus erythematosus (SLE) and discoid lupuserythematosus (DLE). SLE is a chronic inflammatory condition that can affect any of the body'sorgans and systems. Some of the most commonly affected organs and systems are the blood, skin,joints, kidneys, lungs, brain, heart, and lymph nodes. Because of the various systems involved, thedisease ranges from mild to life-threatening (Lupus Foundation of America, Inc., 1992, p. 1).

    DLE affects the skin, with initial lesions appearing as oval or round red patches, referred to as"plaque." These plaque often spread to other areas of the body -- most commonly areas exposed to thesun -- such as the ears, face, scalp, neck, and forearms. In extreme cases, it could spread to theremainder of the trunk. The inflammation can cause permanent scarring, destruction of the hairfollicles and glands, thinning of the skin, and loss of hair. A biopsy is helpful in the diagnosis of DLE(Lupus Foundation of America, Inc., 1992, p. 1).

    Most patients who develop DLE will not develop SLE, although they could have some of thesymptoms typical of SLE. About 20-25% of SLE patients develop discoid skin lesions. About 5% of patients with DLE will develop SLE (Lupus Foundation of America, Inc., 1992, p. 1).

    National Rates of Lupus
    Based on national rates of lupus prevalence in the U.S., SLE is up to four times more common inblacks compared to whites. It is also well recognized that SLE is more common in females, with a ratio of approximately 9:1, but before puberty and after the age of 50 the preponderance of females isless marked. The prevalence rate of lupus in the U.S. is about 30/100,000. Prevalence refers to thetotal number of cases of SLE, new and old, at a given time (point prevalence) or over a given period oftime (period prevalence). Prevalence rates vary depending on both the incidence (number of newcases during a given time period) and the duration of disease; therefore, both disease remission andmortality are crucial factors. National databases indicate that the incidence as well as prevalence rateshave increased over the last few decades (Hopkinson, 1994, p. 290-293). Individual state rates are notavailable.

    SLE, in comparison, is as common as multiple sclerosis (prevalence rate 30/100,000), less commonthan rheumatoid arthritis (1,000/100,000) and insulin-dependent diabetes mellitus (900/100,000)(Holland, Detels, and Knox, 1985), and more common than scleroderma (3/100,000) (Symmons andBacon, 1988). The prevalence rates for SLE have increased over the last few decades from 2-4/100,000 in early studies to 20-50/100,000 in more recent ones (Hopkinson, 1991, p. 292).

    Although SLE can occur at any age (it has been diagnosed at birth and in individuals in the 10thdecade of life) more than 60 % of patients experience the onset of disease between the ages 13 and 40. Among children, SLE occurs three times more commonly in females than in males. In patients in theirteens, twenties, and thirties, 90% to 95% are female. Thereafter, the female preponderance again fallsto that observed before puberty (Wyngaarden and Smith, 1988, p. 2012).

    The disorder is approximately three times more common among American blacks than Americancaucasians. Certain North American Indian tribes (Sioux, Crow, and Arapahoe) have an even greaterpredisposition toward SLE. Asians have been less studied; however, the data suggest that they areaffected to approximately the same extent as American blacks. The overall annual incidence of SLE isabout 6 new cases per 100,000 population per year for relatively low-risk populations and about 35 per100,000 population per year for relatively high-risk populations. The chance of a black femaledeveloping SLE in her lifetime is approximately 1 in 250 (Wyngaarden and Smith, 1988, p. 2012).

    These data suggest that both genetic factors and sex hormones may affect the likelihood of developingSLE. If a family member has SLE, the probability of SLE increases (about 30% for identical twinsand 5% for other first-degree relatives). Although males develop SLE less frequently than do females,their illness is not milder (Wyngaarden and Smith, 1988, p. 2012). The ratio of females to males withlupus is about 10:1. It is believed that the influences of female sex hormones, particularly estrogens,on the immune system make females more susceptible to the development of lupus. Additionalevidence to support this interpretation include the development or worsening of lupus with pregnancyor with the use of birth control pills, instances in which estrogen levels are increased (Aladjem, 1992,p. 2).

    Lupus in children is rare. The age of onset varies but generally falls between 4 and 18 years. Lupus isextremely rare in children under 4. In children, the ratio of females to males with lupus varies from4:1 to 9:1, depending on the clinic. The symptoms are the same in children and adults in most cases(60-90%). Fortunately, most children get better spontaneously. A few adolescents have severe life-threatening disease, whereas others will continue to have relapses and remissions all their lives. Whatdictates the severity of the disease is the extent of organ involvement. The most severe disease oftenoccurs in black female children, although the incidence of the disease is also higher in blacks ingeneral. Three broad manifestations of the disease have a poor prognosis: lupus nephritis (kidneyinvolvement), central nervous system involvement, and persistent systemic manifestations. However,the prognosis for lupus patients has improved considerably and continues to improve each year(Aladjem, 1990, p. 187-189).

    Cause of Lupus is Unknown
    Although it's exact cause is unknown, certain drugs and chemicals can induce in susceptibleindividuals a lupus-like syndrome that disappears when the drug is discontinued (Freni-Titulaer et al.,1989, p. 408). The chemicals associated with lupus fall into four classes: aromatic amines(particularly procainamide, used to treat heart abnormalities), hydrazines, sulfur-containing drugs, andthe hydralazine anti-convulsants. The environmental records do not disclose the presence of thosechemical compounds in the environmental media of RMA at levels of public health significance. Therefore, it's unlikely that cases of lupus could be associated with RMA.

    It bears noting that hydrazine breaks down into nitrosamines rapidly. Nitrosamines have been detectedin wells north of Basin F on RMA, but until recently nitrosamines were not detected downgradient ofthe treatment system. The detection of the nitrosamine N-Nitrosodimethylamine (NDMA) in theOffpost area at very low levels (0.2 - 2 ng/L) has resulted in a commitment by RMA and Shell OilCompany for further monitoring and evaluation in 1995 and early 1996. The significance of this new data is unknown at this time.

    As mentioned earlier, we do not know the cause of lupus. Nonetheless, the importance of geneticfactors in the cause of SLE is clearly demonstrated by studies of monozygotic twins. Rare cases oftwins separated at birth and raised in different environments but both developing SLE within a shorttime of each other are well documented. Recently, rates of 23% for monozygotic twins and 9% fordizygotic twins have been reported (Deapen et al., 1986). These data further support the idea that bothgenetic and environmental factors are important in the development of SLE (Hopkinson, 1991, p.292).

    Several factors, while not causing lupus, may cause lupus flares or tend to aggravate symptoms inpatients already diagnosed with the disease. For example, while ultraviolet (UV) light probably doesnot cause lupus, at least a third of patients are photosensitive and have disease flares following UVexposure. Most lupus patients should avoid all UV light, including the so called "safe" UV-Alight. Uncovered fluorescent bulbs can emit UV light, and some drugs or food containing psoralens cansensitize patients to UV light. Psoralens are chemicals that increase sun sensitivity in patients who aresun sensitive. Some examples of foods with psoralens are celery or celery salt, parsnips, parsley, andfigs (Krieg, 1990, p. 18).

    Many bacterial and viral infections can cause immune activation that could in turn exacerbate lupus. Lupus patients are prone to viral and bacterial infections and sometimes have flares after commoninfections, but this risk has not been documented in clinical studies (Krieg, 1990, p. 18).

    It has been the clinical impression of many physicians caring for lupus patients that severe physical oremotional stress can induce flares. Some patients feel that their lupus symptoms worsen with stress,but others report no difference. This question has yet to be studied clinically, so it is unclear howoften stress aggravates lupus (Krieg, 1990, p. 19).

    Hair dyes contain high levels of hydrazines and other chemicals that are related to procainamide andhydralazine and can be absorbed thorough the scalp. One study has found that patients exposed to hairdyes have a significantly increased risk of lupus (Freni-Titulaer et al., 1989). Further studies areneeded to confirm whether the use of hair dye is a risk factor for SLE (Krieg, 1990, p. 19).

    Some lupus cases have followed the injection or implantation of silicone polymers, such as those usedin breast implants. Although this observation has been made, more studies are needed to follow up onthis finding (Krieg, 1990, p. 19).

    Diagnosis of Lupus
    Lupus can be diagnosed through various blood tests performed by a physician. All lupus cases areindividual and are treated in different ways. The drugs used to control lupus range from aspirin andanti-inflammatory agents (e.g., Motrin) to corticosteroids (e.g., Prednisone) and immunosuppressantdrugs (e.g., Cytoxin). Anti-malarial drugs are also occasionally used. Lifestyle is extremely importantin controlling lupus. Proper nutrition, avoidance of excess stress and sun exposure, and getting bothrest and exercise are all aspects of treatment. Learning to cope with a chronic illness is an importantpart of treatment and may include psychotherapy, support groups, etc. (Lupus Foundation of America,Inc., 1992, p. 3).

    Lupus Research
    For the last four decades, the main focus of lupus research has been aimed at efforts to understandwhat causes the immune system to produce the abnormal antibodies (Aladjem, 1992, p. 2). The twoprimary factors thought to be important in the production of autoantibodies are environmental agentsand genetic factors of the patient. It is likely that mutual dependence of these factors is required forautoantibodies to develop. For instance, a person would need exactly the right combination of genesand contact with a particular environmental agent for autoantibodies to be formed. Several lines ofevidence seem to support this notion. For example, certain drugs (environmental agents) discussedearlier are capable of inducing antinuclear antibodies as well as clinical symptoms of lupus. It is alsobelieved that there are unidentified environmental agents (toxins or allergens, food substances,infectious agents, etc.) that are responsible for lupus. It is also believed that there may not be a singlecause of the disease but rather multiple responsible agents. Several factors provide evidence of theimportance of genetic influences: increased frequency of lupus in identical twins and in certainfamilies with lupus, the increased representation of the disease in certain racial groups, and theidentification of certain genes (HLA genes) associated with the disease (Aladjem, 1992, p. 9). Theother major question in lupus research is why the antibodies that are formed go on to produce clinicaldisease. Researchers hope to answer these questions so that lupus can be better understood.

    For more information, contact the Lupus Foundation of Colorado or the Lupus Foundation ofAmerica, Inc.

    More Information About Diabetes

    Definition of Diabetes
    Diabetes (also known as diabetes mellitus or "sugar" diabetes) is the name given to the chronic diseasethat describes a group of disorders in which the body either does not produce or does not respondappropriately to insulin. Insulin is a hormone produced by beta cells in the pancreas and is used toregulate carbohydrate metabolism by controlling blood glucose (sugar) levels. When insulin is notavailable for this conversion, glucose builds up in the blood. High glucose levels are a common factorin the different types of diabetes (CDPHE, 1992b, p. i).

    Diabetes is the leading cause of blindness among individuals between the ages of 22 and 74, theleading cause of kidney failure, and one of the major risk factors for heart disease and stroke. It is alsoresponsible for one-half of the lower-extremity amputations performed each year (CDPHE, 1992b, p. i).

    There are several types of diabetes. The two major types are Type I, also called Insulin-DependentDiabetes Mellitus, or IDDM, and Type II diabetes, also called Non-Insulin Dependent DiabetesMellitus, or NIDDM (American Diabetes Association, 1988a). A third type of diabetes is GestationalDiabetes (CDPHE, 1992b, p. i).

    Type I Diabetes
    This type of diabetes usually begins in childhood and is often called juvenile diabetes. This type ofdiabetes occurs when the body produces little or no insulin. Therefore, most insulin-dependentdiabetics have to inject insulin into their bodies daily (American Diabetes Association, 1989a). Type Idiabetes can develop at any age, although most cases are generally diagnosed when the patient is lessthan 30 years old (CDPHE, 1992b, p. i; American Diabetes Association, 1989a).

    At the time of diagnosis, they are usually quite ill and display classic symptoms of unexpected weightloss, increased hunger and excessive thirst, frequent urination, irritability, and weakness and fatigue(American Diabetes Association, 1989a; CDPHE, 1992b, p. i). Persons with Type I diabetes are proneto ketosis (accumulation of waste products called ketones) and must take insulin (CDPHE, 1992b, p. i).

    Type I diabetes accounts for approximately 3% of all new cases of diabetes diagnosed each year in theU.S. and accounts for only 10% of all cases of diabetes. Although it is much less common in thegeneral population than Type II diabetes, Type I is by no means rare among children and young adults. With an estimated annual incidence rate among people under age 20 years of 15 per 100,000 people (1new case per 7,000 children per year), Type I diabetes is 3- to 4-fold more common than chronicchildhood diseases such as cystic fibrosis, peptic ulcer, juvenile rheumatoid arthritis, or leukemia, andit is nearly 10-fold more common than nephrotic syndrome, muscular dystrophy, or lymphoma(American Diabetes Association, 1989a).

    After age 20, the yearly incidence decreases to 5 per 100,000. The incidence is similar in men andwomen, lower in blacks than whites, and markedly less common in Hispanics, Asian Americans, andnative Americans (American Diabetes Association, 1989a, 1994). The peak incidence is between 10and 12 years of age in girls and 12 and 14 years of age in boys (CDPHE, 1992b, p. i). Two to 5% ofsiblings of individuals with Type I diabetes will develop the disorder, and among identical twins, oneof whom has Type I diabetes, concordance rates are 50% (American Diabetes Association, 1989a).

    The cause of Type I diabetes is not completely understood. Research points to the immune system asbeing important in the development of Type I diabetes, and several causative agents including virusesand drugs have been proposed, but none have gained widespread acceptance (American DiabetesAssociation, 1989a; CDPHE, 1992b, p. i). The histocompatibility leukocyte antigen (HLA) complex,located on chromosome 6, consists of a cluster of genes that code for transplantation antigens andregulation of the immune response. Inheritance of certain HLA types, principally the DR3 or DR4loci, confers a tendency to develop Type I diabetes. Genetic factors alone are inadequate to causeType I diabetes; i.e., it is the tendency and not the disease itself that is inherited. The fact thatidentical twins are concordant for Type I diabetes only 50% of the time suggest that some externalenvironmental factor(s) is needed to initiate the disease process. These factors and their mode ofaction remain unknown (American Diabetes Association, 1989a).

    Type II Diabetes
    The most common type of diabetes is Type II diabetes, which affects about 90% of individuals withdiabetes. This condition is called maturity-onset diabetes and usually occurs in adults. With non-insulin dependent diabetes, the body produces insulin but not in the necessary amounts (AmericanDiabetes Association, 1989b). Diagnosis of Type II diabetes is often difficult due to the absence ofsymptoms. It is estimated between 6% and 7% of people in the U.S., or up to 1 in 15, have diabetesand are not aware they have it. Type II diabetes occurs more often in the elderly and in minoritypopulations. Colorado data show higher prevalence of diabetes and increased complications in boththese groups. Many with Type II diabetes are obese (having more than 120% of ideal body weight)and have a sedentary lifestyle (CDPHE, 1992b, p. i).

    Persons with Type II diabetes are generally not prone to ketosis; they can produce insulin but just notin sufficient amounts. First-line treatment for them consists of diet and exercise. As necessary,treatment then progresses to the use of oral hypoglycemic medications (pills that lower blood glucose)and insulin (CDPHE, 1992b, p. i).

    Medical experts do not know the exact cause of Type II diabetes. It most frequently occurs in personsover age 30 who have a genetic predisposition to diabetes or a family history of the disease (CDPHE,1992b, p. i). A person can inherit a tendency to get Type II diabetes, but it usually takes anotherfactor, such as obesity, to bring on the disease. Warning signs of Type II diabetes include anysymptoms of Type I diabetes; frequent infections; blurred vision; numbness in legs, feet, and fingers;cuts that are slow to heal; and itching (American Diabetes Association, 1989b).

    Reduction of blood pressure, lowering cholesterol, smoking cessation, and careful control of bloodsugars can dramatically reduce the risk of heart attacks, strokes, and kidney failure. In addition,exercise and weight reduction can improve glucose tolerance and reduce obesity, important risk factorsfor diabetes and other chronic diseases. Early recognition of diabetic eye disease can permit treatmentand preservation of sight. Similarly, planned pregnancies and expert prenatal care can minimize theincidence of birth defects (CDPHE, 1992b, p. i).

    It is important for all individuals with diabetes to monitor their exercise and diet. Insulin-dependentdiabetics must monitor their use of insulin. If a diabetic does not control these factors an imbalancebetween insulin and sugar in the body can create a diabetic emergency. Signals and symptoms of adiabetic emergency include changes in the level of consciousness, rapid breathing and pulse, andfeeling and looking ill (American Diabetes Association, 1989b).

    Gestational Diabetes
    Gestational diabetes is diabetes that is first recognized during pregnancy. Women who have eitherType I or Type II diabetes prior to pregnancy are not included in statistics for this type. Approximately 5% of pregnancies are complicated by gestational diabetes (CDPHE, 1992b, p. i).

    Gestational diabetes significantly increases both morbidity and mortality of offspring. Diagnosis ofgestational diabetes is made by glucose tolerance testing. Treatment consists of dietary modificationand in some cases, insulin injections for the duration of the pregnancy. Gestational diabetes generallyconcludes following pregnancy. Women who have had gestational diabetes have a greatly increasedrisk for developing Type II diabetes later in life (CDPHE, 1992b, p. i).

    Research and Other Information Specific for Colorado
    Currently, research being conducted in Colorado is investigating Type II diabetes in minorities, withan emphasis on Hispanics (ATSDR, 1994d). Hispanics had the highest prevalence of diabetes inColorado compared with whites and blacks. In 1990, the age-adjusted prevalence of diabetes was 51per 1,000 population among Hispanics, 41 per 1,000 among blacks, and 24 per 1,000 among whites(CDPHE, 1993c, p. 1).

    In August 1990, the Colorado Board of Health appointed the Colorado Diabetes Advisory Council toaddress the health needs of Coloradans with diabetes. The council has released information that detailsrecommendations for improving the health and well-being of Coloradans with diabetes. Residentsshould contact the Colorado Department of Health, Diabetes Control Program for a copy of the reportor a list of the council members (CDH, 1992b, p. i).

    The Colorado Department of Health has also published two reports that discuss the risk factors fordiabetes, diabetes prevalence and morbidity specifically related to Colorado residents, andrecommendations for improving the health and well-being of Coloradans with diabetes. Those reportsare Diabetes in Colorado: Approaching the Year 2000 and Diabetes Prevalence and Morbidity inColorado Residents, 1980-1991 (CDH, 1992b and CDH, 1993c). For more information on diabetes orcopies of these reports, residents should contact the Colorado Diabetes Control Program, under thedirection of the Colorado Department of Health.


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