PUBLIC HEALTH ASSESSMENT
ROCKY MOUNTAIN ARSENAL
ADAMS COUNTY, COLORADO
| Category | Definition | Criteria |
| A. Urgent public health hazard | This category is used for sites that pose an urgent public health hazard as the result of short-term exposures to hazardous substances. | |
| B. Public health hazard | This category is used for sites that pose a public health hazard as the result of long-term exposures to hazardous substances. | |
| C. Indeterminate public health hazard | This category is used for sites with incomplete information. | |
| D. No apparent public health hazard | This category is used 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. | |
| E. No public health hazard | This category is used for sites that do not pose a public health hazard. | the site has had an adverse impact on human health. |
TABLE 13 - Alluvial/Unknown Aquifer Contaminants
Specifically created for individual well owners, this appendix contains an evaluation of every chemical found in drinking water wells at a concentration detected above ATSDR's comparison values. Out of the hundreds of drinking and domestic wells currently in use and monitored regularly for RMA and non-RMA contaminants, 23 wells have been identified that produce water containing nitrate or lead at levels of public health concern (see Table 19). Local health officials have notified the users of contaminated wells of the possible health effects that might occur from continued use. The available evidence indicates that Rocky Mountain Arsenal is not the source of those contaminants. The lead in the water could be from several sources such as naturally occurring lead in the groundwater or lead contamination in plumbing. The nitrate could be traced to many sources such as agricultural fertilizers, animal wastes, or private on-site sewage disposal systems. There are also some wells in which RMA contaminants are detected, but the levels of contamination are not of public health concern. Private drinking water wells to the north and northwest will continue to be monitored for both RMA and non-RMA sourced contaminants, and when a well is sampled, the results will be communicated 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 number and specific contaminant and recommended actions are discussed in the Recommendations section of this Assessment. The section contains evaluations of private wells with a single contaminant and private wells with multiple contaminants. The concentrations listed below represented the most recent detections of contaminants for drinking water wells in the Alluvial/Unknown Aquifer based on RMAED 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, 1993 through 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 how the chemical concentration was evaluated for potential health effects. Thereafter, shortened toxicological 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 replacement water 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 domestic purposes, whereas well 583A with a concentration of 14.0 ppb and well 940A with a concentration of 8.29 ppb are used mainly for domestic purposes. The Maximum Contaminant Level (MCL) for arsenic in drinking water is 50 ppb.
Three people use well 565A for drinking water. A daily dose estimate for water containing 5.69 ppb of arsenic is 0.00016 mg/kg/day for adults and 0.00057 mg/kg/day for children. Arsenic is very poorly 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. population in 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 toxic form of arsenic. The EPA has established a chronic oral RfD of 0.0003 mg/kg/day for inorganic arsenic. A study of 17,000 individuals exposed to arsenic-contaminated drinking water in Taiwan determined 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-cancerous health effects (ATSDR, 1993e). Because the type of arsenic in this well water is unspeciated and the estimated daily dose for children is just slightly above the MRL, RfD, and no-effect levels, ingestion of the amount of arsenic in the well water from this well is not expected to result in non-cancerous health 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 have indicated 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 the well water from this well is not expected to result in a significant increase in cancer risk.
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, and bathing). 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 for adults and 0.00083 mg/kg/day for children. Based on 14.0 ppb (well 583A), a daily dose estimate would be 0.00040 mg/kg/day for adults and 0.0014 mg/kg/day for children. Ingestion of the amount of arsenic in those wells would not be expected to result in non-cancerous health effects in adults or children, even if those wells were used for drinking water. In addition, use of those wells is not expected to result in a significant increase in cancer risk.
Atrazine
Well number 373D was detected with 4.53 ppb of atrazine. Since the residents served by this well receive bottled water, the well is used primarily for domestic purposes. Estimates indicate that 5% of the water used is ingested incidentally. According to Table 13, five people use this well. The MCL for atrazine in drinking water is 3 ppb. Under the provisions of the Offpost ROD, this well qualify for connection 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 from dermal contact with the water (TOMES, 1994). A daily dose estimate for water containing 4.53 ppb of atrazine is 0.00013 mg/kg/day for adults and 0.00045 mg/kg/day for children. The acceptable daily ingestion 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 to result in non-cancerous health effects in adults and children, even if this well water were used for drinking.
The EPA has concluded that data from toxicological studies have not indicated that exposure to atrazine through ingestion and inhalation of, or dermal contact with it, causes carcinogenic health effects in people (TOMES, 1994).
Atrazine is currently undergoing review by the EPA, as are other triazines. The potential health effects from widespread use of triazine pesticides, including atrazine, is being re-evaluated. If new health guidelines are established for atrazine, that value will be used to re-evaluate the concentration of atrazine in the water from this well.
Lead
Lead has been detected in the well water from four wells: 372A, 550A, 602A, 603A. All four wells are used mainly for domestic purposes such as cooking, washing, and bathing, since bottled water is supplied 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 of these 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 Action Level for lead in drinking water is 15 ppb.
The source of lead could be from several sources, such as lead contamination in the groundwater or plumbing (lead piping, lead-based solder, and water faucets containing lead). Tea and coffee made with tap water containing lead may have an increased lead concentration due to evaporation of the water, particularly if the coffee or tea sits on a hot plate. The natural background levels of lead in the groundwater near RMA ranges from less than 18.6 ppb to less than 37.2 ppb. The following concentrations 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 lead absorbed 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 evaluating the potential health effects from lead exposure.
The health effects of lead are not immediately apparent. Once in the blood, lead is distributed to the soft tissue (kidneys, bone marrow, liver, and brain) and mineralizing tissue (bones and teeth). Bones and teeth contain about 95% of the total body burden of lead (ATSDR, 1992A; ATSDR, 1993f). It is the total body burden of lead that is related to the risk of adverse health effects. Because the body accumulates lead over a lifetime and releases it slowly, even small doses of lead over time can cause lead poisoning. Further, relatively low blood lead levels can cause adverse health effects, some of which, 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 levels are as low as 7 µg/dL. High levels of blood lead (40 µg/dL) may affect sperm or damage other parts of the 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 women are pregnant, lead stored in their bone marrow can enter their blood stream increasing the amount of lead reaching the fetus, resulting in premature birth, low birth weight, and decreased mental ability. In infants and young children, lead exposure has been shown to decrease intelligence (IQ) scores, slow their growth, and cause hearing problems in cases with blood lead levels less than or equal to 10 µg/dL. These effects can persist as children get older and interfere with successful performance in school (CDC, 1991). Because lead is ubiquitous in the environment, many children have elevated blood lead levels approaching those believed to cause non-cancerous health effects (ATSDR, 1993f and ATSDR, 1992a). Consumption of drinking water containing 50 ppb of lead would correspond to a rise of 10 µg/dL in the blood lead levels of children. But since these are estimates, the increases in blood 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-cancerous health effects. However, because the lead levels in the well water from these wells fluctuated above and below the action level of 15 ppb and some of these lead levels are somewhat high, two aspects of lead exposure are of concern. One is exposure, even once, to extremely high levels of lead. The second is intermittent exposure over an extended period of time, e.g., more than a year. Under these exposure conditions, people can absorb enough lead, even at moderate levels, to raise their body burden of lead to levels that might pose health problems. People swallowing lead contaminated water at 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 health effects (ATSDR, 1992a). Therefore, based on the lead levels detected in these wells, use of these wells for drinking (including infant formula) and/or cooking may result in non-cancerous health effects in children, infants, pregnant women and their fetuses, and other adults. Because well 550A apparently does not qualify for a connection to replacement under the provisions of the Offpost ROD and because the well also not qualify for continuation on the program for interim supply bottled water, a future pathway of human exposure to elevated levels of lead in drinking water may be created. This well has not been sampled for lead since 1991 and it is not known if the present 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 lead in drinking water. If you are concerned about your blood lead levels either because of the lead levels in your drinking water or other possible lead exposure sources, there is a simple medical test available to screen for blood lead levels. People who are concerned about their exposure to lead should see their doctor 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 (a component of the blood), nutritional deficiencies (especially iron and calcium), and neurological or kidney 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 has concluded that human data is inadequate to determine if lead exposure could cause cancerous health effects in people. However, using animal studies, EPA has classified lead as a probable (B2) human carcinogen; although there are sufficient animal studies, there are inadequate human studies that show it causes cancer. Health guidelines for determining possible cancer effects in people exposed to lead have 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 some types of batteries in industrial settings, and in the production of ammunition and some kinds of metal products (such as sheet lead, solder, and pipes). For older wells, the most common use of lead has been in the construction of such wells and associated piping. Some chemicals containing lead, such as tetraethyl 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 phased out. 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 in people and animals. Currently, workers may be exposed to lead in a variety of occupations including smelting 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 that contain lead. Breathing air with dust that contains lead or swallowing lead-containing soils that might be 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 through plumbing work where lead-base solder and brass fixtures are used. Other sources of occupational lead exposure 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 hobbies may 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 children and pregnant women, private well water with lead at 15 ppb or greater should stop drinking the water and/or using it for cooking. Adults drinking well water with 15 to 50 ppb should try to reduce their exposure. For adults drinking well water greater than 50 ppb, they should stop drinking the water and stop using it for cooking.
Additional Health Information
Lead toxicity greatly depends on the route of exposure. Lead must be absorbed into the body to produce 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 lower respiratory tract, lead is almost completely absorbed into the body. Absorption from contaminated sources 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 skin acts as a barrier to lead absorption. Dermal absorption of inorganic lead compounds is much less significant than absorption by inhalation (which would be most significant in the workplace) or ingestion routes of exposure (ATSDR, 1993f). However, organic lead (tetraethyl lead) may be absorbed 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, especially nutritional well-being, figure prominently in the level of lead exposure required to produce effects and indications of toxicity. A number of nutritional factors suppress lead absorption and toxicity in humans (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 body tissues, especially bone. It is the total body burden of lead that is related to toxicity. During pregnancy or in the presence of chronic disease, lead stored in bone tissue can be released and increase concentrations of lead in the blood (ATSDR, 1993f).
The most sensitive target of lead poisoning is the nervous system. The effects in children were discussed earlier. However, central nervous system effects in adults include subtle behavioral changes, fatigue, and impaired concentration. Peripheral nervous system damage is observed, primarily in adults, as a peripheral neuropathy with mild slowing of nerve conduction velocity. Those effects Peripheral 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 than 50 µg/dL from occupational exposure had adverse reproductive effects including decreased prostate/seminal vesicle function, lowered semen volumes, and lower function maturity of sperm (ATSDR, 1992a). An increased likelihood of miscarriage has been associated with occupational lead exposure in pregnant women: Nordstrom et al. (1979) found an increased frequency of miscarriages in women living near or working at a lead smelter.
The fetus has no metabolic or anatomic barrier to lead. Lead absorbed by pregnant women can transfer to the fetus via the placenta; therefore, exposure of pregnant women to lead is unsafe for the fetus. Uptake may occur during the entire pregnancy, including during development of the fetal nervous system and other target organs of lead toxicity. Developmental consequences of prenatal exposure 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 a decrease 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 with erythropoiesis and by diminishing red blood cell survival (ATSDR, 1992a). Anemia is not an early effect of lead poisoning; it is evident only after prolonged periods of significantly elevated blood lead concentrations.
Occupational and general population studies provide strong evidence that a statistically significant association exists between blood lead levels and hypertension (ATSDR, 1993f). The association is most evident in men 40-59 years old and is seen with blood lead levels as low as 7 µg/dL. A mean increase in systolic blood pressure of 1.0 to 2.0 mm Hg appears to result from every doubling in blood lead 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 water and thus your exposure to lead are included below. You cannot see, taste, or smell lead in your drinking water, so it is important to perform these precautionary steps, especially if there is a concern about 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 pipes
for more than four hours should be flushed for three to five minutes, for example, first thing in the
morning and when you arrive home in the evening. A good indication of when to stop flushing the
cold water tap is when the water becomes noticeably colder. Use cold water for cooking or making
infant formula because water from the hot water tap dissolves lead more quickly, which will cause
lead 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 even
after flushing, then you may want to consider taking the following additional measures. You may
chose to use bottled water instead of tap water for drinking or cooking purposes, or you may chose to
use a water purification system. Purification systems range in size and cost from the water pitcher
filtration 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 in those wells would be nearby farms, stockyards, and septic sewer systems north of RMA. As previously noted, the concentration of nitrate in these Offpost wells varies over time and the level of nitrate contamination has been decreasing with time. By June 1996 no drinking water well in this area 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 not continue.
Most of these wells are each used by 3 people. However, wells 332B, 332D, 456A, and 1305A are each used by 2 people, and four people use well 981A. Well 1276A is used by 6 people.
Because the residents of houses served by these wells are not on the bottled water program, the wells are being used for both domestic and drinking water purposes. Of those wells the maximum concentration of nitrate detected was 24,000 ppb in well 1276A. If nitrate levels had remained at the 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 2.40 mg/kg/day for children. Nitrate exposure could occur through ingestion of and dermal contact with water containing nitrate (ATSDR, 1991; IRIS, 1994; and TOMES, 1994). Chronic ingestion of more than 5 mg/kg/day is considered unacceptable for adults and children (TOMES, 1994). EPA has established 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 effects are 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 infants are more susceptible to nitrate exposure than older persons (TOMES, 1994). For example, ingestion of nitrate ranging from 1 mg/kg/day to 15.5 mg/kg/day in 111 infants less than 6 months old was associated with increased methemoglobin levels (i.e., the mean methemoglobin level was measured to be 1.6 percent, with the highest level being 5.3 percent), although none of the children had the typical symptoms of methemoglobinemia (Winton, Tardiff, and McCabe, 1971). Nitrates in well water used to prepare infant feeding formula have been implicated as causing significant (but unspecified) illness in children at 90,000 ppb (Comly, 1987). Therefore, using these wells at pre-1994 nitrate levels for making infant formula might result in non-cancerous health effects in infants, especially those under six 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 total hemoglobin) to a maximum of 10.5% at the 30th week of pregnancy and subsequently declines to normal after delivery. Thus, pregnant women could be more sensitive to the induction of clinical methemoglobinemia 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 result in non-cancerous health effects.
The EPA has concluded that data from toxicological studies do not indicate that ingestion and inhalation 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 nitrates may be absorbed through the skin, dermal exposure cannot be assessed because little information was found pertaining to this route of exposure (ATSDR, 1991, p. 3 and TOMES, 1994). People who are concerned about their exposure to nitrates should see their doctors for more information.
These wells are being used mainly for domestic purposes, because bottled water is supplied to the residences with these wells. All of these wells, except well 547A, qualify for connection to a replacement water supply and use of these wells may not continue. If nitrate levels had remained at the pre-1994 levels, the use of these wells for drinking (including infant formula) and/or cooking may result 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 in most 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 can cause elevation of the concentrations of nitrates in drinking water: 1) nitrogenous waste matter from humans or from dairy cattle or other livestock or poultry and 2) nitrogenous fertilizers, especially those used in irrigated farming. The nitrates used in nitrogen-based fertilizers (including such material as anhydrous ammonia, which can be converted in the soil to nitrates) can seep into the groundwater and contaminate it (Goldsmith, 1991, p. 148). Shallow, rural domestic wells (wells less than 100 feet deep) are most likely to be contaminated with nitrates, especially in areas where nitrogen-based fertilizers are in widespread use. During spring melt or drought conditions, both domestic wells and public water systems using surface water, or wells that are shallow, may have increased nitrate concentrations (ATSDR, 1991, p. 2).
In humans, ingested nitrate is rapidly absorbed from the proximal small bowel and distributed throughout the body. Nitrate enters the large bowel from the blood and is rapidly converted to highly reactive nitrite, in part by fecal microorganisms. Nitrates are rapidly converted in the liver to denitrated metabolites and inorganic nitrites, which are then excreted in the urine. Approximately 60% to 70% of an ingested nitrate dose is excreted in urine within the first 24 hours. About 25% is excreted in saliva through an active blood-nitrate transport system and could be reabsorbed. Half-lives of parent nitrate compounds are usually less than 1 hour; half-lives of metabolites range from 1 hour to 8 hours (ATSDR, 1991, p. 6).
While vegetables seldom are a source of acute toxicity, they account for more than 70% of the nitrates in a typical human diet. Cauliflower, spinach, collard greens, broccoli, and root vegetables such as beets and carrots have naturally greater nitrate contents than other plant foods. The remainder of the nitrate in a typical diet comes from drinking water (approximately 21%) and from meat and meat products (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 not properly transported in the blood, resulting in an intermittent bluish discoloration. Throbbing headache, nausea, vomiting, diarrhea, and irregular heartbeat are common symptoms of nitrate exposure. 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 in children who have eaten sausage heavily treated with nitrates and nitrites. For infants, the major source 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 when nitrate contamination is suspected; evaporation actually increases the nitrate concentration. Increased nitrate levels have been associated with increased levels of coliform bacteria. Water treatment technologies (ion exchange resins or reverse osmosis) used to remove nitrate from water are not adequate to remove other associated contaminants, especially coliform bacteria. Private wells should be 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 by April 1994 indicated that eight of the 14 wells contained levels of lead and nitrate that may individually 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 is expected to occur, because the concentrations of lead required to add to the effects that nitrate may cause are not high enough. Therefore, additional non-cancerous health effects are not expected from simultaneous 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 to multiple chemicals when similar mechanisms of action (biological and chemical) and/or health outcomes 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 of these wells, except well 967A, qualify for connection to a replacement water source and use of these wells may not continue. Evaluation of those individual contaminants indicates that no adverse health effects are expected from the use of those wells, even if they are used for drinking and other domestic purposes. And, a discussion of the chemicals detected in those wells is evaluated elsewhere in this section. 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, to contain chemical concentrations of public health concern will be identified by well number and specific contaminant. Recommended actions for such wells will then be subsequently discussed in the Recommendations 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 for domestic 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 Level for lead in drinking water is 15 ppb.
Chloroform has been detected in this well. Ingestion or inhalation of water containing chloroform, or dermal contact with such water could result in exposure. Inhalation is considered to be just as significant as ingestion (ATSDR, 1993h). A daily dose estimate for water containing 8.34 ppb of chloroform 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 for chloroform is 0.01 mg/kg/day (IRIS, 1994). Ingestion and inhalation of and dermal contact with this concentration 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 inadequate or no human studies to show that a substance causes cancer. Ingestion and inhalation of the level of chloroform detected in this well would not pose a significant increase in cancer risk, even if this well were used for drinking and if this level were chronically inhaled. Evidence associating dermal exposure 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, individuals concerned 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 for drinking, cooking, showering, and other such household activities:
Tetrachloroethylene (TCLEE or PCE) was detected at 2.16 ppb in this well. Ingestion or inhalation of water containing PCE or dermal contact with it could result in PCE exposure. A daily dose estimate for water with this amount of PCE would be 0.000062 mg/kg/day for adults and 0.00022 mg/kg/day for children. ATSDR's intermediate, oral MRL is 0.1 mg/kg/day (ATSDR, 1993g), and EPA's chronic, oral RfD is 0.01 mg/kg/day (IRIS, 1994). Ingestion and inhalation of and dermal contact 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 considered for placement into either the B2 or the C cancer group. The EPA considers B2 carcinogens probable human carcinogens; while animal studies indicate that they cause cancer, there are not adequate human studies to confirm that finding. C Carcinogens are those substances for which no human studies, and only limited animal studies, exist to indicate that they cause cancer. The level of PCE detected in this well (even if used for drinking) would not result in a significant increase in cancer risk. There is no established 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 use 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. 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 26,000 ppb. Although this well is mainly used for domestic purposes, nitrate exposure could occur through ingestion 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 and 2.60 mg/kg/day for children. 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 is used for drinking. 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 their fetuses.
Well 551A
Lead was detected in well 551A at a concentration of 100.0 ppb and nitrate at a concentration of 12,000 ppb. The residence served by this well receives bottled water, so this well is mainly used for domestic purposes. Five residents use this well. This well qualifies for connection to a replacement water supply and use of the well may not continue. The EPA Action Level for lead in drinking water is 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 who use 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 (including using 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 and the 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 mainly used for domestic purposes, nitrate exposure could occur through ingestion of and dermal contact with water from this well (ATSDR, 1991; IRIS, 1994; and TOMES, 1994). A daily dose estimate for water containing 12,000 ppb nitrate is 0.34 mg/kg/day for adults and 1.2 mg/kg/day for children. 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 is used for drinking. However, using this well water at pre-1994 nitrate levels for drinking (including infant formula) or cooking may result in non-cancerous health effects 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 domestic purposes. Five people use well 578A. This well qualifies for connection to a replacement water source and use may not continue. The MCL for PCE and nitrate in drinking water are 5 and 10,000 ppb, 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 water containing PCE or dermal contact with such water could result in exposure to PCE. A daily dose estimate for water with this amount of PCE would be 0.000029 mg/kg/day for adults and 0.0001 mg/kg/day for children. Ingestion and inhalation of, and dermal contact with this amount of PCE are not likely to result 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 significant increase in cancer risk.
Lead has been found at a concentration of 119.0 ppb. Bottled water is supplied to the residents who use 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 (including using 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 and the 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 mainly used for domestic purposes, nitrate exposure could occur through ingestion of and dermal contact with water from this well (ATSDR, 1991; IRIS, 1994; and TOMES, 1994). A daily dose estimate for water containing 14,000 ppb 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 health effects in adults and children, even if this well is used for drinking. However, using this well water at pre-1994 nitrate levels for drinking (including infant formula) or cooking may result in non-cancerous health effects 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. Residents at this well have not been provided bottled water, so it is presumed that the well water is used for both drinking and domestic purposes. Three people use this well. This well qualifies for connection to a replacement water supply and the use of this well may not continue. The MCL for PCE in drinking water 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 water containing PCE or dermal contact with such water could result in exposure to PCE. A daily dose estimate for water with this amount of PCE would be 0.000041 mg/kg/day for adults and 0.00014 mg/kg/day for children. Ingestion and inhalation of, and dermal contact with this amount of PCE are not likely to result 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 significant increase in cancer risk.
Lead has been found at a concentration of 98.8 ppb in well number 579A. Bottled water is not supplied to the residents who use this well, therefore, it is presumed that this well is being used for drinking and other 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 (including using 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 and the possibility for additional lead exposure that might occur from the environment and workplace.
Nitrate has been detected in well 579A. Since bottled water is not provided, it is presumed that this well is used for drinking water and domestic purposes. Nitrate exposure could occur through ingestion of and dermal contact with water from this well. A daily dose estimate for water containing 14,000 ppb 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 health effects 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 and pregnant 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. Since bottled 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 well qualifies for connection to a replacement water source and the use of this well may not continue. The MCL for PCE, atrazine, and nitrate in drinking water are 5, 3, and 10,000 ppb, respectively. The EPA Action Level for lead in drinking water is 15 ppb.
PCE was detected in this well. Ingestion and inhalation of water containing PCE or dermal contact with such water could result in PCE exposure. A daily dose estimate for water containing 1.25 ppb of PCE would be 0.000036 mg/kg/day for adults and 0.00013 mg/kg/day for children. Ingestion and inhalation of and dermal contact with this amount of PCE are not likely to result 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 significant increase in cancer risk.
Atrazine has been detected in well water from well 613A. Atrazine exposure could occur through ingestion and inhalation of and dermal contact with water containing atrazine (TOMES, 1994). A daily dose estimate for water containing 5.81 ppb of atrazine is 0.00017 mg/kg/day for adults and 0.00058 mg/kg/day for children. Ingestion of, inhalation of, and dermal contact with atrazine in this well are not likely to result in non-cancerous health effects in adults and children, even if this well were used for a drinking water supply.
Nitrate has been detected in well 613A. Since bottled water is not provided, it is presumed that this well is used for drinking water and domestic purposes. Nitrate exposure could occur through ingestion of and dermal contact with water from this well. A daily dose estimate for water containing 11,000 ppb nitrate is 0.31 mg/kg/day for adults and 1.1 mg/kg/day for children. Ingestion of the level of nitrate detected in this well is not expected to result in non-cancerous health effects in adults and children. 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 their fetuses.
Well 616A
Well 616A was found to have chloroform at 8.33 ppb, PCE at 1.26 ppb, arsenic at 10.9 ppb, and nitrate at 16,000 ppb. This residence is provided with bottled water, so this well is used mainly for domestic purposes. Ingestion of the well water is estimated to take place 5% of the time. Six residents use this well. This well qualifies for a replacement water source and the use of this well may not continue. The MCL for chloroform, PCE, arsenic, and nitrate in drinking water are 100, 5, 50, and 10,000 ppb, respectively.
Chloroform was detected in this well. A daily dose estimate for water containing 8.33 ppb of chloroform is 0.00024 mg/kg/day for adults and 0.00083 mg/kg/day for children. Ingestion and inhalation of and dermal contact of this concentration of chloroform in this well are not likely to result in 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 significant increase 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 of water containing PCE or dermal contact with such water could result in PCE exposure. A daily dose estimate for water with 1.26 ppb of PCE is 0.000036 mg/kg/day for adults and 0.00013 mg/kg/day for children. Ingestion and inhalation of and dermal contact with this amount of PCE are not likely to result 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 significant increase in cancer risk.
Arsenic has been detected in well 616A at a concentration of 10.9 ppb. Ingestion is the most significant route of exposure from arsenic in this well. A daily dose estimate for water containing this amount of arsenic is 0.00031 mg/kg/day for adults and 0.0011 mg/kg/day for children. Ingestion of the amount of arsenic detected in this well would not be expected to result in non-cancerous health effects in adults or children, even if this well were used for drinking water. In addition, use of this well 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, nitrate exposure could occur through ingestion of and dermal contact with water from this well. A daily dose estimate for water containing 16,000 ppb nitrate is 0.46 mg/kg/day for adults and 1.6 mg/kg/day for children. 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 may result 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, the maximum concentration detected for each chemical will be evaluated, and any well judged to contain chemical concentrations of public health concern will be identified by well number and specific contaminant. Recommended actions for such wells will then be subsequently discussed in the Recommendations section of this Assessment.
Arsenic
Those wells are used for both drinking water and domestic purposes. The maximum concentration detected was measured in well 601A at a concentration of 14.4 ppb; the MCL for arsenic in drinking water is 50 ppb. Each of those wells are used by three people. Based on 14.4 ppb, a daily dose estimate would be 0.00041 mg/kg/day for adults and 0.0014 mg/kg/day for children. Ingestion of the amount 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 in here is not expected to result in a significant increase in cancer risk. All of the listed well, except wells 864A and 1354A, qualify for connection to a replacement water source and the use of these well may not continue.
The level of arsenic detected in this well 595A was 9.59 ppb. The residents using this well are provided with bottled water, so this well water is used mainly for domestic purposes. The well is used by three people. A daily dose estimate for water containing this amount of arsenic is 0.00027 mg/kg/day for adults and 0.00096 mg/kg/day for children. Ingestion of the amount of arsenic detected in this well would not be expected to result in non-cancerous health effects in adults or children, even if this well were used for drinking water. In addition, use of this well is not expected to result in a significant increase in cancer risk. This well qualifies for connection to a replacement water source and 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 15 ppb. This well is used for both drinking and domestic purposes (cooking, washing, and bathing) since bottled water is not provided. 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 (including using 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 the possibility for additional lead exposure that might occur from the environment and workplace. Three people use this well. This well qualifies for connection to a replacement water source and the use of this well may not continue.
Types of Lupus
There are two main types of lupus: systemic lupus erythematosus (SLE) and discoid lupus
erythematosus (DLE). SLE is a chronic inflammatory condition that can affect any of the body's
organs 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, the
disease 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 the sun -- such as the ears, face, scalp, neck, and forearms. In extreme cases, it could spread to the remainder of the trunk. The inflammation can cause permanent scarring, destruction of the hair follicles 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 the symptoms 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 in
blacks 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 is
less marked. The prevalence rate of lupus in the U.S. is about 30/100,000. Prevalence refers to the
total number of cases of SLE, new and old, at a given time (point prevalence) or over a given period of
time (period prevalence). Prevalence rates vary depending on both the incidence (number of new
cases during a given time period) and the duration of disease; therefore, both disease remission and
mortality are crucial factors. National databases indicate that the incidence as well as prevalence rates
have increased over the last few decades (Hopkinson, 1994, p. 290-293). Individual state rates are not
available.
SLE, in comparison, is as common as multiple sclerosis (prevalence rate 30/100,000), less common than 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 and Bacon, 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 10th decade 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 their teens, twenties, and thirties, 90% to 95% are female. Thereafter, the female preponderance again falls to that observed before puberty (Wyngaarden and Smith, 1988, p. 2012).
The disorder is approximately three times more common among American blacks than American caucasians. Certain North American Indian tribes (Sioux, Crow, and Arapahoe) have an even greater predisposition toward SLE. Asians have been less studied; however, the data suggest that they are affected to approximately the same extent as American blacks. The overall annual incidence of SLE is about 6 new cases per 100,000 population per year for relatively low-risk populations and about 35 per 100,000 population per year for relatively high-risk populations. The chance of a black female developing 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 developing SLE. If a family member has SLE, the probability of SLE increases (about 30% for identical twins and 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 with lupus 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. Additional evidence to support this interpretation include the development or worsening of lupus with pregnancy or 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 is extremely rare in children under 4. In children, the ratio of females to males with lupus varies from 4:1 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. What dictates the severity of the disease is the extent of organ involvement. The most severe disease often occurs in black female children, although the incidence of the disease is also higher in blacks in general. Three broad manifestations of the disease have a poor prognosis: lupus nephritis (kidney involvement), 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 susceptible
individuals 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, and
the hydralazine anti-convulsants. The environmental records do not disclose the presence of those
chemical 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 detected in wells north of Basin F on RMA, but until recently nitrosamines were not detected downgradient of the treatment system. The detection of the nitrosamine N-Nitrosodimethylamine (NDMA) in the Offpost area at very low levels (0.2 - 2 ng/L) has resulted in a commitment by RMA and Shell Oil Company 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 genetic factors in the cause of SLE is clearly demonstrated by studies of monozygotic twins. Rare cases of twins separated at birth and raised in different environments but both developing SLE within a short time of each other are well documented. Recently, rates of 23% for monozygotic twins and 9% for dizygotic twins have been reported (Deapen et al., 1986). These data further support the idea that both genetic 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 in patients already diagnosed with the disease. For example, while ultraviolet (UV) light probably does not cause lupus, at least a third of patients are photosensitive and have disease flares following UV exposure. 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 can sensitize patients to UV light. Psoralens are chemicals that increase sun sensitivity in patients who are sun sensitive. Some examples of foods with psoralens are celery or celery salt, parsnips, parsley, and figs (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 common infections, 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 or emotional 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 how often stress aggravates lupus (Krieg, 1990, p. 19).
Hair dyes contain high levels of hydrazines and other chemicals that are related to procainamide and hydralazine and can be absorbed thorough the scalp. One study has found that patients exposed to hair dyes have a significantly increased risk of lupus (Freni-Titulaer et al., 1989). Further studies are needed 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 used in breast implants. Although this observation has been made, more studies are needed to follow up on this finding (Krieg, 1990, p. 19).
Diagnosis of Lupus
Lupus can be diagnosed through various blood tests performed by a physician. All lupus cases are
individual and are treated in different ways. The drugs used to control lupus range from aspirin and
anti-inflammatory agents (e.g., Motrin) to corticosteroids (e.g., Prednisone) and immunosuppressant
drugs (e.g., Cytoxin). Anti-malarial drugs are also occasionally used. Lifestyle is extremely important
in controlling lupus. Proper nutrition, avoidance of excess stress and sun exposure, and getting both
rest and exercise are all aspects of treatment. Learning to cope with a chronic illness is an important
part 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 understand
what causes the immune system to produce the abnormal antibodies (Aladjem, 1992, p. 2). The two
primary factors thought to be important in the production of autoantibodies are environmental agents
and genetic factors of the patient. It is likely that mutual dependence of these factors is required for
autoantibodies to develop. For instance, a person would need exactly the right combination of genes
and contact with a particular environmental agent for autoantibodies to be formed. Several lines of
evidence seem to support this notion. For example, certain drugs (environmental agents) discussed
earlier are capable of inducing antinuclear antibodies as well as clinical symptoms of lupus. It is also
believed 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 single
cause of the disease but rather multiple responsible agents. Several factors provide evidence of the
importance of genetic influences: increased frequency of lupus in identical twins and in certain
families with lupus, the increased representation of the disease in certain racial groups, and the
identification of certain genes (HLA genes) associated with the disease (Aladjem, 1992, p. 9). The
other major question in lupus research is why the antibodies that are formed go on to produce clinical
disease. 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 of America, Inc.
More Information About Diabetes
Definition of Diabetes
Diabetes (also known as diabetes mellitus or "sugar" diabetes) is the name given to the chronic disease
that describes a group of disorders in which the body either does not produce or does not respond
appropriately to insulin. Insulin is a hormone produced by beta cells in the pancreas and is used to
regulate carbohydrate metabolism by controlling blood glucose (sugar) levels. When insulin is not
available for this conversion, glucose builds up in the blood. High glucose levels are a common factor
in 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, the leading cause of kidney failure, and one of the major risk factors for heart disease and stroke. It is also responsible 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-Dependent Diabetes Mellitus, or IDDM, and Type II diabetes, also called Non-Insulin Dependent Diabetes Mellitus, or NIDDM (American Diabetes Association, 1988a). A third type of diabetes is Gestational Diabetes (CDPHE, 1992b, p. i).
Type I Diabetes
This type of diabetes usually begins in childhood and is often called juvenile diabetes. This type of
diabetes occurs when the body produces little or no insulin. Therefore, most insulin-dependent
diabetics have to inject insulin into their bodies daily (American Diabetes Association, 1989a). Type I
diabetes can develop at any age, although most cases are generally diagnosed when the patient is less
than 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 weight loss, 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 prone to 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 the U.S. and accounts for only 10% of all cases of diabetes. Although it is much less common in the general 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 (1 new case per 7,000 children per year), Type I diabetes is 3- to 4-fold more common than chronic childhood diseases such as cystic fibrosis, peptic ulcer, juvenile rheumatoid arthritis, or leukemia, and it 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 and women, lower in blacks than whites, and markedly less common in Hispanics, Asian Americans, and native Americans (American Diabetes Association, 1989a, 1994). The peak incidence is between 10 and 12 years of age in girls and 12 and 14 years of age in boys (CDPHE, 1992b, p. i). Two to 5% of siblings of individuals with Type I diabetes will develop the disorder, and among identical twins, one of 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 as being important in the development of Type I diabetes, and several causative agents including viruses and drugs have been proposed, but none have gained widespread acceptance (American Diabetes Association, 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 and regulation of the immune response. Inheritance of certain HLA types, principally the DR3 or DR4 loci, confers a tendency to develop Type I diabetes. Genetic factors alone are inadequate to cause Type I diabetes; i.e., it is the tendency and not the disease itself that is inherited. The fact that identical twins are concordant for Type I diabetes only 50% of the time suggest that some external environmental factor(s) is needed to initiate the disease process. These factors and their mode of action 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 with
diabetes. 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 (American
Diabetes Association, 1989b). Diagnosis of Type II diabetes is often difficult due to the absence of
symptoms. It is estimated between 6% and 7% of people in the U.S., or up to 1 in 15, have diabetes
and are not aware they have it. Type II diabetes occurs more often in the elderly and in minority
populations. Colorado data show higher prevalence of diabetes and increased complications in both
these 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 not in 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 persons over 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 another factor, such as obesity, to bring on the disease. Warning signs of Type II diabetes include any symptoms 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 blood sugars 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 factors for diabetes and other chronic diseases. Early recognition of diabetic eye disease can permit treatment and preservation of sight. Similarly, planned pregnancies and expert prenatal care can minimize the incidence of birth defects (CDPHE, 1992b, p. i).
It is important for all individuals with diabetes to monitor their exercise and diet. Insulin-dependent diabetics must monitor their use of insulin. If a diabetic does not control these factors an imbalance between insulin and sugar in the body can create a diabetic emergency. Signals and symptoms of a diabetic emergency include changes in the level of consciousness, rapid breathing and pulse, and feeling and looking ill (American Diabetes Association, 1989b).
Gestational Diabetes
Gestational diabetes is diabetes that is first recognized during pregnancy. Women who have either
Type 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 of gestational diabetes is made by glucose tolerance testing. Treatment consists of dietary modification and in some cases, insulin injections for the duration of the pregnancy. Gestational diabetes generally concludes following pregnancy. Women who have had gestational diabetes have a greatly increased risk 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, with
an emphasis on Hispanics (ATSDR, 1994d). Hispanics had the highest prevalence of diabetes in
Colorado compared with whites and blacks. In 1990, the age-adjusted prevalence of diabetes was 51
per 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 to address the health needs of Coloradans with diabetes. The council has released information that details recommendations for improving the health and well-being of Coloradans with diabetes. Residents should contact the Colorado Department of Health, Diabetes Control Program for a copy of the report or 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 for diabetes, diabetes prevalence and morbidity specifically related to Colorado residents, and recommendations for improving the health and well-being of Coloradans with diabetes. Those reports are Diabetes in Colorado: Approaching the Year 2000 and Diabetes Prevalence and Morbidity in Colorado Residents, 1980-1991 (CDH, 1992b and CDH, 1993c). For more information on diabetes or copies of these reports, residents should contact the Colorado Diabetes Control Program, under the direction of the Colorado Department of Health.
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