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1. ATSDR > Public Health Assessments & Consultations

PUBLIC HEALTH ASSESSMENT

MONTICELLO MILL TAILINGS (DOE) AND
MONTICELLO RADIOACTIVELY CONTAMINATED PROPERTIES
(aka MONTICELLO VICINITY PROPERTIES)

APPENDICES

Appendix A

Population Data
Monticello Mill Tailings Site
Monticello Vicinity Properties

Table A1. Population Data Table
Variable	City of Monticello	San Juan County
Total persons	1,806	12,621
Total area, square miles	2.74	7,821
Persons per square mile	659	2
% White	87.5	43.6
% Black	0.1	0.1
% American Indian, Eskimo, or Aleut	4.3	54.3
% Asian or Pacific Islander	0.3	0.3
% Other races	7.8	1.7
% Hispanic origin	12.3	3.5
% Under age 18	41.4	43.3
% Age 65 and older	10.0	7.1
Source: 1990 Census of Population and Housing, Summary Tape File 1B Extract on CD-ROM (Utah) (machine-readable data files). Prepared by Bureau of the Census. Washington, DC: The Bureau (producer and distributor), 1991.

Housing Data
Monticello Mill Tailings Site
Monticello Vicinity Properties

Table A2. Housing Data Table
Variable	City of Monticello	San Juan County
Households*	542	3,375
Persons per household	3.26	3.70
% Households owner occupied	77.9	77.3
% Households renter occupied	22.1	22.7
% Persons in group quarters	2.3	1.0
Median value, owner-occupied households, $	55,300	42,800
Median rent paid, renter-occupied households, $	199	187
* A household is an occupied housing unit. The definition does not include group quarters, such as military barracks, prisons, and college dormitories. Source: 1990 Census of Population and Housing, Summary Tape File 1B Extract on CD-ROM (Utah) (machine-readable data files). Prepared by Bureau of the Census. Washington, DC: The Bureau (producer and distributor), 1991.

Socioeconomic Data
Monticello Mill Tailings Site
Monticello Vicinity Properties

Table A3. Socioeconomic and Housing Variables Table
Variable	City of Monticello	San Juan County
Median household income, $	25,787	17,289
Per capita income, $	8,615	5,907
% Persons below the poverty level	12.6	36.4
% Persons aged >25 with high school equivalency or higher	79.9	59.7
% Occupied housing units lacking complete plumbing	3.7	28.8
% Occupied housing units on public water source	96.0	63.6
% Occupied housing units using private wells or other water source	4.0	36.4
Source: 1990 Census of Population and Housing, Summary Tape File 3 on CD-ROM (Utah) (machine-readable data files). Prepared by Bureau of the Census. Washington, DC: The Bureau (producer and distributor), 1992.

Appendix B

US EPA Contract Laboratory Program Target Compound List

VOLATILE ORGANIC COMPOUNDS	BASE NEUTRAL/ACID EXTRACTABLES
CHLOROMETHANE BROMOMETHAN VINYL CHLORIDE CHLOROETHANE METHYLENE CHLORIDE ACETONE CARBON DISULFIDE 1,1-DICHLORETHENE 1,1-DICHLORETHANE 1,2-DICHLORETHENE(total) CHLOROFORM 1,2-DICHLORETHANE 2-BUTANONE 1,1,1-TRICHLOROETHANE CARBON TETRACHLORIDE VINYL ACETATE BROMODICHLOROMETHANE 1,2-DICHLOROPROPANE cis-1,3-DICHLOROPROPENE TRICHLOROETHENE DIBROMOCHLOROMETHANE 1,1,2-TRICHLOROTHANE BENZENE trans-1,3-DICHLOROPROPENE BROMOFORM 4-METHYL1-2-PENTANONE 2-HEXANONE TETRACHLOROETHENE 1,1,2,2-TETRACHLOROETHANE TOLUENE CHLOROBENZENE ETHYLBENZENE STYRENE XYLENE(total)	PHENOL bis(2-CHLOROETHYL)ETHER 2-CHLOROPHENOL 1,3-DICHLOROBENZENE 1,4-DICHLORBENZENE BENZYL ALCOHOL 1,2-DICHLOROBENZENE 2-METHLYPHENOL bis(2-CHLOROISOPROPYL)ETHER 4-METHYLPHENOL N-NITROSO-D-N-PROPYLAMINE HEXACHLOROETHANE NITROBENZENE ISOPHORONE 2-NITROPHENOL 2,4-DIMETHYLPHENOL BENZOIC ACID bis(2-CHLOROETHOXY)METHANE 2,4-DICHLOROPHENOL 1,2,4-TRICHLOROBENZENE NAPHTHALENE(*) 4-CHLOROANILINE HEXACHLOROBUTADIENE 4-CHLORO-3-METHYLPHENOL 2-METHYLNAPHTHALENE(*) HEXACHLOROCYCLOPENTADIENE 2,4,6-TRICHLOROPHENOL 2,4,5-TRICHLOROPHENOL 2-CHLORONAPHTHALENE(*) 2-NITROANILINE DIMETHYLPHTHALATE ACENAPHTHYLENE(*) 2,6-DINITROTOLUENE	3-NITROANILINE ACENAPHTHENE(*) 1,4-DINITROPHENOL 4-NITROPHENOL DIBENZOFURAN 2,4-DINITROTOLUENE DIETHYLPHTHALATE 4-CHLOROPHENYL-PHENYLETHER FLUORENE(*) 4-NITROANILINE 4,6-DINITRO-2-METHYLPHENOL N-NITROSODIPHENYLAMINE 4-BROMOPHENYL-PHENYLETHER HEXACHLOROBENZENE PENTACHLOROPHENOL PHENANTHRENE(*) ANTHRACENE(*) DI-n-BUTYLPHTHALATE FLUORANTHENE(*) PYRENE(*) BUTYLBENZYLPHTHALATE 3,3'-DICHLOROBENZIDINE BENZO(a)ANTHRACENE(*) CHRYSENE(**) bis(2-ETHYLHEXYL)PHTHALATE DI-n-OCTYLPHTHALATE BENZO(b)FLUORANTHENE(**) BENZO(k)FLUORANTHENE(**) BENZO(a)PYRENE(**) INDENO(1,2,3-cd)PYRENE(**) DIBENZO(a,h)ANTHRACENE(**) BENZO(g,h,i)PERYLENE(**)

Radioactive Contaminants

Uranium. Pure metallic uranium dust is known to be a very strong carcinogenic agent (1). However, pure uranium metal is very reactive chemically so it either oxidizes in air, preventing further oxidation, or ignites spontaneously at room temperature. The size of the granular structure normally determines the outcome; large chunks tarnish, and very small pieces burn. Water also reacts slowly with uranium.

There are a number of uranium oxides of concern at a mill site, as shown in Table C1 (2). UO₂ is uranium dioxide, a component of the various minerals in the raw ore. U₃O₈ is uranium octaoxide, UO₃ is uranium trioxide, and UO₄•2H₂O is uranium peroxide.

Uranium octaoxide is an insoluble radioactive metal oxide. It is odorless and has an olive-green to black color and solid or orthorhombic (trimetric) crystal structure. In milling, exposure to U₃O₈ dust may cause redness and swelling of the eyes and eye damage, with cataract formation occurring anywhere from 6 months to several years after a single exposure. Other short-term chemical acute health effects due to inhalation include lack of appetite, nausea, vomiting, diarrhea, dehydration, weakness, drowsiness, incoordination, twitching, sterility, blood disorders, kidney damage, convulsions, and shock. "Chronic inhalation may affect the lungs and tracheobronchial lymph nodes and may be associated with increased cancer of the lungs, bone, lymphatic, and hemopoietic tissue. The major organ for uranium toxicity is the kidneys"(3).

Typically, uranium compounds taken into the body are more chemically toxic than radioactively toxic. Animal studies have shown that uranium primarily affects two parts of the kidneys, the glomerulus and the proximal tubules (4). The result is a decrease in filtration rate by the glomerulus and a disruption of solute reabsorption by the tubules. Uranium is loosely bound in the kidneys. It clears within a few weeks, and repair processes start. Chronic repeated exposures typical of exposures uranium millers and miners encounter may affect the repair process. Deaths from nephritis and sclerosis have been reported for both uranium millers and miners (5,6). Nephritis is an acute or chronic inflammation of the kidney; a sclerosis is a hardening of the kidney tissue.

Some animal studies also indicate that uranium administered orally (7), by inhalation (8), or subcutaneously (9) may cause minor liver conditions. These include congestion with blood, exaggerated growth of the hepatocyte cells, and blood circulation changes.

Radium and Thorium. Radium and thorium present complications. Because of these complications, we will discuss both elements. Radium has three isotopes. They are radium-228, radium-226, and radium-224. Thorium has four: thorium-234, thorium-232, thorium-230, and thorium-228. The movement of the thorium and radium radionuclides inside the body is different. Radium and thorium exhibit different behaviors because of the various transmutation⁽²⁾ possibilities, i.e., the transition of one isotope to another depends on radiation characteristics, half-lives, decay energies, etc.

The focus here will depend on the radionuclides' retention in the bone. There are two classes of "bone seekers": surface seekers and volume seekers. Thorium tends to accumulate on bone surfaces; while radium tends to locate within the volume of the bone. Bone surface seekers are in the immediate vicinity of blood vessels. Thorium, since it is a bone surface seeker, may cause leukemia. The decay products of thorium may remain in the bone, transfer to other portions of the body, or exit the body entirely.

Radon. The United States Environmental Protection Agency (EPA) has listed radon as the second leading cause of lung cancer in the United States (11). One cannot see, smell, or taste it. Good ventilation is necessary to prevent radon accumulation indoors, but outdoors radon is usually found in very low concentrations and generally should not present a health risk. However, since radon is produced from uranium and thorium, there are fairly large amounts of radon releases near uranium processing sites.

Uranium and thorium are naturally occurring radioactive materials present in all soils. Each decays through a sequence or decay chain of radionuclides that includes radon. The isotopes of radon that are the most abundant in soil are radon-220 and radon-222. Since radon is a nonreactive noble gas, it can pass through the soil and escape into the atmosphere. Radon-222 achieves a higher air concentration, which causes it to be a larger public health hazard. The decay products of radon are electrically charged, so they attract and attach to particles floating in the air. The radioactive contamination in the air arises mainly from the radon-222 parent, its daughters that are attached to dust particles, and its unattached daughters (12). The radon daughters, being heavy metals, react with proteins and can potentially be trapped in the lungs of those breathing radon gas (13).

There are a number of health problems related to radon-220 and radon-222. The lungs retain a large amount of radon decay products produced in them. Radon decay causes radiation exposure of the mucosa of the nose, pharynx, and tracheobronchial tree, and that exposure can lead eventually to cancer. Measurements of the radon concentration in the sinus and mastoid air spaces show that radon and its decay products contribute a significant portion of the total alpha dose to the sinus and mastoid epithelium (10). The healthy human respiratory tract is lined with ciliated cells (cilia are like motorized hairs) and other cells that produce a layer of thick mucus. The beating of the cilia create upward currents in the mucus, forming a mucociliary escalator that carries entrapped hazardous particulate substances upward to where they can be swallowed and eliminated by the digestive tract. In people who smoke and, to a lesser extent, people who have respiratory tract damage from particulate-born acid air pollutants such as sulfurous and sulfuric acid, the cells responsible for this elimination mechanism are damaged. Radon daughters can remain trapped in their lungs for a much longer time (14).

The noble gases radon-220 and radon-222 can diffuse into the bloodstream, where they deposit in the fatty tissues. Cancer and genetic effects are among the long-term delayed effects. However, cancer is most frequently observed in the hematopoietic system, thyroid, bone, and skin (15), with leukemia occurring as the most likely form of malignancy.

Studies of miners (especially of uranium miners) have shown an incidence of lung diseases, including lung cancer, that increases with the concentration and duration of radon exposure (13). These studies associating radon and radon daughters with lung cancer are confounded by the presence of other radionuclides and the silicon dust the miners inhale, and they are also confounded by higher smoking rates among miners than in the general population (13). Efforts to extend the association with cancer reported for the high radon-222 levels (100 to 10,000 picocuries per liter [pCi/L]) to environmental levels (1 to 10 pCi/L) have met with mixed results. Here in the United States, counties with high lung cancer mortality rates (> 8 in 100,000) have lower reported indoor radon levels (0.4 to 2 pCi/L) than the radon levels (0.9 to 4 pCi/L) in counties with low lung cancer mortality rates (< 4 in 100,000); lung cancer deaths decrease with increasing exposure to radon (16, 17). A group of Swedish researchers examined a wider range of indoor radon levels (from less than 1.4 to more than 10.8 pCi/L) and found no significant association with the relative risk of lung cancer in those who never smoked (18). But the relative risk for those who smoked at least 10 cigarettes per day and were exposed to more than 10.8 pCi/L was three times that of the smokers exposed to less than 4 pCi/L, and more than 30 times the risk of the general population exposed to less than 4 pCi/L (18).

Nonradioactive Contaminants in Soil and Sediment

Beryllium. Soil and sediment off site contain 1 milligram (mg) beryllium per kilogram (kg) soil, which is below the reference dose media evaluation guide (RMEG) of 10 parts per million (ppm). An RMEG is a soil environmental media evaluation guide (EMEG) based on EPA's oral reference dose for absence of noncancer effects. Moreover, ingestion of up to 25 mg/kg/day beryllium has failed to produce adverse noncancer effects in animals (19). A 10-pound child would have to consume 250 kg of the soil each day to ingest the maximum amount of beryllium shown not to have these adverse effects. A significant association between beryllium ingestion and cancer has not been shown, probably because absorption from the gut is poor (19, 20). Dermal absorption is also poor, but beryllium is absorbed upon inhalation (20). When inhaled, its primary hazard is to the point of entry -- the lung (20). Inhaled beryllium has been associated with lung cancer in humans and animals. It is classified B2, a probable human carcinogen, with a unit inhalation risk of 2.4 x 10^-3 (µg/m³)^-1 (19). Assuming a 70-kg human inhales 20 cubic meters/day, the inhalation slope factor is 8.4 mg/kg/day. EPA staff members have drafted a method for determining preliminary remediation goals for carcinogens and noncarcinogens in soil based on route of exposure and land use (21). For a soil contaminant that could present a cancer risk by inhalation and/or ingestion, the following formula expresses the soil concentration (in mg contaminant per kg soil, or ppm) associated with a one-in-a-million risk of cancer:

PRG =

TR X AT X 365 days/yr EFX{(SFoX10-6kg/mgXIFsoil/adj) + (SFiXIRage-adjX[1/VF+1/PEF])}

where

PRG is the contaminant concentration in the soil associated with TR, the target risk (10-6) for AT years average exposure at 365 days/year with an exposure frequency (EF) of 350 days/year to a soil contaminant having an oral slope factor of SFo, an inhalation slope factor SFi, and a soil-to-air volatilization factor of VF. The age-adjusted soil ingestion factor, IFsoil/adj, is assumed to be 114 mg-yr/kg-day, the age-adjusted inhalation rate, IRage-adj, is assumed to be 14.6 m3-yr/kg-day, and the particulate emission factor, PEF, is assumed to be 4.63X109 m3/kg (21).

For beryllium, assumed to be present chiefly as the oxides, the particulate contribution will be very much greater than that from volatilization, causing the 1/VF term to drop out. Because beryllium causes cancer by inhalation only at the port of entry (lung) and is poorly absorbed by ingestion with no significant reported associated carcinogenicity, the SF_o term also drops out. Thus, the soil concentration of beryllium associated with a one-in-a-million inhalation risk of cancer for residents who are in this area 350 days/year, 24 hours/day, for their entire lifetimes would be almost 3,000 ppm; the 1 ppm present off site therefore would present no increased risk of lung cancer to the people living in the area.

Lead. Children near the Monticello Mill Tailings Site could play in soil containing as much as 22 ppm lead. These concentrations are close to background and below even the most conservative standards likely to be considered in the near future (22). The exact relationship between the lead concentration in soil and that in children's blood is in dispute among scientists. According to one theory, the average concentration of lead in their blood is unlikely to be increased by as much as 0.1 (µg) lead per deciliter (dl) of blood, although the relationship would depend on many factors, such as the chemical form of the lead, the soil particle size, and the nutritional state of the children (22). In one case, this increase was calculated using the relationship reported between soil and blood lead concentrations observed in Helena Valley in Montana and Silver Valley in Idaho (22). The following equation was derived:

natural log (blood lead in µg/dl) = 0.879 + 0.241 X natural log (soil lead in ppm)

Some factors (soil particle size, chemical species of lead, nonsoil lead sources, population demographics such as age and distribution of wealth, nutritional status, etc.) upon which a soil-lead relationship depends are site specific. By varying assumptions about these and other factors, it is possible to form different conclusions about the potential for lead-induced harm.

Young children are at risk from lead ingestion during the years (ages 2-4 years) they are prone to pica behavior (ingestion of nonnutritive substances, such as soil). Ingestion of small amounts of lead by children is associated with depressed intelligence quotient (IQ) scores, slow growth, and hearing deficits (23). Exposure to larger amounts of lead could harm the fetuses of pregnant women, leading to premature delivery, low birthweight, or miscarriage. Moreover, lead has caused tumors in laboratory animals, suggesting it could cause human cancer (23). Lead is classified by the EPA as B2 (probable human carcinogen), although the available data are not sufficient for quantitative assessment (19). Middle-aged men may become hypertensive from small increases in their blood lead levels (23).

EPA scientists point out that the health effects of lead, especially those on "children's neurobehavioral development, may occur at blood lead levels so low as to be essentially without a threshold" and consider it inappropriate to derive a reference dose (RfD) for oral exposure to lead (19). Because a population's blood lead concentration is directly related to the local soil lead concentration (22), it seems inadvisable to use soil comparison values or standards. Under certain conditions, however, a soil standard may be used. If, as in the case of residents living near the Monticello Mill Tailings Site, there are no lead exposures from additional pathways, young children are probably protected by keeping barren soil near them below 100 ppm, and adults are probably protected from increases in their blood lead levels by keeping soil lead concentrations below 120 to 333 ppm (22). These concentrations are well above the maximum soil concentration found near Monticello.

Thallium. Thallium is no longer used as a rat poison, because the oral dose sufficient to kill half of treated rats is three times greater than that which would have the same proportion of lethality in humans (14). EPA verified an oral RfD of 0.00009 mg thallium (as the sulfate)/kg/day (19). This value resulted from application of an uncertainty factor of 3,000 to the highest oral no-observed-adverse-effects-level (a NOAEL of 0.25 mg thallium sulfate/kg/day) administered to rats for 90 days in the key study (19). All treated rats in this study, down to the lowest dose of 0.01 mg/kg/day, showed hair loss, excessive eye tearing and bulging eyeballs, but EPA did not consider these effects adverse (19). The uncertainty factor of 3,000 included factors of 10 for extrapolation from subchronic to lifetime exposure, 10 to allow for sensitive subpopulations, and 3 to account for lack of reproductive and lifetime toxicity data (19). Moreover, it is not clear that the effects in the study would not be considered adverse to human health. Thallium has been used as a depilatory (hair remover) by some people, but involuntary loss of all hair from the head and body might not be welcomed by all people (14). Finally, reproductive and developmental effects do exist in the thallium toxicity database (19, 24). A strain of rats different from that used in the key study exhibited testicular injury at 0.7 mg thallium/kg/day for 60 days, with no NOAEL identified (19). Pups born to pregnant rats treated with 0.08 mg or more thallium/kg/day exhibited poor learning capacity, with no NOAEL identified, suggesting neurological vulnerability in the developing or young animal (24). For all these reasons, use of the RfD to estimate a soil RfD-based medium evaluation guide would not be unreasonably conservative. If a 10-kg child prone to pica behavior ingested 5 grams (about a teaspoon) of soil per day contaminated by 0.2 ppm thallium, the resulting dose would be the RfD (25). The sample quantitation limit applied to off-site soil is 10 times this RMEG (26). More sensitive analytical methods are available to protect the exposed public (24).

Nonradioactive Contaminants in Groundwater

Arsenic. Arsenic occurs in the environment in both inorganic and organic forms. In the absence of specific information about the form of arsenic in the soil and groundwater, public health would be better protected by assuming that all arsenic found on-site in groundwater and soil is in the much more toxic inorganic form. Chronic human ingestion of as little as 0.01 to 0.06 mg/kg/day (e.g., 350 to 2,000 ppb in drinking water) of inorganic, but not organic, arsenic has been associated with evidence of impaired circulation in the extremities, such as significantly increased incidence of blackfoot disease and symptoms similar to Raynaud syndrome (27). Other noncancer effects of low-level human oral exposure to the inorganic form included abdominal pain, diarrhea, liver damage (hepatomegaly and portal hypertension), skin lesions (melanosis and keratosis), and mild peripheral neuropathy (27). No effects were seen consequent to oral intake of as much as 0.006 mg inorganic arsenic/kg/day (e.g., 21 ppb in drinking water) (27). Human ingestion of 0.009 to 0.04 mg inorganic arsenic/kg/day (e.g., 315 to 1,400 ppb in drinking water) for 12 to 60 years has been associated with increased incidence of cancer of the skin, lung, and liver (27). Although EPA declined to verify an oral slope factor for inorganic arsenic, that agency did derive a unit risk in water of 0.00005/µg/L (19). Because EPA assumes chemical carcinogenesis to be without a threshold, the derived value suggests lifetime exposure to drinking water containing as little as 0.2 ppb inorganic arsenic might result in a low increased cancer rate in the exposed public. Because of pharmacokinetic considerations, ingestion of less than 250 µg/day (0.004 mg/kg/day) does not affect blood arsenic concentration -- i.e., an adverse effect on the public health from arsenic ingestion would be unlikely from concentrations of inorganic arsenic less than 120 ppb in drinking water (28). Drinking water used by residents near the mill site is either supplied by the city from surface water taken upstream of the mill site, or taken from wells that tap the Burro Canyon Aquifer. These water sources have not exceeded 50 ppb (29). Since 1984, the alluvial aquifer has not exceeded 131 ppb off site (29). This value is unlikely to affect the public health adversely for two reasons. First, there is no evidence that any wells that have been supplying potable water tap the alluvial aquifer, although it is possible that some wells might do so now or in the future in the absence of institutional controls, such as ordinances to prevent screening this aquifer. Second, there is little likelihood that this maximum value has been reached with sufficient frequency to result in an average chronic intake in excess of 120 ppb for any individual.

Vanadium. Vanadium is a nonradioactive chemical element that makes up about 0.02% of the earth's crust. After refining, it is a light gray, shapeable, flexible metal that is hardened and embrittled after reaction with oxygen, nitrogen, or hydrogen. Vanadium is found in air, soil, food, plants, and animals. Although some evidence suggests that vanadium may be an essential trace element for mammals, this issue has not been resolved. In the mill operated at Monticello, the vanadium and its compounds were extracted as vanadium pentoxide (V₂O₅). Vanadium pentoxide (red cake) is an odorless, yellow to rust-brown crystalline powder. Vanadium pentoxide and vanadates are the vanadium compounds most likely released from the Monticello Mill Tailings Site onto nearby properties.

Occupational exposure to vanadium-containing dusts is encountered in the mining of vanadium-bearing ores. Most of the vanadium-bearing ores in the United States come from Arkansas, Colorado, Utah, and Idaho. In milling, exposure to vanadium-containing dust can occur on and near the production sites. These dusts can contain numerous vanadium compounds, particularly vanadium pentoxide and, to a lesser extent, the vanadates. Numerous exposures to vanadium compounds have occurred during the cleaning of oil-fired burners, where the dust is generated from the residual oil ash of high-vanadium content oil.

Much of the information on the public health effects of vanadium and its compounds on humans has come from reports of accidental exposures of workers in vanadium processing and manufacturing plants and in boiler cleaning operations. However, some questions posed by these studies have prompted research involving controlled exposures of humans. Table C2 (30) summarizes the health effects of vanadium compounds on humans involved in those controlled exposure experiments. Most of the symptoms and signs indicated in Table C2 are short-term or acute health effects.

Epidemiologic studies of workers exposed for a long time indicate that exposures to vanadium cause health effects similar to those of the short-term studies described above. The acute effects of irritation were reversible after exposure ended. However, more severe chronic or delayed effects, i.e., emphysema and pneumonia, were reported, but the available data make these reports less than reliable. Table C3 (30) summarizes the epidemiologic studies conducted in populations exposed to vanadium compounds, mostly vanadium pentoxide.

Occupational exposure to vanadium and vanadium compounds, especially vanadium pentoxide, produces mainly irritation of the eyes and the upper respiratory tract, often accompanied by productive cough, wheezing, rales, chest pains, difficulty in breathing, bronchitis, questionable pneumonia, and rhinitis (31,32,33,34,35,36,37,38,39,40). There have been occurrences of green-to-black discoloration of the tongue, metallic taste, nausea, and diarrhea (38,39,40). Several studies have reported skin irritation (31,32,41,42,43,44). General fatigue, weakness, headache, and tremors of the hands have also been reported (32,33,39,40,45), but their relationship to vanadium exposure has not been demonstrated. Earlier investigations (40,46) that suggested systemic poisoning effects from vanadium have not been confirmed by later and more detailed studies (32,36,38,39,42).

The most likely routes of exposure that would result in environmental doses of vanadium and its compounds for the residents of Monticello are inhalation, skin contact, eye contact, and ingestion. Doses of vanadium and its compounds can cause short-term acute effects and long-term chronic or delayed effects. The occurrences of these effects depend on the amount of the vanadium and its compounds that are delivered to the body, i.e., the body dose. If the dose is not large enough, there would be no adverse health effects. The residents of Monticello likely were exposed to vanadium pentoxide through the airborne particulate releases from the mill site and resuspension of the released materials. The Occupational Safety and Health Administration (OSHA), the National Toxicology Program, and the International Agency for Research on Cancer do not list vanadium pentoxide as a carcinogen (47). The primary short-term effect (47) that could be caused by inhalation is respiratory irritation, which exacerbates respiratory diseases such as asthma. Low doses may cause other signs and symptoms (48, 49), such as runny nose, sneezing, coughing, asthma, headache, lack of appetite, dizziness, nervousness, and sleeplessness. High doses may cause signs and symptoms (48) such as weight loss, nausea, vomiting, stomach pain, bloody spit, blood in the urine, difficulty breathing, asthma, headache, anemia, dizziness, nervousness, sleeplessness, and for very high doses, even lung damage. Possible long-term effects from exposure (47, 49) are high blood pressure, lung effects, blood disorders, and liver and kidney damage.

Skin contact may cause dermal irritation, including rash and itching. Eye contact may cause eye irritation, including tearing and blurred vision. These signs and symptoms would apply to both short- and long-term effects (47).

Ingestion may cause the following symptoms at low doses: runny nose, metallic taste, blood disorders, high blood pressure, and kidney effects. The following effects may be caused at high doses: nausea, vomiting, diarrhea, stomach pain, and difficulty breathing. The effects that may be caused at very high doses are paralysis, convulsions, and even kidney damage. These signs and symptoms are for short-term effects (47, 49); there is no information available on significant long-term adverse health effects (47). Animal studies indicate that vanadium may be an essential requirement of the diet and that it contributes to glucose balance in animals (49). Vanadium is being investigated as a treatment for diabetes (48,50,51,52).

Table C4 shows occupational exposure limits established for vanadium pentoxide. Table C5 lists the environmental exposure limit and dose limits for the general public established for vanadium and its compounds.

The occupational limits are provided for informational purposes only. These limits are for use in the practice of industrial hygiene as guidelines or recommendations in control of potential health hazards and are not for use in the evaluation or control of community air pollution exposures. Although the OSHA permissible exposure limit is 0.05 mg(V₂O₅)/m³ time weighted average (TWA), a material safety data sheet (46) indicates that direct skin contact with air concentrations of about 0.03 mg(V)/m³ may result in dermal irritation, eczema with intense itching and discharge, generalized rashes such as hives, and possible sensitization resulting in contact dermatitis during acute exposures. During chronic exposures at these concentrations, repeated or prolonged contact may result in allergic eczema, sensitization, and dermatitis. Direct eye contact with air concentrations of greater than or equal to 0.018 mg(V)/m³ may result in eye irritation, profuse tearing, blurred vision, and a burning sensation of the conjunctiva during acute exposures. During chronic exposures at these concentrations, repeated or prolonged exposures may cause inflammation of the conjunctiva.

The signs and symptoms discussed above can also be caused by physical, radioactive, and chemical toxicants other than vanadium and its compounds. Only a medical diagnosis can determine the cause of reported signs and symptoms. Any residents of Monticello who develop any of these signs or symptoms and suspect that they may be caused by exposure to vanadium-containing or radioactive dusts should consult their physicians.

Table C2. Human Research Results on the Health Effects of Vanadium Compounds
SUBSTANCE	DURATION and EXPOSURE ROUTE	CONCENTRATION OF VANADIUM (mg/m3)	REPORTED EFFECTS	REFERENCE
V2O5 (vanadium pentoxide)	Unknown Respiratory	1-48	Respiratory irritation with bronchopneumonia, heart palpitations	53
V2O5	2-5 days Respiratory	10-32	Respiratory irritation, tremors, discolored tongue	54
V2O5	8 hours Respiratory	0.6	Coughing	55
V2O5	5 minutes Respiratory	0.6	Coughing, rales	55
V2O5	8 hours Respiratory	0.1	Coughing	55
V2O5	8 hours Respiratory	0.06	Coughing	55
V2O5, NaVO3 (ammonium metavanadate)	Unknown Respiratory	0.3-1.2	Eye, respiratory irritation	37
V2O5, NH4VO3	Unknown Respiratory	0.04-0.4	Respiratory irritation, discolored tongue	56
V2O5, V2O3 (vanadium trioxide)	1-5 years Respiratory	Unknown	Asthma in 3 of 120 workers	57
Ca3(VO4)2 (calcium vanadate)	1.5 days Respiratory	Unknown	Bronchitis, fever, headache, gastrointestinal (GI) distress	45
V-Al alloy (vanadium aluminum)	Unknown Respiratory	Unknown	Respiratory irritation, discolored tongue	58
VC (vanadium carbide)	Unknown Respiratory	Unknown	Little effect	38
FeV (ferrovanadium)	Unknown Respiratory	Unknown	Eye, respiratory irritation	38
V (vanadium metal)	Unknown Respiratory	Unknown	Respiratory irritation	38
(CHOH)(CO2NH4) (ammonium vanadyl tartrate)	45-68 days Oral	25 mg, 1-4/day	GI discomfort, discolored tongue, increased steroid excretion	59
(CHOH)2(CO2NH4)2 (diammonium vanadotartrate)	6 months Oral	25mg/day,2 wk; 125mg/day, 22 wk	GI discomfort, pharyngitis, tongue ulceration and discoloration	60

Table C3. Summary of Epidemiologic Studies with Vanadium
SUBSTANCE	DURATION and EXPOSURE ROUTE	CONCENTRATION of VANADIUM (mg/m3)	REPORTED EFFECTS	REFERENCE
Vanadium ore	<3 years Respiratory	0.1-2.212	Eye, respiratory irritation	39
V2O5 (vanadium pentoxide), vanadates	2.5 years (mean) Respiratory	0.01-0.52	Respiratory irritation, discolored tongue	38
V2O5	0.5-16 years 6 years (mean) Respiratory	Unknown	Cough, pulmonary effects with chest pain	40
V2O5	2-13 years 6.6 years (mean) Respiratory	Unknown	Eye, respiratory irritation, chest pain, bronchitis, emphysema	61
V2O5	2-3 years Respiratory	Unknown	Eye and respiratory irritation, bronchitis	61

REFERENCES FOR APPENDIX OF TOXICOLOGICAL INFORMATION

1. U.S. Environmental Protection Agency, Office of Radiation Programs. Final environmental impact statement for remedial action standards for inactive uranium processing sites, 40 C.F.R. 192, Volume II, October 1982.

2. Wrenn ME. Radiological surveys in and around Monticello, Utah, 1986.

3. Occupational Health Services, Inc. Material safety data sheet OHS24630 -- substance: uranium octaoxide. New York: Occupational Health Services. April 1994.

4. Agency for Toxic Substances and Disease Registry. Toxicological profile for uranium. Atlanta: U.S. Department of Health and Human Services, Public Health Service; 1990 Dec.

5. National Institute for Occupational Safety and Health, Division of Surveillance, Hazard Evaluation and Field Studies. Mortality patterns among a retrospective cohort of uranium mill workers, November 1983. Cincinnati: U.S. Department of Health and Human Services, Public Health Service, 1983.

6. Waxweiler RJ, Roscoe RJ, Archer VE, et al. Mortality follow up through 1977 of white underground uranium miners cohort examined by USPHS. In: Gomez M, editor. Radiation hazards in mining. New York: Society of Mining Engineers of the AIMMPE Inc., 1981: 823-830.

7. Domingo JL, Llobet JM, Tomas JM, Corbella J. Acute toxicity of uranium in rats and mice. Bull Environ Contam Toxicol 1987; 39(1):168-174.

8. Galibin GP, Pozdnyakov AL, Murav'eva LI. Biological effects of ammonium diruanate following prolonged inhalation. Gig Sanit Hyg Sanit; 31(10-12):338-344.

9. MacNider WDeB. A study of the acquired resistance of fixed tissue cells morphologically altered through process of repair, I. The liver injury induced by uranium nitrate. A consideration of the type of epithelial repair which imparts to the liver resistance against subsequent uranium intoxications J Pharmacol Exp Ther 1936; 56:359-372.

10. Mays CW, Jee WSS, Lloyd RD, Stover BJ, Dougherty GH, Taylor GN. Delayed effects of bone-seeking radionuclides. Salt Lake City: University of Utah Press, 1969.

11. U.S. Environmental Protection Agency. Consumer's guide to radon reduction. Washington, DC: Environmental Protection Agency. Air and Radiation 6604J, August 1992; 402-K92-003.

12. International Atomic Energy Agency. Inhalation risks from radioactive contaminants. Technical Reports Series No. 142, 1973.

13. Agency for Toxic Substances and Disease Registry. Toxicological profile for radon. Atlanta: U.S. Department of Health and Human Services, Public Health Service, December 1990.

14. Amdur MO, Doull J, Klassen C, editors. Casarett and Doull's toxicology, 4th edition. New York:McGraw-Hill Inc., 1991.

15. Occupational Health Services, Inc. Material safety data sheet OHS20081 -- substance: radon 222. New York: Occupational Health Services, April 1994.

16. Cohen BL. Expected indoor ²²²Rn levels in counties with very high and very low lung cancer rates. Health Physics 1989;57(6):897-907.

17. Cohen BL. Relationship between exposure to radon and various types of cancer. Health Physics 1993;65(5):529-531.

18. Pershagen G, Akerblom G, Axelson O, Clavensjo B, Damber L, Desai G, et al. Residential radon exposure and lung cancer in Sweden. New Engl J Med 1994; 330(3):159-164.

19. Environmental Protection Agency. Integrated Risk Information System (IRIS). Online database. Cincinnati, OH: Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, 1994.

20. Agency for Toxic Substances and Disease Registry. Toxicological profile for beryllium. Atlanta: U.S. Department of Health and Human Services, Public Health Service; April 1993.

21. Agency for Toxic Substances and Disease Registry. Attachment to a memorandum to Allan Susten from George C. Buynoski concerning EPA soil clean-up levels. HSED FY92 progress report, cleanup goals for surface soil.

22. Xintaras C. Analysis paper: Impact of lead-contaminated soil on public health. Atlanta: U.S. Department of Health and Human Services, Public Health Service, Agency for Toxic Substances and Disease Registry, May 1992.

23. Agency for Toxic Substances and Disease Registry. Toxicological profile for lead. Atlanta: U.S. Department of Health and Human Services, Public Health Service; June 1990.

24. Agency for Toxic Substances and Disease Registry. Toxicological profile for thallium. Atlanta: U.S. Department of Health and Human Services, Public Health Service; July 1992.

25. Agency for Toxic Substances and Disease Registry. HazDat (Hazardous Substance Release/Health Effects Database). Atlanta: U.S. Department of Health and Human Services, Public Health Service. March 23, 1994.

26. Dames and Moore. Revised final report: Monticello remedial action project. 1991 mill site characterization study. Volume I. February 4, 1992.

27. Agency for Toxic Substances and Disease Registry. Toxicological profile for arsenic. Draft for public comment. Atlanta: U.S. Department of Health and Human Services, Public Health Service; February 18, 1992.

28. Valentine JL, Reisbord LS, Kang HK, Schluchter MD. Arsenic effects on population health histories. In: Mills CF, Bremner I, Chesters JK, editors. Trace elements in man and animals--TEMA 5. Aberdeen, Scotland: Commonwealth Agricultural Bureaux, 1985:289-292.

29. U.S Department of Energy. Monticello Mill Tailings Site environmental reports for calendar years 1984-1995. March 1985-August 1996.

30. Department of Health, Education, and Welfare. NIOSH criteria for a recommended standard....occupational exposure to vanadium. Atlanta: U.S. Public Health Service, Center for Disease Control, National Institute for Occupational Safety and Health, 1977.

31. Zenz C, Bartlett JP, Theide WH. Acute vanadium pentoxide intoxication. Arch Environ Health 1962; 5:542-46.

32. Sjoberg SG. Vanadium pentoxide dust -- a clinical and experimental investigation on its effect after inhalation. Acta Med Scand Suppl 1950; 238:1-188.

33. Massmann W, Opitz H. Industrial medical implications of vanadium dusts. Arch Gewerbepathol Gewerbehyg 1954; 13:353-62 (German).

34. Pielstickler F. Injury to health by vanadium compounds -- symptomatology and prognosis. Arch Gewerbepathol Gewerbehyg 1954; 13:73-96 (German).

35. Symanski H. Status of research on occupational damage caused by vanadium. Arh Hig Rada 1954; 5:360-70 (German).

36. Sjoberg SG. Vanadium dust, chronic bronchitis and possible risk of emphysema -- a follow-up investigation of workers at a vanadium factory. Acta Med Scand 1956; 154:381-86.

37. Gul'ko AG. Characterization of vanadium as an industrial poison. Gig Sanit 1956; 21:24-28 (Russian).

38. Lewis CE. The biological effects of vanadium -- II. The signs and symptoms of occupational vanadium exposure. AMA Arch Ind Health 1959; 19:497-503.

39. Vintinner FJ, Vallenas R, Carlin CE, Weiss R, Macher C, Ochoa, R. Study of the health of workers employed in mining and processing of vanadium ore. AMA Arch Indian Health 1955; 12:653-42.

40. Wyers H. Some toxic effects of vanadium pentoxide. Br J Ind Med 1946; 3:177-82.

41. Browne RC. Vanadium poisoning from gas turbines. Br J Ind Med 1955; 12:57-59.

42. Tedbrock HE, Machle W. Exposure to europium-activated yttrium orthovanadate -- a cathodoluminescent phosphor. J Occup Med 1968; 10:692-96.

43. Fear EC, Tyrer FH. A study of vanadium poisoning in gas workers. Trans Assoc Ind Med Off 1958; 7:153-55.

44. Stokinger HE. Vanadium. In: Patty FA, editor. Industrial hygiene and toxicology. 2nd rev. ed. Toxicology. Fassett DW, Irish DD, editors. New York: Interscience Publishers, 2:1171-82, 1963.

45. Tara S, Cavigneaux A, Delplace Y. Calcium vanadate poisoning. Arch Mal Prof Med Trav Secur Soc 1953; 14:378-80 (French).

46. Dutton WF. Vanadiumism. JAMA 1911; 1:1648.

47. Occupational Health Services, Inc. Material safety data sheet OHS24780 -- substance: vanadium pentoxide. New York: Occupational Health Services; July 1994.

48. Henquin JC, Cartin F, Ongemba LN, Becker DJ. Improvement of mild hypoinsulinaemic diabetes in the rat by low non-toxic doses of vanadate. J Endocrinol 1991; 142(3):555-61.

49. Agency for Toxic Substances and Disease Registry. Toxicological profile for vanadium. Atlanta: U.S. Department of Health and Human Services, Public Health Service; July 1992.

50. Sprietsma JE, Schuitemaker GE. Diabetes can be prevented by reducing insulin production. Med Hypotheses 1994; 42(1):15-23.

51. Domingo JL, Sanchez DJ, Gomez M, Llobet JM, Corbella J. Oral vanadate and iron in treatment of diabetes mellitus in rats: improvements of glucose homeostasis and negative side-effects. Vet Hum Toxicol 1993; 35(6):495-500.

52. Shechter Y, Shisheva A. Vanadium salts and the future treatment of diabetes. Endeavour 1993; 17(1):27-31.

53. Sjoberg SG. Vanadium bronchitis from cleaning oil-fired boilers. AMA Arch Ind Health 1955, 11:505-12.

54. Williams N. Vanadium poisoning from cleaning oil-fired boilers. J Ind Med 1952; 9:50-55.

55. Zenz C, Berg BA. Human responses to controlled vanadium pentoxide exposure. Arch Environ Health 1967; 14:709-12.

56. Hudson TGF. Vanadium -- Toxicology and biological significance. Monograph No. 36, Elsevier Monograph Series. New York: Elsevier Scientific Publishing, 1964, pp 74-76, 126-33.

57. Roshchin IV, Il'nitskaya AV, Lutsenko LV. Effect on organism of vanadium trioxide. Gig Tr Prof Zabol 1964; 28:25-29 (Russian).

58. Roberts WC. The ferroalloy industry -- hazardous of the alloys and semimetallics -- part II. J Occup Med 1965; 7:71-77.

59. Dimond EG, Caravaca J, Benchimol A. Vanadium -- excretion, toxicity, lipid effect in man. Am J Clin Nutr 1963; 12:49-53.

60. Somerville J, Davies B. Effect of vanadium on serum cholesterol. Am Heart J 1962; 64:54-56.

61. Symanski H. Industrial vanadium poisoning, its origin and symptomatology. ARH Hig Rada 1954; 5:360-70 (German).

Appendix D

Other Community Concerns Evaluation

1. What is ATSDR, and what are the agency's responsibilities?

   The Agency for Toxic Substances and Disease Registry (ATSDR) is part of the U.S. Department of Health and Human Services. ATSDR's mission is to prevent exposure and adverse human health effects and diminished quality of life associated with exposure to hazardous substances from waste sites, unplanned releases, and other sources of pollution present in the environment. ATSDR has no regulatory authority, but the agency does recommend public health actions that address potential adverse health effects resulting from environmental releases from hazardous waste sites.

   ATSDR's staff is responsible for preparing public health assessments according to the Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA or Superfund). As mandated by that law, staff members conduct public health assessments of hazardous waste sites listed or proposed for listing on the National Priorities List (NPL) of the U.S. Environmental Protection Agency (EPA). ATSDR also responds to requests (petitions) to conduct public health assessments.

   Three primary sources of information are used in a public health assessment: environmental data, community health concerns, and health outcome data. ATSDR scientists do not routinely perform environmental sampling. The environmental data used in public health assessments come from the Department of Energy (DOE), the EPA, state and local environmental and health agencies, and other groups or individuals. In addition, ATSDR health assessors conduct site visits to make firsthand observations of current conditions at the site, land use, public accessibility, and demographic characteristics of the nearby community.

   Health assessors gather community members' health concerns to determine whether people who live or work near the site are experiencing specific health effects. Information from the public also helps ATSDR assessors determine how people might have been or might be exposed to hazardous substances in the environment. Throughout the public health assessment process, ATSDR staff members talk with people living or working at or near the site about site-related health concerns. Other sources of community health concerns are records from the site's public affairs office, EPA's community relations representative, and state and local health and environmental agencies.

   Health outcome documents identify health effects that occur in populations. Data from those documents, which come from sources such as state tumor registry databases, birth defects databases, vital statistics records, or other records, may provide information about the general health of the community living near a site. Other, more specific information, such as hospital and medical records and records from site-specific health studies, may be used. Demographic data that provide information on population characteristics (e.g., age, sex, and socioeconomic status) are useful in the analysis of health outcome data.

   ATSDR health assessors identify actual and perceived site-related health effects and the level of public health hazard posed by the site. They then make recommendations for the agency to DOE, EPA, and relevant state and local agencies, as appropriate, on preventing or alleviating human exposures to site-related contaminants. When indicated, ATSDR assessors identify a need for any follow-up health activities such as epidemiologic studies, registries, or community health education. Finally, ATSDR staff members provide a mechanism to reevaluate health issues as site conditions change (e.g., after site remediation or changes in land use) or when new information becomes available.

   The public health assessment includes a public health action plan (PHAP). The PHAP contains a description of actions ATSDR representatives and other parties will take at and in the vicinity of the site. The purpose of the PHAP is to provide a plan of action for preventing and mitigating adverse human health effects resulting from exposure to hazardous substances in the environment. ATSDR staff members monitor the implementation of the plan annually. Public health actions may include but are not limited to restricting site access, sampling, surveillance, registries, health studies, environmental health education, and applied substance-specific research.

   Public health assessments are distributed in three phases: an initial release (red cover), a public comment release (brown cover), and a final release (blue cover). The initial release document, which is prepared as part of the process of gathering and analyzing data and drawing conclusions and recommendations from the information evaluated in a public health assessment, goes for review and comment to the DOE component involved, EPA, and state and local environmental and health agencies. This release gives agencies the opportunity to comment on the completeness of information they have provided and the clarity of the presentation. The initial release comment period lasts 45 days. After the initial release, the ATSDR staff prepares the document for distribution to the general public. The public is notified of the document's availability at repositories (e.g., libraries and city halls) in the site area through advertisements and public notices in newspapers. The public comment period lasts 45 days. After public comments, ATSDR staff members address all public comments and revise or append the document as appropriate. The final public health assessment is then released; that document includes written responses to all public comments.

   A public health assessment is an ongoing process. ATSDR staff members revise final documents if new information about the environment, community health concerns, and health outcome data become available and are found to modify previous conclusions and recommendations.

2. Is the aquifer located beneath White Mesa Mill contaminated?

   Staff members of EPA Region VIII, the Nuclear Regulatory Commission, and Energy Fuels are investigating the concern that the aquifer located beneath the White Mesa Mill Site may be contaminated by UMETCO activities.

3. Can you provide additional information about the granary, golf course, and cemetery?

   Uranium mill tailings were found at the golf course and cemetery during the radioactive surveys performed throughout Monticello, and both tailings and ore were found at the granary. The tailings appear to have been introduced as a fill material for depressions or top dressing to improve surface quality. The radioactive surveys used the same type of equipment and methods described below to locate, quantify, and determine the extent of contamination. Contaminated sites were then scheduled for remediation. A summary of the survey equipment and methods appears below, followed by a discussion of remediation efforts and their status for each site.

   Scientists used a gamma scanner, a soil contamination monitor, soil collection and analysis equipment, and a bore hole logging device to assess radioactive levels. The gamma scanner determined the aerial extent of the contamination; the soil contamination monitor estimated the radium-226 concentration and refined the contamination boundaries; the soil collection equipment was used to obtain a column of soil for measuring the depth profile of the contamination; and the bore hole logger provided a rapid estimate of that profile. Table D1 summarizes the ambient levels of gamma radiation and soil radioactivity concentration present in the particular portion of Monticello and the increase above those levels that would cause a property to be included in the remediation program.

The gamma scanner used to locate and define the perimeter of contaminated areas consisted of a 1-1/2" x 1-1/2" sodium iodide detector and a digital rate meter that measures in counts per second. It was checked against a pressurized ion chamber to determine the count rate to dose rate conversion factor. The detector was mounted on a hospital crutch to make it easy to quickly move the detector and reproducible space the detector 3" off the ground. Any reading more than 30% greater than the background level indicated potential contamination and was noted on a property map. The resulting map provided a rough footprint of elevated areas.

Analysts used the Delta Scintillometer soil contamination monitor to estimate the radium concentration in the top 15 centimeters (cm) of soil and define the perimeter of contaminated areas precisely. The monitor measures total counts during a counting interval. It is a one-piece instrument, manufactured by Rust Geotech, that consists of a 2" x 2" sodium iodide detector surrounded by a lead prefilter a few millimeters thick, a count-up and count-down digital scaler with timer, and a 3" x 3" x 1/4" tungsten shield. It was placed in contact with the ground and allowed to collect counts for 2 minutes. The tungsten shield was inserted below the detector to shield the detector from any contamination directly below it and allowed to count backward for 2 minutes. The resulting counts measured contamination directly below the detector. The factor for converting the unit's count rate readings to soil activity concentration was determined on a DOE calibration pad at the Grand Junction, Colorado, airport, where the radium-226 concentration is well documented.

Investigators used either a corer to collect a vertical sample or a bore hole logging device to measure radiation levels at depths under the surface as a basis for determining the depth profile of contamination. The corer is a hollow tube pounded into the ground and then removed to extract a vertical plug of soil, which is subsequently sectioned every two inches and analyzed through the use of a multichannel analyzer. The bore hole logger was a 3" x 3" sodium iodide detector connected to a scaler and adjusted to see gamma ray energies above 500 kiloelectron volts. The process involved digging a hole with a gasoline-powered 4"-diameter auger, and lowering the detector into the hole. Readings were taken at 3-inch intervals from the surface to a maximum depth of 6 feet, although the practical depth was normally limited to 3 feet by the rough and rocky terrain. A correction was made for activity in soil sections above and below the section of interest. Soil concentrations at more than 5 picocuries per gram (pCi/g) in the top 15 cm of soil and more than 15 pCi/g in deeper layers were considered contaminated.

Each area was mapped to show its area size and depth in inches. The tailings were excavated to the prescribed depth through the use of earthmoving equipment, or hand tools near fence posts, and moved to the East Tailings Pile for temporary storage. The excavated areas were then backfilled with clean soil with a concentration below 1 pCi/g and reseeded or resodded.

After remedial action, each excavation area was gridded into roughly 10' x 10' areas and soil samples and Delta Scintillation surveys were taken. Soil aliquots from 9 to 12 areas were blended to represent 100 meters of surface and analyzed in an opposed crystal system (OCS). The OCS is a lead shield containing two 3" x 3" sodium iodide detectors facing each other. The sample was packaged in a metal can, then placed between the detectors and, after 500 seconds, analyzed for the 609 keV peak of 214-Bi, a radium-226 decay product. This method can analyze a nonuniform sample more accurately than a single crystal system can. Any area where the average radium-226 concentration exceeds 5 pCi/g in the top 15-cm of soil or 15 pCi/g in each subsequent 15-cm layer, averaged over 100 square meters, was selected for remediation.

4. Why are uranium mill workers not covered by a federal compensation act when uranium mine workers are?

   Address concerns about the expansion of the Uranium Mine Workers Compensation Act to cover mill workers to the following individuals:
   
   

   Lynda Taylor
   Southwest Research and Information Center
   P.O. Box 4524
   Albuquerque, NM 87106
   (505) 262-1862

   Christine Benally
   Office of Navajo Uranium Workers
   P.O. Box 6035
   Shiprock, NM 87420
   (505) 368-1260

   Address further questions about the scope of the Uranium Mine Workers Compensation Act to the appropriate congressional representatives.

5. How can the residents find more information about the Nevada Test Site and the Utah downwinders study?

   The Utah downwinders study was conducted by representatives of the U.S. Department of Energy's Nevada Operations Office, which is the office responsible for the Nevada Test Site. Concerned residents may request information about the Nevada Test Site and/or about how the downwinders study from the following individual:

   Mr. Chris L. West, Director
   Office of Intergovernmental and External Affairs
   U.S. Department of Energy
   Nevada Operations Office
   P.O. Box 98518
   Las Vegas, NV 89193-8518

Appendix E

Uranium Mill Workers Exposures and Long-Term Health Effects
Compiled by Ken Silver, Boston University

Former workers of the Monticello Mill and area mines have raised questions regarding their long-term risks of chronic, work-related diseases. These concerns are well-founded. Since the 1940s, federal and state authorities, as well as some employers, have conducted periodic evaluations of working conditions and mine and mill workers' health status. The Monticello Mill itself and some area mines have been included in a number of these evaluations. The implications of these historical studies for former workers are discussed in the sections below. Overall, these studies provide an important documentary record of working conditions and health problems in the industry during the time period that is of concern to Monticello residents.

One serious drawback to relying on old government studies is that exposure levels specific to the Monticello Mill are not always available. Most studies provide summary results from several mills, instead of a mill-by-mill breakdown. However, in general terms, Harris et al (1959) states that the older mills that were originally built for the extraction of vanadium "had no great emphasis on dust control." The 1958 industrial hygiene evaluation of the Monticello Mill conducted by National Lead Company (Beverly and McArthur, 1958), which is discussed below, suggests that this generalization was an apt description of the Monticello Mill, which was built for the extraction of vanadium in 1942.

Mill workers are thought to have had relatively little exposure to radon gas and its decay products, because of the open, airy construction of mills in that era and the opportunities for off-gassing by ores in the early steps of transport and processing. Crusher houses were the only mill areas ever considered to pose a radon hazard. Exposures to silica dust, mixed radioactive dusts, metallic components, and acids were commonplace in milling operations. Beginning with the earliest investigations of Wolf (1948) and Holaday et al (1951, 1952), several themes are apparent:

o dry operations, including the handling of finished product, were associated with the highest exposures
o vanadium exposure in certain operations produced upper respiratory tract irritation, resulting in a dry hack, or cough
o vanadium exposure produced a green coating on mucous membranes, tongue and teeth,
o workers in certain operations absorbed uranium
o a high potential for silica exposure existed in certain mills

These investigators also struck several themes regarding industrial hygiene controls that were to be echoed by subsequent reports and studies:

o local exhaust ventilation, if made available, could bring under control many of the hazards in the dustiest operations
o better housekeeping was needed to reduce dust throughout the plants
o vacuuming should replace dry sweeping and compressed air for cleanup
o respirators may be useful as an interim measure, until engineering controls were instituted, or in transient high-exposure situations

An industrial hygiene survey of the Monticello Mill performed by National Lead Company in 1958 (Beverly and McArthur, 1958) reiterated many of these themes. Marked variability in levels of dust was found among different areas of the plant. Levels of airborne radioactive dust exceeded the maximum permissible concentration (at that time 5 x 10^-11 µc/ml) by 2- to 78-fold in air samples obtained in the following areas of the plant: ore sample plant, sample preparation area, crushing area, and yellow cake drying area. Workers in some dusty areas were found to have elevated urinary levels of uranium, but the results were highly variable among individuals with similar external exposures. Exposure to external radiation was highest in areas where yellow cake was handled. The authors recommended major improvements in equipment, such as new dust collectors for the plant crusher building as well as the yellow cake drying and drumming area. After some equipment changes were instituted in July 1958, further air sampling in October of that year revealed mixed results: big decreases were seen in some areas, with modest reductions in others. In a few cases, such as the yellow cake dryer, exposures actually increased.

The most extensive evaluation of the uranium milling industry was conducted by Harris et al (1959). Harris's team from the Atomic Energy Commission's Health and Safety Laboratory in New York inspected 12 mills from the standpoint of worker health hazards, but also took into consideration environmental health hazards. The industrial hygiene survey conducted by Beverly and McArthur (1958) mentions Harris's group as having monitored the Monticello Mill for radiation in April 1957. Therefore, it is safe to assume that the Monticello Mill is one of the 12 mills reported in the Harris et al (1959) study as mills "A through L." But which one? We do not know.

Nevertheless, the Harris et al (1959) report provides an important glimpse into working conditions and health hazards in this industry during the late 1950s. Between one-fourth and one-third of workers were estimated to be exposed to airborne radioactive dust above the Atomic Energy Commission's maximum permissible concentration of 5 x 10^-11 µc/ml. The highest exposures were in initial ore handling and final concentrate packaging. Manual handling of dry yellow cake produced "extremely high" levels of airborne radioactive dust. Workers in adjacent operations were also at risk, as the aforementioned dusty operations were capable of contaminating surrounding work areas. The degree of silica hazard was dependent to a large degree on the percent free silica in the ore, which ranged from 5% to 50% among the 12 mills studied. Vanadium levels were found to be high in the final processing areas. Confirming concerns first raised by Miller et al (1956), Harris' group also noted potential hazards associated with the handling of acids, alkalis, and other chemicals employed in milling operations.

By the end of the 1950s, a large database had accumulated on worker exposure to airborne contaminants in the uranium milling industry (Kusnetz, 1959). The crushing area of the mill was frequently associated with excessive airborne concentrations of silica, radium, and vanadium. In the final product area of the mill, uranium exposures were especially problematic, but vanadium could also pose a hazard. By the early 1970s, when responsibility for following up the health experience of uranium millers had passed to the National Institute for Occupational Safety and Health, Archer et al (1973) detected excess deaths due to lymphatic and hematopoietic cancers. A decade later, Waxweiler et al (1983) confirmed this finding, and also suggested that nonmalignant respiratory disease and chronic kidney disease are elevated among former uranium mill workers. With funding from the U.S. Army, NIOSH is now embarking on a further follow-up study of the long-term health experience of uranium mill workers.

References

Archer VE. Health concerns in uranium mining and milling. J Occup Med 1981; 23(7):502-505.

Archer VE, Magnuson HJ, Holaday DA, Lawrence PA. Hazards to health in uranium mining and milling. J Occup Med 1962; 4(2):55-60.

Archer VE, Wagoner JK, Lundin FE. Cancer mortality among uranium mill workers. J Occup Med 1973; 15(1):11-14.

Beverly RG, McArthur CK. Survey and prevention techniques for control of radioactivity hazards at the Monticello uranium mill, WIN-114. Winchester, MA: National Lead Co., 1958.

Harris WB, Breslin AJ, Glauberman H, Weinstein MS. Environmental hazards associated with the milling of uranium ore, A.M.A. Archives of Industrial Health, 20: 365-382 (1959)

Holaday DA. Progress report (July 1950-December 1951) on the health study in the uranium mines and mills. Salt Lake City, UT: Federal Security Agency, Public Health Service, Division of Occupational Health, 1951.

Holaday DA, David WD, Doyle HN. An interim report of a health study of the uranium mines and mills, May 1952. Salt Lake City, UT: Federal Security Agency, Public Health Service, Division of Occupational Health; Colorado State Department of Public Health, 1952. In: Eichstaedt P. If you poison us: uranium and Native Americans. Santa Fe: Red Crane, 1994; pp. 203-217.

Holaday DA, Rushing DE, Coleman RD, Woolrich PF, Kusnetz HL, Bale WF. Control of radon and daughters in uranium mines and calculations on biologic effects. Washington, D.C.: U.S. Public Health Service, 1957.

Kusnetz HL. Review of environmental studies in uranium mills. In: Hearings on Employee Radiation Hazards and Workmen's Compensation before the Subcommittee on Research and Development of the Joint Committee on Atomic Energy. 86th Congress, March 10-19, 1959. Washington: U.S. Government Printing Office, 1959; pp. 123-127.

Los Alamos Scientific Laboratory, Health Division. Annual report. Los Alamos: Los Alamos Scientific Laboratory, 1951. LA-1256, p. 29

Los Alamos Scientific Laboratory, Health Division. H-Division progress report, August 20, 1950, to September 20, 1950. Los Alamos: Los Alamos Scientific Laboratory, 1950; p. 23.

Miller SE, Holaday DA, Doyle HN. Arch Ind Health 1956; 14: 48-55.

Tsivoglou EC, Bartsch AF, Holaday DA, Rushing DE. Report of survey of contamination of surface waters by uranium recovery plants. September 1955.

Waxweiler RJ, Archer VE, Roscoe RJ, Watanabe A, Thun MJ. Mortality patterns among a retrospective cohort of uranium mill workers. In: Epidemiology applied to health physics. Proceedings of the Sixteenth Midyear Topical Meeting of the Health Physics Society. Albuquerque, NM, January 9-13, 1983, pp. 428-435.

Wolf BS. Medical survey of Colorado raw materials area. Memo to P.C. Leahy, Manager, Colorado Area Office, Atomic Energy Commission. July 19, 1948.

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