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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
VariableCity of MonticelloSan Juan County
Persons per household3.263.70
% Households owneroccupied77.977.3
% Households renteroccupied22.122.7
% Persons in groupquarters2.31.0
Median value, owner-occupied households, $55,30042,800
Median rent paid, renter-occupied households, $199187
* 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
VariableCity of MonticelloSan Juan County
Median household
income, $
Per capita income, $8,6155,907
% Persons below the poverty level12.636.4
% Persons aged >25 with high schoolequivalency or higher79.959.7
% Occupied housing units lackingcomplete plumbing3.728.8
% Occupied housing units on publicwater source96.063.6
% Occupied housing units usingprivate wells or other water source4.036.4
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


(*) - Compound is a polycyclic aromatic hydrocarbon (PAH).
(**) - Compound is considered a carcinogenic PAH.





Appendix C

Additional Toxicological Information

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, preventingfurther oxidation, or ignites spontaneously at room temperature. The size of the granularstructure 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). UO2is uranium dioxide, a component of the various minerals in the raw ore. U3O8 is uraniumoctaoxide, UO3 is uranium trioxide, and UO4•2H2O is uranium peroxide.

Table C1.

Uranium Oxides
OxideColorMethod of Formation
UO2BrownReduction of UO3 by H2
U3O8BlackOxidation of UO2
UO3OrangeIgnition of UO2(NO3)2
UO4•2H2OYellowPrecipitation by H2O2
from solutions of UO22+

Uranium octaoxide is an insoluble radioactive metal oxide. It is odorless and has an olive-greento black color and solid or orthorhombic (trimetric) crystal structure. In milling, exposure toU3O8 dust may cause redness and swelling of the eyes and eye damage, with cataract formationoccurring anywhere from 6 months to several years after a single exposure. Other short-termchemical acute health effects due to inhalation include lack of appetite, nausea, vomiting,diarrhea, dehydration, weakness, drowsiness, incoordination, twitching, sterility, blooddisorders, kidney damage, convulsions, and shock. "Chronic inhalation may affect the lungs andtracheobronchial 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 radioactivelytoxic. Animal studies have shown that uranium primarily affects two parts of the kidneys, theglomerulus and the proximal tubules (4). The result is a decrease in filtration rate by theglomerulus and a disruption of solute reabsorption by the tubules. Uranium is loosely bound inthe kidneys. It clears within a few weeks, and repair processes start. Chronic repeatedexposures typical of exposures uranium millers and miners encounter may affect the repairprocess. Deaths from nephritis and sclerosis have been reported for both uranium millers andminers (5,6). Nephritis is an acute or chronic inflammation of the kidney; a sclerosis is ahardening of the kidney tissue.

Some animal studies also indicate that uranium administered orally (7), by inhalation (8), orsubcutaneously (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 thesecomplications, 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, andthorium-228. The movement of the thorium and radium radionuclides inside the body isdifferent. 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 bonesurfaces; while radium tends to locate within the volume of the bone. Bone surface seekers arein the immediate vicinity of blood vessels. Thorium, since it is a bone surface seeker, may causeleukemia. The decay products of thorium may remain in the bone, transfer to other portions ofthe body, or exit the body entirely.

Radon. The United States Environmental Protection Agency (EPA) has listed radon as thesecond 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 isusually 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 ofradon releases near uranium processing sites.

Uranium and thorium are naturally occurring radioactive materials present in all soils. Eachdecays through a sequence or decay chain of radionuclides that includes radon. The isotopes ofradon that are the most abundant in soil are radon-220 and radon-222. Since radon is anonreactive noble gas, it can pass through the soil and escape into the atmosphere. Radon-222achieves a higher air concentration, which causes it to be a larger public health hazard. Thedecay products of radon are electrically charged, so they attract and attach to particles floating inthe air. The radioactive contamination in the air arises mainly from the radon-222 parent, itsdaughters that are attached to dust particles, and its unattached daughters (12). The radondaughters, 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 alarge amount of radon decay products produced in them. Radon decay causes radiation exposureof the mucosa of the nose, pharynx, and tracheobronchial tree, and that exposure can leadeventually to cancer. Measurements of the radon concentration in the sinus and mastoid airspaces show that radon and its decay products contribute a significant portion of the total alphadose to the sinus and mastoid epithelium (10). The healthy human respiratory tract is lined withciliated 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 escalatorthat carries entrapped hazardous particulate substances upward to where they can be swallowedand eliminated by the digestive tract. In people who smoke and, to a lesser extent, people whohave respiratory tract damage from particulate-born acid air pollutants such as sulfurous andsulfuric acid, the cells responsible for this elimination mechanism are damaged. Radondaughters 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 depositin 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, andskin (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 thepresence of other radionuclides and the silicon dust the miners inhale, and they are alsoconfounded by higher smoking rates among miners than in the general population (13). Effortsto extend the association with cancer reported for the high radon-222 levels (100 to 10,000picocuries 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) havelower reported indoor radon levels (0.4 to 2 pCi/L) than the radon levels (0.9 to 4 pCi/L) incounties with low lung cancer mortality rates (< 4 in 100,000); lung cancer deaths decrease withincreasing exposure to radon (16, 17). A group of Swedish researchers examined a wider rangeof indoor radon levels (from less than 1.4 to more than 10.8 pCi/L) and found no significantassociation with the relative risk of lung cancer in those who never smoked (18). But therelative risk for those who smoked at least 10 cigarettes per day and were exposed to more than10.8 pCi/L was three times that of the smokers exposed to less than 4 pCi/L, and more than 30times 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 oralreference dose for absence of noncancer effects. Moreover, ingestion of up to 25 mg/kg/dayberyllium has failed to produce adverse noncancer effects in animals (19). A 10-pound childwould have to consume 250 kg of the soil each day to ingest the maximum amount of berylliumshown not to have these adverse effects. A significant association between beryllium ingestionand 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 beenassociated with lung cancer in humans and animals. It is classified B2, a probable humancarcinogen, with a unit inhalation risk of 2.4 x 10-3 (µg/m3)-1 (19). Assuming a 70-kg humaninhales 20 cubic meters/day, the inhalation slope factor is 8.4 mg/kg/day. EPA staff membershave drafted a method for determining preliminary remediation goals for carcinogens andnoncarcinogens in soil based on route of exposure and land use (21). For a soil contaminant thatcould present a cancer risk by inhalation and/or ingestion, the following formula expresses thesoil concentration (in mg contaminant per kg soil, or ppm) associated with a one-in-a-millionrisk of cancer:

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

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

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

Lead. Children near the Monticello Mill Tailings Site could play in soil containing as much as22 ppm lead. These concentrations are close to background and below even the mostconservative standards likely to be considered in the near future (22). The exact relationshipbetween 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 beincreased by as much as 0.1 (µg) lead per deciliter (dl) of blood, although the relationship woulddepend on many factors, such as the chemical form of the lead, the soil particle size, and thenutritional state of the children (22). In one case, this increase was calculated using therelationship reported between soil and blood lead concentrations observed in Helena Valley inMontana 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, populationdemographics 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 otherfactors, 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 topica behavior (ingestion of nonnutritive substances, such as soil). Ingestion of small amounts oflead by children is associated with depressed intelligence quotient (IQ) scores, slow growth, andhearing deficits (23). Exposure to larger amounts of lead could harm the fetuses of pregnantwomen, leading to premature delivery, low birthweight, or miscarriage. Moreover, lead hascaused tumors in laboratory animals, suggesting it could cause human cancer (23). Lead isclassified by the EPA as B2 (probable human carcinogen), although the available data are notsufficient for quantitative assessment (19). Middle-aged men may become hypertensive fromsmall increases in their blood lead levels (23).

EPA scientists point out that the health effects of lead, especially those on "children'sneurobehavioral development, may occur at blood lead levels so low as to be essentially withouta threshold" and consider it inappropriate to derive a reference dose (RfD) for oral exposure tolead (19). Because a population's blood lead concentration is directly related to the local soillead concentration (22), it seems inadvisable to use soil comparison values or standards. Undercertain conditions, however, a soil standard may be used. If, as in the case of residents livingnear 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, andadults are probably protected from increases in their blood lead levels by keeping soil leadconcentrations below 120 to 333 ppm (22). These concentrations are well above the maximumsoil concentration found near Monticello.

Thallium. Thallium is no longer used as a rat poison, because the oral dose sufficient to kill halfof treated rats is three times greater than that which would have the same proportion of lethalityin 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 torats for 90 days in the key study (19). All treated rats in this study, down to the lowest dose of0.01 mg/kg/day, showed hair loss, excessive eye tearing and bulging eyeballs, but EPA did notconsider these effects adverse (19). The uncertainty factor of 3,000 included factors of 10 forextrapolation from subchronic to lifetime exposure, 10 to allow for sensitive subpopulations, and3 to account for lack of reproductive and lifetime toxicity data (19). Moreover, it is not clearthat the effects in the study would not be considered adverse to human health. Thallium hasbeen used as a depilatory (hair remover) by some people, but involuntary loss of all hair fromthe head and body might not be welcomed by all people (14). Finally, reproductive anddevelopmental effects do exist in the thallium toxicity database (19, 24). A strain of ratsdifferent from that used in the key study exhibited testicular injury at 0.7 mg thallium/kg/day for60 days, with no NOAEL identified (19). Pups born to pregnant rats treated with 0.08 mg ormore thallium/kg/day exhibited poor learning capacity, with no NOAEL identified, suggestingneurological vulnerability in the developing or young animal (24). For all these reasons, use ofthe RfD to estimate a soil RfD-based medium evaluation guide would not be unreasonablyconservative. If a 10-kg child prone to pica behavior ingested 5 grams (about a teaspoon) of soilper day contaminated by 0.2 ppm thallium, the resulting dose would be the RfD (25). Thesample quantitation limit applied to off-site soil is 10 times this RMEG (26). More sensitiveanalytical 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 absenceof specific information about the form of arsenic in the soil and groundwater, public healthwould be better protected by assuming that all arsenic found on-site in groundwater and soil is inthe much more toxic inorganic form. Chronic human ingestion of as little as 0.01 to 0.06mg/kg/day (e.g., 350 to 2,000 ppb in drinking water) of inorganic, but not organic, arsenic hasbeen associated with evidence of impaired circulation in the extremities, such as significantlyincreased incidence of blackfoot disease and symptoms similar to Raynaud syndrome (27). Other noncancer effects of low-level human oral exposure to the inorganic form includedabdominal pain, diarrhea, liver damage (hepatomegaly and portal hypertension), skin lesions(melanosis and keratosis), and mild peripheral neuropathy (27). No effects were seenconsequent to oral intake of as much as 0.006 mg inorganic arsenic/kg/day (e.g., 21 ppb indrinking water) (27). Human ingestion of 0.009 to 0.04 mg inorganic arsenic/kg/day (e.g., 315to 1,400 ppb in drinking water) for 12 to 60 years has been associated with increased incidenceof cancer of the skin, lung, and liver (27). Although EPA declined to verify an oral slope factorfor inorganic arsenic, that agency did derive a unit risk in water of 0.00005/µg/L (19). BecauseEPA assumes chemical carcinogenesis to be without a threshold, the derived value suggestslifetime exposure to drinking water containing as little as 0.2 ppb inorganic arsenic might resultin a low increased cancer rate in the exposed public. Because of pharmacokineticconsiderations, ingestion of less than 250 µg/day (0.004 mg/kg/day) does not affect bloodarsenic concentration -- i.e., an adverse effect on the public health from arsenic ingestion wouldbe 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 surfacewater 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 notexceeded 131 ppb off site (29). This value is unlikely to affect the public health adversely fortwo reasons. First, there is no evidence that any wells that have been supplying potable watertap the alluvial aquifer, although it is possible that some wells might do so now or in the futurein 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 sufficientfrequency 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 theearth's crust. After refining, it is a light gray, shapeable, flexible metal that is hardened andembrittled 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 essentialtrace 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). Vanadiumpentoxide (red cake) is an odorless, yellow to rust-brown crystalline powder. Vanadiumpentoxide and vanadates are the vanadium compounds most likely released from the MonticelloMill 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 andnear the production sites. These dusts can contain numerous vanadium compounds, particularlyvanadium pentoxide and, to a lesser extent, the vanadates. Numerous exposures to vanadiumcompounds have occurred during the cleaning of oil-fired burners, where the dust is generatedfrom the residual oil ash of high-vanadium content oil.

Much of the information on the public health effects of vanadium and its compounds on humanshas come from reports of accidental exposures of workers in vanadium processing andmanufacturing plants and in boiler cleaning operations. However, some questions posed bythese studies have prompted research involving controlled exposures of humans. Table C2 (30)summarizes the health effects of vanadium compounds on humans involved in those controlledexposure 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 vanadiumcause health effects similar to those of the short-term studies described above. The acute effectsof irritation were reversible after exposure ended. However, more severe chronic or delayedeffects, i.e., emphysema and pneumonia, were reported, but the available data make these reportsless than reliable. Table C3 (30) summarizes the epidemiologic studies conducted in populationsexposed 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 byproductive cough, wheezing, rales, chest pains, difficulty in breathing, bronchitis, questionablepneumonia, and rhinitis (31,32,33,34,35,36,37,38,39,40). There have been occurrences ofgreen-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 theirrelationship 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 itscompounds for the residents of Monticello are inhalation, skin contact, eye contact, andingestion. 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 thevanadium and its compounds that are delivered to the body, i.e., the body dose. If the dose isnot large enough, there would be no adverse health effects. The residents of Monticello likelywere exposed to vanadium pentoxide through the airborne particulate releases from the mill siteand resuspension of the released materials. The Occupational Safety and Health Administration(OSHA), the National Toxicology Program, and the International Agency for Research onCancer 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 diseasessuch 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, andsleeplessness. 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, blooddisorders, and liver and kidney damage.

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

Ingestion may cause the following symptoms at low doses: runny nose, metallic taste, blooddisorders, high blood pressure, and kidney effects. The following effects may be caused at highdoses: nausea, vomiting, diarrhea, stomach pain, and difficulty breathing. The effects that maybe caused at very high doses are paralysis, convulsions, and even kidney damage. These signsand symptoms are for short-term effects (47, 49); there is no information available on significantlong-term adverse health effects (47). Animal studies indicate that vanadium may be anessential 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 C5lists the environmental exposure limit and dose limits for the general public established forvanadium and its compounds.

The occupational limits are provided for informational purposes only. These limits are for use inthe practice of industrial hygiene as guidelines or recommendations in control of potential healthhazards 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 concentrationsof about 0.03 mg(V)/m3 may result in dermal irritation, eczema with intense itching anddischarge, generalized rashes such as hives, and possible sensitization resulting in contactdermatitis during acute exposures. During chronic exposures at these concentrations, repeated orprolonged contact may result in allergic eczema, sensitization, and dermatitis. Direct eye contactwith 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 acuteexposures. During chronic exposures at these concentrations, repeated or prolonged exposuresmay cause inflammation of the conjunctiva.

The signs and symptoms discussed above can also be caused by physical, radioactive, andchemical toxicants other than vanadium and its compounds. Only a medical diagnosis candetermine the cause of reported signs and symptoms. Any residents of Monticello who developany 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 VanadiumCompounds
V2O5 (vanadium pentoxide)Unknown
1-48Respiratory irritationwith bronchopneumonia,heart palpitations53
V2O52-5 days
10-32Respiratory irritation,tremors, discoloredtongue54
V2O58 hours
V2O55 minutes
0.6Coughing, rales55
V2O58 hours
V2O58 hours
NaVO3 (ammonium metavanadate)
0.3-1.2Eye, respiratory irritation37
0.04-0.4Respiratory irritation,
discolored tongue
V2O3 (vanadium trioxide)
1-5 years
UnknownAsthma in 3 of 120workers57
Ca3(VO4)2 (calcium vanadate)1.5 days
UnknownBronchitis, fever,headache,gastrointestinal (GI)distress45
V-Al alloy (vanadium aluminum)Unknown
UnknownRespiratory irritation,
discolored tongue
VC (vanadium carbide)Unknown
UnknownLittle effect38
FeV (ferrovanadium)Unknown
UnknownEye, respiratory irritation38
V (vanadium metal)Unknown
UnknownRespiratory irritation38
(ammonium vanadyl tartrate)
45-68 days
25 mg,
GI discomfort, discoloredtongue, increased steroidexcretion59
(diammonium vanadotartrate)
6 months
25mg/day,2 wk;
125mg/day, 22 wk
GI discomfort,pharyngitis, tongueulceration anddiscoloration60

Table C3.

Summary of Epidemiologic Studies with Vanadium
VANADIUM (mg/m3)
Vanadium ore<3 years
0.1-2.212Eye, respiratory irritation39
V2O5 (vanadiumpentoxide), vanadates2.5 years (mean)
0.01-0.52Respiratory irritation,discolored tongue38
V2O50.5-16 years
6 years (mean)
UnknownCough, pulmonaryeffects with chest pain40
V2O52-13 years
6.6 years (mean)
UnknownEye, respiratoryirritation, chest pain,bronchitis, emphysema61
V2O52-3 years
UnknownEye and respiratoryirritation, bronchitis61

Table C4.

Occupational Exposure Limits for Vanadium Pentoxide
Occupational Safety and
Health Administration
0.05 mg(V2O5)/m3 time-
weighted average (TWA)

Respirable dust and fume

National Institute forOccupational Safety andHealth0.05 mg(V)/m3 15-minuteceiling

Total particulate

American Conference ofGovernmental IndustrialHygienists0.05 mg(V2O5)/m3 TWA

Respirable dust and fume

Table C5.

Vanadium Exposure/Dose Limits for the General Public
Established ByType LimitLimit
ATSDRaMRL (Airborne Exposure)0.0002 mg V/m3
ATSDRaMRL (Oral Dose)0.003 mg V/kg/day
USEPAbRfD (Oral Dose)0.009 mg V/kg/day
NOTE: Table C5 includes the following footnotes and abbreviations:

aAgency for Toxic Substances and Disease Registry. Toxicological profile for vanadium.Atlanta: U.S. Department of Health and Human Services, Public Health Service; 1992.
bEnvironmental Protection Agency. "Integrated Risk Information System," [online database].January 6, 1994. Washington, DC: Environmental Protection Agency; 1994.

MRL = minimal risk level
RfD = reference dose
mg = milligram
V/m3 = vanadium per cubic meter
V/kg/day = vanadium per kilogram per day


  1. U.S. Environmental Protection Agency, Office of Radiation Programs. Finalenvironmental impact statement for remedial action standards for inactive uraniumprocessing 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; 1990Dec.

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

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

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

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

  9. MacNider WDeB. A study of the acquired resistance of fixed tissue cellsmorphologically altered through process of repair, I. The liver injury induced byuranium nitrate. A consideration of the type of epithelial repair which imparts to theliver 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. Delayedeffects 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, August1992; 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 lungcancer rates. Health Physics 1989;57(6):897-907.

  17. Cohen BL. Relationship between exposure to radon and various types of cancer. HealthPhysics 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). Onlinedatabase. Cincinnati, OH: Office of Health and Environmental Assessment,Environmental Criteria and Assessment Office, 1994.

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

  21. Agency for Toxic Substances and Disease Registry. Attachment to a memorandum toAllan Susten from George C. Buynoski concerning EPA soil clean-up levels. HSEDFY92 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 forToxic 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; June1990.

  24. Agency for Toxic Substances and Disease Registry. Toxicological profile for thallium.Atlanta: U.S. Department of Health and Human Services, Public Health Service; July1992.

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

  26. Dames and Moore. Revised final report: Monticello remedial action project. 1991 millsite 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 populationhealth histories. In: Mills CF, Bremner I, Chesters JK, editors. Trace elements in manand animals--TEMA 5. Aberdeen, Scotland: Commonwealth Agricultural Bureaux,1985:289-292.

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

  30. Department of Health, Education, and Welfare. NIOSH criteria for a recommendedstandard....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 EnvironHealth 1962; 5:542-46.

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

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

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

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

  36. Sjoberg SG. Vanadium dust, chronic bronchitis and possible risk of emphysema -- afollow-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 ofoccupational 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 thehealth of workers employed in mining and processing of vanadium ore. AMA ArchIndian 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 -- acathodoluminescent phosphor. J Occup Med 1968; 10:692-96.

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

  44. Stokinger HE. Vanadium. In: Patty FA, editor. Industrial hygiene and toxicology. 2ndrev. 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 MedTrav 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 mildhypoinsulinaemic diabetes in the rat by low non-toxic doses of vanadate. J Endocrinol1991; 142(3):555-61.

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

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

  51. Domingo JL, Sanchez DJ, Gomez M, Llobet JM, Corbella J. Oral vanadate and iron intreatment of diabetes mellitus in rats: improvements of glucose homeostasis andnegative 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 IndHealth 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. ArchEnviron 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, pp74-76, 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 inman. 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 HigRada 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 exposureand adverse human health effects and diminished quality of life associated withexposure to hazardous substances from waste sites, unplanned releases, and othersources of pollution present in the environment. ATSDR has no regulatory authority,but the agency does recommend public health actions that address potential adversehealth effects resulting from environmental releases from hazardous waste sites.

    ATSDR's staff is responsible for preparing public health assessments according to theComprehensive Environmental Response, Compensation, and Liability Act (CERCLAor Superfund). As mandated by that law, staff members conduct public healthassessments of hazardous waste sites listed or proposed for listing on the NationalPriorities List (NPL) of the U.S. Environmental Protection Agency (EPA). ATSDRalso 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. ATSDRscientists do not routinely perform environmental sampling. The environmental dataused in public health assessments come from the Department of Energy (DOE), theEPA, state and local environmental and health agencies, and other groups orindividuals. In addition, ATSDR health assessors conduct site visits to make firsthandobservations of current conditions at the site, land use, public accessibility, anddemographic characteristics of the nearby community.

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

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

    ATSDR health assessors identify actual and perceived site-related health effects and thelevel of public health hazard posed by the site. They then make recommendations forthe agency to DOE, EPA, and relevant state and local agencies, as appropriate, onpreventing or alleviating human exposures to site-related contaminants. Whenindicated, ATSDR assessors identify a need for any follow-up health activities such asepidemiologic studies, registries, or community health education. Finally, ATSDRstaff members provide a mechanism to reevaluate health issues as site conditionschange (e.g., after site remediation or changes in land use) or when new informationbecomes available. 

    The public health assessment includes a public health action plan (PHAP). The PHAPcontains a description of actions ATSDR representatives and other parties will take atand in the vicinity of the site. The purpose of the PHAP is to provide a plan of actionfor preventing and mitigating adverse human health effects resulting from exposure tohazardous substances in the environment. ATSDR staff members monitor theimplementation of the plan annually. Public health actions may include but are notlimited 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 initialrelease document, which is prepared as part of the process of gathering and analyzingdata and drawing conclusions and recommendations from the information evaluated ina public health assessment, goes for review and comment to the DOE componentinvolved, EPA, and state and local environmental and health agencies. This releasegives agencies the opportunity to comment on the completeness of information theyhave provided and the clarity of the presentation. The initial release comment periodlasts 45 days. After the initial release, the ATSDR staff prepares the document fordistribution to the general public. The public is notified of the document's availabilityat repositories (e.g., libraries and city halls) in the site area through advertisements andpublic notices in newspapers. The public comment period lasts 45 days. After publiccomments, ATSDR staff members address all public comments and revise or appendthe document as appropriate. The final public health assessment is then released; thatdocument includes written responses to all public comments.

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

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

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

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

    Uranium mill tailings were found at the golf course and cemetery during theradioactive surveys performed throughout Monticello, and both tailings and ore werefound at the granary. The tailings appear to have been introduced as a fill material fordepressions or top dressing to improve surface quality. The radioactive surveys usedthe same type of equipment and methods described below to locate, quantify, anddetermine the extent of contamination. Contaminated sites were then scheduled forremediation. 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 andanalysis equipment, and a bore hole logging device to assess radioactive levels. Thegamma scanner determined the aerial extent of the contamination; the soilcontamination monitor estimated the radium-226 concentration and refined thecontamination boundaries; the soil collection equipment was used to obtain a columnof soil for measuring the depth profile of the contamination; and the bore hole loggerprovided a rapid estimate of that profile. Table D1 summarizes the ambient levels ofgamma radiation and soil radioactivity concentration present in the particular portion ofMonticello and the increase above those levels that would cause a property to beincluded in the remediation program.

Table D1.

Property Inclusion Limits
Gamma Radiation (µR/hr)Radium-226 in Soil (pCi/g)
Background LevelLimitBackground
Limit Above
Granary17Bkg + 30%15/15
Golf Course14.6Bkg + 30%15/15
Cemetery14.6Bkg + 30%15/15
µR/hr = microroentgen per hour
pCi/g = picocuries per gram
Bkg = background
5/15 = 5 pCi/g in the top 15-centimeter (cm) layer of soil and 15 pCi/g in each subsequent 15-cm layer

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

    Analysts used the Delta Scintillometer soil contamination monitor to estimate theradium concentration in the top 15 centimeters (cm) of soil and define the perimeter ofcontaminated areas precisely. The monitor measures total counts during a countinginterval. It is a one-piece instrument, manufactured by Rust Geotech, that consists of a2" x 2" sodium iodide detector surrounded by a lead prefilter a few millimeters thick, acount-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 anycontamination directly below it and allowed to count backward for 2 minutes. Theresulting counts measured contamination directly below the detector. The factor forconverting the unit's count rate readings to soil activity concentration was determinedon 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 loggingdevice to measure radiation levels at depths under the surface as a basis for determiningthe depth profile of contamination. The corer is a hollow tube pounded into the groundand then removed to extract a vertical plug of soil, which is subsequently sectionedevery two inches and analyzed through the use of a multichannel analyzer. The borehole logger was a 3" x 3" sodium iodide detector connected to a scaler and adjusted tosee 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 thehole. Readings were taken at 3-inch intervals from the surface to a maximum depth of6 feet, although the practical depth was normally limited to 3 feet by the rough androcky terrain. A correction was made for activity in soil sections above and below thesection of interest. Soil concentrations at more than 5 picocuries per gram (pCi/g) inthe top 15 cm of soil and more than 15 pCi/g in deeper layers were consideredcontaminated.

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

    After remedial action, each excavation area was gridded into roughly 10' x 10' areasand soil samples and Delta Scintillation surveys were taken. Soil aliquots from 9 to 12areas were blended to represent 100 meters of surface and analyzed in an opposedcrystal system (OCS). The OCS is a lead shield containing two 3" x 3" sodium iodidedetectors facing each other. The sample was packaged in a metal can, then placedbetween 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 moreaccurately than a single crystal system can. Any area where the average radium-226concentration exceeds 5 pCi/g in the top 15-cm of soil or 15 pCi/g in each subsequent15-cm layer, averaged over 100 square meters, was selected for remediation.

  1. 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 CompensationAct 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 WorkersCompensation Act to the appropriate congressional representatives.

  2. 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. Departmentof Energy's Nevada Operations Office, which is the office responsible for the NevadaTest Site. Concerned residents may request information about the Nevada Test Siteand/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 regardingtheir 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 conductedperiodic 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 theseevaluations. The implications of these historical studies for former workers are discussedin the sections below. Overall, these studies provide an important documentary record ofworking conditions and health problems in the industry during the time period that is ofconcern to Monticello residents.

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

Mill workers are thought to have had relatively little exposure to radon gas and its decayproducts, because of the open, airy construction of mills in that era and the opportunitiesfor off-gassing by ores in the early steps of transport and processing. Crusher houseswere 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 millingoperations. 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 tractirritation, resulting in a dry hack, or cough
    o vanadium exposure produced a green coating on mucous membranes, tongueand 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 thatwere to be echoed by subsequent reports and studies:

    o local exhaust ventilation, if made available, could bring under control many ofthe 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 LeadCompany 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. Levelsof airborne radioactive dust exceeded the maximum permissible concentration (at thattime 5 x 10-11 µc/ml) by 2- to 78-fold in air samples obtained in the following areas of theplant: ore sample plant, sample preparation area, crushing area, and yellow cake dryingarea. Workers in some dusty areas were found to have elevated urinary levels ofuranium, but the results were highly variable among individuals with similar externalexposures. Exposure to external radiation was highest in areas where yellow cake washandled. The authors recommended major improvements in equipment, such as new dustcollectors for the plant crusher building as well as the yellow cake drying and drummingarea. After some equipment changes were instituted in July 1958, further air sampling inOctober of that year revealed mixed results: big decreases were seen in some areas, withmodest reductions in others. In a few cases, such as the yellow cake dryer, exposuresactually increased.

The most extensive evaluation of the uranium milling industry was conducted by Harriset al (1959). Harris's team from the Atomic Energy Commission's Health and SafetyLaboratory in New York inspected 12 mills from the standpoint of worker healthhazards, but also took into consideration environmental health hazards. The industrialhygiene survey conducted by Beverly and McArthur (1958) mentions Harris's group ashaving monitored the Monticello Mill for radiation in April 1957. Therefore, it is safe toassume 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 workingconditions and health hazards in this industry during the late 1950s. Between one-fourthand one-third of workers were estimated to be exposed to airborne radioactive dust abovethe Atomic Energy Commission's maximum permissible concentration of 5 x 10-11µc/ml. The highest exposures were in initial ore handling and final concentratepackaging. Manual handling of dry yellow cake produced "extremely high" levels ofairborne radioactive dust. Workers in adjacent operations were also at risk, as theaforementioned 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 inthe ore, which ranged from 5% to 50% among the 12 mills studied. Vanadium levelswere found to be high in the final processing areas. Confirming concerns first raised byMiller et al (1956), Harris' group also noted potential hazards associated with thehandling of acids, alkalis, and other chemicals employed in milling operations.

By the end of the 1950s, a large database had accumulated on worker exposure toairborne contaminants in the uranium milling industry (Kusnetz, 1959). The crushingarea of the mill was frequently associated with excessive airborne concentrations ofsilica, radium, and vanadium. In the final product area of the mill, uranium exposureswere 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 passedto the National Institute for Occupational Safety and Health, Archer et al (1973) detectedexcess deaths due to lymphatic and hematopoietic cancers. A decade later, Waxweiler etal (1983) confirmed this finding, and also suggested that nonmalignant respiratorydisease 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-upstudy of the long-term health experience of uranium mill workers.


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 andmilling. J Occup Med 1962; 4(2):55-60.

Archer VE, Wagoner JK, Lundin FE. Cancer mortality among uranium mill workers. J Occup Med1973; 15(1):11-14.

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

Harris WB, Breslin AJ, Glauberman H, Weinstein MS. Environmental hazards associated with themilling 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 andmills. Salt Lake City, UT: Federal Security Agency, Public Health Service, Division of OccupationalHealth, 1951.

Holaday DA, David WD, Doyle HN. An interim report of a health study of the uranium mines andmills, May 1952. Salt Lake City, UT: Federal Security Agency, Public Health Service, Division ofOccupational Health; Colorado State Department of Public Health, 1952. In: Eichstaedt P. If you poisonus: 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 anddaughters in uranium mines and calculations on biologic effects. Washington, D.C.: U.S. Public HealthService, 1957.

Kusnetz HL. Review of environmental studies in uranium mills. In: Hearings on Employee RadiationHazards and Workmen's Compensation before the Subcommittee on Research and Development of theJoint 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 ScientificLaboratory, 1951. LA-1256, p. 29

Los Alamos Scientific Laboratory, Health Division. H-Division progress report, August 20, 1950, toSeptember 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 surfacewaters by uranium recovery plants. September 1955.

Waxweiler RJ, Archer VE, Roscoe RJ, Watanabe A, Thun MJ. Mortality patterns among a retrospectivecohort of uranium mill workers. In: Epidemiology applied to health physics. Proceedings of the SixteenthMidyear 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 AreaOffice, Atomic Energy Commission. July 19, 1948.

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