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PETITIONED HEALTH CONSULTATION

Residential Soil, Indoor Dust, and Ambient Air

ELIZABETH COPPER MINE
(a/k/a ELIZABETH MINE)
STRAFFORD, ORANGE COUNTY, VERMONT


BACKGROUND AND STATEMENT OF ISSUES

The Agency for Toxic Substances and Disease Registry (ATSDR) received a petition to addresspublic health concerns from residents living near the Elizabeth Copper Mine Site in Strafford,Vermont. This health consultation addresses the sampling results for indoor dust, ambient air, andadditional soil sampling conducted at three residences near the site.

The Elizabeth Copper Mine, now abandoned, operated sporadically from 1793 to 1958 producingiron sulfate and copper. The site contains open pit mines, extensive underground workings, threetailings areas, and several buildings. Tailings pile #1 (covering 30 acres) and #2 (covering 5 acres)consists of fine-grained tailings from a flotation mill which operated onsite from 1943 to 1958 [1]. Tailings pile #3 consists of coarser mine spoils and is a six-acre waste pile from earlier miningoperations [1]. All three of the tailings piles are within one-half mile of the nearest residences.

Three families living along Old Mine Road, a dirt road adjacent to the site, have expressed concernthat exposures to site-related contaminants are causing a variety of health problems includingelevated blood lead levels. ATSDR previously issued health consultations addressing contaminants found in private drinking water wells and soil at these and other nearby residences [2,3].


DISCUSSION

In November 2000, EPA collected indoor dust and indoor wipe samples from each of threeresidences located on Old Mine Road [4]. Ambient air and residential soil samples were alsocollected in two of the three residential yards. All samples were analyzed for metals. ATSDR'sevaluation of these samples (indoor dust, ambient air, and residential soil) follows.

Indoor Dust

The primary routes of exposure to contaminants in indoor dust are inhalation, dermal contact, andingestion of contaminated foods (or mouthing of contaminated objects by toddlers and infants). Indoor dust samples were obtained using two different collection methods. The first method used avacuum sampler to collect dust from a measured area on the floor in three different living spaceswithin each residence. In the second method, cloth wipes were used to collect dust samples atlocations adjacent to the vacuum sample locations. The highest metal concentrations were primarily found in one sample location [4].

Lead

Based on the vacuum sample results, the lead concentrations detected in indoor dust ranged fromnon-detect to 1600 milligrams per kilogram per square meter (mg/kg/m2) [4]. ATSDR has notestablished a Minimal Risk Level (MRL) for lead nor has EPA established a reference concentrationfor lead. However, the EPA Office of Solid Waste and Emergency Response recommends a 400milligrams per kilogram (mg/kg) screening level for lead in residential soil at Superfund sites [5].

In one of the three residences sampled, one indoor bulk dust sample indicated a lead level (1600mg/kg) significantly greater than the 400 mg/kg screening level. This level does not appear to berepresentative of overall lead levels in the household dust. However, routine exposure to this highestlead level could cause adverse health effects, especially for young children.

The wipe samples indicated that lead loading (lead mass per surface area) ranged from 120-550 micrograms per square meter (µg/m2). For public housing, the U.S. Agency for Housing and Urban Development (HUD) defines a lead dust hazard as a lead level greater than 1080 µg/m2 on surface flooring (hard floors or carpeting) [6]. In a 1998 notice of proposed rule making, EPA defined a lead dust hazard as a level greater than 540 µg/m2 of lead on uncarpeted floors [7]. One of the dust wipe samples collected from the residence noted above showed a level of 550 µg/m2. This level slightly exceeds EPA's proposed definition of a lead dust hazard of 540 µg/m2 for child occupied facilities.

Iron

Dust samples contained levels of iron ranging from 7500 mg/kg to 19,000 mg/kg. ATSDR has notestablished an MRL for iron, however, these levels are less than the EPA Region III Risk BasedConcentration (RBC) for iron in residential soil (23,000 ppm). RBCs are daily exposures that arenot expected to result in any adverse health effects [8]. ATSDR does not anticipate that adversehealth effects would occur from exposure to iron in dust at these levels.

Aluminum, Antimony, Arsenic, Cadmium, Chromium, Manganese, and Zinc

Public health agencies have not established screening values for indoor dust levels of aluminum,antimony, arsenic, cadmium, chromium, manganese, and zinc. However, the highest concentrationfound for each of these contaminants is less than the respective ATSDR soil screening value forpotentially adverse health effects in children (non-pica). As a result, ATSDR does not expect anyadverse health effects in children or adults as a result of exposure to the levels of these metals found in indoor dust.

For example, the concentrations of arsenic detected in the dust samples ranged from 1-7 ppm. Allof the detected levels of arsenic in indoor dust are less than ATSDR's soil screening value forchronic non-cancer effects in children (20 ppm). These arsenic levels do exceed the soil screeningvalue of 0.6 ppm for pica children. However, the screening value for pica children is based onconsumption of 5000 milligrams (or 5 grams) of soil per day and contains a safety factor of three.

Pica is defined as an appetite for substances having no nutritional value, e.g., clay, dried paint,starch, or ice [9]. True pica behavior in children is relatively rare (< 1%), and sporadic, and istypically exhibited only during the first few years of life. It is not to be confused with the commonhabit of all babies and toddlers to mouth objects. Pica children actually swallow large amounts ofnon-nutritive materials; their intentional ingestion of soil, for example, is assumed to be 25 times theincidental ingestion of soil by non-pica children and 50 times that of adults. These values are on thehigh end and overestimate average soil consumption rates (by a factor of 2 or more) for mostchildren.

Children are not likely to find or eat, 5-15 grams of household dust on a daily basis. The ATSDREnvironmental Media Evaluation Guides (EMEGs) for arsenic in soil and water were based on aTaiwanese drinking water study. Since arsenic is several times more bioavailable in drinking waterthan in soil or dust, the soil EMEGs, which do not take bioavailability into account are moreconservative than the drinking water EMEGs which are based on the same study and assume 100%bioavailability. The true margin of safety in all of ATSDR's EMEGs for arsenic (including the soilvalue for pica children) is substantially greater than the uncertainty factor of three would suggest. As a result, no adverse health effects would be expected to result from the ingestion of house dustcontaining 1-7 ppm arsenic, even if a child finds and consumes several grams of household dustevery day.

The concentrations of total chromium detected in indoor dust ranged from 15-51 ppm. Like thosefor arsenic, these levels were less than the ATSDR Reference Dose Media Evaluation Guide(RMEG) soil screening value for chronic non-cancer effects in children (200 ppm). However, thechromium levels found exceed the RMEG for pica children. The reference dose (RfD) on which thisRMEG was based contains a composite safety factor of 900. Therefore, it would be virtuallyimpossible for any child to find and eat enough contaminated household dust (more than one poundper day) to get a dose equivalent to the Lowest Observed Adverse Effects Level (LOAEL) forchromium. The LOAELs are exposure levels associated with adverse health effects that may be serious or relatively subtle.

Another consideration is that the RMEG for chromium addresses the more toxic hexavalentchromium [Cr(VI)]. In environmental samples, trivalent chromium [Cr(III)] levels are typicallyseven times higher than Cr(VI) levels. As a result, we would expect that most of the chromiumfound in the household dust is the less toxic Cr(III).

Magnesium, Phosphorus, Sodium, Titanium

No public health standards have been established for magnesium, phosphorus, sodium, and titaniumin dust or soil. However, magnesium, phosphorus, and sodium are major mineral nutrients; childrenneed about 150, 800, and 200 mg, respectively, in their daily diet. Due to its low toxicity, titaniumand several of its compounds are used in medical therapies for skin disorders as well as in implantmaterials in orthopedics, oral surgery, and neurosurgery. Therefore, ATSDR does not anticipateany adverse health effects from exposure to these constituents at the levels found in the indoor dustsamples.

Ambient Air

Five ambient air samples were collected near two homes located downwind of the tailings piles. Three samples were collected from one yard and two samples were collected from another.

Lead

Lead was found at 0.18 micrograms per cubic meter (µg/m3) near each home. This level is more than 60 times lower than the lowest lowest-observed-adverse-effect levels (LOAEL) found for humans exposed to lead via inhalation (11 µg/m3 ) [10]. As a result, ATSDR does not expect any adverse health effects to occur as a result of the levels of airborne lead found at these residences.

Chromium

Chromium (total) was found in the ambient air near one residence at levels of 0.56 µg/m3 and 0.27 µg/m3. Chromium was also present in the lot blank at 1.4 µg which may indicate that actual ambient chromium levels were lower than the results show. Total chromium includes trivalent chromium [Chromium III or Cr(III)] and the much more toxic hexavalent chromium [Chromium VI or Cr(VI)]. The levels of chromium found in the residential samples exceed the ATSDR Cancer Risk Evaluation Guide (CREG) for cancer effects for hexavalent chromium of 0.00008 µg/m3.

The concentration of total chromium in air [both Cr(III) and Cr(VI)] generally ranges between 0.01 and 0.03 µg/m3 [10]. The arithmetic mean concentrations of total chromium in the ambient air in the United States, urban, suburban, and rural areas monitored during 1977-1984 ranged from 0.005 to 0.525 µg/m3 [11,12]. The highest level of total chromium measured at the Elizabeth Mine site (0.56 µg/m3) is slightly above this range.

Chromium is released into the atmosphere mainly by man-made sources such as the combustion of natural gas, oil, and coal. Only a very small percentage (0.2%) of these chromium emissions are estimated to consist of the more toxic hexavalent chromium (Cr(VI) [13]. Therefore, the highest level of Cr(VI) found in ambient air near one residence could be estimated at 0.00122 µg/m3 (0.2% of 0.56 µg/m3). Since this level is higher than ATSDR's screening level (0.00008 µg/m3), further explanation is needed.

Hexavalent chromium [Cr(VI)] is a known human carcinogen via the inhalation route. The lowest concentration of chromium in air [a mix of Cr(III) & Cr(VI)] reported to be associated with elevated rates of lung cancer in humans is 40 µg/m3 [13]. However, the exposures in that study were occupational and lasted from 1 to 49 years [13,14]. The ATSDR CREG of 0.00008 µg/m3 was extrapolated from apparent effects levels observed in another occupational study [15] and assumes a threshold of zero. It represents a hypothetical 1-in-a-million "risk" level. However, the zero-threshold assumption is not likely to be applicable to Cr(VI) exposure. Inflammation is considered to be essential for the induction of most chromium-induced respiratory effects. Therefore, inflammation may be a necessary precursor for Cr(VI)-induced lung cancer which would suggest that a threshold may exist for the carcinogenic effects of chromium. The lowest human cancer effects level for chromium is 40 µg/m3 which is 20 times higher than the lowest LOAEL for non-cancer respiratory effects (2 µg/m3). Therefore, the highest level of total chromium found near a residence is more than three times lower than the lowest LOAEL for total chromium. Similarly, the highest level of total chromium found is more than 70 times lower than the lowest cancer effect level for total chromium.

Although EPA Region I has not established a comparison value for chromium, the EPA Region III Risk Based Concentration for trivalent chromium [Cr(III)] is 5500 µg/m3 for non-cancer health effects [7]. This level is almost 10,000 times greater than the levels found in the residential samples. As a result, no adverse effects would be expected from exposure to the maximum level of total chromium (0.56 µg/m3).

Residential Soil

Surface soil samples were collected from three residential yards and two background locations [16].

Arsenic

The highest level of arsenic found in any sample collected from a residential yard was 15.8 parts permillion (ppm). [An estimated level of 18.3 ppm was also reported.] Although this level exceeds themost conservative ATSDR comparison values for chronic oral exposure to arsenic, it is not a levelthat is expected to cause adverse health effects.

Using the highest level of arsenic found (15.8 ppm), the estimated ingestion dose for a 10-kilogram(kg) child consuming 200 milligrams (mg) of this maximally contaminated soil every day is0.00032 mg/kg/day. This estimated dose is more than two and a half times lower than the No-Observed-Adverse-Effect-Level (NOAEL) on which ATSDR's Minimal Risk Level (MRL) is based[17]. Neither oral nor dermal health effects from exposure to arsenic levels found in residential soilare expected to be a public health concern.

ATSDR's chronic Environmental Media Evaluation Guides (EMEGs) for arsenic in soil are 20 ppm(child) and 200 ppm (adult) and have a built-in safety factor. These EMEGs were derived, usingdefault values for body weight and soil ingestion rate, from ATSDR's MRL of 0.0003 mg/kg/day(with an uncertainty factor of three). The MRL, derived from a Taiwanese drinking water study,may not be relevant to the potential adverse health effects of drinking water exposures in U.S.populations [17]. Also, arsenic in soil is less bioavailable (< 10%) than arsenic in water (>80%)[17]. Soluble, more readily absorbed, forms of arsenic tend to either be trapped in the soil matrix orleached out by rain, leaving the relatively insoluble, less readily absorbed, forms in the soil. Therefore, the MRL's effective safety margin is much greater for the ingestion of arsenic in soil thanfor arsenic in drinking water.

For example, the concentrations of arsenic detected in the soil samples ranged from 0.7-18.3 ppm. All of the detected levels of arsenic in indoor dust are less than ATSDR's soil screening value forchronic non-cancer effects in children (20 ppm). These arsenic levels do exceed the soil screeningvalue of 0.6 ppm for pica children. However, the screening value for pica children is based onconsumption of 5000 milligrams (or 5 grams) of soil per day. Children are not likely to eat 5-15grams of soil on a daily basis. The ATSDR EMEG for arsenic used here is the same EMEG used inthe previous evaluation for indoor dust. Again, this EMEG is based on a Taiwanese drinking waterstudy. Since arsenic is several times more bioavailable in drinking water than in soil or dust, the soilEMEGs, which do not take bioavailability into account are conservative. The true margin of safetyin all of ATSDR's EMEGs for arsenic (including the soil value for pica children) is substantiallygreater than the safety factor of 3. As a result, no adverse health effects are expected to result from the potential ingestion of the residential soil sampled.

Iron

Iron levels ranging from 12,400 ppm to 170,000 ppm (an average of 51,000 ppm) were found in thesoil samples collected from three residential yards. Many of these levels exceed the EPA Region IIIRisk Based Concentration (RBC) for residential soil (23,000 ppm). RBCs are daily exposures thatare not expected to result in any adverse health effects [8].

Based on the highest concentration of iron found in the soil, the estimated daily intake from soilingestion for a child (non-pica) is 34 milligrams per day (mg/day). This amount of iron is 3.4 timesgreater than the U.S. Department of Agriculture (USDA) Recommended Dietary Allowance (RDA)for iron in children (10 mg/day) [18]. However, using the average iron concentration of 51,000ppm, a child consuming 200 mg soil per day would also ingest 10.2 mg iron per day. Actual soilconsumption is much less than 200 mg per day for most children and the bioavailability of iron insoil is likely to be less than that of iron in food. In addition, the body normally reduces absorption ofiron from the gastrointestinal tract in response to higher concentrations. As a result, the levels ofiron found in the soil are not likely to pose a health hazard to children.

Although ATSDR considers it extremely unlikely, it is conceivable that a pica child could ingestenough of the most-heavily contaminated soil to be exposed to an acutely toxic dose of iron. However, to the authors' knowledge, no case of acute iron toxicity has ever occurred as a directresult of soil consumption. The absence of such cases probably reflects the large amount ofcontaminated soil that would have to be ingested combined with the much lower intestinalabsorption of iron from soil than from food.

Thallium

The highest level of thallium found was 2.6 ppm. This level is less than the EPA Region III RBCfor residential soil (5.5 ppm) [8].ATSDR has not derived any acute, intermediate, or chronic-duration oral Minimal Risk Levels (MRLs) for thallium because no data on effects of chronic-duration oral exposure to thallium were located.

The maximum estimated soil ingestion exposure dose of thallium for a 10-kg pica child at this site isestimated at 0.0013 mg/kg/day. This estimated dose is based on the highest thallium level foundamong all the residential samples collected. Animal studies indicate a NOAEL of 0.20 mg/kg/dayof thallium [19] which is almost 154 times greater than the highest estimated dose that could beexpected from exposure to residential soil levels. Therefore, the thallium levels found are notexpected to cause acute or chronic adverse health effects in children or adults.

Copper

Copper levels found in residential soils ranged from 19.2 ppm (estimated value) to 4690 ppm(estimated value). Only one value (4690 ppm) exceeded the Region VI Human Health ScreeningLevels for copper in residential soils (2900 ppm) [20].

In general, most copper in soil is in mineral form or tightly bound to organic matter. ATSDR doesnot expect that the copper levels found at the site are likely to pose an adverse health threat based onoral or dermal exposure.

Lead

The levels of lead found in the residential soil samples ranged from 11.2 to 316 mg/kg. These levels do not exceed the EPA screening level (400 mg/kg) and are not expected to pose a health hazard.


ATSDR'S CHILD HEALTH INITIATIVE

ATSDR's Child Health Initiative recognizes that the unique vulnerabilities of infants and childrenrequire special emphasis in communities faced with environmental contamination. At this site,sampling has identified lead, iron, arsenic, chromium, and copper as contaminants of concern. Children are particularly sensitive to the harmful effects of lead. ATSDR has taken into account that children live near the site and could be exposed to site-related contaminants.


CONCLUSIONS

  1. Indoor dust levels in the three sampled residences show elevated levels of lead and other metals. Most of these levels are not associated with adverse health effects in children or adults. However, a lead level of 1600 mg/kg found in one bulk dust sample (in Residence #2) is a potential exposure concern, especially for young children.

  2. Based on an analysis of the available ambient air data, there appears to be neither an acute nor chronic health hazard associated with inhalation, dermal exposure to or ingestion of airborne contaminants at residences near the site.

  3. The metals levels found in samples collected from the three residential yards are notexpected to cause adverse health effects based on the most plausible direct exposurescenarios.

RECOMMENDATION

Based on the best available public health practice, the blood lead levels of children younger than six living in Residence #2 should be tested periodically (a minimum of annually).


Table 1.

Off-site Exposure Pathway Elements Elizabeth Copper Mine Site
Pathway Name Exposure Pathway Elements Time Frame
Source Media Point of Exposure Route of Exposure Exposed Population
Completed Exposure Pathways
Indoor Dust Elizabeth Copper Mine site (ECMine) Indoor Dust Residential homes near the ECMine Ingestion Residents near the ECMine Past;
Current;
Future
Air (ambient) ECMine Ambient Air Ambient air near the ECMine Ingestion;
Inhalation;
Dermal
Residents near the ECMine Past;
Current;
Future
Soil ECMine Surface Soil Residential surface soil near the ECMine Ingestion,
Dermal
Residents who disturb surface soils near the ECMine Past;
Current;
Future


Site Map
Figure 1. Site Map


PREPARERS OF REPORT

Gail E. Scogin
Environmental Health Scientist
Petitions Response Section
Exposure Investigation and Consultations Branch
Division of Health Assessment and Consultation

Frank C. Schnell, PhD.
Toxicologist
Petitions Response Section
Exposure Investigation and Consultations Branch
Division of Health Assessment and Consultation


Reviewed By:

Donald Y. Joe, P.E.
Chief, Petitions Response Section
Exposure Investigation and Consultations Branch
Division of Health Assessment and Consultation


REFERENCES

  1. USGS. U.S. Department of the Interior, U.S. Geological Survey. Characterization of Mine Waste at the Elizabeth Copper Mine, Orange County, Vermont. Open-File Report 99-564. July 3, 2000.

  2. ATSDR. Agency for Toxic Substances and Disease Registry. Health Consultation. Residential Soil and Mine Tailings, Elizabeth Copper Mine Site, Strafford, Orange County,Vermont. November 29, 2000.

  3. ATSDR. Agency for Toxic Substances and Disease Registry. Health Consultation. AnEvaluation of Residential Drinking Water Wells Adjacent to the Elizabeth Copper MineSite, Orange County, Strafford, Vermont. September 28, 2000.

  4. Lockheed Martin. Memorandum from Miguel Trespalacios, REAC Sub-Task Leader toAlan Humphrey, U.S. EPA/ERTC Work Assignment Manager. Subject: Elizabeth MineSite. Strafford, Vermont. Work Assignment #0-117 - Amended Trip Report. March 30,2001.

  5. U.S. Environmental Protection Agency, Solid Waste and Emergency Response. RevisedInterim Soil Lead Guidance for CERCLA Sites and RCRA Corrective Action Facilities;Directive #9355.4-12. August 1994.

  6. U.S. Department of Housing and Urban Development. Guidelines for the Evaluation andControl of Lead-Based Paint Hazards in Housing. June 1995.

  7. 63 Federal Register 30353. June 3, 1998.

  8. USEPA. U.S. Environmental Protection Agency Region III Risk-Based ConcentrationsTable. April 12, 1999.

  9. Stedman's Medical Dictionary (26th Ed., 1995)

  10. Griffen TB, Couiston F, Wills H. Biological and Clinical Effects of Continuous Exposure to Airborne Particulate Lead. Arh Hig Toksikol 26:191-208. 1975.

  11. EPA. 1984. Health Assessment Document for Chromium. Research Triangle Park, NC:Environmental Assessment and Criteria Office, U.S. Environmental Protection Agency. EPA 600/8-83-014F.

  12. EPA. 1990. Noncarcinogenic Effects of Chromium: Update to Health AssessmentDocument. Research Triangle Park, NC: Environmental Criteria and Assessment Office,Office of Health and Environmental Assessment, U.S. Environmental Protection Agency. EPA 600/8-87/048F.

  13. ATSDR. Agency for Toxic Substances and Disease Registry. Toxicological Profile forChromium. U.S. Department of Health and Human Services. September 2000.

  14. Langard S. 1980. A Survey of Respiratory Symptoms and Lung Function inFerrochromium and Ferrosilicon Workers. Int Arch Occup Environ Health 46:1-9.

  15. Mancuso TF. 1975. Consideration of Chromium as an Industrial Carcinogen. In:Hutchinson TC, ed. Proceedings of the International Conference on Heavy Metals in theEnvironment. Toronto, Canada: Toronto Institute for Environmental Studies, pp 343-356.

  16. Weston. Memorandum from Eric D. Ackerman, Roy F. Weston, Superfund TechnicalAssessment and Response Team to Elizabeth Mine Site File. Subject: Surficial SoilSampling Event at Three Residential Properties on the Elizabeth Mine Site in Strafford,Orange County, Vermont, 1 and 2 November 2000. Not Dated.

  17. ATSDR. Agency for Toxic Substances and Disease Registry. Toxicological Profile forArsenic. U.S. Department of Health and Human Services. August 1998.

  18. National Academy of Sciences. National Academy of Sciences Press, Washington, D.C. Recommended Dietary Allowances, 10th edition. 1989.

  19. ATSDR. Agency for Toxic Substances and Disease Registry. Toxicological Profile forThallium. U.S. Department of Health and Human Services. July 1992.

  20. USEPA. U.S. Environmental Protection Agency Region VI Human Health Medium-Specific Screening Levels. February 23, 2000.


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