BASELINE HUMAN HEALTH RISK ASSESSMENT FOR THE …

BASELINE HUMAN HEALTH RISKASSESSMENT FOR THE

MURRAY SMELTER SUPERFUND SITE

SITE-WIDE EVALUATION

May 1997

Prepared for:

U.S. Environmental Protection AgencyRegion VHI

One Denver Place999 18th Street, Suite 500

Denver, Colorado 80202-2405

EPA Work Assignment No. 90-8BQ9Document Control No. 04500-090-AOAC

Prepared by:

ROY F. WESTON, INC.215 Union Boulevard, Suite 600Lakewood, Colorado 80228-1622

2075846

TABLE OF CONTENTS

Section Title Page

EXECUTIVE SUMMARY ES-1

1.0 INTRODUCTION 1-1.

1.1 Site Description 1-11.2 Scope and Purpose of This Document 1-41.3 Organization of This Document 1-4

2.0 CHEMICALS OF POTENTIAL CONCERN 2-1

2:1 Selection of Chemicals of Potential Concern 2-12.2 Sampling Plan 2-12.3 Summary of Data 2-4

3.0 EXPOSURE ASSESSMENT . . 3-1

3.1 Conceptual Site Model 3-13.2 Pathway Screening 3-3

3.2.1 Soil/Dust Ingestion 3-33.2.2 Inhalation Exposure to Soil/Dust in Air 3-33.2.3 Dermal Contact with Soil and Dust 3-33.2.4 Ingestion of Home-Grown Vegetables 3-43.2.5 Exposure to Slag Piles 3-43.2.6 Exposure to Surface Water and Sediments 3-43.2.7 Ingestion of Fish from Little Cotionwood Creek 3-43.2.8 Exposure to Groundwater 3-53.2.9 Summary of Pathways of Principal Concern 3-5

3.3 Quantification of Exposure to Arsenic 3-63.3.1 Basic Equation 3-63.3.2 Concentration (C) 3-73.3.3 Human Intake Factors (HIFs) . . 3-12

3.3.3.1 HIF for Soil and Dust Ingestion 3-123.3.3.2 HIF for Slag Ingestion 3-173.3.3.3 HIF for Drinking Water Ingestion 3-19

3.3.4 Dose Calculations 3-203.4 Evaluation of Exposure to Lead 3-20

3.4.1 Exposure of Residential Children 3-203.4.2 Exposure of On-Facility Workers to Lead 3-263.4.3 Exposure of Teenagers to Lead in Slag 3-33

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TABLE OF CONTENTS (Continued)

Section Title Page

4.0 TOXICITY ASSESSMENT 4-1

4.1 Overview 4-14.2 Adverse Effects of Arsenic 4-24.3 Adverse Effects of Lead 4-3

5.0 RISK CHARACTERIZATION 5-1

5.1 Evaluation of Risks from Arsenic . 5-15.1.1 Risks from Arsenic Soil and Dust 5-25.1.2 Risks from Arsenic in Slag 5-45.1.3 Risks from Arsenic in Groundwater 5-4

5.2 Evaluation of Risks from Lead 5-65.2.1 Health Risks from Lead to Residential Children 5-6

5.2.1.1 Risks to Children from Lead in Soil and Dust 5-75.2.1.2 Risks to Children from Lead in Groundwater 5-9

5.2.2 Health Risks from Lead to Pregnant Workers 5-95.2.2.1 Risks to Workers from Lead in Soil and Dust 5-95.2.2.2 Risks to Workers from Lead in Groundwater 5-11

5.2.3 Risks to Teenagers from Ingestion of Lead in Slag 5-12

6.0 UNCERTAINTIES 6-1

6.1 Exposure Uncertainties 6-16.2 Toxicokinetic Uncertainties 6-36.3 Model Uncertainties • . . 6-36.4 Hazard Uncertainties 6-4

7.0 REFERENCES 7-1

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APPENDIX A - EVALUATION OF TARGET ANALYTES FOR HUMAN HEALTH RISKASSESSMENT AT MURRAY SMELTER

\

APPENDIX B - ASSESSMENT OF EXPOSURE FROM HOME-GROWN VEGETABLES

APPENDIX C - ESTIMATION OF LEAD BKSF

APPENDIX D - DETAILED CALCULATION OF EXPOSURE AND RISK

APPENDIX E - SCREENING LEVEL EVALUATION OF RELATIVE RISK FROMINHALATION OF DUST AND DERMAL CONTACT WITH SOIL ORWATER

LIST OF TABLES

TABLE TITLE PAGE

ES-1 Risks from Arsenic in Surface Soil and Dust ES-10ES-2 Potential Risks from Arsenic in Groundwater ES-12ES-3 Risks from Lead in Surface Soil ES-142-1 Lead and Arsenic in Surface Soil 2-52-2 Geochemical Speciation Data for Surface Soil Samples 2-92-3 Lead and Arsenic in Subsurface Soil 2-102-4 Lead and Arsenic in Groundwater 2-123-1 Exposure Point Concentrations for Arsenic in Surface Soil 3-83-2 Exposure Parameters Ingestion of Arsenic in Soil and Dust . 3-143-3 Lead Levels in Residential Area Soil and Dust 3-243-4 Exposure Parameters for IEUBK Model 3-273-5 Lead Levels in Commercial Area Soil and Dust 3-313-6 Model Input Parameters for Estimation of Lead

Exposure in Women Workers 3-345-1 Risks from Arsenic in Surface Soil and Dust 5-35-2 Potential Risks from Arsenic in Groundwater - . 5-55-3 Risks to Children from Lead in Surface Soil and Dust 5-85-4 Risks to Workers from Lead in Surface Soil and Dust 5-10

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LIST OF FIGURES

FIGURE TITLE PAGE

ES-1 Site Map ES-41-1 Site Location 1-22-1 Site Map 2-22-2 Concentrations of Lead in Surface Soil 2-62-3 Concentrations of Arsenic in Surface Soil 2-72-4 Concentrations of Arsenic in Groundwater 2-133-1 Conceptual Site Model for Human Exposure 3-23-2 Relationship Between Arsenic in Dust and Soil 3-103-3 Relationship Between Lead in Dust and Soil 3-23

Baseline Human Health Risk Assessment May 1997

Document Control Number 4500-090-AOAC Page v


LIST OF ACRONYMS AND ABBREVIATIONS

ABA Absolute UnavailabilityAF Absorption FractionAT Averaging timeBDL Below Detection LimitBKSF Biokinetic Slope FactorBW Body weightC Concentration of a chemical in an environmental mediumCI Contact-intensiveCDC Centers for Disease ControlCLP Contract Laboratory ProgramCOPC Chemical of Potential ConcernDI Daily Intake of a chemicalED Exposure DurationEE/CA Engineering Evaluation/Cost AssessmentEF Exposure FrequencyEPA United States Environmental Protection AgencyEPC Exposure point concentrationEU Exposure UnitGM Geometric MeanGSD Geometric Standard DeviationHIF Human Intake FactorHQ Hazard QuotientIEUBK Integrated Exposure, Uptake, Biokinetic ModelIR Ingestion RateIRIS Integrated Risk Information SystemISZ Initial Study ZonekO Concentration in dust not attributable to yard soilks Mass fraction of soil in house dustmg/kg Milligrams per kilogramNCI Non-contact-intensiveNHANES National Health and Nutrition Examination SurveyNPL National Priorities ListPbB, Blood lead level (ug/dL)ppm pans per millionPRG Preliminary Remediation GoalP10 Probability of exceeding a blood lead level of 10 ug/dLPI 1.1 Probability of exceeding a blood lead level of 11.1 ug/dLRBA Relative BioavaiiabiliryRfD Reference DoseRME Reasonable Maximum ExposureSF Cancer Slope FactorTWA Time-weighted AverageUCL Upper Confidence Limit of the Meanug/kg Micrograms per kilogramXRF X-Ray fluorescence

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EXECUTIVE SUMMARY

INTRODUCTION

Site History

The Murray Smelter Superfund Site is located in Murray, Utah, near the intersection of StateStreet and 5300 South Street. Smelting activities began at the facility around 1872 at theGermania Smelter, located in the northwest corner of the facility. The Germania Smelteroperated until 1902, when the newer Murray Smelter (located in the east-central portion of thefacility) began operations. The Murray Smelter operated until about 1949, processing mainlylead and silver ores. The chief solid waste products generated by the smelters were arsenic,cadmium, and slag. Arsenic was sold for use as an insecticide or to the government for warpurposes. Cadmium was sold for use as a paint pigment. Slag was disposed of to the ground.Some portions of the slag were subsequently used for railroad ballast, fill material, and othersimilar uses. However, large masses of slag remain on-faciliry, both exposed at the surface andcovered by fill and by buildings.

Land Use

Following closure of Murray Smelter in 1949, portions of the facility were sold or leased to anumber of different businesses. The facility is currently occupied mainly by industrial orcommercial facilities, but two on-faciliry areas are zoned for residential land use and arecurrently occupied by trailer parks (Doc and Dell's, located on the east side of the facility, andGrandview, located along the southern border of the facility). An area in the Germania Smelterportion of the facility has been proposed as the site of a Murray City police training facility.

The area surrounding the site is mainly residential, with some commercial properties. Thecentral area of the City of Murray is located immediately north of the site, and a city park andthe County fairgrounds are located to the east. A high school is located immediately south ofthe site, and a junior high school is located adjacent to the high school, south-east of the site.

In the future, it is considered likely that current land use patterns will not change in most areas.Specifically, it is believed that the main part of the on-facility area will remainindustrial/commercial, and the off-facility area surrounding the site will remain mixed'residential/commercial. However, it is considered likely that the current on-facility residentialareas (the two trailer parks) will eventually be convened to non-residential uses.

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Surface Terrain

The site is mainly flat, having been leveled over much of its area with slag and other fillmaterial. A steep wall of slag descends to the level of the surrounding terrain on the north andthe east of the site. The only permanent surface water body near the site is Little CottonwoodCreek, which forms the northern boundary of the facility. The creek flows northwest, draininginto the Jordan River about one mile west of the site.

Groundwater

Groundwater at the site occurs in a shallow and an intermediate alluvial aquifer. The shallowalluvial aquifer occurs at an average depth of about 10 feet below the surface, and is about 20feet thick. Beneath the shallow alluvial aquifer is a layer of clay that averages 30 feet inthickness and is apparently continuous across the site. Beneath the clay is a layer of coarsealluvial sediment about 10-20 feet thick, comprising the intermediate alluvial aquifer.Groundwater flow in the shallow alluvial aquifer at the site is mainly north, towards LittleCottonwood Creek, while flow in the intermediate alluvial aquifer is more to the northwest.Groundwater flow rates in the shallow alluvial aquifer are about 0.4 feet/day, and about 1.7feet/day in the intermediate alluvial aquifer. Although the intermediate alluvial aquifer isconfined, the hydraulic gradient is mainly downward (about 0.2-0.6 ft/ft) over most of the site.

Basis for Potential Concern

The U.S. Environmental Protection Agency (EPA) proposed that the Murray Smelter site beplaced on the National Priorities List (NPL) in January, 1994, based on concerns that metalspresent in on-faciliry smelter wastes might be posing a risk to humans or the environment. Thesite is being evaluated as a non-time-critical removal action.

Purpose of this Document

This document is a baseline human health risk assessment for the Murray Smelter site, includingthe site itself (facility) and adjacent off-facility areas that may have been impacted by historicor on-going releases from the site. The objective of the risk assessment is to evaluate potentialhealth risks to humans from site-related chemicals, both now and in the future, if no actions aretaken to reduce contamination or limit exposure to site-related chemicals. The information inthis assessment is intended to help support risk management decisions regarding the potentialneed to undertake remedial actions at the site to ensure protection of human health. Potentialrisk to ecological receptors from site-related chemicals is being assessed separately.

CHEMICALS OF POTENTIAL CONCERN

The chemicals of primary concern at smelting sites are metals. Typically, the environment maybecome contaminated with a wide variety of different metals that were present in the ores orconcentrates smelted at the facility. However, experience at many mining, milling and smelting

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sites has shown that the large majority of risk to humans is usually due to arsenic and/or lead.This conclusion was supported for the Murray Smelter site by an analysis of preliminary dataavailable from early site investigations. On this basis, samples collected to support the humanhealth risk assessment were analyzed for lead and arsenic only.

Soil Data

Prior to sampling, the on-facility area was divided into eleven "exposure units" (EUs), and theoff-facility area was divided into eight Initial Study Zones (ISZs). These areas are shown inFigure ES-1. In the on-facility area, EU-1 to EU-7 are mainly commercial/industrial, while EU-8 to EU-11 contain the two residential trailer parks. In the off-facility area, ISZ-1 to ISZ-8 aremainly residential, although some areas are mixed commercial/residential. Area ISZ-3 includesthe local high school, and ISZ-2 includes the junior high school.

For on-facility sampling within each exposure unit, a total of 10-20 surface soil samples (0-2inches in depth) were collected, depending on the size of the unit. In addition, test pits wereinstalled in several exposure units, using information on existing and historical site structuresand operations to select the location of the pits. At each test pit, a series of samples werecollected at depths of 0-1, 1-2, 2-3, 3-4, and 4-5 feet. Subsurface soil samples collected on-facility at the Grandview Trailer Park (EU-8, EU-9 and EU-10) were from soil borings ratherthan test pits, and the sample depths were 0-2", 2-6", 6-12" and 12-18". The main purpose ofthese test pits and soil borings was to reveal whether there were any consistent concentrationpatterns as a function of depth, and whether any buried sources could be identified. '

For each off-facility ISZ, surface soil samples were collected from 10 to 16 distinct locations(depending on the size of the zone). Each sample was a composite of surface soil from 4 to 6sublocations. In addition, soil borings were collected at two different locations in each ISZ, witheach sample being divided into depths of 0-2", 2-6", 6-12", and 12-18". These borings werecollected to investigate the vertical extent of contamination in each off-facility zone.

Inspection of the data on lead and arsenic in surface soil revealed the following mainobservations:

• On-facility, there is very wide variability in the concentration levels detected forboth lead and arsenic. In most EUs, the range of values from minimum tomaximum is at least 100-fold, and sometimes exceeds 1,000-fold. Often, highconcentrations were detected in close proximity to low concentrations. This on-facility pattern of high variability over small distances is probably a result ofhistoric waste disposal practices, along with activities such as grading and fillingwith mixtures of clean fill and site wastes;

• On-facility, the highest concentrations occur adjacent to the railroad right-of-way.However, high concentrations are detected at individual sampling locations innearly all EUs. The lowest average on-facility levels are observed in the eastern

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BASELINE RISK ASSESSMENT FIGURE ES-1

SITE MAP

215 Union BoulevardSuite 600

Lake-wood. CO 80228(303) 980-6800

MURRAY SMELTER SITEMURRAY, UTAH

portion of the Grandview trailer park and in Doc and Dell's trailer park.

• Off-facility, variability in measured concentrations is considerably smaller than' on-faciliry, with ranges within each ISZ typically falling within a factor of 10.

• Off-facility, the highest average concentrations are observed in those ISZsimmediately west and immediately south of the site. Mean levels in ISZs that arefurther removed from the facility tend to be lower, supporting the view that theclosest off-facility areas have been impacted by the facility.

Inspection of the data on lead and arsenic in sub-surface soil revealed the following mainobservations:

• The pattern of concentration with depth is not uniform. At some locations, bothlead and arsenic concentration tend to increase substantially as depth increases,while at some locations, both lead and arsenic concentrations tend to decrease asdepth increases. At many locations, there appear to be zones of highlycontaminated material inter-layered between zones of lesser contamination.

• There is often a general correspondence between lead and arsenic levels (bothtending to be high or low in the same sample), but this correspondence is notstrong.

• At off-facility locations, variability by depth is generally smaller than on-facility,although it should be noted the depth interval studied was narrower (0-18 inchesvs 0-5 feet). In most cases, there is no clear concentration trend as a function ofdepth, although a few locations appear to show a decrease.

Dust Data

Indoor dust samples were collected from 22 different homes or buildings located in off-facilityareas. Typically, each sample was a composite of dust collected from three areas, each about2 feet by 7 feet. Linear regression analysis of the relationship between the concentration of leadand arsenic in indoor dust at a house to the concentrations in the soil of that house revealed thefollowing best-fit equations:

Lead: C(dust) = 98 ppm + 0.32-C(soil)Arsenic: C(dust) = 16 ppm + 0.17-C(soil)

These data support the view that yard soil contributes to indoor dust contamination, but thatconcentrations in indoor dust are derived only in pan (17%-32%) from yard soil.


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Groundwater Data

A total of twenty wells were installed, 13 in the shallow alluvial aquifer and 7 in theintermediate alluvial aquifer. Several other on-facility wells (7 in the shallow zone and 3 in thedeeper zone) that had been installed in earlier investigations were also redeveloped and sampled.

Inspection of the data on arsenic levels in groundwater reveals that there is very high variabilitybetween different wells, ranging from values below the detection limit (< 5 ug/L) to more than27.000 ug/L. The highest values occur in the shallow alluvial aquifer. The highly variablepattern of groundwater contamination, especially in the shallow zone, suggests that there areprobably several buried on-facility sources of arsenic that are leaching to the shallow alluvialaquifer. A few of the wells screened in the intermediate alluvial aquifer may be slightlyimpacted, although this is difficult to judge without representative background data.

In contrast to arsenic, lead levels in most of the shallow and intermediate alluvial aquifers arerelatively low. This is consistent with the fact that lead is usually much less mobile in soil thanarsenic, and is therefore less likely to migrate from soil into groundwater.

Slag Data

The EPA collected a single composite sample of slag from nine different locations at the facility.The sample was analyzed in duplicate, and the mean concentration values were as follows:

Arsenic 695 ppmLead 11,500 ppm

EXPOSURE ASSESSMENT

When the Germania and Murray smelters were operating, stack emissions presumably containedsubstantial levels of lead and arsenic, which fell to the ground in tiny particles of soot, or werecarried from the air to the ground by rain or snow. In addition, smelting operations generatedsolid wastes including slag, flue dust and dross. These waste materials also contained lead andarsenic (especially flue dust and dross). Extensive slag deposits are evident on-facility, someof which are exposed at the surface and some of which are covered by fill of varying depth.There are no recognizable piles of flue dust or dross presently on the facility, but these materialsmay have been disposed of to soil and subsequently graded and/or covered with slag or fill.Contaminants in these solid wastes may have caused secondary contamination of the surroundingenvironment by several pathways, including wind erosion of fine dust particles into air, watererosion of dissolved or suspended metals into Little Cottonwood Creek, and leaching ofdissolved metals downward into groundwater. In addition, some of the waste materials mayhave been used for purposes such as fill, road base, road sanding, etc.

Because lead and arsenic are not volatile and are not subject to chemical degradation, most ofthe lead and arsenic which were released to the site or to the surrounding area by past smelting

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operations are probably still in place. Thus, on-facility workers (assumed to be located mainlyin EU-1 to EU-7), on-facility residents (located in EU-8 to EU-11), or nearby off-facilityresidents (located in ISZ-1 to ISZ-8) might be exposed to site-related contaminants by a numberof pathways. However, not all pathways that might exist are thought to be of equal concern.Based on quantitative or qualitative analysis of the relative importance of each pathway, thefollowing pathways are judged to be most likely to account for the majority of exposure and riskfrom site-related materials:

• Ingestion of soil/dust (current and future workers and residents)• Ingestion at slag piles (current and future teenagers age 12-18)• Ingestion of groundwater (future workers and residents)

Other exposure pathways to site-related wastes are judged to be sufficiently minor that furtherquantitative evaluation is not warranted.

For on-facility workers, two different exposure scenarios were considered. The first focuses onworkers who spend most of the day indoors. Because such workers are not expected to havefrequent and extensive direct contact with outdoor soil, they are referred to as "Non-ContactIntensive" (NCI) workers. The second scenario focuses on workers who work mainly outdoors,often coming into direct contact with soil. This type of worker is referred to as "Contact-Intensive" (CI). Available information regarding current on-facility workplace activitiesindicates that both types of worker are present at the facility, so both types of worker wereevaluated.

For all populations considered (residents, teenagers, NCI-workers, Cl-workers), it is expectedthat there will be variation between different individuals in the population, depending on theirpersonal habits and the amount of contact they have with environmental media. To account forthis variability between different people, risks were calculated for individuals whose exposureis about typical, and for individuals whose exposure is near the upper end of the range (aboutthe 95th percentile). These two groups are referred to as "Average" and "Reasonable MaximumExposure" (RME), respectively.

TOXICITY ASSESSMENT

Arsenic

Excess exposure to arsenic is known to cause a variety of adverse health effects in humans.Characteristic symptoms of chronic low-level exposure include diarrhea, decreased blood cellformation, injury to blood vessels, damage to kidney and liver, and impaired nerve function thatleads to "pins and needles" sensations in the hands and feet. The most diagnostic sign of chronicarsenic exposure is an unusual pattern of skin abnormalities, including dark and white spots anda pattern of small "corns," especially on the palms and soles.

Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 55.7


The long-term average daily intake of arsenic that produces these noncancer effects varies fromperson to person. In a large epidemiclogical study, skin and vascular lesions were noted inhumans exposed to 0.014 mg/kg/day or more arsenic through drinking water. These effectswere not observed in a control population ingesting 0.0008 mg/kg/day. Based on this, the EPAcalculated a chronic oral reference dose (RfD) of 0.0003 mg/kg/day. This is a dose which isbelieved to be without significant risk of causing adverse noncancer effects in even the mostsusceptible humans following chronic exposure. For situations where only subchronic (and notchronic) exposures are possible, the EPA has proposed a subchronic RfD of 0.006 mg/kg-day.

There have been a number of studies in humans which indicate that chronic oral exposure toarsenic increases the risk of skin cancer and other (internal) cancers. The amount of arsenicingestion that leads to skin cancer is controversial. Based on a study of skin cancer in peopleexposed to arsenic in drinking water, the EPA has calculated a unit risk of 5E-5 (ug/L)"1

corresponding to an oral slope factor of 1.5 (mg/kg/day)'1. However, there are good data toshow that arsenic is metabolized by methylation in the body, and some researchers havesuggested that this could lead to a threshold dose below which cancer will not occur. The EPAis currently reviewing the cancer slope factor for arsenic, but does not believe the data arecurrently adequate to establish that there is a threshold for arsenic-induced cancer.

Lead

Excess exposure to lead is known to cause a variety of adverse effects in humans. The effectusually considered to be of greatest concern is impairment of the developing nervous system ofyoung children and fetuses. Effects of chronic low-level exposure on the nervous system aresubtle, and normally cannot be detected in individuals, but only in studies of groups of children.Common measurement endpoints include various types of tests of intelligence, attention span,hand-eye coordination, etc. Most studies observe effects in such tests at blood lead levels of 20-30 ug/dL, and some report effects at levels as low as 10 ug/dL and even lower. Such effectson the nervous system are long-lasting and may be permanent.

.In addition to effects on the nervous system, excess exposure is also believed to causefetotoxicity and possibly teratogenicity in the fetus, decreased heme synthesis with resultantinhibition of red blood cell formation and synthesis of heme-dependent enzymes, and elevatedsystolic blood pressure in adults. Studies in animals suggest that lead may also cause renalcancer following chronic high dose exposures.

RISK CHARACTERIZATION

Risks from Arsenic

Noncancer risks from arsenic are characterized in terms of a Hazard Quotient (HQ). The HQis the ratio of the dose estimated to occur in a person exposed at the site, compared to aReference Dose (RfD) that is believed to be safe. If the value of HQ is less than or equal toone, it is believed there is no significant risk of noncancer effects occurring, even in the most

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susceptible members of the population. If the value of HQ is greater than one, there is a riskof noncancer effects, but a value above one does not mean that an effect will definitely occur.However, the chances of an effect increase as the value of HQ increases.

Cancer risks from arsenic are described in terms of the probability that a person will developcancer over a lifetime as a consequence of site-related exposures. The level of cancer risk thatis of concern is a matter of individual, community and regulatory judgement. However, theEPA typically considers risks below one in one million to be so small as to be negligible, andrisks above 100 in one million to be sufficiently large that some son of action or interventionis usually needed. Risks between 1 and 100 per million are evaluated on a case by case basis.

Arsenic in Soil.

Potential risks from arsenic in soil were calculated for each EU or ISZ where residentialexposure is considered likely. Because the EUs and ISZs are relatively large compared to thesize of an average residential property, the results should be considered to be generallyrepresentative of conditions within the area, but should not be considered to apply to specificresidential properties, since any one property might have risks either above or below the areaaverage.

For each location, calculations were performed using two different estimates of the concentrationof arsenic in soil. In the first case, the estimate was based on the mean concentration.However, because the true mean concentration cannot be calculated with certainty from a limiteddata set, risks were also calculated based on the upper 95% confidence limit of the mean or themaximum value (whichever was lower). The span in risks between these two approaches helpsindicate the range of uncertainty which exists in the risk estimates.

Table ES-1 summarizes the estimated risks from arsenic in soil. Values are presented fornoncancer and cancer risks to residents who live in an on-facility trailer park (EUS to EU-11)or in an adjacent off-facility area (ISZ-1 to ISZ-8), and to workers who are exposed at on-facility commercial areas (EU-1 to EU-7). For convenience, exposure locations that result inan HQ value above one or a cancer risk estimate above 100 per million have been shaded.Inspection of this table reveals the following main observations:

• For on-facility and off-facility residents, nearly all chronic noncancer risks arebelow a level of concern. This conclusion is supported by the results of a urinaryarsenic study conducted by the Salt Lake City-County Health Department, inwhich urinary arsenic levels in 7 children age 0-7 years and in 17 children age8-17 years living in Doc and Dells (EU-11) or Grandview (EU-9 or EU-10) wereall close to or below detection limits (2 ug/L), which is well within or belownormal ranges. The only location where noncancer risks from arsenic appear tobe of concern to residents is Area EU-8 (HQ = 1 to 9). It should be noted thatalthough EU-8 is pan of the Grandview Trailer Park area, there are no residencescurrently in this EU. Cancer risks to residents mainly range between 1 and 80


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TABLE ES-1 RISKS FROM ARSENIC IN SURFACE SOIL AND DUST

ExposedPopulation

Residents

Non-ContactIntensiveWorker

Contact- .IntensiveWorker

Area

EU-8

EU-9

EU-10

EU-11

ISZ-1

1SZ-2

ISZ-3

ISZ-4

ISZ-5

ISZ-6

ISZ-7

ISZ-8

EU-1

EU-2

EU-3

EU-4

EU-5

EU-6

EU-7

EU-1

EU-2

EU-3

EU-4

EU-5

EU-6

EU-7

Noncancer HQ

Average1

1 ^:;:;;3::'.v::;o:

0.08 0.1

0.05 0.1

0.02 0.05

0.07 0.1

0.02 0.03

0.04 0.08

0.03 0.05

0.03 0.05

0.04 0.08

0.09 0.1

0.05 0.3

0.03 0.1

0.02 0.08

0.3 :"--:::;>:-:2:>;;;i;i:

0.09 1

0.02 0.07

0.1 0.4

0.1 0.3

0.2 0.9

0.1 0.5

3:2 100.6 : .:: :8,;:: ;

:

0.1 0.4

0.7 • • • • " ; . • . ;3',:";

0.6 ; * -: .2 • • • : "

RME1

''•^^••^•V^'i:

0.2 0.4

0.1 0.4

0.05 0.1

0.2 0.4

0.05 0.08

0.1 0.2

0.1 0.2

0.09 0.1

0.1 0.2

0.2 0.3

0.2 0.8

0.04 0.2

0.02 0.09

0.3 ••V^&j||

0.1 1

0.03 0.07

0.1 0.5

0.1 0.3

0.4 r::.:;.v

0.3 1

4 • • ' • • • . • • • , •30- • • ; ; '1 :"-.-.;2bM

0.3 1

1 !:"''«?1S!

1 ;: . :.;;4#'::;v

Estimated Cancer Risk (per million)

Average1

• 60 ;-?;:2bbl5 8

3 8

1 3

4 8

0.9 2

2 4

2 3

2 3

2 5

5 6

3 20

1 5

0.6 3

8 60

3 40

0.8 2

3 10

3 9

6 30

4 20

60 :••• :400V

20 i .300:;;

5 10

20 90

20 60

RME1

: ;600' : 2000

40 80

30 80

10 20

40 80

9 20

20 40

20 30

20 30

20 40

50 60

30 : vv.;200::;.A;

6 30

4 20

50 n.30QB;

20 -'2001

4 10

20 70

20 50

70 ::;..300:;:|;

40 ;i:V200Sf

: 600: :^'4000:A:-;;';200-;. '•;•;. 3006;!

50 : :200; i;

;:;;:200:i : 1000 ;

v.--;200'.:.:.;,-:-:::70o:;'.:-:

Shaded cells indicated locations where risks exceed common guidelines (HQ > 1. cancer risk > 100 per million)

The first value shown is based on the mean concentration, and the second value is based on the EPC (usually the maximumdetected concentration)

Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page ES-10


per million, with risks greater than 100 per million occurring only in area EU-8under both average and RME conditions, and in ISZ-8 (using the EPC and RMEconditions).

• For non-contact intensive workers, chronic noncancer risks are below a level ofconcern in most areas, but HQ values of 2 are observed for area EU-3 using theEPC and assuming RME exposure conditions. Average cancer risks range from0.6 to 60 per million, with RME risks exceeding 100 per million in two areas(EU-3 and EU-4) if the EPC is used.

• For contact intensive on-facility workers, average and/or RME noncancer risksare of potential concern in a number of areas, with some HQ values ranging from2 to 30. Cancer risks based on the EPC exceed the 100 per million level in twoareas (EU-3 and EU-4) for average workers, and in all 7 areas for RME workers,with risk values ranging up to 4,000 per million. If the mean concentration isused, risks are below 100 per million in all locations for the average worker, butstill exceed 100 per million in 4 of 7 areas for the RME worker.

Arsenic in Slag

The population of chief concern for direct exposure to slag is judged to be teenager (age 12-18years). Estimated risks to this population from ingesting arsenic in slag are summarized below:

RiskParameter

Chronic HQ

Cancer Risk (per million)

Estimated Value

Average

0.02

2

RME

0.2

10

As seen, noncancer HQ values do not exceed a level of concern for either average or RMEexposure assumptions. Excess cancer risks range from 2 per million (average) to 10 per million(RME).

Arsenic in Groundwater

At present, it is not believed that water from the shallow or intermediate alluvial aquifer on ornear the site is used for drinking by humans. However, such exposure might conceivably occurin the future.

Table ES-2 summarizes potential noncancer and cancer risks that would exist if water fromvarious on-facility and off-facility wells were used for drinking. As seen, potential noncancerHQ values exceed a value of one at a number of wells, both for residents and for workers. Insome cases the exceedances are relatively small (e.g., HQ = 2), but at some wells the HQ

Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page ES-11THIS DOCUMENT WAS PREPARED BY ROY F WESTON. INC. EXPRESSLY FOR EPA. IT SHALL NOT BE RELEASED ORDISCLOSED IN WHOLE OR IN PART WITHOUT THE EXPRESS WRITTEN PERMISSION OF EPA.

TABLE ES-2: POTENTIAL RISKS FROM ARSENIC IN GROUNDWATER

Population

Resident

Worker

Location

On-facility

Off-facility

Off-facility

On-facility

On-facility

AquiferDepth

Shallow

Shallow

Intermediate

Shallow

Intermediate

WellID

MW-1001

MW-1011

MW-102

MW-103

MW-104

MW-106

MW-101D

MW-104D

MW-102

MW-105

MW-106

MW-107

MW-I08

MW-109

MW-110

MW-111*

MW-112

GW-]

GW-2

Well 1

Well 2

Well 3"

UTBN-1

MW-105D

MW-108D

MW-109D

MW-112D

GW-1A

GW-1AR

GW-2A

Noncancer HQ

Average

0.1

0.3

0.8

::VVio:;.'":,:0.3

;:;,-i-;6oov;::.:;0.1

0.8

0.4

0.3

iV^obir-.-'0.05

0.05

0.3:: :;s6:':;::;V:

^•••".fiO-V:^1

• ' ^SOW1.

••^••W"-;:-'-;:

• '::'.:- •' '4. ••::';.'::-

• • ••'-. -40;-:;.:\::-

::;. ,VS.V.V:

.•.w:sv:v0.5

0.05

1

0.8

-v-:20T::-:!.:;

0.1

X:-;-H'9r:::::fix:

RME

0.2

0.5

:-,:H" .2' - • • : - .

•,-:.-,-20':'::-':::

0.5

;:>.:.C2.obo'::''-:-0.2

.;.^:;;,;..-2\,:^vV-

0.6

0.4

::.^;-:;;:::966:v. -;•:.:;

0.08

0.08

0.5

^ • :8bV:--:-.;-::,,:

rvV'SO;':::: •••-:••.

V'V:^ :• : : ; • ; ' ' .:';:':;;:::4o:.:v-'VV-:.:-:90V::..: :

••• •'•.:'': "7 r: -:":-

V;V60 :.Vl-

•./• :.:'.'.-;8'':.,- :..;,'

••:v::\.-:9. • ' • : . ' • • • ;0.8

0.08:r.:".':''.2r^.-..-.-V

1' •^30 • : • • • • ' • • ]

0.2

%:.;': -.ilO;:::/; ;

Estimated Cancer Risk(per million)

Average

6

10

50

:....:: .-700: ••• ' ' :•

10

;70;000

6

50

10

8

> 20:000 ;: ?

2

2

9

' < • ' " 2,000 ;: :;

: : '...2;000 "•

30

.:•;:;•• rsoo-!:-. •^••:-: : ' v . 2.000 ' • ' •

100:;.: .., 1,000% .. :•

;.;-:'---20o:; • - : . : • .; : : - ' : : "2oa:':; ••:-

20

2

40

30

:,'/-"::-500'. -'•:;

4

•.-::.':'3oo::-;vv

RME

40

100

300

5,000

100

400,000

40

. ::300 ' :

100

70

: 100;000:::

10

10

70

10.000 -

• : ' , -20,000V:,.

. : ' - - -':30oW:--.-^•7,606;?.; ; - ; ': 10X100 "

v;oooi>vto,ooo;:::.

V-;-L.OOO.Rx;:^--Va;ob6:;^:::?-

100

10

• ' ; . • • ! AGO';; : - : . : ' ":;•,-'• -:200:;-:- •

..;:4,ooo:"-.30

^••::-2,000'V:;

Shaded cells indicate wells where risks from arsenic exceed typical EPA guidelines (HQ > 1. cancer risk > 100 per million)

1 Well located in an up-gradiem location' Well is completed in slag

Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page ES-12THIS DOCUMENT WAS PREPARED BY ROY F. WESTON. INC. EXPRESSLY FOR EPA IT SHALL NOT BE RELEASED ORDISCLOSED IN WHOLE OR IN PART WITHOUT THE EXPRESS WRITTEN PERMISSION OF EPA.

values are very high (e.g., 1,000 to 2,000 for residents at well MW-103, and 500 to 900 forworkers at well MW-106). Similarly, potential excess cancer risk values to residents andworkers are quite high at a number of wells, with 4 of 8 wells above the 100 per million risklevel to residents and 14 of 22 wells above 100 per million for workers.

These calculations indicate that use of water from at least several locations, especially in theshallow zone, would pose very substantial risks to human health. Risks from potential futureuse of wells in the intermediate alluvial aquifer are lower than for the shallow zone, but severalwells still exceed the common health-based criteria used by EPA (HQ > 1, cancer risk > 100per million).

Risks from Lead

Health-Based Goals

Risks from lead are not evaluated using a Hazard Quotient approach, but rather are assessed byestimating the likelihood that a random member of an exposed population would have a bloodlead level (PbB) above some specified concentration. For children, the EPA has concluded thatblood lead levels above 10 ug/dL are associated with risks that warrant avoidance, and has setas a goal that the probability of a typical child or group of similarly-exposed children exceedinga blood lead level of 10 ug/dL ("P10") should be no more than 5%.

The EPA has not yet issued formal guidance on the blood lead level that is consideredappropriate for protecting the health of teenagers, adult residents or workers. However, becausefetuses are believed to be as susceptible to the adverse neurological effects of lead as children,it is common to focus concern in these populations on the subpopulation of pregnant women andwomen of child-bearing age, and to set as a goal that there should be no more than a 5% chancethat the fetus of an exposed woman would have a blood lead level over 10 ug/dL. Because theblood lead concentration of a fetus is usually about 90% of that of the mother, a PbB in themother of 11.1 ug/dL corresponds to a PbB in the fetus of 10 ug/dL.

Risks from Lead in Soil

Table ES-3 summarizes the estimated risks to children age 0-84 months and to workers fromexposure to lead in surface soil. The values for children were estimated using EPA's IEUBKmodel, while the results for adults were derived using a model developed by Bowers et al. Forconvenience, locations where risks exceed EPA's target (no more than a 5% chance of exceedinga blood lead level of 10 ug/dL in young children or 11.1 ug/dL in adults) have been shaded.Inspection of this table reveals the following main observations:

• For resident children, predicted risks from lead are higher than EPA's target forall areas except EU-10, ISZ-2, ISZ-4 and ISZ-5. In some cases, the predictedrisk of exceeding the target of 10 ug/dL is quite high (e.g., >99% at EU-8, 53%at ISZ-1, 48% at ISZ-7). Limited blood lead data are available for children

Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC . . Page ES-13THIS DOCUMENT WAS PREPARED BY ROY F. WESTON. INC. EXPRESSLY FOR EPA. IT SHALL NOT BE RELEASED ORDISCLOSED IN WHOLE OR IN PART WITHOUT THE EXPRESS WRITTEN PERMISSION OF EPA.

TABLE ES-3 RISKS FROM LEAD IN SURFACE SOIL

Population

ResidentChild(age 0-84months)

Non-contactIntensiveWorker

Contact-IntensiveWorker

ExposureArea

EU-8

EU-9

EU-10

EU-11

ISZ-1

ISZ-2

ISZ-3

ISZ-4

ISZ-5

ISZ-6

ISZ-7

ISZ-8

EU-1

EU-2

EU-3

EU^»

EU-5

EU-6

EU-7

EU-1

EU-2

EU-3

EU-4

EU-5

EU-6

EU-7

Mean LeadConcentration (ppm)

6177

909

538

814

1299

241

768

391

426

657

1222

1062

2905

2879

9548

1750

2754

2297

2524

2905

2879

9548

1750

2754

2297

2524

Risk of Exceeding TargetBlood Lead Level

^^^:^:>99%-)}^--:--. • - : • ' • • -

:^:^§^\::26%;^:-^ • •

4.0%

1^'UA^19*:--'^" • ' • • : - - :

•^%^^M^3%::'^-y':^, . :..

0.1%

,;:::f;::::::,;C.;V;;::.:;;i5.%:'V. . ' - • ' ' - . . *

0.9%

1.4%

.^?!^f^-=^*6%j •:;::•:.••••?'•. M ' : - :

:4&^:i^;?*8.%^rv:":H -^^?:^^;379t;.: ;:.;;;•;;;:•;••.-;•::

0.9%

0.9%

"^^^V^^P^^V.:;^:;;-^:

0.3%

0.8%

0.5%

0.6%

:^iv=v^:^::59%^:- . ..:;.V?::v:?N^:"--58*';'-:;:^;::-:^i^.::i:^'^:vH^^*^r/^?^:i;

^ ;•.; .^;^-:25%:'^;-:^^j;-;:^M^ ;-r:?:::::.;::55:%::;i-: ;•:•:-:;; ;::'-;

::: ;.::::.;;:

::;,;: ;.c: ::': ;-:42«:.:.; ^^::?;-; r;;:;•;:{;;:•:;. ^^48*»^^;^-

Shaded cells indicated locations where calculated risks exceed the target (5%)


THIS DOCUMENT WAS PREPARED BY ROY F. WESTON, INC. EXPRESSLY FOR EPA. tT SHALL NOT BE RELEASED ORDISCLOSED IN WHOLE OR IN PART WITHOUT THE EXPRESS WRITTEN PERMISSION OF EPA.

living in Grandview (EU-9 and EU-10) and Doc and Dell's (EU-11). Thegeometric mean blood lead values observed in these areas are somewhat lowerthan predicted by the IEUBK model, and the observed incidence of children withblood lead values above 10 ug/dL is also lower than predicted. This suggests thatthe IEUBK model may be over-estimating lead exposure levels in children at thissite, but the number of children is too small to be certain.

• For non-contact intensive workers, risks from lead in surface soil are belowEPA's goal at all locations except EU-3, where the risk is estimated to be about20% of exceeding a blood lead value of 11.1 ug/dL.

• For contact intensive workers, risks from lead in surface soil are above EPA'sgoal at all on-facility locations, with probabilities ranging from 25% to >99%of exceeding a blood lead value of 11.1 ug/dL.

These calculations support the view that lead contamination from past smelter operations maybe posing a health risk both to area children and to on-facility workers who have extensivecontact with soil.

Risks from Lead in Slag

The potential effect of exposure of area teenagers to lead in slag was evaluated using the Bowersmodel. The results are summarized below:

Baseline(No slag)

GM (ug/dL)

1.6

Pl l . l 1

<0.01%

IncludingSlag Exposure*

GM (ug/dL)

2.4

Pl l . l

0.02%

IncrementDue to Slag

GM (ug/dL)

0.8

Pll . l

<0.02%

GM = Geometric mean blood lead (ug/dL)' P l l . l = probability of a teenager exceeding a blood lead of 11.1 ug/dL" Concentration of lead in slag = 11.500 ppm

As seen, direct ingestion of slag is estimated to increase geometric mean blood lead levels byabout 0.8 ug/dL. However, assuming a geometric standard deviation (GSD) of 1.54, this doesnot result in a significant risk of exceeding a blood lead value of 11.1 ug/dL. This suggests thatexposure of area teenagers to lead in slag is not likely to be of significant health concern.

Risks from Lead in Groundwater/

Under typical circumstances, the expected increment in geometric mean blood lead by a childage 0-84 months is about 0.05-0.06 ug/dL per ug/L of lead in water. Nearly all wells locatedin residential areas have lead concentrations less than 10 ug/L, corresponding to increments ingeometric mean blood lead of less than 0.5-0.6 ug/dL. This increment is sufficiently small,



especially compared to the estimated effects of ingesting soil/ dust and/or slag, that blood leadlevels in children and the probability of exceeding 10 ug/dL are not likely to be significantlyaffected by potential future ingestion of groundwater.

For women workers, the expected increment in blood lead in women workers due to ingestionof lead in drinking water is 0.0168 ug/dL per ug/L in water. Most wells located in thecommercial areas of the site have lead levels that are less than 10 ug/L, and potential futureingestion of water from these wells would be expected to cause only a very small increase (<0.2 ug/dL) in blood lead level of workers. However, a few on-facility wells (e.g., MW-111,Well-3) have lead concentrations that appear to be significantly higher than average, andingestion of groundwater from these wells could increase the risk of exceeding the target of 11.1ug/dL in non-contact-imensive workers by about 10%-13%. However, these two wells arecompleted in slag, and may not be representative of actual wells for human use. In contact-intensive workers, the risk of elevated blood lead from contact with soil is sufficiently high thatthe additional exposure from ingestion of lead in water is not expected to be substantial.

UNCERTAINTIES

Quantitative evaluation of the risks to humans from environmental contamination is frequentlylimited by uncertainty (lack of knowledge) regarding a number of important exposure andtoxicity factors. This lack of knowledge is circumvented by making assumptions or estimatesbased on the limited data that are available. Because there are a number of assumptions andestimates employed in the exposure and risk calculations, the results of the calculations arethemselves uncertain, and it is important for risk managers and the public to keep this in mindwhen interpreting the results of a risk assessment. The main sources of uncertainty in the riskcalculations for arsenic and lead at this site include the following:

• Uncertainty in actual human exposure rates, especially to soil, dust and slag

• Uncertainty in the actual mean environmental concentrations of lead and arsenicthat an exposed individual may encounter, especially in soil

• Uncertainty in the extent of absorption (bioavailability) of lead and arsenic fromsoil and slag

• Uncertainty in key input parameters used in the mathematical models forevaluating lead exposure of children and adults, as well as uncertainty in theaccuracy of the models themselves

• Uncertainty in the exposure levels of lead and arsenic that are actually likely tocause significant adverse effects, and the exposure levels that are below a levelof concern

• Uncertainty in future land use patterns

Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page ES-16THIS DOCUMENT WAS PREPARED BY ROY F. WESTON. INC. EXPRESSLY FOR EPA. IT SHALL NOT BE RELEASED ORDISCLOSED IN WHOLE OR IN PART WITHOUT THE EXPRESS WRITTEN PERMISSION OF EPA.

BASELINE HUMAN HEALTH RISK ASSESSMENTFOR THE MURRAY SMELTER SUPERFUND SITE

SITE-WIDE EVALUATION

1.0 INTRODUCTION

A detailed description of the Murray Smelter Superfund Site is provided in Hydrometrics (1996).A summary of information that is important for the evaluation of human risks is presentedbelow.

1.1 SITE DESCRIPTION

Location

The Murray Smelter Superfund Site is located in Murray, Utah, near the intersection of StateStreet and 5300 South Street (Figure 1-1).

Smelting activities began at the site in about 1872 at the Germania Smelter, located in thenorthwest corner of the site. The Germania Smelter operated until 1902, when the newerMurray Smelter (located in the east-central portion of the site) began operations. The MurraySmelter operated until about 1949, processing mainly lead and silver ores. The chief solid wasteproducts generated by the smelters were arsenic, cadmium, and slag. Arsenic was sold for useas an insecticide or to the government for war purposes. Cadmium was sold for use as a paintpigment. Slag was disposed of to the ground. Some portions of the slag were subsequently usedfor railroad ballast, fill material, and other similar uses. However, large masses of slag remainon-facility, both exposed at the surface and covered by fill and by buildings.

When the site was operating, smelter-related on-site facilities included an extensive rail network,several blast furnaces, ore storage bins, several roasters, sinter plants, mills, a power house, anda bag house. Most of the smelter facilities have been demolished, and all that remain are twolarge stacks, one building foundation, and the original office/Engine Room building.

Land Use

Following closure of the smelter in 1949, portions of the facility were sold or leased to a numberof different businesses. The site is currently occupied by a pre-stressed concrete manufacturingplant (Buehner Corporation), a cement plant (Ashgrove), an asphalt operation (Monroe), atelecommunications facility (STS), a Federal Express outlet, and several smaller warehousing,

Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 1-1


,Ji M EA.JD o w KR o o k• A,, \

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SITE LOCATION

y.^'.n m?-=^

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BASELINE RISK ASSESSMENTUnion BoulKvoid

Suile 600lokewnod. CO R0228

9HO-6800MURRAY SMELTER SITE

MURRAY, UTAH

supply and other industrial operations. The on-faciliry area also includes two areas zoned forresidential land use that are currently occupied by trailer parks: Doc and Dells, located on theeast side of the site, immediately adjacent to a steep wall of slag, and Grandview, located alongthe southern border of the site. An area in the Germania Smelter portion of the site has beenproposed as the site of a Murray City police training facility.

The area surrounding the site is mainly residential, with some commercial properties. Thecentral area of the City of Murray is located immediately north of the site, and a city park andthe County fairgrounds are located to the east. A high school is located immediately south ofthe site, and a junior high school is located adjacent to the high school, south-east of the sue.

In the future, it is considered likely that current land use patterns will not change in most areas.Specifically, it is believed that the main part of the on-faciliry area will remainindustrial/commercial, and the off-facility area surrounding the site will remain mixedresidential/commercial. However, it is considered likely that the current on-facility residentialareas (the two trailer parks) will eventually be convened to non-residential uses.

Surface Terrain

The site is located in the Salt Lake Valley, between the Oquirrh Mountains on the west and theWasatch Mountains on the east. The valley generally tends to slope gently to the north-northwest, towards the Great Salt Lake. The site itself is mainly flat, having been leveled overmuch of its area with slag and other fill. A steep wall of slag descends to the level of thesurrounding terrain on the north and the east of the site.

Surface Water

The only permanent surface water body near the site is Little Cottonwood Creek, which formsthe northern boundary of the site. The creek originates in the mountains to the east of the siteand flows northwest, draining into the Jordan River about one mile west of the site. The creekcontains water year-round, with highest flows occurring during spring snowmell.

Groundwater

Groundwater at the site occurs in three distinct units: the shallow alluvial aquifer, theintermediate alluvial aquifer, and the deep principal aquifer. The shallow alluvial aquifer isunconfmed, occurring in surface sediments and fill material that average about 20 feet thick.The average depth to the shallow alluvial aquifer surface is about 10 feet. Beneath the shallowalluvial aquifer is a layer of Bonneville Blue Clay that averages 30 feet in thickness and isapparently continuous across the site. Beneath the clay is a layer of coarse alluvial sedimentabout 10-20 feet thick, comprising the intermediate alluvial aquifer (Hydrometrics 1995b). Thedeep principal aquifer is artesian, and is recharged mainly by water infiltrating from thesurrounding mountains. This aquifer typically occurs several hundred feet below the surface,

Baseline Human Health Risk Assessment . May 1997Document Control Number 4500-090-AOAC Page 1-3

THIS DOCUMENT WAS PREPARED BY ROY F. WESTON. INC EXPRESSLY FOR EPA. IT SHALL NOT BE RELEASED ORDISCLOSED IN WHOLE OR IN PART WITHOUT THE EXPRESS WRITTEN PERMISSION OF EPA.

and is the main source of drinking water for most residents in the Salt Lake Valley (Taylor andLeggette 1949).

Groundwater flow in the shallow alluvial aquifer at the site is mainly north, towards LittleCortonwood Creek. Flow in the intermediate alluvial aquifer is more to the northwest.Groundwater flow rates in the shallow aquifer are about 0.4 feet per day, and in the intermediateaquifer are about 1.7 feet per day. Although the intermediate alluvial aquifer is confined, thehydraulic gradient is mainly downward (about 0.2-0.6 ft/ft) over most of the site, withoccasional locations where the vertical hydraulic gradient is slightly upward (Hydrometrics1995b).

Basis for Potential Concern

The U.S. Environmental Protection Agency (EPA) proposed that the Murray Smelter site beplaced on the National Priorities List (NPL) in January, 1994, based on concerns that metalspresent in on-facility smelter wastes might be posing a risk to humans or the environment. Thesite is being evaluated as a non-time-critical removal action.

1.2 SCOPE AND PURPOSE OF THIS DOCUMENT

This document is a baseline human health risk assessment for the Murray Smelter site, includingthe site itself and adjacent off-facility areas that might be impacted by historic or ongoingreleases from the site. The objective of the assessment is to characterize the risks to humansfrom site-related chemicals that would exist, either now or in the future, if no remedial actionsare taken. The information in this assessment is intended to help support risk managementdecisions regarding the potential need to undertake remedial actions at the site.

A streamlined human health risk evaluation was completed previously for the site of a proposedpolice training facility, expected to be constructed in 1997 (WESTON 1996). Potential risks toecological receptors and the environment are being evaluated separately (WESTON 1997).

1.3 ORGANIZATION OF THIS DOCUMENT

In addition to this introduction, this report is organized into the following sections:

Section 2 This section discusses the chemicals of potential concern to human health, andprovides a summary of the available data on the levels of these chemicals in on-facility and off-facility media:

Section 3 This section discusses how humans may be exposed to site-related chemicals, nowor in the future, and provides equations for quantifying the level of exposure forthose pathways that are considered to be of potential significance.

Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC . Page |_4


Section 4 This section summarizes the characteristic cancer and noncancer health effects ofthe chemicals of potential concern, and provides quantitative toxicity factors thatcan be used to calculate cancer and noncancer risk levels.

Section 5 This section combines data on the level of exposure to chemicals of potentialconcern in on-faciliry and off-facility media (Section 3) with information of thetoxicity of each chemical (Section 4) to yield quantitative estimates of the risk ofcancer and noncancer health effects occurring in humans exposed to site-relatedcontaminants.

Section 6 This section reviews the sources of uncertainty in the risk estimates for humans,and evaluates which sources of uncertainty are likely to underestimate and whichare likely to overestimate risk.

Section 7 This section provides full citations for EPA guidance documents and scientificpublications referenced in the risk assessment.

Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page j.j


2.0 CHEMICALS OF POTENTIAL CONCERN

2.1 SELECTION OF CHEMICALS OF POTENTIAL CONCERN

The chemicals of principal concern at smelting sites are metals. Typically, the environment maybecome contaminated with a wide variety of different metals that were present in the ores orconcentrates smelted at the facility. However, experience at many mining, milling and smeltingsites has shown that the large majority of risk to humans is usually due to arsenic and/or lead.Based on preliminary data available from early site investigations, the EPA performed screeninglevel calculations to investigate whether lead and arsenic were the chief chemicals of concernat this site. This analysis is presented in Appendix A. The results of the analysis supported theconclusion that lead and arsenic were the only chemicals likely to be of substantial concern tohumans. Based on this, analysis of samples collected to support the human health riskassessment was focused on lead and arsenic.

2.2 SAMPLING PLAN

Data on lead and arsenic levels in surface and subsurface soil, indoor dust, and groundwaterwere collected during a Engineering Evaluation/Cost Assessment (EE/CA) investigation of theMurray Smelter site. This EE/CA investigation was performed by Asarco, in accord withdirection provided by the EPA (Hydrometrics 1995c, 1996).

Soil and Dust

The site investigation for surface soil, subsurface soil and dust is detailed in Hydrometrics(1995a). Prior to sampling, the on-facility area was divided into eleven "exposure units" (EUs),based mainly on current property boundaries. Similarly, the off-facility area was divided intoeight "Initial Study Zones" (ISZs), based on a consideration of the predicted pattern of historicair deposition from the site (WESTON 1995a), along with current street and land-use features.These exposure units and study zones are shown in Figure 2-1. The exact boundaries of theEUs and ISZs were somewhat arbitrary, but an attempt was made to follow current propertylines (on-facility) or to use existing streets to define neighborhood areas (off-facility).

For on-facility sampling within each exposure unit, a total of 10-20 surface soil samples (0-2inches) were collected, depending on the size of the unit. In addition, test pits were excavatedin several exposure units, using existing and historical features to select the location of the pits.Special emphasis was placed on EU6 (the former location of the Murray Smelter), since this isthe area where potential sources such as flues, the bag house, waste transfer facilities, etc. werelocated. At each test pit, a series of samples were collected at depths of 0-1, 1-2, 2-3, 3-4 and4-5 feet. Subsurface soil samples collected on-facility at the Grandview Trailer Park (EU-8, 9and 10) were from soil borings rather than test pits, and the sample depths were 0-2", 2-6", 6-12" and 12-18". The main purpose of these test pits and soil borings was to reveal whether

Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 2-1THIS DOCUMENT WAS PREPARED BY ROY F. WESTON. INC EXPRESSLY FOR EPA. IT SHALL NOT BE RELEASED ORDISCLOSED IN WHOLE OR IN PART WITHOUT THE EXPRESS WRITTEN PERMISSION OF EPA.

ON-FACIIJTY

x

/ BRUNTfljuip

WORKS

BASELINE RISK ASSESSMENT FIGURE 2-1

SITE MAP

215 UnionSuite 600

lokewood, CO 80228(303) 960--6800

MURRAY SMELTER SITEMURRAY, UTAH

there were any consistent contaminant patterns with depth, and whether any buried sources couldbe identified.

In the EE/CA workplan, EPA specified that all soil samples be prepared for analysis by sievingto isolate the fine (less than 250 um) fraction. This is because it is considered likely that humanexposure is mainly to this fine fraction. However, on-facility soils were ground (and not sieved)prior to analysis (Hydrometrics 1995a). In order to evaluate the potential impact of this change,portions of some samples were prepared by each method (sieving or grinding), and the resultinglead and arsenic levels were compared. In general, there was reasonable agreement between thetwo preparation methods, although sieved samples tended on average to be about 20% higherfor lead and 10% higher for arsenic than ground samples (Hydrometrics 1995a). This indicatesthat use of the data from the ground soil samples could cause a small underestimation ofexposure and risk to fine-grained contaminants in site soil, but this is not considered to be asubstantial concern, especially compared to the degree of uncertainty in several other exposureand toxicity terms.

For each off-facility study zone, surface soil samples were collected from 10 to 16 distinctlocations (depending on the size of the zone). Each sample was a composite of surface soil from4 to 6 sublocations. In addition, soil borings were collected at two different locations in eachISZ, with each sample being divided into depths of 0-2", 2-6", 6-12", and 12-18". Theseborings were collected to investigate the vertical extent of contamination in each off-facilityzone. All off-facility soil samples were sieved (not ground) prior to analysis.

Indoor dust samples were collected from 22 different homes or buildings located in off-facilityareas (Hydrometrics 1995a). Samples were collected using a hand-held vacuum. Typically,each sample was a composite of dust collected from three areas, each about 2 feet by 7 feet.

Groundwater

The site investigation for groundwater is detailed in Hydrometrics (1995b). A total of twentywells were installed, 13 in the shallow alluvial aquifer and 7 in the intermediate alluvial aquifer.Each well was developed by pumping an average of 60 gallons from shallow wells and 180gallons from deep wells. Samples for chemical analysis were collected using a low-flowperistaltic pump or a 12-volt submersible pump. A minimum of three bore volumes were purgedbefore collection of each sample, although some wells (e.g. GW-1A) were pumped dry beforethis volume could be purged. Several other on-facility wells (7 in the shallow zone and 3 in thedeeper zone) that had been installed in earlier investigations were also redeveloped and sampled.

Slag

The EPA collected a single composite sample of slag from nine different locations at MurraySmelter (EPA 1996, WESTON 1996b). Two of the subsamples were from the GermaniaSmelter Slag Pile (EU-1), six were from the face of the slag monolith located adjacent to EU-2,



and one was from the slag at the base of the pile adjacent to Doc and Dell's Trailer Park (EU-11). This composite sample was used to measure the relative and absolute bioavailability of leadand arsenic in the slag sample, using young swine as the experimental animal (EPA 1996).

2.3 SUMMARY OF DATA

Surface Soil

Concentrations of lead and arsenic in surface soil (0-2") were measured using x-ray fluorescence(XRF). Detailed data are presented in Appendix D (Part 1), and summary statistics are providedin Table 2-1. Maps of the measured values are shown in Figure 2-2 (lead) and Figure 2-3(arsenic). The color codes used to indicate increasing concentration are arbitrary, withgradations from green to blue to yellow to red to magenta representing increasing concentration(and increasing potential concern).

Inspection of these data reveals the following main points:

• On-facility, there is very wide variability in the concentration levels detected forboth lead and arsenic. In most EUs, the range of values from minimum tomaximum is at least 100-fold, and sometimes exceeds 1,000-fold. Often, highconcentrations were detected in close proximity to low concentrations. This on-facility pattern of high variability over small distances is probably a result ofhistoric waste disposal practices, along with activities such as grading and fillingwith mixtures of clean fill and site wastes.

• On-facility, the highest concentrations occur in EU-3 and EU-8, adjacent to therailroad right-of-way. However, high concentrations are detected at individualsampling locations in nearly all EUs. The lowest average on-facility levels areobserved in the eastern portion of the Grandview Trailer park (EU-9 and EU-10)and in Doc and Dell's trailer park (EU-11).

• Off-facility, variability in measured concentrations is considerably smaller thanon-facility, with ranges within each ISZ typically falling within a factor of 10.

• Off-facility, the highest average concentrations are observed in those ISZsimmediately west of the site (ISZ-1 and ISZ-8) and immediately south of the site(ISZ-7). Mean levels in ISZs that are further removed from the site (ISZ-2, ISZ-4, ISZ-5, ISZ-6) tend to be lower, with mean arsenic values ranging from 16-55ppm and mean lead values ranging from 240-660 ppm. This spatial patternsupports the view that off-facility areas have been impacted by the site, and thatthe impact tends to decrease as distance from the site increases.


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TABLE 2-1: LEAD AND ARSENIC IN SURFACE SOIL

Location

On-facility

Off-faciliry

Area

EU-1

EU-2

EU-3

EU-4

EU-5

EU-6

EU-7

EU-8

EU-9

EU10

EU-11

ISZ-1

ISZ-2

ISZO

ISZ^

ISZ-5

ISZ-6

ISZ-7

ISZ-8

Arsenic

DetectionFrequency*

13/19

13/17

18/18

13/20

19/20

19/20

19/19

10/10

10/10

9/10

8/10

19/19

7/10

10/10

16/16

16/16

11/12

10/10

7/12

Average(ppm)

130

79

1172

418

100

432

418

1674

118

69

19

106

16

55

43

42

52

126

76

Range(ppm)

BDL"-630

BDL-360

9-7700

BDL-5400

BDL-520

BDL-5100

18-2200

64-5000

29-210

BDL-220

BDL-78

13-340

BDL-37

7-110

8-170

7-130

BDL-120

59-180

BDL-450

Lead

DetectionFrequency

19/19

17/17

18/18

20/20

20/20

20/20

19/19

10/10

10/10

10/10 .

10/10

19/19

10/10.

10/10

16/16

16/16

12/12

10/10

12/12

Average(ppm)

2905

2879

9548

1750

2754

2297

2524

6177

909

538

814

1299

241

768

377

426

657

1222

1062

Range(ppm)

83-15000

98-9900

74-33000

37-15000

110-10000

71-7600

92-12000

570-25000

340-2000

150-1100

100-5700

250-3200

80^10

110-1600

110-780

130-640

120-1800

720-1800

66-7300

All data from Hydrometrics 1995a.1 TotaJ number of samples withb BDL = Below detection limit

detectable levels over total number of samples analyzed,(about 5 ppm).

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> - .UKI[ I : . I . I | • I I I .

• k * A» / ^i

Logend

it? < 75 ppm

*[• > - .75 and < 350 ppm

O > - 350 and < 1,000 ppm

• > - WOO and < 2,000 ppm

9 > - 2,000 ppm

0" - 2' Depth

Figure 2-3-B..UWIP.I. 03.juH.nl

EPA.

In order to gain information on the physical and chemical nature of the lead and arsenic presentin surface soil, the EPA collected 10 samples from locations on and near the site. Thesesamples were dried and sieved to yield the fine fraction (< 250 um), and submitted thesesamples for geochemical characterization by electron microprobe analysis (Drexler 1996). Theresults are summarized in Table 2-2. Inspection of this table reveals that lead occurs in a varietyof different forms, most commonly as lead phosphates, lead silicates, lead oxides, iron-leadoxides, lead arsenic oxide, and lead sulfide (galena). In contrast, arsenic occurs mainly asferric-lead-arsenic oxide and lead-arsenic oxide, with only small amounts of other arsenicspecies. The lead- and arsenic-bearing particles were mainly smaller than 20 um. with about80% of all the lead or arsenic-bearing grains existing in a liberated or cemented state, with onlyabout 20% existing within a rock or glass matrix (Drexler 1996).

Subsurface Soil

Data on lead and arsenic levels in subsurface samples are detailed in Appendix D (Part 2) andsummary statistics are provided in Table 2-3. Inspection of the data in Appendix D reveals thefollowing main points:

• The pattern of concentration with depth is not uniform. At some locations, bothlead and arsenic concentration tend to increase substantially as depth increases(e.g., EU1-2, EU6-8). At some locations, both lead and-arsenic-concentrationstend to decrease as depth increases (e.g., EU6-3, EU6-13, EU6-19, EU7-4). Atmany locations, there appear to be zones of highly contaminated material inter-layered between zones of lesser contamination (e.g., EU6-10, EU6-12, EU6-15,EU6-18). In some cases, elevated concentration levels in subsurface soil appearto correlate with the presence of slag, but other types of on-facility waste (fluedust, ore, etc.) may also have contributed to the subsurface contamination.

• There is often a general correspondence between lead and arsenic levels (bothtending to be high or low in the same sample), but this correspondence is notstrong. For example, the ratio of arsenic to lead ranges from a minimum of 5ppm/12,000 ppm (0.0004) to a maximum of 4,700 ppm/79 ppm (59.5). Further,the correlation coefficient (R2) value for the linear regression line through thepaired data (arsenic vs lead) is only 0.016, indicating that the quantitative degreeof correlation is quite low.

• At off-facility locations, variability by depth is generally smaller than on-facility,although it should be noted the depth interval studied was narrower (0-18 inchesvs 0-5 feet). In most cases, there is no clear concentration trend as a function ofdepth, although a few locations appear to show a decrease (e.g., 249 West Vinein ISZ-8), and a few show an apparent increase (e.g., ISZ-3-10).



TABLE 2-2: GEOCHEMICAL SPECIAT1ON DATA FOR SURFACE SOIL SAMPLES

Relative Lead Mass (Approximate Percent of Total)

Mineral Form

PbOCalciteFe-Pb OxideGalenaPbAsOPb PhosphateSlapFe-Pb SulfatePb(M)OClavPbSiO4

Mn-Pb OxidePbOOHNative LeadAnelesitePbCr04Pb Solder

Soil Sample Number (Concentration of Lead, ppm)

1(56)964

2(1130)

101918

.48T224

311040)

11

3

192T1

T

5811

4(1090)

216

487T4

T

84

6

5(219)

2059113

2

6(57)

2138

2

42

7(830)

37

159

3

1

8(250)

5

332119742

44

5

9(485)

5

1228296i

6

53

10T

10(3080)

9

341223

T4T28T14

2

2

T

Relative Arsenic Mass (Approximate Percent of Total)

Mineral Form

Fe-Pb-As-Oxide

PbAsOPb-As PhosphatePvrite

SlagFe-Pb-As SulfateAs(M)OClav

Pb PhosphateMn-Pb OxideMn-Pb-As OxideCalciteArsenopvritePbSi04

Soil Sample Number (Concentration of Arsenic, ppm)1

(BDL)

2

(162)6416122

4

T1

3(124)

59291

8

T5

4(236)

581912

6T

T

18

5(21)888T

T8

6(17)

99

T

T

7(73)37

5

60

8(37)

907T

T2

T

9(65)

631911T16

T

10(267)

522916

3

T

T

T

Trace

Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 2-9THIS DOCUMENT WAS PREPARED BY ROY F. WESTON. INC. EXPRESSLY FOR EPA. IT SHALL NOT BE RELEASED ORDISCLOSED IN WHOLE OR IN PART WITHOUT THE EXPRESS WRITTEN PERMISSION OF EPA.

TABLE 2-3: LEAD AND ARSENIC IN SUBSURFACE SOIL

Locaiion

On-facility

Off-facility

Area

EU-1

EU-2

ELU

EU-5

EU-6

EU-7

EU-8

EU-9

EU10

ISZ-1

ISZ-2

ISZ-3

ISZ"^

ISZ-5

ISZ-6

ISZ-7

1SZ-8

Numberof siaiions

2

1

1

1

19

4

2

2

2

2

2

2

2

2

i

2

2

DepthIntervals

0-1 ft1-2 ft2-3 ft3-4 ft4-5 ft

0-2 in2-6 in

6-12 in12-18 in

0-2 in2-6 in

6-12 in12-18 in

Arsenic

Average(ppm)

448

272

158

25

1224

3005

2851

1240

107

69

73

214

68

81

47

185

132

Range(ppm)

BDL-1500

130-340

BDL-620

BDL-56

BDL-48000

BDL-34000

64-7200

13-7500

45-140

17-230

27-170

53-610

6-150.

44-120

BDL-70

86-480

BDL-450

Lead

Average(ppm)

8243

9480

1656

222

2259

3793

2751

6858

634

334

1089

520

486

443

588

2659

165

Range(ppm)

50-16000

8200-10000

66^*800

61-600

57-22000

63-14000

520-9000

75^0000

430-1200

240-420

150-3200

87-1600

290-710

230-560

120-1000

550-7300

140-190

All data from Hydromeirics 1995a.BDL = Below detection limit (about 5 ppm).

J


Indoor Dust

Indoor dust samples were collected from 22 different homes or buildings located in areassurrounding the Murray Smelter site (Hydrometrics 1995a). Detailed data are provided inAppendix D (Part 3). Summary statistics are presented below:

Chemical

Arsenic

Lead

Numberof

Samples

22

21'

Concentration in Dust (ppm)

Average

27

303'

Range

5-94

83-7571

* Excludes one data point for lead with an anomalously high value (5.315 ppm)

Slag

The composite slag sample collected by EPA (1996) was analyzed in duplicate using ContractLaboratory Program (CLP) methods. The mean values of the duplicate analyses are as follows:

ArsenicLead

Groundwater

695 ppm11,500 ppm

Data on total lead and arsenic concentrations in groundwater collected in October, 1995, aresummarized in Table 2-4. Values for dissolved lead and arsenic are very similar (Hydrometrics1995b), suggesting that very little of either chemical exists as suspended paniculate matter orsediment. Inspection of the data in Table 2-4 reveals that there is very high variability in arsenicconcentrations between different wells, ranging from values below the detection limit (< 5ug/L) to more than 27,000 ug/L. The spatial pattern of arsenic contamination is shown inFigure 2-4. Wells screened in the shallow alluvial aquifer are indicated by circles, and wellsscreened in the intermediate alluvial aquifer are shown by triangles. The highly variable patternof groundwater contamination, especially in the shallow zone, suggests that there are probablyseveral buried on-facility sources of arsenic that are leaching to the shallow alluvial aquifer. Thedata suggest that a few wells screened in the intermediate alluvial aquifer are probably alsoimpacted (e.g., GW-1A, GW-2A, MW-109D, MW-112D), although this is difficult to judgewithout representative background data. In contrast to arsenic, lead levels in most of the shallowand intermediate alluvial aquifers are relatively low. This is consistent with the fact that leadis usually much less mobile in soil than arsenic, and therefore less likely to migrate from soilinto groundwater. Although the distribution of lead values expected in background wells is notknown with certainty, it appears that many of the wells are probably at or near background,although a few of the shallow wells may have been impacted (e.g., MW-111, Well 3).

Baseline Human Health Risk Assessment May 1997Document Control Number 450CW»90-AOAC Page 2-11THIS DOCUMENT WAS PREPARED BY ROY F. WESTON. INC. EXPRESSLY FOR EPA. IT SHALL NOT BE RELEASED ORDISCLOSED IN WHOLE OR IN PART WITHOUT THE EXPRESS WRITTEN PERMISSION OF EPA.

TABLE 2-4: LEAD AND ARSENIC IN GROUNDWATER

AquiferZone

Shallowalluvia]aquifer

Intermediatealluvialaquifer

WellID

MW-1001

MW-1011

MW-102

MW-103

MW-104

MW-105

MW-106

MW-107

MW-108

MW-109

MW-110

MW-ll l"

MW-112

GW-1

GW-2

Well 1

Well 2

Well 3"

UTBN-1

JMM-08

MW-101D

MW-104D

MW-105D

MW-108D

MW-109D

MW-112D

GW-1A

GW-1AR

GW-2A

Concentration (ug/L) (total)

Arsenic

<56

18.4

270613

27,180

<5<514

2,347

2,903

521,287

2,870

2161,974

23627078<5

1925<569

39790

6439

Lead

84

<2

3367

2824

212

16.5

3<29

3150504

714

104

6

86

5<2

All data are based on a single measurement (Hydrometrics 1995b).

1 Well is located in an up-gradient locationb These wells are completed in slag


< Sue"

TH t.civ .li. > - 5 and < 50 ug/L

> - 50 and < 250 ug/L

@ A >-250 and <2,500 ugA.

> - 2,500 and < 25,000 ug/L

O A > - 25«» ug/1.

iKl ii^mi&ysiMw-ioaH^^ ••'•C'!ir~'i,-^-i = ^"^ i in""1 ' / . • i?, £5?'wi®1 .•'•ss%»B {• '•

r P lg -JlL-i' ^MMfe.;/te'/feKS%^'ii-jn =-Jgt;.:>s.4 fi'5

^y-EflUasst-'' ! JiiTK

3.0 EXPOSURE ASSESSMENT

3.1 CONCEPTUAL SITE MODEL

Figure 3-1 presents a conceptual model showing the main pathways by which smelting activitiesat the site may have resulted in environmental contamination, and the scenarios by which currentor future workers at the site (EU-1 to EU-8), residents living on the facility (EU-8 to EU-11),or residents living near the facility (ISZ-1 to ISZ-8) might reasonably be exposed to lead orarsenic.

When the smelters were operating, stack emissions presumably contained substantial levels oflead and arsenic, which fell to the ground in tiny particles of soot, or were carried from the airto the ground by rain or snow. In addition, smelting operations generated solid wastes includingslag, flue dust and dross. These waste materials (especially flue dust and dross) also containedlead and arsenic. Extensive slag deposits are evident on-faciliry, some of which are exposed atthe surface and some of which are covered by fill of varying depth. There are no recognizablepiles of flue dust or dross presently on the site, but these materials may have been disposed ofto soil and subsequently graded and/or covered with slag or fill. Contaminants in these solidwastes may have caused secondary contamination of the surrounding environment by severalpathways, including wind erosion of fine dust panicles into air, water erosion of dissolved orsuspended metals into Little Cottonwood Creek, and leaching of dissolved metals downward intogroundwater. In addition, some of the waste materials may have been used for purposes suchas fill , road base, road sanding, etc.

Because lead and arsenic are not volatile and are not subject to chemical degradation, most ofthe lead and arsenic which was released to the site or to the surrounding area by past smeltingoperations are probably still in place. Thus, on-faciliry workers and on-faciliry or nearby off-facility residents might be exposed to site-related contaminants by a number of pathways,including the following:

Contaminated Medium

Soil and Dust

Exposed Slag

Air

Surface water, sediment

Vegetables grown in contaminated soil

Fish from contaminated creek

Potential Human Exposure Pathways

IngestionDermal contact


Inhalation of air-borne paniculate matter


Ingestion

Ingestion

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Not all of these exposure pathways are believed to be of equal concern. Those that areconsidered to be most likely to be of concern are shown in Figure 3-1 by boxes with a cross-hatch design, and greatest attention is focused on these pathways. Pathways which contributeonly occasional and minor exposures are shown by boxes with single hatching. Section 3.2(below) presents a more detailed description of each of these exposure scenarios, and presentsthe basis for concluding that some pathways are minor.

3.2 PATHWAY SCREENING

3.2.1 Soil/Dust Ingestion

Although few humans intentionally ingest soil, a number of studies show that most people doingest small amounts of soil and/or dust derived from the soil. Young children are thought tobe especially likely to ingest soil and dust, mainly through hand-to-mouth activities, includingmouthing of objects (toys, pacifier, etc.) that have soil or dust on them. Adults are also believedto ingest soil and dust through hand-to-mouth contact, both at home and in the workplace. Thispathway is most likely to be important in areas of exposed surface soil, but may also occur evenin areas (such as Doc and Dell's) where most soil is covered. This is because soil canaccumulate on paved surfaces and lead to contact just as if the area were unpaved. Soilingestion is believed to be one of the most important mechanisms by which humans can beexposed to environmental contaminants, and this pathway was evaluated quantitatively.

3.2.2 Inhalation Exposure to Soil/Dust in Air

Lead and arsenic are not volatile and do not exist in air except as pan of soil or dust paniclesthat become suspended in air as a result of wind or mechanical erosion. However, except underconditions of extreme soil erosion to air, this pathway is normally a minor source of exposure.For example, using screening level estimates of human exposure recommended by EPA (1991d),the intake of soil from the inhalation pathway is less than 0.01 % of the ingested dose (seeAppendix E). Based on this, it is concluded that inhalation exposure to lead and arsenic byinhalation of airborne panicles is likely to be minimal at this site, and inhalation exposure wasnot considered further in this assessment.

3.2.3 Dermal Contact with Soil and Dust

Humans can be exposed to contaminated soil by getting it on their skin while working or playingoutdoors, and may also have dermal contact with dust while indoors. However, current data ondermal absorption rates from soil or dust are not adequate to allow reliable estimation of theamount of most metallic contaminants (including both lead and arsenic) absorbed across the skin(EPA 1992b). On this basis, this pathway was not evaluated quantitatively in this assessment.Although data are sparse, it is generally considered that metals in soil do not rapidly cross the

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skin, and exclusion of this pathway is not likely to cause a significant underestimate of exposureand risk (see Appendix E).

3.2.4 Ingestion of Home-Grown Vegetables

Area residents can be indirectly exposed to smelter-related contaminants via consumption ofvegetables grown in contaminated soil. No data exist on the concentration of lead or arsenic invegetables grown near the Murray Smelter, so it is necessary to use a mathematical model toestimate the concentration of lead and arsenic which might occur in locally-grown vegetables.Screening level calculations (presented in Appendix B) reveal that the dose of lead fromingestion of garden vegetables by children is probably no more than 4%-7% of that fromingestion of soil and dust, and that the dose of arsenic ingested from garden vegetables is nomore than 1 % in children and 4-7% in adults. Based on these estimates, this pathway is judgedto be sufficiently minor (at least in comparison to direct exposure via soil and dust ingestion)that it was not retained for further quantitative evaluation.

3.2.5 Exposure to Slag Piles

There are extensive areas of the site where slag is exposed at the surface. It is not consideredlikely that on-facility workers or other adults will spend much time in areas of exposed slag, sodirect worker and residential adult exposure to slag is likely to be minimal. However, areateenagers have been observed to visit the site in areas where slag is exposed, so this pathwayis judged to be of potential concern for this sub-population and was retained for quantitativeanalysis. It is also possible that area children (especially current or future residents at Doc andDell's trailer park) might play in areas of exposed slag, although it is suspected that this wouldnot be a frequent event. As with dermal contact with soils, dermal absorption of lead andarsenic from slag is likely to be a minor source of exposure, at least in comparison to the oralpathway, and was not considered further in this assessment.

3.2.6 Exposure to Surface Water and Sediments

Contaminants can be dissolved or carried as particles by run-off from waste piles and othersources into Little Cottonwood Creek. While area children or other humans could be exposedto contaminated surface water and/or sediment while playing along the banks of the creek nearthe site, exposure is most likely to be mainly by the dermal route, with only low opportunity fororal intake. Further, exposure is likely to be relatively infrequent. Based on this, exposure tosurface water and sediments are both judged to be of sufficiently low concern that they were notevaluated further in this assessment.

3.2.7 Ingestion of Fish from Little Cottonwood Creek

At present, there is no information to indicate that people catch edible fish from LittleCottonwood Creek in the vicinity of the site. Therefore, exposure via this pathway is not

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believed to be of significant concern at present. This absence of edible fish is probably due toa combination of factors, including not only potential stress from site-related releases but alsothe impact of numerous upstream urban sources as well as current water management practiceswhich do not tend to foster a good fish habitat.

Current surface water monitoring data reveal an increase in arsenic concentration (from < 5ug/L to about 100-300 ug/L) in Linle Cottonwood Creek as it passes the site (Hydrometrics1996). The concentration of lead does not show a measurable increase. If the creek becamea suitable habitat for edible fish in the future, it is possible the fish might accumulate low levelsof arsenic in edible tissues. However, even if this were to occur, it is considered likely that thenumber of fish caught and consumed from the impacted reach of the creek would be sufficientlysmall that it would not be an important source of human exposure. On this basis, this pathwayis considered to be sufficiently minor that it was not considered further in this assessment.

3.2.8 Exposure to Groundwater

Current commercial and residential properties in the vicinity of the site are supplied with waterfrom a municipal water system, so exposure to contaminants in ground water beneath the site isnot currently believed to be occurring. In the future, it is considered very likely that any newresidences or commercial properties constructed on or near the site will also be supplied withwater from the municipal system. However, it is plausible that some businesses or residentsmight wish to install private wells, and if so, these wells might be installed in areas wheregroundwater has been impacted by leaching from site-related wastes. In this event, exposureto lead or arsenic could occur either by ingestion of drinking water or by dermal contact whileshowering or bathing. Of these, the ingestion pathway is of greatest concern, and is retainedfor quantitative evaluation. Screening level calculations reveal that the absorbed dermal dosefor both lead and arsenic while showering or bathing is less than 0.2% of the absorbed dosefrom ingestion of water (see Appendix E). Based on this, dermal exposure was not consideredfurther in this assessment.

3.2.9 Summary of Pathways of Principal Concern

Based on the considerations above, the following pathways for exposure of workers and/orresidents to smelter-related wastes are judged to be of sufficient potential concern to warrantquantitative exposure and risk analysis:

• Ingestion of soil/dust (current and future workers and residents)• Ingestion at areas of exposed slag (current and future teenagers)• Ingestion of groundwater (future workers and residents)

Other exposure pathways to site-related wastes are judged to be sufficiently minor that furtherquantitative evaluation is not warranted.

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3.3 QUANTIFICATION OF EXPOSURE TO ARSENIC

The EPA has developed a standard method for quantifying human exposure to mostenvironmental contaminants at Superfund sites (EPA 1989a). This method is applied below forexposure to arsenic at this site. The EPA recommends a modified exposure assessment approachfor lead, as detailed in Section 3.4.

3.3.1 Basic Equation

The magnitude of human exposure to chemicals in an environmental medium is described interms of the average daily intake (DI), which is the amount of chemical which comes intocontact with the body by ingestion, inhalation, or dermal contact. The general equation forcalculating the daily intake from contact with an environmental medium is (EPA 1989a):

DI = C • IR • EF • ED/(BW • AT)

where:

DI = daily intake of chemical (mg/kg-d)C = concentration of chemical in an environmental medium (e.g., mg/kg)IR = intake rate of the environmental medium (e.g., kg/day)EF = exposure frequency (days/yr)ED = exposure duration (years)BW =. body weight (kg)AT = averaging time (days)

For mathematical and computational convenience, this equation is often written as:

DI = C • HIF

where:

HIF = "Human Intake Factor". The units of HIF are kg/kg-day for soil, dustand slag ingestion, and L/kg-day for water ingestion. The value of HIFis given by:

HIF = IR • EF • ED/(BW • AT)

There is often wide variability in the amount of contact that different populations (teenagers,workers, residents, etc.) have with environmental media, so separate HIF factors are needed foreach population. In addition, there is often substantial variability between different individualswithin a population. Thus, human contact with an environmental media is best thought of as a

Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC f>age 3.6


distribution of possible values rather than a specific value. Usually, emphasis is placed on twodifferent portions of this distribution:

Average or Central Tendency (CT) refers to individuals who have average or typicalintake of environmental media. ,

Upper Bound or Reasonable Maximum Exposure (RME) refers to people who are at thehigh end of the exposure distribution (approximately the 95th percentile). Thisevaluation is intended to assess exposures that are conservative (i.e., higher thanaverage), but are still within a realistic range of exposure.

3.3.2 Concentration (C)

Soil

The concentration term used in the equation above is the arithmetic mean concentration of acontaminant, averaged over the location where exposure is presumed to occur during thespecified time interval (EPA 1989a). This is referred to as the Exposure Point Concentration(EPC). Because the true mean concentration cannot be calculated with certainty from a limitedset of measurements, the EPA recommends that the upper 95th confidence limit (UCL) of thearithmetic mean concentration be used as the EPC in calculating exposure and risk (EPA 1992a).If the calculated UCL is higher than the highest measured value, then the maximum value isused as the EPC instead of the UCL (EPA 1992a).

The method used to calculate the UCL of a data set depends on whether the data are distributednormally or lognormally (EPA 1992a). Based on the observation that most environmentalconcentration values tend to be right skewed and are more nearly lognormal than normal, allUCL values were derived based on the assumption of lognormality.

Appendix D (Pan 1) details the concentration data used for estimating exposure to arsenic insurface soil in each exposure unit and initial study zone. The resulting mean, maximum, UCLand EPC values are summarized in Table 3-1.

Dust

As discussed in EPA (1995a), indoor dust contamination can arise from three types of sources:area sources, local yard soils, indoor sources. Based on this, the following mass-balanceequation describes the concentration of contaminant in indoor dust:

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TABLE 3-1 EXPOSURE POINT CONCENTRATIONS FORARSENIC IN SURFACE SOIL

Location

On-facility

Off-facility

Area

EU-1

EU-2

EU-3

ELM

EU-5

EU-6

EU-7

EU-8

EU-9

EU10

EU-11

ISZ-1

ISZ-2

ISZ-3

ISZ-4

ISZ-5

ISZ-6

ISZ-7

ISZ-8

Arsenic Concentration (ppm)

Mean

130

79

1172

418

100

432

418

1674

118

69

19

106

16

55

43

42

52

126

76

Max

630

360

7700

5400

520

5100

2200

5000

210

220

78

340

37

110

170

130

120

180

450

UCL

1424

681

57840

7618

285

1788

1220

25568

222

383

62

222

57

128

73

65

162

158

2117

EPO

630

360

7700

5400 .

280

1800

1200

5000

210

220

62

220

37

110

73

65

120

160

450

1 EPC = exposure point concentration (UCL or maximum value, which ever is lower)

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c -

where:

m = mass of material in dust derived from yard soils (m,), area sources (ma),or indoor sources (mi).

C = concentration of contaminant in interior dust (Cd), yard soils (Cs), areasources (CJ, or indoor sources (Q).

This equation can be re-written as follows:

ksC5

where:

k = mass fraction in dust of material derived from area sources (kj, yard soil(k,) and indoor sources (k|).

In theory, this basic equation can then be used to estimate the best fit values of k,, k,, and k;

from a site-specific data set in which paired data are available for the concentration ofcontaminants in dust, yard soil and indoor sources (if relevant). In practice, however, data arerarely available on the concentration of chemicals in indoor sources, so it is frequently difficultto separate the relative contribution of indoor sources from those of area sources. Thus, it isusually simplest to analyze paired soil-dust data using a two-parameter model, as follows:

where:

k(, = contribution to indoor dust from non-yard soil sources (ppm)k, = mass fraction of yard soil in indoor dust (unitless)Cs = Concentration in yard soil (ppm)

As described in Section 2, paired soil-dust samples were collected from 22 off-facility locations,and these data were used to analyze the average relationship between levels of arsenic in soil anddust. The data are shown in Figure 3-2, along with the best fit straight line through the datacalculated by linear regression. As discussed in EPA (I995a), analysis of soil/dust relationshipsby linear regression is complicated by the problem of measurement error, which tends to leadto an underestimate of slope and an overestimate of intercept. On this basis, the best-fit slope


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Figure 3-2 Relationship BetweenArsenic in Dust and Soil

100

80

r 6°Q

o 40'cQ)(/>

<20

0

Best-Fit Linear Regression:Dust= 16 + 0.17*Soil

0 50 100

Arsenic in Soil (mg/kg)150 200

was rounded upwards and the intercept was rounded downwards to yield the followingapproximation of the mean soil-dust relationships:

Parameter

k<v (ppm)

k, (ppm per ppm)

Value for Arsenic

Linear Regression

17

0.17

Adjusted'

10

0.20

1 Adjusted by rounding k, up and rounding k« down to account for measurement error.

Groundwater

Exposure to ground water is usually assumed to occur at discrete well locations, since people whoare employed at a business or who live at a residence are likely to ingest most of their drinkingwater from the well which serves their building. Thus, averaging across different wells is notusually appropriate. Table 2-3, presented previously, lists the concentrations of arsenic detectedin each well. For the purposes of this assessment, these wells were used to evaluate residentialand worker exposures as follows:

Population

Resident

Workers

Location

On-facility

Off-facility

On-facility

Wells

MW-102 (south of Doc and Dell's)MW-106 (west of Grandview)

MW-100MW-101 and 101DMW-103MW-104 and 104D

MW-1021

MW-105 and 105DMW-1061

MW-107MW-108 and 108DMW- 109 and 109DMW-110M W - l l l b

MW-112 and 112DGW-1, 1A and 1ARGW-2 and 2AWell 1Well 2Well 3"UTBN-1

' On-facility well used for both residential and worker evaluation" These wells are completed in slag, and may not be representative of actual future wells.

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19973.)]

Slag

As discussed in Section 2.4, one composite slag sample was collected by EPA (1996) from ninedifferent locations along the face of the exposed slag. The concentration value of arsenic,averaged over two duplicate analyses, was 695 ppm.

3.3.3 Human Intake Factors (HIFs)

As noted earlier, intake rates for environmental media differ from population to population,depending on the types and durations of activities that each population engage in. At this site,there are three populations of chief concern: residents (both on-facility and off-facility), workers(on-facility), and area teenagers who may trespass on-facility. Residents are assumed to beexposed mainly in the vicinity of their homes during routine activities. The level of exposurewhich workers experience is probably highly variable, depending on their specific jobresponsibilities. EPA refers to workers who spend all or most of the day indoors as "non-contact intensive", and workers who spend all or most of each work-day outdoors and who havefrequent and extensive opportunity for contact with soil are referred to as "contact-intensive".Because both types of worker are likely to be employed at the site (e.g., office workers and yardworkers), the risk assessment considered both types of workplace exposure scenario. These twogroups of workers are abbreviated "NCI" (non-contact intensive) and "CI" (contact intensive).

Presented below is a description of how the estimated average and RME HIF values arecalculated for each population for each of the exposure pathways of concern at this site.

3.3.3.1 HIF for Soil and Dust Ingestion

Based on the assumption that the concentration of contaminants is the same in soil and dust, theEPA usually evaluates exposure to soil and dust in a single step. The basic equation is asfollows:

1£-06

BWEF., -EDsd

AT

where:

DIsd = Daily intake of chemical from soil and dust (mg/kg-day)Csd = Concentration of chemical in soil and dust (mg/kg)IR,d = Intake rate of soil plus dust (mg/day)1E-06 = Conversion factor (kg/mg)BW = Body weight (kg)EF = Exposure frequency (days/yr)

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ED = Exposure duration (years)AT = Averaging time (days)

For residents, both chronic and lifetime average intake rates are time-weighted to account forthe possibility that an adult may begin exposure as a child when intake rates are higher than inadulthood (EPA 1989a, 1991a, 1993), as follows:

TWA-DI, = C,id

IR- lE-06 EF-ED, IR • 1£-06 EF-ED n

BV.'c (ATc + ATC) BWa (ATC - ATa)

where:

TWA-DIsd = Time-weighted average daily intake of chemical from soil/dust (mg/kg-day)Csd = Concentration of chemical in soil and dust (mg/kg)IR,,) = Intake rate of soil plus dust (mg/day) when a child (IRJ or an adult (IRJ1E-06 = Conversion factor (kg/mg)BW = Body weight (kg) when a child (BWC) or an adult (BWJEF = Exposure frequency (days/yr) when a child (EFJ or an adult (EFJED = Exposure duration (years) when a child (EDC) or an adult (EDJAT = Total averaging time (days) as child (ATC) and adult (ATJ

The value selected for the averaging time depends on whether non-cancer or cancer effects arebeing assessed. For non-cancer effects, the averaging time is equal to the exposure duration(i.e., the calculation yields the average dose rate during the time interval when exposure isoccurring). For evaluation of cancer risks, the averaging time is always equal to 70 years, andthe dose calculation yields an estimate of the average exposure rate over the entire lifetime.

Default values and assumptions recommended by EPA (1989a, 1991a, 1993a) for evaluation ofresidential and occupational exposure to soil and dust are listed in Table 3-2. It should be notedthat data on soil and dust intake rates by humans are quite limited, especially for adult residentsand workers (both NCI-workers and Cl-workers). Thus, the selection of the default valuesinvolves considerable professional judgement, and all of the soil/dust intake rates shown shouldbe considered to be uncertain.

Studies at a number of mining/smelting sites in the western United States have shown that theaverage concentration of contaminants in indoor house dust is sometimes lower than in the soilof the yard, and available data indicate that this is true for arsenic at this site (see Section 3.3.2,above). In this case, it becomes necessary and appropriate to evaluate exposure to soil and dustseparately, as follows:

Bucline Human Health Risk Aisessmem May 1997Documem Control Number 4JOO-090-AOAC Page 3-13


TABLE 3-2 EXPOSURE PARAMETERS FOR INGESTION OF ARSENIC IN SOIL AND DUST

Exposure Parameter

IR as child (mg/d)

IR as adult (rng/day)

BW as child (kg)

BW as adult (kg)

EF (days/yr)

ED as child (years)

ED as adult (years)

RBA of arsenic in soil and dusi

AT (noncancer effects)' (days)

AT (cancer effects) (days)

Average

Resident

100

50

15

70

234

2

7

0.26

9 - 3 6 5

70 • 365

NCI-Worker

--

50

--

70

219

--

5

0.26

5 - 3 6 5

70 • 365

Cl-Worker

--

240'

--

70

185"

--

5

0.26

5 - 3 6 5

70 • 365

RME

Resident

200

100

15

70

350

6

24

0.26

30 • 365

70 • 365

NCI-Worker

--

50

--

70

250

--'

25

0.26

25 • 365

70 • 365

Cl-Worker

--

480

-

70

211"

--

25

0.26

25 • 365

70 • 365

All values from EPA I993a and EPA I99la, except as noted

1 Extrapolated from default RME value based on assumed ratio of 2:1 for RME to averageb Based on da la which indicate that the ground is frozen or snow-covered about 57 days/yr.c The averaging time for noncancer effects in residents is the sum of the exposure durations as a child and an adult.

com

Cd-HIFd

where:

DI$d = Daily intake of chemical from soil plus dust (mg/kg-day)C = Concentration of chemical in soil (C,) or dust (Cd) (mg/kg)HIF = Human intake factor for soil (HIF5) or dust (HIFJ (kg/kg-day)

i .

Data on the relative contribution of soil and dust are sparse, but limited data support the viewthat total intake is composed of about 45% soil and 55% dust in children (EPA 1994a). Byextrapolation, this ratio is also assumed to apply to adults residents. In the absence of data onthe relative intake of soil and dust by indoor workers, a ratio of 50%:50% was assumed.

There are no default recommendations for the average amount of soil and dust ingested by a Cl-worker, so a value of 1/2 the default RME value (480 mg/day) was assumed. Because CI-workers are exposed mainly outdoors, it was assumed that all of this total intake was soil. Itwas assumed Cl-workers are exposed to soil outdoors essentially every day that they are atwork, except for days when the ground is frozen or snow-covered. Data provided by the UtahClimate Center indicates that, on average, the ground in the Salt Lake City area is frozen orsnow-covered about 57 days per year (Campbell 1996). Thus, the exposure frequencies assumedfor NCI-workers were multiplied by a factor of (365-57)/(365) = 0.84 to estimate the numberof days that Cl-workers would have the opportunity for direct contact with outdoor soil.

HIF Values

Based on the exposure parameters shown in Table 3-2 and the equations above, the HIFs forexposure of residents and workers to soil and dust are as follows:

Population

Resident

NCI-Worker(non-contactintensive)

Cl-Worker(contactintensive)

ExposureDuration

Chronic

Lifetime

Chronic

Lifetime

Chronic

Lifetime

Average

Soil

5.9E-07

7.6E-08

2.1E-07

1.5E-08

1.7E-06

1.2E-07

Dust

7.2E-07

9.2E-08

2.1E-07

1.5E-08

—

—

RME

Soil

1.6E-06

7.1E-07

2.5E-07

8.7E-08

4.0E-06

1.4E-06

Dust

2.0E-06

8.6E-07

2.5E-07

8.7E-08

—

—

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Relative Bioavailabilitv Adjustment

Default approaches for estimating exposure and risk from arsenic in soil assume that arsenicexists in a form that can be absorbed by the body (e.g., arsenic dissolved in water). However,there are several studies which indicate that arsenic in soil is less well absorbed than arsenic inwater, and on this basis EPA Region VIII recommends a default relative bioavailabiliry (RBA)factor for arsenic in soil of 80% (EPA 1993b).

At this site, the RBA of arsenic has been evaluated for a composite sample of surface soil. Thissample was prepared by mixing 16 different soil samples collected at on-facility locations,mainly in EU-1 and EU-5. The composite sample was fed to young swine for 15 days, and theamount of arsenic excreted in the urine of animals exposed to soil was compared to that foranimals exposed to a soluble reference material (sodium arsenate). Preliminary results indicatethat the RBA of arsenic in the soil samples is 26%, with a 90% confidence interval from 21 %to 33% (Weisetal . 1996).

Because the sample fed to the swine was collected mainly from EU-1 and EU-5, it is uncertainwhether the RBA value derived for the sample should be considered representative for soilsamples from other on-facility or off-facility locations. Comparison of the arsenic speciationdata for the test sample with the speciation data for the 10 soil samples shown in Table 2-2suggests that the test sample might be somewhat enriched in arsenic oxides (58%) compared toother soil samples (generally about 25%-40%). If arsenic oxide is more bioavailable than otherarsenic forms, the RBA value for the test sample might be somewhat higher than appropriate forother soils. However, in the absence of additional data, the site-specific arsenic RBA value(26%) based on the soil composite was assumed to apply to all samples of soil and dust.

Final Dose Equation

Based on the data and assumptions above, the dose of arsenic to a person from soil and dust(combined) may be expressed as:

DIs.d = C S -HIF S -RBA, + C d -HIF d -RBA d

where:

Cd = 10 + 0.2-C,

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3.3.3.2 HIF for Slag Ingestion

The basic equation for evaluating exposure from ingestion of material from slag piles is:

DJ.slag -slag AT

The EPA has not established any default parameters for human exposure to slag, so parameterswere estimated as described below.

There are no data on the amount of material that may be ingested by area teenagers who visitareas where slag is exposed. The intake rate presumably depends on the amount of materialwhich adheres to the hands, and the amount of hand-to-mouth contact which occurs while thecontamination remains on the hands. In the absence of data, average and RME intake rates of50 and 100 mg/event were assumed. It is not known if these assumptions are higher or lowerthan actual intake rates.

BW

Based on the assumption that area teenagers are the most likely sub-population to be exposed toon-facility slag deposits, an age range of 12-18 years was chosen to represent this group. Basedon data reported in EPA (1991c), the average body weight for boys and girls ages 12-18 yearsis 57 ke.

EF,•lag

There are no data on the frequency of teenagers visiting areas of exposed slag. In the absenceof data, it was assumed that exposure occurs an average of about 25 times per year, with amaximum of about 50 times per year. It is not known if these assumptions are higher or lowerthan actual exposure frequencies.

ED

Assuming that teenagers visit the site mainly over the age range 12-18 years, the exposureduration for this pathway is 7 years.


AIThe averaging time for evaluation of noncancer effects from contaminants in slag is equal to theassumed exposure duration (7 years • 365 days/yr = 2555 days). For evaluation of cancer risks,the averaging time is 70 years (25,550 days).

HIF Values

Based on these exposure parameters, the HIF for exposure of teenagers (age 12-18) to wastepiles are as follows:

ExposureDuration

Chronic

Lifetime

HIF for Slag Ingestion (kg/kg-d)

Average

6.0E-08

6.0E-09

RME

2.4E-07

2.4E-08

Relative Bioavailabilitv Adjustment

As noted above, the default bioavailability of arsenic in soils and other similar materials(including slag) recommended by EPA Region VIII is 0.80 (80%). At this site, the relativebioavailability (RBA) of arsenic in slag has been evaluated in a composite sample of slagcollected from nine different on-facility locations (EPA 1996, WESTON 1996b). Thiscomposite sample was fed to young swine for 15 days, and the amount of arsenic excreted inthe urine of animals exposed to slag was compared to that for animals exposed to a solublereference material (sodium arsenate). Preliminary results indicate that the RBA for arsenic inslag is about 45%, with a 90% confidence interval of 23% -71% (Weis et al. 1996). Althoughpreliminary, this value (45%) was used in the exposure calculations for slag.

Final Dose Equation

Based on the data and assumptions above, the dose of arsenic to a teen from slag may beexpressed as:

= Csla< • HIFslllg •

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3.3.3.3 HEF for Drinking Water Ingestion

The basic equation for calculation of the HIF for ingestion of drinking water is (US EPA 1989a):

EF • ED

BW -AT

where:

HIFW = Human intake factor for water (L/kg-day)IR, = Ingestion rate for water (L/day)EF = Exposure frequency (days/yr)ED = Exposure duration (years)BW = Body weight (kg)AT = Averaging time (days)

Standard EPA defaults (EPA 1989a, 1991a, 1993a) for evaluation of water ingestion by residentsand workers are as follows:

Parameter

IR fL/dav)

BW (kg)

EF (days/yr)

ED (years)

AT (noncancer effects) (days)

AT (cancer effects) (days)

Resident

Average

1.4

70

234

9

9-365

70 • 365

RME

2.0

70

350

30

30 • 365

70 • 365

Worker

Average

0.7

70

219

5

5-365

70 - 365

RME

1.0

70

250

25

25 • 365

70 • 365

Based on these exposure parameters, the HIF values for exposure of residents and workers togroundwater are as follows:

ExposedPopulation

Resident

Worker

ExposureDuration

Chronic

Lifetime

Chronic

Lifetime

HIF for Water Ingestion (L/kg-d)

Average

1.3E-02

1.7E-03

6.0E-03

4.3E-04

RME

2.7E-02

1.2E-02

9.8E-03

3.5E-03

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Final Dose Equation

In the case of arsenic dissolved in water there is no adjustment needed for bioavailability, so thefinal dose equation is simply:

3.3.4 Dose Calculations

Combining the estimates of concentration summarized in Section 3.3.1 with the human exposureassumptions described in Section 3.3.2 yields the dose estimates for arsenic shown in AppendixD (Part 4).

3.4 EVALUATION OF EXPOSURE TO LEAD

Lead is widely distributed in the environment as a result of both natural and man-made sources.Consequently, humans are exposed to lead from many different media, not just those that havebeen impacted at a site. Because of this, and because the most common way for quantifyinghuman exposure to lead is in terms of blood lead level (PbB), the EPA has developed anIntegrated Exposure Uptake and Biokinetic (IEUBK) model for predicting blood lead levels inthe blood of children exposed at residential locations (EPA 1994a). Section 3.4.1, below,describes the application of the IEUBK model to on-facility and off-facility residential childrenat this site. The EPA has not yet developed an analogous model that is applicable to adultresidents or workers, but simplified models based on similar concepts are available. Section3.4.2 describes the application of one such model to evaluate lead exposures in on-facilityworkers.

3.4.1 Exposure of Residential Children

Overview of the Model

The IEUBK model developed by EPA predicts the level of lead in the blood of a child or apopulation of children under a specified set of exposure conditions, taking all sources of leadexposure into account. Detailed discussions of the structure of the model and how to use themodel to assess lead exposures at a site are provided in the "Guidance Manual for the IntegratedExposure Uptake Biokinetic Model for Lead in Children" (EPA 1994a).

In brief, the model is composed of two main parts. The first part is the exposure section. Inthis pan, the amount of lead which a child ingests or inhales is calculated from data on a) theconcentration of lead in each relevant environmental medium (e.g. soil, dust, food, water andair), and b) information on how much of each of these media is ingested or inhaled by a child



each day. The second part of the model is the biokinetic section. This pan predicts the bloodlead level that will result in the child from the specified exposures. This prediction is based ondata regarding a) how much of the ingested or inhaled lead is actually absorbed into the body,b) how much of the absorbed lead enters each of the different "compartments" of the body (e.g.,blood, bone, soft tissue, etc.), and c) how rapidly lead is removed from the body by excretionin urine or feces.

If all of the exposure and biokinetic parameters were accurately known for an individual child,it is expected that the model would predict a reasonable point estimate of the blood lead valuefor that individual child. However, exposure and biokinetic parameters are not known forindividuals at a site, but are only available as group statistics from population studies (e.g.,estimated mean soil intake rate, estimated mean gastrointestinal absorption fraction, estimatedmean body weight, etc.). Because of this, the model does not seek to accurately predict theblood lead level of any one specific individual, but rather seeks to predict the typical (geometricmean) blood lead level that would be expected in an "average" child. Blood lead levels in theentire population of all children, especially those that are at the upper pan of the distribution(e.g., the 95th percentile) are then estimated by generating the approximate distribution from theestimated geometric mean. This is achieved by assuming the distribution is approximatelylognormal in shape, and by applying an estimate of the degree of variability between differentchildren. This descriptor of variability is the Geometric Standard Deviation (GSD).

In general, the model is intended to evaluate situations where exposure is on-going, and theexposure levels can be reasonably described in terms of long-term averages. In this case, thepredicted blood lead level is the expected long-term average value. This long-term averagevalue is generally considered to be the most appropriate basis for evaluating health risks fromlead. The model is not presently intended to allow evaluation of occasional or transitory leadexposures that cause "spikes" in blood lead level (EPA 1994d).

Input Parameters

The EPA has developed a set of recommended "default" input parameters for the IEUBK model,based on data from a wide variety of exposure and biokinetic studies (EPA 1990). However,site-specific data must be entered for environmental lead concentrations in each exposurelocation, and other parameters may be revised based on site-specific data, as appropriate.These site-specific inputs are discussed below.

Concentration of Lead in Soil and Dust

Typically, the exposure location used to evaluate exposure of a residential child is the home andyard where the child resides. In this case, data are not available for individual homes andresidences, but only for representative sample locations from within each EU and.ISZ where


residential children are or might be exposed (see Table 2-1). Therefore, these area-wideaverages are used in these calculations. Because of the variability within locations, somechildren might be exposed to higher levels and some to lower levels.

The normal assumption used in the IEUBK model is that the concentration of lead in indoor dustis 70% of that in outdoor soil (EPA 1994a). However, this assumption has been found tooverestimate lead concentrations in dust at some mining-related sites. As described in Section2, paired soil-dust samples were collected from 22 off-facility locations, and these data wereused to analyze the average relationship between levels of metals in soil and in dust. The datafor lead are shown in Figure 3-3, along with the best fit straight lines through the data calculatedby linear regression. As noted, one data point was considered an outlier (dust lead = 5315ppm, soil lead = 718 ppm). and this point was not used when calculating the best-fit equation.As discussed in EPA (1995a), analysis of soil/dust relationships by linear regression iscomplicated by the problem of measurement error, which tends to lead to an underestimate ofslope and an overestimate of intercept. On this basis, the best-fit slopes are rounded upwardsand the intercepts are rounded downwards to yield the following approximations of the meansoil-dust relationships:

Parameter

ko (ppm)

k, (ppm per ppm)

Value for Lead

Linear Regression

98

0.32

Adjusted'

90

0.35

1 Adjusted by rounding k, up and k<j down to account for measurement error.

Table 3-3 summarizes the soil and dust concentration values used to assess exposure ofresidential children.

Bioavailabilirv of Lead in Soil and Dust

The EPA has conducted a study of the bioavailability of lead in a composite soil sample fromthe Murray Smelter site (EPA 1996). Estimates of RBA based on four different endpoints (leadin blood, liver, kidney, and bone) were obtained. Because these estimates did not preciselyagree in all cases, judgment must be used in interpreting the data. In general, EPA recommendsgreatest emphasis be placed on the RBA estimates derived from the blood lead data. This isbecause blood lead data are more robust and less susceptible to random errors than the tissuelead data, so there is greater confidence in RBA estimates based on blood lead. In addition,absorption into the central compartment is an early indicator of lead exposure, is the mostrelevant index of central nervous system exposure, and is the standard measurement endpointin investigations of this sort. However, data from the tissue endpoints (liver, kidney, bone) alsoprovide valuable information. EPA considers the plausible range to extend from the RBA based

Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Pige 3.22THIS DOCUMENT WAS PREPARED BY ROY F. WESTON. INC. EXPRESSLY FOR EPA. IT SHALL NOT BE RELEASED ORDISCLOSED IN WHOLE OR IN PART WITHOUT THE EXPRESS WRITTEN PERMISSION OF EPA.

Figure 3-3 Relationship BetweenLead in Dust and Soil

1000

800

600

13Q

•£ 400 I

Best-Fit Linear Regression:Dust = 98 + 0.32*Soil

One outlier excluded(Dust = 5315, Soil = 780)

(00)

200 |

0

0 500 1000Lead in Soil (mg/kg)

1500 2000

jo u

TABLE 3-3: LEAD LEVELS IN RESIDENTIAL AREA SOIL AND DUST

ExposureArea

EU-8

EU-9

EU-10

EU-11

ISZ-1

ISZ-2

ISZ-3

ISZ-4

ISZ-5

ISZ-6

ISZ-7

ISZ-8

Mean Lead Concentration (ppm)

Surface Soil

6177

909

538

814

1299

241

768

391

426

657

1222

1062

Indoor Dust1

2252

408

278

375

545

174

359

227

239

320

518

462

Calculated from mean soil level as follows:C(dust) = 90 + 0.35-C(soil)

Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Pjge 3.24


on blood AUC to the mean of the other three tissues (liver, kidney, bone). The preferred rangeis the interval from the RBA based on blood to the mean of the blood RBA and the tissue meanRBA. The suggested point estimate is the mid-point of the preferred range. These values arepresented below:

RBA in Site Soil

Plausible Range

Preferred Rai.^e

Suggested Point Estimate

Value

0.67-0.84

0.67-0.75

0.71

As seen, although there is uncertainty in the estimate, the relative bioavailability for soil isprobably about 70%, slightly higher than the default value used in the IEUBK model. Basedon this value, and assuming that lead in food and water is about 50% absorbed by children (EPA1990), this RBA value corresponds to an absolute bioavailability of 35% (0.35).

GSD

A study of blood lead levels in Sandy, Utah, indicate that variability between different childrencan be described by an individual geometric standard deviation of 1.4 (EPA 1995b). Becausethe population of Sandy is believed to be generally similar to the population of Murray, thisvalue (GSD = 1.4) is considered to be more relevant and a better approximation of the true site-specific value than the default value (1.6), so the site-specific value is used in place of thedefault value.

Dietary Intakes

Recent dietary data collected by the FDA (Gunderson 1995, Bolger et al. 1996) support the viewthat dietary intake levels of lead are now lower than the default values provided in the IEUBKmodel. The revised values are as shown below. These data were used in the IEUBK modelcalculation of lead exposure levels in residential children.

Age

6-1 1 months

1 year

2 years

3 years

4 years

5 years

6 years

Intake (ug/day)

1.82

1.90

1.87

1.80

1.73

1.83

2.02

Biseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 3.25


' Summary of Input Parameters

Table 3-4 summarizes the input parameters used in the IEUBK model to evaluate risks tochildren from lead in soil and dust.

Results — Predicted Exposure to Lead in Soil and Dust

The IEUBK model input parameters discussed above (summarized in Tables 3-3 and 3-4) wereused to predict the geometric mean and 95th percentile blood lead values in children exposedat residential areas. The detailed calculations are presented in Appendix D (Part 5), and thefindings are discussed in Section 5.2.1.1.

3.4.2 Exposure of On-Facilitv Workers to Lead

There are several mathematical models which have been proposed for evaluating lead exposurein adults, including those developed by Bowers et al. (1994), O'Flaherty (1993), Leggett (1993),and the State of California (CEPA 1992). Of these, the biokinetic slope factor approachdescribed by Bowers et al. has been identified by EPA's Technical Workgroup for Lead as areasonable interim methodology for assessing risks to adults from exposure to lead and forestablishing preliminary remedial goals that will protect adults from lead in soil. For thisreason, this method was used for estimating the blood lead level that could occur in workersexposed at this site. Because the fetus of a pregnant woman is believed to be at least assusceptible to the adverse neurological effects of lead exposure as the child (and more susceptiblethan either the mother or other adult workers), the worker subpopulation selected for evaluationare pregnant women or women of child-bearing age.

Basic Equation

The Bowers model predicts the blood lead level in an adult exposed to lead in a specifiedoccupational setting by summing the "baseline" blood lead level (PbB<,) (that which would occurin the absence of any occupational exposures) with the increment in blood lead that is expectedas a result of occupational exposure to soil or dust. The latter is estimated by multiplying theabsorbed dose of lead from occupational soil/dust exposures by a "biokinetic slope factor"(BKSF). Thus, the basic equation is:

PbB = PbB0 + BKSF • [C, • IR, • EFS • AF5 + Cd • IR, • EFd • AFd]

where:

PbB = Geometric mean blood lead level (ug/dL) in a population of adults exposedto lead-contaminated soil or dust via occupational activities

Baseline Human Health Risk Assessment M 199-jDocument Control Number 4500-090-AOAC j^ 3 26


n in c =-r 3 5o o ** **1/1 O ~ X

° C ? 3

TABLE 3-4 EXPOSURE PARAMETERS USED FOR IEUKK MODEL

P

a:o

H Tj

•A*

otopn

Medium

Air .

Diet

DrinkingWater

Soil/Dust

All

Parameter

Breathing Rate (mVhr)

Time outside (hr/day)

CJCM

Absorption Fraction

Default concentration (ug/m3)

Daily lead intake (ug/day)

Absorption fraction

Ingestion Rate (L/day)

Absorption fraction

Default concentration (ug/L)

Total daily intake (mg/d)

Fraction of total thai is soil

Absorption fraction

GSD'

Age (years)

0.5-1

2

\

0.30

0.32

O.I

1.82

0.50

0.20

0.50

4

85

0.45

6.35

1.4

1-2

3

2

0.30

0.32

O.I

1.90

0.50

0.50

0.50

4

135

0.45

0.35

1.4

2-3

5

3

0.30

0.32

0.1

1.87

0.50

0.52

0.50

4

135

0.45

0.35

1.4

3-4

5

4

0.30

0.32

0.1

1.80

0.50

0.53

0.50

4

135

0.45

0.35

1.4

4-5

5

L 4

0.30

0.32

0.1

1.73

0.50

0.55

0.50

4

100

0.45

0.35

1.4

5-6

7

4

0.30

0.32

O.I

1.83

0.50

0.58

0.50

.4

90

0.45

0.35

1.4

6-7

7

4

0.30

0.32

0.1

2.02

0.50

0.59

0.50

4

85

0.45

0.35

1.4

All values from EPA 1994a

PbB0 = Geometric mean "baseline" blood lead level in adults not exposed to lead-contaminated scil via occupational activities, but including otherbackground exposures, including residential exposure

BKSF = Biokinetic slope factor (ug/dL increase in blood lead per ug/day leadabsorbed)

C = Arithmetic mean concentration (ug/g) of lead in soil (Cs) or dust (Cd).averaged over the workplace location where exposure occurs

IR = Mean daily intake rate of soil (IR,) or dust (IRJ during occupationalactivities in areas of contamination (g/day)

EF = Exposure frequency (days/day) to soil (EF5) or dust (EFd) duringoccupational in areas of contamination

AF = Absolute absorption fraction (bioavailability) of lead in soil (AFS) or dust

Note that this equation does not depend on exposure duration. This is because it is assumed thatindividuals are exposed long enough to reach a steady-state blood lead level, and the equationis designed to predict that steady-state value. The exposure duration needed to reach orapproach this steady state level is not known, but is probably at least several weeks.

Once the geometric mean blood lead value is calculated, the full distribution of likely blood leadvalues in the population of all exposed women workers can then be estimated by assuming thedistribution is lognormal with some specified geometric standard deviation (GSD). Specifically,the 95th percemile of the predicted distribution is given by the following equation (Aitchison andBrown 1957):

95th = GM-GSD1 6 4 5

Input Parameters

The following sections summarize what is known about each of the model input parameters, andthe basis for the estimated mean values selected for use in calculating exposure of on-facilityworkers.

Background Blood Lead Level (PbBn)

As discussed above, it is assumed the subpopulation of workers of greatest potential concern forrisks from lead are women of child-bearing age. One source of information on baseline bloodlead levels in women of child-bearing age is the NHANES III study (Brody et al. 1994). The

Baseline Human Health RisV Assessment May 1997Documeni Control Number 4500-090-AOAC Page 3-28


geometric mean PbB values (ug/dL) reported for women aged 20-49 was 1.7 for whites, 2.2 forblacks, and 2.0 for Hispanics. In a study of blood lead levels in Sandy, Utah, a geometric meanblood lead value of 2.3 was observed in a group of 33 adult women (EPA 1995b). It is assumedthat the value observed in women in Sandy is more likely to be appropriate for the residents ofMurray than the national average value, so a value of 2.3 ug/dL was assumed for PbBo.

Geometric Standard Deviation (GSDJ

Data collected during the NHANES III survey indicate that the GSD for all women is about 2.1(Pirkle et al. 1994). Data collected during a study of the residents of Sandy, Utah (EPA 1995b)indicates the GSD for blood lead levels in adult women was 1.54. Because the residents ofSandy are likely to be more similar to the residents of Murray that the general population of theU.S.. the GSD value of 1.54 from Sandy was used to estimate the full distribution of blood leadvalues in the exposed population.

Biokinetic Slope Factor (BKSF)

The biokinetic slope factor proposed by Bowers et al. is 0.375 ug/dL per ug/day absorbed. Thisvalue is estimated from an observed slope of 0.06 ug/dL increase in blood lead of adult men perug/L of lead in first draw water (Pocock et al. 1983). Calculation of the BKSF from the Pocockdata requires a number of assumptions regarding how much total water was ingested, how muchof this was first draw and how much was drawn after the pipes were flushed, the decrease inlead concentration when the pipes were flushed, and the amount of lead absorbed from theingested water. Appendix C presents an analysis of the range of possible BKSF values whichmight be derived from the Pocock study, depending on the input assumptions. Based on thisanalysis, EPA believes the Pocock study data are consistent with a mean BKSF of about 0.4ug/dL per ug/day absorbed. A similar value of 0.444 can be derived from the data ofRabinowitz et al. (1974), although this study is based on only two male individuals, so theresulting value may not be highly representative. Calculations performed using thepharmacokinetic model developed by O'Flaherty (1993) show that BKSF is not a constant forall humans, but depends on age, sex, and lead body burden. Estimated values range from 0.25to 0.53 for a 25 to 35 year-old woman, assuming an absorption fraction of 0.08 (Gradient 1995).Based on this information, a value of 0.4 ug/dL per ug/day absorbed is selected as being areasonable estimate of the mean BKSF value for women of child-bearing age.

Concentration of Lead in Soil (C.) and Dust (Cd)

As noted above, the value of Q to be used in the calculations is the arithmetic mean of leadlevels in surface soil (EPA 1994a), averaged over an area where exposure is assumed to berandom. Table 2-1 summarizes these mean values for each on-facility exposure unit whereworkers could be exposed. As noted earlier, the concentration of lead in surface soil is highlyvariable from location to location, so estimates of the mean should be considered uncertain.



As discussed in Section 3.4.1, data from a number of off-facility locations around MurraySmelter indicate that the level of lead in interior dust is approximately related to the level of leadin soil by the following equation:

Cdusl = 0.35-Csoil

This equation is assumed to be applicable to indoor dust levels in on- facility workplaces. Theresulting soil and dust concentrations for on-faciliry commercial areas are summarized in Table3-5.

Ingesiion Rate of Soil (IR.) and Dust (IR.)

As noted earlier, the EPA (1993a) has issued draft guidance on recommended default soil anddust intake by workers, as follows:

Worker Type

Non-contact intensive

Contact intensive

Estimated Soil and Dust Intake (mg/day)

Average

50

240'

RME

50

480

1 Data are considered insufficient to derive a default recommendation; value shown isextrapolated from the RME value based on an assumed ratio of 2:1 (RME:average).

As noted above, the intake parameter required for use in this model is the mean intake, so avalue of 50 mg/day total is selected for the non-contact intensive worker. There are no data onhow the total is distributed between soil and dust in non-contact intensive workers, so it isassumed that the amount of soil and dust are each 50% of the total. Thus, the mean intake ofsoil and dust are each assumed to be 25 mg/day (0.025 g/day) for the non-contact intensiveworker. Because the contact intensive worker is assumed to be exposed mainly outside, it isassumed that all of the intake is soil (240 mg/day).

Exposure Frequency (EF)

There are no site-specific data on the number of days each year an on-facility worker will likelybe at work, so the standard mean default value of 219 days/yr (219/365 days/day) is assumedfor the non-contact intensive worker (EPA 1993a). For the contact-intensive worker, it wasassumed outdoor exposure occurs essentially every day that they are at work, except for dayswhen the ground is frozen or covered with snow. As noted earlier, meteorological data fromthe Salt Lake City area indicate that this is about 57 days per year (Campbell 1996), so exposurefrequencies of Cl-workers to outdoor soil were adjusted by multiplying by a factor of(365-57)/(365) = 0.84.

Baseline Human Health Risk Assessment May [997Document Control Number 4500-090-AOAC Page 3.30

THIS DOCUMENT WAS PREPARED. BY ROY F. WESTON. INC. EXPRESSLY FOR EPA. IT SHALL NOT BE RELEASED ORDISCLOSED IN WHOLE OR IN PART WITHOUT THE EXPRESS WRITTEN PERMISSION OF EPA.

TABLE 3-5 LEAD LEVELS IN COMMERCIAL AREA SOIL AND DUST

ExposureArea

EU-1

EU-2

EU-3

EU-4

EU-5

EU-6

EU-7

Mean Lead Concentration (ppm)

Surface Soil

2905

2879

9548

1750

2754

2297

2524

Indoor Dust*

1107

1098

3432

703

1054

894

973

" Calculated from mean soil level as follows:C(dust) = 90 + 0.35-C(soil)

MayBaseline Human Health Risk AssessmentDocument Control Number 4500-090- AOAC p^e 3.3 ,


Absorption Fraction (AF)

"Baseline" Absorption Fraction (AFo). A number of studies have been published on theabsorption of lead by adults. In a study with 5 adult male volunteers, Rabinowitz et al. (1980)found that the absorption fraction depended on whether the lead was ingested along with foodor was ingested 9 hours after the last meal. For lead ingested along with food (or for leadingested in the diet), the absorption fraction was 8-10%. For lead ingested by 9-hr fastedsubjects, the absorption fraction was 30-37%. (No food was ingested by these subjects until hour16). O' Flaherty (1993) reviewed several reports (including Rabinowitz et al. 1980) andconcluded that gastrointestinal absorption of lead in adults ingesting mixed diets is 4-11 %, witha mean of about 8-9%.

Clearly the choice of the most appropriate absorption fraction depends on what is assumedregarding the time of lead ingestion in relation to the time of the previous meal. For workers,it seems reasonable to assume that most will arrive at work shortly after having breakfast, andwill also ingest food at lunch time. Thus, a value of 10% seems likely to be representative ofthe baseline absorption fraction in most workers, and this value (0. 10) is selected for use in thesecalculations.

Adjustment for Bioavailability in Soil. As noted above, the EPA has measured the relativebioavailability of lead in a composite soil sample from the Murray Smelter site (EPA 1996), andpreliminary results suggest the value is probably about 0.71 (71%). Based on this, the absolutebioavailability (ABA) of lead in site soils is estimated to be:

ABA = 0.10-0.71 = 0.07 (7%)

Exposure to Lead in Groundwater

Based on the model of Bowers et al. (1994), the increment in geometric mean blood lead (AGM)due to water ingestion is given by the following equation:

AGM = BKSF • Cw • HV EF/365 • AFW

As discussed previously, values for these parameters for workers are as follows:

BKSF = 0.40 ug/dL per ug/day absorbedIPs, = 0.7 L/day (average)EF = 219 days/year (average)AFW = 0.10

Baseline Human Health Risk Assessment ' j^ay 1997Document Control Number 4500-090-AOAC Page 3.37


Based on this, the increment in GM blood lead is:

AGM = 0.0168-Cwug/dL

Summary of Inputs

Table 3-6 lists the model input parameters used to estimate blood lead levels in the populationof on-faciliry women workers.

Results — Predicted Blood Lead Levels in Workers

The predicted blood lead levels in workers exposed at on-faciliry locations are detailed inAppendix D (Pan 5) and are discussed in Section 5.2.2.2.

3.4.3 Exposure of Teenagers to Lead in Slag

As noted in Section 2.4, the concentration of lead in a composite slag sample from the site is11.500 ppm. This concentration is sufficiently high that intake by local teenagers could be ofpotential concern. However, the IEUBK model is not appropriate for evaluation of leadexposure in older children and teenagers, so the adult model of Bowers et al. used above toassess worker exposure was also used to assess risks to teenagers. The basic equation is:

PbB = PbB0 + BKSF • [CI.lag1 t-F $Uj • Ar jiagj

where:

PbB

PbB0

BKSF

IR,,ag

EFslig

AFslag

= Geometric mean blood lead level (ug/dL) in a population of teenagersexposed to lead-contaminated slag

= Geometric mean "baseline" blood lead level in teenagers not exposed tolead-contaminated slag, but including other background exposures,including residential exposure

= Biokinetic slope factor (ug/dL increase in blood lead per ug/day leadabsorbed)

= Arithmetic mean concentration (ug/g) of lead in slag

= Mean daily intake rate of slag (g/day)

= Exposure frequency (days/day) to slag

= Absolute absorption fraction (bioavailability) of lead in slag


Document Control Number 4500-090-AOAC Page 3-33


TABLE 3-6: MODEL INPUT PARAMETERS FOR ESTIMATION OF LEADEXPOSURE IN WOMEN WORKERS

Model Input

Geometric mean baseline blood lead

Biokinetic slope factor

Ingestion rate of soil

Ingestion rate of dust

Exposure frequency at work

Absorption fraction from soil and dust

Geometric standard deviation

Abbr.

PbB0

BKSF

IR,

IRd

EF

AF,. AFd

GSD

Units

ug/dL

ug/dL per ug/d

mg/day

mg/day

days/day

—

—

Value

NCI-Worker

2.3

0.4

25

25

219/365

0.07

1.54

CI-Worker

2.3

0.4

240

—

185/365

0.07

1.54



Input Parameters

There are no site-specific data on the geometric mean blood lead value in area teenagers, so datafrom the NHANES III study (Brody et al. 1994) were employed. As reported in this study, theGM for children age 12-19 is 1.6 ug/dL.

BKSF

As discussed above, the estimated BKSF is 0.4 ug/dL per ug/day absorbed.

As discussed above, the measured concentration of lead in a composite slag sample is 11.500ppm.

IE,las

As discussed above, the average ingestion rate of slag by area teenagers who visit the site isassumed to be 50 mg/event.

EF, lag

As discussed above, the exposure frequency for teenagers who visit the site is assumed to be anaverage of 25 days/year.

AZsIa

The oral absorption fraction of lead in slag from this site has been studied in animals (youngswine) by the EPA (1996). Preliminary results are summarized below:

RBA

Plausible Range

Preferred Range

Suggested Point Estimate

Value

0.47-0.55

0.51-0.55

0.53

Based on the suggested point estimate above (53%), and assuming teenagers absorb about 10%of dissolved lead in food and water, the absolute absorption fraction of lead from slag bychildren is estimated to be 53% • 10% = 5.3%.

Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC . Page 3.35


GSD

Observed GSD values in children and adults range from 1.4 to 1.54 in residents of Sandy, Utah.To be conservative, the value of 1.54 was assumed to apply to teenagers as well as adults.

Results — Predicted Blood Lead Levels in Teenagers

The predicted blood lead levels in teenagers exposed to slag at on-facility locations are detailedin Appendix D (Pan 5) and are discussed in Section 5.2.3.


Document Control Number 450CMD90-AOAC Page 3.3$


4.0 TOXICITY ASSESSMENT

4.1 OVERVIEW

The toxic effects of a chemical generally depend not only upon the inherent toxic ity of thecompounds and the level of exposure (dose), but also on the route of exposure (oral, inhalation,dermal) and the duration of exposure (subchronic, chronic or lifetime). Thus, a full descriptionof the toxic effects of a chemical includes a listing of what adverse health effects the chemicalmay cause, and how the occurrence of these effects depend upon dose, route, and duration ofexposure.

When data permit, the EPA derives numeric values that are useful in quantifying the risk ofnoncancer and cancer effects of a chemical. For noncancer health effects, the values are termedReferences Doses (RfDs). These are route- and duration-specific estimates of the average dailyintake (mg chemical/kg-day) that may occur without appreciable risk of any adverse effect.

For cancer, the EPA assigns a weight-of-evidence category which summarizes the overallstrength of the data supporting the conclusion that each chemical causes cancer in humans.These categories and their meanings are summarized below.

Category

A

Bl

B2

C

D

Meaning

Known human carcinogen

Probable human carcinogen

Probable human carcinogen

Possible human carcinogen

Cannot be evaluated

Description

Sufficient evidence of cancer in humans.

Suggestive evidence of cancer incidence in humans.

Sufficient evidence of cancer in animals, but lack of datainsufficient data from humans.

or

Suggestive evidence of carcinogenicity in animals.

No evidence or inadequate evidence of cancer in animalshumans.

or

For chemicals which are classified in Group A, B, or C, the EPA derives (if the data permit)a numeric descriptor of carcinogenic potency referred to as a Slope Factor (SF). These areroute-specific estimates of the slope of the cancer dose-response curve at low doses. It isassumed that at low doses the curve is linear and passes through the origin. The units of the SFsare (mg/kg-day)'1.

The following sections summarize the characteristic cancer and noncancer effects for lead andarsenic, and list available toxiciry parameters for each.

Baseline Human Health Risk Assessment May 1997Documeni Control Number 4500-090-AOAC Pagt 4.]

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4.2 ADVERSE EFFECTS OF ARSENIC

Excess exposure to arsenic is known to cause a variety of adverse health effects in humans.These effects depend on exposure level (dose) and also on exposure duration. The followingsections discuss the most characteristic of these effects.

Noncancer Effects

Oral exposure to high doses of arsenic produces marked acute irritation of the gastrointestinaltract, leading to nausea and vomiting. Symptoms of chronic ingestion of lower levels of arsenicoften begin with a vague weakness and nausea. As exposure continues, symptoms become morecharacteristic and include diarrhea, vomiting, decreased blood cell formation, injury to bloodvessels, damage to kidney and liver and impaired nerve function that leads to "pins and needles"sensations in the hands and feet. The most diagnostic sign of chronic arsenic exposure is anunusual pattern of skin abnormalities, including dark and white spots and a pattern of small"corns," especially on the palms and soles (ATSDR 1991).

The long-term (chronic) average daily intake of arsenic that produces these effects varies fromperson to person. In a large epidemiological study, Tseng et al. (1968) reported skin andvascular lesions in humans exposed to 0.014 mg/kg/day or more arsenic through drinking water.These effects were not observed in a control population ingesting 0.0008 mg/kg/day. Based onthis, the EPA calculated a chronic oral reference dose (RfD) of 3.0E-04 mg/kg/day (IRIS 1996).This is a dose which is believed to be without significant risk of causing adverse noncancereffects in even the most susceptible humans following chronic exposure.

For situations where only subchronic (and not chronic) exposures are possible, the EPA hasproposed a subchronic RfD of 6E-03 mg/kg-day (Benson 1995). This value is based on reviewof a number of reports of toxicity in humans exposed for time intervals ranging from 6 monthsto 10-15 years. These data indicate that adverse effects may occur in humans exposed to dosesof 0.06 mg/kg-day for as little as 6 months. Applying a safety factor of 10 yields a subchronicreference dose of 6E-03 mg/kg-d.

Carcinogenic Effects

There have been a number of epidemiological studies in humans which indicate that chronicinhalation exposure to arsenic is associated with increased risk of lung cancer (EPA 1984,ATSDR -1991). In addition, there is strong evidence from a number of human studies that oralexposure to arsenic increases the risk of skin cancer (EPA 1984, ATSDR 1991). The mostcommon type of cancer is squamous cell carcinoma, which appears to develop from some skincorns. In addition, basal cell carcinoma may also occur, typically arising from cells notassociated with the corns. Although these cancers may be easily removed, they can be painfuland disfiguring and can be fatal if left untreated. Although the evidence is limited, there aresome reports which indicate that chronic oral arsenic exposure may also increase risk of internal


cancers, including cancer of the liver, bladder and lung, and that inhalation exposure may alsoincrease risk of gastrointestinal, renal or bladder cancers (ATSDR 1991).

The amount of arsenic ingestion that leads to skin cancer is controversial. Based on a study ofskin cancer incidence in Taiwanese residents exposed to arsenic in drinking water (Tseng et al.1968, EPA 1984), the EPA has calculated a unit risk of 5E-5 (ug/L)'1 corresponding to an oralslope factor of 1.5 (mg/kg/day)'1 (IRIS 1996). This study has been criticized on severalgrounds, including uncertainty about exposure levels, possible effects of poor nutrition in theexposed population, potential exposure to other substances besides arsenic and lack of blindingin the examiners. Consequently, some quantitative uncertainty exists in the cancer potencyfactor derived from the Tseng data. Nevertheless, these criticisms do not challenge thefundamental conclusion that arsenic ingestion is associated with increased risk of skin cancer,and the Tseng study is considered to be the best study currently available for quantitativeestimation of skin cancer risk.

There are good data to show that arsenic is metabolized by methylation in the body, and someresearchers have suggested that this could lead to a threshold dose below which cancer will notoccur. Although there are data which are consistent with this view, the EPA has reviewed theavailable information (EPA 1988b) and has concluded that the data are insufficient at present toestablish that there is a threshold for arsenic-induced cancer.

4.3 ADVERSE EFFECTS OF LEAD

Neurological Effects

The effect of lead usually considered to be of greatest concern in humans is impairment of thenervous system. Many studies have shown that animals and humans are most sensitive to theeffects of lead during the time of nervous system development. Thus, the fetus, infants andyoung children are particularly vulnerable. Effects of chronic low-level exposure on the nervoussystem are subtle, and normally cannot be detected in individuals, but only in studies of groupsof children. Common measurement endpoints include various types of tests of intelligence,attention span, hand-eye coordination, etc. Most studies observe effects in such tests at bloodlead levels of 20-30 ug/dL, and some report effects at levels as low as 10 ug/dL and even lower.Such effects on the nervous system are long-lasting and may be permanent.

Effects on Pregnancy and Fetal Development

Studies in animals reveal that high blood lead levels during pregnancy can cause fetotoxic andteratogenic effects. Some epidemiologic studies in humans have detected an association betweenelevated blood lead levels and endpoints such as reduced fetal heme synthesis, decreased fetalsize or weight, shortened gestation period, decreased birth weight, congenital abnormalities,spontaneous abortion and stillbirth (EPA 1986). However, these effects are not detectedconsistently in different studies, and some researchers have detected no significant association


between blood lead levels and signs of fetotoxicity. On balance, these data provide suggestiveevidence that blood lead levels in the range of 10-15 ug/dL may cause small increases in the riskof undesirable prenatal as well as postnatal effects, but the evidence is not definitive.

Effects on Heme Synthesis

A characteristic effect of chronic high lead exposure is anemia stemming from lead-inducedinhibition of heme synthesis and a decrease in red blood cell life span. ACGIH (1995)concluded that decreases in ALA-D activity (a key early enzyme involved in heme synthesis) canbe detected at blood lead levels below 10 ug/dL. Heme synthesis is inhibited not only in redblood cells but in other tissues. Several key enzymes that contain heme, including those neededto form vitamin D, also show less activity following lead exposure (EPA 1986). The Centersfor Disease Control (CDC 1991) reviewed studies on the synthesis of an active metabolite ofvitamin D and found that impairment was detectable at blood lead levels of 10 - 15 ug/dL.

Effects on Blood Pressure

A number of studies have detected a weak association between blood lead level and increasesin both systolic and diastolic blood pressure in adults. EPA (1986) stated that although thechanges in blood pressure associated with moderate lead exposures are small (about 0.5 to 3 mmpressure with a rise in blood lead from 20 to 40 ug/dL), the increased risk of stroke or heartattack from this increase makes this an effect of concern at the population level. In contrast,ACGIH (1995) concluded that the public health significance of a rise of 0.5 to 3 mm in bloodpressure in the occupational populations is unknown but is expected to be small. The currentliterature suggests an association between blood lead and blood pressure, but until issuesapplying confounding factors are resolved, the relationship cannot be classified as definitive(ACGIH 1995).

Cancer Effects

Studies in animals indicate that chronic oral exposure to very high doses of lead salts may causean increased frequency of rumors of the kidney (EPA 1989b, ACGIH 1995). However, thereis only limited evidence suggesting that lead may be carcinogenic in humans, and thenoncarcinogenic effects on the nervous system and on hematopoiesis (heme synthesis) are usuallyconsidered to be the most important and sensitive endpoints of lead toxicity (EPA 1988a). EPAhas classified lead as a Group B2, probable human carcinogen, based on sufficient informationfrom animal studies with inadequate information on humans. EPA has not developed slopefactors for inhalation or oral exposure to lead. ACGIH (1995) states that there is insufficientevidence to classify lead as a human carcinogen.

Baseline Human Healih Risk Assessment M ]997

Documem Control Number 4500-090-AOAC pa 4-4


5.0 RISK CHARACTERIZATION

5.1 EVALUATION OF RISKS FROM ARSENIC

The basic equations recommended by EPA (1989a) to predict the risk from arsenic in soil anddust are as follows:

Noncancer Risk

HQ = DI/RfD

where:

HQ = Hazard QuotientDI = Daily intake (mg/kg-day)RfD = Reference dose (mg/kg-day)

If the value of HQ is less than or equal to one (1E+00), it is believed there is no significant riskof noncancer effects occurring, even in the most susceptible members of the population. If thevalue of HQ is greater than 1E+00, there is a risk of noncancer effects, but a value aboveIE+ 00 does not mean that an effect will definitely occur. However, the chances of an effectincrease as the value of HQ increases.

Cancer Risk

Risk = l-exp(-DI-SF)

where:

Risk = risk that cancer will occur in a person over a lifetime as a consequence of site-related exposures. For example, a risk of 1E-05 means there is a risk of 1 outof 10s (1/100,000) that a cancer will occur.

DI = Daily intake (mg/kg-day), averaged over a lifetime (70 years)

SF = Oral slope factor (mg/kg-d)'1

The level of cancer risk that is of concern is a matter of individual, community and regulatoryjudgement. However, the EPA typically considers risks below 1E-06 to be so small as to benegligible, and risks above 1E-04 to be sufficiently large that some sort of action or interventionis usually needed (EPA 1991b). Risks between 1E-04 and 1E-06 usually do not require


environmental remediation (EPA 1991b), although other forms of risk management may bejudged helpful to minimize human exposure.

Using these equations, the estimated daily intake values calculated as described in Section 3.3were combined with the toxicity factors discussed in Section 4.1. The detailed calculations arepresented in Appendix D (Pan 4). Results are summarized below.

5.1.1 Risks from Arsenic in Soil and Dust

In accord with EPA guidelines, risks to residents and workers from exposure to arsenic in soilwere evaluated for each EU or ISZ based on an exposure point concentration (EPC) which wasthe UCL of the mean or the maximum concentration value (whichever was lower). Becausevariability was high in most areas, the majority of the EPC values were equal to the maximumvalue, so estimates based on the EPC might tend to overestimate risk in some cases. To helpprovide perspective on the range of risk values which might be credible, risks were alsocalculated based on the mean values in each area.

The detailed calculations are presented in Appendix D, and the results are summarized in Table5-1. Inspection of this table reveals the following main observations:

• For on-facility and off-facility residents, nearly all chronic noncancer risks arebelow a level of concern. This conclusion is supported by data from a urinaryarsenic study conducted by the Salt Lake City-County Health Department, inwhich urinary arsenic levels in 7 children age 0-7 and in 17 children age 8-17living in Doc and Dell's (EU-11) or Grandview (EU-9 or EU-10) were all closeto or below detection limits (2 ug/L), which is well within or below normalranges. Even though these data are limited by the small number of participantsand by the fact that Urinary arsenic levels reflect only recent exposures, theresults do not suggest that above-average intake and/or absorption of arsenicare common. The only location where noncancer risks from arsenic appear tobe of concern is Area EU-8 (HQ = 1 to 9). It should be noted that althoughEU-8 is pan of the Grandview Trailer Park area, there are no residencescurrently in this sublocation. Cancer risks to residents mainly range between1E-07 and 8E-05, with risks greater than 1E-04 occurring in area EU-8 underboth average and RME conditions, and in ISZ-8 (using the EPC and RMEconditions).

• For non-contact intensive workers, chronic noncancer risks are below a levelof concern in most areas, but HQ values of 2 are observed for area EU-3 usingthe EPC and assuming RME exposure conditions. Average cancer risks rangefrom 6E-07 to 6E-05, with RME risks exceeding 1E-04 in two areas (EU-3 andEU-4) if the EPC is used.

Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 5-2THIS DOCUMENT WAS PREPARBD BY ROY F. WESTON. INC EXPRESSLY FOR EPA. IT SHALL NOT BE RELEASED ORDISCLOSED IN WHOLE OR IN PART WITHOUT THE EXPRESS WRITTEN PERMISSION OF EPA.

TABLE 5-1: RISKS FROM ARSENIC IN SURFACE SOIL AND DUST

Population

Resident

NCI-Worker

Cl-Worker

Location

On-faci l i ty

Off-facility

On facility

On-facility

Area

EU-8EU-9

F.U-IO

E U - I I

ISZ-I

ISZ 2

ISZ 3ISZ 4

ISZ 5

ISZ 6

ISZ-7

ISZ-g

EU 1

EU-2

F.U-3

EU 4

EU-5

EU-6

EU-7

EU 1

EU-2

EU-3

EU^i

EU-5

EU 6

EU-7

Arsenic Concentration (ppni)

Mean Max EPC

1674 5 < X X > 5<XX>

118 210 210

f>9 220 220

19 78 62

106 340 222

16 37 37

55 110 110

45 170 75

42 130 65

52 120 120

126 IRO 158

76 450 450

1 30 630 630

79 360 360

1172 7700 771X1

418 54(X) 54(X)

100 520 285

432 5100 1788

418 2200 1220

130 630 630

79 360 360

1172 7700 7700

4 1 8 5400 5400

100 520 285

432 5100 1788

418 2200 1220

Noncancer IIQ'

AvgIE + 00 ::::3E;fOO:

8F.-02 IEJOI

5E-02 \E4 \

2E02 5E-02

7E02 IE 01

2E-02 3E-02

4E-02 8E-02

3E-02 5E-02

3E-02 5E-02

4E02 8E029E02 IE-01

5E-02 3E^)I

3E02 IE-01

2E-02 8E-02

3E-OI JE+W;

9E-02 JE +00

2E-02 7E02

IE-01 4E-OI

1E^)I 3 E O I

2E-OI 9EOI

\E-0\ 5E-0\2E+'oo: ;;iE*oi ;isE^oi JEtpp;IE-01 4EX)I

7E01 :::;3B*;QO:

6E-01 :: ;:: 26*00 :•

RME;3E+pO ••:• . . 9E+00

2 E O I 4 E O I

IE-01 4E01

5E-02 IE 01

2 E O I 4E-OI

5E02 8E-02

IE-01 2E-OII E O I 2 E O I

9E4)2 I E O I

IE-01 2E-OI

2E-OI 3E-OI

2E-OI 8E^)14E-02 2 E O I

2E02 9EW

3 E O I ; ; ; ; 2E4-00:;I E O I JE-i-'oO

3E02 7E-02

I E O I 5E-OI

IE-01 3E-OI

4E-OI : 2E400

3 E O I IE + 00

4E40Q ".': ."'3EfplV.1E + 66 ••'. 2E+OI ;

3E-OI IE + 00

IE + 00 : 6E*00 :

IE + 00 I ;:4E + iD6: ;

Cancer Risk*

Avg6E-415 ;j 28-04:

5E-06 8E-06

3E4>6 8E-06

IE 06 3E^)6

4E06 RE06

9E-07 2E-06

2E06 4E-062E06 3E06

2E 06 3E 062E06 5E-06

5Efl6 6E-06

3E-06 2E-05

IE-06 5E-06

6E-07 3E-06

8E-06 6E-05

3E06 4EX)5

8E-07 2E-06

3E^X> IE-05

3E^)6 9E-06

6E-06 3E-05

4E06 2E-05

6E05 4EXM2E05 3&04

5E-06 JE-05

2E05 9E-05

2E4J5 6E-05

RME'.6B-04 ;;••;-:; ::-2B-fl3-i

4E05 8E-05

3E05 RE-05

IE-05 2E-05

4E-05 8E-05

9E4)6 2E-05

2E^)5 4E^)5

2EX15 3E^)5

2E-05 3Efl5

2EX)5 4E^)5

5E-05 6E05

3E-05 i ; ; :2EXM ;:

6E06 3E^)5

4EX)6 2E-05

5E-05 Is|-3E^4;::,;::2E-05 |::|2&fl4:;;

:'

4E^)6 IE-05

2E-05 7E-05

2E-05 5E-05

7E-05 ; : 3E-04

4E-05 -: . 2E-04

6E^)4 ; ::4E-03 ;

••?i&<)4.:v;;:::3EX)3--.

5E-05 2E^)4

2B-04 : JB-03

: Zfi-04 7E-04 ;

Shaded cells indicate locations where risks from arsenic exceed typical EPA guidelines ( I IQ > IE+ (X), cancer risk > IE-04)

' The first value shown is based on the mean concentration, and the second value shown is based nn the EPC (usual ly (he maximum)

For contact intensive on-facility workers, average and/or noncancer risks areof potential concern in a number of areas, with some HQ values ranging from2 to 30. Cancer risks based on the EPC exceed the 1E-04 level in 2 areas foraverage workers and in all 7 areas for RME workers, with risk values rangingup to 4E-03. If the mean concentration is used, risks are below 1E-04 in alllocations for the average worker, but still exceed 1E-04 in 4 of 7 areas for theRME worker.

5.1.2 Risks from Arsenic in Slag

Estimated arsenic risks to area teenagers (age 12-18) from direct ingestion of slag aresummarized below:

RiskParameter

Chronic HQ

Cancer Risk

Estimated Value

Average

5E-02

2E-06

RME

2E-01

IE-OS

As seen, noncancer HQ values do not exceed a level of concern for either average or RMEexposure assumptions. Excess cancer risks range from 2E-06 (average) to 1E-05 (RME).

5.1.3 Risks from Arsenic in Groundwater

Table 5-2 summarizes the average and RME risks to residents and workers from potential futureingestion of arsenic in groundwater. Inspection of this table reveals the following mainobservations:

• For wells located in or near residential areas, noncancer risks to residents aremainly below a level of concern (HQ < 1E+00). However, smallexceedances of the target occur at wells MW-102 (HQ = 2E+00) and MW-104D (HQ = 2E+00). Substantially larger exceedances occur at wells MW-103 (HQ = 2E+01) and MW-106 (HQ = 2E+03). Excess cancer risk levelsto the average resident mainly range between 6E-06 and 5E-05, with riskestimates greater than 1E-04 at wells MW-103 (7E-04) and MW-106 (7E-02).For residents with reasonable maximum exposure, excess cancer risks rangefrom 4E-05 to 4E-01, with 4 of 8 wells above a level of 1E-04.

• For on-facility workers, there are number of wells where ingestion of arsenicin groundwater would be of potential health concern. For noncancer effects,average and/or RME HQ values exceed 1E+00 for shallow wells MW-106,



5997

e 5.4

TABLE 5-2: POTENTIAL RISKS FROM ARSENIC IN GROUNDWATER

Population

Resident

Worker

Location

On-site

Off-site

On-site

Aquifer

Shallow

Intermediate

Shallow

Intermediate

Well

MW-10O1

MW-10TMW-102MW-103MW-104MW-106MW-101DMW-104D

MW-102MW-105MW-106MW-107MW-108MW-109MW-110M W - l l l b

MW-112GW-1GW-2Well 1Well 2Well 3b

UTBN-1MW-105DMW-108DMW-109DMW-112DGW-1AGW-1ARGW-2A

Concentration

3618

2706

27,180319

1813

27,1803314

2,3472,903

521,2872,870216

1,974236270253

6939

7906

439

Chronic HQAvg RME

1E-01 2E-013E-01 5E-018E-01:;;:2E-fOa

: :;iE+oi;H2E*Qi3E-01 "'"""" 5E:41

:::|:;i£+Q3.::i::;:2E*031E-01 2E-018E-01 ;2E*OQ

4E-01 6E-013E-01 4E-01

::::5E*02::;::;9E*025E-02 " 8E-025E-02 8E-023E-01 5E-01

5E+OI; 8E+016E+01 .9E+01iE+ob:.2E-f:oo

:3E4-01 4E+016E+01- 9E+014E+00 7.E+00

:4E*bH6E-fOl:5E+Od \: 8E+005E+00 9E+00

5E-01 8E-015E-02 8E-02

1E+00:;2E+008E-01 1E+00

2E+OI-:: 3E+011E-01 2E-01

•:9E-t-00 IE-f-01

Cancer RiskAvg RME

6E-06 4E-051E-05 1E-045E-05 :3E-04

:-7E-04 5E-031E-05 1E-04

:. E-02 ••"• 4E-Q16E-06 4E-055E-05 3E-*4

1E-05 1E-048E-06 7E-05

, :2E-02 1E-012E-06 ' 1E-052E-06 1E-059E-06 7E-05

;2E4)3 ;:;::l£-Q2.::2E-05::>:::.2E-02

3E-Q5;'-:-3E-M;8E-04::; 7E-032E-03 :P:1E4>2

lE-04/, \rlEr031E-03: i:iE-H02

.2E-04;;:;;1E-«32E-04 i !E-fl32E-05 1E^042E-06 IE-OS4E-05:;.-4E-043E-05: :-2E-W

;;:5E-04; i 4EiO34E-06 3E-05

F3E-04::: ;:-2E-03:

Shaded cells indicate wells where risks from arsenic exceed typical EPA guidelines (HQ > IE+00. cancer risk> 1E-04)

' Well located in an up-gradient location" Well is completed in slag

Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC p^e 5.5


MW-110, MW-111, MW-112. GW-1, GW-2, Well-1, WelI-2, Well-3, andUTBN-1, and for intermediate wells GW-1 A, GW-2A and MW-109D. Excesscancer risks to workers from arsenic in groundwater range from 2E-06 to1E-01, with 10 of 15 shallow wells and 4 of 7 intermediate wells having RMErisk values above 1E-04.

In some cases, arsenic levels in groundwater are sufficiently high to pose very substantial risksto any population who might drink the water. For example, at well MW-106, the RME HQvalue for an adult resident is 2E+03, and RME cancer risks range from 1E-01 to 4E-01 (10%-40%). Ingestion of such water would almost certainly result in severe health effects, both short-term and long-term.

5.2 EVALUATION OF RISKS FROM LEAP

As discussed earlier, in areas where land use is or might be residential, lead risk assessmentstypically focus on young children, since young children tend to have higher lead exposures thanolder children or adults, because young children tend to absorb more lead than do adults, andbecause young children are more susceptible to the adverse effects of lead on the nervoussystem. In areas where land use is not residential but commercial/industrial, the population ofchief concern is usually workers rather than children, with special attention to pregnant womenand women of child-bearing age. Section 3.4.1 above discussed the use of EPA's IEUBK modelto predict the expected distribution of blood lead values in populations of children living atcurrent on-facility residential areas (EU-8, EU-9, EU10 and EU-11), and at nearby off-facilityresidential areas (ISZ-1 to ISZ-8). Section 3.4.2 described the use of the model by Bowers etal. (1994) to predict blood lead levels in on-facility workers exposed at areas EU-1 to EU-7,while Section 3.4.3 discusses use of the Bowers model to evaluate lead exposure in teenagers.Detailed calculations are presented in Appendix D (Part 5). The following sections comparesthese predicted blood lead levels with current health-based guidelines in order to determine iflead is of potential concern in any of these locations.

5.2.1 Health Risks from Lead to Residential Children

It is currently difficult to identify what degree of lead exposure, if any, can be considered safefor infants and children. As discussed in Section 4.2, some studies report subtle signs of lead-induced effects in children beginning at around 10 ug/dL or even lower, with population effectsbecoming clearer and more definite in the range of 30-40 ug/dL. Of special concern are theclaims by some researchers that effects of lead on neurobehavioral performance, heme synthesis,and fetal development may not have a threshold value, and that the effects are long-lasting (EPA1986). On the other hand, some researchers and clinicians believe the effects that occur inchildren at low blood lead levels are so minor that they need not be cause for concern.

After a thorough review of all the data, the EPA has identified 10 ug/dL as the concentrationlevel at which effects begin to occur that warrant avoidance, and has set as a goal that there

Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 5.^THIS DOCUMENT WAS PREPARED BY ROY F. WESTON. INC. EXPRESSLY FOR EPA. IT SHALL NOT BE RELEASED ORDISCLOSED IN WHOLE OR IN PART WITHOUT THE EXPRESS WRITTEN PERMISSION OF EPA.

should be no more than a 5% chance that a typical child or group of similarly-exposed childrenwill have a blood lead value above 10 ug/dL (EPA 1994c, 1994d). This approach focuses onthe risks to a person at the upper bound (about the 95th percentile) of the exposure distribution,very much the same way that the approach used for other chemicals focuses on risks to theReasonably Maximally Exposed (RME) individual (EPA 1989). The CDC has also establisheda guideline of 10 ng/dL in preschool children which is believed to prevent or minimize lead-associated cognitive deficits (CDC 1991).

The following sections compare the predicted blood lead levels in resident children to thesehealth-based criteria. In the absence of site-related exposures to lead, most children are expectedto have blood lead values in the 3-5 ug/dL range, with about 7-10% above 10 ug/dL (Brody etal. 1994)

5.2.1.1 Risks to Children from Lead in Soil and Dust

Table 5-3 summarizes the predicted blood lead levels in children (age 0-84 months) exposed tolead in soil and dust at on-facility and off-facility residential areas. Inspection of this tablereveals that the probability that a random child would have a blood lead level higher than 10ug/dL (this is referred to here as "P10") is greater than EPA's goal of 5% at all locations exceptfor EU-10, ISZ-2, ISZ-4 and ISZ-5. In some cases the degree of exceedance is relatively small(e.g., 9% at ISZ-6), but is well above the goal (e.g., 15%-99%) in most other exposure areas.This suggests that risks to current and future children from lead in surface soil and dust in moston-facility and nearby off-facility areas are of potential concern.

In 1995. the Salt Lake City-County Health Department conducted a study in which blood leadlevels were measured in 10 children age 0-7 living in Doc and Dell's (EU-11) or Grandview(EU-9 or EU-10). The results are presented below, compared to the predicted values derivedfrom the IEUBK model:

Area

Doc and Dell's

Grandview

Observed

N

1

9

CM (ug/dL)

4.7

4.8

N > 10 ug/dL

--

0

Predicted

GM (ug/dL)

7.5

6.9

PIO

19%

13%

As seen, the geometric mean blood lead values predicted by the IEUBK model for the on-facilitytrailer park areas appear to be somewhat higher than observed, and the observed incidence ofchildren with blood lead values above 10 ug/dL (0%) is lower than predicted (13%-19%). Thissuggests that the IEUBK model may be over-predicting blood lead exposure levels in childrenat this site. However, because of the small number of children (only 9 at Grandview and oneat Doc and Dell's), and because only a single blood sample was collected from each child (asopposed to multiple samples over time), this conclusion is not certain.


TABLE 5-3: RISKS TO CHILDREN FROM LEAD IN SURFACE SOIL AND DUST

ExposureArea

EU-8

EU-9

EU-10

EU-11

ISZ-1

ISZ-2

ISZ-3

ISZ-4

ISZ-5

ISZ-6

ISZ-7

ISZ-8

Mean LeadConcentration

(ppm)

6177

909

538

814

1299

241

768

391

426

657

1222

1062

Predicted Blood Lead Distribution in Children

GM (ug/dL)

28.6

8.1

5.6

7.5

10.4

3.4

7.2

4.6

4.8

6.5

10.0

9.0

95th (ug/dL)

50

14

10

13

18

5.9

13

8.0

8.0

11

17

16

P101

•:••'. ••.•.-•>99%y.:-- •

- - : .•26%-:::.;:::

4%

; . . . ' - ,19%;;. . . . . . :

• • ' : : : ' • 53:%::;-y:3-:':-v0.1%

-;•••• W M;15& P: ; • • • • '

0.9%

1.4%

" ' • • ' - ; ' :9:0% " • • ' • • • • • - '

•""• : • '-'48% : • • • ' . ' -

' - . . . ' . ' :.37%: '••

P10 = probability of a child exceeding a blood lead level of 10 ug/dL (%). Shaded cells identifylocations where the value of P10 is higher than EPA's goal of no more than 5%.

Baseline Human Health Risk Assessment j^ay 1997Document Control Number 4500-090-AOAC Pjge 5.3


5.2.1.2 Risks to Children from Lead in Groundwater

Under typical conditions (soil lead levels in the range of 500-1000 ppm), the expected incrementin geometric mean blood lead by a child age 0-84 months predicted by the IEUBK model isabout 0.06 ug/dL per ug/L of lead in water. As shown in Table 2-4, nearly all wells locatedin residential areas have lead concentrations less than 10 ug/L, corresponding to increments ingeometric mean blood lead of less than 0.6 ug/dL. This increment is sufficiently small,especially compared to the estimated effects of ingesting soil and dust, that blood lead levels andthe probability of exceeding 10 ug/dL are not likely to be significantly affected by ingestion ofgroundwater.

5.2.2 Health Risks from Lead to Pregnant Workers

The EPA has not yet issued formal guidance on the blood lead level that is consideredappropriate for protecting the health of adult residents or workers. However, because fetusesare believed to be as susceptible to the adverse neurological effects of lead as children, it iscommon to focus concern on the subpopulation of pregnant women and women of child-bearingage, and to set as a goal that there should be no more than a 5% chance that the fetus of anexposed woman would have a blood lead level over 10 ug/dL.

The relationship between fetal and maternal blood lead concentration has been investigated ina number of studies. Goyer (1990) reviewed a number of these studies, and concluded that therewas no significant placental/fetal barrier for lead, with fetal blood lead values being equal to orjust slightly less than maternal blood lead values. The mean ratio of fetal PbB to maternal PbBin three recent studies cited by Goyer was 0.90. Based on this, the PbB in the mother whichcorresponds to a PbB in the fetus of 10 ug/dL is then 10/0.90 = 1 1 . 1 ug/dL. That is, in orderto ensure that the 95th percentile blood lead value in the fetus does not exceed 10 ug/dL, the95% percentile of the blood lead distribution in exposed women workers should not be higherthan 11.1 ug/dL.

5.2.2.1 Risks to Workers from Lead in Soil and Dust

Table 5-4 summarizes the predicted geometric mean blood lead levels in women workersexposed to lead in soil and dust at each of the commercial areas of the site. Inspection of thistable reveals that for non-contact intensive workers the value of "PI 1.1" (the probability ofexceeding the target blood lead level of 11.1 ug/dL) is equal to or less than 5% in all locationsexcept EU-3. However, for contact-intensive workers, the value of PI 1.1 exceeds the target of5% in all areas, with most areas having a probability of more than 40% of having anexceedance. These results suggest that risks to indoor workers from lead are not likely to beof concern for most areas, but risks to outdoor workers could be of concern across the entiresite.



TABLE 5-4: RISKS TO WORKERS FROM LEAD IN SURFACE SOIL AND DUST

ExposureArea

EU-1

EU-2

EU-3

EU-4

EU-5

EU-6

EU-7

Mean LeadConcentration

(ppm)

2905

2879

9548

1750

2754

2297

2524

Predicted Blood Lead Distributionin NCI-Workers

CM(ug/dL)

4.0

4.0

7.8

3.3

3.9

3.6

3.8

95th(ug/dL)

8.1

8.1

16

6.8

7.9

7.4

7.7

pn.r

0.9%

0.9%

;::;?;:20fc: ;;.•;;;

0.3%

0.8%

0.5%

0.6%

Predicted Blood Lead Distributionin Cl-Workers

GM(ug/dL)

12

12

35

8.3

12

10

11

95th(ug/dL)

25

25

71

17

24

21

22

P l l . r

59%

r.::58%.:: :

• ,-: 99S -V.-

"' :23£- i

.:::::::S5%:' >•,.,..;42.%...:....

;•• :48%V

P l l . l = probability of a worker exceeding a blood lead level of 11.1 ug/dL. For convenience, values above 5%have been shaded

Baseline Human Health Risk Assessment M,., 1997Document Control Number 4500-090-AOAC p^ 5.]0


In addition, it is important to recall that test pits installed at the site indicated that there arelocations where subsurface soil lead levels are significantly higher than are currently at thesurface, reaching values of 10,000-40,000ppm in some locations (see Section 2.4 and AppendixD, Pan 2). Such very high lead levels might be of concern if there were a pathway by whichworkers might come into contact with this soil. For example, if future excavation activitiesresulted in subsurface soil at an average level of 10,000 ppm being spread on the surface, therisk of a woman exceeding the target blood lead level would be nearly 23% for the NCI-workerand essentially 100% for the Cl-worker. Therefore, future excavation activities at the site whichcould bring contaminated subsurface soils to the surface and distribute those soils where humancontact might occur could be of potential concern, depending on the concentration and amountof material brought to the surface, and the degree of mixing with current surface soils.

5.2.2.2 Risks to Workers from Lead in Groundwater

As discussed previously (see Section 3.4.2), the increment in GM blood lead in women workersdue to ingestion of lead in drinking water is:

AGM = 0.0168-Cw ug/dL

As shown in Table 2-4, most wells located in the commercial areas of the site have leadconcentrations that are less than 10 ug/L. For these wells, the increment in blood lead causedby ingestion of groundwater is nearly negligible (< 0.2 ug/dL). However, a few wells (MW-111, Well-3, UTBN-1) have concentrations that appear to be significantly higher than average,and ingestion of groundwater from these wells could cause increases in blood lead levels ofpotential concern. The results for NCI-workers (calculated using the Bowers model) aresummarized below.

Well ID

MW-111

Well 3

UTBN-1

LeadCone.(ug/L)

212

150

50

Area

EU-4

EU-2

EU-1

Lead inSoil'

(ppm)

1750

2879

2905

Lead inDust"(ppm)

703

1098

1107

Baseline (no water)

GM

3.3

4.0

4.0

P l l . l

0.3%

0.9%

0.9%

Including Water

GM

6.9

6.5

4.8

P l l . l

13%

11%

3%

' Mean lead level in the exposure area" Calculated using the equation C(dusi) = 90 + 0.35 • C(soil)

As seen, for wells MW-111 and Well-3, ingestion of groundwater by NCI-workers would resultin a moderate increase (10%-13%) in the risk of exceeding the target blood lead level of 11.1ug/dL. For well UTBN-1, the increased risk (about 3%) is not of concern. For Cl-workers,risks of elevated blood lead from contact with soil are much higher, and the increment causedby ingestion of lead in water at these wells is relatively small, as shown below.

Baseline Human Health Risk Assessment May 1997Document Control Number 4SOO-090-AOAC Page 5-11THIS DOCUMENT WAS PREPARED BY ROY F WESTON, INC. EXPRESSLY FOR EPA IT SHALL NOT BE RELEASED ORDISCLOSED IN WHOLE OR IN PART WITHOUT THE EXPRESS WRITTEN PERMISSION OF EPA.

Well ID

MW-111

Well 3UTBN-1

LeadCone.(ug/L)

21215050

Area

EU-4

EU-2EU-1

Lead inSoil1

(ppjn)

175028792905

Lead inDust"(ppm)

703

10981107

Baseline (no water)

GM

3.3

12.112.2

Pl l . l

25%

58%59%

Including Water

GM

11.814.613.0

P l l . l

56%

74%64%

• Mean lead level in the exposure area* Calculated using the equation C(dusi) 90 + 0.35 • C(soil)

5.2.3 Risks to Teenagers from Ingestion of Lead in Slag

As discussed in Section 3.4, it is assumed that teenagers (age 12-18) may be exposed to slagwhile visiting the site. The potential effect of this exposure was evaluated using the Bowersmodel. The results are summarized below:

Baseline

(No slag)

GM

1.6

P l l . l 1

<0.01%

Including

Slag Exposure11

GM

2.4

P l l . l

0.02%

Increment

Due to Slag

GM

0.8

P l l . l

<0.02%

' P l l . l = probability of a teenager exceeding a blood lead of 11.1 ug/dLh Concentration of lead in slag = 11.500 ppm

As seen, direct ingestion of slag may increase geometric mean blood lead levels in teenagers byabout 0.8 ug/dL. However, assuming a GSD of 1.54, this does not result in a significant riskof exceeding a blood lead value of 11.1 ug/dL. This suggests that exposure of area teenagersto lead in slag is not likely to be of significant health concern.

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6.0 UNCERTAINTIES

Quantitative evaluation of the risks to humans from environmental contamination is frequentlylimited by uncertainty (lack of knowledge) regarding a number of important exposure andtoxicity factors. This lack of knowledge is circumvented by making assumptions or estimatesbased on the limited data that are available. Because there are a number of assumptions andestimates employed in the exposure and risk calculations, the results of the calculations arethemselves uncertain, and it is important for risk managers and the public to keep this in mindwhen interpreting the results of a risk assessment. The following sections review the mainsources of uncertainty in the risk calculations for arsenic and lead at this site.

6.1 EXPOSURE UNCERTAINTIES

Accurate calculations of risk require accurate estimates of the level of human exposure that isoccurring. However, because humans activity patterns are so variable, it is difficult to measureand difficult to predict exposures to most environmental sources of contamination.

Soil and Dust Intake

Ingestion exposure to soil and dust is usually considered to be one of the most importantexposure pathways at a site. However, reliable quantitative data on soil and dust ingestion ratesby humans is sparse, especially for adult residents and workers (both non-contact intensive andcontact intensive). The risk calculations reported here employ "default" soil and dust ingestionrates estimated by EPA, but because these defaults are developed from such a limited database,the values must be viewed as rather uncertain. It is usually supposed that the default soil anddust intake values employed are more likely to be high than low, but even this qualitativeconclusion is uncertain. There is also uncertainty in many of the other key human exposureparameters (exposure frequency, exposure duration, body weight), but these uncertainties areprobably small compared to the uncertainty in soil and dust intake rates.

Concentration Uncertainties

In all exposure calculations, the desired input parameter is the true mean concentration in amedium averaged over the area where random exposure occurs. There are two types ofuncertainty which influence the confidence in an estimate of the mean: 1) the accuracy of thesample analyses, and 2) the representativeness of the samples collected. At this site, thesampling and analysis program was well-planned and generally well-implemented, as detailedin the data quality reports for each medium (Hydrometrics, 1996). In general, there were nosignificant problems in the analysis of either soil or water samples, and none of the sampleresults for lead or arsenic were rejected during the data validation process. This indicates thatanalytical variability and error is unlikely to be a significant source of uncertainty at this site.

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However, there is significant uncertainty regarding the representativeness of the samples. First,all of the EUs and ISZs used to evaluate exposure are rather large, so even if the mean for eacharea were known with certainty, the value might not be representative of sub-areas or individualproperties within the area. In addition, there were a number of cases where the degree ofvariation between field duplicates was higher than specified in the data quality objectives.Because the data show there is very high spatial variability in concentration values betweendifferent sampling locations, it is probable that this variability in field duplicates is due toauthentic differences between the field duplicate samples rather than high variability in thesample analysis. Thus, the largest source of uncertainty in the estimated mean concentrationvalues for a location stems from the inherent variability of samples and the statistical difficultyin estimating the true mean concentration from a highly variable data set. In accord with EPAguidance, the best estimate of the mean concentration is used for assessing exposure to lead, sorisk estimates based on these values might be either too high or too low. In the case of arsenic,the upper 95th confidence limit of the mean is the recommended value rather than the bestestimate of the mean. In all cases at this site, the UCL of the mean is substantially higher thanthe best estimate of the mean, and sometimes the UCL exceeds the maximum measured value.Thus, use of the UCL or maximum (whichever is lower) is more likely to overestimate thanunderestimate the true level of exposure and risk.

In addition to the inherent uncertainty in concentration values in soil, there is even greateruncertainty in the relationship between soil contamination and dust contamination. In general,the data from paired soil and dust samples indicates that soil contributes to dust contamination,but that the strength of the correlation is not strong and the magnitude of the contribution isrelatively small. Thus, outdoor soil concentrations of lead or arsenic may not always be a goodpredictor of human exposure inside buildings. Further, there is uncertainty in the estimate ofthe average contribution of soil to dust, since estimates derived by linear regression analysis aresubject to bias that results from measurement error.

Water Exposure

As noted earlier, there are no persons who are currently using groundwater from the site fordrinking water, so risks to humans from this medium are not presently of concern. Risk levelswere calculated for this pathway because it is plausible that future residents or workers mightinstall wells, but this is not considered to be likely.

Pathways Not Quantified

As discussed in Section 3, humans may be exposed to environmental contaminants by a widevariety of pathways, but not all of these are likely to be equally important. At this site,exposures through inhalation of dust in air, dermal contact with soil and water, ingestion ofsurface water and sediment, and ingestion of chemicals in local foods (e.g., fish, gardenvegetables) were not evaluated quantitatively. Omission of these pathways will tend tounderestimate total exposure and risk, but it is believed that the magnitude of the exposure

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through these pathways (and hence the magnitude of the risk) is small compared to the exposureand risk due to the pathways that were evaluated (ingestion of soil and dust, ingestion ofgroundwater).

6.2 TOXICOKINETIC UNCERTAINTIES

Bioavailabilitv

As noted above, it is often proposed that metallic contaminants in ingested soil and slag are notwell absorbed into the body. In order to investigate this, the EPA performed a study of lead andarsenic absorption from soil and slag from the Murray Smelter site, using young swine as thetest species. Use of these preliminary site-specific bioavailability estimates from these studiesrather than the default values is believed to increase accuracy in the exposure and riskcalculations, but it must be understood that the measured RBA values are themselves uncertain.This uncertainty has many sources, most important of which is experimental variability betweenanimals, and the possibility that RBA values measured in swine might not be entirely equivalentto values in humans. It is not known if the site-specific RBA values used for lead and arsenicin soil and slag are likely to be higher or lower than the true values. Further, it is not knownif the measured values (each based on a single composite sample) are representative of the entiresite and of off-facility areas.

Other Toxicokinetic Parameters

In the case of lead, exposure calculations performed by the IEUBK model require not only dataon bioavailability, but also on distribution and clearance rate constants, body compartment sizes,etc. The IEUBK model employs values for these parameters derived from a variety of sources,employing human data whenever possible. However, because of limitations and gaps in thedata, each of these parameters is also uncertain. Thus, the predictions of the IEUBK modelshould be viewed as uncertain.

Similarly, the Bowers model used to assess lead exposures in adults requires a compositetoxicokinetic parameter (the biokinetic slope factor) to predict the effect of exposure on bloodlead levels. This value is derived mainly from studies in adult males, and it is not certain thatthe value is accurate for women in general and pregnant women in particular.

6.3 MODEL UNCERTAINTIES

The absorption, distribution and clearance of any chemical in the human body is an extremelycomplicated process, and any mathematical model intended to simulate the actual processes islikely to be an over-simplification. In this case, two different mathematical models were usedto evaluate risks from lead: EPA's IEUBK model was used to assess risks to children residents,and the model developed by Bowers et al. (1994) was used to assess lead risks to womenworkers.

Baseline Human Health Risk Assessmtm May 1997Document Control Number 4500-090-AOAC Pa-j 5.3


IEUBK Model

The internal structure of the IEUBK model is similar to most pharmacokinetic models, beingcomprised on a number of body "compartments". The lead concentration in each compartmentat any one time is determined by the balance between intake rate and the removal rate. Repeatedcalculations over time of flux in and flux out are then used to track how ingested lead isdistributed and cleared from the various compartments. Uncertainty is introduced into the modelby the use of generalized body compartments to represent highly heterogeneous tissues, and bythe lack of definitive data on the rate of uptake and removal of lead from each compartment.In addition, the final distribution of predicted blood lead values employs an estimated value forGSD|. This parameter cannot be measured directly, and so must be estimated from populationstudies. If the value employed is too high, this can result in a substantial overestimate of thefraction of the population above the health-based criterion. Thus, the predictions of the IEUBKmodel are uncertain and should not be interpreted or applied without considering thisuncertainty.

Bowers Model

The Bowers model is intentionally very simple, and is intended only for screening calculations.The chief simplifying assumptions used by this model are that a simple linear relationship existsbetween blood lead and environmental concentration values, and that the increment caused bysite-related exposures is simply additive with "background" blood lead levels. Theseassumptions are probably approximately correct for low dose exposures, but are likely tooverestimate responses at high dose. Thus, the predicted geometric mean blood lead values andthe corresponding estimated PI 1.1 values are likely to be too high for exposure units with veryhigh lead levels.

6.4 HAZARD UNCERTAINTIES

Arsenic

Even if the actual doses of arsenic ingested by residents and workers were known with certainty,there is still uncertainty regarding the health risks that these exposures would cause. Forexample, there is on-going debate regarding the correct cancer slope factor to use for arsenic,and whether humans can detoxify low doses of arsenic by methylation (ATSDR, 1991). If so,the cancer risk estimates provided above might be too high. On the other hand, the cancer riskestimates presented above do not account for the potential increase in internal tumors, so riskestimates might be too low. In order to account for these and other uncertainties associated withthe evaluation of toxiciry data, both RfDs and SFs are derived by EPA in a way that isintentionally conservative; that is, risk estimates based on these RfDs and SFs are more likelyto be high than low. In addition, both RfDs and SFs are intended to apply to the most

Basclmt Human Health Risk Assessment May 1997

Document Control Number 4500-090-AOAC Pa?e 6-4


susceptible members of a population, so average persons may not be affected to the degreepredicted by the toxiciry factors.

Lead

Similarly, even if it were possible to predict blood lead levels in exposed children and workerswith great accuracy, there is still uncertainty regarding the actual health risk to the fetus posedby those blood lead levels. It is important to note that the choice of 10 Mg/dL as the upper 95thpercentile limit for the child and the fetus does not imply that exposures above this definitelycause unacceptable health effects and that levels below this are definitely without risk. Rather,there is a graded increase in the severity of adverse effects as blood lead levels increase.Typically, frank clinical effects are not observed in children at blood lead levels less than 60-80pig/dL, and effects that occur at blood levels of about 10 ^g/dL are subtle and are generallyobservable only in well-designed population studies. Therefore, there are differences in opinionbetween health professionals as to what blood lead level should be treated as the acceptable limit.The choice of a health limit of 10 ^g/dL by EPA is based on a consensus among agencyscientists that effects which begin to appear at this exposure level are sufficiently undesirable towarrant avoidance (EPA, 1988a).

Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC p™ 5.5


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Brody DJ, Pirkle JL, Kramer RA, Flegal KM, Matte TD, Gunter EW, Paschal DC. 1994.Blood Lead Levels in the US Population. Phase 1 of the Third National Health and NutritionExamination Survey (NHANES III, 1988 to 1991). JAMA 272:277-283.

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EPA. 1991c. U.S. Environmental Protection Agency, Office of Health and EnvironmentalAssessment. Exposure Factors Handbook. Washington, D.C. Review Draft, July 1991.

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EPA. 1992b. Dermal Exposure Assessment: Principles and Applications. Interim Report.Office of Research and Development, Washington, DC. EPA/600/8-91/01 IB.

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EPA. 1994d. Guidance on Residential Lead-Based Paint, Lead Contaminated Dust, and Lead-Contaminated Soil. U.S. Environmental Protection Agency, Office of Prevention, Pesticides andToxic Substances. Memorandum from Lynn R. Goldman, M.D., Assistant Administrator. July14, 1994. °

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Hydrometrics. 1995a. Soil Technical Memorandum I. Former Murray Smelter Site, Murray.Utah. Revised Draft I. Report prepared for Asarco, Inc., by Hydrometrics, Inc. December1995.

Hydrometrics. 1995b. Groundwater Technical Memorandum No. 2. Former Murray SmelterSite, Murray, Utah. Draft. Report prepared for Asarco, Inc., by Hydrometrics, Inc.December 1995.

Hydrometrics. 1995c. Engineering Evaluation/Cost Analysis Work Plan Documents for FormerMurray Smelter Site, Murray Utah, September, 1995. Prepared by Hydrometrics, Inc., forAsarco Incorporated.

Hydrometrics. 1996. Site Characterization Report for the Former Murray Smelter Site,Murray, Utah. Report prepared for Asarco, Inc., by Hydrometrics, Inc. April, 1996.

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Tseng WP, Chu HM, How SW, et al. 1968. Prevalence of Skin Cancer in an Endemic Areaof Chronic Arsenism in Taiwan. J. Natl. Cancer Inst. 40:453-463.

Weis, CP, Henningsen G, Griffin S. 1996. Preliminary Bioavailabiliry Values for Arsenic inSoil and Slag from the Murray Smelter Superfund Site. Memo from Christopher P. Weis. GerryHenningsen and Susan Griffin to Bonnie Lavelle, dated 8/19/96.

WESTON. 1995a. Proposed Off-Facility Study Area Boundary, Murray Smelter Site, MurrayCity, Utah. Prepared by Roy F. Weston, Inc. for the USEPA Region VIII. March 24, 1995.Document Control No. 04800-051-0055.

WESTON. 1995b. Phase II Bioavailability Studies Sample Preparation and Analysis Report,Section 5 - Murray Smelter Site, Murray City, Utah. Prepared by Roy F. Weston, Inc. for theUSEPA Region VIII. June, 1995. Document Control No. 04800-030-0126.

WESTON. 1996. Streamlined Evaluation of Risks to Workers at the Proposed Murray PoliceTraining Facility. Prepared by Roy F. Weston, Inc. for the USEPA Region VIII. April 8,1996. Document Control No. 04800-051-0172.

WESTON. 1997. Ecological Risk Assessment for the Murray Smelter Superfund Site. Reportin preparation by Roy F. Weston, Inc. for the USEPA Region VIII.



APPENDIX A

EVALUATION OF TARGET ANALYTES FOR HUMAN HEALTHRISK ASSESSMENT AT MURRAY SMELTER

December, 1994

PROJEC^FILE

EVALUATION OF TARGET ANALYTES FOR HUMAN HEALTHRISK ASSESSMENT AT MURRAY SMELTER

Document Control Number 4800-051-0016

SECTION 1.0INTRODUCTION

Murray Smelter is a Superfund site located in the city of Murray, about 10 miles south of SaltLake City, Utah. This site is of potential concern because of the historic release of metals fromthe smelter to the environment.

Several preliminary site investigations have been performed which provide data on the type andconcentration of metal contamination at the site. The results of these studies are summarizedin Attachment 1. In brief, most of the studies have assumed that the principle chemicals ofpotential human health concern are lead and arsenic, and most samples that have been analyzedwere analyzed for lead and arsenic only using X-ray fluorescence emission spectroscopy.

While there is linle question that lead and arsenic are likely to be the primary sources of humanhealth risk at a smelter site such as this, it is not always true that risks from other inorganicchemicals are negligible. Therefore, a review of available data was performed in order todetermine whether future site investigations intended to support the human health risk assessmentshould focus on lead and arsenic, or should include a broader suite of inorganics.

SECTION 2.0EVALUATION OF SITE-SPECIFIC DATA

A total of 25 samples from the Murray site were located for which full metal analyses had beenperformed. These samples were categorized into three groups, as follows:

Medium

On-site Soils

Off-site Soils

On-site Slags

Number

10

10

5

Attachment 2 provides a listing of the raw data for these samples, and Table 1 presents summarystatistics. These data were used to estimate the likely importance of each chemical as a sourceof noncancer and cancer risk. The results are presented below.

Evajiuuoo of Ttrfct Aniiyiu for Humin Hearth Riik Ancumcai December 1994

Murray Smelter Siu, Mumy. Utih Pt|c 1THIS DOCUMENT WAS PREPARED BY ROY F. WESTON. INC. EXPRESSLY FOR EPA. PT SHALL NOT BE RELEASED OR DISCLOSED INWHOLE OR IN PART wrrHoirr THE EXPRESS WRITTEN PERMISSION OF EPA.cpmreiireporu*4I_J M6. dec

Table I. Summary Statistics for Inorganic Concentration Levels* at Murray Smelter

METALAluminumAntimony

ArsenicBariumBerylliumCadmium

CalciumChromiumCobalt

Copper

IronLeadMercuryMagnesium

ManganeseNickel

PotassiumSelenium

Silver

SodiumThalliumVanadium

Zinc

On Site Soils

N Mean Mai Min9

1010109

109

109

101010109

1099

10109

101010

658815

4989821.045

514682010

47753932

29750 7

68651299

162188

1 412

7883 278

10835

8950

492246

32503.0246

136628

5227

1172173256

89542 0

86105928

312979

2 828

164590361

34072

4670

255

1400 3

716600

94

9910000

4250.2

4620234

81700

0 31

2501013

330

Off-Site Soili

N Mean Mai Min7

10

10

10

7107

107

101010

10

7

10

77

10107

101010

101065

10314008

1245135

187

14223671

55810

11435352II

3634

5 95

12523 624

361

1621417

1921971038

757143312

25051900

15593 0

26571429

214976540

101853

90

38714

5780

12695

031

486393

7610 100

290 1

6020283

82000

0 12

2500.5

9100

SlagN Mean Mai Min05550505055550500550555

--20

10734241

--246

--

14--

127016142034908

2 1--

2161

----

13726--

124131

71944

—38

412315530

—1057

—22-

2630250600

7384069-

3864----

27.7

65--

567293

123200

—

4156861

—

0—

6—

80283WX)14130

00-

715---

4 812--

0 1

3238890

o)oO

I

' All concentration values expressed in units of mg/kg (ppm)

2.1 NQNCANCER RISK

Table 2 presents estimated Reasonable Maximum Exposure (RME) Hazard Quotient (HQJ valuesfor an adult resident who ingests 100 mg of soil or slag per day, 350 days per year. As seen,except for arsenic in on-site soil and slag, none of the HQ values exceed 1E+00. regardless ofwhether the calculation is based on the average or the maximum value detected in the samples.Even if the noncancer effects of all the chemicals were additive (they are not), the Hazard Index(HI) value for all non-arsenic chemicals does not exceed 1E+00 except for the highest slagsample. In all cases, arsenic contributes 70-90% of the total screening level HI.

Table 3 shows the results of a screening level evaluation of exposure to beneficial nutrients insoils and slag. As seen, none of the expected doses from site-related materials significantlyexceed a level that is considered safe.

2.2 CANCER RISK

Of the chemicals detected in site samples, the following are currently ranked as carcinogens byEPA:

Chemical

Arsenic

Beryllium

Cadmium

Chromium

L«>j

Nickel

OrmJ

X

X

X

Inhalation

X

X

X

X

X

X

Table 4 shows the estimated RME cancer risks to an adult resident who ingests 100 mg of soilper day and-who breaths 20 m3 of air per day containing 0.2 Mg/m3 of respirable dust panicles.350 days per year for 30 years. As seen, the inhalation risks are very small compared to theoral risks, and essentially all of the total cancer risk is contributed by arsenic.

2.3 CONCLUSIONS BASED ON SITE DATA

The calculations presented in Sections 2.1 and 2.2 strongly support the conclusion that, withrespect to the human health risk assessment at this site, it is reasonable to restrict attention toarsenic and lead, and that risk estimates based only on these two chemicals will not significantlyunderestimate the total risk from all chemicals combined, either for cancer or noncancer effects.

EviJujuoo of Turct ADiJyui for Hunuo Hufth Riik AneiimeolMurray Smeller Site. Murray. UubTHIS DOCUMENT WAS PREPARED BY ROY F. WESTON. INC. EXPRESSLY FOR EPA.WHOLE OR IN PART WITHOUT THE EXPRESS WRITTEN PERMISSION OF EPA.cpa \ArciMTponjt4 8 51^16.dec

December 1994Pifc 3

IT SHALL NOT BE RELEASED OR DISCLOSED IN

Table 2. Evaluation ofNoncancer Risks'

METALAluminumAntimonyArsenicBan urnBerylliumCadmiumChromiumCobaltCopperLeadMercuryManganeseNickelSilverThalliumVanadiumZinc

RfDb

—4.0E-043.0E-047.0E-025.0E-03l.OE-035.0E-03

—3.7E-02

—3.0E-04l.OE-012.0E-025.0E-037.0E-057.0E-033.0E-01

HQ From Arsenic AloneSum of all other HQsTotal of all HQs% Attributable to Arsenic

RME Hazard Quotum (HQ)On-Site Soil

Mean

—0.052.270.020.000.060.01

—0.02-

0.000.020.000.000.060.020.052.270.312.58

88

Max

—0.1710.260.060.000.340.01

—0.04

—0.010.080.000.010.180.070.16

10.261.13

11.3990

Off-Site SoilMean

—0.020.470.000.000.020.00

—0.01

—0.000.000.000.000.070.000.000.470.130.60

78

Max

—0.060.880.000.000.050.01

—0.01

—0.010.010.000.000.180.010000.880.341.22

72

SlagMean

—0.074.900.08

—0.340.00

—0.05

—0.010.03

—0.010.240.030.334.901.186.08

81

Max

—0.13

18.830.30_

1.450.01_

0.10

—0.030.05

—0.021.110.060.56

18.833.82

22.6483

1 Assumes mgesiion of 100 mg of soil/dust per day by a 70-kg adult, 350 days/yrb RfD = Reference Dose (mg/kg-d)

Evthuuan of Tirjct AnAivui for HUOLU HctAta Ruk Aucitmau December 1944Mumy Smeller Siu. Mumy. Uuh fift 4IMS DOCUMENT WAS PREPARED BY ROY F. WESTON. INC. EXPRESSLY FOR E?A. IT SHALL NOT BE RELEASED OR DISCLOSED [NWHOLE OR IN PART WITHOUT THE EXPRESS WRITTEN PERMISSION OF EPA.

Table 3. Beneficially Screen

METALCalciumIronMagnesiumPotassiumSeleniumSodium

RDA*1200.0

15.0350.0

2000.00.1

500.0

Ratio of Estimated Daily Intake (ing/day) to RDA*On-Site SoilMean

0.000.360.000.000.000.00

Max0.011.160.000.000.000.00

Off-Site SoilMean) Max

0.000.160.000.000.010.00

0.010.350.010.000.080.00

SlagMean Mai

—1.08-

—0.02-

—1.67

—_

004-

RDA = Recommended Daily Allowance (mg/day)

EviJuiuoo el T»rfO Aaatytci for Humm HuAta Ruk Auunxai December 1994Mumy Smeller Site. Mumy, Uub p,jc jTHIS DOCUMENT WAS PREPARED BY ROY P. WESTON. INC. EXPRESSLY FOR EPA. IT SHALL NOT BE RELEASED OR DISCLOSED INWHOLE OR rN PART WITHOUT THE EXPRESS WRITTEN PERMISSION OF EPA.cpi \artivrcporut4l_51_16. dec

Table 4. Analysis of Cancer Risks

OralExposure'ArsenicBerylliumLeadTotal'/•Arsenic

oSF*1.8E+004.3E-KX)

Estimated RME Ezcesi Lifetime Cancer RiskOn-Site Soil

Mean5.1E-042.5E-06

5.1E-0499.5

Max2.3E-037.6E-06

2.3E-03997

Off-Site Soil

Mean1.1E-042.0E-06

1.1E-0498.2

Max2.0E-042.5E-06

2.0E-0498 7

Slag

Mean Max1.1E-03

ND

1.1E-03100.0

4.2E-03ND

4.2E-03100.0

InhalationExposure'ArsenicBerylliumCadmiumChromiumLeadNickelTotal% Arsenic

iSF-1.5E+018.4E-HX)6.3E-KK)4.2E-K)!

-•84E-OI

On-Site SoilMean

1.9E-072.2E-1074E-092.2E-08

-3.4E-102.2E-07

86.7

Max8.7E-076.5E-104.0E-085.6E-08

—6.7E-109.7E-07

89.9

Off-Site SoilMean

4.0E-081.7E-101.9E-092.0E-08

-2.3E-106.2E-08

64.5

Max7.4E-082.2E-106.2E-093.6E-08

-4.6E-101.2E-07

63.6

SlagMean

4.2E-07ND

4.0E-081.5E-08

—ND

4.7E-0788.3

Max1.6E-06

ND1.7E-072.4E-08

..ND

1.8E-0689.1

Total Exposure(Oral + Inhalation)ArsenicBervlliumCadmiumChromiumLeadNickelTotal'/» Arsenic•/.Oral

On-Site SoilMean

5.1E-042.5E-067.4E-092.2E-08

«3.4E-105.1E-04

99.51000

Max2.3E-037.6E-064.0E-085.6E-08

-67E-10

. 2.3E-0399.7

100.0

Off-Site SoilMean

1.1E-042.0E-061.9E-092.0E-08

~2.3E-101.1E-04

98.1

99.9

Max2.0E-042.5E-066.2E-093.6E-08

—4.6E-102.0E-04

98.7

999

SlagMean

1.1E-03ND

40E-081.5E-08

—ND

1.1E-03100.0100.0

Max42E-03

ND1.7E-072.4E-08

—ND

4.2E-03100.0100.0

' Assumes ingestion of 100 mg/day by a 70-kg adult, 350 d/yr for 30 yr' oSF = Oral slope factor (mg/kg-d)'1

e Assumes 0.2 ug/m' of soil in air, with inhalation of 20 mVday by a 70-kg adult, 350 d/yrfor 30 yr

" iSF = Inhalation slope factor (mg/kg-d)"'

Evthuuon of TufO AaiJyu* for Humu Hufth Ruk AiiuoacatMumy Smcter Site. Mumy, UubTHIS DOCUMENT WAS PREPARED BY ROY F. W1STON. INC. EXPRESSLY FOR EPA.WHOLE OR IN PART wrrHOirr THE EXPRESS WRITTEN PERMISSION OF EPA.

_Jl_16.doc

December 1994Pifc 6

FT SHALL NOT BE RELEASED OR DISCLOSED IN

SECTION 3.0INTER-SITE COMPARISON

An alternative method for evaluating the relative importance of the risks contributed byinorganics other than lead and arsenic is to examine the risk estimates obtained at a site similarto the Murray Smelter site. The risk assessment previously performed at the Midvale Slag Site(Operable Unit 1) was selected for this comparison because it is believed that both sites smeltedsimilar ores using similar smelting processes.

3.1 COMPARISON OF COT

If the inter-site comparison is to be considered relevant, it is necessary that the levels ofcontamination be similar at the two sites. As shown in Figure 1, the concentration of thecontaminants in on-site soils tend to be somewhat higher and more variable at the Murray sitethan at the Midvale site, but the range of concentration values overlap in all cases.

3.2 SUMMARY OF RISK CALCULATIONS

Table 5 summarizes the results of the noncancer risk assessment at Midvale Slag OU1. As seen,arseni accounts for the majority of the screening level total HI, and there are no locationswhere a non-arsenic chemical (other than lead) was of potential noncancer concern but arsenicwas not of concern.

At this site, cancer risk was evaluated only for the soil/dust ingestion pathway. (As notedabove, the inhalation pathway contributes very little additional cancer risk). Thus, only arsenicand beryllium contributed to the risk. In all cases, arsenic accounted for 97% or more of thetotal cancer risk.

3.3 CONCLUSIONS BASED ON INTER-SITE COMPARISON

The risk calculations at Midvale Slag OU1 show that only arsenic and lead contributesignificantly to potential human health risk. Based on the similarity in contamination betweenMidvale Slag and Murray Smelter, it is considered likely that the same conclusion will apply atMurray Smelter.

EvtJuiuoo of Tirfet Aoilyui for Humu Health Rilk Aneitmoii December 1944Muniy Smeller Snc. Mumy, Uub P«jc ^THIS DOCUMENT WAS PREPARED BY ROY F. WESTON. INC. EXPRESSLY FOR EPA. IT SHALL NOT BE RELEASED OR DISCLOSED ENWHOLE OR IN PART WITHOUT THE EXPRESS WRITTEN PERMISSION OF EPA.

51 16.dec

bo O

I 2,

Figure 1. Comparison of Concentrationsat Murray Smelter and Midvale Slag

•- > 3 B a

's « 1 f Ifrig- 1

g> 1 1a! f§"* IP ip j5 ni §o «

o K

>0

>

M

rz3tn

PP

GoX)

O

§ "

8 1m T> -*

lit

1E5

1E4

Q. 1E3

S:Coco 1E2

"c0)0

o 1E10

1EO

1E-1

Al

' As

Sb

-

-l-H-H-l-HA B A B A E

MnMax

CdMean

Ni

Co AgMin

Tl

Be

I-H-H-H-I-H I! I I I I I l-l-l I I I I I l-l-l I I I I I I I I I M I I IAB AB AB AB AB AB AB AB AB AB AB AB AB AB

Site (A = Murray, B = Midvale)

Table 5. Noncancer Risk Results for Midvale Slag OU1 °

ChemicalAntimonyArsenicBariumBerylliumCadmiumCyanideManganeseMercuryNickelSilverThalliumVanadiumHQ for ArsenicSum of all other HQsTotal of all HQs% Attributable to Arsenic

Hazard Quotient by AreaWE-CRA

0.111.130.050.000.290.000.070.210.010.060.040.021.130.851.9857%

WE-SEA0.515.800.030.000.320.000.040.070.000.020.080.015.801.096.8984%

LF0.153.400.020.000.290.000.040.060.010.010.100.023.400.694.0983%

LG0.42

12.430.030.000.760.000.030.100.010.030.050.01

12.431.43

13.8790%

LR-West0.173.03

• 0.020.000.440.000.040.050.010.020.030.013.030.793.8279%

LR-SEA0.505 470.020000.710.000.030.030.010010.080.025.471.416.88

' 79%

Data from Life Systems Inc (1992)

EviJuiuoo of Tufct AnaJyut for Hunun Health Riik Ain-iiroml December 19*4Murray Smeller Sat, Murray. Uuh PIJC 'THIS DOCUMENT WAS PREPARED BY ROY P. WESTON, INC. EXPRESSLY FOR EPA. IT SHALL NOT BE RELEASED OR DISCLOSED INWHOLE OR IN PART WITHOUT THE EXPRESS WRITTEN PERMISSION OF EPA.cpii*rciircporut4> 51 16.dec

SECTION 4.0RECOMMENDATIONS

Based on the risk calculations using preliminary site-specific data (Section 2), and supported bythe findings of a risk assessment at a similar site (Section 3), it is concluded that human healthrisks (both cancer and noncancer) at Murray Smelter from inorganics iher than lead are \s rvlikely to be dominated by arsenic. Consequently, it is recommended that arsenic and lead beselected as the chemicals of potential human health concern at this site, and that future site-characterization studies intended to support the human health risk assessment be restricted toinvestigations of the level and distribution of these two chemicals. It should be noted that thisconclusion may not be appropriate for investigations intended to support an ecological riskassessment.

Evtluiuoa of Ttrgci AaiMct for Husun Huttb Hoi Aiieiimeat December 1994Murray Smelter Silt. Murray, Hub Pifc 10THIS DOCUMENT WAS PREPARED BY ROY F- WESTON, INC. EXPRESSLY FOR EPA. IT SHALL NOT BE RELEASED OR DISCLOSED INWHOLE OR IN PART WITHOUT THE EXPRESS WRITTEN PERMISSION OF EPA.cpii*rtivrcporuUI_51 _l 6.dec

ATTACHMENT 1

SUMMARY OF PRELIMINARY DATA COLLECTED AT MURRAY SMELTER

Attachment 1Table I

Fit Data 1984

Medium

Soil slag

G round -water

Sediment

SurfaceWater

Location

On-sileN. of creekMurray HS

On-sile(shallow)On-sile (deep)

UpstreamDownstream

UpstreamDownstream

Numberof

Samples

31-2 ?3-4?

32

11

11

DataQuality

l^vel III ICP/AALevel III ICP/AALevel 111 ICP/AA

Level III ICP/AALevel III ICP/AA

Uvel III ICP/AAUvel III ICP/AA

Uvel III ICP/AALevel III ICP/AA

Analyle

Full suiteFull suiteFull suite

Full suiteFull suite



Concentration RangeSoil/Sed in mg/kg;

Waters >tg/f

As (345-860); Pb (5928 8954)As (26-92); Pb (29-370)As(99-J92); Pb (238- 1559)

As (9.0U-9.5); Pb (4.5U)As (9.0U); Pb (4.5U)

As (5VJ), Pb (76)As (24); Pb (2348)

As (14); Pb(4.5U)As (9U); Pb (4.5U)

Comments

—

Suggests no impacts; however,coverage is poor.

Suggests site-related impacts.

Suggests no impacts for theseelements.

cp

Attachment 1Table 2

KRB Trailer Park Sampling

Medium

SurfaceSoil

Slag

HouseDust

Tap Waler

l^ocalion

Grand view

Shady Grove

Grand viewShady Grove

Doc & Dels

Grandview

Grand view

Numberof

Samples

56

10

62

2

28

28

DataQuality

XRF

XRF

Ijcvcl III AA/ICPLevel III AA/ICP

XRF

Unknown

Uvel III AA/ICP

Analyle

Pb/As

Pb/As


Special ion

Pb/As

Pb

Concentration RangeSoil/Scd in mg/kg;

Waters /jg/f

As (NA); Pb (90-2500)

As(NA); Pb(l80U^60)

As (55-386); Pb (425-2500)As (45 65); Pb (365-740)

N/A

N/A

Pb(5U-l7)

Comments

Pb acceptable for RA; As isrejected.Pb acceptable Tor RA; As isrejected.All acceptable.All acceptable.

N/A

Pb acceptable; As is rejected.

All acceptable.

N/A = Nnl Applicable

l dau Ibl

Attachment 1Table 3

Independent Investigationof 5100 S. Stale Street

• Medium

Soil

G round -water

Location

0-2'28 '

8-I21

from 2 on-sileboreholes

Numberof

Samples

1419

5

2

DataQuality

Uvcl III ICPUvel III ICTUvcl III ICP

Level III ICP

Analyle

As/PbAs/l'bAs/Pb

As/Pb

Concentration RangeSoil/Sed in nig/kg;

Waters pg/f

As (5. 4-69); Pb (13-2000)As (7. 3-700); Pb (15 670)As (1.7-230); Pb (11-420)

As (26-52); Pb (80-140)

Comments

All results acceptable.All results acceptable.All results acceptable.

All results acceptable.

Mil d»u Ibl

Attachment 1Table 4

Independent Site AssessmentMonroe, Inc.

'Medium

SurfaceSoil

SubsurfaceSoil

G round -water

location

Unknown

Unknown

Unknown

Numberof

Samples

3

4

3

DataQuality

l,evel 111

Level III

[>cvcl III

Analylc

TCl.P-Pb

TCLP-Pb

IMi(dissolved)

Concentration RangeSoil/Scd in mg/kg;

Waters pg/f

PbTCLP(< 100 10,000)

PbTCLP(<l003I.OOO)

Pb(< 10-30)

C'oinnienls

Not applicable to riskassessment.

Not applicable to riskassessment.

Acceptable.

il ikU Ibl l'.tc <

Attachment ITable 5

UI)KQ/I)ERR Site Investigation1992

Medium

Soil

Soil

Soil

Soil

Location

Doc & Dell

Grandvjew

Murray HS

Background S.of Doc & Dell

Numberof

Samples

3

3

3

1

DataQuality

l^vel III AA/ICP

Level III AA/ICP

\jcvel III AA/ICP

l>evel III AA/ICP

Analyte

Full suite

Full suite

Full suite

F'ull suite

Concentration RangeSoil/Sed in mg/kg;

Waters /jg/f

As (156-284); Pb (22,170 32,820)

As (560-4123); Pb (670 73.840)

As (59.1 186); Pb (299-783)

As (10.6); Pb(14.5)

Comments

Acceptable

Acceptable

Acceptable

Acceptable

cpHfil d>U.lbl

ATTACHMENT 2

RAW DATA FOR SAMPLES FROM MURRAY SMELTERTHAT WERE ANALYZED FOR MULTIPLE METALS

ATTACHMENT 2

METAL

Aluminum

Antimony

Arsenic

Harium

Deryllium

Cadmium

Calcivim

Chioinium

Cobalt

Copper

Iron

lead

Mercury

Magnesium

Manganese

Nickel

Potassium

Selenium

Silver

Sodium

lliulliuin

Vanadium

Zinc

Study I';&L/IAT(I993)

Malrii Soil

ID No. GV-SO-18

Location Grandview

On site

89500

2 4

550

1520

0.5

69

257000

90

41)

990

120000

4 2 5 0

0.6

71400

2820

HO

23000

0 3

1 0

9000

20

160

3300

Soil

(iV-SO-20

Giandvicw

On site

63900

2 8

7 3 0

- 2 5 1 0

0 5

7 4

2.11000

II 0

4 0

2500

1 12000

K400

O K

63700

324 0

100

IHOOO

1 0

60

2500

1 3

1 5 0

1 260 (I

Soil

(iV-SO-32

Grand view

(.hi site

46700

60

1560

299 0

0 3

21 2

170000

90

4 0

2000

100000

9700

0 5

46200

2420

100

17000

1 6

4 0

2500

2 0

1 3 0

8060

Soil

GV-SO-36

Grand view

On site

65400

30

2920

3850

0 3

269

372000

140

50

2830

128000

17300

07

79400

3 1 5 0

150

2000.0

1.7

90

2500

1 0

170

14500

Soil

GV-SO-44

Grandview

On site

49100

70

1890

161 0

0 3

140

289000

no4 0

1)70

II 1000

8000

06

86100

2340

90

18000

2 1

50

2500

50

130

931 0

Soil

GV-SO-50

Grandview

On site

49400

90

3860

5640

0 3

39 1

166000

II 0

40

3890

122000

25500

09

59300

2580

140

17000

2 8

1 3 0

5000

5 0

160

1 1 90 0

Soil

SG-SO-OI

Shady (rrove

Off site

60500

40

650

1970

03

1 1 7

467000

130

40

2170

1 1 300 0

7400

06

73800

3090

110

25000

10

80

5000

4 0

170

6K30

SoilSG-S(M)9

Shady Glove

Off site

57800

1 3

450

1570

0 3

4 1

356000

90

3 0

900

IOKKIO

3650

0 5

6020 0

2830

HI)

20OOO

0 3

60

2500

07

90

7 1 4 0

Note: All concentration values are in unils ofmgAg (ppm)

Non-delects are recorded as one/half the detection limit

ATTACHMENT 2

Study FIT Report (EPA 1985)

Malrii Soil . SoilID No. S-8 S-7

Location 77 77METAL On site On site

AluminumAnlimonyArsenicBariumBerylliumCadmiumCalciumChromiumCobaltCopperIronLeadMercuryMagnesiumManganeseNickelPotassiumSeleniumSilverSodiumThalliumVanadiumZinc

73200270

345032220

20150

9536003 5 0160

92801314430

592800 2

6443059280

18028450

06210

1603020

1650340720

6919049.0

378.032500

3.0170

13662805202 1 0

110501732560

895400 2

6395014940

2 5 02564 0

06280

144203 0

361.0339540

Soil SoilS-6 S-5

77 North of siteOn site Off site86560

3908600

139202 0

590817200

380270

117201295700

688202 0

8333.03597.0

31 029790

06250

1645090

151 0338170

1621403 5

2601570

1010

757140330120930

22643029.00 1

2657104290

21.042430

063 0

164300 5

3801000

SoilS-4

Murray MSOfTsile77720

80920980

1090

67935020060

820130980

370005

907604180

8 527010

0650

1489030

2102060

SoilS-3

Murray MSOff site121800

1101920I860

10190

33333023090

1670193590

833010

1 1090 04230

8 548140

0660

1853050

3204680

SoilS-2

Murray IISOff site129760

17.018501370

10380

48630230100

2500207140

1559030

607103040

8 549760

540100

1613090

3105480

SoilS-l

Murray MSOff site97670

3 5990

15101050

51802027080

760181980

23800 3

1383703780

8 542030

0650

1419030

3702620

Note. All concentration values are in units of mg/kg (ppm)Non-delects are recorded as one/half the detection limit

An ACUMEN! 2

METALAluminumAntimonyArsenicHariuinBerylliumCadiiiiiunCalciumChromiumCobaltCopperIron1 cudMercuryMagnesiumManganeseNickelPotassiumSeleniumSilverSodiumThalliumVanadiumZinc

study DDI;Q/DI;RR iIVUlrii Slog

ID No. MS SO II

Location Doc & DellsOn site

1 8 21560

155300

0 4

60

1 1 5 7 0206700 0

31 38000 1

3 3 2 3 0

4 81 2 2

0 11650

1232000

992Slag

' MS-SO- 12Doc A Dells

On sile

27 I244 0

20630

300

21 8

898 02506000

32H20000

3864 0

1 2 81 7 5

0 12930

90740 0

SlagM:, • • ' '

Doc&iOn site

1 2 42840

17500

1 1 3 0

13 1

802083600021370(1

0 7

13350

10021 8

1 81290

632700

Slag

3764 1 2 3 09990

10570

104

263001648000738400

69

15670

2 7 7

65 1

567

3 2 2388900

Slag/SoilMS-SO- 15Urandview

On sile

3956008610

31 8

18 1

86401014000

1413003 1

7150

13 I13 1

3 43 3 7

436200

SoilMS-SO- 16Grand view

On sile

2 122460

1400

2460

103

2050357500

67000 3

3160

2 33 7

16178

5420

SoilMS-SO 17

Murray IISOffsile

1 5I860953

157

105

1690205000

783030

3630

084 2

6.5167

2960

SoilMS SO- 18

Murray IISOffsile

0759 1990

5.0

108

1690519000

299004

284.0

0 32 4

1 <>204

1500

SoilMS-SO 19MumyllS

Offsile

09770

1190

6 5

1 1 4

1050489000

36600 4

3270

0 11 7

202 1 7

1780

Note: All concentration values are in units ofmgAg (ppm)Non-delecis are recorded as one/half (lie detection limit

APPENDIX B

ASSESSMENT OF EXPOSURE TO LEAD AND ARSENICFROM HOME-GROWN VEGETABLES

APPENDIX B

ASSESSMENT OF EXPOSURE TO LEAD AND ARSENICFROM HOME-GROWN VEGETABLES

Basic Equations

Exposure of residents through ingestion of home-grown garden vegetables depends on theconcentration of chemical which is taken up from soil into the vegetable and how much of thevegetable is ingested by a resident. Both these parameters vary from vegetable to vegetable.Thus, the basic dose equation is:

DIV, = E(C,,-HIF,)

where:DIV I = Daily intake of contaminant "x" from homegrown vegetables (mg/kg-d)Cj., = Concentration of contaminant "x" in vegetable type "i" (mg/kg)HIE, = Human intake factor for vegetable type "i" (kg/kg-d)

The basic equation for calculating the concentration of a chemical in a vegetable due to uptakefrom soil is as follows:

C = C - P U F*-!.« ^S r UI 1.1

where:Cs = Concentration of chemical "x" in soil (mg/kg)PUF, t = Plant uptake factor for chemical "x" into vegetable type "i"

Combining these two equations yields:

DIV, = C^

Vegetable Classes

For this analysis, vegetables are classified into four categories:

Category

Leafv vegetables

LegumesRoot vegetables

Garden fruits

Example

Lettuce, cabbageBeans

CarrotsTomatoes

Baseline Human Health Risk Assessment May 1997Documem Control Number 4500-090-AOAC Page B-lTHIS DOCUMENT WAS PREPARED BY ROY F. WESTON. INC. EXPRESSLY FOR EPA. IT SHALL NOT BE RELEASED ORDISCLOSED IN WHOLE OR IN PART WITHOUT THE EXPRESS WRITTEN PERMISSION OF EPA.

Plant Uptake Factors

Plant uptake factors (PUFs) are measured empirically by calculating the ratio of theconcentration of contaminant in the edible tissues of a plant grown to the concentration ofcontaminant in soil (mg/kg) where the plant is grown:

PUF = CVCJ/Qoijsoil

The value of PUF depends on many parameters, including the chemical of concern, the type ofvegetable, the type of soil the vegetable is grown in, and the conditions under which the plantis grown. Further, the value of PUF often depends on the concentration of the chemical in soil.That is, the concentration of chemical in plant tissue often does not increase linearly withincreases in soil concentration. Thus, values for PUFs reported in the literature may varysubstantially from report to report, usually because of differences in one or more of the variablesabove. Consequently, when more than one PUF value is available from the literature, selectingthe most appropriate value for use at a site should take into consideration the applicability of thereported data.

Two principal reports are available that provide data on PUFs:

• EPA (1992) performed a detailed review of data on plant uptake of metals as part of thedevelopment of regulations for land disposal of sewage sludge. However, many of thedata in this report deal specifically with soils amended with sewage sludge. Sludge-amended soil is typically high in organic content, and so may not be a good model formountain soils contaminated with mine wastes.

• Baes et al. (1984) reviewed a wide variety of literature reports, and provide default PUFvalues for all metals of common concern. PUF values are given for two categories ofvegetable tissue: "reproductive" and "vegetative". According to Baes el al, "vegetative"tissues (Bv) include only leafy vegetables (lettuce), while "reproductive" tissues (Br)include all other tissue types (garden fruits, roots and legumes).

Data on plant uptake factors for arsenic and lead are summarized below:

Chemical

Arsenic

Lead

Baes et al. 1984

Vegetative(Bv)

0.04

0.045

Reproductive(Br)

0.006

0.009

USEPA 1992

Leafy

0.018

--

Legumes

0.001

--

For arsenic, the data from USEPA (1992) were selected for use because the values appeared tobe based on a more thorough literature review than for Baes, and because the sources of

Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page B-2


information were better documented and justified,employed since no other data were located.

For lead, the values from Baes were

The PUF values discussed above are expressed as mg of chemical per kg dry weight ofvegetable per ppm in soil. In order to apply these data to human exposure estimates, it is mostconvenient to convert the values to a wet-weight basis. Based on data reported in EPA (1989),the average dry-weight/wet-weight ratios for these vegetable types are as follows:

Leafy (Lettuce): 0.06 gigLegumes (Beans): 0.21 gigRoots (Carrots): 0.14 gigFruits (Tomatoes): O . lOg /g

Using these conversion factors, the wet-weight adjusted PUFs for common vegetable types areas shown below:

Chemical

Arsenic

Lead

PUF (wet weight)

Leafy

1.1E-03

2.7E-03

Legumes

2.1E-04

1.9E-03

Roots

5.6E-04

1.3E-03

Fruii

l.OE-04

9.0E-04

Human Intake Factors (HIFs)

The basic equation for calculation of human intake of home-grown vegetables is:

HIF =IR, -CF

BWEF-ED

AT

where:

HIF, =IR =CF =BW =EF =ED =AT =

Human Intake Factor for vegetable type "i" (kg wet weight/kg-day)Intake rate of vegetable type "i" (g wet weight/day)Conversion factor (1E-03 kg/g)Body weight (kg)Exposure frequency of intake from home garden (days/yr)Exposure duration (years)Averaging time (days)

Baseline Human Health Risk AssessmentDocumem Control Number 4500-090-AOAC


1997

3.3

Vegetable Intake Rates

National data on the average amount of each type of vegetable ingested per day as a functionof age are available in EPA (1989). The values for children (age 2 years) and adults (age 25-30years) are shown below:

Vegetable Type

Leafy (Lettuce)

Legumes (Beans)

Roots (Carrots)

Fruits (Tomatoes)

National Average Intake(g wet weight/day)

Child (age 2 yr)

7.2

20.1

5.1

15.9

Adult (age 25-30)

39.1

41.7

12.3

49.0

Exposure Frequency to Home-Grown Vegetables

The EPA recommends the following default values for evaluation of home-grown gardenvegetable intake when site-specific data are not available:

Fraction home-grown 25% (Central tendency)40% (RME)

These home-grown fractions are equivalent to assuming an exposure frequency to home-grownvegetables of about 91 days/year (central tendency) or 146 days /year (RME).

Other Parameters

Other parameters needed to calculate human exposure via garden vegetables are the standardassumptions recommended by EPA for residents:

Parameter

BW (kg)

ED (years)

AT (Noncancer) (years)

AT (Cancer) (years)

Child

Mean

15

2

2

NA

RME

15

6

6

NA

Adult

Mean

70

9

9

70

RME

70

30

30

70

Based on these input parameters, the values of the term E(PUF-HIF) for each chemical are asshown below. For convenience, this term is referred to as the "Vegetable Intake factor" (VIF).



Population

Child

Adult

Chemical

Arsenic

Lead

Arsenic

Lead

V1F (kg/kg-day)

Average

6.01E-08

2.86E-07

4.91E-08

1.91E-07

RME

1.80E-07

8.57E-07

1.47E-07

5.73E-07

The dose from garden vegetables for each chemical "x" is then calculated as:

DI,, =C5 , -E(PUF,,-HIF i)

= Q.-VIF,

Relative Risk

The relative importance of exposure through the garden vegetable pathway can be assessed bycalculating the ratio of the ingested dose of each chemical in vegetables compared to the dosefrom ingestion of soil and dust. The default soil plus dust intake assumptions recommended byEPA for residents (EPA 1991) yield the following human intake factors:

Population

Child Resident

Adult Resident

Default Soil/Dust Intake (kg/kg-d)

Average

6.4E-06

6.8E-07

RME

1.3E-05

3.7E-06

Based on these values, the ratios of the doses from vegetables to those from soil/dust intake areshown below.

Chemical

Arsenic

Lead

Child

Avg

0.01

0.04

RME

0.01

0.07

Adult

Avg

0.07

0.28

RME

0.04

0.15

As seen, for both lead and arsenic the contribution from vegetables is a relatively small fractionof that from soil/dust intake. On this basis, it is concluded that the garden vegetable pathway

Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC pjge g-5THIS DOCUMENT WAS PREPARED BY ROY F. WESTON. INC. EXPRESSLY FOR EPA. IT SHALL NOT BE RELEASED ORDISCLOSED IN WHOLE OR IN PART WITHOUT THE EXPRESS WRITTEN PERMISSION OF EPA.

is not large enough relative to the soil/dust ingestion pathway to warrant quantification in thisrisk assessment.

References

Baes C, Sharp RD, Sjoreen AL, Shor RW. 1984. A Review and Analysis of Parameters forAssessing Transport of Environmentally Released Radionuclides Through Agriculture. Preparedby Oak Ridge National Laboratory' for the U.S. Department of Energy. ORNL-5786.

EPA. 1989. Development of Risk Methodology for Land Application and Distribution andmarketing of Municipal Sludge. U.S. Environmental Protection Agency Office of Health andEnvironmental Assessment. May 1989. EPA 600/6-89/001.

EPA. 1991. U.S. Environmental Protection Agency, Office of Solid Waste and EmergencyResponse. Human Health Evaluation Manual, Supplemental Guidance: "Standard DefaultExposure Factors". Washington, D.C. OSWER Directive 9285.6-03.

EPA. 1992. Technical Support Document for Land Application of Sewage Sludge. Volume1. Prepared for the U.S. Environmental Protection Agency by Eastern Research Group.November 1992. NTIS Document Number PB93-100575.



APPENDIX C

ESTIMATION OF LEAD BKSF

APPENDIX C

ESTIMATION OF LEAD BKSF

Introduction

Pocock et al. (1983) observed a strong correlation between blood lead level in over 7.300 adultmales and the concentration of lead in first draw water. The slope was 0.60 ug/dL per ug/L.This slope can be used to estimate the biokinetic slope factor (BKSF) for lead by dividing by theaverage absorbed dose of lead per ug/L in first draw water. However, a number of assumptionsare required to estimate the average absorbed dose. The basic equation is:

where:

C = Concentration in first draw water (C,sl) or flushed water (Cf)AF = Absorption fraction from first draw water (AFltl) or flushed water (AFr)IR = Ingestion rate of first draw water (IR,J or flushed water (IRf)

Assumptions regarding each of these parameters are discussed below.

Water Ingestion

There are no data from the Pocock study of how much water of either type (first draw orflushed) was ingested, or on the reduction in concentration in flushed water compared to firstdraw. However, based on observations at other sites (White 1995), it is probably reasonableto expect that no more than 30% of the total water ingested is first draw. Assuming a totalwater intake of 1.4 L/day. this corresponds to intakes of 0.42 L/day (first draw) and 0.98 L/day(flushed).

Concentration in Flushed Water

Pocock et al. did not report the concentration of water after flushing the pipes, but observationsat other sites suggest that the concentration of lead in flushed water is usually about 25% of thatin first draw water (White, 1995).

Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page C-l


Absorption Fraction

As discussed in the main text of this assessment, the absorption fraction for lead in adults rangesfrom about 10% (if the lead is ingested along with food) to about 35% (if the lead is ingestedafter a fast) (Rabinowitz et al. 1980). No information is available on whether the men in thePocock study ingested water with or without food, but it seems plausible to suppose that firstdraw water would be ingested early in the day, perhaps before breakfast, so an absorptionfraction of 0.3 was assumed for this water. For flushed water ingested during the remainder ofthe day, it seems reasonable to assume that this will be ingested along with food, or at leastwithin several hours of eating, so an absorption fraction of 10% was assumed for this water.

Summary and Results

The input parameters used to estimate BKSF from the data of Pocock are summarized below.

Parameter

c/c,,,dri.IR (L/day)

AF

1st Draw

1.00

(0.3)(1.4)=0.42

0.3

Flushed

0.25

(0.7)(1.4)=0.98

0.1

Based on this, the daily absorbed dose is 0.15 ug/day per ug/L in first draw water, and thecorresponding BKSF is 0.40 ug/dL per ug/day absorbed. On this basis. Region VIII feels thatthe Pocock data are consistent with a BKSF of 0.4 ug/dL per ug/day absorbed.

References

Pocock SJ, Shaper AG, Walker M, Wale CJ, Clayton B, Delves T, Lacey RF, Packham RF,Powell P. 1983. Effects of Tap Water Lead, Water Hardness, Alcohol, and Cigarettes onBlood Lead Concentration. J. Epidemiol. Commun. Health 37:1-7.

Rabinowitz MB, Wetherill GW, Kopple JD. 1980. Effect of Food Intake and Fasting onGastrointestinal Lead Absorption in Humans. Am. J. Clin. Nutrit. 33:1784-1788.

White P. Written comments provided to EPA Region VIII by Paul White, EPA ExposureAssessment Group (3/21/95)

1997Baseline Human Health Risk AssessmentDocument Control Number 4500-090-AOAC _


APPENDIX D

DETAILED CALCULATION OF EXPOSURE AND RISK

Pan 1: Concentration Data for Surface SoilPan 2: Concentration Data for Subsurface SoilPart 3: Concentration Data for Paired Soil and Dust SamplesPart 4: Exposure and Risk from ArsenicPan 5: Exposure and Risk from Lead

Appendix D

Part 1

Concentration Data for Surface Soil

APPENDIX D - PART 1

SURFACE SOIL (0-2") DATA FROM MURRAY SMELTERLOCATION EU1

ParameterhitstotalmmmaxavgUCL

SITE_CODE Location CodeEU1S-1EU1S-10EU1S-11EU1S-12EU1S-13EU1S-14EU1S-15EU1S-16EU1S-17EU1S-18EU1S-19EU1S-2EU1S-3

EU1S-5EU1S-6EU1S-7EU1S-SEU1S-9

SOIL_DEPT REMARKS0-2 in0-2 in.0-2 in.0-2 in.0-2 in0-2 in.0-2 in0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in

0-2 in.0-2 in.0-2 in.0-2 in.0-2 in0-2 in

TYPE_NAMESoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoil

Arsenic1319

2.5630130

1424

AS_TOT FLAG_85 U6

41355 U

580335 U

110550

5 U55 U

54

63095 U7

390

Lead191983

150002905

16147

PB_TOT FLAGJO280

210

5908600

110

5800

50013000

670

3700

100

170

831000

4600

130

360

300

15000

p:\brattin\murray\surfsoil.xls Page D-1-1

APPENDIX D - PART 1

SURFACE SOIL (0-2") DATA FROM MURRAY SMELTERLocation EU2

Parameterhitstotalmmmaxavg

UCL

SITE CODE Location Code 'SOIL DEPT REMARKS TYPE NAMEEU2S-1EU2S-10EU2S-11EU2S-12EU2S-13EU2S-14EU2S-15EU2S-16EU2S-17EU2S-2EU2S-3EU2S-4EU2S-5EU2S-6EU2S-7EU2S-8EU2S-9

0-2 in.0-2 in.0-2 in.0-2 in0-2 in.0-2 in0-2 in.0-2 in.0-2 in.0-2 in0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in0-2 in

SoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoil

Arsenic1317

2.536079

681

AS_TOT FLAG_824

230360

5 U5 U

70120

833345 U

1799

5 U22

25072

Lead171798

99002879

19140

PB_TOT FLAGJO180

9900

8900

98

3100

7100

290360

560340

130

270

7300

440

390

9000590

p:\bratlin\murray\surfsoil.xls Page D-1-2

APPENDIX D - PART 1

SURFACE SOIL (0-2") DATA FROM MURRAY SMELTER

Location EU3

SITE_CODE Location CodeEU3S-1EU3S-2EU3S-3EU3S-4

EU3S-5EU3S-6EU3S-7EU3S-8EU3S-9EU3S-10EU3S-11EU3S-12EU3S-13EU3S-14EU3S-15EU3S-16EU3S-17EU3S-18

SOIL_DEPT0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in0-2 in.0-2 in0-2 in.0-2 in.0-2 in.0-2 in0-2 in0-2 in0-2 in0-2 in0-2 in0-2 in

Parameter

hitstotalminmax

avg

UCL

REMARKS TYPE_NAMESoilSoilSoilSoil

WET CHEM SoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoil

Arsenic18

18

9

77001172

57840

AS_TOT FLAG_816

11

1511

9

19

49

230

19001800260029007700670

13001100100

660

Lead

18

18

74

330009548

531032

PB_TOT FLAGJO95

130

130

17074

150

520

16001700019000330002400023000260008500780059004800


APPENDIX D - PART 1


SITE_CODE Location CoaeEU4S-1EU4S-10EU4S-11EU4S-12EU4S-13EU4S-14

ELMS- 15EU4S-16EU4S-17EU4S-18EU4S-19EU4S-2EU4S-20EU4S-3EU4S-4EU4S-5EU4S-6EU4S-7EU4S-8EU4S-9

Parameter

hitstotalmm

max

avg

UCL

SOIL_DEPT REMARKS0-2 in.0-2 in0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in0-2 in.0-2 in.0-2 in0-2 in.0-2 in0-2 in.0-2 in0-2 in0-2 in.0-2 in.

TYPE_NAMESoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoil

Arsenic13

20

2.5

5400418

7618

AS_TOT FLAG_81100

5 U23

5 U5 U

104

14

5 U1100

3214

59

97

16

5 U120

5400260

5 U5 U

Lead20

20

37

1500017507623

PB_TOT FLAGJO9200

46

52

170

1600320

260

66

630

820

160

11002500230

37

160015000

770

140

92


APPENDIX D - PART 1

SURFACE SOIL (0-2-) DATA FROM MURRAY SMELTER

Location EU5

SITE_CODE Location Code

EU5S-1

EU5S-10

EU5S-11

EU5S-12

EU5S-13EU5S-14

EU5S-15

EU5S-16EU5S-17

EU5S-18

EU5S-19

EU5S-2EU5S-20

EU5S-3EU5S-4

EU5S-5

EU5S-6EU5S-7

EU5S-S

EU5S-9

Parameter

hits

total

mmmaxavgUCL

SOIL_DEPT REMARKS

0-2 in

0-2 in.

0-2 in.

0-2 in

0-2 in.

0-2 in

0-2 in.

0-2 in

0-2 in.

0-2 in.

0-2 in.

0-2 in

0-2 in.

0-2 in.

0-2 in.

0-2 in

0-2 in.

0-2 in

0-2 in.

0-2 in.

TYPE_NAME

Soil

Soil

Soil

Soil

Soil

Soil

Soil

Soil

Soil

Soil

Soil

Soil

Soil

Soil

Soil

Soil

Soil

Soil

Soil

Soil

Arsenic

1920

2.5520100285

AS_TOT FLAG_8

2124077

1005 U

140120

1654139

520100

19130100140488953

Lead

2020

110100002754

7253

PB_TOT FLAG_10

5300

39OO

1900

10000

1900

1600

3800

2000

8301100

1200

2000

2400

1108200

6206600

230280

1100


APPENDIX D - PART 1

SURFACE SOIL (0-T) DATA FROM MURRAY SMELTERLocation EU6

Parameter

hitstotalminmaxavgUCL

SITE_CODE Location Code SOIL_DEPTEU6S-1 0-2 in.EU6S-10 0-2 in.EU6S-11 0-2 in.EU6S-12 0-2 in.EU6S-13 0-2 inEU6S-14 0-2 in.EU6S-15 0-2 in.EU6S-16 0-2 in.EU6S-17 0-2 in.EU6S-18 0-2 in.EU6S-19 0-2 in.EU6S-2 0-2 in.EU6S-20 0-2 in.EU6S-3 0-2 in.EU6S-4 0-2 in.EU6S-5 0-2 in.EU6S-6 0-2 in.EU6S-7 0-2 inEU6S-8 0-2 inEU6S-9 0-2 in.

REMARKS

WET CHEM

TYPE_NAMESoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoil

Arsenic1920

2.55100432

1788

AS_TOT FLAG_851004002666

220234972

2305 U

210120012012098

7

130250170150

Lead202071

760022978717

PB_TOT FLAGJO23001000480780

6100190250270840

716100480

760049002800

150530530030002800


APPENDIX D - PART 1


Location EU7Parameter

hits

totalmmmaxavg

UCL

SITE_CODE Location Code

EU7S-1

EU7S-10EU7S-11

EU7S-12

EU7S-13EU7S-14

EU7S-15

EU7S-16EU7S-17

EU7S-18

EU7S-19

EU7S-2

EU7S-3EU7S-4

EU7S-5EU7S-6EU7S-7

EU7S-8

EU7S-9

SOIL_DEPT REMARKS

0-2 in.

0-2 in.0-2 in.

0-2 in.0-2 in.0-2 in0-2 in.0-2 in0-2 in.0-2 in.0-2 in0-2 in.0-2 in.0-2 in0-2 in.0-2 in.0-2 in0-2 in.0-2 in

TYPE_NAMESoil

SoilSoil

SoilSoil

Soil

SoilSoil

Soil

Soil

Soil

Soil

Soil

Soil

Soil

Soil

Soil

SoilSoil

Arsenic191918

22004181220

AS_TOT FLAG_8

51031

370840520470410130310500

2118

460180250220110400

2200

Lead

1919

921200025246644

PB_TOT FLAG_10

4700

92610

1400140014002800

160018006900

2202200

7400

12000

670510370580

1300


APPENDIX D - PART 1


ParameterhitstotalminmaxavgUCL

SITE_CODE Location Code SOIL_DEPTEU8-1 0-2 inEU8-10 0-2 in.EU8-2 0-2 inEU8-3 0-2 in.EU8-4 0-2 in.EU8-5 0-2 in.EU8-6 0-2 in.EU8-7 0-2 in.EU8-6 0-2 in.EU8-9 0-2 in

REMARKS TYPE_NAMESoilSoilSoilSoilSoilSoilSoilSoilSoilSoil

Arsenic101064

5000167425568

AS_TOT FLAG_873064

26003500330083068

4505000

200

Lead1010

57025000

617728783

PB_TOT FLAGJO1800570900025000740010000900230031001700


APPENDIX D - PART 1


Location EU9Parameter Arsenic Leadhits 10 10total 10 10mm 29 340max 210 2000avg 118 909UCL 222 1615

SITE_CODE Location Code SOIL_DEPT REMARKS TYPE_NAME AS_TOT FLAG_8 PB_TOT FLAGJOEU9-1 0-2 in Soil 170 880EU9-10 0-2 in. Soil 190 1600EU9-2 0-2 in. Soil 38 390EU9-3 ' 0-2 in. Soil 100 620EU9-4 0-2 in. Soil 180 590EU9-5 0-2 in. Soil 210 2000EU9-6 0-2 in Soil 100 340EU9-7 0-2 in. Soil 62 370EU9-8 0-2 in Soil 96 600EU9-9 0-2 in. Soil 29 1700

p:\brattin\murray\surtsoil.xls Page D-1-9

APPENDIX D - PART 1

SURFACE SOIL (0-7') DATA FROM MURRAY SMELTERLocation EU10

SITE_CODE Location CodeEU10-1EU10-10EU10-2EU10-3EU10-4

EU10-5EU10-6EU10-7EU10-8EU10-9

SOIL.DEPT0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in0-2 in0-2 in0-2 in.0-2 in



Arsenic9

102.5220

69383

AS_TOT FLAG_87635

22012027418437455 U

Lead1010

1501100538932

PB_TOT FLAGJO680520

1100810150300540490610180


APPENDIX D - PART 1

SURFACE SOIL (0-D DATA FROM MURRAY SMELTER

Location EU11Parameter Arsenic Lead

hits 8 10

total 10 10

mm 2.5 100

TTWX 76 5700

avg 19 814

UCL 62 1950

SITE_CODE Location Code SOIL_DEPT REMARKS TYPE_NAME AS_TOT FLAG_8 PB_TOT FLAGJO

EU11-1 0-2 in Soil 5U 5700EU11-10 0-2 in. Soil 10 ' 170

EU11-2 0-2 in. Soil 30 280

EU11-3 0-2 in. Soil 78 670

EU11-4 0-2 in. Soil 10 220

EU11-5 0-2 in. Soil 12 260

EU11-6 0-2 in. Soil 12 160

EU11-7 0-2 in. Soil 9 290

EU11-8 0-2 in Soil 27 290

EU11-9 0-2 in. Soil 5 U 100


APPENDIX D - PART 1

SURFACE SOIL (0-2") DATA FROM MURRAY SMELTERLocation IS21

SITE_CODE150W BERG150 W BERG171 WBERG171 W BERG171 W BERG174 W BERG175 WBERG175 WBERG175 W BERG179 WBERG184 W BERG248 W VINE275 W BERG275 W BERG491 3 S 300491 3 S 3005061 S 3005061 S 3005061 S 300

Location

ISZ-1ISZ-1ISZ-1ISZ-1ISZ-1ISZ-1ISZ-1ISZ-1ISZ-1ISZ-1ISZ-1ISZ-1ISZ-1ISZ-1ISZ-1ISZ-1ISZ-1ISZ-1ISZ-1


SOILJDEPT REMARKS0-2 in.0-2 in0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in0-2 in.0-2 in0-2 in.0-2 in

TYPE_NAMESoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoil

Arsenic191913

340

106222

AS_TOT FLAG_895

140

51 J4180 J4340 J456

190

290

29

230

110

13

17

13

47

14

64

57

84

Lead1919

250320012991997


21003200

76019002200550

27001500280320250

120010001100840

1100

p:\brattin\murray\surfsoil.xls PageD-1-12

APPENDIX D - PART 1

SURFACE SOIL (0-2") DATA FROM MURRAY SMELTERLocation ISZ2


Arsenic7

102.5371657

Lead101080

410241369

SITE_CODE115 E 5460166 E53005350 S HILLSIDE

LocationISZ-2ISZ-2ISZ-2

5370 S HILLSIDE ISZ-25410 S HILLSIDE ISZ-2ISZ-2-1 ISZ-2ISZ-2-2 ISZ-2ISZ-2-3 ISZ-2ISZ-2-4 ISZ-2ISZ-2-5 ISZ-2

SOIL_DEPT0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in0-2 in.0-2 in.


AS_TOT FLAG_85 U

105 U5 U

37 .272329

717 J4

PB_TOT FLAG_1019080

150190380250410230120410


APPENDIX D - PART 1

SURFACE SOIL (0-2-) DATA FROM MURRAY SMELTER

Location ISZ3Parameter Arsenic Leadhits 10 10total 10 10mm 7 110max 110 1600avg 55 768UCL 128 1757

SITE_CODE Location SOIL_DEPT REMARKS TYPE_NAME AS_TOT FLAG_8 PB_TOT FLAGJOISZ-3-1 ISZ-3 0-2 in Soil 61 890ISZ-3-10 ISZ-3 0-2 in. Soil 110 1100ISZ-3-2 ISZ-3 0-2 in. Soil 44 840ISZ-3-3 ISZ-3 0-2 in. Soil 80 1100ISZ-3-4 ISZ-3 0-2 in. Soil 100 1600ISZ-3-5 ISZ-3 0-2 in. Soil 19 230ISZ-3-6 ISZ-3 0-2 in. Soil 39 500ISZ-3-7 ISZ-3 0-2 in. Soil 7 110ISZ-3-8 ISZ-3 0-2 in. Soil 40 640ISZ-3-9 ISZ-3 0-2 in Soil 48 670

pAbrattin\murray\surfsoil.xls Page D-1-14

APPENDIX D - PART 1


SITE_CODE11 WROSE25 E WILSO26WWILSO3 E ROSE C3 E ROSE C31 WROSE31 WROSE43 E ROSE5479 S SPU5484 S SPU8E WASHIN8 E WASHIN91 WWASHI91 WWASHI5531 S SPURR

LocationISZ-4ISZ-4ISZ-4ISZ^»ISZ-4ISZ-4ISZ-4ISZ-4ISZ-4ISZ-4

ISZ-4ISZ-4ISZ-4ISZ-4ISZ-4

Parameterhitstotalmmmaxavg

UCL •

SOIL_DEPT REMARKS0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in0-2 in.0-2 in0-2 in.0-2 in.0-2 in0-2 in.0-2 in.0-2 in.0-2 in.

TYPE_NAMESoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoil

Arsenic15158

1704575

AS_TOT FLAG_8

170

6611

2821

31

24

26

33

22

97

4344

49

8

Lead15

15110780391

518

PB_TOT FLAGJO

360

780

340

350

390

410

420

440

270

110

500

620

370

330

170


APPENDIX D - PART 1

SURFACE SOIL (OrD DATA FROM MURRAY SMELTERLocation ISZ5

SITE_CODE112 W WASH112 W WASH141 AMERIC1 BOW WASH19 W HILLCREST19WHILLCREST44 W WASHI

53WAMERI53 W AMERI74 W WASHI74 W WASHI85 W AMERI89 W AMERI9 E WASHIN9E WASHIN9 E WASHIN

Location

ISZ-5ISZ-5ISZ-5ISZ-5ISZ-5ISZ-5ISZ-5ISZ-5ISZ-5ISZ-5ISZ-5ISZ-5ISZ-5ISZ-5ISZ-5ISZ-5


SOIL_DEPT REMARKS0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in

TYPE_NAMESoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoil

Arsenic16167

130

42

65

AS_TOT FLAG_813034

33

41

38

7

5834

26

28

28

3367

62

46

12

Lead16

16

130

640

426

531

PB_TOT FLAGJO440

500

360

350

360

210

480

640

360

420

460

430

560

590

520

130


APPENDIX D - PART 1


SITE_CODE1 19 W WOOD122AMERIC1 25 W 53251 37 W 53251 37 W 5325142 AMERIC190 AMERIC5365 S RIL5380 S HILLCRES72 AMERICA

93 W WOODR93 W WOODR

LocationISZ-6ISZ-6ISZ-6ISZ-6ISZ-6ISZ-6ISZ-6ISZ-6ISZ-6ISZ-6ISZ-6ISZ-6

Parameterhitstotalmm

maxavgUCL

SOIL_DEPT REMARKS0-2 in"0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in0-2 in0-2 in.0-2 in.

TYPE_NAMESoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoil

Arsenic11

122.512052

162

AS_TOT FLAG_812052

100158065272949

595 U

25

Lead1212

1201800657

1148

PB_TOT FLAG_101800460

1500270830450340710560390120450


APPENDIX D - PART 1


SITE_CODE116 WOODRO

123 W 5300

141 W5300

151 W53005310SHILLCRES ISZ-757 W 5300

64 WOODROW81 W 530090 WOODROW

97 W 5300

LocationISZ-7

ISZ-7

ISZ-7ISZ-7

ISZ-7ISZ-7

ISZ-7ISZ-7

ISZ-7

ISZ-7

SOIL_DEPT

0-2 in.0-2 in.0-2 in.0-2 in0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.0-2 in.

Parameter

hits

totalmmmaxavg

UCL

REMARKS

COMPOSITE

TYPE_NAMESoil

Soil

Soil

SoilSoil

Soil

Soil

SoilSoil

Soil

Arsenic10

1059

180126

158

AS_TOT FLAG_8

59

170

140

120

120

110

160

100

100

180

Lead1010

720180012221597

PB_TOT FLAG_10760

1600730910

1400

1100

1800

7201400

1800


APPENDIX D - PART 1



Location SOIL_DEPT REMARKS TYPE_NAMEISZ-8 0-2 in. SoilISZ-8 0-2 in. SoilISZ-8 0-2 in. SoilISZ-8 0-2 in. SoilISZ-8 0-2 in. SoilISZ-8 0-2 in. SoilISZ-8 0-2 in. SoilISZ-fl 0-2 in. SoilISZ-8 0-2 in. SoilISZ-8 0-2 in. SoilISZ-8 0-2 in SoilISZ-8 0-2 in. ' Soil

SITE_CODE249 W VINE5125 S 3005135 S 3005135 S 3005139S 3005139 S 3005201 S 300ISZ-8-1ISZ-8-2ISZ-8-3ISZ-S^JISZ-8-5

Arsenic7

122.5450

762117

AS_TOT FLAG_8450677546

220355 U5 U5 U5 U5 U8

Lead121266

730010625877


1200870

110077066

120140110100120


Appendix D

Part 2

Concentration Data for Subsurface Soil

APPENDIX D -- PART 2

LEAD CONCENTRATIONS IN ON-SITE SUBSURFACE SOIL AT MURRAY SMELTER

Ar9a':.:-;:::i-;:-:-:;:-:';:-?

CommercialZone

•;-«uvs*1

2456

7

CODE- •;••';.•EU1-1EU1-2EU2-1EU4-1EU5-1EU6-1EU6-2EU6-3EU6-4EU6-5EU6-6EU6-7EU6-8EU6-9EU6-10EU6-1 1EU6-12EU6-13EU6-14EU6-15EU6-16EU6-17EU6-18EU6-19EU7-1EU7-2EU7-3EU7-4

v-;.;::;::0'l:ft'-180050

1000032009963

240039009208500780051007281808403100400

2200030040002100310820850011000630020002300

•;;:.-;-•;: -^2 ft6500590

100004800

6179

1300180073

400044041002100180087012003800110970022000280012001100023001200010003900570

,-::•: : .:: 2-3 ft ;12000140001000015026074796882

47002600580

1100012026001506406779260320077011087

99002407072

...v-;:3-4'ft:

1500092006690628315084

910078460

11000621202701800768691220578192

140007413076

; ••:• 4^5 ft

16000820066600731009794769290

19000681201107073821002408885100

12000639275

ResidentialTrailerDarks

;.«??eU:v?:::

8

9

10

Code.: : '•• : :-:;B.-;j: :;: • : : : O^j - '. 2-6"}:: : r ' -6ii2>|:ir:hv: r!l:2*18"EU8-2 9000 3400 3500' 3000EU8-10 570 920 1100- 520EU9-3 620 170' 75! 96EU9-10 1600 6500 5800: 40000EU10-6 540 560 530. 530EU10-8 610 1200: 670' 430

p:\brattm\murray\subsoil.xls Page D-2-1


ARSENIC CONCENTRATIONS IN ON-SITE SUBSURFACE SOIL AT MURRAY SMELTER

Ar«8- - '::" -''^'.vCommercial

• > . : -EHN:;ii

Zone24

56

7

Cod*-:- 'H:::

EU1-1EU1-2EU2-1EU4-1

EU5-1EU6-1

EU6-2EU6-3EU6-4

EU6-5EU6-6EU6-7EU6-8EU6-9EU6-10EU6-11EU6-12EU6-13EU6-14

EU6-15EU6-16EU6-17

EU6-18EU6-19EU7-1EU7-2EU7-3EU7-4

::;:'.:'.0-t.fr::'::

295

3205

11

83

280092012064

64095

167

69

440

2702700

15590

1000310

80

48000120

42002400

34000

.-.-<.: -:1T2: ft ;.!v59

340

6205

120

7600300

10

26028

1700

480300150

662600

25

120018001200

24001500

1000033

730

370014000

; - : - -2*3f t - ' : :35

1000270

41

4676

470014

16

650310

813800

281600

9

8705

527

1100900

7

120140140

25490

•^••- 3-4 ft ;•::"

1000130

63

55

200023

31180

874

22008

9017

220013

1510

33

1207

22

618

150380

- 4-6 ft

1500300

62

56

20600

1377

569

36005

220

1627

2117

9

36

19018

83

510

200360

ResidentialTrailerparks

:S£U.::::K|:-::::;Code.;-!F O '*jirf • : • • • ' • • '• • •-. <% A«* I--. .;.. ^ ••^•Mfi-1 \ • • • • .:'.;:;.:•: Z*6--.:j !:':•.: . • • ' iVi :":6--1-2*- 12-18"

8 EU8-2 2600 7200 6300 6200;EU8-10 64: i 10! 200 . 130'

9 EU9-3 100' 14i 19 131

EU9-10 190; 1200' 880' 7500!10 EU10-6 84: 140 140' 110!

EU10-8 45: 130! 120: 831

p:\brattin\murray\subsoil.xls Page D-2-2


SUBSURFACE DATA FROM OFF-SITE LOCATIONS

Murray Smelter

ARSENIC CONCENTRATION (poml SUMMARY STATISTICS

ArBai::;S::;;::':;:.;

ISZ-lISZ-1ISZ-2ISZ-2ISZ-3ISZ-3ISZ-4ISZ-4

ISZ-5ISZ-5ISZ-6ISZ-6ISZ-7

ISZ-7ISZ-8ISZ-8

---s-;:':-:S!SITE:>COD£-;:::;:::':171 W BERG275 W BERG5410 S HILLSIDEISZ-2-1ISZ-3-10ISZ-3-4

5479 S SPU8 E WASHIN44 W WASHI

89 W AMERI122 AMERIC93 W WOODR151 W 530081 W 5300249 W VINEISZ-8-2

.'....• :-:"::<h2i|li

51173727

1 10100

3397

5867

525

120

100450

5

--!".• .:::-:.2*-iri120

185350

320120

3612044

1106132

160

210260

1 1

;•;;:; ™;-:;-8yl2::!n230

2292

110290110

18150

79

1207054

120200240

18

:*•:•:;. :-*2*1 8**4944

17041

61053

687

100675249

86480

54

15

!::•:-:•;:-: ;:-:i.;;-Avs!;-v- -Mm69 17

Mai

230

73 27 170

214 53 610

68 6 150

81 44 120

47 5 70

185 86 480

132 5 450

LEAD CONCENTRATION (ppml SUMMARY STATISTICSocation Cad

ISZ-1ISZ-1ISZ-2ISZ-2ISZ-3ISZ-3ISZ-4ISZ-4

ISZ-5ISZ-5ISZ-6ISZ-6I S Z - 7ISZ-7

ISZ-8ISZ-8

?•;*•• ••SSITESCODE*':**-:171 W BERG275 W BERG5410 S HILLSIDEISZ-2-1ISZ-3-10ISZ-3-4

5479 S SPU8 E WASHIN44 W WASHI

89 W AMERI122 AMERIC93 W WOODR151 W 530081 W 5300249 W VINEISZ-8-2

;:;,;:; Stt2;.|n: :•:?:;::•:790320380250

1 1001600

270500480560

460120910720

7300140

:•;:: '2^6 th-.-i1300

240380210

1500

970280640360530440330900

1400

4400

140

:; 6-12-iri-;:----:1800

300310700

1600

680120710440510

440410

1000

1300

2800190

--:-12ii8::«:K420320420150

320015087

290470230370420610

2800550190

(,,,:,.,,,Av8|::..- Ufa

334 240

.•;-:•:::•::••:-: Max

420

1089 150 3200

520 87 1600

486i 2901 710

443i 230i 560

588i 120 1000

2659: 550 7300

165 140 190

p:\brattin\murray\subsoil.xls Page D-2-3

Appendix D

Part 3

Paired Soil and Dust Samples


SOIL DUST RELATIONSHIP AT MURRAY SMELTERArsenic

Index Location1 171 W. Berger2 174W. Berger3 5135 S 300 W.4 5370 Hillside

. 5 5410 Hillside6 HillcrestJHS7 91 W. Washington8 5479 Spurrier9 8 E. Washington

10 25 E Wilson11 275 W. Berger12 89 W American13 44 W Washington14 5380 S. Hillcrest15 190 W. American16 93 W. Woodrow17 74 W. Washington18 Murray HS19 151W. 5300S20 123W. 5300 S21 64 Woodrow22 81 W 5300 S

Nondetects shown by shaded cells:

MeanStdev

Raw loll data: nonxietects evaluated at 1/2 detection Nrntt (6 ppm)

515675

3727443397661767584927

2861120170160100

1807446

2349

43

13

2844

29 17 38

51 80 100 39 40 48

MeanCone (ppm)

Soil (0-2)1155650605

2 537023546533070.066015067058049.02702 5

280522

1200170016001000

622459

Dust - Raw d43232913

SitlSi'S-112

18*1394231324271928242449471551

Raw data; NO eval at 1/2 DL (10 ppm)

12

18 29 18

MeanCone(ppm)

Dust432329135

125

11.5139423

1252427192824

222549471551

26820 1

file = c:\qpw\murray\soildust.wb1


SOIL DUST RELATIONSHIP AT MURRAY SMELTERLead

LeadIndex Location1 171 W. Berger2 174W Berger3 5135 S 300 W4 5370 Hillside5 54 10 Hillside6 Hillcrest JHS7 91 W. Washington8 5479 Spurrier9 8 E. Washington

10 25 E. Wilson1 1 275 W. Berger12 89 W American13 44 W Washington14 5380 S. Hillcrest15 190W. American16 93 W Woodrow17 74 W. Washington18 Murray HS19 151 W 5300 S20 123 W 5300 S21 64 Woodrow22 81 W 5300 S

MeanStdev

Raw toll790760

1200190380250370270500780320560480560340120420890910

16001800720

data21001000870

410330

620

250

460840

230 120 410 440

850 1100 1600 500 110 640 670

MeanCone, (ppm)

Soil (0-2)14458801035190380310350270560780285560480560340120440

) 80091016001800720

673458

Raw data In Dust - Lead42620367614910121520392 74199

5315508257 143232256219216178221 207 219757522276496

310

MeanCone, (ppm)

Dust426203676149101215203

83199

5315 Outlier508200232256219216178239757522276496

530 (with outlier)1084 (with outlier)

303 (without outlier)186 (without outlier)

file = c:\qpw\murray\soildust.wb1

APPENDIX D- -PART 3

REGRESSION ANALYSIS

ARSENIC

Regression Output:Constant 16.39StdErrofYEst 19.08R Squared 0.15No. of Observations 22Degrees of Freedom 20

X Coefficient(s) 0.168Std Err of Coef. 0.091

LEAD

Regression Output:ConstantStd Err of Y EstR SquaredNo. of ObservationsDegrees of Freedom

X Coefficient(s)Std Err of Coef.

(Excludes outlier)97.98

143.590.56

96

0.3180.121

SUMMARY STATISTICS

ArsenicLeadLead

N222221

Mean27530303

Min58383

Max94

5315 <-- Note: includes outlier757 <-- Note: excludes outlier

file: c:\murray\soildust.wb1

Appendix D

Part 4

Exposure and Risk from Arsenic

APPENDIX D - PART 4

MURRAY SMELTER - CALCULATION OF EXPOSURE AND RISK FROM ARSENIC

CONCENTRATION DATA FOR ARSENIC IN SURFACE SOIL (ppm)

LocationEU-1EU-2EU-3EU-4EU-5EU-6EU-7EU-8EU-9EU-10EU-11IS2-1ISZ-2ISZ-3ISZ-4ISZ-5ISZ-6ISZ-7ISZ-8

Max630360

77005400

520510022005000

210220

78340

37110170130120180450

Avg13079

1172418100432418

16741186919

1061655454252

12676

' UCL1424681

578407618

28517881220

2556822238362

22257

1287565

162158

2117

EPC630 (max)360 (max)

7700 (max)5400 (max)

285178812205000 (max)

210 (max)220 (max)

62222

37 (max)110 (max)7565

120 (max)158450 (max)

CONCENTRATION DATA FOR ARSENIC IN SLAG (ppm)Composite 591

CONCENTRATION DATA FOR ARSENIC IN GROUNDWATER (mg/L)

Aquifer

Shallow

Intermediate

Well ID

GW-1GW-2JMM-08MW-100MW-101MW-102MW-103MW-104MW-105MW-106MW-107MW-108MW-109MW-110MW-111MW-112UTBN-1Well 1Well 2Well 3

GW-1 AGW-1ARGW-2AMW-101DMW-104DMW-105DMW-108DMW-109DMW-112D

TOTALCone Qual

1.2872.87

0.0780.005 U0.006

0.01840.27

0.0060.01327.180.005 U0.005 U0.0142.3472.9030.052

0.270.2161.9740.236

0.790.0060.4390.005 U0.0190.0250.005 U0.0690.039

Adj

1.2872.87

00780.00250.006

00184027

0006001327.18

000250.00250.0142.3472.9030.052

0.270.2161.9740.236

. 0.790.0060439

0.00250.0190.025

0.00250.0690.039

DISSOLVEDCone Qual

1.5342.9940.05

0.005 U0.005 U0.0120.1810.0060.01228.930005 U0.005 U0.0212.3442.8610.0450.2580.28

1.9380.207

0.6360.005 U0.3110.005 U0.014

0.020.005 U0.0440.038

Adj

1.5342.994

0.050.00250.00250.0120.18100060.01228.93

0.00250.00250.0212.3442.8610.0450.2580.28

1.9380.207

0.6360.00250.311

0.00250.0140.02

0.00250.0440.038

p:\brattin\murray\as-risk.xls Page D-4-1

APPENDIX D-PART 4


Oral Toxicity factorsRfDs RfDc oSF

Arsenic 6.0E-03 3.0E-04 1.5

Bioavailability factorsSoil Dust Slag

Arsenic 0.26 0.26 0.45

Soil/Dust RelationshipDO Ksd

Arsenic 10 0.20


APPENDIX D - PART 4


HUMAN EXPOSURE PARAMETERS AND HIFs

ScenarioIngestion ofsoil ana dust

Soil + Dust

Soil

Dust

ScenarioIngestion ofslag by teen(age 12-18)

ScenarioIngestion ofGrounowater

ParameterIR (mg/d) total as childIR (mg/d) total as adultFraction soilBW (kg) as childBW (kg) as adultEF(d/yr)ED (yr) as childED (yr) as adultED (y) totalAT (chronic)AT (lifetime)

cHIFsIHIFs

cHIFsIHIFs

cHIFdIHIFd

ParameterIR (mg/d)BW (kg)EF(d/yr)ED (yr)AT (chronic)AT (lifetime)

cHIFgIHIFg

ParameterIR (L/d)BW(kg)EF(d/yr)ED (yr)AT (chronic)AT (lifetime)

cHIFwIHIFw

AVERAGE SCENARIOResident

10050

0.451570

23427

99

70

1.31 E-061.68E-07

5.88E-077.56E-08

7 18E-079.23E-08

Teen505725

7

7

70

6.01E-086.01 E-09

Resident1.4

70

234

9

970

1.28E-021.65E-03

NCI-Worker

500.5

70219

55

. 570

4.29E-073.06E-08

2.14E-071.53E-OB

2.14E-071 53E-08

Worker0.770

21955

70

600E-034.29E-04

Cl-Worker

2401.0

70185

555

70

1.74E-061.24E-07

1.74E-061.24E-07

O.OOE+00O.OOE+00

RME SCENARIOResident NCI-Worker

20050100

0.451570

3506

24303070

3.65E-061.57E-06

1.64E-067.05E-07

2.01 E-068.61 E-07

0.5

70250

25252570

4.89E-071.75E-07

2.45E-078.74E-08

2.45E-078.74E-08

Teen1005750

77

70

2.40E-072.40E-08

Resident2

70350

303070

2.74E-021 17E-02

Worker1

70250

252570

9.78E-033.49E-03

Cl-Woreer

4801.0

70211

25252570

3.96E-061.42E-06

3.96E-061 42E-06

O.OOE+00O.OOE+00

p:\brattin\murray\as-risk.xls Page

APPEt.,.,,> PART 4

MURRAY .LTER -- CALCULATION OF EXPOSURE AND RISK FROM ARSENIC

MEDIUM: SURFACE SOIL AND OUSTPOPULATION: RESIDENTS

Chronic Exposure (Noncincer Risk) Bated on EPC (UCL or Max)

ExposureLocationEU-8

EU 9

EU-10

EU-11

ISZ-1

ISZ-2ISZ-3ISZ-4

ISZ-5ISZ-6ISZ 7ISZ 8

ConeEPC

5000

210

220

62

222

37

110

75

65120158

450

HIFs588E 07588E-07

5 88E-0758BE 07588E-07588E-07S88E-075 88E -07588E-075 B8E-0758BE-07S88E-07

HIFd7 18E-07

7 18E 07

7 18E-077 18E-07

7 18E-077 18E-077 18E-077 18E-077 18E-077 18E-077 18E 077 18E 07

RBAs026

026

026

026

0 26

0.26

026

026

026026

0 26026

RBAd

026

026

026

026

026

026

026

026

0260 26026

026

Average

DO

10

10

1010

to10

1010

10

10

to10

Ksd

020

020

020

020

020

020

020020

020

0 20020020

Dlsd9 5E 04

4 2E-054 4E-051 4E 05

4 4E-0589E 06

23E-051 6E-05t 4E-0525E 0532E-058 7E-05

cRfD30E-0430E 04

30E-0430E 04

30E-04

3 OE 04

3 OE-043 OE-0430E 04

30E 0430E 0430E 04

HQsd3E«00IE 01

1E-01

5E 02

1E-01

3E028E-025E-025E-02BE 021E 013E 01

Lifetime Exposure (Cancer Risk)

ExposureLocationEU 6

EU9

EU-10

EU-11

ISZ-1

ISZ-2ISZ-3

ISZ -4

ISZ-5

ISZ-8ISZ-7ISZ-8

ConeEPC

5000

210

220

62

222

37

110

75

65

120

158

450

HIFs7 56E 08

7 56E-08

7 56E-087 56E-08

7 56E-08

7 56E 08

7 56E-087 56E-08

7 56E-08

7 56E-087 56E-087 56E-08

HIFd

923E-OB

9 23E OB

9 23E-08

923E-OB923E 08

923E 08

9 23E-089 23E-08

9 23E-08

9 23E-089 23E-089 23E-08

RBAs

026

026

026

026

026

026

026

026

026

026

026

026

RBAd

026

026

026

026

026

026

026

0.26

026

026

0 26

026

AverageDO

10

to10

10

10

to10

10

10

10

10

10

Ksd

020

020

020

020

020

020

020

020

020

020

020020

Dlsd

t :E 045 4 E 0 65 6E-06

1 7E-065 7E 06

1 1E-08

2 9E-06

2 1E-06

1 BE-06

3 2E 06

4 1E-06

1 1E-05

oSF

1 5E'00

t 5E'001 5E»00

1 5E'00 -1 5E'00

1 SE'OO1 SE'OO

1 SE'OO1 SE'OO

1 SE'OO1 SE'OO

1 SE'OO

Risk

2E-04

BE 06

BE 063E 06

8E-062E 06

4E 06

3E-063E-06

5E-066E-062E-05

ConeEPC

5000210

220

62

22237

11075

65

120158450

ConeEPC

5000210

220

62

222

37

110

75

65

120

158

450

HIFs164E061 64E-06

164E 06

1 64E-061 64E-06

1 64E 06

1 64E-061 64E 06

1 64E-061 64E-061 64E-061 64E-06

HIFs7 05E-07

7.05E-077 05E-07

705E 077.05E 07

705E 07

705E-07705E-07

7.05E-07

705E-07705E-07705E 07

HIFd201E06201E-06201E-06201E-06

201E-06201E-06

201E-06201E-06201E-06201E-06201E-06201E-06

HIFd861E 07

861E 07

861E-07B61E 07

861E-07

B61E 07

B61E-07861E 07

861E-07

861E-07861E07

861E-07

RBAs026

026

026

026

028

026

026

026

026026026

026

RBAs

026

026

026

026

026

026

026

026

026

026

026

0.26

RME

RBAd026

0.26

026

026

026

026

028

0.26

026

026026026

RME

RBAd026

026

026

0.26

026

028

026

0.26

026

026

026

026

DO

1010

10

10

10

10

10

1010

101010

DO

10

10

to10

to10

10

10

10

10

to10

Kid

020020

020

020

020

0.20

020

020020

0.20

020020

Kid

020

020

020

020

020

020

020

020

020

020

020

020

Dlsd27E-031 2E-04

1 2E-043 BE-051 2E-04

2 5E-0584E 05

4 5E-0540E-056 BE-0589E-052 4E-04

Dlsd

1 1E-03

50E05

5 2E-051 6E 05

53E 05

1 IE 05

2 7E-051 9E-05

1 7E-053 OE-053 BE-051 OE 04

cRfD3.0E 04

30E 0430E-04

3 OE-043 OE-043 OE-043 OE 04

3 OE-043 OE-043 OE-043 OE-0430E-04

oSF

1 5E«00

1 SE'OO

1 5E»001 5E«001 5E«001 SE'OO

1 5E»00

1 5E«001 SE'OO

1 SE'OO1 SE'OO1 SE'OO

HQsd9E»004E 01

4E 01

1E-01

4E 01

BE 02

2E 012E 01

1E-012E01

3E-018E-01

Risk

2E-03

8E 05

8E-OS2E05

BE 05

2E 05

4E05

3E-053E-05

4E-056E052E-04

p \brattinVnurrayVas-risk.xl! PageD-4-4

APPEND PART 4

MURRA> ..TER - CALCULATION OF EXPOSURE AND RISK FROM ARSENIC

MEDIUM: SURFACE SOIL AND DUSTPOPULATION: NCI-WORKER

Chronic Eiposure (Noncancer Risk) Based on EPC (UCL or Man)

Eiposure Cone AverageLocationEU-1

EU-2

EU3EU-4

EU-5

EU-8

EU-7

EPC630

36077005400

2851788

1220

HIFs2 14E-072 14E-072 14E-072 14E-072 14E-072 14E-072 14E-07

HIFd2 14E 072 14E-072 14E-072.14E-07

2.14E-072 14E-072 14E-07

RBAs026026

026026

026026

026

RBAd026026

026026

026026

026

DO1010

1010

10to10

Ksd020

020020

020020

020

020

Dlsd43E

2 5 E

52E36E

20E1 2E

82E

050504

04

0504

05

cRfD3 OE-0430E 04

30E-043.0E-043 OE 04

3 OE-043 OE 04

HQsdIE 01BE-022E«001E»007E-024E-01

3E-01

Llfetlms Exposure (Cancer Risk)

EiposureLocationEU-1

EU2EU 3EU4

EU 5

EU-6

EU-7

MEDIUM:

ConeEPC630

36077005400

285

1788

1220

POPULATION:

HIFs53E-08

53E0853E 0853E 0853E 08

53E0853E 08

SURFACE

HIFd1 53E-08

1 53E 0853E OB53E 08

53E 0853E-0853E-OB

RBAs026

0260260260 26

026

026

RBAd026

026026026

026

026

026

AverageDO10

• 101010

10

10

10

Ksd

020020

0200 200 20

020

020

Dlsd30E

1 BE3 7E26E1 4E

B6E

0606

050506

06

5 9E-06

oSF

SE'OO5E»005E»005E»00SE'OO5E»005E»00

Risk5E-063E-066E-054E-OS2E-06

IE 05

9E-06

SOIL AND DUSTCI-WORKER

Chronic Exposure (Noncancer Risk)


EU-2

EU-3

EU-4

EU-5

EU6EU-7

ConeEPC630

36077005400285

1788

1220

HIFs1 74E-061 74E-061 74E-061 74E-061 74E-061 74E-061 74E 06

HIFdOOOE*00O.OOE*00OOOE'OOOOOE'OOO.OOE'OOOOOE»00OOOE«00

RBAs026

0.26

026026

026

026

026

RBAd0.26

026026

026

026

026026

AverageDO10to10

10

1010

10

Ksd020

0 20020

020

020

020020

Dlsd28E 041 6E-0435E

24E

1 3E

B IE

5 5E

030304

04

04

cRfD3 OE-0430E-043 OE-043 OE-0430E 04

3 OE-043 OE-04

HOsd9E-015E-01

1E+01

BE+004E-01

3E»002E*00



EU-2

EU-3

EU-4

EU-5

EU6EU-7

ConeEPC630

360

77005400

285

1788

1220

HIFs1 24E-07

1 24E 07

1 24E 071 24E-071 24E-071 24E-07

1 24E-07

HIFd

OOOE»00OOOE»00OOOE'OO0 OOE«00

OOOE»000 DOE « 00

OOOE'OO

RBAs026

026

026

026

026

026

026

RBAd026

026

026

026

026

026

026

AverageDO10

10

to10

10

10

10

Ksd

020

0 20

020

020

020

020

020

Dlsd20E

1 2E

2 5E

1 7E

92E

5 BE

39E

05

05

04

04

06

05

05

oSF

5E»00SE'OO5E*00

SE'OO

SE'OO

SE'OO5E»00

Risk

3E-052E-054E-O4

3E-04

1E-05

9E-05

6E 05

ConeEPC630

36077005400

285

1788

1220

ConeEPC

630

36077005400285

1788

1220

ConeEPC

630360

77005400

285

1788

1220

ConeEPC

630

360

7700

5400

285

1788

1220

HIFs245E-072 45E-07245E-07245E-072.45E072.45E-072 45E-07

HIFs

8 74E 08B.74E 088 74E 088 74E 088 74E-OB8 74E-088 74E-08

HIFs396E 083 96E 083 96E 06

3 96E 06

3 96E-063 96E 06

3 96E-06

HIFs1 42E 06

1 42E 06

1 42E 06

1 42E 06

1 42E-06

1 42E 06

1 42E-06

HIFd245E07245E-07245E-07245E-072 45E-072.45E-07245E-07

HIFd8 74E-088 74E 08B74E 088 74E 08

8 74E-088 74E-088 74E-08

HIFd0 OOE'OOOOOE'OOOOOE«000 OOE*00OOOE'OOOOOE'OO

0 OOE«00

HIFdOOOE'OOOOOE'OOOOOE'OO

OOOE'OO

OOOE'OO

OOOE'OOOOOE'OO

RBAs026026026

026026

028

026

RBAs026

026026026

028

026026

RBAs028026026

028

026

026

026

RBAs028

026

026

026

026

026

026

RMERBAd

026026

026

0.26

026

026026

RMERBAd

026

026026026

026026

026

RME

RBAd026026026

026

026

026

026

RME

RBAd026

026

026

026

026

026

026

DO101010

101010

10

DO

1010

101010

10

10

DO

10101010

10

10

10

DO

10

10

10

10

10

10

10

Ksd020020020020

0200.20

020

Ksd020020

020020020

020

020

Ksd

020020020

020

020

020

020

Ksd

020

020

020

020

020

020

020

Dlsd4 9E-052.8E-055.9E-044 1E-04

2 2E-051 4E-0494E05

Olsd1.7E-051 OE-052 1E-041 5E-048 OE-06

49E-053.3E-05

Dtsd65E 04

37E-0479E-0356E-032 9E-04

1 BE 03

1 3E-03

Dlsd2 3E-04

1 3E 04

2BE-03

20E-03

1 OE 0466E04

4 5E-04

cRID3 OE-0430E 043 OE-0430E-0430E0430E043 OE 04

oSF

1 SE'OO1 5E«001 5E»001 SE'OO1 SE'OO1 SE'OO1 5E»00

cRID3 OE-043 OE-043 OE 043 OE-04

3 OE-04

3 OE 04

3 OEM

oSF

1 SE'OO1. SE'OO

1 SE'OO

1 SE'OO

1 SE'OO

1 SE'OO1 SE'OO

HQsd2E01

9E 022E'001E«007E 025E01

3E 01

Risk

3E-052E053E 042E 04IE 057E 055E05

HQsd

2E*001E«003E+012E»011E«008E*004E»00

Risk

3E^4

2E-044E-033E-032E-041E-037E-04

p \braltirt\murray\as-nsk.xls Page D-4-5

ENW*rAPPENfPPfr> -PART 4

MURR, jMELTER -- CALCULATION OF EXPOSURE AND RISK FROM JENIC

MEDIUM:POPULATION:

SLAGTEEN (Age 12-18)


Exposure Cone AverageLocation EPC HIFslag RBAslag Dlsd cRfD HQsdAll 591 6.01 E-08 045 1.6E-05 3.0E-04 5E-02

Cone RMEEPC HIFslag RBAslag Dlsd cRfD HQsd591 240E-07 045 6.4E-05 3 OE-04 2E-01


Exposure Cone AverageLocation EPC HIFslag RBAslag Dlsd oSF RiskAll 591 6.01E-09 0.45 1.6E-06 1.5E+00 2E-06

Cone RMEEPC HIFslag RBAslag Dlsd oSF Risk591 240E-08 0.45 6.4E-06 1 5E+00 1E-05


MURR>

APPEND^ i" - PART 4

jMELTER -- CALCULATION OF EXPOSURE AND RISK FROM JENIC

MEDIUM: GROUNDWATERPOPULATION: RESIDENTS


AquiferDepthShallow

Intermediate

Lifetime

AquiferDepthShallow

Intermediate

WellIDMW-100MW-101MW-102MW-103MW-104MW-106MW-101DMW-104D

WellIDMW-100MW-101MW-102MW-103MW-104MW-106MW-101 DMW-104D

As Conemg/L

000250.006

001840.27

0.00627 18

000250019

As Conemg/L

0.00250006

0.0184027

000627 18

000250019

AveragecHIF

1.28E-021 28E-021 28E-021.28E-021 28E-021.28E-021 28E-021.28E-02

cDI3.2E-057.7E-052.4E-043 5E-037.7E-053.5E-013.2E-052.4E-04

cRfD3.0E-0430E-043.0E-043.0E-0430E-043.0E-0430E-0430E-04

HQ1E-013E-018E-011E+013E-OV1E+031E-018E-01

AverageIHIF

1.65E-031.65E-031.65E-031.65E-03165E-031.65E-031.65E-031.65E-03

IDI4.1E-069.9E-063.0E-054.5E-0499E-064.5E-024.1E-063.1E-05

oSF1.51.51.51.51.51.51.51.5

Risk6E-061E-055E-057E-041E-057E-026E-065E-05

cHIF274E-02274E-02274E-022.74E-022 74E-022 74E-02274E-022 74E-02

cHIF1.17E-021.17E-021 17E-021.17E-021 17E-021 17E-021.17E-021 17E-02

RMEcDI

6 8E-051 6E-0450E-047.4E-031 6E-047.4E-0168E-0552E-04

RMEIDI

2.9E-0570E-052.2E-0432E-037.0E-053.2E-012.9E-0522E-04

cRfD3.0E-0430E-043.0E-043.0E-0430E-0430E-0430E-043.0E-04

oSF1.5151.51.51.5

•1.51.51 5

HQ2E-015E-012E+002E+015E-012E+032E-012E+00

Risk4E-051E-043E-04,5E-031E-044E-014E-053E-04

On-site well, used to assess on-site residents


MURRAY. .ER - CALCULATION OF EXPOSURE AND RISK FROM ARSENIC

MEDIUM: GROUNDWATERPOPULATION: WORKERS

Chronic Exposure (Noncancer Rltk)

AquiferDepthShallow

Intermediate

Lifetime

AquiferDepthShallow

Intermediate

WellID

MW-102MW 105MW-106MW-107MW-108MW-109MW-110MW-111MW-112GW-1GW-2Well 1Well 2Well]UTBN-tMW-1050MW-10SDMW-1090MW-I12DGW-1 AGW-1ARGW-2A

WellID

MW-102MW-105MW-106MW-107MW-108MW-109

MW-110MW-111MW-112GW-1GW-2Well 1Well 2Well 3UTBN-1MW-105DMW-1080MW-109DMW-112DGW-1 AGW-1ARGW-2A

At Conemg/L

00184001327 18

0002500025

00142347

290300521 287287

02161 9740236027

00250002500690039079

00060439

A» Conemg/L

001840013

27 180002500025

0.014

2347290300521 287

2.87

0216

1 974

0236027

00250002500690039079

00060439

AvtrageCHIP

6 DOE -03600E-036 OOE-036 OOE-036 OOE-036 OOE-036 OOE-036 OOE-036 OOE-036 OOE-036 OOE-036 OOE-036 OOE-036 OOE-036 OOE 036 OOE-036 OOE-036 OOE-036 OOE-036 OOE-036 OOE-036 OOE-03

cDI

1 1E-04

/ BE 051 6E-011 SE-OS1 5E-05B 4E-051 4E-021 7E-023 1E-047 7E-031 7E-021 3E-031 2E-021 4E-031 6E-031.5E-041 SE-054 IE-CM2 3E-044 7E-0336E-052 6E-03

cRfD3 OE-0430E043 OE-043 OE-043.0E-043 OE-043 OE-043 OE-043 OE-043 OE-043 OE-043 OE-043 OE-043 OE-043 OE-043 OE-043 OE-043 OE-043 OE-043 OE-043 OE-043 OE-04

HO4E-01

3E 01

5E«025E-025E-023E-01

5EKM6E+011E«003E+016E«O14E«OO4E+015E»005E»005E-015E-021E*00BE Ot

2E»OI1E-01

9E*00

CHIP978E-039 7BE-039 7BE-039 7BE-039 7BE-039 78E-039 78E-03

9 78E-03978E-039 78E-039 78E-039 78E-039 78E-039 78E-039 78E-039 78E 039 7BE-039 78E-039 7BE-039 78E-039 78E-039 76E-03

AverageIHIF

4 29E-044.29E-044 29E-044.29E-044.29E-04429E-044 29E-044 29E-044.29E-044.29E-044 29E-044.29E-04429E-044 29E-044 29E-044 29E-044 29E-044 29E-044 29E-044 29E-044.29E-044.29E-04

101

7 9E-0656E-061 2E-021 1E 061 1E-066 OE-061 OE 031 2E-032 2E-055 5E-041 2E-039 3E-058 SE-041 OE-041 2E-041 IE 05

1 1E-063 OE-051 7E-0534E-04

2.6E-061 9E-04

oSF

1 51 51 51 51 51 5

1 51 5

1.51 5

1 5

151.51.51 5

1 5

1 5

1.51.51 5

1 5

1 5

RlikIE-OS8E-062E-022E-062E-069E-062E-032E-033E-05BE-042E-031E-041E-032E-042E-042E-052E-064E-053E-05SE-044E-063E-04

cHIF349E-03349E-03349E-033 49E 033 49E-03349E 033 49E-033 49E-033 49E-033 49E-033 49E-033 49E-033 49E-033 49E-033 49E-033 49E-033 49E-033 49E-033 49E-03349E-033 49E-033 49E-03

RME

cDI

1 8E-041 3E-042 7E-0124E 0524E-051.4E-04

2 3E-022 8E-025 1E-04

1 3E-022 8E-022 1E-031 9E-022 3E-032 6E-032 4E-0424E-056 8E 043 8E-047 7E-035 9E-054 3E-03

RME

IDI

64E-054 5E-0595E 028 7E-0687E-064 9E-0582E-031 OE-021 8E-044 5E-031 OE-027 5E-046 9E-038 2E-049 4E-04

8 7E-058 7E-062 4E-041 4E-042 8E-032 IE-OS1 SE-03

cRfD3 OE-043 OE-043 OE-043 OE-043 OE-043.0E-043 OE-043 OE-043 OE-043 OE-043 OE-043 OE-043 OE-043 OE-043 OE-043 OE-043 OE-043 OE-043 OE-043 OE-043 OE-043 OE-04

oSF

1 51 51 S1 515

1 5

1 5

1 S1 S1 S1 5

1 51 S

1.5

15

15

1 51.5

1.5

1.5

1 S

15

HQ

6E-014E-01

9E+02BE-028E-025E-01

8E+01»E»012E+004E»01SE+017E+006E+01BE+009E»008E-018E-02

2E+001E*003E+012E-01

1E+01

RlekIE -04

7E-051E-011E-05IE-OS7E-051E-022E-023E-047E-031E-021E-03

1E-021E-031E-031E-04

IE-OS4E-042E-04

4E-033E-052E-03

p \brittin\murray\ai-risk.ids Page D-4-8

ApPt^Brrn .. PART 4

MURRA -TER - CALCULATION OF EXPOSURE AND RISK FROM ARSENIC

MEDIUM: SURFACE SOIL AND OUSTPOPULATION: RESIDENTS

Chronic Exposure (Noncancer Risk) Bated on Average Concentrations

E»posureLocationEU8

EU-9

EU-10EU-11

IS2-1

ISZ-2IS2-3ISZ-4 •

ISZ-5ISZ-6ISZ-7IS2-8

ConeMean167«

116

69

19

106

1655

45

42

52

12876

HIFs5 88E-07

588E 075 88E-07588E07588E-07588E-07568E-07588E-0758BE-07588E-07588E-07588E-07

HIFd7 18E-07

7 18E-077 18E-077.18E-077 1BE 077 18E-07

7 18E-077 18E 077 18E-077 18E-077 1BE 077 1BE-07

RBAa

026

026

026

026

026

026

026

026

026

026

026026

RBAd026

026

026

026

026

026

026

026

026

026

026026

Average

DO

10

10

10

to10

10

toto10

toto10

Ksd

020

020

020

020

020

0 20020

020

020

020

020

020

Dlsd32E 0424E 051 SE 055 SE 062 2E-054 9E 061 2E-051 OE 059 9E-061 2E-0526E 051 6E-05

cRfD30E-043 OE-04

3 OE-043 OE-043 OE-043 OE-043 OE-04

3 OE-043 OE-043 OE-043 OE-043 OE-04

HQsd1E»00

8E-02SE 022E-02

7E-022E 024E-023E 023E 024E-029E 025E-02

Lltetlm* Exposure (Cancer Risk)


EU-9

EU-10

EU-11IS2-1

ISZ-2

ISZ-3ISZ-4

ISZ-5ISZ-6ISZ-7ISZ-8

ConeMean1674

118

69

19

106

16

55

45

42

52

126

76

HIFi

7 56E-087 56E-08

7 56E 087 S6E-087 56E-087 56E-08

7 56E-08

7.56E-087 56E-08

7 56E-087 56E-087.56E-OB

HIFd9 23E-OB923E-OB

923E-089 23E-OB923E-089 23E 089 23E-08

9 23E-08

9 23E-08

9.23E-089.23E-089 23E-08

RBA«

026

026

026

026

026

026

026

026

026

026

026026

RBAd026026

026

026

026

026

026

026

026

026

026

026

AverageDO10

10

10

10toto10

10

10

10

10

10

Ksd

020

020

020

020

020

020

020

020

020

020

020

020

Dlsd4 IE-OS3 1E-061 9E-06! 1E-0728E 066 3E-07

1 6E-061 3E 061 3E-06

1 5E-063 3E-062 1E-06

oSF

1 5E»001 SE'OO1 SE'OO

1 5E«001 5E»001 5E»001 5E»001 5E»00

1. SE'OO

1 5E*001 5E«001.5E»00

Risk6E-055E-063E06

1E-064E 069E 072E-06

2E-06

2E-062E 065E-063E-06

ConeMean1674118

69

19

106

16

55

45

42

52128

76

ConeMean1674

118

69

19

106

16

55

45

42

52

126

76

HIFs1 64E-061 64E-06

1 64E-061 64E 061 64E 061 64E 061 64E-06

1 64E 061 64E-06

1 64E-061 64E-061 64E-06

HIFs7 05E-077 05E 07705E-07

7 OSE-077 05E 077 05E-07

7 05E 07705E07

7.05E-07

7 05E-07

705E-077 05E-07

HIFd2.01E-062.01E-06

201E-06201E-06201E-06201E-06

201E082.01E-06

201E-06201E-062.01E-06201E06

HIFd8.61E-07861E-07

861E-07

861E-07881E-07861E-07B.61E-07

861E-07

861E-07881E-07

861E-07881E-07

RBAs026

028

026

026

026

026

026

026

026

026

026

0.28

RBAs026

026

026

026

026

026

026

026

026

0.26026

026

RME

RBAd026

026

026

026

026

026

026

026

026

026

026028

RMERBAd

026

026

026

026

028028

028

026

026

026

026

026

DO

10

10

10

1010

10

10

10

10

10

10

10

DO

1010

10

1010

10

10

10

to10

10

10

Ksd

020

020

020

020020

020

020

020

020

020

020

020

Ksd020

020

020

020020

020

020

0.20020

020

020

020

Dlsd9 OE-04

68E-054 2E 051 5E 056 2E-OS1 4E-0534E-OS

2 BE-052 8E-053 3E 0572E-054 6E-05

Dlsd3 BE 042 9E-051 8E-0566E-06

2 6E-055.8E-061 5E-05

1 2E-051 2E 051 4E-053 1E 0520E-05

cRfDJ OE-04) OE-04

JOE 04)OE 045 OE 04i.OE-04

3 OE 043 OE-0430E 043 OE-043 OE-0430E 04

oSF5E*005E»005E»005E«005E»005E«005E«00

5E«00

5E*00

5E*005E»005E»00

HQsd3E»002E 011E-01SE 022E 015E 02IE 011E-019E-02IE 012E 012E-01

Risk8E-044E 053E 051E-054E 059E 062E-05

2E05

2E-05

2E055E053E05

p \brattin\murray\as-nik2 xls Page D-4-9

ApppJK; n .. PART 4

MURRAY .TER - CALCULATION OF EXPOSURE AND RISK FROM ARSENIC

MEDIUM: SURFACE SOIL AND DUSTPOPULATION: NCI-WORKER

Chronic Eiposure (Noncincer Risk) Based on Average Concentrations

EiposureLocationEU-1EU-2EU-3EU-4EU-5EU-6EU-7

ConeMean

13079

1172418100432418

2222222

HIFi14E-0714E-0714E-0714E-0714E-0714E-07

.14E-07

HIFd2 14E-072 14E 072 14E-072 14E-072 14E-072 14E 072 14E-07

RBAs026026026026026026026

RBAd026026026026026026026

AverageDO10101010101010

Ksd020020020020020020020

Dlsd92E 0659E 067 9E 052BE-057 2E-0629E-0529E-05

cRfD3 OE-043 OE 0430E 043 OE-043 OE-043 OE 043 OE-04

HQsd3E-022E 023E-019E-022E-021E 011E-01

Lifetime Eipoiure (Cincer Risk)

EiposureLocationEU-1EU-2EU-3EU-4EU 5EU-8EU-7

MEDIUM:

ConeMean

13079

1172418100432418

1111111

HIFs53E-0853E-0853E-OB53E-OB53E OB53E-0853E 08

SURFACEPOPULATION:

HIFd1 53E-081 53E 081 53E-081 53E-OB1 53E 081 53E-081 53E 08

RBAs0260260260260260 260 26

RBAd026026026026026026026

AverageDO1010101010io10

Ksd0200200200200200 20020

Dlsd66E-0742E-075 6E-062 OE-065 2E-072 1E-0620E 06

oSF1 5E»001 5E»001 5E«001 SE'OO1 5E»001 SE'OO1 5E«00

Risk1E-0666-07BE 063E-06BE -073E 063E 06

SOIL AND DUSTCI-WORKER

Chronic Eiposure (Noncancer Risk)

EiposureLocationEU-1EU-2EU-3EU-4EU-5EU-6EU-7

ConeMean

13079

1172418100432418

HIFs74E-0674E-0674E-0674E-0674E-0674E-0674E-06

HIFdOOOE+00OOOE'OOOOOE*00OOOE'OOOOOE»00OOOE + 00OOOE'OO

RBAs026026026026026026026

RBAd026026026026026026026

AverageDO10101010101010

Ksd020020020020020020020

Dlsd5.9E-053 6E 0553E 041 9E 044 5E-0520E-041 9E 04

CRfD30E-0430E-043 OE-043 OE 0430E 043 OE-043 OE-04

HQsd2E-011E-01

2E+006E-01IE 017E-016E-01


ExposureLocationEU-1EU-2EU-3EU-4EU-5EU-6EU-7

ConeMean

13079

1172418100432418

11

HIFs24E-0724E-0724E-0724E-0724E-0724E-0724E-07

HIFdOOOE'OOOOOE'OO0 OOE»00OOOE'OOOOOE*00OOOE»00OOOE*00

RBAs028026026026026026026

RBAd026026026026026026026

AverageDO10101010101010

Ksd020020020020020020020

Dlsd4 2E-0626E-063BE-051 3E-053 2E 061 4E-051 3E 05

oSF1 5E»001 5E»001 5E*001 5E«001 5E*001 5E*001 5E«00

Risk6E-064E-066E 052E-055E-062E-052E-05

ConeMean

13079

1172418100432418

ConeMean

13079

1172418100432418

ConeMean

13079

1172418100432418

ConeMean

13079

1172418100432418

HIFs245E-07245E-07245E-07245E-072 45E-072 45E-072 45E-07

HIFs8 74E-088 74E-088 74E 088 74E-08B74E-OB8 74E-088 74E 08

HIFs396E-083 96E-06396E-063 96E-06396E-06396E-06396E-06

HIFs1 42E-061 42E-061 42E 061 42E-061 42E-061 42E 061 42E 06

HIFd2.45E-07245E 07245E 07245E-07245E-07245E-072 45E-07

HIFd8 74E-088 74E-088 74E-088 74E-088 74E-OB8 74E-088 74E 08

HIFdOOOE*00OOOE'OOOOOE'OOOOOE'OO0 OOE»000 OOE'OOOOOE'OO

HIFd0 OOE»00OOOE'OOOOOE'OOOOOE'OOOOOE'OOOOOE'OOOOOE'OO

RBAs026026026026026026026

RBAs026026026026026026026

RBAs026026026026026026026

RBAs026026026026026026028

RMERBAd

0260260260260260260.26

RMERBAd

026026028026026026026

RMERBAd

0280.28026026026026026

RMERBAd

026026026026026026026

DO10101010101010

DO10101010101010

DO10101010101010

DO10101010101010

Ksd0200200200200200.200.20

Ksd0200200200200200.20020

Ksd0200200200.200.20020020

Ksd020020020020020020020

Dlsd1 IE-OS6 7E-0690E-OS33E-058.2E-0634E-053 3E-05

Dlsd38E-062 4E 0832E 051 2E-0529E-061 2E 051 2E 05

Olsd1 3E-048 2E-051 2E-034 3E-041 OE-044 5E-044 3E-04

Dlsd4 BE 052 9E-054 3E-041 5E-0437E-051 6E-041 5E 04

cRfD3 OE-043 OE-043 OE-0430E 0430E 043 OE-043 OE-04

oSF1 5E*001 5E«00

5E<005E*005E<005E«005E>00

CRfD30E-0430E043 OE-043 OE-0430E 0430E 043 OE-04

oSF1 5E«00

5E»005E«005E«005E«005E«005E»00

HQsd4E-022E-023E-011E01

3E-021E-011E-01

Risk6E-064E 065E 052E-054E-062E052E 05

HQsd4E-013E-01

4E*001E*00.3E-011E«001E»00

Risk7E 054E-056E-042E-O45E-052E-042E-04

p VbraninVnurray\as-risk2 xls PageD-4-10

Appendix D

Parts

Exposure and Risk from Lead

APPENDIX D - PART 5

CALCULATION OF BLOOD LEAD LEVELS IN RESIDENT CHILDRENAT MURRAY SMELTER

Calculation of PbB performed using IEUBK model (LEAD 0.99d)

EVALUATION OF RISK FROM SOIL AND DUST

Parameter Value UnitsDO 90 ppmKsd 0.35 ppm per ppmGSD 1.4 -RBA 70%ABA 35%

From IEUBKLocation Soil (ppm) Dust (ppm) GM 95th P10EU-8 6177 2252 28.6 50 >99%EU-9 909 408 8.1 14 26%EU-10 538 278 5.6 10 4.0%EU-11 814 375 7.5 13 19%IZS-1 1299 545 10.4 18 53%ISZ-2 241 174 3.4 5.9 0.1%ISZ-3 768 359 7.2 13 15%ISZ-4 391 227 4.6 8.0 0.9%

•ISZ-5 426 239 4.8 8 1.4%ISZ-6 657 320 6.5 11 9%ISZ-7 1222 518 10.0 17 48%ISZ-8 1062 462 9.0 16 37%

EVALUATION OF RISK FROM WATERAssume Cw = 10 ug/L

Baseline (no H2O) With Water Inc. from WaterCsoil Cdust GM P10(%) GM P10(%) GM P10(%)

500 265 6.0 6.2 6.6 10.2 0.6 4.01000 440 9.4 40.9 10.0 47.8 0.6 6.9

File = p:\brattin\murray\sitewide\riskcalc\childpb.wb1

APPENDIX D - PART 5

CALCULATION OF BLOOD LEAD LEVELS IN NON-CONTACT INTENSIVE WORKERSAT MURRAY SMELTER

EVALUATION OF RISK FROM SOIL/DUST

Bas/c equations:PbB(GM) = PbBO + BKSF*(Cs*IRs*EFs/365*AFs+Cd*IRd*EFd/365*AFd)PbB(GM) = PbBO + BKSF*(Cs*A+Cd*B)95th = PbB(GM)*GSDA1.645

Parameter Value UnitsPbBO(GM) 2.3 ug/dLBKSF 0.4 ug/dL per ug/dayIRs 25 mg/dayEFs 219 days/yrAFs 0.07 -DO 90 ppmKsd 0.35 ppm per ppmIRd 25 mg/dayEFd 219 d/yrAFd 0.07 -GSD 1.54

A 1.05E-03B 1.05E-03

LOCATION Cs Cd GM 95th PM1.1EU-1 2905 1107 3.98 8.11 0.9%EU-2 2879 1098 3.97 8.08 0.9%EU-3 9548 3432 7.75 15.77 20.3%EU^ 1750 703 3.33 6.78 0.3%EU-5 2754 1054 3.90 7.93 0.8%EU-6 2297 894 3.64 7.41 0.5%EU-7 2524 973 3.77 7.67 0.6%

PRG 5497 2014 545 11.10 5.0%

EVALUATION OF RISK FROM WATER

Basic equation. (PbB -PbBO)=BKSF*(CWIRw'EFw/365*AFw)

BKSF 0.4 ug/dL per ug/dayCw 1 ug/LIR 0.7 L/dEF 219 d/yrAF 0.1

Delta PbB 0.017 ug/dL per ug/L

File = p:Vbrattin\murray\sitewide\nskcalc\adultpbb.wb1

APPENDIX D - PART 5

CALCULATION OF BLOOD LEAD LEVELS IN CONTACT-INTENSIVE WORKERSAT MURRAY SMELTER

EVALUATION OF RISK FROM SOIL/DUST

Basic equations:PbB(GM) = PbBO + BKSF*(Cs*IRs*EFs/365*AFs+Cd*IRd*EFd/365*AFd)PbB(GM) = PbBO + BKSF*(Cs*A+Cd*B)95th = PbB(GM)*GSDA1.645

Parameter Value UnitsPbBO (GM) 2.3 ug/dLBKSF 0.4 ug/dL per ug/dayIRs 240 mg/dayEFs 185 days/yrAFs 0.07 -DO 90 ppmKsd 0.35 ppm per ppmIRd 0 mg/dayEFd 185 d/yrAFd 0.07 -GSD 1.54

A 8.52E-03B O.OOE+00

LOCATIONEU-1EU-2EU-3EU-4EU-5EU-6EU-7

PRG 927 414 5.46 11.10 5.0

EVALUATION OF RISK FROM WATER

Basic equation: (PbB -PbBO)=BKSF*(Cw*IRWEFw/365*AFw)

BKSF 0.4 ug/dL per ug/dayCw 1 ug/LIR 0.7 L/dEF 219 d/yrAF 0.1

Delta PbB 0.017 ug/dL per ug/L

File = p:\brattin\murray\sitewide\riskcalc\adultpbb.wb1

Cs2905287995481750275422972524

Cd1107109834327031054894973

GM12.1912.1134.828.2611.6810.1210.90

95th24.8124.6370.8516.8123.7620.6022.17

P>11.158.658.099.624.754.741.648.3

APPENDIX D - PART 5

CALCULATION OF BLOOD LEAD LEVELS IN TEENAGERSAT MURRAY SMELTER

EVALUATION OF RISK FROM SLAG EXPOSURE

Basic equations:PbB(GM) = PbBO + BKSF*(Cslag'IRslag*EFslag/365*AFslag)PbB(GM) = PbBO + BKSF*(Cs*A+Cd*B)95th = PbB(GM)*GSDA1.645

Parameter Value UnitsPbBO(GM) 1.6 ug/dLBKSF 0.4 ug/dL per ug/dayIRslag 50 mg/dayEFslag 25 days/yrAFslag 0.053 -GSD 1.54

A 1.82E-04B

LOCATION Cslag GM 95th P>11.1All 11500 2.43 4.95 0.02

APPENDIX E

SCREENING LEVEL EVALUATION OF RELATIVE RISK FROMINHALATION OF DUST AND DERMAL CONTACT WITH SOIL OR WATER

APPENDIX E

SCREENING LEVEL EVALUATION OF RELATIVE RISK FROMINHALATION OF DUST AND DERMAL CONTACT WITH SOIL OR WATER

1.0 EXPOSURE VIA INHALATION OF PARTICIPATES IN AIRf

The basic equation recommended by EPA (1989a) for evaluation of inhalation exposure is:

DIair = Ca • BR, • EF • ED/(BW • AT)where:

DIair = Daily intake from air (mg/kg-d)Ca = Concentration of substance in air (mg/m3)BR, = Breathing rate of air (nrVday)EF = Exposure frequency (days/yr)ED = Exposure duration (yrs)BW = Body weight (kg)AT = Averaging time (days)

Recommended data defaults are as summarized below.

Parameter

BR

EF

ED

BW

AT

Source Documents

RAGS (EPA 1989b)

RAGS Supplemental Guidance (EPA 1991)

RAGS Supplemental Guidance (EPA 1991)

RAGS (EPA 1989b)

RAGS (EPA 1989b)RAGS Supplemental Guidance (EPA 1991)

Typical RME Values forResidential Adulf

20 mVday

350 days/yr

30 years

70 kg

30 years (noncancer)70 years (cancer)

The relative magnitude of the inhaled dose of arsenic and lead from air can be compared to theincested dose from soil as follows:

CS-IRS

Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page E-lTHIS DOCUMENT WAS PREPARED BY ROY F. WESTON. INC. EXPRESSLY FOR EPA IT SHALL NOT BE RELEASED ORDISCLOSED IN WHOLE OR IN PART WITHOUT THE EXPRESS WRITTEN PERMISSION OF EPA.

where:

DI^, = Daily intake from air (mg/kg-d)Ca = Concentration of substance in air (mg/m3)BR., = Breathing rate of air (mVday)Cs = Concentration in soilIR, = Ingestion rate of soil (kg/day)

The EPA recommends a screening level soil to air transfer factor of 2E-10 kg/m3 (EPA 1991a)and a soil ingestion rate by adults of 100 mg/day (1E-04 kg/day) (EPA 1991b). Based on thesevalues, the ratio of the mass of soil inhaled to that ingested is:

DI __ 2£-10*g/m3 .20m> f day __ 4£_Q5

DI, 1E-04 kg/day

As seen, the inhaled dose of soil is very small compared to the ingested dose, so the inhalationpathway is not considered to be of significant concern at this site.

2.0 DERMAL EXPOSURE VIA WATER

The basic equation recommended by EPA (1989a, 1992) for evaluation of dermal exposure towater based on this model is:

ADU. = Cw • SA • PC • t • EF • ED/(BW • AT)

where:

ADU = Absorbed dose from water (mg/kg-d)Cw = Concentration of chemical in water (mg/cm3)SA = Surface area exposed (cm2)PC = Chemical-specific permeability constant (cm/hr)t = Exposure time (hi/event)EF = Exposure frequency (days/yr)ED = Exposure duration (yrs)BW = Body weight (kg)AT = Averaging time (days)

Recommended data defaults are as summarized below.

Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page £.2THIS DOCUMENT WAS PREPARED BY ROY F. WESTON, INC. EXPRESSLY FOR EPA. IT SHALL NOT BE RELEASED ORDISCLOSED IN WHOLE OR IN PART WITHOUT THE EXPRESS WRITTEN PERMISSION OF EPA.

Parameter

SA

PC

(

EF

ED

BW

AT

Source Documents

Dermal Exposure Guidance (EPA 1992)Exposure Factors Handbook (EPA 1989a)

Dermal Exposure Guidance (EPA 1992)

RAGS (EPA 1989b)Exposure Factors Handbook (EPA 1989a)Dermal Exposure Guidance (EPA 1992)

Dermal Exposure Guidance (EPA 1992)RAGS Supplemental Guidance (EPA 1991)

Dermal Exposure Guidance (EPA 1992)RAGS Supplemental Guidance (EPA 1991)



Typical RME Values forResidential Adult1

20.000 cnr

Chemical specific

12 minutes

350 days/yr

30 years

70kg

30 years (noncancer)70 years (cancer)

' Values shown are for the bathing/showering pathway. Other values may be applicable for scenarios such as wadingor swimming.

For a residential population exposed to water-borne contaminants by both ingestion and dermalcontact via the showering/bathing scenario, the relative magnitude of the absorbed dosefollowing dermal exposure to water (ADd) and oral (ingestion) exposure (AD0) to water is givenbv:

ADSA-PC- lIR-AF.

where:

SA = Surface area exposed (cnr)PC = Chemical-specific permeability constant (cm/hr)t = Exposure time (hr/day)IR^ = Ingestion rate of water (cnvVday)AF0 = Oral absorption fraction

Incorporating representative values for the whole-body surface area of an adult (20,000 cm2) andfor time spent bathing or showering (0.2 hr), and assuming a water ingestion rate of 2 L/day(2.000 cnrVday), yields the following:



paee

AD.AD,

2-PC~AF~

For lead and arsenic, measured and recommended default values of AF0 and PC are listedbelow, along with the calculated ratio of absorbed doses (ADd/AD0):

Chemical

Lead

Arsenic

PC (cm/hr)

' 4E-06'

1E-03"

AF0

0.10°

Iff

ADa/AD0

8E-05

2E-03

• Measured value (USEPA 1992)" USEPA (1992) recommends a default value of 1E-03 cm/hr for inorganics for which data are not available1 Owen (1990)

As seen, the ratio of dermal to oral absorbed dose is quite small for both lead (0.08%) andarsenic (0.2%). Based on this, it is concluded that the dose contributed by the dermal pathwayis likely to be sufficiently minor compared to the ingestion pathway that it need not be quantifiedfor the residential population.

3.0 DERMAL EXPOSURE VIA SOIL

The basic equation recommended for estimation of dermal dose from contact with soils is asfollows (EPA 1989b, 1992):

ADS01| = Cs • SA • AF • ABS • EF • ED/(BW • AT)

where:

C5 = concentration of chemical in soil (mg/kg)

SA = surface area in contact with soil (cm2)AF = soil adherence factor (kg/cm:)ABS = absorption fraction (unitless)

At the present time, data are very limited on the value of the ABS term, and the EPA (1992)has concluded that there are only three chemicals for which sufficient data exist to estimatecredible ABS values, as shown below:

1997Baseline Human Health Risk Assessment .Document Control Number 4500-090-AOAC


Chemical

Dioxms

PCBs

Cadmium

ABS

0.1-3%

0.6-6%

0.1-1%

It is important to realize that even these values are rather uncertain, due to a variety ofdifferences between the exposure conditions used in laboratory studies of dermal absorption andexposure conditions that are likely to occur at Superfund sites. For example, most laboratorystudies use much higher soil loadings on the skin (e.g., 5-50 mg/cm2) than are expected to occurat sites (0.2-1 mg/cm2). Also, most studies investigate the amount absorbed after a relativelylengthy contact period (16-96 hours), while it is expected that most people would wash off soilon the skin more promptly than this. Because of these difficulties in extrapolation fromexperimental measurements to "real-life" conditions, the values above are only consideredapproximate, and are more likely to be high than low. With respect to estimating ABS valuesfor other chemicals (those for which there are no reliable experimental measurements), the EPAconcludes that current methods are not sufficiently developed to calculate values from availabledata such as physical-chemical properties.

If values of ABS were available for lead and arsenic, the relative magnitude of the dermal doseto the oral dose would be calculated as follows:

ADd

~AD~_

SA-AF-ABS-EF

where:

SAAFABS

AF

EF0

surface area in contact with soil (cm2)soil adherence factor (kg/cnr)absorption fraction (unitless)Ingestion rate of water (cm'/day)Oral absorption fractionDermal exposure frequency (days/yr)Dermal exposure frequency (days/yr)

Assuming that 10% of the body area (2,000 cm2) is covered with soil (1 mg/cm: = 1E-06kg/cnr) for 50 days/yr, the ratio of the predicted dermal absorbed dose to the oral absorbed doseis given by:

Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page E-5


-AD,

-=

ABS

If, by extrapolation from cadmium, ABS is assumed to be 0.1-1 % for lead and arsenic, then theratio of dermal dose from soil to oral dose from soil are as follows:

Chemical

Arsenic

Lead

ABS(assumed)

0.001-0.01

0.001-0.01

AFo

1

0.1

Dose Ralio(dermal/oral)

0.3-3%

3-28%

Because the value of ABS is not available for lead or arsenic, these values should not beconsidered to be reliable. However, this calculation does support the conclusion that dermalabsorption of lead and arsenic from dermal contact with soil is likely to be relatively minorcompared to the oral pathway, and omission of this pathway is not likely to lead to a substantialunderestimate of exposure or risk.

Baseline Human Health Risk AssessmentDocument Control Number 4500-090-AOACTHIS DOCUMENT WAS PREPARED BY ROY F. WESTON. INC. EXPRESSLY FOR EPA. IT SHALL NOT BE RELEASED ORDISCLOSED IN WHOLE OR IN PART WITHOUT THE EXPRESS WRITTEN PERMISSION OF EPA.

page

4.0 REFERENCES

EPA. 1989a. Exposure Factors Handbook. Office of Health and Environmental Assessment,Washington, DC. EPA/600/8-89/043.

EPA. 1989b. Risk Assessment Guidance for Superfund. Volume I: Human Health EvaluationManual Part A. Interim Final. Office of Solid Waste and Emergency Response (OSWER),Washington, DC. OSWER Directive 9285.701A.

EPA. 199la. Risk Assessment Guidance for Superfund. Volume I: Human Health EvaluationManual (Part B, Development of Risk-Based Preliminary Remediation Goals). Interim. Officeof Research and Development, Washington, DC EPA/540/R-92-003.

EPA. 19915. "Standard Default Exposure Factors." Supplemental Guidance for Risk AssessmentGuidance for Superfund, Volume I: Human Health Evaluation Manual. OERR, Washington, DC.OSWER Directive 9285.6-03.

EPA. 1992. Dermal Exposure Assessment: Principles and Applications. Interim Report. Officeof Research and Development, Washington, DC. EPA/600/8-91/01 IB.

Owen BA. 1990. Literature-derived Absorption Coefficients for 39 Chemicals via Oral andInhalation Routes of Exposure. Reg. Toxicol. Pharmacol. 11:237-252.

Baseline Human Health Risk Assessment May 1997Document Conuol Number 4500-090-AOAC Page E-7


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