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Home My WebLink AboutDERR-2024-008632BASELINE HUMAN HEALTH RISKASSESSMENT FOR THEMURRAY SMELTER SUPERFUND SITE SITE-WIDE EVALUATION May 1997 Prepared for: U.S. Environmental Protection AgencyRegion VIEOne Denver Place999 18th Street, Suite 500Denver, 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 TABLE OF CONTENTS Section Title 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 ................................. 3-33.2.1 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 Cottonwood Creek ............ 3-43.2.8 Exposure to Groundwater ......................... 3-53.2.9 Summary of Pathways of Principal Concern .............. 3-53.3 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) ...................... 3-123.3.3.1 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 ............. 3-193.3.4 Dose Calculations .............................. 3-203.4 Evaluation of Exposure to Lead .......................... 3-203.4.1 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 Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page iiTHIS 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 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 ................... 5-45.2 Evaluation of Risks from Lead .......................... 5-65.2.1 Health Risks from Lead to Residential Children ........... 5-65.2.1.1 Risks to Children from Lead in Soil and Dust ...... 5-75.2.1.2 Risks to Children from Lead in Groundwater ...... 5-95.2.2 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 hi Groundwater ...... 5-115.2.3 Risks to Teenagers from Ingestion of Lead hi 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 Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page iiiTHIS 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 OF CONTENTS (Continued) 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 LeadExposure 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 Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page ivTHIS 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 OF CONTENTS (Continued) 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 1997Document Control Number 4500-090-AOAC Page vTHIS 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. LIST OF ACRONYMS AND ABBREVIATIONS ABA Absolute BioavailabilityAF Absorption FractionAT Averaging timeBDL Below Detection LimitBKSF Biokinetic Slope FactorBW Body weightC Concentration of a chemical in an environmental mediumCI Contact-intensive •CDC 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 parts 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 BioavailabilityRfD Reference DoseRME Reasonable Maximum ExposureSF Cancer Slope FactorTWA Time-weighted AverageUCL Upper Confidence Limit of the Meanug/kg Micrograms per kilogramXRF X-Ray fluorescence Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page viTHIS 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. 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 hi 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-facility, both exposed at the surface andcovered by fill and by buildings. Land Use Following closure of Murray Smelter hi 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-facility 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, andGrand view, located along the southern border of the facility). An area hi 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 pan of the on-facility 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 converted to non-residential uses. Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page ES-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. 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 fGroundwater 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 hi 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-facility 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 Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page ES-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. V_^- 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 concentration\~s patterns 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 mamobservations: • 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 hi 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 hinearly all EUs. The lowest average on-facility levels are observed hi the eastern Baseline Human Health Risk Assessment May 1997Document Control Number 4500090-AOAC Page ES-3THIS 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. Color Map(s) The following maps contain color thatdoes not appear in the scanned images.To view the actual images pleasecontact the Superfund Record Centerat (303) 312-6473. BASEUNE RISK ASSESSMENT FIGURE ES-1 SITE MAP 215 Union BoulevardSuite 600Lokewood. 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 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 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 nichesvs 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:Arsenic:C(dust) = 98 ppm + 0.32-C(soil)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 part (17%-32%) from yard soil. Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page ES-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. 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 hi the shallow alluvial aquifer. The highly variablepattern of groundwater contamination, especially hi 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 ah* 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 hi these solid wastes may have caused secondary contamination of the surroundingenvironment by several pathways, including wind erosion of fine dust particles into ah-, 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 Baseline Human Health Risk Assessment May 1997Document Control Number 450WJ90-AOAC Page ES-6THIS 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. 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 then-personal 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 hi 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 ES-7THIS 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. The long-term average daily intake of arsenic that produces these noncancer effects varies fromperson to person. In a large epidemiological 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 hi 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)r'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 hi 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 hi 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 hi 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 Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page ES-8THIS 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. 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 sort 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 (EU8 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 part of the Grandview Trailer Park area, there are no residencescurrently in this EU. Cancer risks to residents mainly range between 1 and 80 Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page ES-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 ES-1 RISKS FROM ARSENIC IN SURFACE SOIL AND DUST ExposedPopulation Area Noncancer HQ Average*RME1 Estimated Cancer Risk (per million) Average1 RME» Residents EU-8 1 60EU-9 0.08 0.1 0.2 0.4EU-10 0.05 0.1 0.1 0.4EU-11 0.02 0.05 0.05 0.1ISZ-1 0.07 0.1 0.2 0.4 ISZ-2 0.02 0.03 0.05 0.08 0.9ISZ-3 0.04 0.08 0.1 0.2ISZ-4 0.03 0.05 0.1 0.2ISZ-5 0.03 0.05 0.09 0.1ISZ-6 0.04 0.08 0.1 0.2ISZ-7 0.09 0.1 0.2 0.31SZ-8 0.05 0.3 0.2 0.8 20 40 8030801020408020 20 402030 20 302040506030 Non-ContactIntensiveWorker EU-1 0.03 0.1 0.04 0.2EU-2 0.02 0.08 0.02 0.09 0.6 EU-3 0.3 0.3 60EU-4 0.09 0.1 40 EU-5 0.02 0.07 0.03 0.07 0.8 EU-6 0.1 0.4 0.1 0.5 10EU-7 0.1 0.3 0.1 0.3 30205020 1020702050 Contact-IntensiveWorker EU-1 0.2 0.9 0.4 30EU-2 0.1 0.5 0.3 20EU-3 60 7040 EU-4 0.6 20EU-5 0.1 0.4 0.3 10 50EU-6 0.7 20 90EU-7 0.6 20 60 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-10THIS 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. 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) iftthe 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 hi slag are summarized below: RiskParameter Chronic HQCancer Risk (per million) Estimated ValueAverage 0.022 RME 0.210 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 w Population Resident Worker Location On-facility Off-facility Off-facility On-facility On-facility AquiferDepth WellID Shallow Shallow Intermediate Shallow Intermediate MW-1001 MW-101"MW-102MW-103MW-104MW-106MW-101DMW-104DMW-102MW-105MW-106MW-107MW-108MW-109MW-110MW-lll"MW-112GW-1GW-2WelllWell 2Well 3h UTBN-1MW-105DMW-108DMW-109DMW-112DGW-1AGW-1ARGW-2A Noncancer HQ Average 0.10.30.8 0.3 0.10.80.40.3-- - 0.050.050.3 0.50.05 0.8 0.1 RME 0.20.5 0.5 0.2 0.60.4 0.080.080.5 0.80.08 0.2 Estimated Cancer Risk(per million)Average 1050 10 5010 30 100 20 4030 RME 40100 100 40 10070 101070 iii 10010 30 Shaded cells indicate wells where risks from arsenic exceed typical EPA guidelines (HQ > 1, cancer risk > 100 per million) • Well located in an up-gradient 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 hi 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 lOug/dL is quite high (e.g., >99% atEU-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-8EU-9EU-10EU-11ISZ-1ISZ-2ISZ-3ISZ-4ISZ-5ISZ-6ISZ-7ISZ-8 EU-1EU-2EU-3EU-4EU-5EU-6EU-7 EU-1EU-2EU-3EU-4EU-5EU-6EU-7 Mean LeadConcentration (ppm) 6177909538814129924176839142665712221062 2905 287995481750275422972524 2905287995481750275422972524 Risk of Exceeding TargetBlood Lead Level 4.C 0.1% 0.9%1.4 0.9%0.9% 0.3%0.8%0.5%0.6% Shaded cells indicated locations where calculated risks exceed the target (5%) Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page ES-14THIS 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. 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 hi children at thissite, but the number of children is too small to be certain. • For non-contact intensive workers, risks from lead hi 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 hi slag was evaluated using the Bowersmodel. The results are summarized below: Baseline(No slag)GM (ug/dL) 1.6 Pll.l' <0.01% IncludingSlag Exposure* GM (ug/dL) 2.4 Pll.l 0.02% IncrementDue to SlagGM (ug/dL) 0.8 Pll.l <0.02% GM = Geometric mean blood lead (ug/dL)* Pll.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 hi slag is not likely to be of significant health concern. Risks from Lead hi Groundwater Under typical circumstances, the expected increment hi geometric mean blood lead by a childage 0-84 months is about 0.05-0.06 ug/dL per ug/L of lead hi water. Nearly all wells locatedhi residential areas have lead concentrations less than 10 ug/L, corresponding to increments higeometric mean blood lead of less than 0.5-0.6 ug/dL. This increment is sufficiently small, Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page ES-15THIS 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. 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-intensive 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 hi the extent of absorption (bioavailability) of lead and arsenic fromsoil and slag • Uncertainty in key input parameters used hi the mathematical models forevaluating lead exposure of children and adults, as well as uncertainty in theaccuracy of the models themselves • Uncertainty hi 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 rA 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). History 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, suiter 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 (Monroc), atelecommunications facility (STS), a Federal Express outlet, and several smaller warehousing, Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 1-1THIS 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. LOCATION SCALE: 1 = 2000'from: USGS 7.5' QUAD., SALT LAKE CITY SOUTH, UTAH. BASELINE RISK ASSESSMENT FIGURE 1-1 SITE LOCATION 215 Union BoulevardSuite 600® Lakewood, CO 80228oesGNERS/coNSUiMMS (2>03) 980-6800MURRAY SMELTER SITEMURRAY, UTAH supply and other industrial operations. The on-facility 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 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 pan of the on-facility 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 converted 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 snowmelt. 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 isunconfined, 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 1-3THIS 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 LittleCottonwood 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 hi 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 hi 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 hi the future, if no remedial actionsare taken. The information hi 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 die 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 hi 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 1-4THIS 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. 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-facility 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 1-5THIS 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. 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, die 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 historicah- 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 4300-090-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. BASELINE RISK ASSESSMENT FIGURE 2-1 SITE MAP 215 Union BoulevardSuite 600Lakewood. CO 80228(303) 980-6800 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 hi 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, Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 2-3THIS 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 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 jn 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 die 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 hi 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. Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 2-4THIS 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 2-1: LEAD AND ARSENIC 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 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) BDLb-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 80-410 110-1600 110-780 130-640 120-1800 720-1800 66-7300 All data from Hydrometrics 1995a.1 Total number of samples with detectable levels over total number of samples analyzed.b BDL = Below detection limit (about 5 ppm). Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 2-3THIS 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. c c Legend < 500 ppm > - 500 and < 2,500 ppm O > - 2,500 and < 5,000 ppm > - 5,000 and < 10,000 ppm > -10,000 ppm Map base features and analytical data fromHydrometrics, Inc., Helena, MT., 1995. Murray Smelter SltaConcentrations ofLoad in Surface Soil 0" - 2" DepthFigure 2-2DCN: 4603-051-021-6420 M002 Ravteten Data: 03-JUN-1896ERA Legend < 75 ppm > - 75 and < 350 ppm O > - 350 and < 1,000 ppm > - 1,000 and < 2,000 ppm > - 2,000 ppm Map base features and analytical data fromHydrometrics, Inc., Helena, MT., 1995. Murray Smelter SiteConcentrations ofArsenic In Surface Soil 0" - 2" DepthFigure 2-3DCN: 4603-051-021-6420 M003 Revision Date: O3-JUN-1996 WJVtMtM \^ljrn*f PUMHiMJCOHflJ Legend Shallow IntermediateZone Zone 5ug/L > - 5 and < 50 ug/L A > - SOand < 250 ug/L > - 250 and < 2,500 ug/L A > - 2,500 and < 25^)00 ug/L A > - 25,000 ug/L Map base features and analytical data fromHydrometrics, Inc., Helena, MT., 1995. Murray Smelter SitewOnoentrfltionv ofAraenio (total) in Qroundwater Figure 2-4 murrev2/mBp«/8»1/mBP1________Bavlrion Data: 26-OCT96ERA In order to gain information on the physical and chemical nature of the lead and arsenic presenthi 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 urn), 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 hi 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 hi Appendix D (Part 2) andsummary statistics are provided hi Table 2-3. Inspection of the data hi 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 Vinehi ISZ-8), and a few show an apparent increase (e.g., ISZ-3-10). ^""^^ Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 2-8THIS DOCUMENT WAS PREPARED BV 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 2-2: GEOCHEMICAL SPECIATION DATA FOR SURFACE SOIL SAMPLES Relative Lead Mass (Approximate Percent of Total) Mineral Form PbOCalciteFe-Pb OxideGalenaPbAsOPb PhosphateSlagFe-Pb SulfatePb(M)OClayPbSiO4Mn-Pb OxidePbOOHNative LeadAnglesitePbCrO4Pb Solder Soil Sample Number (Concentration of Lead, ppm)1(56)964 2(1130) 10191848T224 3(1040)11 '• 3 192T1 T 5811 4(1090) 216487T4T 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 122829626 53 10T 10(3080)9 341223 T4T28T1422 T Relative Arsenic Mass (Approximate Percent of Total) Mineral Form Fe-Pb- As-OxidePbAsOPb-As PhosphatePyriteSlagFe-Pb-As SulfateAs(M)OClayPb PhosphateMn-Pb OxideMn-Pb-As OxideCalciteArsenopyritePbSiO4 Soil Sample Number (Concentration of Arsenic, ppm)1(BDL)2(162)6416122 4T1 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 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 Location On-facility Off-facility Area EU-1 EU-2 EU-4 EU-5 EU-6 EU-7 EU-8 EU-9 EU10 ISZ-1 ISZ-2 ISZ-3 ISZ-4 1SZ-5 ISZ-6 ISZ-7 ISZ-8 Numberof stations 2 1 1 1 19 4 2 2 2 2 2 2 2 2 2 2 2 DepthIntervals CF 0-1 ft1-2 ft2-3 ft3-4 ft4-5 ft 0-2 in2-6 in6-12 in12-18 in 0-2 in2-6 in6-12 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 BDL48000 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 66-4800 61-600 57-22000 63-14000 520-9000 75-40000 430-1200 240-420 150-3200 87-1600 290-710 230-560 120-1000 550-7300 140-190 All data from Hydrometrics 1995a.BDL = Below detection limit (about 5 ppm). Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 2-10THIS 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. 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 ArsenicLead Numberof..Samples22211 Concentration in Dust (ppm)Average 27303' Range 5-9483-757* * 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 hi 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 hi most of the shallowand intermediate alluvial aquifers are relatively low. This is consistent with the fact that leadis usually much less mobile hi 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 4500-090-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 AquiferZoneShallowalluvialaquifer Intermediatealluvialaquifer WellIDMW-KXfMW-iorMW-102MW-103MW-104MW-105MW-106MW-107MW-108MW-109MW-110MW-lllk MW-112GW-1GW-2Well 1Well 2Well 3b UTBN-1JMM-08MW-101DMW-104DMW-105DMW-108DMW-109DMW-112DGW-1AGW-1ARGW-2A Concentration (ug/L) (total)Arsenic <5618.427061327,180<5<5142,3472,903521,2872,8702161,97423627078<51925<569397906439 Lead 84<23367282421216.53<2931505047141046865<2 All data are based on a single measurement (Hydrometrics 1995b). ' Well is located in an up-gradient locationb These wells are completed in slag Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 2-12THIS 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. 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 au-to the ground by ram 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-facility, 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 particles 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-facility workers and on-facility 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 AirSurface water, sediment Vegetables grown in contaminated soilFish from contaminated creek Potential Human Exposure Pathways IngestionDermal contact IngestionDermal contactInhalation of air-borne paniculate matterIngestionDermal contactIngestion Ingestion Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 3-1THIS 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. 00 X CL Ul 0o RA N S P O R T AT H W A Y S O OLJo: o£§§en o o tc.O 5 i Si 8 uJ . Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 3-2THIS 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 FT>A 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 hi 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 part of soil or dust particlesthat become suspended in air as a result of wind or mechanical erosion. However, except underconditions of extreme soil erosion to ah*, 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 particles 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 then- 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 Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 3-3THIS 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. 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 leadvand arsenic which might occur hi locally-grown vegetables.Screening level calculations (presented hi 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 hi 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 hi 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 hi 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 hi 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 hi 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 hi the vicinity of the site. Therefore, exposure via this pathway is not Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 3-4THIS 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. 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 Little 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 h\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 groundwater 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. Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 3-5THIS 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. 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 hi 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 Page 3-6THIS 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. distribution of possible values rather than a specific value. Usually, emphasis is placed on twodifferent portions of this distribution: Average or Central Tendency (CD 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 (O 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 lognonnally (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 (Part 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 hi Table 3-1. Dust As discussed hi 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: ^"""^ Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 3-7THIS 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 3-1 EXPOSURE POINT CONCENTRATIONS FORARSENIC IN SURFACE SOIL Location On-facility Off-facility Area EU-1EU-2EU-3EU-4EU-5EU-6EU-7EU-8EU-9EU10EU-11 ISZ-1ISZ-2ISZ-3ISZ-4ISZ-5ISZ-6ISZ-7ISZ-8 Arsenic Concentration (ppm)Mean13079« 117241810043241816741186919 106165543425212676 Max6303607700540052051002200500021022078 34037110170130120180450 UCL 1424681578407618285178812202556822238362 2225712873651621582117 EPC' 6303607700540028018001200500021022062 22037110r~ 7365120160450 1 EPC = exposure point concentration (UCL or maximum value, which ever is lower) Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 3-8THIS 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. (ms + ma + m,. where: m = mass of material in dust derived from yard soils (m,), area sources (n\),or indoor sources (m). C = concentration of contaminant in interior dust (Cd), yard soils (Cs), areasources (C,), or indoor sources (Cj). This equation can be re-written as follows: where: k = mass fraction in dust of material derived from area sources (kj, yard soil(k,) and indoor sources (kj). 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: ko = contribution to indoor dust from non-yard soil sources (ppm)k, = mass fraction of yard soil in indoor dust (unitless)C, = 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 (1995a), 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 Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 3-9THIS 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. c c c grfj » fc ia i?§=, 100 80- Figure 3-2 Relationship BetweenArsenic in Dust and Soil Best-Fit Linear Regression:Dust=16 + 0.17*Soil 50 100 150Arsenic in Soil (mg/kg)200 was rounded upwards and the intercept was rounded downwards to yield the followingapproximation of the mean soil-dust relationships: Parameter ko(ppm)k, (ppm per ppm) Value for ArsenicLinear Regression170.17 Adjusted*100.20 1 Adjusted by founding k, up and founding ko down to account for measurement error. Groundwater Exposure to groundwater 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 then* 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: PopulationResident Workers LocationOn-facility Off-facility On-facility WellsMW-102 (south of Doc and Dell's)MW-106 (west of Grandview)MW-100MW-101 and 101DMW-103MW-104 and 104DMW-1021 MW-105 and 10SDMW-106*MW-107MW-108 and 108DMW-109 and 109DMW-110MW-111"MW- 112 and 112DGW-1, 1A and 1ARGW-2 and 2AWell 1Well 2Well 3b UTBN-1 • On-facility well used for both residential and worker evaluationb These wells are completed in slag, and may not be representative of actual future wells. Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 3-11THIS 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. 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: IE-06BW -EDAT where: = Daily intake of chemical from soil and dust (mg/kg-day)C,d = Concentration of chemical in soil and dust (mg/kg)IRjd = Intake rate of soil plus dust (mg/day)IE-06 = Conversion factor (kg/mg)BW = Body weight (kg)EF = Exposure frequency (days/yr) Baseline Human Health Risk Assessment May 1997Document Control Number 450CWJ90-AOAC Page 3-12THIS 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. 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-DIsd IRC-IE-06 EFC-EDC IRa - IE-06 EFa-EDaBWC (ATC + ATC) BW0 (ATC + ATa) where: TWA-DI^ = Time-weighted average daily intake of chemical from soil/dust (mg/kg-day)CH, = Concentration of chemical in soil and dust (mg/kg)IR,,, = Intake rate of soil plus dust (mg/day) when a child (IR,) or an adult (IRJIE-06 = Conversion factor (kg/mg)BW = Body weight (kg) when a child (BWC) or an adult (BW.)EF = Exposure frequency (days/yr) when a child (EFJ or an adult (EFJED = Exposure duration (years) when a child (EDC) or an adult (ED,)AT = 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 tune is equal to the exposure duration(i.e., the calculation yields the average dose rate during the tune interval when exposure isoccurring). For evaluation of cancer risks, the averaging tune 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 hi 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: Baseline Human Health Risk Assessment May 1997Document Control Number 45QO-090-AOAC Page 3-13THIS 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. s> id 8 8 B VO cs 1 a i fll ± a Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 3-14THIS 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. Dlsd Ct-WFs where: = Daily intake of chemical from soil plus dust (mg/kg-day)C = Concentration of chemical in soil (C,) or dust (Cj) (mg/kg)HIF = Human intake factor for soil (HIF,) or dust (HIF,,) (kg/kg-day) fData 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 CI-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. IE-07 l.SE-08 1.7E-06 1.2E-07 Dust 7.2E-07 9.2E-08 2. IE-07 1.5E-08 — — RME Soil 1.6E-06 7. IE-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 — — Baseline Hunan Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 3-15THIS DOCUMENT WAS PREPARED BY ROY F. WESTON. INC. EXPRESSLY FOR EPA. FT SHALL NOT BE RELEASED ORDISCLOSED IN WHOLE OR IN PART WITHOUT THE EXPRESS WRITTEN PERMISSION OF EPA. 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 hi soil is less well absorbed than arsenic inwater, and on this basis EPA Region Vni recommends a default relative bioavailability (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 hi the soil samples is 26%, with a 90% confidence interval from 21%to 33% (Weis et al. 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 hi 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, hi 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: DI!+d = C^fflP.-RBA, + C where: Cd = 10 + 0.2-C, Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 3-16THIS 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. 3.3.3.2 HIT for Slag Ingestion The basic equation for evaluating exposure from ingestion of material from slag piles is: EF..-EDDI.slag slagAT The EPA has not established any default parameters for human exposure to slag, so parameterswere estimated as described below. IBslag 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 kg. 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. ID Assuming that teenagers visit the site mainly over the age range 12-18 years, the exposureduration for this pathway is 7 years. ^~*"^ Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 3-17THIS 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. A! The 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: Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 3-18THIS 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. 3.3.3.3 HIF for Drinking Water Ingestion The basic equation for calculation of the HIF for ingestion of drinking water is (US EPA 1989a):IR^-EF -EDBW -AT where: HIFW = Human intake factor for water (L/kg-day)11^ = 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 (L/day) BW(kg) EF (days/yr)ED (years)AT (noncancer effects) (days)AT (cancer effects) (days) ResidentAverage 1.4 70 2349 9 '36570-365 RME 2.0 70 350 30 30 '36570-365 Worker Average 0.770 2195 5-36570-365 RME 1.070 25025 25-36570 • 365 Based on these exposure parameters, the HIF values for exposure of residents and workers toground water are as follows: ExposedPopulation Resident Worker ExposureDuration ChronicLifetime ChronicLifetime HIF for Water Ingestion (L/kg-d) Average 1.3E-021.7E-036.0E-034.3E-04 RME 2.7E-02 1.2E-02 9.8E-03 3.5E-03 Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 3-19THIS 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. Final Dose Equation In the case of arsenic dissolved in water there is no adjustment needed for bioavailability, so thefinal dose equation is simply: = Cwater-HIF,water 3.3.4 Dose Calculations e 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 in'\^^ the 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 part, the amount of lead which a child ingests or inhales is calculated from data on a) theconcentration of lead hi 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 ^•^ Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 3-20THIS 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. each day. The second part of the model is the biokinetic section. This part 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 "compartments11 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 part 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 Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 3-21THIS 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. 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 hi 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 LeadLinear Regression 980.32 Adjusted' 900.35 * Adjusted by Founding k, up and ko down to account for measurement error. Table 3-3 summarizes the soil and dust concentration values used to assess exposure ofresidential children. Bioavailabilitv of Lead in Soil and Dust The EPA has conducted a study of the bioavailability of lead hi a composite soil sample fromthe Murray Smelter site (EPA 1996). Estimates of RBA based on four different endpoints (leadhi blood, liver, kidney, and bone) were obtained. Because these estimates did not preciselyagree hi all cases, judgment must be used hi 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 hi 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 endpointhi 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 Page 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. c 0 c 1000 800 IO)E, 600*-»COQ.£ 400030) 200 - - Figure 3-3 Relationship BetweenLead in Dust and Soil Best-Fit Linear Regression:Dust = 98 + 0.32*Soil One outlier excluded(Dust = 5315, Soil = 780) 500 1000Lead in Soil (mg/kg)1500 2000 TABLE 3-3: LEAD LEVELS IN RESIDENTIAL AREA SOIL AND DUST ExposureArea EU-8EU-9EU-10EU-11ISZ-1ISZ-2ISZ-3ISZ-4ISZ-5ISZ-6ISZ-7ISZ-8 Mean Lead Concentration (ppm) Surface Soil 6177909538814129924176839142665712221062 Indoor Dust" 2252408278375545174359227239320518462 ' 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 Page 3-24THIS 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 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 RangePreferred Range 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 mat 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 PDA (Gunderson 1995, Bolger et al. 1996) support the viewthat dietary intake levels of lead are now lower than the default values provided hi the IEUBKmodel. The revised values are as shown below. These data were used hi the IEUBK modelcalculation of lead exposure levels in residential children. Age6-11 months1 year2 years3 years4 years5 years6 years Intake (ug/day)1.821.901.871.801.731.832.02 Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 3-25THIS 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. 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 (PbBo) (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 = PbBo + BKSF-IC.-IIVEF.-AF, + C<rmd-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 May 1997Document Control Number 4500-090-AOAC Page 3-26THIS 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. s& •o 03 (N g r o « {! 00 8 i s 8 tn to I I Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 3-27THIS 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. PbBo = Geometric mean "baseline" blood lead level in adults not exposed to lead-contaminated soil 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 (EF,) or dust (EFj) 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 percentile of the predicted distribution is given by the following equation (Aitchison andBrown 1957): 95th = GM-GSD1645 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 (PbB^ 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 HI study (Brody et al. 1994). The Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 3-28THIS 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. 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 19955). 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 PbB,,. Geometric Standard Deviation (GSD) Data collected during the NHANEg HI 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 (C4) As noted above, the value of C, 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. Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 3-29THIS DOCUMENT WAS PREPARED BY ROY P. WESTON. INC. EXPRESSLY FOR EPA. IT SHALL NOT BE RELEASED ORDISCLOSED IN WHOLE OR IN PART WITHOUT THE EXPRESS WRITTEN PERMISSION OF EPA. As discussed hi Section 3.4.1, data from a number of off-facility locations around MurraySmelter indicate that the level of lead hi ulterior dust is approximately related to the level of leadhi soil by the following equation: C = 90 4- 0 35 • C •*~dust — -'*' ' U.JJ ^--ioil This equation is assumed to be applicable to indoor dust levels in on-facility workplaces. Theresulting soil and dust concentrations for on-facility commercial areas are summarized hi Table3-5. Ingestion 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 intensiveContact intensive Estimated Soil and Dust Intake (rag/day)Average502401 RME 50480 * 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 hi 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 hi 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 1997Document Control Number 4500-090-AOAC Page 3-30THIS 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-1EU-2EU-3EU-4EU-5EU-6EU-7 Mean Lead Concentration (ppm) Surface Soil 2905287995481750275422972524 Indoor Dust* 1107109834327031054894973 * 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 Page 3-31THIS 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. 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 hi 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 hi 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 hi geometric mean blood lead (AGM)due to water ingestion is given by the following equation: AGM = BKSF-Cw-IRw-EF/365-AFwAs discussed previously, values for these parameters for workers are as follows: BKSF = 0.40 ug/dL per ug/day absorbedIR^ = 0.7 L/day (average)EF = 219 days/year (average)AFW = 0.10 Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 3-32THIS 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. 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-facility women workers.*Results — Predicted Blood Lead Levels in Workers The predicted blood lead levels in workers exposed at on-facility locations are detailed inAppendix D (Part 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 = where: PbB = Geometric mean blood lead level (ug/dL) in a population of teenagersexposed to lead-contaminated slag PbB0 = Geometric mean "baseline" blood lead level in teenagers not exposed tolead-contaminated slag, but including other background exposures,including residential exposure BKSF = Biokinetic slope factor (ug/dL increase in blood lead per ug/day leadabsorbed) Citag = Arithmetic mean concentration (ug/g) of lead in slag = Mean daily intake rate of slag (g/day) EFtlag = Exposure frequency (days/day) to slag AF$lag = Absolute absorption fraction (bioavailability) of lead hi slag . Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 3-33THIS 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 3-6: MODEL INPUT PARAMETERS FOR ESTIMATION OF LEADEXPOSURE IN WOMEN WORKERS Model Input Geometric mean baseline blood lead Biokinetic slope factor Digestion rate of soil Ingestion rate of dust Exposure frequency at work Absorption fraction from soil and dust Geometric standard deviation Abbr. PbBo BKSF IR, IRdEF AF,, AFdGSD Units ug/dL ug/dL per ug/d tag/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 Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 3-34THIS 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. 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. lEs.ag As discussed above, the average ingestion rate of slag by area teenagers who visit the site isassumed to be 50 mg/event. As discussed above, the exposure frequency for teenagers who visit the site is assumed to be anaverage of 25 days/year. 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 RangePreferred RangeSuggested Point Estimate Value 0.47-0.550.51-0.550.53 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 3-35THIS 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. 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 (Part 5) and are discussed in Section 5.2.3. ^"^^ Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 3-36THIS 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. 4.0 TOXICITY ASSESSMENT 4.1 OVERVIEW The toxic effects of a chemical generally depend not only upon the inherent toxicity 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 pennit, 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 ABl62 CD Meaning Known human carcinogenProbable human carcinogenProbable human carcinogen Possible human carcinogenCannot 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 data orinsufficient data from humans.Suggestive evidence of carcinogenicity in animals.No evidence or inadequate evidence of cancer in animals orhumans. 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 toxicity parameters for each. Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 4-1THIS 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. 4.2 ADVERSE EFFECTS OF ARSENIC Excess exposure to arsenic is known to cause a variety of adverse health effects hi 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 argenic 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 "phis 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 hi humans exposed for tune intervals ranging from 6 monthsto 10-15 years. These data indicate that adverse effects may occur hi 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 Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 4-2THIS 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. 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 hi 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 hi 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 Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 4-3THIS 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. 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 hi bloodpressure hi 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 hi annuals indicate that chronic oral exposure to very high doses of lead salts may causean increased frequency of tumors 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 Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 4-4THIS 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. 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: rNoncancer 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 above\^ 1E+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 IE-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 IE-06 to be so small as to benegligible, and risks above IE-04 to be sufficiently large that some sort of action or interventionis usually needed (EPA 1991b). Risks between IE-04 and IE-06 usually do pot require ^*^ Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 5-1THIS 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. 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 hi Section 4.1. The detailed calculations arepresented in Appendix D (Part 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, hiwhich urinary arsenic levels in 7 children age 0-7 and hi 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 part of the Grandview Trailer Park area, there are no residencescurrently in this sublocation. Cancer risks to residents mainly range betweenIE-07 and 8E-05, with risks greater than IE-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 hi 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 IE-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 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. c c cfTABLE 5-1: RISKS FROM ARSENIC IN SURFACE SOIL AND DUST Population Resident NCI-Worker Cl-Worker ^ocation On-facility Off-facility On-facility On-facility Area EU-8EU-9EU-10EU-11ISZ-1ISZ-2ISZ-3ISZ-4ISZ-5ISZ-6ISZ-7ISZ-8EU-1EU-2EU-3EU-4EU-5EU-6EU-7EU-1EU-2EU-3EU-4EU-5EU-6EU-7 Arsenic Concentration (ppm) Mean Max EPC1674 5000 5000118 210 21069 220 22019 78 62106 340 22216 37 3755 110 11045 170 7542 130 6552 120 120126 180 15876 450 450130 630 63079 360 3601172 7700 7700418 5400 5400100 520 285432 5100 1788418 2200 1220130 630 63079 360 3601172 7700 7700418 5400 5400100 520 285432 5100 1788418 2200 1220 NoncancerHQ* Avg1E+008E-02 """"ffpgf""5E-02 IE-012E-02 5E-027E-02 IE-012E-02 3E-024E-02 8E-023EXJ2 5E-023E-O2 5E-024E-02 8E-029E-02 IE-015E-02 3E-013E-02 IE-012E-02 8E-02 ^2E-02 7E-02IE-01 4E-01IE-01 3E-012E-01 9E-01IE-01 5E-01 7E-01 pSfHiJiSHI;6E-01 RME:|:3|ipJ;;;;;:;;;;i:ii;;!ffi*:M:if2§li 41-01IE-01 4E-015E-02 IE-012E-01 4E-015E-02 8E-02IE-01 2E-01IE-01 2E-019E-02 IE-01IE-01 2E-012E-01 3E-012E-01 8E-014E-02 2E-012E-02 9E-02 IE-01 JE+iSb3E-02 7E-02IE-01 5E-01IE-01 3E-014E-01 gl^^OGJII;3E-01 1E+00^4SS?SSli^3M^8i^i 3EO1 s'x':il+bf:"'1E+00lE+oo iiiiiiii Cancer Risk* Avg6E-05SE-oe "'""ifoe™"3E-06 8E-06IE-06 3E-064E-O6 8E-069E-07 2E-062E-06 4E-062E-06 3E-062E-06, 3E-062E-06 5E-065E-06 6E-063E-06 2&05IE-06 5E-066E-07 3E-068E-06 6E-053E-06 4E-058E-07 2E-063E-06 IE-053E-06 9E-066E-06 3E-054E-06 2E-05 2E-055E-06 "'"ti^OS""2E-05 9E-052E-05 6E-05 RME •;:W:''X:-'X:X:o:X:X:Xv-y;x;:XrX:X;X:Xw:4E-05 8E-053E-05 8E-OSIE-05 2E-OS4E-05 8E-059E-06 2E-OS2E-05 4E052E-05 3E-OS2E05 3E-OS2E-05 4E-055E-05 6E-053E-056E-06 3E-054E-06 2E-05 2E-05 l|l;t]llil|||i:4E-06 ™™if^J5"K"2&O5 7E-052E-05 5E-05a ! \ I Shaded cells indicate locations where risks from arsenic exceed typical EPA guidelines (HQ > 1E+00, cancer risk > IE-04) ' The first value shown is based on the mean concentntion, and the second value shown is based on the EPC (usually the 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 IE-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 IE-04 in alllocations for the average worker, but still exceed IE-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 HQCancer Risk Estimated Value Average 5E-022E-06 RME 2E-01IE-05 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 IE-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 hi 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 IE-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 IE-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, Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 5-4THIS 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 5-2: POTENTIAL RISKS FROM ARSENIC IN GROUNDWATER Population Location Aquifer Well Concentration Chronic HQAvg RME Cancer RiskAvg RME Resident On-site Off-site Shallow Intermediate MW-lOffMW-101'MW-102MW-103MW-104MW-106MW-101DMW-104D 3618270627,180319 IE-01 2E-013E-01 5E-01 6E-06 4E-05IE-05 IE-045E-05 8E-01I 5E-05 Worker On-site Shallow Intermediate MW-102MW-105MW-106MW-107MW-108MW-109MW-110MW-111"MW-112GW-1GW-2Well 1Well 2Well 3b UTBN-1MW-105DMW-108DMW-109DMW-112DGW-1AGW-1ARGW-2A 181327,18033142,3472,903521,2872,8702161,97423627025369397906439 4E-013E-01 5E-023E-01 6E-014E-01 8E-025E-01 IE-05 IE-048E-06 7E-05 2E-069E-06 IE-057E-05 SE-02 8E-021E+008E-01 IE-05 Shaded cells indicate wells where risks from arsenic exceed typical EPA guidelines (HQ > IE+00, cancer risk> IE-04) * Well located in an up-gradient locationb Well is completed in slag Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 5-5THIS 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. MW-110, MW-111, MW-112. GW-1, GW-2, Well-1, Well-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 toIE-01, with 10 of IS shallow wells and 4 of 7 intermediate wells having RMErisk values above IE-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+Q3, and RME cancer risks range from IE-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 LEAD 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 hi 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 hichildren 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 5-6THIS 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 pg/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 hi 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 hi 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'sGrandview ObservedN 1 9 GM (ug/dL) 4.74.8 N > 10 ug/dL — 0 PredictedGM (ug/dL) 7.56.9 P10 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 hi 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 tune), this conclusion is not certain. Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 5-7THIS 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 5-3: RISKS TO CHILDREN FROM LEAD IN SURFACE SOIL AND DUST ExposureArea EU-8EU-9EU-10EU-11 ISZ-1 ISZ-2 ISZ-3 ISZ-4 ISZ-5 ISZ-6 ISZ-7 ISZ-8 Mean LeadConcentration(ppm) 6177 909538 8141299 241 768 391 426 657 1222 1062 Predicted Blood Lead Distribution in Children CM (ug/dL) 28.68.15.6 7.510.43.4 7.24.6 4.8 6.5 10.09.0 95th (ug/dL) 501410 13 185.9138.08.011 17 16 P101 4% 0.1% 0.9%1.4% 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 . May 1997Document Control Number 4500-090-AOAC Page 5-8THIS 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. 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 locatedhi residential areas have lead concentrations less than 10 ug/L, corresponding to increments higeometric 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 hia 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 PbBhi three recent studies cited by Goyer was 0.90. Based on this, the PbB hi the mother whichcorresponds to a PbB hi the fetus of 10 ug/dL is then 10/0.90 =11.1 ug/dL. That is, hi 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 hi 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% hi all locationsexcept EU-3. However, for contact-intensive workers, the value of PI 1.1 exceeds the target of5% hi 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. Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 5-9THIS 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 5-4: RISKS TO WORKERS FROM LEAD IN SURFACE SOIL AND DUST ExposureArea EU-1 EU-2 EU-3EU-4 EU-5 EU-6 EU-7 Mean LeadConcentration(ppm) 2905 2879 95481750 27542297 2524 Predicted Blood Lead Distributionin NCI-Workers GM(ug/dL) "4.0 4.0 7.83.3 3.9 3.6 3.8 95th(ug/dL) 8.1 8.1 166.8 7.97.4 7.7 Pll.l1 0.9%0.9% 0.3% 0.8% 0.5% 0.6% Predicted Blood Lead Distributionin Cl-WorkersGM(ug/dL) 1212 358.3 1210 11 95th(ug/dL) 25 25 7117 24 21 22 Pll.l1 PI 1.1 — 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 May 1997Document Control Number 4500-090-AOAC Page 5-10THIS 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. 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 10,000-40,000 ppm in some locations (see Section 2.4 and AppendixD, Part 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 hi blood lead levels ofpotential concern. The results for NCI-workers (calculated using the Bowers model) aresummarized below. Well ID MW-111Well 3UTBN-1 LeadCone.(ug/L)21215050 Area EU-4EU-2EU-1 Lead inSoil'(ppm)175028792905 Lead inDust*(ppm)703109S1107 Baseline (no water)GM 3.34.04.0 Pll.l 0.3%0.9%0.9% Including WaterGM 6.96.54.8 Pll.l 13%11%3% * Mean lead level in the exposure area* Calculated using the equation C(dust) = 90 + 0.35 • C(soil) As seen, for wells MW-111 and Well-3, ingestion of groundwater by NCI-workers would resulthi a moderate increase (10%-13%) hi 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 hi water at these wells is relatively small, as shown below. Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-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-111Well 3UTBN-1 LeadCone.(ug/L)21215050 Area ElMEU-2EU-1 Lead inSoil*(ppm)175028792905 Lead inDust"(ppm)70310981107 Baseline (no water)GM 3.312.112.2 Pll.l 25%58%59% Including WaterGM 11.814.613.0 Pll.l 56%74%64% • Mean lead level in the exposure area' Calculated using the equation C(dust) «= 90 + 0.35 • C(soil)t5.2.3 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 Pll.l' <0.01% IncludingSlag Exposure*GM 2.4 Pll.l 0.02% IncrementDue to Slag GM 0.8 . Pll.l <0.02% ' Pll.l = probability of a teenager exceeding a blood lead of 11.1 ug/dL11 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 hi a significant riskof exceeding a blood lead value of 11.1 ug/dL. This suggests that exposure of area teenagersto lead hi slag is not likely to be of significant health concern. Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 5-12THIS 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. 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 hi 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 hi 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. Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 6-1THIS 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. 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 hi 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 hi 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 Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 6-2THIS 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. V^/' 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 ParametersWIn 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 Assessment May 1997Document Control Number 4500-090-AOAC Page 6-3THIS 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. 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 fate of uptake and removal of lead from each compartment.In addition, the final distribution of predicted blood lead values employs an estimated value forGSDj. 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 toxicity 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 Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 6-4THIS 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. susceptible members of a population, so average persons may not be affected to the degreepredicted by the toxicity 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 /ig/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 60-80pg/dL, and effects that occur at blood levels of about 10 /zg/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 pg/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 Page 6-5THIS 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. 7.0 REFERENCES Aitchison J, Brown JAC. 1957. The Lognormal Distribution - University of CambridgeDepartment of Applied Economics Monograph. Cambridge University Press. ACGIH. 1995. American Conference of Governmental Industrial Hygienists, Inc. Lead,inorganic dust and fumes. Recommended BEI (7/24/95 draft). c-ATSDR. 1991. Agency for Toxic Substances and Disease Registry. Toxicological Profile forArsenic. Atlanta, GA: Agency for Toxic Substances and Disease Registry. Benson. 1995. Subchronic Reference Dose for Arsenic. Memo from Robert Benson, Ph.D.,to Chris Weis, Ph.D., dated 9/12/95. Bolger PM, Yess NJ, Gunderson EL, Troxell TC, Carrington CD. 1996. Identification andReduction of Sources of Dietary Lead in the United States. Food Additives and Contaminants,Vol. 13, No 1, 53-60. Bowers TS, Beck BD, Karam HS. 1994. Assessing the Relationship Between EnvironmentalLead Concentrations and Adult Blood Lead Levels. Risk Analysis 14:183-189. 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 in, 1988 to 1991). JAMA 272:277-283. Campbell. 1996. Ground Freeze/Snow Cover Data. Memo from Kent R. Campbell, UtahClimate Center, Utah State University, to Karen Holliway. July 18, 1996. CDC. 1991. Preventing Lead Poisoning in Young Children. US Department of Health andHuman Services, Centers for Disease Control. CEPA. 1992. California Environmental Protection Agency, Department of Toxic SubstancesControl. Supplemental Guidance for Human Health Multimedia Risk Assessment of HazardousWaste Sites and Permitted Facilities. Sacramento, California. Drexler JW. 1996. Laboratory Report: Metal Speciation for Lead and Arsenic. Reportprepared for Roy F. Weston Inc., by Dr. John Drexler, University of Colorado Department ofGeological Sciences. WESTON Project File Number 4800-51-171. EPA. 1984. U.S. Environmental Protection Agency. Office of Health and EnvironmentalAssessment. Health Assessment Document for Inorganic Arsenic. Final report. ResearchTriangle Park, NC: U.S. Environmental Protection Agency. EPA 600/8-83-021F, Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 7-1THIS 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. EPA. 1986. U.S. Environmental Protection Agency. Office of Health and EnvironmentalAssessment. Air Quality Criteria for Lead. June, 1986, and Addendum, September, 1986.Research Triangle Park, NC: U.S. Environmental Protection Agency. EPA 600/8-83-028F. EPA. 1988a. U.S. Environmental Protection Agency. Drinking Water Regulations: MaximumContaminant Level Goals and National Primary Drinking Water Regulations for Lead andCopper; Proposed Rule. Fed. Register August 18, 1988. 53:31516-31578. EPA. 1988b. U.S. Environmental Protection Agency. Office of Health and EnvironmentalAssessment. Special Report on Ingested Inorganic Arsenic: Skin Cancer; NutritionalEssentiality. Washington, DC: U.S. Environmental Protection Agency. EPA/625/3-87/013. EPA. 1989a. U.S. Environmental Protection Agency, Office of Emergency and RemedialResponse. Risk Assessment Guidance for Superfund. Volume I. Human Health EvaluationManual (Part A). EPA Document EPA/540/1-89/002. EPA. 1989b. U.S. Environmental Protection Agency, Office of Health and EnvironmentalAssessment. Evaluation of the Potential Carcinogenicity of Lead and Lead Compounds.EPA/600/8-89/045A. EPA. 1990. U.S. Environmental Protection Agency, Technical Support Document on Lead.ECAO-CIN-757. Cincinnati, OH: EPA Office of Environmental Criteria and AssessmentOffice. September. EPA. 1991a. 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. 1991b. U.S. Environmental Protection Agency, Office of Solid Waste and EmergencyResponse. Role of the Baseline Risk Assessment in Superfund Remedy Selection Decisions.Washington, D.C. OSWER Directive 9355.0-30. EPA. 1991c. U.S. Environmental Protection Agency, Office of Health and EnvironmentalAssessment. Exposure Factors Handbook. Washington, D.C. Review Draft, July 1991. EPA. 1991d. U.S. Environmental Protection Agency, Office of Emergency and RemedialResponse. Risk Assessment Guidance for Superfund. Volume I. Human Health EvaluationManual (Part B, Development of Risk-Based preliminary Remediation Goals). EPA DocumentEPA/540/R-92/003. EPA. 1992a. U.S. Environmental Protection Agency, Office of Solid Waste and EmergencyResponse. Supplemental Guidance to RAGS: Calculating the Concentration Term. Publication9285.7-081. Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 7-2THIS DOCUMENT WAS PREPARED BY ROY F. WESTON, INC. EXPRESSLY FOR EPA. IT SHALL NOT BE RELEASED ORDISCLOSED IN WHOLE OR IN PART WTTHOUT THE EXPRESS WRITTEN PERMISSION OF EPA. EPA. 1992b. Dermal Exposure Assessment: Principles and Applications. Interim Report.Office of Research and Development, Washington, DC. EPA/600/8-91/011B. EPA. 1993a. U.S. Environmental Protection Agency. Superfund's Standard Default ExposureFactors for the Central Tendency and Reasonable Maximum Exposure. Draft, dated 11/04/93. EPA. 1993b. U.S. Environmental Protection Agency. Region 8 Superfund Technical Section.Clark Fork Position Paper on the Bioavailability of Arsenic. Prepared by Life Systems Inc.,under subcontract to Sverdrup Corporation, for US EPA Region VIII. EPA. 1994a. U.S. Environmental Protection Agency, Office of Emergency and RemedialResponse. Guidance Manual for the Integrated Exposure Uptake Biokinetic Model for Lead inChildren. EPA Publication No. 9285.7-15-1. EPA. 1994b. U.S. Environmental Protection Agency, Technical Review Workgroup for Lead.Comments and Recommendations on a Methodology for Estimating Risk Associated with AcuteLead Exposures at Superfund Sites. EPA. 1994c. U.S. Environmental Protection Agency, Office of Solid Waste and EmergencyResponse. Revised Interim Soil Lead Guidance for CERCLA Sites and RCRA CorrectiveAction Facilities. OSWER Directive 9355.4-12. Elliot P. Laws, Assistant Administrator. July14. 1994. 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. EPA. 1995a. U.S. Environmental Protection Agency, Region 8 Superfund Technical Section.Standard Operating Procedure. Evaluating Exposure from Indoor Dust. EPA. 1995b. U.S. Environmental Protection Agency, Region 8 Superfund Technical Section.Evaluation of the Risk from Lead and Arsenic. Sandy Smelter Site, Sandy, Utah. EPA. 1996. U.S. Environmental Protection Agency, Region 8 Superfund Technical Section.Bioavailability of Lead in Soil and Slag from the Murray Smelter Superfund Site. Goyer RA. 1990. Transplacental Transport of Lead. Environ. Health Perspect. 89:101-105. Gradient. 1995. Comments on Leadville Commercial and Recreational Scenarios. Commentssubmitted by Dr. Brian Murphy, Gradient Corporation, to the Technical Advisory Committeeon the Baseline Human Health Risk Assessment for the California Gulch Superfund Site. Letterdated January 9, 1995. Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 7-3THIS 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. V_y Gunderson EL. 1995. PDA Total Diet Study, July 1986-April 1991, Dietary Intakes ofPesticides, Selected Elements, and Other Chemicals. Journal of AOAC International Vol. 78,No. 6, 1353-1363. 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. IRIS. 1996. Retrieval from EPA's Integrated Risk Information System (IRIS). May 1, 1996. Leggett. 1993. An Age-Specific Kinetic Model of Lead Metabolism in Humans. Environ.\^ Health Perspectives 101:598. O'Flaherty FJ. 1993. Physiologically Based Models for Bone-Seeking Elements. IV. Kineticsof Lead Disposition in Humans. Toxicol. Appl. Pharmacol. 118:16-29. Pirkle JL, Brody DJ, Gunter EW, Kramer RA, Paschal DC, Flegal KM, Matte TD,. 1994. TheDecline in Blood Lead Levels in the United States. The National Health and NutritionExamination Surveys. JAMA 272:284-291. 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 M, Wetherill GW, Kopple JD. 1974. Studies of Human Lead Metabolism by Useof Stable Isotope Tracers. Environ. Health Perspect. 7:145-153. 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. Taylor GH, Leggette RM. 1949. Ground Water in the Jordan Valley, Utah. Geological SurveyWater-Supply Paper 1029. U.S. Geological Survey, United States Department of the Interior. ^-"'^ Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 7-4THIS 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. 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 Bioavailability 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 n 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 Vffl. 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 Vin. Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page 7-5THIS 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. APPENDIX A EVALUATION OF TARGET ANALYTES FOR HUMAN HEALTHRISK ASSESSMENT AT MURRAY SMELTER December, 1994 PROJECT EVALUATION OF TARGET ANALYTES FOR HUMAN HEALTHRISK ASSESSMENT AT MURRAY SMELTER Document Control Number 4800-051-0016 °5 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 little question that lead and arsenic axe 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. Evaluation of Target Anilyto for Human Health Kiik Aueumcnt December 1994Murray Smelter Site, Murray, Utah Page 1THIS 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.epaXarci\reporU\4»_S t_16.dec c c c Table 1. Summary Statistics for Inorganic Concentration Levels * at Murray Smelter METALAluminumAntimonyArsenicSariumBerylliumCadmiumCalciumChromiumCobaltCopperIronLeadMercuryMagnesiumManganeseNickelPotassiumSeleniumSilverSodiumThalliumVanadiumZinc On-Site SoilsN Mean Max Min91010109109109101010109109910109101010 6588IS4989821.0455146820104775393229750.7686512991621881.4127883.27810835 895049224632503.02461366285227117217325689542.0861059283129792.82816459.036134072 46702551400.37166009499100004250.24620234817000.312501.013330 Off-Site SoilsN Mean Mix Min71010107107107101010107107710107101010 10106 51031400.81245135187142236715581.0114353521136345.9512523.624361 16214 171921971.0387571433122505190015593.02657142921497654.01018539.038714 5780126950.31486393761010029O.I602028382000O.I22500.59100 si>eN Mem Max Min05550505055550500550555 —2010734241—246—14—1270161420349082.1-2161 —-13.726-12.413171944 —38412315530—1057 —22—2630250600738406.9—3864—-27.765-56.7293123200 —4156861—0—6~80283600141300.0—715—-4.812—O.I3238890 * All concentration values expressed in units of mg/kg (ppm) 2.1 NONCANCER RISK Table 2 presents estimated Reasonable Maximum Exposure (RME) Hazard Quotient (HQ) 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 by Chemical ArsenicBeryllium Cadmium Chromium LeadNickel Oral X X X Inhalation XX X XX 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 /*g/m3 of respirable dust particles,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. 23 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. Evaluation of Target Aaalytes for Human Health Riik Aueiimeat December 1994Murray Smelter Site, Murray, Utah Pige 3THIS 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.epa\arci\reportaVU_51_I6.dec Table 2. Evaluation of Noncancer Risks ' METALAluminumAntimonyArsenicBariumBerylliumCadmiumChromiumCobaltCopperLeadMercuryManganeseNickelSilverThalliumVanadiumZinc 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-01HQ From Arsenic AloneSum of all other HQsTotal of all HQs% Attributable to Arsenic RME Hazard Quotient (HQ)On-Site SoilMean—0.052.270.020.000.060.01-0.02—0.000.020.000.000.060.020.052.270.312.5888 Max—0.1710.260.060.000.340.01—0.04-0.010.080.000.010.180.070.1610.261.1311.3990 off-site SOBMean—0.020.470.000.000.020.00-0.01—0.000.000.000.000.070.000.000.470.130.6078 Max-0.060.880.000.000.050.01—0.01-0.010.010.000.000.180.010.000.880.341.2272 SlagMean—0.074.900.08-0.340.00—0.05—0.010.03 0.010.240.030.334.901.186.0881 Max_0.1318.830.30—1.450.0 1—0.10—0.030.05 0.021.110.060.5618.833.8222.6483 * Assumes ingestion of 100 mg of soil/dust per day by a 70-kg adult, 350 days/yrb RfD = Reference Dose (mg/kg-d) Evihuiion of Target Anilyiei for Human Hetttt Riik Aimiment December 1994Mumy Smelter Site. Murny, Utah p««e *THIS DOCUMENT WAS PREPARED BY ROY F. WESTON. INC. EXPRESSLY FOR EPA. FT SHALL NOT BE RELEASED OR DISCLOSED INWHOLE OR IN PART WITHOUT THE EXPRESS WRITTEN PERMISSION OF EPA.cpi\trci\rcportiV4S_)l_lti.4cc Table 3. Beneficiality Screen METALCalciumIronMagnesiumPotassiumSeleniumSodium RDA*1200.015.0350.02000.00.1500.0 Ratio of Estimated Daily Intake (ing/day) to RDA'On-Site SoilMean0.000.360.000.000.000.00 Max0.011.160.000.000.000.00 Off-Site SoilMean0.000.160.000.000.010.00 Max0.010.350.010.000.080.00 SlagMean Max—1.08——0.02— ~1.67-_0.04- * RDA = Recommended Daily Allowance (mg/day) Evaluation of Tuftt Aufytc* far Humtn Hetfih Riak Aueumeot December 1994Murray Smelter She. Murray. Utah ftte J THIS DOCUMENT WAS PREPARED BY ROY F. WESTON. INC. EXPRESSLY FOR EPA. TT SHALL NOT BE RELEASED OR DISCLOSED INWHOLE OR IN PART WITHOUT THE EXPRESS WRITTEN PERMISSION OF EPA.J l_16.dec Table 4. Analysis of Cancer Risks OralExposure*ArsenicBerylliumLeadTotal% Arsenic oSF*1.8E+OQ4.3E-KK) Estimated RME Excess Lifetime Cancer RiskOn-Site SoilMean5.1E-042.5E-06 5. IE-0499.5 Max2.3E-037.6E-06 2.3E-0399.7 Off-Site SoilMean1. IE-042.0E-06 1. IE-0498.2 Max2.0E-042.5E-06 2.0E-0498.7 SlagMean Max1. IE-03ND 1. IE-03100.0 4.2E-03ND 4.2E-03100.0 InhalationExposure*ArsenicBerylliumCadmium^_'ftfflint^yyyiLeadNickelTotal•A Arsenic iSF1 1.5E+018.4E+006.3E-KW4.2E-HH 8.4E-01 On-Site SoilMean1.9E-072.2E-107.4E-092.2E-08 3.4E-102.2E-0786.7 Max8.7E-076.5E-104.0E-085.6E-08 6.7E-109.7E-0789.9 Off-Site SoilMean4.0E-08l.TE-101.9E-092.0E-08 2.3E-106.2E-0864.5 Max7.4E-082.2E-106.2E-093.6E-08 4.6E-101.2E-0763.6 SlagMean4.2E-07ND4.0E-081.5E-08 ND4.7E-0788.3 Max1.6E-06ND1.7E-072.4E-08 ND1.8E-0689.1 Total Exposure(Oral + Inhalation)ArsenicBerylliumfjiAmiamChromiumLeadNickelTotal•A Arsenic•A Oral On-Site SoilMean5. IE-042.5E-067.4E-092.2E-08 3.4E-105.1E-0499.5100.0 Max2JE-037.6E-064.0E-085.6E-08 6.7E-102.3E-0399.7100.0 Off-Site SoilMean1.1E-042.0E-061.9E-092.0E-08 2.3E-101. IE-0498.199.9 Max2.0E-042.5E-066.2E-093.6E-08 4.6E-102.0E-0498.799.9 SlagMean1. IE-03ND4.0E-081.5E-08 ND1. IE-03100.0100.0 Max4.2E-03ND1.7E-072.4E-08 ND4.2E-03100.0100.0 1 Assumes ingestion of 100 mg/day by a 70-kg adult, 350 d/yr for 30 yrb oSF - Oral slope factor (mg/kg-d)'1 e Assumes 0.2 ug/mj of soil in air, with inhalation of 20 mVday by a 70-kg adult, 350 d/yr for 30 yrd iSF - Inhalation slope factor (mg/kg-d)*1 Evaluation of Target Aailytti for Humin Health Risk Aueumeat December 1994Murray Smeller Site. Murray, Ulab Pf* *THIS 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. 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 CONTAMINANT IJE 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. Evaluation of Target Anarytes for Human Health Riit Aueument December 1994Murray Smeller She, Murray, Utah hfe ^THIS DOCUMENT WAS PREPARED BY ROY F. WESTON. INC. EXPRESSLY FOR EPA. IT SHALL NOT BE RELEASED OR DISCLOSED INWHOLE OR IN PART WTTHOUT THE EXPRESS WRITTEN PERMISSION OF EPA.ep» \arci\reporu\4J_Jl_16.dee C c Figure 1 . Comparison of Concentrationsat Murray Smelter and Midvale Slag Al |K!18:IpFl«S|11!g|I^8* 1 1E4 g r As Pb* I » Mn ..Ba Max »•- - a i I . v.O ' MeanS« "S 1E25g •*= I Ni j § Sb ] Co ] Ag l Min q o 1E1--••••---•- • '•••-•-••• ••-•••••• •-••••••-••- -I--- -..-....•-..--.....-....-..-.. - •• - -r-0 T r I- j |TIBe Hg8 1EO I6o _ 1E-1 -H-H-H-H-hH-l-HH-H-H-l-K-H-f-H-Hf-hl-H-t-f-}-I-+4-*-H-AB AB AB AB AB AB AB AB AB AB AB AB AB ABB ,», Site (A = Murray, B = Midvale)si5 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-CRA0.111.130.050.000.290.000.070.210.010.060.040.021.130.851.9857% 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% LG0.4212.430.030.000.760.000.030.100.010.030.050.0112.431.4313.8790% LR-West0.173.030.020.000.440.000.040.050.010.020.030.013.030.793.8279% LR-SEA0.505.470.020.000.710.000.030.030.010.010.080.025.471.416.8879% • Data from Life Systems Inc (1992) EvihuuooofT»ii«AB«lyie»forHunMaH«aIthRJikAMeMmeal December 1994Murray Smeller Site. Murray. Utah Pt*t 'THIS DOCUMENT WAS PREPARED BY ROY F. WESTON, INC. EXPRESSLY FOR EPA. TT SHALL NOT BE RELEASED OR DISCLOSED INWHOLE OR IN PART WITHOUT THE EXPRESS WRITTEN PERMISSION OF EPA.ept\irci\rcportsV4S_51_l«.dcc 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 ther than lead are verylikely 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. Evihmkc of Target Acilytci for Hurnm Health Kit Auenment December 1994Mumy Smelter Site, Munxy. Utah P««e 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.epi\irciVfeportiV«S_51_l6.dec ATTACHMENT 1 SUMMARY OF PRELIMINARY DATA COLLECTED AT MURRAY SMELTER c c cAttachment 1Table 1Fit Data 1984 Medium Soil slag Ground-water Sediment SurfaceWater Location On-siteN. of creekMurray MS On-site(shallow)On-site (deep) UpstreamDownstream UpstreamDownstream NumberofSamples 31-2?3-4? 32 11 11 DataQuality Level III ICP/AALevel III ICP/AALevel III ICP/AA Level III ICP/AALevel III ICP/AA Level III ICP/AALevel III ICP/AA Level III ICP/AALevel III ICP/AA Analyte Full suiteFull suiteFull suite Full suiteFull suite Full suiteFull suite Full suiteFull suite Concentration RangeSoil/Sed in mg/kg;Waters pg/l As (345-860); Pb (S928-89S4)As (26-92); Pb (29-370)As (99-192); Pb (238-1559) As (9.0U-9.5); Pb (4.5U)As (9.0U); Pb (4.5U) As (5U); 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. ep«\fri d»U.ltH P»fcl c c c Attachment 1Table 2ERB Trailer Park Sampling Medium SurfaceSoil Slag HouseDust Tap Water Location Grandview Shady Grove GrandviewShady Grove Doc & Dels Grandview Grandview NumberofSamples 56 10 62 2 28 28 DataQuality XRF XRF Level III AA/ICPLevel III AA/ICP XRF Unknown Level III AA/ICP Analyte Pb/As Pb/As Full suiteFull suite Speciation Pb/As Pb Concentration RangeSoil/Sed in mg/kg;Waters jig/f As (NA); Pb (90-2500) As (NA); Pb (180U-660) As (55-386); Pb (425-2500)As (45-65); Pb (365-740) N/A N/A Pb (5U-I7) Comments Pb acceptable for RA; As isrejected.Pb acceptable for RA; As isrejected.All acceptable.All acceptable. N/A Pb acceptable; As is rejected. All acceptable. N/A = Not Applicable ep*Vfil-<liU.lbl hie 2 c c Attachment 1Table 3Independent Investigationof 5100 S. State Street Medium Soil Ground-water Location 0-2*2-8'8-12* from 2 on-siteboreholes NumberofSamples 14195 2 DataQuality Level III ICPLevel III ICPLevel III ICP Level III ICP Analyte As/PbAs/PbAs/Pb As/Pb Concentration RangeSoil/Sed in mg/kg;Waters pglt 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. epi\(H dM.lbl F.JCJ c cAttachment 1Table 4Independent Site AssessmentMonroc, Inc. Medium SurfaceSoil SubsurfaceSoil Ground-water Location Unknown Unknown Unknown NumberofSamples 3 4 3 DataQuality Level HI Level III Level III Analyle TCLP-Pb TCLP-Pb Pb(dissolved) Concentration RangeSoil/Sed in mg/kg;Waters pg/t PbTCLP(< 100-10.000) PbTCLP(< 100-3 1,000) Pb(< 10-30) Comments Not applicable to riskassessment. Not applicable to riskassessment. Acceptable. Pice 4 c c Attachment 1Table 5UDEQ/DERR Site Investigation1992 Medium Soil Soil Soil Soil Location Doc & Dell Grandview Murray HS Background S.of Doc & Dell NumberofSamples 3 3 3 1 DataQuality Level III AA/ICP Level III AA/ICP Level HI AA/ICP Level III AA/ICP Analyte Full suite Full suite Full suite Full suite Concentration RangeSoil/Scd in mg/kg;Waters pg/f As (156-284); Pb (22,370-32,820) 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 ep«\fd dMi.tbl P*C<5 ATTACHMENT 2 RAW DATA FOR SAMPLES FROM MURRAY SMELTERTHAT WERE ANALYZED FOR MULTIPLE METALS c c c ATTACHMENT 2 METALAluminumAntimonyArsenicBariumBerylliumCadmiumCalciumChromiumCobaltCopperIronLeadMercuryMagnesiumManganeseNickelPotassiumSeleniumSilverSodiumThalliumVanadiumZinc Study E&E/TAT(I993)Matrii SoilID No. OV-SO-18Locution GrandviewOn site8950.02.455.0IS2.00.56.925700.09.04.099.0120000425.00.671400282.08.02300.00.31.0900.02.0160330.0 SoilGV-SO-20GrandviewOn site6390.02.873.0251.00.57.424100.01104.0250011200.08400086370032401001800.0106025001.315.01260.0 SoilGV-SO-32GrandviewOn site4670.06.0156.0299.00.321.217000.09.04.0200.010000.097000.54620.0242.010.01700.01.64.0250.02.013.0806.0 SoilGV-SO-36GrandviewOn site6540.03.0292.0385.00.326.937200.014.05.0283.012800.01730.00.77940.0315.015.02000.01.79.0250.01017.01450.0 SoilGV-SO-44GrandviewOn site4910.07.0189.0161.00.314.028900.011.04.0137.01 1 1000800.00.68610.0234.09.01800.02.15.0250.05.013.0931.0 SoilGV-SO-50GrandviewOn site4940.09.03860564.00.339.116600.011.04.0389.012200.02550.00.95930.0258.014.01700.02813.0500.05.01601190.0 SoilSG-SO-OIShady GroveOff site6050.04.065.0197.00.311.746700.013.04.0217.011300.0740.00.673800309.01102500.01.08.050004.017.0683.0 SoilSG-SO-09Shady GroveOff site5780.01.3450157.00.34135600.09.03.090.010100036500560200283080200000.36.025000.7907140 Note: All concentration values are in units of mg/kg(ppm)Non-detects are recorded as one/half the detection limit c c c ATTACHMENT 2 Study FIT Report (EPA 1985)Matrii Soil . SoilID No. S-8 S-7Location 77 7?METAL On site On siteAluminumAntimonyArsenicBariumBerylliumCadmiumCalciumChromiumCobaltCopperIronLeadMercuryMagnesiumManganeseNickelPotassiumSeleniumSilverSodiumThalliumVanadiumZinc 7320.027.0345.03222.02.015.095360.035.016.0928.0131443.05928.00.26443.05928.018.02845.00.621.01603.02.0165.034072.0 6919.049.0378.03250.03.017.0136628.052.021.01105.0173256.08954.00.26395.01494.025.02564.00.628.01442.03.0361.033954.0 Soil SoilS-6 S-57? North of siteOn site Off site8656.039.0860.01392.02.059.081720.038.027.01172.0129570.06882.02.08333.03597.031.02979.00.625.01645.09.0151.033817.0 16214.03.526.0157.01.01.075714.033.012.093.022643.029.0O.I26571.0429.021.04243.00.63.01643.00.538.0100.0 SoilS-4Murray HSOff site7772.08.092.098.01.09.067935.020.06.082.013098.0370.00.59076.0418.08.52701.00.65.01489.03.021.0206.0 SoilS-3Murray HSOfTsite12180.011.0192.0186.01.019.033333.023.09.0167.019359.0833.01.011090.0423.08.54814.00.66.01853.05.032.0468.0 SoilS-2Murray HSOfTsite12976.017.0185.0137.01.038.04863.023.010.0250.020714.01559.03.06071.0304.08.54976.054.010.01613.09.031.0548.0 SoilS-lMurray HSOff site9767.03.599.0151.01.05.051802.027.08.076.018198.0238.00.313837.0378.08.54203.00.65.01419.03.037.0262.0 Note: All concentration values are in units of mg/kg (ppm)Non-defects are recorded as one/half the detection limit c c c ATTACHMENT 2 Study UDEQ/DERR 1992Murrii Slag Slag SlagIDNa. MS-SO-ll 'MS-SO-12 M.S " ' 'Locution Doc & Dells Doc & Dells Doc&iMETAL On site On site On siteAluminumAntimonyArsenicBariumBerylliumCadmiumCalciumChromiumCobaltCopperIronLeadMercuryMagnesiumManganeseNickelPotassiumSeleniumSilverSodiumThalliumVanadiumZinc 18.2156.015530.0 0.4 6.0 11570206700.031380.00.1 3323.0 4.8122 01165.0123200.0 27.1244.02063.0 30.0 21.8 898.0250600.032820.00.0 3864.0 12.817.5 O.I293090740.0 12.4284.01750.0 113.0 13.1 802.083600.022370.00.7 1335.0 10.021.8 1.8129.063270.0 Slag Mv " ,»., ..uc 37.64123.0999.0 1057.0 10.4 2630.0164800.073840.06.9 1567.0 27.7651 56.732.238890.0 Slag/SoilMS-SO-15GrandviewOn site 3.9560.0861.0 31.8 18.1 8640101400014130.03.1 715.0 13.113.1 3.433.743620.0 SoilMS-SO-16GrandviewOn site 2.12246.0140.0 246.0 10.3 205.035750.0670.00.3 316.0 2.33.7 1.617.8542.0 SoilMS-SO-17Murray HSOff site 1.5186.0953 15.7 10.5 169.020500.0783.03.0 363.0 0.84.2 6.516.7296.0 SoilMS-SO-18Murray HSOff site 0.759.199.0 5.0 10.8 169.051900.0299.00.4 284.0 0.32.4 1.920.4150.0 SoilMS-SO-19Murrey HSOfTsite 0.977.0119.0 6.5 114 105.048900.036600.4 327.0 O.I1.7 2.02171780 Note: All concentration values are in units of mg/kg (ppm)Non-detects are recorded as one/half the deleclion 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 rExposure 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: DI¥, = E^-HIFi) where:DIV x = Daily intake of contaminant "x" from homegrown vegetables (mg/kg-d)Cj tll = Concentration of contaminant "x" in vegetable type "i" (mg/kg)HIFj = 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: Cu = C,.PUFUwhere:C, = Concentration of chemical "x" in soil (mg/kg)PUFU = Plant uptake factor for chemical "x" into vegetable type "i" Combining these two equations yields: Vegetable Classes For this analysis, vegetables are classified into four categories: CategoryLeafy vegetablesLegumesRoot vegetablesGarden fruits ExampleLettuce, cabbageBeansCarrotsTomatoes Baseline Human Health Risk Assessment May 1997Document 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 = C^/C^, 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 et 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 ArsenicLead Baes et al. 1984Vegetative(Bv) 0.040.045 Reproductive(Br) 0.0060.009 USEPA 1992Leafy 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 4500490-AOAC Page B-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. information were better documented and justified. For lead, the values from Baes wereemployed since no other data were located. 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):Legumes (Beans):Roots (Carrots):Fruits (Tomatoes): 0.06 g/g,0.21 g/g0.14g/g0.10 g/g Using these conversion factors, the wet-weight adjusted PUFs for common vegetable types areas shown below: Chemical ArsenicLead PUF (wet weight)Leafy 1. IE-032.7E-03 Legumes 2. IE-041.9E-03 Roots 5.6E-041.3E-03 Fruit l.OE-049.0E-04 Human Intake Factors (HIFs) The basic equation for calculation of human intake of home-grown vegetables is: HIFi CFBW EF-AT where: 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 (IE-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 Assessment May 1997Document Control Number 4500-090-AOAC Page B-3THIS 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. Vegetable Intake Rates National data on the average amount of each type of vegetable ingested per day as a functionof age are available hi 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) 7.220.1 5.115.9 Adult (age 25-30) 39.141.712.349.0 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) ChildMean 1522NA RME 1566NA AdultMean 709970 RME 70303070 Based on these input parameters, the values of the term E(PUF • HIP7) for each chemical are asshown below. For convenience, this term is referred to as the "Vegetable Intake factor" (VIF). Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page B-4THIS 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. Population Child Adult Chemical ArsenicLeadArsenicLead VIF (kg/kg-day)Average6.01E-082.86E-074.91E-081.91E-07 RME1.80E-078.57E-071.47E-075.73E-07 The dose from garden vegetables for each chemical "x" is then calculated as: DIV., = CM-E(PUFu.HIFi) 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 hi 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 Page B-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. EEPA. 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. Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page B-6THIS 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. 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 (Ci „) or flushed waterAF = Absorption fraction from first draw water (AF1$t) or flushed water (AFf)IR = Ingestion rate of first draw water (IR,5t) 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 hi concentration hi 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 thathi first draw water (White, 1995). Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page C-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. 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. Parameterc/clit(hmwIR (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 VIE 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 Vffl by Paul White, EPA ExposureAssessment Group (3/21/95) Baseline Human Health Risk Assessment May 1997Document Control Number 4SOO-090-AOAC Page C-2THIS DOCUMENT WAS PREPARED BY ROY F. WESTON, INC. EXPRESSLY FOR EPA. FT SHALL NOT BE RELEASED ORDISCLOSED IN WHOLE OR IN PART WITHOUT THE EXPRESS WRITTEN PERMISSION OF EPA. APPENDIX D DETAILED CALCULATION OF EXPOSURE AND RISK Pan 1: Concentration Data for Surface SoilPan 2: Concentration Data for Subsurface SoilPan 3: Concentration Data for Paired Soil and Dust SamplesPan 4: Exposure and Risk from ArsenicPan 5: Exposure and Risk from Lead Appendix D Parti Concentration Data for Surface Soil APPENDIX D - PART 1 SURFACE SOIL (0-r) DATA FROM MURRAY SMELTERLOCATION EU1 SITE.CODE Location CodeEU1S-1EU1S-10EU1S-11EU1S-12EU1S-13EU1S-14EU1S-15EU1S-16EU1S-17EU1S-18EU1S-19EU1S-2EU1S-3EU1S-4EU1S-5EU1S-6EU1S-7EU1S-8EU1S-9 ParameterhitstotalminmaxavgUCL SOILJJEPT 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.0-2 in.0-2 in.0-2 in. TYPE.NAMESoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoil Arsenic13192.56301301424 AS_TOT FLAG_8SU841355U560335 U1105505 U55U5463095U7390 Lead19198315000290516147 PB_TOT FLAGJO28021059086001105800500130006703700100170831000460013036030015000 p:\brattin\rnurTay\surfsoil.xls Page D-1-1 APPENDIX D - PART 1 SURFACE SOIL (0-2") DATA FROM MURRAY SMELTERLocation EU2 ParameterhitstotalminmaxavgUCL SITE_CODE Location CodeEU2S-1EU2S-10EU2S-11EU2S-12EU2S-13EU2S-14EU2S-15EU2S-16EU2S-17EU2S-2EU2S-3EU2S-4EU2S-5EU2S-6EU2S-7EU2S-8EU2S-9 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.0-2 in. TYPE_NAMESoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoil Arsenic13172.536079681 AS_TOT FLAG_8242303605U5U70120833345 U17995U2225072 Lead1717989900287919140 PB_TOT FLAGJO18099008900983100710029036056034013027073004403909000590 p:\brattin\murray\surfsoil.xls Page D-1-2 APPENDIX D - PART 1 SURFACE SOIL (0-2") DATA FROM MURRAY SMELTERLocation EU3 ParameterhitstotalminmaxavgUCL SITE_CODE Location Code SOIL_DEPTEU3S-1 0-2 in.EU3S-2 0-2 in.EU3S-3 0-2 in.EU3S-4 0-2 in.EU3S-5 0-2 in.EU3S-6 0-2 in.EU3S-7 0-2 in.EU3S-8 0-2 in.EU3S-9 0-2 in.EU3S-10 0-2 in.EU3S-11 0-2 in.EU3S-12 0-2 in.EU3S-13 0-2 in.EU3S-14 0-2 in.EU3S-15 0-2 in.EU3S-16 0-2 in.EU3S-17 0-2 in.EU3S-18 0-2 in. REMARKS WETCHEM TYPE_NAMESoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoil Arsenic181897700117257840 ASJTOT FLAG_816111511919492301900180026002900770067013001100100660 Lead181874330009548531032 PB_TOT FLAGJO951301301707415052016001700019000330002400023000260008500780059004800 p:\brattin\murray\surfsoil.xls Page D-1-3 APPENDIX D - PART 1 SURFACE SOIL (0-2") DATA FROM MURRAY SMELTERLocation EU4 SITE.CODE Location CodeEU4SMEU4S-10EU4S-11EU4S-12EU4S-13EU4S-14EU4S-15EU4S-16EU4S-17EU4S-18EU4S-19EU4S-2EU4S-20EU4S-3EU4S-4EU4S-5EU4S-6EU4S-7EU4S-8EU4S-9 ParameterhitstotalminmaxavgUCL SOIL_DEPT REMARKS0-2 hi.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_NAMESoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoil Arsenic13202.55400418761B AS_TOT FLAG_811005U235U5U104145U110032145997165U12054002605U5U Lead2020371500017507623 PB_TOT FLAGJO92004852170160032026066630820160110025002303718001500077014092 p:\brattin\murray\surfsoil.xls Page D-1-4 APPENDIX D - PART 1 SURFACE SOIL (0-2') DATA FROM MURRAY SMELTERLocation EU5 SITE.CODE Location CodeEU5S-1EU5S-10EU5S-11EU5S-12EU5S-13EU5S-14EU5S-15EU5S-16EU5S-17EU5S-16EU5S-19EU5S-2EU5S-20EU5S-3EU5S-4EU5S-5EU5S-6EU5S-7EU5S-8EU5S-9 ParameterhitstotalminmaxavgUCL 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.0-2 in.0-2 in.0-2 in.0-2 in. TYPE_NAMESoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoil Arsenic19202.5520100285 AS_TOT FLAG_821240771005U140120165413952010019130100140488953 Lead20201101000027547253 PB_TOT FLAGJO5300390019001000019001600380020008301100120020002400110820062066002302801100 p:\brattin\murray\surfsoil.xls Page D-1-5 APPENDIX D - PART 1 SURFACE SOIL (0-2") DATA FROM MURRAY SMELTERLocation EU6 SITE.CODE Location CodeEU6S-1EU6S-10EU6S-11EU6S-12EU6S-13EU6S-14EU6S-15EU6S-16EU6S-17EU6S-18EU6S-19EU6S-2EU6S-20EU6S-3EU6S-4EU6S-5EU6S-6EU6S-7EU6S-8EU6S-9 ParameterhitstotalminmaxavgUCL SOIL_DEPT REMARKS0-2 in"0-2 in.0-2 in.0-2 In.0-2 in.0-2 in.0-2 in. WETCHEM0-2 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_NAMESoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoil Arsenic19202.551004321788 AS_TOT FLAG_8~510040026682202349722305U2101200120120987130250170150 Lead202071760022978717 PB_TOT FLAGJO230010004807806100190250270840716100480760049002800150530530030002800 p:\brattin\murray\surfsoil.xls Page D-1-6 APPENDIX D - PART 1 SURFACE SOIL (0-2") DATA FROM MURRAY SMELTERLocation EU7 SITE.CODE Location CodeEU7S-1EU7S-10EU7S-11EU7S-12EU7S-13EU7S-14EU7S-15EU7S-16EU7S-17EU7S-18EU7S-19EU7S-2EU7S-3EU7S-4EU7S-5EU7S-6EU7S-7EU7S-8EU7S-9 ParameterhitstotalminmaxavgUCL 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.0-2 in.0-2 in.0-2 in. TYPEJJAMESoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoil Arsenic19191822004181220 AS_TOT FLAG.85103137084052047041013031050021184601802502201104002200 Lead1919921200025246644 PB_TOT FLAGJO470092610140014001400280016001800690022022007400120006705103705801300 p:\brattin\murray\surfsoil.xls Page D-1-7 APPENDIX D - PART 1 SURFACE SOIL (0-2") DATA FROM MURRAY SMELTERLocation EU8 ParameterhitstotalminmaxavgUCL SITE_CODE Location Code SOIL_DEPTEU8-1 0-2 in.EU8-10 0-2 in.EU&-2 0-2 in.EU&-3 0-2 in.EU8-4 0-2 in.EU8-5 0-2 in.EU8-6 0-2 in.EU8-7 0-2 in.EU8-8 0-2 in.EU8-9 0-2 in. REMARKS TYPE_NAMESoilSoilSoilSoilSoilSoilSoilSoilSoilSoil Arsenic1010645000167425568 AS.TOT FLAG_873064260035003300830684505000200 Lead101057025000617728783 PB_TOT FLAGJO1800570900025000740010000900230031001700 p:\brattin\murray\surfsoil.xls Page D-1-8 APPENDIX D - PART 1 SURFACE SOIL (0-r) DATA FROM MURRAY SMELTERLocation EU9 Parameter Arsenic Leadhits 10 10total 10 10min 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\surfsoil.xls Page D-1-9 APPENDIX D - PART 1 SURFACE SOIL (0-2") DATA FROM MURRAY SMELTERLocation EU10 ParameterhitstotalminmaxavgUCL Arsenic9102.522069383 Lead1010ISO1100538932 SITE.CODE Location Code SOIL.DEPTEU10-1 0-2 in.EU10-10 . 0-2 in.EU10-2 0-2 in.EU10-3 0-2 in.EU10-4 0-2 in.EU10-5 0-2 in.EU10-6 0-2 in.EU10-7 0-2 in.EU10-8 0-2 in.EU10-9 0-2 hi. REMARKS TYPE_NAMESoilSoilSoilSoilSoilSoilSoilSoilSoilSoil AS_TOT FLAG_8763522012027418437455 U PB_TOT FLAGJO6805201100810150300540490610180 p:\brattin\murray\surfsoil.xls PageD-1-10 APPENDIX D - PART 1 SURFACE SOIL (0-2") DATA FROM MURRAY SMELTERLocation EU11 Parameter Arsenic Leadhits 8 10total 10 10min 2.5 100max 78 5700avg 19 814UCL 62 1950 SITE_CODE Location Code SOIL_DEPT REMARKS TYPE_NAME AS_TOT FLAG_8 PB_TOT FLAGJOEU11~1 0-2 in" Soil 5U 5700EU11-10 0-2 in. Soil 10 170EU11-2 0-2 in. Soil 30 280EU11-3 0-2 in. Soil 78 670EU11-4 0-2 in. Soil 10 220EU11-5 0-2 in. Soil 12 260EU11-6 0-2 in. Soil 12 160EU11-7 0-2 in. Soil 9 290EU11-8 0-2 in. Soil 27 290EU11-9 0-2 in. Soil 5U 100 p:\brattin\murray\surfsoil.xls Page D-1-11 APPENDIX D - PART 1 SURFACE SOIL (0-2") DATA FROM MURRAY SMELTERLocationISZ1 SITE_CODE150 W BERG150 W BERG171 W BERG171 W BERG171 W BERG1 74 W BERG1 75 W BERG175 W BERG1 75 W BERG1 79 W BERG184 W BERG248 W VINE275 W BERG275 W BERG4913 S 3004913 S 3005061 S 3005061 S 3005061 S 300 LocationISZ-1ISZ-1ISZ-1ISZ-1ISZ-1ISZ-1ISZ-1ISZ-1ISZ-1ISZ-1ISZ-1ISZ-1ISZ-1ISZ-1ISZ-1ISZ-1ISZ-1ISZ-1ISZ-1 ParameterhitstotalminmaxavgUCL 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.0-2 in.0-2 in.0-2 in. TYPE_NAMESoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoil Arsenic191913340106222 AS_TOT FLAG_89514051 J4180 J4340 J456190290292301101317134714645784 Lead1919250320012991997 PB_TOT FLAGJO120017007902100320076019002200550270015002803202501200100011008401100 p:\brattin\murray\surfsoil.xls Page D-1-12 APPENDIX D - PART 1 SURFACE SOIL (0-Z1) DATA FROM MURRAY SMELTERLocation ISZ2 ParameterhitstotalminmaxavgUCL SITE_CODE115E5460166E53005350 S HILLSIDE ISZ-25370 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 Location SOIL.DEPT REMARKS TYPE_NAMEISZ-2 0-2 In. SoilISZ-2 0-2 in. Soil0-2 in. Soil0-2 in. Soil0-2 in. Soil0-2 in. Soil0-2 in. Soil0-2 in. Soil0-2 in. Soil0-2 in. Soil Arsenic7102.5371657 AS_TOT FLAG_85U105U5U37272329717 J4 Lead101080410241369 PB_TOT FLAGJO19080150190380250410230120410 p:\brattin\murray\surfsoil .xls PageD-1-13 APPENDIX D - PART 1 SURFACE SOIL (0-2") DATA FROM MURRAY SMELTERLocation ISZ3 Parameter Arsenichits 10total 10min 7max 110avg 55UCL 128 SITE.CODE Location SOIL_DEPT REMARKS TYPE_NAME AS_TOT FLAG_8ISZ-3-1 ISZ-3 0-2 in. Soil 61ISZ-3-10 ISZ-3 0-2 in. Soil 110ISZ-3-2 ISZ-3 0-2 in. Soil 44ISZ-3-3 ISZ-3 0-2 in. Soil 80ISZ-3-4 ISZ-3 0-2 in. Soil 100ISZ-3-5 ISZ-3 0-2 in. Soil 19ISZ-3-6 ISZ-3 0-2 in. Soil 39ISZ-3-7 ISZ-3 0-2 in. Soil 7ISZ-3-8 ISZ-3 0-2 in. Soil 40ISZ-3-9 ISZ-3 0-2 in. Soil 48 Lead101011016007681757 PBJTOT FLAGJO890110084011001600230500110640670 p:\brattin\murray\surfsoil.xls Page D-1-14 APPENDIX D - PART 1 SURFACE SOIL (0-2") DATA FROM MURRAY SMELTERLocation ISZ4 ParameterhitstotalminmaxavgUCL Arsenic151581704575 SITE.CODE11 W ROSE25EWILSO26WWILSO3 E ROSE C3 E ROSE C31 W ROSE31 W ROSE43 E ROSE5479 S SPU5484 SSPU8EWASHIN8EWASHIN91WWASHI91 WWASHI5531 S SPURR LocationISZ-4ISZ-4ISZ-4ISZ-4ISZ-4ISZ-4ISZ-4ISZ-4ISZ-4ISZ-4ISZ-4ISZ-4ISZ-4ISZ-4ISZ-4 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. TYPE.NAMESoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoil AS_TOT FLAG_8170661128213124263322974344498 Lead1515110780391516 PB_TOT FLAGJO360780340350390410420440270110500620370330170 p:\brattin\murray\surfsoil.xls PageD-1-15 APPENDIX D - PART 1 SURFACE SOIL (0-r) DATA FROM MURRAY SMELTERLocationISZ5 SITE_CODE1 12 W WASH112WWASH141 AMERIC180 W WASH19WHILLCREST19WHILLCREST44 W WASH!53WAMERI53WAMERI74WWASHI74 W WASH!85WAMERI89WAMERI9EWASHIN9EWASHIN9EWASHIN LocationISZ-5ISZ-5ISZ-5ISZ-5ISZ-5ISZ-5ISZ-5ISZ-5ISZ-5ISZ-5ISZ-5ISZ-5ISZ-5ISZ-5ISZ-5ISZ-5 SOIL.DEPT0-2 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. ParameterhitstotalminmaxavgUCL REMARKS TYPE_NAMESoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoilSoil Arsenic161671304265 ASJTOT FLAG_813034334138758342628283367624612 Lead1616130640426531 PB_TOT FLAGJO440500360350360210480640360420460430560590520130 p:\brattin\murray\surfsoil.xls Page D-1-16 APPENDIX D - PART 1 SURFACE SOIL (0-21 DATA FROM MURRAY SMELTERLocation SITE_CODE119 W WOOD122AMERIC125 W 5325137W5325137 W 5325142AMERIC190AMERIC5365 SRIL5360 S HILLCRES ISZ-672 AMERICA ISZ-693WWOODR ISZ-693WWOODR ISZ-6 ISZ6 Parameter Arsenichits 11total 12min 2.5max 120avg 52UCL 162 Location SOILJDEPT REMARKS TYPE_NAME ASJTOT FLAG.8ISZ-6 0-2 in. Soil 120ISZ-6 0-2 in. Soil 52ISZ-6 0-2 in. Soil 1000-2 in. Soil 150-2 in. Soil 800-2 In. Soil 650-2 in. Soil 270-2 in. Soil 290-2 in. Soil 490-2 in. Soil 590-2 In. Soil 5 U0-2 in. Soil 25 ISZ-6ISZ-6ISZ-6ISZ-6ISZ-6 Lead121212018006571148 PB_TOT FLAGJO18004601500270830450340710560390120450 p:\brattin\murray\surfsoil.xls Page D-1-17 APPENDIX D - PART 1 SURFACE SOIL (0-7) DATA FROM MURRAY SMELTERLocation ISZ-7 SITE_CODE116WOODRO123W5300141 W 5300151 W 5300531OSHILLCRES ISZ-757 W 5300 IS2-764WOODROW IS2-781 W 5300 ISZ-790WOODROW ISZ-797 W 5300 ISZ7 Parameter Arsenichits 10total 10min 59max 180avg 126UCL 158 Location SOIL.DEPT REMARKS TYPE_NAME ASJTOT FLAG_8ISZ-7 0-2 In. Soil 59ISZ-7 0-2 in. Soil 170ISZ-7 0-2 in. Soil 1400-2 in. Soil 1200-2 in. Soil 1200-2 in. Soil 1100-2 in. Soil 1600-2 in. Soil 1000-2 in. Soil 100COMPOSITE Soil 180ISZ-7 0-2 in. Lead1010720180012221597 PBJTOT FLAG_10760160073091014001100180072014001800 p:\brattin\murray\surfsoil.xls PageD-1-18 APPENDIX D - PART 1 SURFACE SOIL (0-2") DATA FROM MURRAY SMELTERLocation ISZ8 ParameterhitstotalminmaxavgUCL Arsenic7122.5450762117 Lead121266730010625877 SITE_CODE Location SOIL_DEPT REMARKS TYPE_NAME AS_TOT FLAGjB249 W VINE ISZ-8 0-2 in. Soil 4505125 S 300 ISZ-8 0-2 In. Soil 675135 S 300 ISZ-8 0-2 in. Soil 755135 S 300 ISZ-8 0-2 in. Soil 465139 S 300 ISZ-8 0-2 in. Soil 2205139 S 300 ISZ-8 0-2 in. Soil 355201S 300 ISZ-8 0-2 in. Soil 5UISZ-8-1 ISZ-8 0-2 in. Soil 5 UISZ-8-2 ISZ-8 0-2 in. Soil 5 UISZ-8-3 ISZ-8 0-2 in. Soil 5 UISZ-8-4 ISZ-8 0-2 in. Soil 5UISZ-8-5 ISZ-8 0-2 in. Soil 8 PB_TOT FLAGJO73008501200870110077066120140110100120 p:\brattin\murray\surfsoil.xls PageD-1-19 Appendix D Part 2 Concentration Data for Subsurface Soil APPENDIX D -- PART 2 LEAD CONCENTRATIONS IN ON-SITE SUBSURFACE SOIL AT MURRAY SMELTER IHlftillllCommercialZone ResidentialTrailerparks iiiiiit1 2456 7 8 9 10 iillliiiliEU1-1EU1-2EU2-1EU4-1EU5-1EU6-1EU6-2EU6-3EU6-4EU6-5EU6-6EU6-7EU6-8EU6-9EU6-10EU6-1 1EU6-12EU6-13EU6-14EU6-15EU6-16EU6-17EU6-18EU6-19EU7-1EU7-2EU7-3EU7-4 EU8-2EU8-10EU9-3EU9-10EU10-6EU10-8 18005010000320099632400390092085007800510072818084031004002200030040002100310820850011000630020002300fliiiiiliiill90005706201600540610 lllllillli650059010000480061791300180073400044041002100180087012003800110970022000280012001100023001200010003900570 Iliilltilal340092017065005601200 1200014000100001502607479688247002600580110001202600150640677926032007701108799002407072 35001100755800530670 iiiiliHili 150009200669062831508491007846011000621202701800768691220578192140007413076iiiiiilllijli30005209640000530430 iiililiiiii 160008200666007310097947692901900068120110707382100240888510012000639275 p:\brattin\murray\subsoil.xls Page D-2-1 APPENDIX D -- PART 2 ARSENIC CONCENTRATIONS IN ON-SITE SUBSURFACE SOIL AT MURRAY SMELTER CommercialZone ResidentialTrailerparks Ililllllll1 2456 7 iittia^i8 9 10 EU1-1EU1-2EU2-1EU4-1EU5-1EU6-1EU6-2EU6-3EU6-4EU6-5EU6-6EU6-7EU6-8EU6-9EU6-10EU6-1 1EU6-12EU6-13EU6-14EU6-1 5EU6-16EU6-17EU6-18EU6-19EU7-1EU7-2EU7-3EU7-4 EU8-2EU8-10EU9-3EU9-10EU10-6EU10-8 illlllllllill 295320511832800920120646409516769440270270015590100031080480001204200240034000 2600641001908445 llllllilllll 59340620512076003001026028170048030015066260025120018001200240015001000033730370014000iiiiiiliiii7200110141200140130 llillllllli 35100027041467647001416650310813800281600987055271100900712014014025490 llllllllll630020019880140120 lliHlllfiil 1000130635520002331180874220089017220013151033120722618150380 Illtfilliii!620013013750011083 iiiiiimii 1500300625620600137756936005220162721179361901883510200360 p:\brattin\murray\subsoil.xls Page D-2-2 APPENDIX D - PART 2 SUBSURFACE DATA FROM OFF-SITE LOCATIONSMurray Smelter ISZ-1ISZ-1ISZ-2ISZ-2ISZ-3ISZ-3ISZ-4ISZ-4ISZ-5ISZ-5ISZ-6ISZ-6ISZ-7ISZ-7ISZ-8ISZ-8 mmmm*ISZ-1ISZ-1ISZ-2ISZ-2ISZ-3ISZ-3ISZ-4ISZ-4ISZ-5ISZ-5ISZ-6ISZ-6ISZ-7ISZ-7ISZ-8ISZ-8 i ARSENIC CONCENTRATION (p 171 WBERG275 W BERG541 OS HILLSIDEISZ-2-1ISZ-3-10ISZ-3-45479 S SPU8 E WASHIN44 W WASH!89 W AMERI122AMERIC93 W WOODR151 W530081 W 5300249 W VINEISZ-8-2 171 WBERG275 W BERG541 OS HILLSIDEISZ-2-1ISZ-3-10ISZ-3-45479 S SPU8 E WASHIN44 W WASH!89 W AMERI122AMERIC93 W WOODR151 W530081 W 5300249 W VINESZ-8-2 51173727110100339758675251201004505 silSsiiSilsSii1201853503201203612044110613216021026011 23022921102901101815079120705412020024018 m)iWiilltii 49441704161053687100675249864805415 LEAD CONCENTRATION (ppm)Miiifcii790320380250110016002705004805604601209107207300140 1300240380210150097028064036053044033090014004400140 18003003107001600680120710440510440410100013002800190 4203204201503200150872904702303704206102800550190 SUMMARY STATISTICSi^lll^SSli69 73 214 68 81 47 185 132 ;ii!i;iiS!17 27 53 6 44 5 86 5 tllliifiiSl230 170 610 150 120 70 480 450 SUMMARY STATISTICSisiiiilll334 1089 520 486 443 588 2659 165 illiisi240 150 87 290 230 120 550 140 420 3200 1600 710 560 1000 7300 190 p:\brattin\murray\subsoil.xls Page D-2-3 Appendix D Part3 Paired Soil and Dust Samples c cAPPENDIX D - PART 3 SOIL DUST RELATIONSHIP AT MURRAY SMELTERArsenic Index Location1 171 W. Berger2 174 W. Berger3 5135 S. 300 W.4 5370 Hillside5 5410 Hillside6 HillcrestJHS7 91 W. Washington8 5479 Spurrier9 8 E. Washington10 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 151 W. 5300 S20 123 W. 5300 S21 64 Woodrow22 81W. 5300 S Nondetects shown by shaded cells: MeanStdev m«*m515675KSSSSSSffSSiStyssssfsKffSt3727443397661767584927 2861120170160100 :<B»QI?;ini9!P*!ei'5t?S;Sy»Il:^^1807446 23 29 7 17 3849 43 13 2844 51 80 100 39 7 40 48 C MeanCone (ppm)Soil (0-2) HI115.565.060.52.537.0 m23.546.5 $^33.070.066.015.067.058.049.027.02.528.052.2120.0170.0160.0100.0 S¥»WSiS!SWW^^:WS^lW43232913 12 13942313 12242719282424 1849471551 MeanConc (PPm) 43232913512511.513942312.5242719282429 18 22.2549471551 62.245.9 26.820.1 file = c:\qpw\murray\soildust.wb1 c cAPPENDIX D - PART 3 SOIL DUST RELATIONSHIP AT MURRAY SMELTERLead Index Location1 171 W. Berger2 174 W. Berger3 5135 S. 300 W.4 5370 Hillside5 5410 Hillside6 HiDcrestJHS7 91 W. Washington8 5479 Spurrier9 8 E. Washington10 25 E. Wilson11 275 W. Berger12 89 W.American13 44 W.Washington14 5380 S. Hiflcrest15 190 W.American16 93W. Woodrow17 74 W.Washington18 Murray HS19 151 W. 5300 S20 123 W. 5300 S21 64 Woodrow22 81 W. 5300 S MeanStdev mam790760120019038025037027050078032056048056034012042089091016001800720 21001000870 410330 620 250 460840 230 120 410 440 850 1100 1600 500 110 640 673458 C MeanCone, (ppm)I!! Soil (0-2)14458801035190380310350270560780285560480560340120440670 80091016001800720 ^jjiii^ifiii^42620367614910121520392 741995315508257 143232256219216178221 207 219 310757522276496 MeanCone, (ppm)Dust42620367614910121520383199+m^&$m508200232256219216178239757522276496 530 (with outlier)1084 (with outlier) 303 (without outlier)186 (without outlier)file = c:\qpw\murray\soildustwb1 c REGRESSION ANALYSIS ARSENIC Regression Output:ConstantStdErrofYEstR SquaredNo. of ObservationsDegrees of Freedom X Coefficients)Std Err of Coef. 16.3919.080.152220 0.1680.091 C cAPPENDIX D ~ PART 3 LEAD Regression Output:ConstantStdErrofYEstR SquaredNo. of ObservationsDegrees of Freedom X Coefficients)Std Err of Coef. (Excludes outlier)97.98143.590.56 96 0.3180.121 SUMMARY STATISTICS ArsenicLeadLead N Mean Min Max22 27 5 9422 530 83 5315 <- Note: includes outlier21 303 83 757 <~ 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-11ISZ-1ISZ-2ISZ-3ISZ-4ISZ-5ISZ-6ISZ-7ISZ-8 Max630360770054005205100220050002102207834037110170130120180450 Avg13079117241810043241816741186919106165545425212676 UCL14246815784076182851788122025568222383622225712875651621582117 EPC630 (max)360 (max)7700 (max)5400 (max)285178812205000 (max)210 (max)220 (max)6222237 (max)110 (max)7565120 (max)158450 (max) CONCENTRATION DATA FOR ARSENIC IN SLAG (ppm)Composite 591 CONCENTRATION DATA FOR ARSENIC IN GROUNDWATER (mg/L) Adj 1.2872.870.0780.00250.0060.01840.270.0060.01327.180.00250.00250.0142.3472.9030.0520.270.2161.9740.236 0.790.0060.4390.00250.0190.0250.00250.0690.039 Aquifer Shallow Intermediate Well ID GW-1GW-2JMM-08MW-100MW-101MW-102MW-103MW-104MW-105MW-106MW-107MW-108MW-109MW-110MW-111MW-112UTBN-1Well!Well 2Well 3 GW-1AGW-1ARGW-2AMW-101DMW-104DMW-105DMW-108DMW-109DMW-112D TOTALCone Qual 1.2872.870.0780.005 U0.0060.01840.270.0060.01327.180.005 U0.005 U0.0142.3472.9030.0520.270.2161.9740.236 0.790.0060.4390.005 U0.0190.0250.005 U0.0690.039 DISSOLVEDCone dual 1.5342.9940.050.005 U0.005 U0.0120.1810.0060.01228.930.005 U0.005 U0.0212.3442.8610.0450.2580.281.9380.207 0.6360.005 U0.3110.005 U0.0140.020.005 U0.0440.038 Adj 1.5342.9940.050.00250.00250.0120.1810.0060.01228.930.00250.00250.0212.3442.8610.0450.2580.281.9380.207 0.6360.00250.3110.00250.0140.020.00250.0440.038 p:\brattin\murray\as-risk.xls Page CM-1 APPENDIX D-PART 4MURRAY SMELTER - CALCULATION OF EXPOSURE AND RISK FROM ARSENIC Oral Toxicity factorsRfDs RfDc oSFArsenic 6.0E-03 3.0E-04 1.5 Bioavailability factorsSoil Dust SlagArsenic 0.26 0.26 0.45 Soil/Dust RelationshipDO KsdArsenic 10 0.20 p:\brattin\murray\as-risk.xls Page D-4-2 APPENDIX D-PART 4MURRAY SMELTER - CALCULATION OF EXPOSURE AND RISK FROM ARSENIC HUMAN EXPOSURE PARAMETERS AND HIFs ScenarioIngestion ofsoil and dust Soil + Dust Soil Dust ScenarioIngestion ofslag by teen(age 12-18) ScenarioIngestion ofGroundwater AVERAGE SCENARIO RME SCENARIOParameterIR (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(oVyr)ED(yr)AT (chronic)AT (lifetime) cHIFgIHIFg ParameterIR (L/d)BW(kg)EF(d/yr)ED(yr)AT (chronic)AT (lifetime) cHIFwIHIFw Resident100500.451570234279970 1.31E-061.68E-07 5.88E-077.56E-08 7.18E-079.23E-08 Teen5057257770 6.01 E-086.01 E-09 Resident1.4702349970 1.28E-021.65E-03 NCI-Worker 500.5 70219 55- 570 4.29E-073.06E-08 2.14E-071.53E-08 2.14E-071.53E-08 Worker0.7702195570 6.00E-034.29E-04 Cl-Worker 2401.0 70185 55570 1.74E-061.24E-07 1.74E-061.24E-07 O.OOE+00O.OOE+00 Resident2001000.451570350624303070 3.65E-061.57E-06 1.64E-067.05E-07 2.01 E-068.61 E-07 Teen10057507770 2.40E-072.40E-08 Resident270350303070 2.74E-021.17E-02 NCI-Worker 500.5 70250 25252570 4.89E-071.75E-07 2.45E-078.74E-08 2.45E-078.74E-08 Worker170250252570 9.78E-033.49E-03 Cl-Worker 4801.0 70211 25252570 3.95E-061.42E-06 3.96E-061.42E-06 O.OOE-t-00O.OOE+00 p:\brattin\murray\as-risk.xls Page D-4-3 MURRA^ APPENDIXD-PART4 JLTER - CALCULATION OF EXPOSURE AND RISK FROM ARSENIC IDIXJ3 MEDIUM: SURFACE SOIL AND DUSTPOPULATION: RESIDENTS Chronic Exposure (Noncancw Risk) Based on EPC (UCL or Max) ExposureLocationEU-8EU-9EU-10EU-11ISZ-1ISZ-2ISZ-3ISZ-4ISZ-5ISZ-6ISZ-7ISZ-8 ConeEPC500021022082222371107565120158450 HIFs5.88E-075.88E-075.88E-075.88E-075.88E-075.88E-075.88E-075.88E-075.88E-075.88E-075.88E-075.88E-07 HIFd7.18E-077.18E-077.18E-077.18E-077.18E-077.18E-077.18E-077.18E-077.18E-077.18E-077.18E-077.18E-07 RBAs0.260.260.260.260.260.260.260.260.260.260.260.26 fRBAd0.260.280.260.260.260.260.260.260.260.260.260.26 wwsg<DO101010101010101010101010 I Ksd0.200.200.200.200.200.200.200.200.200.200.200.20 Dlsd9.5E-044.2E-OS4.4E-051.4E-OS4.4E-058.9E-062.3E-051.6E-051.4E-052.5E-053.2E-058.7E-05 CRTD3.0E-04t;ii;3.0E-043.0E-043.0E-043.0E-043.0E-043.0E-043.0E-043.0E-043.0E-043.0E-043.0E-04 HQsdJjE+OlS;"lE-011E-01SE-021E-013E-028E-025E-025E-028E-021E-013E-01 Ufetbm Exposure (Cancer Risk) ExposureLocationEU-8EU-9EU-10EU-11ISZ-1ISZ-2ISZ-3ISZ-4ISZ-5ISZ-6ISZ-7ISZ-8 ConeEPC500021022062222371107565120158450 HIFS7.56E-087.56E-087.56E-087.56E-087.56E-087.56E-087.56E-087.56E-087.56E-087.56E-087.56E-087.56E-08 HIFd9.23E-089.23E-089.23E-089.23E-089.23E-089.23E-089.23E-089.23E-089.23E-089.23E-089.23E-089.23E-08 RBAs0.260.260.260.260.260.260.260.260.260.260.260.26 /RBAd0.260.260.260.260.260.260.260.260.260.280.260.26 Wfctt^DO101010101010101010101010 a Ksd0.200.200.200.200.200.200.200.200.200.200.200.20 Dlsd12E-045.4E-065.6E-061.7E-085.7E-061.1 E-062.9E-062.1E-061.8E-063.2E-064.1E-061.1E-05 OSF1.5E+OOpj?1.5E+001.5E+001.5E+001.5E+001.5E+001.5E+0015E+001.5E+001.5E+001.5E+001.5E+00 Rhk2^-648E-068E-063E-068E-082E-064E-063E-063E-065E-066E-062E-05 c ConeEPC500021022062222371107565120158450 ConeEPC500021022062222371107565120158450 HIFs1.64 E-061.64E-061.64E-061.64E-061.64E-081.64E-061.64E-061.64E-061.64E-061.64E-061.64E-061.64E-08 Hlrs7.05E-077.05E-077.05E-077.05E-077.05E-077.05E-077.05E-077.05E-077.05E-077.05E-077.05E-077.05E-07 HIFd2.01 E-062.01 E-062.01 E-062.01 E-082.01 E-062.01 E-062.01 E-062.01 E-062.01 E-062.01 E-062.01 E-062.01 E-08 HIFd8.61 E-078.61 E-078.61 E-078.61 E-078.61E-078.81 E-078.61E-078.61 E-078.61E-078.61 E-078.61 E-078.61E-07 RBAs0.260.260.260.260.260.260.260.260.260.260.260.26 RBAS0.260.260.260.260.260.260.260.260.260.260.260.26 RMERBAd0.260.260.280.260.260.260.260.260.260.260.260.26 RMERBAd0.260.260.260.260.260.260.260.260.260.260.260.26 DO101010101010101010101010 DO101010101010101010101010 Ksd0.200.200.200.200.200.200.200.200.200.200.200.20 Ksd0.200.200.200.200.200.200.200.200.200.200.200.20 Dlsd2.7E-031.2E-041.2E-0438E-051.2E-042.5E-056.4E-054.SE-054.0E-056.9E-058.9E-052.4E-04 Dlsd1.1E-035.0E-055.2E-051.6E-055.3E-051.1E-052.7E-051.9E-051.7E-053.0E-053.8E-051.0E-04 cRfD3.0E-04 33.0E-043.0E-043.0E-043.0E-043.0E-043.0E-043.0E-043.0E-043.0E-043.0E-043.0E-04 OSF1.5E+001.5E+001.5E+001.5E+001.5E+001.5E+001.5E+001.5E+001.5E+001.5E+001.5E+001.5E+00;'/ HQsdpffiEfBS">E-bV4E-011E-014E-018E-022E-012E-01IE-012E-013E-018E-01 Risk2E-038E-058E-052E-058E-052E-054E-053E-053E-054E-056E-05L^t-fr*: p:\bcattin\inurray\as-rfsk.xls PageD-4-4 APPENDIX D-PART 4 iLTER - CALCULATION OF EXPOSURE AND RISK FROM ARSENIC c cMEDIUM: SURFACE SOIL AND DUSTPOPULATION: NCI-WORKER Chronic Exposure (Noncancer Risk) SasetfonEPCft/CLorMn^ ExposureLocationEU-1EU-2EU-3ElMEU-5EU-6EU-7 ConeEPC6303607700540028517881220 HIFs2.14E-072.14E-072.14E-072.14E-072.14E-072.14E-072.14E-07 HIFd2.14E-072.14E-072.14E-072.14E-072.14E-072.14E-072.14E-07 RBAS0.260.260.260.260.260.260.26 RBAd0.260.260.260.260.260.260.26 AverageDO10101010101010 Ksd0.200.200.200.200.200.200.20 Dlsd43E-052.5E-055.2E-043.6E-042.0E-0512E-048.2E-05 cRfD3.0E-043.0E-043.0E-04J*!:;3.0E-043.0E-043.0E-043.0E-04 HQsdIE-018E-02tzSMIBi1E+007E-024E-013E-01 Lifetime Exposure (Cancer Risk) ExposureLocationEU-1EU-2EU-3ElMEU-5EU-6EU-7 MEDIUM: ConeEPC6303607700540028517881220 HIFs1.53E-081.53E-081.53E-081.53E-081.53E-081.53E-081.53E-08 HIFd1.53E-081.53E-081.53E-081.53E-081.53E-081.53E-081.53E-08 RBAs0.260.260.260.260.260.260.26 RBAd0.260.260.260.260.260.260.26 AverageDO10101010101010 Ksd0.200.200.200.200.200.200.20 Dlsd3.0E-061.8E-063.7E-052.6E-051.4E-068.6E-065.9E-06 OSF1.5E+001.5E+001.5E+001.5E+001.5E+001.5E+001.5E+00 Risk5E-063E-066E-054E-052E-061E-059E-06 SURFACE SOIL AND DUSTPOPULATION:CI-WORKER Chronic Exposure (Noncancer Risk) ExposureLocationEU-1EU-2EU-3ElMEU-5EU-6EU-7 ConeEPC6303607700540028517881220 HIFs1.74E-061.74E-061.74E-061.74E-061.74E-061.74E-061.74E-06 HIFdO.OOE+00O.OOE+00O.OOE+00O.OOE+00O.OOE+00O.OOE+00O.OOE+00 RBAs0.260.260.260.260.260.260.26 RBAd0.260.260.260.260.260.260.26 AverageDO10101010101010 Ksd0.200.200.200.200.200.200.20 Dlsd2.8E-041.6E-043.5E-032.4E-031.3E-048.1E-045.5E-04 eRfO3.0E-043.0E-043.0E-04 i>>:3.0E-04JS1 3.0E-043.0E-04;! !3.0E-04|:;; HQsd9E-015E-01BE+OO:4E-01;t3l*60]?2t*SLifetime Exposure (Cancer Risk) ExposureLocationEU-1EU-2EU-3ElMEU-5EU-6EU-7 ConeEPC6303607700540028517881220 HIFs1.24E-071.24E-071.24E-071.24E-071.24E-071.24E-071.24E-07 HiFoO.OOE+00O.OOE+00O.OOE+00O.OOE+00O.OOE+00O.OOE+00O.OOE+00 RBAs0.260.260.260.260.260.260.26 RBAd0.260.260.260.260.260.260.26 AverageDO10101010101010 Ksd0.200.200.200.200.200.200.20 Dlsd2.0E-051.2E-052.5E-041.7E-049.2E-065.8E-053.9E-05 oSF1.5E+001.5E+001.5E+00|i|1.5E+00|-I1.5E+001.5E+001.5E+00 Risk3E-052E-05; 4E-041-3&6IIE-OS9E-056E-05 ConeEPC6303607700540028517881220 ConeEPC6303607700540028517881220 HIFs2.45E-072.45E-072.45E-072.45E-072.45E-072.45E-072.45E-07 HIFs8.74E-088.74E-088.74E-088.74E-088.74E-088.74E-088.74E-08 HIFd2.45E-07245E-072.45E-072.45E-072.45E-072.45E-072.45E-07 HIFd8.74E-088.74E-088.74E-088.74E-088.74E-088.74E-088.74E-08 RBAs0.260.260.260.260.260.260.26 RBAs0.260.260.260.260.260.260.26 RMERBAd0.260.260.260.260.260.260.26 RMERBAd0.260.260.260.260.260.260.26 DO10101010101010 DO10101010101010 Ksd0.200.200.200.200.200.200.20 Ksd0.200.200.200.200.200.200.20 Dlsd4.9E-052.8E-055.9E-044.1E-042.2E-051.4E-049.4E-05 Dlsd1.7E-051.0E-052.1E-041.5E-048.0E-084.9E-053.3E-05 cRID30E-043.0E-043.0E-043.0E-043.0E-043.0E-043.0E-04 OSF1.5E+001.5E+001.5E+001.5E+001.5E+001.5E+001.5E+00 HQsd2E-019E-022E+001E+007E-025E-013E-01 Risk3E-052E-053E-042E-04IE-OS7E-055E-05 ConeEPC6303607700540028517881220 ConeEPC6303607700540028517881220 HIFs3.96E-063.96E-063.96E-063.96E-063.96E-06396E-063.96E-06 HIFs1.42E-061.42E-061.42E-061.42E-061.42E-061.42E-061.42E-06 HIFdO.OOE+00O.OOE+00O.OOE+00O.OOE+00O.OOE+00O.OOE+00O.OOE+00 HIFdO.OOE+00O.OOE+00OOOE+00O.OOE+00O.OOE+00O.OOE+00O.OOE+00 RBAs0.260.260.260.260.260.260.26 RBAs0.260.260.260.260.260.260.26 RMERBAd0.260.260.260.260.260.260.26 RMERBAd0.260.260.260.260.260.260.26 DO10101010101010 DO10101010101010 Ksd0.200.200.200.200.200.200.20 Ksd0.200.200.200.200.200.200.20 Dlsd6.5E-043.7E-047.9E-035.6E-032.9E-041.8E-031.3E-03 Dlsd2.3E-041.3E-042.8E-032.0E-031.0E-046.6E-044.5E-04 cRfD3.oE-o4p:;;3.0E-043.0E-04F3.0E-04!r<3.0E-043.0E-04^3.0E-04U oSF1.5E+OOJ1.5E+OOJr1.5E+OOp1.5E+OOSl-SE+OOi;i.5E+ooy-1.5E+00& HQsd«2?P>1E+00-smmsf:26*bll1E+00^ee*§8:mmf. RiskJ>t-3§*4HCzE-Oi;:tf::4&oi:rivisifeoiftiiE-w:siHie-oi:ste& p:\txattinVnurray\as-rlsk.xls PageD-4-5 -lC <SENIC \APPENDIX-PART4MURft. . SMELTER - CALCULATION OF EXPOSURE AND RISK FRO MEDIUM: SLAGPOPULATION: TEEN (Age 12-18) Chronic Exposure (Noncancer Risk) Exposure Cone Average Cone RMELocation EPC HIFslag RBAslag Dlsd cRfD HQsd EPC HIFslag RBAslag Dlsd cRfD HQsdAll 591 6.01 E-08 0.45 1.6E-05 3.0E-04 5E-02 591 2.40E-07 0.45 6.4E-05 3.0E-04 2E-01 Lifetime Exposure (Cancer Risk) Exposure Cone Average Cone RMELocation EPC HIFslag RBAslag Dlsd oSF Risk EPC HIFslag RBAslag Dlsd oSF RiskAll 591 6.01 E-09 0.45 1.6E-06 1.5E+00 2E-06 591 2.40E-08 0.45 6.4E-06 1.5E+00 1E-05 p:\brattin\murray\as-risk.xls Page D-4-6 APPENDIX^-PART4MURftv.. SMELTER - CALCULATION OF EXPOSURE AND RISK FROli ;SENtC CMEDIUM: GROUNDWATERPOPULATION: RESIDENTS Chronic Exposure (Noncancer Risk) AquiferDepthShallow Intermediate Lifetime AquiferDepthShallow Intermediate WellIDMW-100MW-101iMW-titeinJ'(^163MW-104sixfoil?!MW-101DMW-104D WellIDMW-100MW-101iMvVlJlOJfeSMW-103 "MW-104pMr1p6f;fRMW-101DMW-104D As Conemg/L0.00250.0060.01840.270.00627.180.00250.019 As ConemgIL0.00250.0060.01840.270.00627.180.00250.019 AveragecHIF1.28E-021.28E-021.28E-021.28E-021.28E-021.28E-021.28E-02B1.28E-02* cDI3.2E-057.7E-052.4E-043.5E-037.7E-053.5E-01ijJ^&OS,2.4E-04 cRfD3.0E-043.0E-043.0E-043.0E-04!3.0E-043.0E-04I3.0E-043.0E-04 HQ1E-013E-018E-01f|||11ffpl43J=loi 1E-018E-01 AverageIHIF1.65E-031.65E-031.65E-031.65E-031.65E-031.65E-031.65E-031.65E-03 IDI4.1E-069.9E-063.0E-054.5E-049.9E-064.5E-024.1E-063.1E-05 oSF1.51.51.51.5 j1.51.5J1.51.5 Risk6E-061E-055E-05IptiitliOji£6s" 6E-065E-05 cHIF2.74E-022.74E-022.74E-022.74E-022.74E-022.74E-022.74E-022.74E-02 cHIF1.17E-021.17E-021.17E-02•^"i i" i*i'**yci'- fto'•' 'f »' 1 f »3twfc'1.17E^021.17E-021.17E-021.17E-02 RMEcDI6.8E-051.6E-045.0E-047.4E-031.6E-047.4E-016.8E-055.2E-04 RMEIDI2.9E-057.0E-052.2E-043.2E-037.0E-053.2E-012.9E-052.2E-04 cRfD3.0E-043.0E-043.0E-04j3.0E-0413.0E-043.0E-04,3.0E-043.0E-04! oSF1.51.51.51.51.51.51.51.5 HQ2E-015E-01|pi£;SK*C|(|:;|i||2|fQ^"""'""' 5E*-bli~. /.'. *'..'-,; 'Ocfjiiirt^i-''Ptk"i'i:'^^fcC^«\IOs"^^ioTMW& Risk4E-051E-04I11||E5&1|p;lf|:5Jgl03i1E-04jjcsi^E-ifl" 4E-05£.;i:y43E-Q4j ; On-site well, used to assess on-site residents p:\brattin\murray\as-risk.xls Page D-4-7 MURRA'.LTER - CALCULATION OF EXPOSURE AND RISK FROM ARSENIC APPENDIX^-PART 4 MEDIUM: GROUNDWATERPOPULATION: WORKERS Chronte Exposure (Nonc*ne*f Risk) AquiferDepthShallow Inla !••>• iliiiliniBiiiwuiw AquiferDepthShallow Intermedial WellIDMW-102MW-105MW-106MW-107MW-108MW-109MW-110MW-111MW-112GW-1GW-2WaH1WsN2WsH3UTBN-19 MW-105DMW-108DMW-109DMW-112DGW-1AGW-1ARGW-2A UU*IIflrVIlIDMW-102MW-105MW-106MW-107MW-108MW-109MW-110MW-111MW-112GW-1GW-2WHI1Wed 2Well 3UTBN-1a MW-105DMW-108DMW-109DMW-112DGW-1AGW-1ARGW-2A As Conemgft.0.01840.01327.180.00250.00250.0142.3472.9030.0521.2872.870.2161.9740.2360.270.0250.00250.0690.0390.790.0060.439 A* Conerog'L0.01840.01327.180.00250.00250.0142.3472.9030.0521.2872.870.2161.9740.2360.270.0250.00250.0690.0390.790.0060.439 eHIF6.00E-036.00E-036.00E-036.00E-036.00E-036.00E-036.00E-036.00E-036.00E-036.00E-036.00E-036.00E-036.00E-036.00E-036.00E-036.00E-036.00E-036.00E-036.00E-036.00E-036.00E-036.00E-03 AVVCMCD)1.1E-047.8E-051.6E-011.5E-051.SE-058.4E-OS1.4E-021.7E-023.1E-047.7E-031.7E-021.3E-031.2E-021.4E-031.6E-03asm.1.5E-054.1E-042.3E-044.7E-033.6E-OS2.6E-03 f»cRfD3.0E-043.0E-043.0E-041;3.0E-043.0E-043.0E-043.0E-04 !3.0E-04|f3.0E-04*3.0E-04rr3.0E-04C3.0E-04I3.0E-043.0E-04I-3.0E-04|3.0E-043.0E-043.0E-043.0E-04 HQ4E-013E-015E+025E-025E-023E-01SE+Oi6E+dt|1E+003B*ol;B^4-bt''M 6E+00SE+W)'5E-015E-021E+008E-013.0E-04fr2l+Oi3.0E-043.0E-04|1E-01*m eHIF9.78E-039.78E-039.78E-039.78E-039.78E-039.78E-039.78E-039.78E-039.78E-039.78E-039.78E-039.78E-039.78E-039.78E-039.78E-039.78E-039.78E-039.78E-039.78E-039.78E-039.78E-039.78E-03 AverageIMIF4.29E-044.29E-044.29E-044.29E-044.29E-044.29E-044.29E-044.29E-044.29E-044.29E-044.29E-044.29E-044.29E-044.29E-044.29E-044.29E-044.29E-044.29E-044.29E-044.29E-044.29E-044.29E-04 ID)7.9E-065.6E-061.2E-021.1E-081. IE-066.0E-061.0E-031.2E-032.2E-055.5E-041.2E-039.3E-058.5E-041.0E-041.2E-041.1E-051. IE-063.0E-051.7E-053.4E-042.6E-061.9E-04 oSF1.51.51.5 K1.51.51.51.5*1-5 1;1.5ISjf.5".5.5ft.9 x•5|.5".5.5.5.5|.5•*:ii Risk1E-058E-062E-022E-062E-069E-06•US'3E-05*8E-042E-03IE-04iE-032E-04i 25-04]2E-OS2E-064E-053E-05^86*1'4E-063E-<>4 eHIF3.49E-033.49E-033.49E-033.49E-033.49E-033.49E-033.49E-033.49E-033.49E-033.49E-033.49E-033.49E-033.49E-033.49E-033.49E-033.49E-033.49E-033.49E-033.49E-033.49E-033.49E-033.49E-03 RMEcDI1.8E-041.3E-042.7E-012.4E-052.4E-051.4E-042.3E-022.8E-025.1E-041.3E-022.8E-022.1E-031.9E-022.3E-032.6E-032.4E-042.4E-OS6.8E-043.8E-047.7E-03S.9E-054.3E-03 RME1016.4E-054.SE-059.5E-028.7E-068.7E-064.9E-058.2E-031.0E-021.8E-044.5E-031.0E-027.5E-046.9E-038.2E-049.4E-048.7E-058.7E-062.4E-041.4E-042.8E-032.1E-051.5E-03 CRfD3.0E-043.0E-043.0E-04 ;,;U3.0E-043.0E-043.0E-043.0E-04 W|3.0E-04 f3-3.0E-04|i'-$3.0E-04|I-I3.0E-04|!|3.0E-04J.3*3.0E-04pi3.0E-04H;|3.0E-04p!23.0E-043.0E-043.0E-04;,::v;3.0E-043.0E-04Ji.'H3.0E-043.0E-04 J j;; oSF1.51.5.5 \,,r'i.5'".5.5.5pfsfcii:'!;•5 •**•.5 f.?41.5pl1.5pf1 5 fc;« t£1.51.51.5 fc,-1.5 !&1.5^';1.5 1.5i:S; HQ6E-014E-0191+028E-028E-025E-01SE+619Eioi;-*MliiVY:^IC*Vl|!JIE-KrljdE^OIt7E+00OE+OI8E+009E+008E-018E-02yi^dd:il+oo3E+bi2E-01«« RtakIE-047E-05^E-pi"1E-051E-057E-05-JWfflbI-2B-OZ?-f:0&dfS'TfrbJ?C|E»lKEIti-wtfciE^2! ll&iDj!ilE-03!IE-041E-05<E-04'2E-044E-033E-052E-03 p:\bfatHn\murray\awisk.xls P«osD-4-8 MURRAv APPENDI)Ln-PART4 .cLTER - CALCULATION OF EXPOSURE AND RISK FROM ARSENIC IDDLn MEDIUM: SURFACE SOIL AND DUSTPOPULATION: RESIDENTS Chronic Exposure (Noncancer Risk) Btstd on Avenge Concentrations Exposure1 *t-ft*ttft*tUOCoTKH)EU-8EU-9EU-10EU-11ISZ-1ISZ-2ISZ-3ISZ-4ISZ-5ISZ-6ISZ-7ISZ-8 ConeMean16741186919106165545425212676 HIFs5.88E-075.88E-075.88E-075.88E-075.88E-075.88E-075.88E-07S.88E-075.88E-07588E-075.88E-075.88E-07 HIFd7.18E-077.18E-077.18E-077.18E-077.18E-077.18E-077.18E-077.18E-077.18E-077.18E-077.18E-077.18E-07 RBAs0.260.260.260.260.260.260.260.260.260.260.260.26 RBAd0.260.260.260.260.260.260.260.260.260.260.260.26 AverageDO101010101010101010101010 Kid0.200.200.200.200.200.200.200.200.200.200.200.20 Dlsd3.2E-042.4E-051.5E-055.5E-062.2E-054.9E-061.2E-051.0E-059.9E-061.2E-052.6E-0516E-05 cRfD3.0E-043.0E-043.0E-043.0E-0430E-043.0E-043.0E-043.0E-043.0E-043.0E-043.0E-043.0E-04 HQsd1E+008E-025E-022E-027E-022E-024E-023E-023E-024E-029E-025E-02 Lifetime Exposure (Cancer Risk) ExposureLocationEU-8EU-9EU-10EU-11ISZ-1ISZ-2ISZ-3ISZ-4ISZ-5ISZ-6ISZ-7ISZ-8 ConeM&««Mean16741186919106165545425212676 HIFs7.56E-087.56E-087.56E-087.56E-08756E-087.56E-087.56E-087.56E-087.56E-087.56E-087.56E-087.56E-08 HIFd9.23E-089.23E-089.23E-089.23E-089.23E-089.23E-089.23E-089.23E-089.23E-089.23E-089.23E-089.23E-08 RBAs0.260.260.260.260.260260.260.260.260.260.260.26 RBAd0.260.260.260.260.260.260.260.260.260.260.260.26 AverageDO101010101010101010101010 Ksd0.200.200.200.200.200.200.200.200.200.200.200.20 DM4.1E-053.1E-061.9E-067.1E-072.8E-068.3E-071.6E-061.3E-061.3E-061.5E-063.3E-062.1E-06 OSF1.5E+001.5E+00.5E+00.5E+00.5E+00.5E+00.5E+00.5E+00.5E+00.5E+00.5E+001.5E+00 Risk6E-055E-063E-06IE-064E-089E-072E-062E-062E-062E-065E-063E-06 c ConeMean16741186919106165545425212676 ConeUA«Mmean16741186919106165545425212676 HIFs1.64E-061.64E-061.64E-061.64E-061.64E-061.64E-061.64E-081.64E-061.64E-061.64E-061.64E-061.64E-06 HIFS7.05E-077.05E-077.05E-077.05E-077.05E-077.05E-077.05E-077.05E-077.05E-077.05E-077.05E-077.05E-07 HIFd2.01 E-062.01E-062.01 E-062.01E-062.01 E-062.01 E-062.01E-062.01 E-062.01 E-062.01 E-062.01 E-062.01 E-06 HIFd8.81 E-078.61E-078.61 E-078.61 E-078.61 E-078.61 E-078.61E-078.61 E-078.61 E-078.61E-078.61 E-078.61 E-07 RBAs0.260.260.260.260.260.260.260.260.260.260.260.26 RBAs0.260.260.260.260.260.260.260.260.260.260.260.26 RMERBAd0.260.260.260.260.260.260.260.260.260.260.260.26 RMERBAd0.260.260.260.260.260.260.260.260.260.260.260.26 DO101010101010101010101010 DO101010101010101010101010 Ksd0.200.200.200.200.200.200.200.200.200.200.200.20 Ksd0.200.200.200.200.200.200.200.200.200.200.200.20 Dtod9.0E-046.8E-054.2E-051.5E-056.2E-051.4E-053.4E-052.9E-052.8E-053.3E-057.2E-0546E-05 Dlsd3.8E-042.9E-051.8E-056.6E-062.6E-055.8E-0815E-051.2E-051.2E-051.4E-053.1E-052.0E-05 cRfD3.0E-04 •3.0E-043.0E-043.0E-043.0E-043.0E-043.0E-043.0E-043.0E-043.0E-043.0E-043.0E-04 OSF1.5E+00->1.5E+001.5E+001.5E+001.5E+001 5E+001.5E+001.5E+001.5E+001.5E+001.5E+001.5E+00 HQsd3G+M2E-011E-015E-022E4115E-02IE-011E-019E-021E-012E-012E-01 RiskJ:\ClpS?4E-053E-051E-054E-059E-062E-052E-052E-052E-055E-053E-05 p:\ixattln\mutray\as-f1sk2.xls PageD-4-9 MURRffv APPENDIX-"-PART 4 .cLTER - CALCULATION OF EXPOSURE AND RISK FROM ARSENIC YDJX-"cMEDIUM: SURFACE SOIL AND DUSTPOPULATION: NCI-WORKER Chronic Exposure (Noncancer Risk) 0ase<f oft Average Concefifratfo/is Exposure Cone AverageLocation Mean HIFs HIFdEU-1 130 2.14E-07 2.14E-07EU-2 79 2.14E-07 2.14E-07EU-3 1172 2.14E-07 2.14E-07EU-4 418 2.14E-07 2.14E-07EU-5 100 2.14E-07 2.14E-07EU-6 432 2.14E-07 2.14E-07EU-7 418 2.14E-07 2.14E-07 Lifetime Exposure (Cancer Risk) Exposure ConeLocation Mean HIFs HIFdEU-1 130 .53E-08 1.53E-08EU-2 79 .S3E-08 1.53E-08EU-3 1172 .53E-08 1.S3E-08EU-4 418 .S3E-08 1.53E-08EU-5 100 .53E-08 1.53E-08EU-6 432 1.53E-08 1.53E-08EU-7 418 153E-08 1.53E-08 RBAs0.260.260.260.260.260.260.26 RBAs0.260.260.260.260.260.260.26 RBAd0.260.260.260.280.260.260.26 RBAd0.260.260.260.260.260.260.26 DO10101010101010 AverageDO10101010101010 Ksd0.200.200.200.200.200.200.20 Ksd0.200.200.200.200.200.200.20 Dlsd9.2E-065.9E-067.9E-052.8E-057.2E-082.9E-052.9E-05 Dlsd6.6E-074.2E-075.6E-062.0E-06S.2E-072.1E-062.0E-06 cRfD3.0E-043.0E-043.0E-043.0E-043.0E-043.0E-043.0E-04 oSF1. SE+001. SE+001.5E+001. SE+001.5E+001.5E+001.5E+00 HQsd3E-022E-023E-019E-022E-021E-01IE-01 Risk1E-066E-078E-063E-088E-073E-063E-08 MEDIUM: SURFACE SOIL AND DUSTPOPULATION: CMWORKER Chronic Exposure (Noncancer Risk) Exposure ConeLocation Mean HIFs HIFdEU-1 130 1.74E-08 O.OOE+00EU-2 79 1.74E-06 O.OOE+00EU-3 1172 1.74E-OB O.OOE+00EU-4 418 1.74E-06 O.OOE+00EU-5 100 1.74E-08 O.OOE+00EU-6 432 1.74E-06 O.OOE+00EU-7 418 1.74E-OB O.OOE+00 Lifetime Exposure (Cancer Risk) Exposure ConeLocation Mean HIFs HIFdEU-1 130 1.24E-07 O.OOE+00EU-2 79 1.24E-07 O.OOE+00EU-3 1172 1.24E-07 O.OOE+00EU-4 418 1.24E-07 O.OOE+00EU-5 100 1.24E-07 O.OOE+00EU-6 432 1.24E-07 O.OOE+00EU-7 418 1.24E-07 O.OOE+00 RBAs0.260.260.260.260.260.260.26 RBAS0.260.260.260.260.260.260.26 RBAd0.260.260.260.260.260.260.26 RBAd0.260.260.260.280.260.260.26 AverageDO10101010101010 AverageDO10101010101010 Ksd0.200.200.200.200.200.200.20 Ksd0.200.200.200.200.200.200.20 DlsdS.9E-OS3.6E-05S.3E-041.9E-044.5E-052.0E-041.9E-04 Dlsd4.2E-082.6E-083.8E-051.3E-053.2E-061.4E-051.3E-05 CRfD3.0E-043.0E-043.0E-04HS3.0E-043.0E-043.0E-043.0E-04 OSF1. SE+001.5E+001. SE+001.5E+001.5E+001.5E+001.5E+00 HQsd2E-011E-012E+OQ6E-011E-017E-016E-01 Risk6E-064E-066E-052E-055E-082E-052E-05 ConeH__MPTCHII130791172418100432418 ConeMcsn130791172418100432418 HIFs2.4SE-072.45E-072.45E-072.45E-072.45E-072.45E-072.45E-07 HIFs8.74E-088.74E-088.74E-088.74E-088.74E-088.74E-088.74E-08 HIFd2.45E-072.45E-072.45E-072.45E-072.45E-072.45E-072.45E-07 HIFd8.74E-088.74E-088.74E-088.74E-088.74E-088.74E-088.74E-08 RBAs0.260.260.260.260.260.260.26 RBAs0.260.260.260.260.260.260.26 RMERBAd0.260.280.260.260.260.280.26 RMERBAd0.260.260.260.260.260.260.26 DO10101010101010 DO101010101010 '10 Ksd0.200.200.200.200.200.200.20 Ksd0.200.200.200.200.200.200.20 DlsdLIE-OS6.7E-069.0E-053.3E-058.2E-063.4E-053.3E-05 Dlsd3.8E-062.4E-063.2E-051.2E-052.9E-061.2E-051.2E-05 cRfD3.0E-043.0E-043.0E-043.0E-043.0E-043.0E-043.0E-04 OSF1.5E+001.5E+00.SE+00.5E+00.5E+005E+005E+00 HQsd4E-022E-023E-011E-013E-02IE-011E-01 Risk6E-064E-065E-052E-OS4E-062E-052E-05 ConeMean130791172418100432418 ConeMean130791172418100432418 HIFs3.96E-063.96E-063.96E-063.96E-063.96E-063.96E-063.96E-06 HIFs1.42E-061.42E-081.42E-061.42E-061.42E-061.42E-061.42E-06 HIFdO.OOE+00O.OOE+00O.OOE+00O.OOE+00O.OOE+00O.OOE+00O.OOE+00 HIFdO.OOE+00O.OOE+00O.OOE+00O.OOE+00O.OOE+00O.OOE+00O.OOE+00 RBAs0.260.260.260.260.280.260.26 RBAs0.260.260.280.260.260.260.26 RMERBAd0.260.260.260.260.260.280.26 RMERBAd0.280.260.260.260.260.260.26 DO10101010101010 DO10101010101010 Ksd0.200.200.200.200.200.200.20 Ksd0.200.200.200.200.200.200.20 Dlsd1.3E-048.2E-OS1.2E-034.3E-041.0E-044.5E-044.3E-04 Dlsd4.8E-052.9E-054.3E-041.5E-043.7E-051.6E-041.5E-04 cRfD3.0E-043.0E-043.0E-04P3.0E-043.0E-043.0E-043.0E-04 oSF.5E+005E+00.SE+00 1?.5E+OOP.5E+00.5E+00 i.5E+OOp HQsd4E-013E-014E+00"li+oo3E-011E+001E+00 Risk7E-054E-05;fe'SE"8$:;:S2E-04;"'"slPos'V::2EmjV!J&04] p:\bratBn\rnwTay\as-risk2jds Pag«D-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 ofPbB 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 P10(%)EU-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\riskcatc\childpb.wb1 APPENDIX D - PART 5 CALCULATION OF BLOOD LEAD LEVELS IN NON-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 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 P>11.1EU-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-4 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 5.45 11.10 5.0% EVALUATION OF RISK FROM WATER Basic equation: (PbB -PbBO)=BKSF*(Cw*IRw*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:\brattin\murray\sitewide\riskcalc\adultpbb.wb1 APPENDIX D-PART 5 V y 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 = PbBfGMpGSDM^S 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*IRw*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:\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 = ParameterPbBO(GM)BKSFIRslagEFslagAFslagGSD AB Value Units1.6 ug/dL0.4 ug/dL per ug/day50 mg/day25 days/yr0.053 -1.54 1.82E-04 LOCATIONAll Cslag11500 GM2.43 95th4.95 P>11.10.02 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 AIR The basic equation recommended by EPA (1989a) for evaluation of inhalation exposure is: DIair = Ca • BR, • EF • ED/(BW - AT)where: DI^ = Daily intake from air (mg/kg-d)C, = Concentration of substance in air (mg/m3)BRj = 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 BREFEDBWAT 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 Adult* 20 mVday350 days/yr30 years70kg30 years (noncancer)70 years (cancer) The relative magnitude of the inhaled dose of arsenic and lead from air can be compared to theingested dose from soil as follows:DI air •BR.DI oral C.-R, 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: Daily intake from air (mg/kg-d)Ca = Concentration of substance in air (mg/m3)BR, = Breathing rate of air (mVday)C, = 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 (IE-04 kg/day) (EPA 1991b). Based on thesevalues, the ratio of the mass of soil inhaled to that ingested is: 2E-10 kg/m3 -20 nIE-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: ADW = Cw-SA-PC-t-EF-ED/(BW-AT) where: ADW = 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 (hr/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 E-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 PCt 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)RAGS (EPA 1989b)RAGS Supplemental Guidance (EPA 1991)RAGS (EPA 1989b)RAGS Supplemental Guidance (EPA 1991) Typical RME Values forResidential Adult* 20.000 cm2 Chemical specific12 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 (ADj) and oral (ingestion) exposure (AD0) to water is givenby: SA-PC't where: SAPCt AFn Surface area exposed (cm2)Chemical-specific permeability constant (cm/hr)Exposure time (hr/day)Ingestion rate of water (cmVday)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: Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page E-3THIS 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. AD,AD.2-PCAF. 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 LeadArsenic PC (cm/hr) * 4E-061 IE-03* AF00.10=1.0= ADd/AD08E-05 2E-03 • Measured value (USEPA 1992)b USEPA (1992) recommends a default value of IE-03 cm/hr for inorganics for which data are not availablee 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 (FJ>A 1989b, 1992): = C5-SA-AF-ABS'EF-FJ)/(BW-AT) = concentration of chemical in soil (mg/kg)= surface area in contact with soil (cm2)= soil adherence factor (kg/cm2)= absorption fraction (unitless) where: C,SAAFABS 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: Baseline Human Health Risk Assessment May 1997Document Control Number 4500-090-AOAC Page E-4THIS 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. Chemical Dioxins 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 hi 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 SA-AF'ABS-EFaAD0 IR-AF0-EF0 where: SAAFABS AF0 =EFd =EF = surface area in contact with soil (cm2)soil adherence factor (kg/cm2)absorption fraction (unitless)Ingestion rate of water (cmVday)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/cm2 = IE-06kg/cm2) 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-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. AD 2.86 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 Ratio(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 Assessment May 1997Document Control Number 4500-090-AOAC Page E-6THIS 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. 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. r-EPA. 1991a. 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. 1991b. "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/600/8-91/011B. 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 Control Number 4500-090-AOAC Page E-7THIS 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.