; remedial planning activities at selected … · the recommendation, currently being implemented,...

EBASCO

REM III PROGRAM

; REMEDIAL PLANNING ACTIVITIESAT SELECTED UNCONTROLLED

HAZARDOUS SUBSTANCE DISPOSAL SITES

-•*

EPA CONTRACT 68-01-7250

EBASCO SERVICES INCORPORATED

EPA WORK ASSIGNMENT NUMBER: 199-2L38EPA CONTRACT NUMBER: 68-01-7250


FINAL

PUBLIC HEALTH EVALUATIONVESTAL WELL 1-1 SITEVESTAL, NEW YORK

MAY 1990

NOTICE

The information in this document has been funded by the United StatesEnvironmental Protection Agency (USEPA) under REM III Contract No. 68-01-7250 to Ebasco Services Incorporated (Ebasco). This document has beenformally released by Ebasco to the EPA. This document does notrepresent, however, the EPA position or policy and has not been formallyreleased by EPA.

EBASCO ENVIRONMENTALA Division ol EBASCO SERVICES INCORPORATED

FRAfifO•«•" fc^«*^^

2111 Wilson Blvd., Suite 1000, Arlington, VA 22201, (703) 358-8900

May 16, 1990RMOII-90-096Response Requested

Mr. M Shaheer Alvi, PERegional Project ManagerU.S. Environmental Protection Agency26 Federal PlazaNew York, New York 10278

Mr. Ed AlsRemedial Project ManagerU.S. Environmental Protection Agency26 Federal PlazaNew York, New York 10278

Subject: REM III PROGRAM - EPA CONTRACT 68-01-7250VESTAL WELL 1-1 SITEWORK ASSIGNMENT NO. 199-2L38FINAL PUBLIC HEALTH EVALUATION REPORT

Dear Mr. Alvi and Mr. Als:

Ebasco Services Incorporated (Ebasco) is pleased to submit thisFinal Publich Health Evaluation Report. The report includesrevisions made in response to comments provided by EPA andNYSDEC.

If you have any questions or comments regarding this report,please do not hesitate to call Jonathan Weiss at (703) 358-8958.

Very truly yours.

Dev R. Sachdev, PhD,Regional Manager, Region II

DRS/JSW/SSSEnclosure

cc R. Heffernan (EPA)M. Stotler (EPA)R. T. FellmanF. TsangJ. S. WeissFile

Mr. M. Shaheer Alvi, PEMr. Ed Als

Subject: REM III PROGRAM - EPA CONTRACT 68-01-7250VESTAL WELL 1-1 SITEWORK ASSIGNMENT NO. 199-2L38FINAL PUBLIC HEALTH EVALUATION REPORT

ACKNOWLEDGMENT OF RECEIPT

Please acknowledge receipt of the enclosure on the duplicatecopy of this letter and return it to the sender.

M. Shaheer Alvi, PE DateRegional Project Officer

jit

EPA WORK ASSIGNMENT NUMBER: 199-2L38EPA CONTRACT NUMBER: 68-01-7250


FINAL

PUBLIC HEALTH EVALUATIONVESTAL WELL 1-1 SITEVESTAL, NEW YORK

MAY 1990

Prepared by: Approved by:

Andrew WarnerClement Associates, Inc.

Dev R. Sachdev, Ph.D., PrE.Regional Manager, Region IIEbasco Services Incorporated

Jonathan WeissSite ManagerEbasco Services Incorporated

TABLE OF CONTENTS

Section Page

1.0 INTRODUCTION........................................... 1

2.0 SELECTION OF CHEMICALS OF POTENTIAL CONCERN............ 22.1 Site Description................................. 22.2 Sampling and Analysis Results.................... 4

3.0 EXPOSURE ASSESSMENT.................................... 123.1 Identification of Exposure Pathways.............. 123.2 Estimation of Exposure Point Concentrations...... 18

4.0 TOXICITY ASSESSMENT.................................... 344.1 Health Effects Classification and Criteria

Development.................................... 344.2 Toxicity Summary................................... 41

5.0 RISK CHARACTERIZATION.................................. 725.1 Comparison to Potential Applicable or Relevant

and Appropriate Requirements (ARARs)........... 725.2 Quantitative Risk Assessment Methodology......... 775.3 Potential Exposures and Risks to Workers in

Excavated Soils................................ 795.4 Potential Exposures and Risks from Generation of

Dusts During Construction...................... 895.5 Potential Exposures and Risks from Future Use of

Groundwater.................................... 905.6 Evaluation of Inorganics Detected in Monitoring

Wells...... .................................... 99

6.0 DEVELOPMENT OF TARGET CLEANUP LEVELS................... 110

7.0 UNCERTAINTIES.......................................... 115

8.0 SUMMARY AND CONCLUSIONS................................ 118

9.0 REFERENCES............................................. 128

/" " LIST OF TABLES

, Table Page

2-1 Summary of Organic Chemicals Detected in Soil. ......... 5

; 2-2 Summary of Inorganic Chemicals Detected in Soil........ 8

2-3 Background Concentrations of Inorganic Chemicalsin Soil .............................................. 9

2-4 Summary of Inorganic Chemicals Detected in Groundwater. 11

2-5 Background Concentrations of Inorganic Chemicalsin Groundwater ....................................... 13

2-6 Summary of Chemicals of Potential Concern. ............. 14

3-1 Average and Plausible Maximum Case Soil Concentrations. 21

3-2 Chemical -Physical Parameters Used in the SoilVolatilization Model. ................................ 25

3-3 Site Specific Parameters Used in the Air Modeling ...... 26,*******%• 3-4 Estimated Air Concentrations For Construction Workers

Exposed to Volatile Chemicals During TrenchingOperations ........................................... 28

I 3-5 Input Parameters Used in the Box Model for PredictingAir Concentrations from Construction Activities ...... 30

3-6 Air Concentrations Due to Fugitive Dust GenerationDuring Construction Activities ....................... 31

3-7 Parameters Used in the Groundwater Leaching Model...... 35

3-8 Estimated Groundwater Concentrations Due to Leachingfrom Soil — Area 1 .................................... 36




ii

oA>

LIST OF TABLES (Continued)

Table Page

4-1 Summary of Health Effects Criteria for Chemicals ofPotential Concern. ................................... 42

5-1 Potential Groundwater ARARs ............................ 75

5-2 Assumptions Used in Estimating Dermal ContactExposure ............................................. 81

5-3 Assumptions Used in Estimating Incidental IngestionExposure ............................................. 83

5-4 Potential Exposures and Risks from Dermal Absorption,Incidental Ingestion, and Inhalation by On- SiteWorkers — Area 1 ...................................... 85

5-5 Potential Exposures and Risks from Dermal Absorption,Incidental Ingestion, and Inhalation by On-SiteWorkers — Area 2 ...................................... 86

5-6 Potential Exposures and Risks from Dermal Absorption,Incidental Ingestion, and Inhalation by On-SiteWorkers — Area 3 ...................................... 87

5-7 Potential Exposures and Risks from Dermal Absorption,Incidental Ingestion, and Inhalation by On-SiteWorkers — Area 4. ..................................... 88

5-8 Potential Exposures and Risks from Inhalation ofDust by Future On-Site Workers — Area 1. .............. 91




5-12 Parameters Used in the Shower Model. ................... 100

5-13 Potential Exposures and Risks from Future Use ofGroundwater — Area 1 .................................. 101

iii

LIST OF TABLES (Continued)

Table Page



5-16 Potential Exposures and Risks from Future Use ofGroundwater — Area 4 .................................. . 104

5-17 Potential Exposures and Risks from Ingestion ofGroundwater at Concentrations Detected inMonitoring Wells ..................................... 105

5-18 Estimated Blood Lead Concentrations for 2-Year-OldsExposed to Lead in Drinking Water at ConcentrationsEqual to Levels Detected in Monitoring Wells. ........ Ill

6-1 Health-Based Target Cleanup Levels. .................... 113

8-1 Risk Assessment Summary — Vestal Well 1-1 Site. ......... 123

iv

1.0 INTRODUCTIONThis Public Health Evaluation (PHE) addresses the potential impacts to

human health associated with the Vestal Well 1-1 Site in the absence ofremedial (corrective) actions. This assessment therefore constitutes anevaluation of the no-action alternative required under Section 300.68 (f)(v)of the National Contingency Plan (NCP). Such an assessment will enable adetermination to be made of whether remedial actions are required. Thisassessment deals primarily with soil contamination in the four identifiedsource areas in relation to their potential for additional contamination ofgroundwater in the future and other potential future exposures and risksdirectly related to soil. The PHE also reviews the levels of inorganicsdetected in groundwater relative to potential health effects and drinkingwater standards. Current levels of volatile organic groundwater contaminationhave been addressed by previous studies (Ecology and Environment 1986) and arenot considered here.

This PHE has been conducted using conservative assumptions according tothe general guidelines outlined by USEPA. The purpose of using conservativeassumptions is to explore the potential for adverse health effects usingconditions that tend to overestimate risk. Consequently, the final estimateswill usually be near or higher than the upper end of the range of actualexposures and risks. As a result, this risk assessment should not beconstrued as presenting an absolute estimate of risk to human populations.Rather, it is a conservative analysis intended to indicate the potential foradverse impact to occur.

This assessment follows EFA guidance for risk assessment in general andfor Superfund sites in particular (EPA 1986a,b,c) and is based on datagenerated during the Supplemental Remedial Investigation (RI) conducted in theSummer and Fall of 1988. The assessment is organized as follows:

• Section 2.0 Selection of Site Related Chemicals . A briefdescription of the site and its environs is presented. Chemicals |detected in environmental media sampled during the RI (i.e. soil and ^groundwater) are identified. Those chemicals present at levels abovebackground and attributable to past site activities are identified for -,evaluation in the risk assessment. ~*

/"x,• Section 3.0 Exposure Assessment. Potential pathways by which

populations may be exposed to contaminants from the site areidentified. Concentrations of chemicals in environmental media at

' potential exposure points are estimated. In the case of groundwaterand air, models are developed to estimate the potential migration ofcontaminants from soils.

• Section 4.0 Toxicity Assessment. In this section, the toxiccharacteristics of the site-related chemicals are discussed andtoxicity criteria are identified. The methodology for thequantitative risk assessment is also reviewed.

• Section 5.0 Risk Characterization. As one measure of risk,concentrations of chemicals at points of exposure are compared toApplicable or Relevant and Appropriate Requirements (ARARs) such asMaximum Contaminant Levels (MCLs) and NY State Drinking VaterStandards. Since ARARs are not available for all chemicals in allmedia, quantitative risk estimates are also developed, by combiningthe estimated intakes of potentially exposed populations with healtheffects criteria.

• Section 6.0 Development of Health-Based Target Cleanup Levels. Foreach exposure pathway and chemical that results in an estimated riskthat exceeds EFA target risk levels (as defined in Section 4.0) orexceeds a drinking water standard, the exposure models are used to

'"""*" back-calculate a health-based level in soils that corresponds to thetarget risk level for the given conditions of exposure.

• Section 7.0 Uncertainties. The uncertainties and limitations of theFHE are discussed.

• Section 8.0 S"TffaYy and Conclusions. In this section the mainfeatures and conclusions of the FHE are summarized.

2.0 SELECTION OF CHEMICALS OF POTENTIAL CONCERN2.1 SITE DESCRIPTION

The Vestal Well 1-1 site is located in the town of Vestal, 5 milessouthwest of Binghamton in South Central New York. The water supply for thecity of Vestal comes from a series of wells located near the river. Samplingand analysis of the well water in 1979 following a spill of1,1,1-trichloroethane in Endicott, New York (north of Vestal) revealed thepresence of chlorinated organic compounds. The New York Department of

Environmental Conservation (NYDEC) performed a remedial investigation todefine the extent of the groundwater contamination. Their study resulted inthe recommendation, currently being implemented, to treat the water fromWell 1-1 through packed-tower aeration and discharge to the Susquehanna.Other investigations concluded that the source of contamination of the Vestalwells was not the 1,1,1-trichloroethane spill. A variety of chlorinated andnonchlorinated volatile organics were detected in Vestal wells 1-1, 4-2 andmonitoring wells throughout the area. The primary contaminants detected weretetrachloroethylene, trichloroethylene, and 1,1-dichloroethane. From thepattern of contamination it appeared that the source of the contamination wasin the vicinity of the Stage Road Industrial Park. Consequently, the currentinvestigation was undertaken primarily to characterize the levels ofchlorinated volatiles remaining in soils in these potential source areas.

The Stage Road Industrial Park consists of several small and medium-sizedcommercial and industrial buildings. Most of the site is paved, either byroads or parking areas. Four potential source areas were identified forinvestigation within the industrial park: (1) Area 1, a shallow dump site inthe vicinity of well S-2, (2) Area 2, a truck parking area in the vicinity ofthe Vestal Asphalt Company where high levels of chlorinated organics weredetected in groundwater and soil, (3) Area 3, the leach field that may havebeen used for disposal of solvents north of Chenango Industries, anelectroplating operation, and (4) Area 4 the parking area south of ChenangoIndustries.

The industrial park is located approximately 1,700 feet southeast of thewell 1-1. The area is underlain by various layers of glacial sand, gravel,and clay. Below the glacial deposits is a bedrock of shale and sandstone.The bedrock occurs at a depth of approximately 45 feet below ground surface atthe industrial park and slopes downward to a depth of approximately 130 feetat well 1-1. Groundwater occurs at depth of about 10 to 20 feet below theground surface at the industrial park. Groundwater flow follows the bedrockslope and flows in a southeast to northwest direction from the source areas t<

ooo

the well field. Thus contaminants leached from soils in the source areascould potentially reach the Vestal supply wells.

2.2 SAMPLING AND ANALYSIS RESULTSDuring the supplemental remedial investigation, soil samples were collect

from soil borings in each of the four areas within the industrial park.Sample depths ranged from two feet below ground surface to 24 feet. Sampleswere subjected to both a field screening for five volatile organics using agas chromatograph (DQO Level II data) and off-site laboratory analysis (DQOLevel IV data) for full Target Compound List parameters. Because ofdiscrepancies between Level II and Level IV data, only the higher qualityLevel IV data are used in the PHE. In Area 1, seven borings and a total ofeight soil samples were analyzed by CLP. In Area 2, eight borings and a totalof seventeen samples were analyzed by CLP. Nine borings yielding elevensamples were taken in Area 3, and twenty-five samples from 12 borings fromArea 4 were analyzed. Surface soil samples are not reported due to theabsence of complete exposure pathways for surface soil (see Section 3.0). Theresults of the analysis for organics are summarized in Table 2-1. The tablelists, for each detected chemical, the frequency of detection (i.e., thenumber of positive detected values out of the total number of samplesanalyzed), the geometric mean1 value of the concentration for the samplegroup, and the maximum detected value for the group. The following guidelineswere used in evaluating the data presented in Table 2-1:

• Samples flagged with an R by laboratory validation reviewers were notincluded in the summary. The R indicates that the data are unreliablebecause of quality control problems. The R flag indicates uncertaintyin both the identity of the compound and its measured value.

lDue to the low frequency of detection of most chemicals, it was notpossible to definitively determine if the data follow a normal or log-normaldistribution. Several researchers, however, have indicated that manycollections of measurements of environmental contaminants are log-normallydistributed (Dean 1981, Ott 1988). Therefore, geometric means have been usedin this assessment.

"y

U1 L.VC.L LUU

TABU 2-1

SUMMARY OF ORGANIC CHEMICAIS OFJFCTFD IN SUBSURI AflV f S T A I Will 1-1 S I T E

(Al l concentrations in iw|/laj)

c>0ll

AREA 1 ARIA I ARIA S Alt) A -1

GeometricF requency Mean

VI HE CHEMICALS

tonetenejtanonejroben/enejroformDichloroe thaneDichloroethylene

is-1 ,2-Dichloroethylene

nylene Chloride/ene. 2 . 2 - let rach loroethanerachloroethylenejene,1-Trichloroethanerhloroethyleneene (total)romod ich loromethane

Max imum

0/92/92/21/91/90/90/92/92/9NO0/90/90/95/90/90/91/90/9

0.0030.034

NRNR----

. 0.0030.005

--—--.-

0.005

--0.007

--

0.0040.060.0010.001

--.-

0.0040.046

--------

0 043----

0.054--

GeometricFrequency Mean

o/i72/171/10/171/172/172/178/176/171/171/172/175/173/174/177/177/170/17

NR0 026

--NRNRNR

0.1180.0870 049

NR0.040.0680.0640.0750.1710.197

--

Max imum

0.0040.026

0.0070.0260 006

113 70 220.0060.0491 2

0.331215016

Geometricfrequency Mean

9/110/112/3

0/110/112/111/114/110/114/110/110/110/113/111/116/110/110/11

2.961

0 01

NRNK

0.013

0 032

NRNR

0.022

Maximum

32

0.01/

0 0040.0030.025

0 22

0 0090 0020.078

Gfomt'tr tcFrequency Mean Maximum

10/^tl0/2H0/90/280/282/282/280/280/287/?H0/280/281/285/2810/2813/280/281/28

I ,'1B2

0.12NR

0 146

NRNR

0.1580 176

0 118

0 680.015

1.7

0 00?0 0064 299

0.740

I-VOLATILE CHEMICALS

zoic acid(2-ethylhexyl)phthalateylbenzylphthalateh loro- 3-methy Ipheno 1enzofuran- 0 ich lorobenzenen butylphthalaten octylphthalatephoronee thy Ipheno 1ethy Ipheno 1carcinogenic PAHs (a)cinogenic PAHs (b)tachtorophenolnol.4 I rich lorobenzene.5- Irichlorophenol

1242l?481260

0/80/70/80/82/80/80/83/80/81/80/82/82/80/80/80/80/80/80/80/8

------

0.470----

0.366--NR--

3.9301.100

.----------

------

9.300----

1.100--

0.081--

101.2009.200

--------

- -

0/101/171/171/173/171/172/170/170/170/171/17

11/174/171/171/170/171/170/171/172/17

0.4000 410

NR0 340

NRNR--- ---NR

2 2101 500

NRNR

1 500

0 0'.00 100

0.7301.2000.2400.7800.0500.110

------

0.29027

2.8000.0420.056

0 055

0 4.!00 220

1/11 NR 0.061 1/28 NR 0 0754/lt 170 1 100 7/28 0.210 11 0001/11 NR 0.086 0/280/11 -- -- 1/2B NR 0 OBI0/11 -- -- 0/280/11 -- -- 0/2H1/11 0.220 0.330 0/28l / l l NR 0210 0/280/11 - - 2/15 0220 Jf>00/11 - -- 0/280/11 I/2M 0 200 0 1001/11 NR 0.320 ' I/2H 0 200 0 2*0l/ll NR 0042 0/2H1/11 NR 0 110 0/2M0/11 --- -- 0/2H0/11 - 1/2H NR 0 0410/11 - - 0/2K0/11 I//H 0 O'.O () '.'.()0 /11 0/2H0/11 0 /2H

Anthracene, aLeiidphtl.i-iiu, f luoi anthene. fluorene, 2 methy Inaphtha lene, naphthalene. phi-Nan threw-, pyieiiel!t-n/u(a)anthracene. Inn/o(a)pyiene, i:hrysene- Not leported lit-uiii. 'i n. mean is qieater than maximum detected value due to t-r.l HIM ted values he low the deti-Lt ion l imn

• Samples flagged with a J or N by laboratory validation reviewers wereincluded in the summary. These flags indicate that the chemical wasdetected, but that the reported levels were estimated. Although theseestimated results may add an additional degree of uncertainty to theconcentration levels (i.e., may: overestimate or underestimate actualvalues), they are considered valid results and have been used in thisassessment.

• Analyte concentrations were compared to analyte concentrations infield and trip blanks. If the blank contained detectable levels ofcommon laboratory contaminants (methylene chloride, acetone, toluene,or phthalate esters), the analyte concentration in the sample was usedonly if the sample concentration was greater than ten times the blankconcentration. If the sample concentration was less than ten timesthe blank concentration, then the sample was treated as a non-detect.If the blank contained detectable levels of other analytes, thecorresponding sample concentration was used only if it was five timesthe concentration in the blank. If the sample concentration of theanalyte was less than five times the blank concentration, then thesample was treated as a non-detect.

• Concentrations reported for duplicate samples of a given samplingpoint were averaged by calculating a geometric mean of the sample andits duplicate. The mean was considered as a single value ingenerating the mean and frequency of detection for an area. In thecase where a chemical was detected in the sample but not in theduplicate (or vice-versa), if the geometric mean was below the sampledetection limit, the sample was treated as a non-detect.

• To calculate the geometric mean for an area, non-detects were includedby using one-half the sample-specific detection limit. Thisarbitrarily selected value (one-half) is commonly assigned tonondetects when averaging data for risk assessment purposes, since theactual value can be between zero and a value just below the detectionlimit. EPA recommends a value of one-half for monitoring at RCRAsites (EPA 1986d). This may result in mean values that are less thanthe minimum detected value where detection limits are low. Othermeans may be greater than the maximum detected values and are,therefore, not reported or used in the assessment.

A total of forty-three organic chemicals were detected in soil samplesfrom among the four areas. (The three FOB Aroclor mixtures are considered as

/**"'v one chemical.) Seventeen of these chemicals2 were detected in only one or twosamples from the total of sixty-four samples analyzed. This low frequency of

j detection suggests that exposure to these chemical will also be infrequent,and consequently, the chemicals would not be expected to contribute to risk asmuch as the more frequently detected compounds. In addition, most of thesechemicals are not related to known activities at the site, i.e., solvent usageor asphalt manufacture. The methyl phenols and chlorinated phenols aregenerally associated with pesticides and wood preservatives. Of these 16chemicals, only chloroform, and 1,1,2,2-tetrachloroethane (PCA) may be relatedto solvent usage. Consequently, chloroform and PCA are retained as chemicalsof potential concern. The other infrequently detected chemicals are notincluded in the assessment. One additional chemical—di-n-octylphthalate—isalso eliminated from further evaluation since there are no established healthcriteria for this chemical. The remaining organic chemicals are retained aschemicals of potential concern.

Table 2-2 presents a summary, by area, of inorganic chemicals detected insoils. As with organics the table presents the frequency of detection,

/•""--. geometric mean and maximum. The criteria listed above for the evaluation oforganic data were followed in developing the summary for inorganics. In

I selecting inorganic chemicals of potential concern, the criteria used are1 (1) comparison to naturally occurring background levels and (2) the

availability of toxicity criteria. No site-specific background samples were4 taken during the RI. Table 2-3 presents background levels based on samplesa

collected by USGS from soils at four locations in south-central New York andnorth-central Pennsylvania (Boergnen & Shacklette 1981). The mean or maximumvalues from the site sampling must exceed the USGS background by a factor oftwo in order to be considered sufficiently above background to represent achemical of potential concern. Only four chemicals—chromium, calcium,

2Chlorobenzene, chloroform, dibromochloromethane, styrene, 1,1,2,2tetrachloroethane, benzole acid, butylbenzyl phthalate, 4-chloro-3-methylphenol, methylene chloride, 1,4-dichlorobenzene, isophorone, 2-methylphenol, 4-methylphenol, pentachlorophenol, phenol, 1,2,4-trichlorobenzene, and 2,4,5-trichlorophenol.

TABU 2-2

SUMMARY OF INORGANICS OF1EC1FD IN SOUVESIAl WEll 1-1 Silt

(All concentrations in mg/kcj)

AREA 1 AREA Z AREA 3 ARtA 4

GeometricFrequency Mean

GeometricMaximum Frequency Mean

GeometricMaximum frequency Mean

AluminumArsenicBariumBerylliumCadmiumCalciumChromiumCobaltCopperIronleadMagnesiumManganeseNickelPotassiumSeleniumSi IverSodiumThalliumVanadiumZinc

8/88/88/88/80/87/78/88/80/08/85/58/88/88/88/80/81/80/80/88/8 •1/1

10,3001566

0.69--

2,1002411--

25,00014

3.30047020680--0.6----16--

13.700511301.1--

49.50017517--

42.00019

3.8801.270

24894--1.9----20827

17/1717/1717/1717/171/175/5

11/1117/179/917/1717/1717/1717/1717/1717/172/160/170/170/1717/178/8

10.3006.157

0.530.433.900

471223

23,80015

3.400620289000.17

---.--1571

13.00016198085.7

37.1001.13010663

29.10092

4,3006,440

1391,0600.76

------1999

5/55/65/65/60/66/65/65/66/65/66/65/65/65/65/63/60/66/63/65/66/6

Maximum(leant'l ru:

Frequency Mean Max nnum

10,3001.234

0.32--8909.28

7.76.500

7.61.300

75144080 07

--324

0.167.648

13.1003.51410 58

--2.130

161221

34.40014

3.830785255220.6--8870 54

1290

25/2525/2525/2525/?59/2525/2525/2525/2525/2525/?525/?525/2525/2525/2525/252/250/25

21/256/2525/2525/25

10,4006.6440404

1.100201146

23.00014

4.HOO46025710

0 096

820 14

1167

13.700351220 71.2

73.00054916

4H729.000

6121.000

73734

1.0400 14

--.ii'O0 67

14543

TABLE 2-3BACKGROUND CONCENTRATIONS OF INORGANIC CHEMICALS IN SOu

VESTAL WELL i-1 SITE

BACKGROUND CONCENTRATION (a!

ALUMINUMANTIMONYARSENICBARIUMBERYLLIUMCADMIUMCALCIUMCHROMIUMCOBALTCOPPERIRONLEADMAGNESIUMMANGANESEMERCURYNICKELPOTASSIUMSELENIUMSILVERSODIUMTHALLIUMVANADIUMZINC

RANGE

(mg/kg)

50.000-100,000<1

8.2-16200-500

1-21-11

1500-250030-10010-1515-20

15.000-50,00015-30

3000-7000300-700

0.08-0.1415-30

10,000-21.0000.2-0.60.7-5700012.3750-15075-101

GEOMETRICMEAN

(mg/kg)

70.400--

11.12801.51.61940401116

20.30023

42004600.10

2114.400

0.42.47000

--7286

(a) Exept for Cadmium and Silver, values are takenfrom Boerngen and Shacklette (1981) for four samplelocations: two locations in Chenango Co.. NY. onelocation in Tioga Co.. NY, and one location inSusquehanna Co., PA. Cadmium and Silver are range andmean for the conterminous US.

y—V

magnesium, and copper—exceeded the maximum USGS background concentration inmore than two samples. In the case of copper, the mean sample value in Area 4was also greater than the background. Chromium and copper are thereforeretained as chemicals of potential concern. No health criteria have beenestablished for calcium or magnesium. These chemicals are essential nutrientsin the human diet. The body generally has adequate physiological mechanismsto maintain a proper equilibrium over a wide range of intake levels.Consequently these chemicals are not retained as chemicals of potentialconcern. Six other.chemicals—arsenic, cobalt, manganese, nickel, lead, andzinc—exceeded the maximum USGS level by a factor of two in only one or twosamples. In all cases the mean values were below twice the USGS means. Thesechemicals are not considered significantly above background to warrantinclusion as chemicals of potential concern for soil. All other inorganicswere below USGS background levels, and are therefore not retained as chemicalsof potential concern.

Table 2-4 summarizes the results of the sampling of inorganics ingroundwater at the Vestal site. The table presents frequency of detection,geometric mean and range for total (unfiltered) and dissolved (filtered)samples. The data were organized based on the criteria listed above fororganics in soil. The criteria used for the selection of chemicals ofpotential concern for inorganics in groundwater are the same as those used forinorganics in soil—the availability of toxicity criteria, frequency ofdetection, and comparison to naturally occurring background levels. Cadmium,selenium and silver occurred in only one of twenty-four samples, and aretherefore not retained as chemicals of potential concern based on lowfrequencies of detection. As noted for inorganics in soil, no toxicitycriteria have been established for aluminum, calcium, cobalt, iron,3

magnesium, potassium, or sodium. Therefore, these chemicals cannot beevaluated in a quantitative assessment. Regional background levels forgroundwater were not available from USGS or the New York State Soil Survey.

.̂ 3A Secondary Maximum Contaminant Level of 300 pg/liter has beenestablished for. Iron based on organoleptic criteria.

10

TABLE 2-4

SUMMARY OF INORGANIC CHEMICALS DETECTED IN GROUNDWATER(All concentrations in ing/liter)

AluminumAnt imonyArsenicBariumBerylliumCadmiumCalciumChromiumCobaltCopperIronLeadMagnesiumManganeseMercuryNickelPotassiumSeleniumSilverSodiumThalliumVanadiumZinc

Frequency

22/234/249/1124/2414/242/2423/238/1022/2423/2413/1521/2324/2422/2317/2422/2423/232/201/2424/243/2416/2420/21

Total

GeometricMean

1.04E+013.05E:026.98E-031.76E-012.61E-032.85E-038.94E+012.67E-023.02E-027.16E-022.14E+012.57E-021.78E+011.19E+002.09E-037.57E-025.45E+002.25E-034.81E-032.39E+013.93E-033.66E-023.08E-01

Maximum

4.63E+026.35E-022.89E-023.33E+002.28E-02l.OOE-014.50E+021.50E-015.58E-011.58E+007.34E+011.91E-012.25E+025.14E+012.04E-016.19E+002.46E+012.50E-035.00E-036.99E+015.00E-036.89E-016.67E+00

Frequency

8/83/235/2222/2313/230/2322/225/2211/2310/2314/183/2123/2321/229/235/2323/231/111/2323/232/235/238/10

Dissolved

GeometricMean

1.84E-013.07E-024.84E-036.17E-028.50E-04--

5.34E+014.46E-031.47E-029.95E-035.2BE-012.41E-039.41E+002.25E-017.70E-042.19E-022.51Et-002.47E-034.95E-032.21E+013.96E-031.80E-021.19E-02

Maximum

3.01E+005.94E-021.22E-023.01E-012.50E-03—

2.36E+026.00E-032.50E-023.66E-021.84E+011.38E-023.11E+014.14E+002.12E-015.89E-012.67E+012.50E-035.00E-036.77E+015.00E-032.50E-023.48E-01

11

/̂•s. Consequently, the background levels used for comparison were taken fromsamples collected from the Vestal supply wells and analyzed by the BroomeCounty Health Department.'* These results are summarized in Table 2-5. Onlysamples from untreated water have been included. The values may notaccurately reflect background groundwater conditions since the supply wellsare near the Susquehanna and draw surface water through the alluvium.Therefore, there is some degree of uncertainty in the use of these values.Comparison to the levels presented in Table 2-4 indicates that arsenic,barium, chromium, lead, manganese, mercury, and zinc exceed backgroundconcentrations. These chemicals are therefore retained as chemicals ofpotential concern. Five additional chemicals—antimony, beryllium, nickel,thallium, and vanadium—were not analyzed for in the Vestal city well samples.Therefore, background levels could not be estimated. In keeping with the

'"!•

conservative nature of the PHE, these chemicals are retained for evaluation.Table 2-6 summarizes the chemicals of potential concern for the Vestal

site.

i_s 3.0 EXPOSURE ASSESSMENT

3.1 IDENTIFICATION OF EXPOSURE PATHWAYSExposure pathways describe the mechanisms by which humans may come in

I contact with (be exposed to) contaminants. An exposure pathway will depend onthe physical and chemical properties of the contaminants, use of the site andsurrounding area., and site characteristics such as geology, hydrology, soilproperties and climate. EPA guidance on Superfund risk assessments (1986c)defines an exposure pathway as consisting of the following elements: (1) asource and mechanism of chemical release to the environment; (2) anenvironmental transport medium for the released chemical (e.g., air,groundwater}, (3) a point of potential human contact with the contaminatedmedium (referred to as an exposure point); and (4) a route of exposure at theexposure point (e.g., ingestion, dermal contact). If all of the elements of

*The supply wells have not shown any contamination with inorganics andcan therefore be vised as background.

12

TABLE 2-5BACKGROUND CONCENTRATIONS OF INORGANIC CHEMICALS IN GROUNDWATER

i/ESTAL WELL 1-i SITE( a - ' concentrations in mg/1iter)

ALUMINUMANTIMONYARSENICBARIUMBERYLLIUMCADMIUMCALCIUMCHROMIUMCOBALTCOPPERIRONLEADMAGNESIUMMANGANESEMERCURYNICKELPOTASSIUMSELENIUMSODIUMTHALLIUMVANADIUMZINC

VESTAL «Eu.i

RANGE

NANA

<0.002<0.1-0.3

NA<0.001

NA<O.OC5

NA<0. 025-2.1<0. 05-0. 51

<0. 005-0. 008NA

<0. 025-0. 34<0.0002

NANA

<0.0028.2-22

NANA

<0. 025-0. 033

BACKGROUND (a)

GEOMETRICMEAN

NANA

<0.0020.08NA

<O.OC1NA

<0.005NA

0.050.100.004NA

0.04<0.0002

NANA

<0.00212.9NANA

0.017

(a) Results of five samples from Vestal City wells (1-1. 5-1, 1-3,1-2, 4-4) collected 11/88.

NA * chemical not anayzed for.<X * Chemical not detected where x is the detection limit.

13

TABLE 2-6CHEMICALS OF POTENTIAL CONCERN

VESTAL WELL 1-1 SITE

SOIL (a) GROUNDWATER (b)

Acetone AntimonyBenzene Arsenic2-Butanone BariumChloroform Beryllium1,1-Dichloroethane Chromium1,1-Dichloroethylene • Leadtrans-1,2-Dichloroethylene ManganeseEthylbenzene Mercury1.1,2,2-Tetrachloroethane ., NickelTetrachloroethylene ThalliumToluene Vanadium1,1,1-Trichloroethane ZincTrichloroethyleneXyleneBis(2-ethylhexyl)phthalateDi-n-butylphthalateNoncarcinogenic PAHsCarcinogenic PAHsPCBsChromiumCopper

(a) These chemicals selected from soil samples in the four source areas.(b) These chemicals selected from the inorganics detected in monitoring wells.

14

the exposure pathway are present, then that pathway is said to be "complete."Complete exposure pathways are subject to evaluation in the PHE. For thepurposes of this assessment, the sources of contamination at the Vestal Siteare the four identified source areas. The following sections address releaseand transport mechanisms, potentially exposed populations, and exposure routesrelative to each of the potential exposure media—soil, surface water, air,and groundwater.

In this assessment, both current and potential future exposure pathwaysare considered. Current activity patterns at the site are examined toidentify current potential exposures to residents, workers, or biota from thesite as it currently exists. In developing future exposure pathways, it isassumed that no further remedial actions will be undertaken, and that futuredevelopment of the site will be unrestricted. Under this scenario it isassumed that a commercial or light industrial building, such as thosecurrently present at the Industrial Park, may be constructed on the sourceareas and that exposures to contaminants in soils may occur during theconstruction.

Air. Under current site use, potential exposures via the air pathway arelimited at the Vestal site. Volatiles in soil or groundwater may diffuse intothe unsaturated zone. However, two of the three source areas are paved,effectively preventing any release to the atmosphere. Any contaminantsreleased from the- limited uncovered areas would be quickly dispersed in theatmosphere. This was confirmed qualitatively during the RemedialInvestigation conducted in 1986. In that investigation, ambient airmonitoring with a photoionization detector did not detect the presence ofvolatiles. Trace levels of volatiles were detected in some surface soils inthe 1986 RI; however, volatiles in near-surface soils were generally notdetected (Ecology and Environment 1986). Relatively high levels of volatileswere detected by the Level II screening analysis of surface soils during thesupplemental RI. However, based on modeling performed by Hwang (1986)volatiles are expected to be depleted from soils relatively rapidly, and wouldnot contribute significantly to long-term exposures. Because of the paving

15

and lack of non-volatile contamination in surface soil, wind erosion is notcurrently a potential release mechanism at this site. Based on thisdiscussion, air exposures are not considered significant under current uses,and are not addressed in this assessment.

Under future redevelopment, excavation at the site may result involatiles in soils being released to the air within the area being excavated.Workers involved in excavation or the construction of a foundation or basementnay then be exposed. Once the soils are removed from the excavation, loadingor grading operations may generate dust resulting in exposure of workersoutside the excavation pit through inhalation. These represent potentialcomplete exposure pathways under future land-use conditions, and they will beevaluated in the assessment.

Surface Water. Surface water" bodies in the immediate vicinity of thesite include Choconut Creek, approximately 0.4 miles west of the source areas,the Susquehanna River to the north, and two wetland areas to the south andeast of the source areas. The two wetlands drain into the Susquehanna viadrainage ditches. The creek is located outside the area of groundwatercontamination and is not downgradient of the source areas. Therefore,contamination from the study areas is unlikely to reach the creek. Samplingof the surface water and sediments in the wetlands and drainage ditches inprevious investigations did not reveal any contamination with volatiles.Volatiles were detected in a surface water sample collected at the outlet ofthe wetland area south of the source areas. However, the results were notconfirmed by groundwater samples in the area and were therefore not consideredrelated to the groundwater contamination (Ecology and Environment 1986). Anyadditional releases to groundwater from the four source areas may be capturedby Well 1-1 prior to entering the Susquehanna River. Future constructionactivities would not be expected to cause any releases to surface waterassuming that normal erosion control practices are used. Based on the abovediscussion, no significant surface water exposure pathways are present undercurrent or potential future site-use scenarios at the Vestal site.

16

Groundwater. Previous investigations and the current remedial actionhave addressed current volatile organic contamination of groundwater and Well1-1 at the Vestal site. Consequently, these exposures are not included in

w

this assessment. However, in considering future exposure pathways, it isassumed that contaminants in soil in source areas may leach to groundwaterresulting in additional contamination. This potential exposure pathway isaddressed in this assessment. Two exposure points are considered for thisexposure pathway: (1) groundwater directly below the source areas — as a worstpossible case in which a future well is placed below the source areas, and(2) groundwater from Well 1>1 — to assess the potential impact at the currentpoint of focus of remedial actions. The primary routes of exposure forgroundwater are ingestion and inhalation of volatiles while showering. Otherexposures may occur as a result of washing clothes or dishes or otherhousehold use of water. However, models are not available to reliablyquantify these exposures.

The sampling of monitoring wells during the supplemental RI revealed thepresence of inorganics that appear to significantly exceed backgroundconcentrations . As a means of determining if the detected contaminationrepresents a potential risk to public health that may warrant additionalinvestigation or other actions, the PHE contains a screening analysis of thesampling results. In the screening analysis the detected levels are comparedto drinking water standards and health criteria. This represents an upper -bound exposure in which it is assumed that drinking water would be obtainedfrom the location of the monitoring wells. Since drinking water is suppliedby the town of Vestal, this analysis represents a screening case in which thepotential for adverse effects to occur is assessed, rather than an actual orpotential complete exposure pathway.

Soils. As noted above, volatiles in surface soils are not expected toremain in soil for long periods. A large portion of the study area is paved,prevening direct contact with surface soils. Thus, under current site use; nosignificant exposures from direct contact by trespassers or workers would beexpected. Exposure to subsurface soils may occur as a result of excavation or

/•"""N

17 5

construction activities under potential future redevelopment of the site.Exposure may occur through direct contact with exposed skin (hands, forearms)and absorption of contaminants from soil through the skin, and from incidentalingestion of soil by workers who smoke, eat, or drink following contact withsoil.

In summary, the following potential exposure pathways will be evaluatedin the Public Health Evaluation:

1. Potential exposure to future construction workers engaged inexcavation or other subsurface activities. Exposure may occurthrough incidental soil ingestion, dermal absorption of contaminants,and inhalation of volatiles released from excavated soils.

2. Potential exposure to construction workers engaged in above-groundactivities. Exposure may occur as a result of inhalation ofcontaminated dusts generated from loading or grading of excavatedsoils.

3. Potential future leaching of contaminants from soils to groundwaterwith potential exposure directly below the site and at the wellfield. The routes of exposure considered are ingestion andinhalation of volatiles released while showering.

4. Potential exposure from ingestion of inorganics in groundwater at thelevels detected in monitoring wells.

I1 3.2 ESTIMATION OF EXPOSURE POINT CONCENTRATIONS

Concentrations of contaminants of concern at the exposure pointsj identified in the previous section must be estimated in order to assess risk.

The development of exposure point concentrations may be accomplished in one oftwo ways: (1) direct use of monitoring data from environmental media (soil),or (2) development of pollutant transport models to predict the migration ofcontaminants .

For the exposure pathway involving direct contact with soils by futureconstruction workers, exposure point concentrations may be taken directly fromthe sampling. However, three exposure pathways require that models bedeveloped to estimate the release of contaminants from soil. These are:(1) release of volatiles to the air within an area of soil excavation,

on

18

-«"*,,(2) release of dust from the excavation and loading of contaminated soils, and(3) leaching of contaminants from soil to groundwater. The models used to

. estimate these exposures are discussed below.In keeping with EFA guidance on exposure assessments (EPA 1988a), the PHE

examines two exposure cases for each exposure pathway: (1) an average case,and (2) a plausible maximum case. The average case uses average (butconservative) exposure parameters, and as such, represents a typical or likelyexposure for most individuals or for the exposed population as a whole. Theplausible maximum case uses reasonable upper bound limits for exposureparameters, and as such, represents a reasonable (but not absolute) worst caseexposure. The plausible maximum case is less likely to apply to the exposedpopulation as a whole, but may apply to smaller subsets of the population orto the "maximally exposed individual," the single individual subject to thehighest exposure (EPA 1988a). The purpose of using two exposure cases is tohighlight the variability of the exposure parameters. Many parameters used inthe exposure assessment are not known, but must be estimated. Consequently,there is some degree of uncertainty as to the actual value. Where ̂ uncertaintyexists it is more appropriate to provide a range of values than to rely on asingle estimate. By using a range of values, the sensitivity of theassessment to the various parameters can be evaluated. The plausible maximumcase may be used to determine if exposure and risk are significantly belowtarget risk levels even at the upper limits of possible exposure. However, ifthe risk estimates based on the plausible maximum case exceed target risklevels, this should not automatically be taken as a cause for concern, sincethis case represents an upper bound on possible exposure.

In estimating exposure point concentrations for the average case, thegeometric mean soil concentration, calculated using one-half the detectionlimit for non-detect samples, is used as input. For the plausible maximumcase, the geometric mean of only the samples in which the chemical.wasdetected are used. In some cases, the geometric mean of detected samples wasless than the mean including non-detects. In these cases, the higherconcentration was used as the plausible maximum case, and the lower value for

onn

19

/"""̂ the average case. In cases where the mean was above the highest detectedvalue due to high detection limits in non-detect samples, the highest value

; was used for both the average and plausible maximum cases. This may lead toan overestimation of exposure and risk in these cases. The soilconcentrations used to estimate exposure point concentrations are shown inTable 3-1.

; 3.2.1 Release of Volatiles from Soil During ConstructionIn estimating the release of volatiles from soil during construction it

was assumed that exposure would occur within a construction trench or pit.Excavation of the pit exposes additional surface area from whichvolatilization can occur. The pit was assumed to be 12 feet deep with a baseof 6 feet x 100 feet. Thus, the total surface area is the sum of surface area

;V

for each of the 4 walls in the pit and the pit floor.A soil volatilization model developed by Hwang (1986), recommended for

use by the EPA _986e), was used to estimate an emission rate for each of thechemicals detected in soil. A chemical can exist in the soil in three phases:

.-—>•-, (1) adsorbed to soil particles; (2) as a liquid in the soil pore spaces; and(3) as a vapor in the soil pore spaces. The model assumes that there is anequilibrium between the three phases of the chemical present in the soil. The

| following series of equations were applied to estimate the amount of chemicalvapor in the soil pore spaces (phase 3). The equilibrium concentration of a

I chemical in the liquid in the soil pores is calculated by:

C. C,

where

Cx — concentration of chemical in solution (g/ml);

C, - concentration of chemical adsorbed to soil (g/g); and

Ka - soil/liquid partition coefficient (cm3/g)- K̂ *̂ .

20

TABLE 3-1AVERAGE AND PLAUSIBLE MAXIMUM SOIL CONCtNTRAIIONS FOR EXPOSURE MODELING

VESTAL WELL II S ITE

CHEMICALAREA 1 AREA 2

Average Case (a) Plausible Average Case (a)Maximum Case (b)

(mg/kg) (mg/kg) (mg/kg)

ft ft ft

0.003 0.003 0.003 c0.034 0.034 0.026 e

* * 0.007 e* * 0.009 c* * 0.003 c

ylene 0.003 0.003 0.1180.005 0.022 0.087

hane " * 0.04 c* * 0.0670.005 0.01 0.052

* * 0.0750.171

0.007 0.054 e 0.197a late * * 0.4

* * 0.065 c3.9 95.8 3.41.1 ' 5.5 0.8 c

* * 0.1524 24 47

• * * 23

PlausibleMaximum Case (b)

(mg/kg)

*

0.0030.026 e0.007 e0.0090.003 c0.3120.1590.04 d0.2980.330.4255.0452 . 0380 730.0655.161 5 d

0.3784723

AREA 3

Average Case (a)

(mg/kg)

0.195*

0.01*

0.004 c0.003 e0.004 c

A

ft

ft

ft

0.002 eft

*

0.39*

0.32 e0 05 e

A

9.27.7

AREA 4

Plausible Average Case (a)Maximum Case (b)

(mg/kg) (mg/kg)

7.08 1.382ft ft

0.012ft ft

0.004 0.120.003 e 0.005 c0.013 d *

* •

ft «

* 0.002 e« •

0.002 e 0 ISB* 0.134* *

1 . 1 0 2.3A ft

0.32 e 020.05 e

• 0.0514.2 207.7 46

PlausibleMaximum Case (b)

(mg/kg)

12.852ft

ft

ft

0.1860.005

ft

t

A

0 002 e•

0.2160.864

*

3 /82*

0.23 e•

0 SS e2046

AcetoneBenzene2-ButanoneChloroform1 . 1-Oichloroethanel.l-Dichloroethylenetrans-1.2-0ich1oroelhyleneEthylbenzeneI . I ,2,2-Tetrachloroulhane1 et rach loroethy leneToluene1.1. 1-TrichloroethaiK?T rich loroethy leneXyleneBis(2-ethylhexy Uphlli.) lateDi-n-butylphthalateNoncarcinogenic PAHsCarcinogenoc PAHsPCBsChromiumCopper

' Chemical not detected in this area.(«) Geometric, mean wi th one half the detection limit for non-detects unless otherwise noted.(b) Geometric mean ol detected values only, unless otherwise noted.(c) Geometric mean ol detected values only.(d) Geometric mean w i t h non-detects.(e) Only detected v.i iue

LUU

where

Koc - organic carbon partition coefficient (cm3/g)i and

foe - fraction of organic carbon in the soil (dimensionless).

The vapor phase concentration of a chemical in the soil pore spaces iscalculated by:

Cg -

where

Cg - concentration of chemical in the vapor phase [g/cm3],

H - Henry's Law Constant [atm.m3/n>ol],

R - universal Gas Constant ['8.19xlO~5 atm.m3/mol K],

T - soil temperature [293 K].

Substituting for Cx from the previous equation gives the vapor-phaseconcentration:

(Cs)(H')(Koc)(foe)

C3 the initial concentrations of chemical adsorbed to the soil, are taken asthe geometric mean concentration with nondetects for the average case and thegeometric mean of the detected values for the plausible maximum case as givenin Table 3-1.

To estimate emission rates for each chemical, it is assumed that a column(of infinite depth) in the soil initially contains the chemical vapor evenlydistributed throughout the entire column with the surface vapor phaseconcentration at zero. A flux equation predicts the migration of the chemicalup through the soil column toward the surface, and ultimately the flux of thechemical vapor into the air. This flux equation is dependent upon theeffective diffusivity which is dependent on the physicochemical

22

characteristics of the chemical being modeled as well as soil characteristics.The effective diffusivity is given by:

Ds - Di * E1/3

where

DA - vapor-phase diffusion coefficient in air for the ith chemical(cmVg); and

E soil porosity.

The flux rate of vapors from the soil surface into the overlying air isobtained by solving a mass balance equation for a vertical element of thesoil. The average flux rate for a given time period, tj is given by

N - 2 (E)(Ds)(H1)(C.0)(« a t)1/2 Kd

where

Na — average flux over the time period tj (g/m2-sec);

H! - nondimensional Henry's Law Constant;

C80 - initial chemical concentration in soil (g/g) ;

t - flux rate period, (sec);

Kj - soil/liquid partition coefficient - K^ * foe (cm3/g) I

o - [D, * E]/E+P. * (1-E) (Kd/Hi)] (cm2/s) where;

P, - true soil density (g/cm3) .

Once the emission rate is calculated, it is necessary to determine how thisflux of chemical vapors from the soil surface will effect the air quality inthe pit. Indoor air pollution concepts were applied to the pit since it wasassumed that the pit is analogous to a semi -confined structure such as a house

•with windows or doors on one side. The average number of air changes per hourfor houses are estimated to range from 0.5 to 2 (Wadden and Scheff 1983). A

o23

value of 1.0 is used to represent a house with windows or exterior doors onone side. Therefore, the air within the pit would be entirely exchangedwithin a 1 hour period. The ambient air concentration in the pit is given by:

N. A X

Erwhere

C. - chemical- specific ambient air concentration (mg/m3);

N. - chemical- specific average flux rate (g/cm2-sec);

A - total surface area of the excavated trench (cm2) ;

Er - exchange rate in the trench (cm3/sec) .

X - 109 (mg/m3)/(g/cm3)

The exchange rate in the pit is calculated by:

volume of Air exchanged (volume of Pit)•_fcr ~1 hour (time for one air exchange) (3600 sec/hr)

Table 3-2 lists the physicochemical parameters (Koc, Di) used for each ofthe chemicals of potential concern. Table 3-3 lists the various site-specificparameters (foe, E, Area) used in the modeling. The estimates of ambient airconcentrations in the pit for each of the four source areas are listed inTable 3-4.

3.2.2 Generation of Dust from Construction ActivitiesA two part model was used to develop concentrations of chemicals in air

resulting from dust generated during construction activities. First, achemical emission rate is estimated from the dust emission rate and theconcentration of contaminants in the soil. Second, an air dispersion model isused to estimate concentrations of contaminants in the air at the site.

24

TABLE 3-2

CHEMICAL-PHYSICAL PARAMETERS USED I* THESOIL VOLATILIZATION MODEL AT THE VESTAL WELL 1-1 SITE

CHEMICAL

AcetoneBenzeneBis(2 ethylhexyOphthatate2-ButanoneChloroformDi-n-butyl phthalate1,1-Di chloroethane1 ,1-Dichloroethylenetrans-1 ,2-DichtoroethyleneEthylbenzeneMethylene ChlorideCarcinogenic PAHs [BaP]Noncarcinogenic PAHsPCBs-1248Tetrach loroethyleneTolueneTrich loroethylene1,1,2,2-Tetrachloroethane1,1, 1 -Tri chloroethaneXylene

OIFFUS1VITY(cm2/sec)

0.114980.093200.035420.089440.088680.043830.095900.100770.099800.066670.085800.046530.082050.054980.074040.078280.081160.072880.079650.07164

HENRY'SLAW CONSTANT(atm-mB/mole)

3.67E-055.43E-034.40E-075.14E-053.80E-031.30E-065.70E-031.54E-016.60E-037.90E-032.60E-033.72E-052.38E-074.40E-042.30E-026.60E-038.90E-034.70E-042.80E-025.10E-03

ORGANIC CARBONCOEFFICIENT (Koc)

2.283

874004.544

13903065592208.8

5500000940

277000364300126118152238

25

TABLE 3-3

SITE-SPECIFIC PARAMETERS USED INTHE AIR MODELING FOR THE VESTAL WELL 1-1 SITE

PARAMETER VALUE

Parameters used in thesoil volatilization model: Dry Bulk Density of soil

soil (kg/m3) 1330

Fraction of organic carbonin the soil (X) 0.15

Porosity of the soil (X) 46?v

Moisture contentin the soil (X) 0

Source Area (cm2) 2.90E+06

Parameters used inthe box model: Wind Speed (m/sec) 4.6

Parameters used in thetrench constructionscenario (an indoor airdispersion model wasused): Total Surface Area

of Pit (cm2)

Volume ofPit (cm3/sec)

2.90E+06

2.04E+08

26

During "heavy construction dust emissions are generated by a variety ofactivities including excavation, cut and fill operations, and equipment"raffic. The level of fugitive dust emissions is dependent on the size of theconstruction site and the amount of construction activity. The dust emissionrate is also dependent on soil characteristics such as silt content and soilmoisture. An appropriate dust emission rate for large construction operationshas been developed based on field measurements of airborne dust emissionsassociated with large construction activities. According to the EPA (1985a) ,the approximate dust emission level is given by as 1.2 tons of dust per acreof activity per month of activity. This value is applicable to constructionactivities with a medium activity level, moderate silt content in the soil,and a semi -arid climate. The Vestal area receives more rainfall than a semi-arid climate which would help to suppress dust levels. Thus, the emissionrate is a conservative one for this site. In this exposure scenario, it wasassumed that the size of the area under construction was 0.34 acres (based onthe size of buildings already present in the industrial park, approximately100 ft by 100 f t . ) , and the excavation would take 6 weeks at 5 days per week .Thus the total amount of dust released during the construction period is

1.2 tons /month/acre x 0.34 acres x 1 month/2 . 6xl06 sec x 1 . 016xl03kg/ton- 1.6x10'* kg/sec

The chemical emission rate is simply the mass fraction of contaminant inthe soil times the dust emission rate. The concentrations of chemicals ofpotential concern listed in Table 3-1 were used as the contaminant massfraction for the average and plausible maximum cases.

An air dispersion box model was used to estimate concentrations ofcontaminants from the fugitive dust. The box model assumes steady andspatially uniform conditions of dispersion so that the chemical emissions(estimated as described above) uniformly distribute throughout a box definedby the area of the source and the mixing height which is determined bymeteorological conditions. The model requires steady- state chemical emission

o

27

TABLE 3-4

ESTIMATED AIR CONCENTRATIONS FOR CONSTRUCTIONWORKERS EXPOSED TO VOLATILE CHEMICALS DURINGTRENCHING OPERATIONS AT THE VESTAL, NY SITE (a)

ro00

CHEHICALAREA 1 AREA 2 AREA 3

Average Maximum Average Maximum Average Maximum

(a) All concentrations reported In mg/m3.* - Chemical not detected In surface soils

AREA 4

Average Maximum

AcetoneBenzene2-ButanoneChloroform1,1-Dlchloroethane1 , l-D1chloroethy lenetrans-l,2-D1chloroethy1eneEthylbenzene1 , 1 , 2 , 2-TetrachloroethaneTet rach toroethy leneToluene1,1. 1-Tr IchloroethaneTrichloroethyleneXyleneB1s(2-ethylhexyl)phtha1ateDi-n-butylphthalateNoncarclnogenic PAHsCarcinogenic PAHsPCBs

*3.20E-021.22E-01***4.87E-023.04E-02**5.26E-02**3.22E-02**6.19E-022.06E-03*

*3.20E-021.Z2E-01***4.87E-021.34E-01**1.03E-01**2.49E-01**1.48E+001.03E-02*

*3.20E-029.34E-028.87E-022.18E-017.63E-011.92E+005.31E-017.22E-027.01E-015.47E-011.59E+001.79E+009.08E-012.S8E-041.41E-035.16E-021.55E-034.74E-03

*3.20E-029.34E-028.87E-022.18E-017.63E-015.07E+009.70E-017.22E-023.12E+003.46E+009.03E+005.28E+019.38E+005.16E-041.41E-037.94E-022.84E-031.20E-02

9.85E-01*

3.61E-02*9.70E-027.63E-016.50E-02***

••*' *4.24E-02**2.79E-04

4.95E-039.28E-05*

3".57E+01*4.32E-02*9.70E-027.63E-012.1 IE-01****4.24E-02**7.74E-04*4.95E-039.28E-05*

6.96E+00***2.89E+001.27E+00***2.09E-02*

3.35E+001.40E+00*

1.6SE-04*

3.09E-03*1.60E-03

6.48E+01***4.51E+001.27E+00***2.09E-02*

4.58E+009.03E+00*

2.69E-03*3.56E-03

' *

1.75E-02

rates, a constant wind vector, and also that the crosswind distance of thearea source is large in comparison to the downwind distance of the receptor.To meet these requirements, all chemical emission rates were calculated forsteady state, the wind speed was chosen to be the annual average wind speedrecorded at the Binghampton, NY airport, and the area of the box was taken tobe the area of the excavation (0.34 acres). The equation used to determinethe box height is:

X - 6.25 ZQ [(H/Z0) In (H/ZQ) - 1.58(H/ZQ) + 1.58))]where

Z0 - roughness height (m);

X - downwind distance (m); and

H - box height (m).

The on-site air concentration is calculated using:

C. -HWU

where

C. - The concentration on-site for the i contaminant (mg/m );

0 . - The emission rate of the i contaminant (mg/s);

U - Average wind speed in the box (m/s);

H - Height of the box (m);

W - Crosswind width of the area source (m); and2

A - Size of the area source (m ). •

The input parameters to the model are listed in Table 3-5. Table 3-6gives the estimated ambient air concentrations of particle-bound chemicals ofpotential concern for each of the four source areas.

29

TABLE 3-5

INPUT PARAMETERS USED IN THE BOX MODEL FOR PREDICTING AIRCONCENTRATIONS FROM CONSTRUCTION ACTIVITIES

AT THE VESTAL WELL 1-1 SITE

PARAMETER VALUE

Wind Speed (m/sec) 4.6

Width of Box (m) 37'!V

Roughness Height (m) 1

Length of Box (m) 37

Area Encompassed by the Box <m2) 1400

30

TABU 3-6

AIR CONCENTRATIONS Dllf TO FUGITIVE OUST G f N F R A T I O NDURING CONSTRUCTION A C T I V I I I fS AT lilt V E S I A I SIM

1

HEMICAL

cetoneenzeneis (?-ethy1 hexyl) phi ha lateButanone

arcinogenic PAHs, l-Oichloroethatie,1-Dichloroethene,2-Oichloroethene (trjns)i-n-butyl phthalatethyl benzeneoncarcinogenic PAHsCBs (1242)etrachloroethene. 1.2.2-Tetrachloroethuneoluenerichloroethene, 1, 1-Trichloroethaneylenes

AREA 1

GeometricMean (a)

*

9.78E-I6*

1.11E-I43.59E-134

*

9.78E-16ft

1.63E-151.27E-12

.63E-I5

2.28E-15

Maximum

*9*11*»9*33

1

78E-16

HE-1479E-12

78E-16

26E-1512E-11

26E-15

76E-14

ARIA 2

GeometricMean

*918229322I42I1526

78E 1630E-I348E-IS61E 1393E-1578E-1685E-1412E-I484E-14HE-1289E-1418E-1430E-1470E-1457E-1444E-1442E-14

Maximum

A

3 ?6E2 . 3818.48E4 89E2 93E9.78E1.02E2.12FS.I8E1 66F1 23E9 71E1.30E1.08E1 6411.39E6.64E

-O/-13-15-13

IS-16-13-14

14-12-13-14-14

13-12

13-13

ARFA 3

GeometricMean

t>.J6F•1 ?7E3 Z6E1 63E1 30E9 78E1 30F -

04E-

G.S2E-ft

14

13IS141516IS

13

16

Maximum

?. JIFA

.3 S9E3.91E1 (13F1 30E9 . 78E4 .Z4E

04E

6 S2E*

1?

-1.115

-14IS

-16-IS

-13

-16

AKI A

Geome t r11Mean

4 Ml I:•/ Mil N

3 . 9 U - - MI f,.(l IS

I 1.31 146. Si'1 16

4 VI 14'j l',l 14

MAX imum

4 . I 9 E - 1 ?

K 06E-I4I 63E-IS

7 '.OE-14I Ml H6.WI-16

? 8?l -137 041 14

a) All concentrat10, s reported in mg/m3.

* - Chemical not deletled in this area.

/*""""v- 3.2.3 Leaching of Contaminants to GroundwaterA two part model was used to develop concentrations of chemicals of

: potential concern in groundwater as a result of leaching from soil. First,the concentration of contaminant in the pore water infiltrating the site isestablished assuming equilibrium conditions between the pore water and thesoil. Second, a mass balance relationship is used to estimate the mixing ofinfiltration with groundwater and the resultant concentration of chemical in

the groundwater.The pore water concentrations were determined assuming an equilibrium

partitioning between soil and water described as follows:

Cw

Kd

whereCw — concentration of contaminant in the pore water (mg/liter); andCs - concentration of contaminant in soil (mg/kg); andKd - (Koc)(foc);

whereKoc - organic carbon partition coefficient (I/kg); andfoe - fraction of organic carbon in soil (dimensionless).

For copper and chromium, soil-water partition coefficients were obtainedfrom the literature. A coefficient of 35 was used for copper (Baes et al.1984) and a coefficient of 37 was used for chromium (Baes et al. 1983,Gerritse et al. 1982) assuming the chromium exists in the +6 oxidation state.This assumption could over-estimate chromium concentrations in groundwater aschromium VI is more mobile and less common in soils than chromium III.

This method assumes that the concentrations of contaminants in the soilas measured by the samples from the source areas represent the totalcontaminant concentration, i.e., both the contaminant sorbed to the soil andthe dissolved portion capable of leaching to groundwater over time.

32

/*"*"%The groundwater concentration is then determined from the following mass

balance equation:I Cw(Ow)

Cgw - (Qw + Qgw)

where

Cgw - concentration in the groundwater (mg/liter);

Qw — volumetric flow rate of recharge from pore water into thegroundwater (ft3/day);

Qgw - volumetric flow rate of groundwater (ft3/day); and

Cw - contaminant concentration in the pore water (mg/liter).

Qw was calculated from the interstitial pore-water velocity and the areaof the site (ft2). First, infiltration is calculated by the water balanceequation:

I - P - E - Rwhere

I - infiltration (in/yr);P - total annual precipitation (in/yr);E - evapotranspiration (in/yr); andR - runoff (in/yr).

The volumetric flow rate of infiltration is calculated byQw - A.lt, x I

Where A,it, is the area of the site.The volumetric flow rate of groundwater beneath the site is determined by

Darcy's Law:Qgw - AK(dh/dl)

whereA - cross sectional area of the site perpendicular to flow (ft2);K - hydraulic conductivity (ft/ day); and .2dh/dl - hydraulic gradient (ft/ft). ^

oo

33

The Vestal well field is approximately 1,700 feet dovmgradient of thesource areas. Based on the observed concentrations of total volatile organics(Ebasco 1989), which is approximately 10,000 ppb below the source areas and100 ppb at the well field, it is conservatively assumed that contaminantconcentrations will decrease by a factor of 100 (10,000/100 - 100) as theymigrate from the source areas to the well field. The site areas were takenfrom the location of soil borings in the four source areas. Since the modeluses area and length of the site parallel to groundwater flow, the modelresults will be different depending on the shape and size chosen for thesource areas. This results in different predicted concentrations fordifferent source areas, although the soil concentrations may be the same.

Table 3-7 lists the values of .these parameters and their sources. Tables3-8 through 3-11-present the estimated groundwater concentrations for each ofthe four source areas based on the model.

4.0 TOXICITY ASSESSMENT

4.1 HEALTH EFFECTS CLASSIFICATION AND CRITERIA DEVELOPMENTFor risk assessment purposes, individual pollutants are separated into

two categories of chemical toxicity depending on whether they exhibitnoncarcinogenic or carcinogenic effects. This distinction relates to thecurrently held scientific opinion that the mechanism of action for eachcategory is different. EPA has adopted, for the purpose of assessing risksassociated with potential carcinogens, the scientific position that a smallnumber of molecular events can cause changes in a single cell or a smallnumber of cells that can lead to tumor formation. This is described as a no-threshold mechanism, since there is essentially no level of exposure (i.e., athreshold) to a carcinogen which will not result in some finite possibility ofcausing the disease. In the case of chemicals exhibiting noncarcinogeniceffects, however, it is believed that organisms have protective mechanismsthat must be overcome before the toxic endpoint is manifested. For example,if a large number of cells perform the same or similar functions, it would be

/—V

34

TABLE 3-7PARAMETERS USED IN THE GROUNOWATER LEACHING MODEL


PARAMETER VALUE SOURCE

Bulk density, b

Porosity, f

Fraction of organic carbon, foe

Precipitation, P

Evapotranspiration, E

Runoff. R

Site areas. Asite

Length of area perpendicularto groundwater flow;A - Length x 30 ft (aquiferdepth)

Hydraulic gradient, dh/dl

Hydraulic conductivity. K

1.33 g/ml

0.46

0.0015

36 in/yr

26.3 in/yr

3 in/yr

Area 1: 10,500 ft2Area 2: 10,500 ft2Area 3: 32,400 ft2Area 4: 47,300 ft2

Area 1:Area 2:Area 3:Area 4:

165 ft165 ft370 ft445 ft

NY Soil Survey 1989

NY Soil Survey 1989*

Average of 10 on-site samples.

EBASCO 1990

Pan evaporation rate of 37.5in/yr (U.S. Weather Bureau)times an adjustment factor of0.7 (USEPA 1987).

U.S. Soil ConservationService curve number method,modified by Stewart et al.(1976 as reported by Mills etal. 1985). Curve number » 89(hard surfaces, moderatelylow runoff potential).

EBASCO 1990. Figure 1-4.


0.008 ft/ft

Average case: 300 ft/dayPlausible maximum case: 30 ft/day


E&E 1986

35

TABLE 3-8ESTIMATED GROUNDWATER CONCENTRATIONS DUE TO LEACHING FROM SOIL

AREA 1VESTAL WELL 1-1 SITE

CHEMICALSOIL CONCENTRATION

ESTIMATEDGROUNDWATER CONCENTRATION

DIRECTLY BELOW THE SOURCE AREA


AT THE WELL FIELD

Average Case PlausibleMaximum Case

(mg/kg) (mg/kg)


(mg/1) (mg/1)


(mg/1) (mg/1)

AcetoneBenzene2-ButanoneChloroform1 . 1-Dich loroethane1,1-Dichloroethylenetrans-1 ,2-DichloroethyleneEthylbenzene1,1,2, 2-TetrachloroethaneTetrachloroethyleneToluene1,1, 1-Tr ichloroethaneTrichloroethyleneXyleneBis(2-ethy1hexyl)phthalateDi-n-butylphthalateNoncarcinogenic PAHsCarcinogenoc PAHsPCBsChromiumCopper

*3.00E-033.40E-02*

*

*

3.00E-035.00E-03

• *

*

5.00E-03*

*

7.00E-03*

*

3.90E+001 . 10E+00*

2.40E+01*

*

3.00E-033.40E-02*

*

*

3.00E-032.20E-02*

*

l.OOE-02**5.40E-02**9.58E+015.50E+00*2.40E+D1*

it

3.25E-056.78E-03*

it

*

4.S7E-052.04E-05*

*

1.50E-05*«2.62E-05**3.73E-031.80E-07*8.75E-04*

*3.21E-04S.70E-02*

*

*

4.52E-048.88E-04**2.96E-04**2.00E-03**9.05E-018.88E-06*

8.64E-03*

*

3.25E-076.78E-05*

*

*

4.57E-072.04E-07**1.50E-07*

*

2.62E-07**3.73E-051.80E-09*

8.75E-06*

*

3.21E-066.70E-04*

*

*

4.52E-068.88E-06*

*

2.96E-06*

* '

2.00E-05*

*

9.05E-038.88E-08*

8.64E-05*

Chemical not detected in this area.

o>J

36

/*••


AREA 2VESTAL WELL FIELD

f*U?UT f ft 1


SOIL CONCENTRATION DIRECTLY BELOW THE SOURCE AREA


AcetoneBenzene2-ButanoneChloroform1 . 1 -D i ch loroethane1.1-Dichloroethylenetrans-l,2-Dich1oroethy1eneEthylbenzene1.1,2 , 2-Tetrachl oroethaneTetrachloroethyleneToluene1,1,1-TrichloroethaneTrichloroethyleneXyleneBis(2-ethy1hexyl)phtha1ateDi-n-butylphthalateNoncarcinogenic PAHsCarclnogenoc PAHsPCBsChromiumCopper

(mg/kg)

*3. ODE-032.60E-027.00E-039.00E-033.00E-031.18E-018.70E-024.00E-026.70E-025.20E-027.50E-021.71E-011.97E-014.00E-016.50E-023.40E+008.00E-011.50E-014.70E+012.30E+01

(mg/kg)

*

3.00E-032.60E-027.00E-039.00E-033.00E-033.12E-011.59E-014.00E-022.98E-013.30E-014.25E-015.04E+002.04E+007.30E-016.50E-025.16E+001.50E+003.78E-014.70E+012.30E+01


(mg/D

*3.25E-055.18E-031.43E-042.70E-044.15E-051.80E-033.55E-043.05E-041.65E-041.56E-044.44E-041.22E-037.38E-044.11E-064.20E-053.25E-031.31E-072.14E-051.71E-03B.86E-04

(mg/1)

*3.21E-045.12E-021.41E-032.66E-034.10E-044.70E-026.42E-033.01E-037.27E-039.77E-032.48E-023.56E-017.54E-027.42E-054.15E-044.68E-022.42E-065.33E-041.69E-028.75E-03


AT THE WELL FIELD


(mg/1)

*

3.25E-075.18E-051.43E-062.70E-064.15E-071.80E-053.55E-063.05E-061.65E-061.56E-064.44E-061.22E-057.38E-064.11E-084.20E-073.25E-051.31E-092.14E-071.71E-058.B6E-06

(mg/1)

*

3.21E-065.12E-041.41E-052.66E-054.10E-064.70E-046.42E-053.01E-057.27E-059.77E-052.48E-043.56E-037.54E-047.42E-074.15E-064.88E-042.42E-085.33E-061.69E-048.75E-05

Chemical not detected in this area.

*t

J

37



PLJCU T f A I


SOIL CONCENTRATION DIRECTLY BELOW THE SOURCE AREA


AcetoneBenzene2-ButanoneChloroform1,1-Dichloroethane1 , 1-Dichloroethylenetrans-l,2-Dichloroethy1eneEthyl benzene1,1.2. 2-TetrachloroethaneTetrachloroethyleneToluene1,1,1-TrichloroethaneTrichloroethyleneXyleneBis(2-ethylhexyl)phthalateDi-n-butylphthalateNoncarcinogenic PAHsCarcinogenoc PAHsPCBsChromiumCopper

(mg/kg)

1.95E-01*

l.OOE-02*

4.00E-033.00E-034.00E-03*

*

*

*

2.00E-03*

*

3.90E-01*3.20E-015.00E-02*9.20E+007.70E+00

(mg/kg)

7.08E+00*1.20E*02*4.00E-033.00E-031.30E-02****2.00E-03**1.10E+00*

3.20E-015.00E-02*1.42E+017.70E+00


(mg/1)

1.10E-01*

2.74E-03*

1.65E-045.71E-058.38E-05****1.63E-05**5.52E-06*4.21E-041.12E-08*4.61E-044.08E-04

(mg/D

3.91E+01*3.24E-02*

1.62E-035.61E-042.68E-03****1.60E-04**1.53E-04*4.14E-031.11E-07*

7.00E-034.01E-03

ESTIMATED6ROUNDWATER CONCENTRATION

AT THE WELL FIELD


(mg/D

1.10E-03*

2.74E-05*

1.65E-065.71E-078.38E-07****

1.63E-07*

it

5.52E-08*

4.21E-061.12E-10*

4.61E-064.08E-06

(mg/1)

3.91E-01*

3.24E-04*

1.62E-05.5.61E-062.68E-05*

*

*

*

1.60E-06*

*

1.53E-06#

4.14E-051.11E-09*

7.00E-054.01E-05

* Chemical not detected in this area.

38



SOIL CONCENTRATIONCHEMICAL ——————— - ——————————— -


(mg/kg) (mg/kg)

Acetone 1.38E+00 1.29E+01Benzene * *2-Butanone * *Chloroform * *1,1-Dichloroethane 1.20E-01 1.86E-011,1-Dichloroethylene 5.00E-03 5. ODE-03trans-1.2-Dichloroethylene * *Ethylbenzene * *1,1,2,2-Tetrachloroethane * *Tetrachloroethylene 2.00E-03 2.00E-03 .Toluene * *1,1,1-Trichloroethane 1.58E-01 2.16E-01Trichloroethylene 1.34E-01 8.64E-01Xylene * *B1s(2-ethylhexyl)phthalate 2.30E-01 3.78Et-00Di-n-butylphthalate * *Noncarcinogenic PAHs 2.00E-01 2.30E-01Carcinogenoc PAHs * *PCBs 5.00E-02 5.50E-01Chromium 2.00E+01 2.00E+01Copper 4.60E+01 4.60E-t-01

* Chemical not detected in this area.

_


DIRECTLY BELOW THE SOURCE AREA


(mg/1) (ipg/1)

9.42E-01 8.59E+01* *

* *

* *

6.00E-03 9.12E-021.15E-04 1.13E-03* ** ** *8.24E-06 8.08E.-05* *1.56E-03 2.09E-021.60E-03 1.01E-01* *

3.95E-06 6.36E-04* *3.19E-04 3.60E-03« *1.19E-05 1.28E-031.22E-03 1.19E-022.96E-03 2.90E-02

-

t/\


AT THE WELL FIELD


(mg/1) (mg/1)

9.42E-03 8.59E-01* *

* *

* *

6.00E-05 9.12E-041.15E-06 1.13E-05* ** ** *8.24E-08 8.08E-07* *1.56E-05 2.09E-041.60E-05 1.01E-03* *3.95E-08 6.36E-06* *3.19E-06 3.60E-05* *1.19E-07 1.28E-051.22E-05 1.19E-042.96E-05 2.90E-04

|

D

OOn

necessary for significant damage or depletion of these cells to occur beforean effect could be seen. This threshold view holds that a range of exposuresfrom just above zero to some finite value can be tolerated by the organismwithout appreciable risk of causing the disease (EPA 1986c).

A.1.1 Health Effects Criteria for NoncarcinogensHealth criteria for chemicals exhibiting noncarcinogenic effects are

generally developed using risk reference doses (RfDs) developed by the EPA RfDWork Group as listed in EPA's Integrated Risk Information System* (IRIS) database, or RfDs obtained from Health Effects Assessments (HEAs). The RfD,expressed in units of mg/kg/day, is an estimate of the daily exposure to thehuman population (including sensitive subpopulations) that is likely to bewithout an appreciable risk of deleterious effects during a lifetime. These

•fr

RfDs are usually derived either from human studies involving workplaceexposures or from animal studies, and are adjusted using uncertainty factors.The RfD provides a benchmark to which chemical intakes by other routes (e.g.,via exposure to contaminated environmental media) may be compared.

4.1.2 Health Effects Criteria for Potential CarcinogensCancer potency factors, developed by EPA's Carcinogen Assessment Group

(CAG) for potentially carcinogenic chemicals and expressed in units of(mg/kg/day)'1, are derived from the results of human epidemiological studiesor chronic animal biosssays. The animal studies must usually be conductedusing relatively high doses in order to detect possible adverse effects.Since humans are expected to be exposed at lower doses than those used in theanimal studies, the data are adjusted by using mathematical models. The datafrom animal studies are typically fitted to the linearized multistage model toobtain a dose-response curve. The 95th percentile upper confidence limitslope of the dose-response curve is subjected to various adjustments and aninterspecies scaling factor is applied to derive the cancer potency factor forhumans. Thus, the actual risks associated with exposure to a potentialcarcinogen quantitatively evaluated based on animal data are not likely to

sJJ

40

i/̂ *"*N- exceed the risks estimated using these cancer potency factors, but they may bemuch lower. Dose-response data derived from human epidemiological studies are

] fitted to dose-time-response curves on an ad hoc basis. These models providerough, but plausible, estimates of the upper limits on lifetime risk. Cancerpotency factors based on human epidemiological data are also derived usingvery conservative assumptions and, as such, they.too are unlikely tounderestimate risks. Therefore, while the actual risks associated withexposures to potential carcinogens are unlikely to be higher than the riskscalculated using a cancer potency factor, they could be considerably lower.

EFA assigns weight-of-evidence classifications to potential carcinogens.Under this system, chemicals are classified as either Group A, Group Bl, GroupB2, Group C, Group D, or Group E. Group A chemicals (human carcinogens) areagents for which there is sufficient evidence to support the causalassociation between exposure to the agents in humans and cancer. Groups £1and B2 chemicals (probable human carcinogens) are agents for which there islimited (Bl) or inadequate (B2) evidence of carcinogenicity from animalstudies. Group C chemicals (possible human carcinogens) are agents for which

,""*""-••• there is limited evidence of carcinogenicity in animals, and Group D chemicals(not classified as to human carcinogenicity) are agents with inadequate human

. and animal evidence of carcinogenicity or for which no data are available.I Group £ chemicals (evidence of non-carcinogenicity in humans) are agents for

which there is no evidence of carcinogenicity in adequate human or animalstudies.<

Table 4-1 summarizes the toxicity criteria used in this assessment alongwith their associated safety factors (for noncarcinogens) and weight-of-evidence classifications (for carcinogens). The table also lists the sourceof the criteria.

4.2 TOXICITY SUMMARIESIn this section, brief descriptions of the human and animal toxicity of

the chemicals that will be evaluated in this assessment are presented together

,-w-S.

41

tABIt 4 - 1

SUMMARY OF HEALTH EFFECTS CRITFRIA FOR CHfMICAIS OF P01ENTIAI CONCERNVESTAL WELL II SHE

K>

BENZENE1,1-OICHLOROETHANE1.1-OICHLOROETHYLENETRANS-1.2-DICETHYL BENZENETETRACHLOROETHYI ENETOULENE1.1,1-TRICHLOROTTHANETRICHLOROETHYLIHEXYLENESBIS(2-ETHYLHCARCINOGENIC PAIIs (e)NONCARCINOGEACETONE2-BUTANONEDI-N-BUTYLPHTHAIATE1.1,2.2-TETRANTIHONYARSENICBAR IUNBERYLLIUMCHROMIUM (g)COPPER (h)LEAD (i)MANGANESEMERCURYNICKELSELENIUMTHALLIUMVANADIUMZINCPCBs

ORAL CRITERIA ;

ReferenceDose Safety Source (b)

ICAL (RfD) Factor (a)(mg/kg/d)

NELENEIROETHYLENE

ENE

THANEE

JPHTHALATEis (e)PAHs (f)

ATEOROETHANE

*1. OOE-019.00E-032.00E-021. OOE-01l.OOE-023.00E-019.00E-027.35E-03 *2.00E+002.00E-02

--4. OOE-01l.OOE-OI5.00E-021. OOE-01

--4.00E-04l.OOE-03 *5.00E-025. ODE -03

.OOE+03

.OOE+03

.OOE+03

.OOE+03

.OOE+03

.OOE+02

.OOE+03

.OOE+03

.OOE+02

.OOE+03—

.OOE+02

.OOE+03

.OOE+03

.OOE+03--

.OOE+03

.OOE+00

.OOE+02

.OOE+025.00E-03 5. OOE+023.70E-02

2. OOE-01 1 OOF »0?3.00E-04 l.OOE+032.00E-02 3.00E«023.00E-03 1.50E+017.00E 05 3. OOE+037.00E-03 1.00E«022. OOE-01 1. OOE+01

IRISHEAIRISIRISIRISIRISIRISIRISHA

IRISIRIS--

HEAIRISIRISIRIS-.

IRISHEAIRISIRISIRISHEA

HEAHEAIRISHEAHEAHEAHEA

EPA/CAGCancer WeightPotency ofFactor Evidence (c)

(mg/kg/dH

2.90E-029.IOE-026. OOE-01

----

5.10E-02----

1.10E-02--

1.40E-021.I5E401

--------

2.00E-02--

1.75EtOO-.----- -----------------

ACC

--B2

- -B2-.B2B2----

--C--A._----.-B2------._--

- -

INHALATION CRMIKIA

Reference IPA/CAGDose Safety Source (li) (.ancer Weight(RfO) Factor (a) Potency of

(mg/kg/d) Factor Evidence (c)

- (d)l .OOE-OI

l.OOE-03

1 OOF«03

1 OOE+00 1 OOE+033.OOE-01 1 OOE+03

4.DOE-01 I OOE+03

9.00E-02 l.OOE+03

HEA

HEAHI A

HEA

HEA

l.OOE-04 l.OOE-03 HtA

3.00E-04 1 OOE+02 HFA

OOE+01 HEA

(mg/kg/d)-1

2 90E-02

I .?OE+00

3.30E-03

4.60E-03

AB?C

n?

B2

B26 10E+00 ' B?

2 OOE-01

5.OOE+01

8.40E+004 10E+OI

C

A

B2A

7.70F+00 *

tABLE 41 (Continued)

SUMMARY OF HEALTH EFFECTS CRIIERIA FOR CHEMICALS OF POTENTIAL CONCERNVESTAL Wtll I I S H E

(a) Safety factors used to develop reference doses consist of multiples of 10; each factor representing a specific area of uncertainty inherentin the <l<iic) available. The standard uncertainty factors include:

o A Inn-fold factor to account for the variation in sensitivity among the members ol the human population,o A ten-fold factor to account for the uncetainty in extrapolating animal data to the case of humans;o A ten-fold factor to account for the uncertainty in extrapolating from less than chronic No Observed Adverse Effects level;, (NOAEls) to

' chronic NOAELs; ando A ton-fold factor to account for the uncertainty in extrapolating from lowest Observed Adverse Effect Levels (LOAEIs) to NOAf.Ls.

(b) Sources ol Reference Doses: IRIS = chemical files of the Integrated Risk Informal ioti System (May I. 1989); HLA = HealthEffects Assessments; HA = Health Advisory.

(c) Weight of evidence classification scheme for carcinogens:A -- Human Carcinogen, sufficient evidence from human epidemiological studies;Bl -- Ciobable Human Carcinogen, limited evidence from epidemiological studies and adequate evidence from animal studies;B2 -- I'tobable Human Carcinogen, inadequate evidence from epidemiological studies and adequate evidence from animal studies;C -- Possible Human Carcinogen, limited evidence in animals in the absence of human studies;0 -- Not Classified as to human carcinogenicity; andE -- Evidence of Noncarcinogenicity.

(d) -- Indicates that no criteria have been established in IRIS. HEA. or HA for this chemical via this route of exposure.(e) Based on the toxicity of benzo(a)pyrene. CPAHs detected at the Vestal site are ben/o(a)pyrene. benzo(a)anthracene. and chrysene.

(f) Based on Hie toxicity of naphthalene. NCPAHs deleted at the Vestal site are naphthalene, phenanthrene. fluoranthene, pyrene, anthracene, fluorene.2-methy lii jphtha lene.

(g) Criteria .ire for CrVI.(h) This dose is equivalent to the reported drinking water standard of 1.3 mg/liter, assuming a 70 kg person Ingests 2 liters of water per day.

The prinking Water Criteria Document concluded that toxicity data were Inadequate for calculation of an RfD for copper.

(i) Lead is evaluated by the biokinetic uptake model. See text.* Review pending.

with available toxicity values which have been developed for evaluation ofexposure to these chemicals under specific circumstances.

ACETONEAcetone is absorbed in humans and animals following oral or inhalation

exposure (EPA 1984a) . Acetone vapors as high as 2,150 ppm produce irritationof the mucosal membranes in humans (EPA 1984a) . In rats , slight increases inorgan weights and decreases in body weights have been observed following long-term exposure to acetone (EPA 1986f).

EPA (1989a) derived an oral reference dose (RfD) for acetone of0.1 mg/kg/day based on a study sponsored by the EPA Office of Solid Waste (EPA1986f ) in which increased liver and kidney weights and nephrotoxicity wereobserved in rats exposed orally to acetone; an uncertainty factor of 1,000 was'*,-used to derive the RfD.

ANTIMONYAntimony is a metal which occurs both in the trivalent and pentavalent

oxidation states (EPA 1980a) . Absorption of this metal via oral andinhalation routes of exposure is low (EPA 1980a) . Humans and animals exposedacutely orally or through inhalation to either trivalent or pentavalent forms

i - of antimony displayed electrocardiogram (ECG) changes and myocardial lesions(EPA 1980a) . Pneumoconiosis has been observed in humans exposed by acute

1 inhalation and dermatitis has occurred in individuals exposed either orally ordermally. Oral administration of therapeutic doses in humans has beenassociated with nausea, vomiting, and hepatic necrosis (EPA 1980a) . Chronicexposure by inhalation of antimony has led to respiratory effects includingmacrophage proliferation and activity, fibrosis and pneumonia in animals (EPA1980a). A single report (Balyeava 1967) noted an increase in spontaneousabortions, premature births, and gynecological problems in 318 female workersexposed to a mixture of antimony metal, antimony trioxide, and antimonypentasulfide dusts.

§

44

EPA (1989a) derived an oral RfD of 4x10"* mg/kg/day for antimony based ona chronic oral study (Schroeder et al. 1970) in which rats given the metal indrinking water had altered blood glucose and blood cholesterol levels anddecreased lifespan. An uncertainty factor of 1,000 and a LOAEL of0.35 mg/kg/day were used to derive the oral RfD.

ARSENICBoth inorganic and organic forms of arsenic are readily absorbed via the

oral and inhalation routes. Soluble forms are more readily absorbed than theinsoluble forms (EPA 1984b). Approximately 95% of soluble inorganic arsenicadministered to rats is absorbed from the gastrointestinal tract (Coulson etal. 1935, Ray-Bettley and O'Shea 1975). Approximately 70%-80% of arsenicdeposited in the respiratory tract of humans has been shown to be absorbed(Holland et al. 1959). Dermal absorption is not significant (EPA 1984b).Acute exposure of humans to metallic arsenic has been associated withgastrointestinal effects, hemolysis, and neuropathy (EPA 1984b). Chronicexposure of humans to this metal can produce toxic effects on both theperipheral and central nervous systems, keratosis, hyperpigmentation,precancerous dermal lesions, and cardiovascular damage (EPA 1984b). Arsenicis embryotoxic, fetotoxic, and teratogenic in several animals species (EPA1984b). Arsenic is a known human carcinogen. Epidemic logical studies ofworkers in smelters and in plants manufacturing arsenical pesticides haveshown that inhalation of arsenic is strongly associated with lung cancer andperhaps with hepatic angiosarcoma (EPA 1984b). Ingestion of arsenic has beenlinked to a form of skin cancer and more recently to bladder, liver, and lungcancer (Tseng 1977, Tseng et al. 1968, Chen et al. 1986).

EPA has classified arsenic in Group A—Human Carcinogen—and hasdeveloped inhalation (EPA 1989a) and oral cancer potency factors (EPA 1989c)of 50 (mg/kg/day)"1 and 1.75 (mg/kg/day)"1, respectively. The inhalationpotency factor is the geometric mean value of potency factors derived fromfour occupational exposure studies on two different exposure populations (EPA1984b). The oral cancer potency factor was based on an epidemiological study

45

I/"""N in Taiwan which indicated an increased incidence of skin cancer in individuals

exposed to arsenic in drinking water (Tseng 1977). EPA (1989b) has reportedI an oral reference dose (RfD) of IxlO"3 mg/kg/day based on the study by Tseng

(1977) in which blackfoot disease was observed in humans exposed to arsenic intheir drinking water. An uncertainty factor of 1 was used to develop the RfD.The EPA is currently reviewing the oral RfD (EPA 1989a).

BARIUMAdverse effects in humans following oral exposure to soluble barium

compounds include gastroenteritis, muscular paralysis, hypertension,.̂.'"Ventricular fibrillation, and central nervous system damage (EPA 1984c, Perryet al. 1983). Inhalation of barium sulfate or barium carbonate inoccupationally exposed workers has been associated with baritosis, a benign

•iV

pneumoconiosis (Goyer 1986). Experimental animals exposed chronically tobarium in drinking water developed increased blood pressure (EPA 1984c).Inhalation of barium carbonate dust by experimental animals has beenassociated with reduced sperm count, increased fetal mortality, and atresia of

X-.V the ovarian follicles (EPA 1984c, Tarasenko et al. 1977).EPA (1989a) derived an oral reference dose (RfD) based on a chronic rat

study in which a lowest-observed-adverse-effect level (LOAEL) for increasedj blood pressure was observed (Perry et al. 1983). Using the LOAEL of

5.1 mgAg/day and an uncertainty factor of 100, an oral RfD of] 5xlO~2 mg/kg/day was calculated. EPA (1989b) has also developed an inhalation

RfD of 1.4xl(T4 mg/kg/day for barium based on a study by Tarasenko et al.(1977). In this study rats were exposed to barium carbonate dust at airborneconcentrations of up to 5.2 mg/m3 for 4-6 months. Adverse effects noted atthis concentration included decreased body weight, alterations in liverfunction, and increased fetal mortality. An uncertainty factor of 1,000 wasused in developing the RfD.

OTO

46 °

/—\ BENZENEBenzene is readily absorbed following oral and inhalation exposure (EPA

i 1985b). The toxic effects of benzene in humans and other animals followinga

exposure by inhalation include central nervous system effects, hematologicaleffects, and immune system depression. In humans, acute exposures to highconcentrations of benzene vapors has been associated with dizziness, nausea,vomiting, headache, drowsiness, narcosis, coma, and death (NAS 1976). Chronicexposure to benzene vapors can produce reduced leukocyte, platelet, and redblood cell counts (EPA 1985b). Benzene induced both solid tumors andleukemias in rats exposed by gavage (Maltoni et al. 1985b). Many studies havealso described a causal relationship between exposure to benzene by inhalation(either alone or in combination with other chemicals) and leukemia in humans(IARC 1982).

Applying EPA's criteria for evaluating the overall evidence ofcarcinogenicity to humans, benzene is classified in Group A (Human Carcinogen)based on adequate evidence of carcinogenicity from epidemiological studies.EPA (1989a) derived both an oral and an inhalation cancer potency factor for

"̂-x benzene of 2.9xlO"2 (mg/kg/day)"1. This .value was based on several studies inwhich increased incidences of nonlymphocytic leukemia were observed in humansoccupationally exposed to benzene principally by inhalation (Rinsky 1981, Ott

] 1978, Wong 1983). EPA (1989a) is currently reviewing an oral RfD for benzeneand its status is pending.

t

BERYLLIUMBeryllium is not readily absorbed by any route of exposure. Occupational

exposure to beryllium results in bone, liver and kidney disposition (EPA1986g). In humans, acute respiratory effects due to beryllium exposureinclude rhinitis, pharyngitis, tracheobronchitis, and acute pneumonitis.Dermal exposure to soluble beryllium compounds can cause contact dermatitis,ulceration and granulomas (Hammond and Beliles 1980). Ocular effects includeconjunctivitis and corneal ulceration from splash burns. The most commonclinical symptom caused by chronic beryllium exposure is granulomatous lung

50

47

inflammation (1ARC 1980, EPA 1986g) . Chronic skin lesions sometimes appearafter a long latent period in conjunction with the pulmonary effects.

] Systemic effects from beryllium exposure may include right heart enlargementwith accompanying cardiac failure, liver and spleen enlargement, cyanosis,digital clubbing, and kidney stone development (EPA 1986g). Beryllium hasbeen shown to be carcinogenic in experimental animals resulting primarily inlung and/or bone tumors when given by injection, intratracheal administration,or inhalation (EPA 1986g) . Several epidemiological studies have suggestedthat occupational exposure to beryllium may result in an increased lung cancerrisk although the data are inconclusive (EPA 1986g) .

Beryllium has been classified by EPA in Group B2- -Probable HumanCarcinogen based on increased incidences of lung cancer and osteosarcomas inanimals (EPA 1989a) . EPA (1989a),has calculated an inhalation cancer potencyfactor of 8.4 (mg/kg/day)"1 based on the relative risk for lung cancer,estimated from an epidemiological study by Wagoner et al. (1980). EPA (1989a)has also developed an oral reference dose (RfD) for beryllium of 5.0 x 10"3

mg/kg/day based on a study by Schroeder and Hitchner (1975) in which rats/*""*"""• exposed to 0.54 mg/kg/day beryllium sulfate (the highest dose tested) in

• drinking water for a lifetime did not exhibit adverse effects; an uncertaintyfactor of 100 was used to develop the RfD.

]J

BI S ( 2 - ETHYLHEXYL) PHTHALATEsf

Bis(2-ethylhexyl)phthalate, also known as di-ethylhexyl phthalate (DEHP) ,is readily absorbed following oral or inhalation exposure (EPA 1980b) .Chronic exposure to relatively high concentrations of DEHP in the diet cancause retardation of growth and increased liver and kidney weights inlaboratory animals (NTP 1982, EPA 1980b, Carpenter et al. 1953). Reducedfetal weight and increased number of resorptions have been observed in ratsexposed orally to DEHP (EPA 1980b) . DEHP is reported to be carcinogenic inrats and mice, causing increased incidences of hepatocellular carcinomas orneoplastic nodules following oral administration (NTP 1982) .

48

DEHP has been classified in Group B2—Probable Human Carcinogen (EPA1986h, 1989a). EPA (1989a) calculated an oral cancer potency factor for DEHP

- 2 - 1] of 1.4x10 (mg/kg/day) based on data from the NTP (1982) study. EPA hasrecommended an oral reference dose (RfD) for DEHP of 0.02 mg/kg/day based on astudy by Carpenter et al. (1953) in which increased liver weight was observedin female guinea pigs exposed to 19 mg/kg bw/day in the diet for 1 year(EPA 1989a); an uncertainty factor of 1,000 was used to develop the RfD.

2-BTJTANONE (METHYL ETHYL KETONE)Absorption of methyl ethyl ketone from the gastrointestinal tract and

from the lungs has been inferred from systemic toxic effects observedfollowing acute oral exposure and acute and subchronic inhalation exposures(Lande et al. 1976). Schwetz et al. (1974) reported that rats exposed toinhaled methyl ethyl ketone at concentrations of 3,000 ppm displayed retardedfetal development and teratogenic effects (acaudia, imperforate anus, andbrachygnathia). Inhaled methyl ethyl ketone also produces hepatotoxicity andneurological effects in rats (Cavender et al. 1983, Takeuchi et al. 1983).

/***"*v EPA (1989a) determined an oral reference dose (RfD) of 5xlO"2 mg/kg/dayfor methyl ethyl ketone based on a subchronic study by LaBelle and Brieger(1955) in which no adverse effects were observed in rats exposed to 235 ppm(693 mg/m3 or 46 mg/kg/day) methyl ethyl ketone for 12 weeks. Higher doseshave resulted in fetotoxic effects in rats exposed to methyl ethyl ketone viainhalation (1958 mg/m3 or 130 mg/kg/day) (Schwetz et al. 1974). EPA (1989b)also derived an inhalation RfD of 9xlO"2 mg/kg/day based on the LaBelle andBrieger (1955) study in which central nervous system effects were noted. Anuncertainty factor of 1,000 was used to calculate both oral and inhalationRfDs.

CHLOROFORMChloroform, a trihalomethane, is rapidly absorbed through the respiratory

and gastrointestinal tracts in humans and experimental animals; dermalabsorption from contact of the skin with liquid chloroform can also occur (EPA

49

/******• 1985c). In humans, acute exposures to chloroform may result in depression ofthe central nervous system, hepatic and renal damage and death caused by

i ventricular fibrillation following an acute ingested dose of 10 ml (EPA1984d) . Acute exposure to chloroform may also cause irritation to the skin,eyes, and gastrointestinal tract (EPA 1984d, 1985c) . In experimental animals,chronic exposure may lead to fatty cyst formation in the liver (Heywood etal. 1979), renal, and cardiac effects and central nervous system depression(EPA 1985c). Chloroform has been reported to induce renal epithelial tumorsin rats (Jorgenson et al. 1985) and hepatocellular carcinomas inmice (NCI1976a) . Suggestive evidence from human epidemiological studies indicates thatlong-term exposure to chloroform and other trihalomethanes in contaminatedvater supplies may be associated with an increased incidence of bladder tumors(EPA 1985c).

Chloroform has been classified by EPA as a Group B2 Carcinogen (ProbableHuman Carcinogen) (EPA 1989a) . EPA (1989a) developed an oral cancer potencyfactor for chloroform of 6.1xlO"3 (mg/kg/day)"1 based on a study in whichkidney tumors were observed in rats exposed to chloroform in drinking water(Jorgenson et al. 1985). An inhalation cancer potency factor of S.lxlO"2

(mg/kg/day)"1 has been developed by EPA (1989a) based on an NCI (1976a)bioassay in which liver tumors were observed in mice. EPA (1989a) alsoderived an oral reference dose (RfD) of 0.01 mg/kg/day for chloroform based ona chronic bioassay in dogs in which liver effects were observed at12.9 mg/kg/day (Heywood et al. 1979); an uncertainty factor of 1,000 was usedto derive the RfD.

CHROMIUMChromium exists in two states, as chromium (III) and as chromium (VI).

Following oral exposure, absorption of chromium (III) is low while absorptionof chromium (VI) is high (EPA 1987a) . Chromium is an essential micronutrientand is not toxic in trace quantities (EPA 1980c). High levels of solublechromium (VI) and chromium (III) can produce kidney and liver damage following Jacute oral exposure; target organs affected by chronic oral exposure remain

50

f unidentified (EPA 1984e). Chronic inhalation exposure may cause respiratorysystem damage (EPA 1984e). Further, epidemiological studies of worker

I populations have clearly established that inhaled chromium (VI) is a humancarcinogen; the respiratory passages and the lungs are the target organs(Mancuso 1975, EPA 1984e). Inhalation of chromium (III) or ingestion ofchromium (VI) or (III) has not been associated with carcinogenicity in humansor experimental animals (EPA 1984e). Certain chromium salts have been shown

- to be teratogenic and embryotoxic in mice and hamsters following intravenousor intraperitoneal injection (EPA 1984e).

EFA has classified inhaled chromium (VI) in Group A--Probable HumanCarcinogen by the inhalation route (EPA 1989a). Inhaled chromium (III) andingested chromium (III) and (VI) have not been classified with respect tocarcinogenicity (EPA 1989a). EPA (1989a) developed an inhalation cancerpotency factor of 41 (mg/kg/day)'1 for chromium (VI) based on an increasedincidence of lung cancer in workers exposed to chromium over a 6 year period,and followed for approximately 40 years (Mancuso 1975). EPA (1989a) derivedan oral reference dose (RfD) of S.OxlO"3 mg/kg/day for chromium (VI) based on

,--"~v a study by MacKenzie et al. (1958) in which no observable adverse effects wereobserved in rats exposed to 2.4 mg chromium (VI)/kg/day in drinking water for1 year. A safety factor of 500 was used to derive the RfD. EPA (1989a)developed an oral RfD of 1 mg/kg/day for chromium (III) based on a study inwhich rats were exposed to chromic oxide baked in bread; no effects due tochromic oxide treatment were observed at any dose level (Ivankovic andPreussman 1975). A safety factor of 1000 was used to calculate the oral RfD.

COPPERCopper is an essential element. A daily copper intake of 2 mg is

considered to be adequate for normal health and nutrition; the minimum dailyrequirement is 10 Mg/kg (EPA 1985d). In humans, absorption of copperfollowing oral exposure is approximately 60% and is influenced by competition

; .4

with other metals and the level of dietary protein and ascorbic acid in both ? Ihumans and animals (EPA 1984f). Copper is absorbed following inhalation

51

exposures, although quantitative data on the extent of absorption areunavailable (EPA 1984f). Adverse effects in humans resulting from acuteexposure to copper at concentrations that exceed these recommended levels byingestion include salivation, gastrointestinal irritation, nausea, vomiting,.hemorrhagic gastritis, and diarrhea (ACGIH 1986). Dermal or ocular exposureof humans to copper salts can produce irritation (ACGIH 1986). Acuteinhalation of dusts or mists of copper salts by humans may produce irritationof the mucous membranes and pharynx, ulceration of the nasal septum, and metalfume fever. The latter condition is characterized by chills, fever, headache,and muscle pain. Limited data are available on the chronic toxicity ofcopper; however, chronic over-exposure to copper by humans has been associatedwith anemia (ACGIH 1986) and local gastrointestinal irritation (EPA 1987b).Results of several animal bioassays suggest that copper compounds are notcarcinogenic by oral administration; however, some copper compounds can induceinjection-site tumors in mice (EPA 1985d).

EPA (1989b) has reported the drinking water standard of 1.3 mg/liter asan oral reference dose (RfD) based on local gastrointestinal irritation (EPA1987b). Assuming a 70-kg adult ingests 2 liters of water per day, thisconcentration is equivalent to a.dose of 3.7xlO~2 mg/kg/day. However, EPA(1987b) concluded toxicity data were inadequate for the calculation of a.reference dose (RfD) for copper.

1,1-DICHLOROETHANE1,1-DCA is probably less toxic than the 1,2-isomer (EPA 1980d). At one

time, the compound was used as an anesthetic, but it induced cardiacarrhythmias and its use was discontinued. It is probable that human exposureto sufficiently high levels of 1,1-DCA would cause central nervous systemdepression and respiratory tract and skin irritation, since many of thechlorinated aliphatics cause these effects (Parker at al. 1979). However, nodose-response data concerning these effects are available. Renal damage wasobserved in cats exposed by inhalation in a subchronic study (Hofmann et al.1971). Inhalation exposure of pregnant rats to high doses of 1,1-DCA

52

(6,000 ppm) retarded fetal development (Schwetz et al. 1974). Acarcinogenicity bioassay of 1,1-DCA was limited by poor survival of bothtreatment and control groups, and the physical conditions of the treatedanimals was markedly stressed. Dose-related marginal increases in mammarygland adenocarcinomas and in hemangiosarcomas were seen in female rats, and astatistically significant increase in endometrial stromal polyps was seen infemale mice; however, these data were not interpreted as providing conclusiveevidence for the carcinogenicity of 1,1-DCA because of the previouslymentioned limitations of the bioassay (NCI 1978a).

EPA (1989b) has classified 1,1-DCA as a Group B2 agent (Probable HumanCarcinogen) and reported an oral cancer potency factor of 9.1xlO"2

(mg/kg/day)"1. This potency factor is based on structure-activityrelationship to the isomer 1,2-dichloroethane, a Group B2 carcinogen and onthe increased incidence of hemangiosarcomas observed in rats administered1,1-DCA via gavage (NCI 1978a). EPA (1989b) developed an oral and inhalationreference dose of 0.1 mg/kg/day based on adverse renal effects seen in catsfollowing subchronic inhalation exposure (Hofmann et al. 1971). A safetyfactor of 1000 was used to develop the RfD.

1,1-DICHLOROETHYLENE1,1-Dichloroethylene (1,1-DCE) is rapidly absorbed after oral and

inhalation exposures (EPA 1984g, 1987c). Humans acutely exposed to 1,1-DCEvapors exhibit central nervous system depression. In animals, the liver isthe principal target of 1,1-DCE toxicity. Acute exposures result in liverdamage which ranges from fatty infiltration to necrosis (EPA 1987c). Workerschronically exposed to 1,1-DCE in combination with other vinyl compoundsexhibit liver dysfunction, headaches, vision problems, weakness, fatigue andneurological sensory disturbances (EPA 1987c). Chronic oral administration of1,1-DCE to experimental animals results in both hepatic and renal toxicity(EPA 1984g, Quast et al. 1983). Inhalation or oral exposure of rats andrabbits has produced fetotoxicity and minor skeletal abnormalities, but onlyat maternally toxic doses. 1,1-DCE vapors produced kidney tumors and leukemia

53

in a single study of mice exposed by inhalation, but the results of otherstudies were equivocal or negative (EPA 1987c, Maltoni et al. 1985b).

EPA has classified 1,1-DCE as a Group C agent (Possible Human Carcinogen)and has developed inhalation and oral cancer potency factors of 1.2(mg/kg/day)'1 and 0.6 (mg/kg/day)"1, respectively (EPA 1985e, 1989a). Theinhalation potency factor was based on the increased incidence of renaladenocarcinomas in male mice exposed to 1,1-DCE via inhalation for 52 weeksand observed for a total of 121 weeks (Maltoni et al. 1985b). The oralpotency factor was derived by estimating an upper-limit value from negativebioassay data and assuming that a carcinogenic response occurs via ingestion,although there is no direct evidence that this is true. EPA (1989a) developedan oral reference dose (RfD) of 9xlO~3 mg/kg/day based on the occurrence ofhepatic lesions in rats chronically exposed to 1,1-DCE in drinking water(Quast et al. 1983). A safety factor of 1000 was applied to the lowest-observed-adverse-effect level (LOAEL) of 9 mg/kg/day to derive the oral RfD.

trans -1,2 - DICHLOROETHYLENEtrans-l,2-Dichloroethylene is expected to be absorbed by any route of

exposure. Information on the health effects of trans-l,2-dichloroethylene islimited. In humans, trans-l,2-dichloroethylene is a central nervous systemdepressant, and exposure to high concentrations can result in anestheticeffects (Irish 1963). Inhalation exposure of rats to 200 ppm has beenassociated with pneumonic infiltration of the lungs and progressive fattydegeneration of the liver (Freundt et al. 1977). Acute exposure to higherdose levels can cause narcosis and death in rats (Torkelson and Rowe 1981).

EPA (1985c) proposed a maximum contaminant level goal (HCLG) of70 jig/liter for both cis- and trans-l,2-dichloroethylene based on the adjustedacceptable daily intake (AADI) of 350 pg/liter, assuming 20% of the exposureis via drinking water. EPA (1989a) has derived an oral reference dose (RfD)of 2xlO~2 mg/kg/day for trans-l,2-dichloroethylene based on a 90-day drinkingwater study conducted in mice (Barnes et al. 1985). A no-observed-adverse-

54

effect level (NOAEL) of 17 mg/kg/day for increased serum alkaline phosphataseand an uncertainty factor of 1,000 were used to derive the RfD.

Dl-n-BUTYL PHTHALATEDi-n-butyl phthalate is readily absorbed following oral and inhalation

exposure (EPA 1980b). Acute exposures of di-n-butyl phthalate aerosol in micehave produced irritation of the eyes and upper respiratory tract mucousmembranes. Extreme exposures result in labored breathing, ataxia, paresis,convulsions and death from paralysis of the respiratory system (ACGIH 1986).Workers chronically exposed to di-n-butyl phthalate in combination with otherphthalate plasticizers have exhibited pain, numbness and spasms in the upperand lower extremities. Further evaluation revealed vestibular dysfunction andpolyneuritis (ACGIH 1986). Reduced fetal weight, increased numbers ofresorptions, and dose-related musculoskeletal abnormalities have been observedamong fetuses from rats and mice exposed to very high doses of di-n-butylphthalate during gestation (Shiota and Nishimura 1982).

EPA (1989a) calculated an oral reference dose (RfD) for di-n-butylphthalate based on a study by Smith (1953) in which male Sprague-Dawley ratswere fed a diet containing dibutyl phthalate for a period of 1 year. One-halfof all rats receiving the highest dibutyl phthalate concentration (1.25% ofdiet, or 600 mg/kg/day) died during the first week of exposure. The remaininganimals survived the study with no apparent adverse effects. Using a NOAEL of125 mg/kg/day (0.25% dibutyl phthalate in diet) and an uncertainty factor of1,000, an oral reference dose (RfD) of 0.1 mg/kg/day was derived; a LOAEL of600 mgAg/day (1.25% dibutyl phthalate in diet) was observed in this study.

ETHYLBENZENEEthylbenzene is absorbed via inhalation and distributed throughout the

body in rats; the highest levels were detected in the kidney, lung, adiposetissue, digestive tract, and liver (Chin et al. 1980). In humans, short-terminhalation exposure to 435 mg/m3 ethylbenzene for 8 hours can result insleepiness, fatigue, headache, and mild eye and respiratory irritation

55

(Bardodej and Bardodejova 1970); eye irritation has also been observed inexperimental animals exposed to ethylbenzene (EPA 1987d). Increased weightsand cloudy swelling were observed in the liver and kidney of rats exposed toethylbenzene by stomach tube at a dose of 408 mg/kg/day for 182 days (Volf etal. 1956). A single oral dose of ethylbenzene administered by stomach tube tomale and female Wistar-derived rats was reported to have an LD50 of 3,500mg/kg body weight, with systemic effects occurring primarily in the liver andkidney (Wolf et al. 1956). Maternal toxicity was observed in rats exposed byinhalation to 4,348 mg/m3 ethylbenzene for 6-7 hours/day during the first 19days of gestation (Hardin et al. 1981).

EPA (1989a) derived an oral reference dose of 0.1 mg/kg/day forethylbenzene based on the chronic study by Wolf et al. (1956) in which noliver or kidney effects were observed in rats exposed to 136 mg/kg/day. Anuncertainty factor of 1,000 was applied to the no-observed-effect-level toderive the reference dose.

MANGANESEManganese is absorbed at low levels following oral or inhalation exposure

(EPA 1984h). The effects following acute exposure to manganese are unknown.Chronic oral and inhalation exposure of humans to high levels of manganesecauses pneumonitis in exposed workers and has been associated with a conditionknown as manganism, a progressive neurological disease characterized by speechdisturbances, tremors, and difficulties in walking (Kawamura et al. 1941).Altered hematologic parameters (hemoglobin concentrations, erythrocyte counts)have also been observed in persons exposed chronically. Chronic oral exposureof rats to manganese chloride results in central nervous system dysfunction(Leung et al. 1981, Lai et al. 1982). Manganese has not been reported to beteratogenic; however, this metal has been observed to cause depressedreproductive performance and reduced fertility in humans and experimentalanimals (EPA 1984h). Certain manganese compounds have been shown to be

•4

mutagenic in a variety of bacterial tests. Manganese chloride and potassium _fpermanganate caused chromosomal aberrations in mouse mammary carcinomal cells.

Oo56

< Manganese was moderately effective in enhancing viral transformation of Syrianhamster embryo cells (EPA 1984h,i).

EPA (1989b) established an oral reference dose (RfD) of 2.0X10"1

ng/kg/day for manganese based on no observed adverse effects (NOAEL) in rats,exposed chronically to manganese in drinking water (Leung et al. 1981, Lai etal. 1982). An uncertainty factor of 100 was used to derive the referencedose. EPA (1989b) calculated an inhalation reference dose based upon anoccupational study conducted by Saric et al. (1977). Using a NOAEL of2.1 mg/day and an uncertainty factor of 100, an inhalation RfD of3.0x10"* mg/kg/day was derived. Both the inhalation and oral intake valuesare based upon central nervous system effects (EPA 1989b).

MERCURYIn humans, inorganic mercury is absorbed following inhalation and oral

exposure, however only 7% to 15% of administered inorganic mercury is absorbedfollowing oral exposure (EPA 1984J, Rahola et al. 1971, Task Group on MetalAccumulation 1973). Organic mercury is almost completely absorbed from thegastrointestinal tract and is assumed to be well absorbed via inhalation inhumans (EPA 1984J). A primary target organ for inorganic compounds is thekidney. Acute and chronic exposures of humans to inorganic mercury compoundshave been associated with anuria, polyuria, proteinuria, and renal lesions(Hammond and Bellies 1980). Chronic occupational exposure of workers toelemental mercury vapors (0.1 to 0.2 mg/m3) has been associated with mentaldisturbances, tremors, and gingivitis (EPA 1984J). Animals exposed toinorganic mercury for 12 weeks have exhibited proteinuria, nephrotic syndromeand renal disease (Druet et al. 1978). Rats chronically administeredinorganic mercury (as mercuric acetate) in their diet have exhibited decreasedbody weights and significantly increased kidney weights (Fitzhugh et al.1950). The central nervous system is a major target for organic mercurycompounds. Adverse effects in humans, resulting from subchronic and chronicoral exposures to organic mercury compounds have included destruction ofcortical cerebral neurons, damage to Purkinje cells, and lesions of the

oD

57

cerebellum. Clinical symptoms following exposure to organic mercury compoundshave included paresthesia, loss of sensation in extremities, ataxia, andhearing and visual impairment (WHO 1976). Embryotoxic and teratogeniceffects, including malformations of the skeletal and genitourinary systems,have been observed in animals exposed orally to organic mercury (EPA 1984j).Both organic and inorganic compounds are reported to be genotoxic ineukaryotic systems (Leonard et al. 1984).

EPA (1989b) has reported an oral RfD for methyl mercury of3x10"* mg/kg/day based on studies investigating central nervous system effectsin humans exposed to mercury (EPA 1980f); an uncertainty factor of 10 was usedto develop the RfD. EPA (1989b) has also reported an oral reference dose of3x10"* mg/kg/day for inorganic mercury based on a chronic rat study in whichkidney effects were observed (Fitzhugh et al. 1950). An uncertainty factor of1,000 was used to derive the RfD.

NICKELNickel compounds can be absorbed following inhalation, ingestion, or

dermal exposure. The amount absorbed depends on the dose administered and thechemical and physical form of the particular nickel compound (EPA 1986i).Dermal exposure of humans to nickel produces allergic contact dermatitis (EPA19861). Adverse effects associated with acute exposure in animals haveincluded depressed weight gain, altered hematological parameters, andincreased iron deposition in blood, heart, liver, and testes (EPA 1987e).Chronic or subchronic exposure of experimental animals to nickel has beenassociated with reduced weight gain, degenerative lesions of the malereproductive tract, asthma, nasal septal perforations, rhinitis, sinusitis,hyperglycemia, decreased prolactin levels, decreased iodine uptake, andvasoconstriction of the coronary vessels (EPA 1986i). Teratogenic andfetotoxic effects have been observed in the offspring of exposed animals (EPA19861). Inhalation exposure of experimental animals to nickel carbonyl ornickel subsulfide induces pulmonary tumors (EPA 19861). Several nickel saltscause localized tumors when administered by subcutaneous injection or

58

implantation. Epidemiological evidence indicates that inhalation of nickelrefinery dust and nickel subsulfide is associated with cancers of the nasalcavity, lung, larynx, kidney, and prostate (EPA 1986i).

Nickel refinery dust and nickel subsulfide are both categorized in GroupA--Human Carcinogens. These classifications are based on an increaseincidence of lung and nasal tumors observed in workers occupationally exposedto nickel refinery dust. These materials have inhalation cancer potencyfactors of 0.84 (mg/kg/day)"1 and 1.7 (mg/kg/day)"1. respectively (EPA 1989a).Nickel carbonyl is categorized in Group B2—Probable Human Carcinogen;however, a potency factor has not been derived for nickel carbonyl (EPA1989a). EPA (1989a) derived an oral reference dose (RfD) for nickel of2xlO"2 mg/kg/day based on a study by Ambrose et al. (1976) in which ratsadministered 5 mg/kg/day (NOAEL) nickel in the diet for 2 years did notexperience decreased weight gain observed in animals administered 50 mg/kg/day(LOAEL). A safety factor of 300 was used to calculate the RfD.

POLYCYCL1C AROMATIC HYDROCARBONS (Noncarcinogenic)Polycyclic aromatic hydrocarbons (PAHs) occur in the environment as

complex mixtures of which only a few components have been adequatelycharacterized. Only limited information is available on the relativepotencies of the "noncarcinogenie" PAHs. However, many have been shown tohave some weak carcinogenic activity, or to act as promoters or cocarcinogens.

PAH absorption following oral and inhalation exposure is inferred fromthe demonstrated toxicity of PAHs following these routes of administration(EPA 1984k). PAHs are also absorbed following dermal exposure (Kao et al.1985). Acute effects from direct contact with PAHs and related materials arelimited primarily to phototoxicity; the primary effect is dermatitis (NIOSH1977a). PAHs have also been shown to cause cytotoxicity in rapidlyproliferating cells throughout the body; the hematopoietic system, lymphoidsystem, and testes are frequent targets (Santodonato et al. 1981). Some ofthe noncarcinogenic PAHs have been shown to cause systemic toxicity but theseeffects are generally seen at high doses (Santodonato et al. 1981). Slight

ooSI

59

morphological changes in the liver and kidney of rats have been reportedfollowing oral exposure to acenaphthene for 40 days (EPA 1984k). Subchronicoral administration of naphthalene to rabbits and rats has resulted incataract formation (EFA 19841). EFA (1989b) developed an oral reference doseof 0.4 mg/kg/day for naphthalene based on the development of ocular andsystemic lesions in rats (Schmahl 1955, EFA 1986j) and occupational data oncoke oven workers. An uncertainty factor of 100 was applied to the animaldata in the development of the reference dose.

*

POLYCYCLIC AROMATIC HYDROCARBONS (Carcinogenic)FAHs occur in the environment as complex mixtures containing numerous

FAHs of varying carcinogenic potencies. Only a few components of thesemixtures have been adequately characterized, and only limited information isavailable on the relative potencies of different compounds.

PAH absorption following oral exposure is inferred from the demonstratedtoxicity of PAHs following ingestion (EPA 1984k). PAH absorption followinginhalation exposure is inferred from the demonstrated toxicity of PAHsfollowing inhalation (EPA 1984k). FAHs are also absorbed following dermalexposure (Kao et al. 1985). It has been suggested that simultaneous exposureto carcinogenic PAHs such as benzo[a]pyrene and particulate matter canincrease the effective dose of the compound (ATSDR 1987). Acute effects fromdirect contact with FAHs and related materials are limited primarily tophototoxicity; the primary effect is dermatitis (NIOSH 1977a). PAHs have alsobeen shown to cause cytotoxicity in rapidly proliferating cells throughout thebody; the hematopoietic system, lymphoid system, and testes are frequenttargets (Santodonato et al. 1981). Destruction of the sebaceous glands,hyperkeratosis, hyperplasia, and ulceration have been observed in mouse skinfollowing dermal application of the carcinogenic PAHs (Santodonato etal. 1981). The carcinogenic FAHs have also been shown to have animmunosuppressive effect in animals (ATSDR 1987). Nonneoplastic lesions havebeen observed in animals exposed to the more potent carcinogenic FAHs but onlyafter exposure to levels well above those required to elicit a carcinogenic

60 »

response. Carcinogenic PAHs are believed to induce tumors both at the site ofapplication and systemically. Neal and Rigdon (1967) reported that oraladministration of 250 ppm benzo[a]pyrene for approximately 110 days led toforestomach tumors in mice. Thyssen et al. (1981) observed respiratory tracttumors in hamsters exposed to up to 9.5 mg/m3 benzo[a]pyrene for up to 96weeks.

Benzo[a]pyrene is representative of the carcinogenic PAHs and isclassified by EPA in Group B2—Probable Human Carcinogen--based on sufficientevidence of carcinogenicity from animal studies and inadequate evidence fromepidemiological studies (EPA 1984m). EPA (1984k) calculated an oral cancerpotency factor of 11.5 (mg/kg/day)" for carcinogenic PAHs (specificallybenzo[a]pyrene) based on the study by Neal and Rigdon (1967). EPA (1984k)calculated an inhalation cancer potency factor of 6.1 (mg/kg/day) for

*•

benzo[a]pyrene based on the study by Thyssen et al. (1981). These potencyfactors are currently undergoing a reevaluation (EPA 1989a).

POLYCHLORINATED BIPHENYLS (PCBs)PCBs are complex mixtures of chlorinated biphenyls. The commercial PCB

mixtures that were manufactured in the United States were given the trade nameof "Aroclor." Aroclors are distinguished by a four-digit number (for example,Aroclor 1260). The last two digits in the Aroclor 1200 series represent theaverage percentage by weight of chlorine in the product.

PCBs are readily absorbed through the gastrointestinal (G.I.) tract andsomewhat less readily through the skin; PCBs are presumably readily absorbedfrom the lungs, but few data are available that experimentally define theextent of absorption after inhalation (EPA 1985h). Dermatitis and chloracne(a disfiguring and long-term skin disease) have been the most prominent andconsistent findings in studies of occupational exposure to PCBs. Severalstudies examining liver function in exposed humans have reported disturbancesin blood levels of liver enzymes. Reduced birth weights, slow weight gain,reduced gestational ages, and behavioral deficits in infants were reported ina study of women who had consumed PCB-contaminated fish from Lake Michigan

oo

61 -»

ii (EPA 1985h). Reproductive, hepatic, immunotoxic, and immunosuppressiveeffects appear to be the most sensitive end points of PCS toxicity in

{ nonrodent species, and the liver appears to be the most sensitive target organfor toxicity in rodents (EPA 1985h). A number of studies have suggested thatPCB mixtures are capable of increasing the frequency of tumors including livertumors in animals exposed to the mixtures for long periods (Kimbrough et al.1975, NCI 1978b, Schaeffer et al. 1984, Norback and Weltman 1985). Studieshave suggested that PCB mixtures can act to promote or inhibit the action ofother carcinogens in rats and mice (EPA 1985h).

EPA (1984n, 1989a) classified PCB as a Group B2 agent (Probable HumanCarcinogen) based on sufficient evidence in animal bioassays and inadequateevidence from studies in humans. The EPA Carcinogen Assessment Group (EPA1989a) calculated a low-level cancer potency factor of 7.7 (mg/kg/day)"1 forPCBs based on the incidence of hepatocellular carcinomas and adenocarcinomasin female Sprague-Dawley rats exposed to a diet containing Aroclor 1260 asreported in a study by Norback and Veltman (1985).

SELENIUMResults of studies with humans and experimental animals indicate that

certain selenium compounds are readily absorbed from the gastrointestinaltract following oral exposure (EPA 1984o). The pulmonary absorption ofselenium following inhalation exposure has not been well studied, althoughthere are reports suggesting that selenium is absorbed to some extent by this

*

route (EPA 1984o). Selenium is an essential element and therefore is nontoxicat doses necessary for normal health and nutrition. NAS (1980) reported thatan adequate and safe selenium intake for an adult human ranges from 0.05mg/day to 0.2 mg/day. However, exposure to selenium at levels that exceedthese standards has been associated with adverse health effects. Such effectsobserved in experimental animals following subchronic or chronic oral exposureto various selenium compounds have included anemia, reduced growth, increasedmortality, and lesions of the liver, heart, kidney, and spleen (EPA 1984o).In humans, chronic oral exposure to selenium has been associated with

O62 »

alopecia, dermatitis, discoloration of the skin, loss of fingernails, musculardysfunction, convulsions, paralysis, and increased incidences of dental caries(EPA 1984o). Headaches and respiratory irritation have been noted in humans .following acute inhalation exposure (EPA 1984o). Studies with a variety ofanimals have suggested that selenium may be teratogenic; however, thesestudies are limited in that exposure levels are not well characterized (EPA1984o).

Oral and inhalation reference doses (RfD) of 3.0xlO~3 mg/kg/day andl.OxlO"3 mgAg/day, respectively, have been derived by EPA (1984o, 1989b).The oral RfD value was based on a study by Yang et al. (1983) in which humansexposed to selenium in the diet at doses of 3.2 mg/day developed loss of hair,loss of fingernails, dermatitis, and muscular dysfunction. By applying anuncertainty factor of 15 and a LOAEL of 3.2 mg/day, EPA (1989b) determined theoral RfD value of 3xlO"3 mg/kg/day. The oral RfD is currently under review bythe oral RfD Work Group at EPA (1989b). The inhalation RfD value was based onan occupational study by Glover (1967) in which workers exposed to airborneconcentrations of selenium developed dermatitis and gastrointestinaldisturbances. An uncertainty factor of 10 was used to determine theinhalation RfD (EPA 1989b).

1,1,2,2-TETRACHLOROETHANEIn humans, absorption of a single inhalation dose of

1,1,2,2, -tetrachloroethane vapor was reported to be 97%; absorption of thischemical from the gastrointestinal tract is inferred from studies in which anincreased incidence of liver tumors was reported in mice exposed in the diet(EPA 1984p). The effects associated with occupational exposure to1,1,2,2-tetrachloroethane by inhalation or dermal routes are primarilyneurological and include, tremors, headache, numbness, excessive perspiration,and anorexia (EPA 1984p). In experimental animals, subchronic inhalationexposure to 1,1,2,2-tetrachloroethane is associated with liver effects,decreased hemoglobin content of red blood cells, decreased hematocrit, andfluctuations in white blood cell count (Schmidt et al. 1972, Navrotskiy et al.

O0

63

1971, Horiuchi et al. 1962). 1,1,2,2-Tetrachloroethane is a liver carcinogenwhen administered orally to mice (NCI 1978).

EPA (1989a) classified 1,1,2,2-tetrachloroethane in Group C—PossibleHuman Carcinogen based on increased incidence of hepatocellular carcinoma in .mice. EPA (1989a) developed an oral cancer potency factor of0.2 (mg/kg/day)"1 based on the study conducted by NCI (1978c) in which ahighly significant dose-related increase in the incidence of hepatocellularcarcinomas was observed in both male and female mice. An inhalation cancerpotency factor of 0.2 (mg/kg/day)'1 was also calculated from these data (EPA1989a).

TETRACHLOROETHYLENETetrachloroethylene is absorbed following inhalation (IARC 1979) and oral

(EPA 19851,j) exposure. Tetrachloroethylene vapors and liquid also can beabsorbed through the skin (EPA 1985h,i). The principal toxic effects oftetrachloroethylene in humans and animals following acute and longer-termexposures include central nervous system (CNS) depression and fattyinfiltration of the liver and kidney with concomitant changes in serum enzymeactivity levels indicative of tissue damage (EPA 1985i,j). Humans exposed todoses of between 136 and 1,018 mg/m3 for 5 weeks develop central nervoussystem effects, such as lassitude and signs of inebriation (Stewart et al.1974). The offspring of female rats and mice exposed to high concentrationsof tetrachloroethylene for 7 hours daily on days 6-15 of gestation developedtoxic effects, including a decrease in fetal body weight in mice and a smallbut significant increase in fetal resorption in rats (Schwetz et al. 1975).Mice also exhibited developmental effects, including subcutaneous edema anddelayed ossification of skull bones and stemebrae (Schwetz et al. 1975). Ina National Cancer Institute bioassay (NCI 1977), increased incidences ofhepatocellular carcinoma was observed in both sexes of B6C3F1 miceadministered tetrachloroethylene in corn oil by gavage for 78 weeks.Increased incidences of mononuclear cell leukemia and renal adenomas and

64

carcinomas (combined) have also been observed in long term bioassays in whichrats were exposed to tetrachloroethylene by inhalation (NTP 1986b).

EPA (1989b) classifies tetrachloroethylene as a Group B2 carcinogen(Probable Human Carcinogen). EPA (1989a, 1985i) has derived an oral cancer

-2 -1potency factor (q,*) of 5.1x10 (mg/kg/day) based on liver tumors observedin the NCI (1977) gavage bioassay for mice. The inhalation cancer potencyfactor for tetrachloroethylene of 3.3xlO~3 (mg/kg/day)"1 is based on an NTP(1986b) bioassay in rats and mice in which leukemia and liver tumors wereobserved (EPA 1989b). Both cancer potency factors are currently-under reviewby EPA (1989a). EPA (1989a,b) also has derived an oral reference dose (RfD)of IxlO"2 mg/kg/day for tetrachloroethylene based on a gavage study by Bubenand O'Flaherty (1985). In this study, liver weight/body weight ratios weresignificantly increased in mice and rats treated with 71 mg/kg/daytetrachloroethylene but not in animals treated with 14 mg/kg/day. Using aNOAEL of 14 mg/kg/day and applying an uncertainty factor of 1,000, the RfD wasderived.

THALLIUMThallium and its salts are readily and rapidly absorbed through the skin,

lungs, and mucous membranes of the mouth and gastrointestinal tract.Percutaneous absorption has also been reported to occur through rubber gloves(Rumack 1986). Thallium is acutely toxic to humans regardless of the chemicalform of the compound or route of administration. Hundreds of cases ofthallotoxicosis due to ingestion of thallium-based pesticides have beenreported (ACGIH 1986) . Children poisoned by thallium ingestion have exhibitedneurological abnormalities including mental retardation and psychoses (ACGIH1986). The effects of thallium toxicity are similar in humans and animals.The most commonly noted response to thallium exposure is alopecia, butneurological and gastrointestinal findings are frequently found. Such effectsinclude ataxia, lethargy, painful extremities, peripheral neuropathies,convulsions, endocrine disorders, psychoses, nausea, vomiting, and abdominal

•

pains (Bank 1980). It has been noted that the degree and duration of exposure

65

to thallium and its salts can influence the clinical picture of thalliumintoxication. Subchronic feeding studies conducted with weanling ratsobserved marked growth depression and a nearly complete loss of hair (Claytonand Clayton 1981) . Exposure to thallium salts during critical developmentalstages in chicks and rats has been reported to be associated with theinduction of adverse developmental outcomes (Karnofsky et al. 1950). Pre- andpostnatally exposed rat pups have exhibited hydronephrosis, fetal weightreduction and growth retardation (Clayton and Clayton 1981, Gibson and Becker1970). Thallium has also been shown to cross the placenta and, presumably,enter the fetal blood system (Clayton and Clayton 1981). Thallium has notbeen demonstrated to be carcinogenic in humans or experimental animals and mayhave some antitumor activity (Clayton and Clayton 1981).

EPA (1989b) developed an oral reference dose (RfD) for thallium of7xlO"5 mg/kg/day based on a subchronic feeding study in which rats received0.20 mg/thallium/kg/day administered as thallium sulfate (MRI 1986, EPA1986f). Increased blood chemistry parameters (SCOT and serum LDH) andalopecia were observed. An uncertainty factor of 3,000 was used to calculatethe RfD. EPA (1989a) also derived oral RfDs for certain thallium salts (i.e.,thallium acetate, thallium carbonate, thallium chloride, thallium nitrate,thallium selenite and thallium (I) sulfate) of between 8-9xlO"5 mg/kg/daybased on the same EFA (1986k) 90 day subchronic rat study. The same endpointsof toxicity were observed and an uncertainty factor of 3,000 was used toderive the RfDs.

TOLUENEToluene is absorbed in humans following both inhalation and dermal

exposure (EPA 1985k). In humans, the primary acute effects of toluene vaporare central nervous system (CNS) depression and narcosis. These effects occurat concentrations of 200 ppm (754 mg/m3) (von Oettingen et al. 1942a,b). Inexperimental animals, acute oral and inhalation exposures to toluene canresult in central nervous system (CNS) depression and lesions of the lungs,liver, and kidneys (EPA 1987f). The earliest observable sign of acute oral

rjO

66

toxicity in animals is depression of the CNS, vhich becomes evident atapproximately 2,000 mg/kg (Kimura et al. 1971). In humans, chronic exposureto toluene vapors at concentrations of approximately 200 and 800 ppm has beenassociated with CNS and peripheral nervous system effects, hepatomegaly, andhepatic and renal function changes (EPA 1987f). Toxic effects followingprolonged exposure of experimental animals to toluene are similar to thoseseen following acute exposure (Hanninen et al. 1976, von Oettingen et al.1942a). A dose-related reduction in hematocrit values was observed in ratschronically exposed to toluene (CUT 1980). There is some evidence in micethat oral exposure to greater than 0.3 ml/kg toluene during gestation resultsin embryotoxicity (Nawrot and Staples 1979). Inhalation exposure of up to1,000 mg/m3 by pregnant rats during gestation has been associated withsignificant increases in skeletal retardation (Hudak and Ungvary 1978).

EFA (1989a) has derived an oral risk reference dose (RfD) of0.3 mg/kg/day for toluene based on a 24-month inhalation study in which ratswere exposed to concentrations as high as 300 ppm (29 mg/kg/day) andhematological parameters were examined (CUT 1980). No adverse effects wereobserved in any of the treated animals. Using a no-observed-adverse-effectlevel (NOAEL) of 29 mg/kg/day and an uncertainty factor of 100, the oral RfDwas derived. EPA (1989b) reported an inhalation RfD for toluene of 1.0mg/kg/day also based on this CUT study in which CNS effects were noted and anuncertainty factor of 100 was used.

1,1.1-TRICHLOROETHANELike other chlorinated aliphatic hydrocarbons, 1,1,1-trichloroethane

(1,1,1-TCA, methyl chloroform) is rapidly and completely absorbed followingboth the oral and inhalation exposure. Pulmonary absorption is initiallylarge and gradually decreases to a steady-state condition. Absorption throughthe skin is slow. 1,1,1-TCA distributes throughout the body and readily

—f

crosses the blood-brain barrier (EPA 1984q). The most notable toxic effects .Jof 1,1,1-TCA inhalation exposure in humans and animals are central nervoussystem depression, including anesthesia at very high concentrations, and .̂

67

impairment of coordination, equilibrium, and judgment at lower concentrations(350 ppm and above). In both humans and animals, cardiovascular effects,including premature ventricular contractions, decreased blood pressure, andsensitization to epinephrine-induced arrhythmia can result from acute exposureto high concentrations of 1,1,1-TCA vapor (EPA 19851). Fatty liver changes.,have been reported in guinea pigs following subchronic inhalation exposure(Torkelson et al. 1958). NTP (1984) reported preliminary results of bioassaysin rats and mice indicating that oral administration of 1,1,1-TCA increasesthe incidence of hepatocellular carcinomas in female mice but not for malerats. This study was inadequate to evaluate the carcinogenicity of 1,1,1-TCAin female rats and male mice.

EPA (1989a) calculated an oral reference dose (RfD) for 1,1,1-trichloroethane based on an inhalation study by Torkelson et al. (1958) inwhich rats, rabbits, guinea pigs and monkeys were exposed to 1,1,1-TCA vapor.A no-observed-adverse-effect (NOAEL) of 500 ppm (2,730 mg/m3, or 90 mgAg/day)was identified from this study. Using the NOAEL of 90 mg/kg/day and anuncertainty factor of 1,000, a RfD of 9xlO"2 mg/kg/day was derived. Aninhalation RfD of 0.3 mg/kg/day for 1,1,1-TCA also has been determined by EPA(1989b) based on this same study, in which hepatotoxicity was observed inguinea pigs. An uncertainty factor of 1,000 was used in calculating the RfD.

TRICHLOROETHYLENEAbsorption of trichloroethylene (TCE) from the gastrointestinal tract is

virtually complete. Absorption following inhalation exposure is proportionalto concentration and duration of exposure (EPA 1985m). TCE is a centralnervous system depressant following acute and chronic exposures. In humans,single oral doses of 15 to 25 ml (21 to 35 grams) of TCE have resulted invomiting and abdominal pain, followed by transient unconsciousness (Stephens1945). High-level exposure can result in death due to respiratory and cardiacfailure (EPA 1985m). Hepatotoxicity has been reported in human and animalstudies following acute exposure to TCE (EPA 1985m). Nephrotoxicity has beenobserved in animals following acute exposure to TCE vapors (ACGIH 1986,

68

Torkelson and Rowe 1981). Subacute inhalation exposures of mice have resultedin transient trichloroethylene-induced increased liver weights (Kjellstrand etal. 1983). Industrial use of TCE is often associated with adversedermatological effects including reddening and skin burns on contact with theliquid form, and dermatitis resulting from vapors. These effects are usuallythe result of contact with concentrated solvent, however, and no effects havebeen reported after exposure to TCE in dilute, aqueous solutions (EPA 1985m).Trichloroethylene has caused significant increases in the incidence ofhepatocellular carcinomas in mice (NCI 1976b) and renal tubular-cell neoplasmsin rats exposed by gavage (NTP 1983), and pulmonary adenocarcinomas in micefollowing inhalation exposure (Fukuda et al. 1983). Trichloroethylene wasmutagenic in Salmonella typhiourium and in E. coli (strain K-12), utilizingliver microsomes for activation (Greim et al. 1977).

EPA (1989a) classified trichloroethylene in Group B2--Probable HumanCarcinogen based on inadequate evidence in humans and sufficient evidence ofcarcinogenicity from animals studies. EPA (1989a) derived an oral cancerpotency factor of l.lxlO"2 (mg/kg/day)'1 and an inhalation cancer potency

- -3 -1factor of 4.6x10 (mg/kg/day) based on the mouse liver tumor data in theNCI (1976b) and NTP (1983) gavage studies. EPA (1987g) developed an oralreference dose (RfD) of 7.35x10 mg/kg/day based on a subchronic inhalationstudy in rats in which elevated liver weights were observed following exposureto 55 ppm, 5 days/week for 14 weeks (Kimmerle and Eben 1973). A safety factorof 1,000 was used to calculate the RfD. However, this RfD is currently underreview by EPA.

VANADIUMPentavalent vanadium compounds are generally considered to be more toxic

than other valence states. Many incidents of short term and long termoccupational exposures to vanadium, mainly vanadium pentoxide dust, have beenreported. Inhalation causes respiratory tract irritation, coughing, wheezing,labored breathing, bronchitis, chest pains, eye and skin irritation anddiscoloration of the tongue (NIOSH 1977b, NAS 1974). Effects seen in

69

experimental animals following chronic inhalation exposure include fattydegeneration of the liver and kidneys, hemorrhage, and bone marrow changes(Browning 1969).

EPA (1989b) has derived an oral reference dose (RfD) of 7xlO"3 mg/kg/daybased on a chronic study in which rats received vanadium in their drinkingwater (Schroeder et al. 1970). A no-observed-adverse-effect level (NOAEL) of0.77 mg/kg/day and an uncertainty factor of 100 were used to develop the RfD.EPA (1989a) has established an oral RfD for vanadium pentoxide of 9xlO~3

mg/kg/day. This value is based on a chronic rat study in which a NOAEL of0.89 mg vanadium pentoxide/kg/day was noted. The only reported effect was adecrease in the amount of cystine in the hair (Stokinger et al. 1953). Anuncertainty factor of 100 was used to calculate the vanadium pentoxide RfD.EPA has not developed inhalation criteria for vanadium.

XYLENESThe three xylene isomers, compounds that have the same chemical

constituents in a different configuration, have similar toxicologicalproperties and are discussed together. Data from animals and humans suggestthat approximately 60% of an inhaled dose is absorbed. Inference frommetabolism and excretion studies suggests that absorption of orallyadministered xylene is nearly complete. Dermal absorption is reported to beminor following exposure to xylene vapor but may be significant followingcontact with the liquid (EPA 1985n). In humans, acute inhalation exposures torelatively high concentrations of xylene adversely affect the central nervoussystem and lungs and can irritate mucous membranes (EPA 1987h). Savolainen etal. (1980) observed that body balance and manual coordination were impaired ineight male students following inhalation exposure to m-xylene. However,tolerance against the observed effects developed during one work week. Inexperimental rats, long-term inhalation exposure to o-xylene resulted inhepatomegaly (Tatrai et al. 1981). Oral exposure to 200 mg/kg xylene in thediet for up to 6 months was also associated with liver toxicity, specificallythe development of intracellular vesicles (Bowers et al. 1982). Prolonged

70

oral exposures in mice resulted in hyperactivity, a manifestation of CNStoxicity (NTP 1986c). Xylene appears to be fetotoxic and may increase theincidence of visceral and skeletal malformations in offspring of exposedexperimental animals (Mirkova et al. 1983). There is suggestive evidence thatxylene is carcinogenic in experimental animals when exposed by oral gavage(Maltoni et al. 1985).

EPA (1989a) calculated an oral reference dose (RfD) for mixed xylenes of2 mgAg/day based on an NTP (1986c) study in which male rats given a gavagedose of 179 mg/kg/day for 103 weeks did not exhibit hyperactivity, decreasedbody weight or a significant increased mortality. The oral RfD was derivedusing the no-observed-adverse-effect level (NOAEL) of 179 mg/kg/day and anuncertainty factor of 100. EPA (1989b) reported an inhalation RfD for mixedxylenes of 0.4 mg/kg/day based on a study in which no effects were observed inrats exposed to 398 mg/m3 for 13 weeks (Carpenter et al. 1975); an uncertaintyfactor of 1,000 was used to develop the RfD.

ZINCZinc is absorbed in humans following oral exposure; however, insufficient

data are available to evaluate absorption following inhalation exposure (EPA1984r). Zinc is an essential trace element that is necessary for normalhealth and metabolism and therefore is nontoxic in trace quantities (Hammondand Beliles 1980). However exposure to zinc at concentrations that exceedrecommended levels has been associated with a variety of adverse effects.Chronic and subchronic inhalation exposure of humans to zinc has beenassociated with gastrointestinal disturbances, dermatitis, and metal fumefever, a condition characterized by fever, chills, coughing, dyspnea, andmuscle pain (EPA 1984r). Chronic oral exposure of humans to zinc may causeanemia and altered hematological parameters. Reduced body weights have beenobserved in studies in which rats were administered zinc in the diet. Thereis no evidence that zinc is teratogenic or carcinogenic (EPA 1984r).

EPA (1989b) has derived an oral reference dose (RfD) of 2x10'* mg/kg/daybased on studies in which anemia and reduced blood copper were observed in

-O

71

humans exposed to oral zinc doses of 2.14 mg/kg/day (Pories et al. 1967,Prasad et al. 1975). A safety factor of 10 was used in developing the RfD.

5.0 RISK CHARACTERIZATION

According to guidelines for preparing risk assessments as part of theRI/FS process (EPA 1986a), the potential adverse effects on human healthshould be assessed where possible by comparing chemical concentrations foundat or near the site with applicable or relevant and appropriate requirements(ARARs) or other guidance that has been developed for the protection of humanhealth or the environment. If ARARs are available for all chemicals in allenvironmental media, then a comparison to ARARs constitutes the riskassessment. If not, quantitative risk estimates must be developed in additionto the comparison to ARARs. The quantitative assessment includes both thechemicals with ARARs and those without ARARs. For the Vestal site, ARARs areavailable only for groundwater; therefore, in addition to a comparison toARARs, a quantitative assessment is presented below for exposure to soils,air, and groundwater.

5.1 COMPARISON TO POTENTIAL APPLICABLE OR RELEVANT AND APPROPRIATEREQUIREMENTS (ARARS)

Section 121(d) of CERCLA, as amended by the Superfund Amendments andReauthorization Act of 1986 (SARA), requires that remedial actions at CERCLAsites comply with requirements or standards under federal and stateenvironmental laws that are "applicable" or "relevant and appropriate" to thehazardous substances, pollutants, or contaminants at a site or to thecircumstances of the release. A requirement may be either applicable orrelevant and appropriate to a remedial action, but not both. An applicablerequirement is one that specifically addresses a hazardous substance,pollutant, contaminant, remedial action, location, or other circumstance at aCERCLA site. Relevant and appropriate requirements, while not applicable,address problems or situations sufficiently similar to those encountered at aCERCLA site that their use is well suited to the particular site (52 FR 32497,

72

August 27, 1987). EPA makes the final determination on the applicability orrelevance and appropriateness of a requirement based on such factors as thecharacteristics of the remedial action and the physical circumstances of thesite. EPA has, however, issued guidance on the use of water standards aschemical-specific ARARs (52 FR 32496-32499). This guidance is used in thisPHE as the basis for the comparison to estimated future groundwaterconcentrations for the Vestal site.

SARA explicitly mentions three kinds of water standards with whichcompliance is potentially required: Maximum Contaminant Level Goals (MCLGs),Federal Water Quality Criteria (FWQC), and alternate concentration limits(ACLs). EPA guidance describes these potential ARARs as follows (52 FR32499):

MCLGs are developed under the Safe Drinking Water Act as chemical-specific health goals used in setting enforceable drinking waterstandards, known as Maximum Contaminant Levels (MCLs), for publicwater supply systems. MCLGs are based entirely on healthconsiderations and do not take cost or feasibility into account.Moreover, as health goals, MCLGs are set at levels where no known oranticipated health effects may occur, including an adequate marginof safety. MCLs are required to be set as close as feasible to therespective MCLG, taking into consideration the best technology,treatment techniques, and other factors (including cost). However,as the standard for public water supplies, MCLs are fully protectiveof human health and (for carcinogens) fall within the acceptablerisk range of 10"* to 10"7. Furthermore, for noncarcinogens, whichare the majority of contaminants, MCLs will nearly always be set atthe same level as the respective MCLGs. Also, these standardsassure that even sensitive populations will experience no adversehealth effects. Thus, there will be no difference in theprotectiveness of MCLGs and MCLs for most contaminants5, and asdiscussed above, MCLs provide a sufficient level of protectivenesseven for carcinogens.

FWQC are developed under the Clean Water Act as guidelines fromwhich States determine their water quality standards. DifferentFWQC are derived for the protection of human health and protectionof aquatic life.

M̂CLGs are set at zero for carcinogens to reflect the no-thresholdposition as discussed in Section 4.1.

73

/*""**•% ACLs are one of three possible standards available under the SubpartF Groundwater Protection Standards of RCRA. For setting both atrigger and a cleanup level for remediating groundwater

I contamination, an ACL, the background concentration, or for a smallgroup of chemicals the MCL can be selected for a given site.

ACLs are health-based standards that are derived for a specific point ofcompliance at a facility boundary or within a contaminant plume to beprotective of a specific point of exposure. Guidance on the use of ACLs asARARs has not yet been issued.

MCLs are enforceable standards for public water supply systems and assuch will generally be considered applicable. HCLGs are not enforceable andbased on the discussion presented above are treated as "other guidance." Theuse or potential use of the groundwater must also be considered in determiningpotential ARARs. Groundwater at the Vestal site would be classified either asClass I (highly vulnerable drinking water source) or Class II (current orpotential source of drinking water). According to the previously citedguidance, MCLs will generally be considered ARARs for all Class I or Class IIgroundwater.

/"**""""N The New York Department of Environmental Conservation has alsoestablished classifications for groundwater. The Vestal site falls under

) Classification GA—potable, fresh groundwaters found in the saturated zone ofi1 unconsolidated deposits and consolidated rock or bedrock (10 NYCRR Part, 703.5). State standards require that no wastes be deposited in Class GAI waters that would impair its designated use. In addition, numerical standards

have been established for individual contaminants. Table 5-1 lists MCLs andNew York State groundwater standards for the chemicals of potential concern.Comparison of the potential ARARs in Table 5-1 with the groundwater

•*• concentrations predicted by the leaching model (Tables 3-8 to 3-11) indicates

the following:

• The estimated maximum concentrations of trichloroethylene below thesource in Areas 2 and 4 exceed the MCI and the New York standard.

• The estimated maximum concentrations of PCBs below the source in Area:2 and 4 exceed the New York standard.

74

TABLE 5-1POTENTIAL ARARS AND OTHER GUIDANCE


GROUNOWATERCHEMICAL

MCL (a)(mg/1)

AcetoneBenzene 0.0052-ButanoneChloroform 0.100 (d)1,1-Dichloroethane1.1-Dichloroethylene 0.007trans-l,2-DichloroethyleneEthylbenzene1 , 1 , 2 , 2-TetrachloroethaneTetrachloroethyleneToluene1.1.1-Trlchloroethane 0.200Trichloroethylene 0.005XyleneBis(2-ethy1hexyl)phthalateDi-n-butylphthalateNoncarcinogenic PAHsCarcinogenoc PAHsPCBsAntimonyArsenic 0.050Barium 1.000BerylliumChromium 0.050 (e)CopperLead 0.050 (f)ManganeseMercury 0 . 002NickelThalliumVanadiumZinc

a MCL = Safe Drinking Water Act Maximum Contaminantb NY State regulatory criteria for Class GA waters.ic HYDEC Air Guide-1: Guidelines for the Control of

NY STATESTANDARD (b)

(mg/D

„

ND--0.100«—--———----.010—4.2000.770—ND

0.0001--0.0251.000—0.0501.0000.0250.3000.002——--

5.00

Level. 40 CFR 142.10 NYCRR 703.5.

AIR

NY STATEAAL (cj(ug/m3)

35600100

1967(d) 167--

66.7145023.31116750038000900

1450—

166.71.67

;,9,99• iggggg9999(g

Toxic Ambient Air Contaminantsd MCL is for total trihalomethanes (chloroform, bromodichloromethane.le Standard is for CrVI.If Proposed MCL is 0.005 (See text).§ Inorganics not considered for air exposure.- not detectable by methods specified in 10 NYCRR

— « no MCL or state criteria promulgated.703.4.

dibromochloromethane, and bromoform)

75

Comparison of potential ARARs to the concentrations of inorganicsdetected in monitoring wells (Table 2-4) reveals the following:

• The maximum concentrations of total (unfiltered) barium, chromium, •and lead exceed both MCLs and New York standards and the geometricmean concentration of total lead exceeds the New York standard.

• For mercury the maximum total concentration, geometric mean totalconcentration, and maximum dissolved (filtered) concentrations exceedMCLs and New York standards.

• The maximum and geometric mean total concentrations of manganeseexceed the New York standards as does the maximum dissolvedconcentration of manganese .

• The maximum total concentrations of arsenic, copper, and zinc exceedthe New York standard.

In general ARARs have not been established for soils. However, TSCA PCBspill cleanup limits have been cited as potential ARARs. Comparison of PCBconcentrations detected in Areas 2 and 4 indicate that the concentrations arebelow the TSCA limits of 10 mg/kg for unlimited access sites and 25 mg/kg forsites with restricted access.

EPA guidance cited above has defined National Ambient Air QualityStandards (NAAQS) as ARARs for Superfund risk assessments. NAAQS are airquality standards developed for the protection of human health (includingsensitive individuals); they are available for six chemicals or chemicalgroups and for airborne particulate matter. However, no NAAQS values areavailable for the chemicals of potential concern in air at the Vestal site.

The New York State Department of Environmental Conservation (NYSDEC) hasdeveloped acceptable ambient levels (AALs) for many chemicals in air. AALsare not standards but, rather, are guideline values that represent theincremental average annual ambient concentrations above background that shouldnot be exceeded. The AALs are based on chemical -specific toxicity analysesor, in the absence of such analyses, are derived from the American Conferenceof Industrial Hygienists (ACGIH) threshold limit values (TLVs) using safetyfactors (NYSDEC 1986). The NYSDEC (1986) defines an AAL as:

76

The contaminant concentration which is considered to be anacceptable average concentration at a receptor on an annualaverage basis. These values are developed as guidelines tosafeguard receptors against potential chronic effects result-ing from continuing exposures .

NYSDEC (1986) has developed AALs for many of the chemicals of potentialconcern at the Vestal site, and these are listed in Table 5-1. Comparison ofthese levels with the estimated air concentrations associated with soilexcavation presented in Table 3-4 indicates the following:

• In Area 1, the maximum case concentration of noncarcinogenic PAHs isgreater than the AAL.

• In Area 2 , AALs are exceeded by the average case and maximum caseconcentrations of 1, 1-dichloroethylene, 1,1,2,2-tetrachloroethane,trichloroethylene, and PCBs and by the maximum case concentrations oftetrachoroethylene and xylene.

• In Area 3 , AALS are exceeded by the average case and maximum caseconcentrations of 1 , 1-dichloroethylene and by the maximum caseconcentration of acetone.

• In Area 4 , AALs are exceeded by the average case and maximum caseconcentrations of 1, 1-dichloroethylene and trichloroethylene, and bythe maximum case concentration of PCBs .

All estimated air concentrations due to fugitive dust generation (Table 3-6)are well below AALs.

5.2 QUANTITATIVE RISK ASSESSMENT METHODOLOGYTo quantitatively assess the potential risks to human health associated

with the exposure scenarios considered in this assessment, the exposure pointconcentrations developed in the previous sections are converted to chronicdaily intakes (CDIs). CDIs are expressed as the amount of a substance takeninto the body per unit body weight per unit time, or mg/kg/day. A GDI isaveraged over a lifetime for carcinogens (EPA 1986b) and over the exposureperiod for noncarcinogens (EPA 1986c) . As with exposure point concentrations,two cases are considered — an average case and a plausible maximum case. Theaverage case is based on average (but conservative) conditions of exposure and

JL^ - the average exposure point concentrations based on the geometric mean chemicalconcentration. The plausible maximum case is based on upper-bound conditionsof exposure and the plausible maximum exposure point concentration based onthe geometric mean of the detected samples, and as such represents the extremeupper limit of potential exposure. For potential carcinogens, excess lifetimecancer risks are obtained by multiplying the daily intake of the contaminantunder consideration by its cancer potency factor. EPA has implemented actionsunder Superfund associated with total cancer risks ranging from 10"* to 10~7

(i.e., the probability of one excess cancer is one in 10,000 or 10,000,000,respectively, under the conditions of exposure). A risk level of 10"6,representing a probability of one in 1,000,000 that an individual couldcontract cancer due to exposure to the potential carcinogen, is often used asa benchmark level of concern by regulatory agencies.

Potential risks for noncarcinogens are presented as the ratio of thechronic daily intake exposure to the reference dose (CDI:RfD). The sum of theCDI:RfD ratios of chemicals under consideration is called the hazard index.The hazard index is useful as a reference point for gauging the potentialeffects of environmental exposures to complex mixtures. In general, hazard

/""**••-.1 indices which are less than one are not likely to be associated with anyhealth risk, and are therefore less likely to be of concern than hazardindices greater than one. The conclusion should not be categorically drawn,however, that all hazard indices less than one are "acceptable" or that hazard

• indices of greater than one are "unacceptable." This is a consequence of theperhaps order of magnitude or greater uncertainty inherent in estimates of theRfD and GDI in addition to the fact that the uncertainties associated with theindividual terms in the hazard index calculation are additive.

In accordance with EPA's guidelines for evaluating the potential toxicityof complex mixtures (EPA 1986c), it was assumed that the toxic effects of thesite related chemicals would be additive. Thus, lifetime excess cancer risksand the GDI:RfD ratios were summed to indicate the potential risks associatedwith mixtures of potential carcinogens and noncarcinogens, respectively. In

•

the absence of specific information on the toxicity of the mixture to be

78

assessed or on similar mixtures, EPA guidelines generally recommend assumingthat the effects of different components of the mixture are additive whenaffecting a particular organ or system. Synergistic or antagonisticinteractions may be taken into account if there is specific information onparticular combinations of chemicals. In this risk assessment, it was assumedthat the potential effects of site-related chemicals would be additive.

In the case of noncarcinogens, a CDI:RfD ratio of greater than one for aparticular chemical will indicate a potential risk associated with thatchemical. When the Hazard Index exceeds one, the chemicals should beregrouped according to their toxicity endpoints, and the index recalculated todetermine if the hazard index for any of the groups exceeds one.

5.3 POTENTIAL EXPOSURES AND RISKS TO WORKERS IN EXCAVATED SOILS

Workers in excavated soils may be exposed to contaminants in the soilthrough three possible routes: (1) dermal absorption through direct contactwith soil on the hands and arms, (2) incidental ingestion of soil if theworker eats, drinks, or smokes following contact with soil, and (3) inhalationof volatile chemicals within a pit within the excavated soil. The exposuresfrom each of these routes are calculated separately and are then summed togive the total potential exposure.

5.3.1 Dermal ExposureThe exposure assumptions used in determining the dermal contact exposure

are presented in Table 5-2. It was assumed that a future on-site constructionworker would work in a pit such as an excavated building foundation for a6-week period, 5 days per week, and that the worker would be involved in amanual task which would result in dermal contact with soil. Significantexposure via dermal absorption of inorganics Is not expected, because of thelow permeability of skin to metal ions (Schaefer et al. 1983). However, theorganic chemicals of potential concern are more likely to be absorbed throughskin. Non-steady state dermal absorption data for short-duration exposures ofhumans to soils containing the organic chemicals of potential concern are not

79

A.available. However, based on analogy with 2,3,7,8-TCDD, the data from Poigerand Schlatter (1980) can be used to approximate dermal absorption factors for

, PAHs, PCBs, and bis(2-ethylhexyl) phthalate. Insufficient data are availablet '

to develop dermal absorption factors for the volatile organics. A value of10% is assumed based on analogy to other chemicals and chemical-physicalproperties. Similarly, for di-n-butyl phthalate rates of 5% are used for bothaverage and maximum cases based on analogy and chemical-physical properties.

Values of 990 mg/day and 2970 mg/day are Used for the amount of soilcontacting the skin of exposed workers under the average and plausible maximumcases, respectively based on Schaum's exposure ranges of 0.5 to 1.5 mg/cm2

(1984) multiplied by the appropriate area of uncovered skin, i.e., 1,980 cm2

for the forearms and hands of an adult (EPA 1988b). The assumptions outlinedabove and the following chemical intake equation were used to derive thedermal exposure GDI:

(Cs)(CD)(E)(DE)(Z)(DAF)V-<U-L dermal ———————————————————————

(BW)(DY)(AVG)

where

CDIdttmal - chronic daily intake (mgAg/day);1 Cs - concentration of chemical in soil (mg/kg);

CD - contact rate for soil (mg/day);

| E - frequency of exposure (days/year);

DE - duration of exposure (years);

Z - conversion factor (kg/10$ mg);

DAF - dermal absorption factor (percent/100);

BW - average body weight (kg) ,

DY - conversion factor (365 days/year), and >.-4

AVG - averaging period (years).

80

TABLE 5-2

ASSUMPTIONS USED TO ESTIMATE DERMAL CONTACT EXPOSUREVESTAL WELL 1-1 SITE

PARAMETER

Contact rate, mg/d (a)Frequency of exposure, days/yearDuration of exposure, yearsDermal absorption factors, %

Volatile* (b)Phthalates (c)PCBs (c)PAHS (c)Inorganics (d)

Body weight. Kg (e)

Averaging period, yearsCarcinogens (e)Noncarcinogens

AVERAGECASE

990301

100.37

0.90

70

7530/365 = 0.08

VALUE

PLAUSIBLEMAXIMUMCASE

2970

30

1

10372070

7530/365 * 0.08

(a! Schaum (1984) and EPA (1988).(b) Assumed value based on analogy to other chemicals and chemical-

physical properties.(c) Poiger and Schlatter (1980) analogy to PCDDs/PCDFs.d) Skog and Wahlberg (1964).e) EPA 1988.

81

5.3.2 Incidental IngestionThe exposure assumptions used in determining the incidental ingestion GDI

are presented in Table 5-3. The duration of exposure was assumed to be thesame as given above for dermal absorption: 6 weeks, 5 days per week. It was.assumed that a worker would be involved in a manual task which would result insoil contact with the hands and incidental ingestion of soils following eatingor smoking. Soil ingestion rates of 50 mg/day and 100 mg/day presented inLaGoy (1987) were for use in this assessment to evaluate the average andplausible maximum cases, respectively. PAHs, PCBs, and phthalates are likelyto be strongly sorbed to the soil and consequently may be less bioavailable inthe gastrointestinal tract than they would be if they were present in drinkingwater or food, which are the typical media in animal studies used to derivetoxicity criteria. Values of 15% and 50% are used in the average and maximumcases to reflect this diminished bioavailability based in physicochemicalproperties and analogy to studies by Poiger and Schlatter (1980) and Umbreitet al. (1986) with 2,3,7,8-TCDD. For the volatiles and inorganic chemicalsdetected on site a conservative value of 100 percent bioavailability is used.

The assumptions outlined above and the following chemical intake equationused to derive the incidental ingestion exposure GDI:

(Cs)(I)(OAF)(E)(YR)(X)^ioral ~ ______________________

(BW)(DY)(AVG)

where

CDIorsl - chronic daily intake for exposure via incidental ingestion(mgAg/day) ;

Cs - concentration of chemical in soil (mg/kg) ;

I - amount of soil ingested (mg/event) ;

OAF — oral absorption factor (unitless) ;

The remaining parameters are as defined for the dermal exposure.

,,****%

82

f—,TABLE 5-3

ASSUMPTIONS USED TO ESTIMATE INCIDENTAL 1NGESTION EXPOSUREVESTAL WELL 1-1 SITE

PARAMETER

Ingestion rate, mg/d (a)

Oral absorption factors. %PAHs/PCBs (b)All others

Frequency of exposure, days/year

Duration of exposure, years

Body weight, <g (c)

Averaging period, yearsCarcinogens (c)Noncarcinogens

VALUE

AVERAGECASE

50

1510030

1

70

7530/365


100

50100

30

1

70

7530/365

fa) La-joy (1987).(b) Poiger and Schlatter (1980) and Umbrelt et al. (1986).(c) E?A (1988).

83

5.3.3 Inhalation ExposureIn determining the inhalation exposure GDI it was assumed that a future

on-site construction worker potentially would be exposed to VOCs viainhalation over 30 work days for 8 hours a day, for one year. It was alsoassumed that workers would engage in light to moderate activities during whichhe would inhale 7 m3 and 20 m3 of air (per day) for the average and plausiblemaximum exposure scenarios (EPA 1988b) . For the purpose of this analysis, itis further assumed that the chemicals inhaled are 100 percent bioavailable inthe lungs . * .

The assumptions outlined above and the following chemical intake equationused to derive the inhalation GDI:

(Ca)(V)(IAF)(FE)(DE)"

(BW)(DY)(AVG)

where

CDIair - chronic daily intake for exposure via inhalation(mg/kg/day) ;

Ca - concentration of chemical in air (mg/m3) ;

V - ventilation rate (m3/day) ;

IAF = inhalation absorption factor (unitless) .

The remaining parameters are as defined for the dermal and ingestionexposures.

Tables 5-4 through 5-7 present the chronic daily intakes and estimatedrisks for the combined dermal contact, incidental soil ingestion, andinhalation exposures for each of the four source areas. Excess lifetimecancer risks range from 2x10"* to IxlO"6 for the average case and 5x10"* to2xlO"5 for the plausible maximum case. In Area 1 (Table 5-4) carcinogenic |FAHs result in an excess lifetime cancer risk of greater than the target risklevel of 10"6 for the average and plausible maximum cases. In Area 2 §(Table 5-5) a risk level of greater than 10"6 is associated with

\3

TABLE 5-4

POTENTIAL EXPOSURES AND RISKS FROM DERMAL ABSORPTION. INCIDENTAL IN6ESTION,AND INHALATION OF VOLATILES - FUTURE CONSTRUCTION SCENARIO


CHEMICALS EXHIBITINGPOTENTIAL CARCINOGENICEFFECTS

BenzeneBis 2 (ethyl hexyl) phthalate1.1-Dichloroethane1,1-DlchloroethylenePCBsTetrachloroethylene1,1.2. 2-TetrachloroethaneTrichloroethyleneCarcinogenic PAHs

CHRONIC DAILY INTAKEFOR DERMAL ABSORPTION

AND INGEST I ON(mg/kg/day)

PLAUSIBLEAVERAGE MAXIMUMCASE CASE

7.00E-12 1.86E-11*******

1.63E-10 9.42E-09

ORALCANCERPOTENCYFACTOR(rog/kg/day)-l

2.9E-021.4E-029. IE-026.0E-017.7E+005. IE-022.0E-011. IE-021.2E+01

CHRONIC DAILY INTAKEFOR INHALATION(mg/kg/day)

AVERAGECASE

3.51E-06*******

2.26E-07


l.OOE-05

3.23E-06

INHALATIONCANCERPOTENCYFACTOR(mg/kg/day)-l

2.9E-02****

1.2E+00**3.3E-032.0E-014.6E-036.1E+00

TOTAL:

COMBINED EXCESSUPPER -BOUND LIFETIME

CANCER RISK

AVERAGECASE

1;OE-07

1.4E-06

IE-06

PLAUSIBLEMAXIMUM 'CASE

2.9E-07

**2.0E-05

2E-05

00Ul

CHEMICALS EXHIBITINGPOTENTIAL NONCARCINOGENICEFFECTS

AcetoneBis 2 (ethyl hexyl) phthalate2-Butanone1 , 1-Dtchloroethane1 . 1-Olchloroethylene1,2-Dlchloroethylene (trans)Dt-n-butyl phthalateEthyl BenzeneTetrachloroethyleneTolueneTrichloroethylene1 , 1 , 1-Tr IchloroethaneXyleneNoncarclnogenic PAHs


AND INGEST ION(mg/kg/day)


* ** *

5.95E-09 1.58E-08* ** *

5.25E-10 1.40E-09* *8.75E-10 1.03E-08* *8.75E-10 4.66E-09* ** *

1.22E-09 2.52E-087.06E-08 2.57E-05

ORALREFERENCEDOSE

(mg/kg/day)-!

l.OE-012.0E-025.0E-02l.OE-019.0E-032.0E-02l.OE-01l.OE-01l.OE-023.0E-017.3E-039.0E-022.0E+004.0E-01


AVERAGECASE

**

l.OOE-03**

4.00E-04*

2.50E-04*4.32E-04**

2.65E-045.09E-04


**

2.86E-03**

1.14E-03*

3.15E-03*2.42E-03*

*

5.85E-033.48E-02

INHALATIONREFERENCEDOSE

(mg/kg/day)-l

****

9.0E-02l.OE-01**********

l.OE+00**3.0E-014.0E-01*»

HAZARD INDEX:

COMBINED CDI

AVERAGECASE

*

*

1. IE-02*

*

2.6E-08*

8.7E-09*4.3E-04*

*

6.6E-041.8E-07

1.2E-02

:RfD RATIO


**3.2E-02*

*

7.0E-08*l.OE-07*

2.4E-03*

*

1.5E-026.4E-05

4.9E-02

Inhalation toxlcity criteria were not available.

* * Chemical not detected In this area.

UtL LOU

00

TABLE 5-5POTENTIAL EXPOSURES AND RISKS FROM DERMAL ABSORPTION. INCIDENTAL INGEST10N.

AND INHALATION OF VOLATILES - FUTURE CONSTRUCTION SCENARIOAREA 2



BenzeneBis 2 (ethyl hexyl) phthalate1,1-Dtchloroethane1,1-DichloroethylenePCBsTetrachloroethylene1,1,2, 2-TetracnloroethaneTrlchloroethyleneCarcinogenic PAHs


AND INGEST I ON(mg/kg/day)


7.00E-12 1.86E-116.23E-10 2.84E-092.10E-11 5.59E-117.00E-12 1.86E-113.50E-10 2.35E-091.56E-10 1.85E-099.33E-11 2.49E-103.99E-10 3.14E-085.05E-10 2.57E-09

CANCERPOTENCYFACTOR(mg/kg/day) -1

2.9E-021.4E-029. IE-026.0E-017.7E+005. IE-022.0E-011. IE-021.2E+01



3.51E-06 l.OOE-052.83E-08 1.62E-072.39E-05 6.83E-058.36E-05 2.39E-045.19E-07 3.76E-067.68E-05 9.77E-047.91E-06 2.26E-051.96E-04 1.65E-021.70E-07 8.89E-07


2.9E-02****

1.2E+00**3.3E-032.0E-014.6E-036.1E+00

TOTAL:

COMBINED EXCESS UPPER-BOUNDLIFETIME CANCER RISK

AVERAGECASE

l.OE-078.7E-121.9E-12l.OE-042.7E-092.5E-071.6E-069.0E-07l.OE-06

IE-04

PLAUSIBLEMAXIMUM

CASE

2.9E-074.0E-115. IE-122.9E-041.8E-083.2E-064.5E-067.6E-055.5E-06

4E-04


AcetoneBis 2 (ethyl hexyl) phthalate2-Butanonel.l-Dlchloroethane1.1-Dichloroethylene1,2-Dichloroethylene (trans)Dl-n-butyl phthalateEthyl BenzeneTet rach loroethy leneTolueneTrlchloroethylene1,1. 1-Tr ichloroethaneXyleneNoncarcinogenic PAHs


AND INGESTION(mg/kg/day)


* *4.67E-08 2.13E-074.55E-09 .21E-081.57E-09 .20E-095.25E-10 .40E-092.06E-08 .45E-077.59E-09 .90E-081-.52E-08 .41E-081.17E-08 .39E-079.10E-09 .54E-072.99E-08 2.35E-061.31E-08 1.98E-073.45E-08 9.50E-076.16E-08 1.38E-06

ORALREFERENCEDOSE

(mg/kg/day)-l




* *

2.12E-06 1.21E-057.68E-04 2.19E-031.79E-03 5.12E-036.27E-03 1.79E-021.58E-02 1.19E-011.16E-05 3.31E-054.36E-03 2.28E-025.76E-03 7.33E-024.50E-03 8.13E-021.47E-02 1.24E+001.31E-02 2.12E-017.46E-03 2.20E-014.24E-04 1.86E-03


(mg/kg/day) -1

****

9.0E-02l.OE-01**********

l.OE+00**3.0E-014.0E-01**

HAZARD INDEX:

COMBINED CDI

AVERAGECASE

*2.3E-068.5E-031.8E-025.8E-08l.OE-067.6E-081.5E-071.2E-064.5E-034. IE-064.4E-021.9E-021.5E-07

9.3E-02

:RfO RATIO


*

1. IE-052.4E-025. IE-021.6E-077.3E-061.9E-077.4E-071.4E-058. IE-023.2E-047. IE-015.5E-013.5E-06

1.4E+00

Inhalation toxicity criteria were not availaole.* = Chemical not detected In this area.

LUU Muni

oo

TABLE 5-6

POTENTIAL EXPOSURES AND RISKS FROM DERMAL ABSORPTION, INCIDENTAL INGESTION.AND INHALATION OF VOLATILES - FUTURE CONSTRUCTION SCENARIO



BenzeneBts 2 (ethyl hexyl) phthalate1,1-Dlchloroethane1 , 1-DichloroethylenePCBsTet rach loroethy lene1 , 1 ,2,2-TetrachloroethaneTr 1 ch loroethy leneCarcinogenic PAHs


AND INGEST ION(mg/kg/day)


* *6.08E-10 4.28E-099.33E-12 2.49E-117.00E-12 1.86E-11* ** ** ** *

7.42E-12 8.56E-11

CANCERPOTENCYFACTOR(mg/kg/day)-l

2.9E-021.4E-029. IE-026.0E-017 . 7E+005. IE-022.0E-011. IE-021.2E+01


AVERAGECASE

*

3.06E-081.06E-058.36E-05****

1.02E-08


*

2.42E-073.04E-052.39E-04****

2.91E-08


2.9E-02****

1.2E+00**3.3E-032.0E-014.6E-036.1E+00

TOTAL:


AVERAGECASE

*

8.5E-128.5E-13l.OE-04****6.2E-08

IE-04


*

6.0E-112.3E-122.9E-04*

*

*

*

1.8E-07

3E-04


AcetoneBis 2 (ethyl hexyl) phthalate2-Butanone1,1-Dlchloroethane1 , 1-Dichloroethy lene1,2-Oich loroethy lene (trans)01-n-butyl phthalateEthyl BenzeneTetrach loroethy leneTolueneTrichloroethylene1 , 1 , 1-Tr ichloroethan^XyleneNoncarclnogenic PAHs




2.44E-08 2.88E-062.61E-08 2.56E-071.25E-09 4.89E-095.00E-10 1.63E-093.75E-10 1.22E-095.00E-10 5.30E-09* ** ** ** ** *

2.50E-10 8.15E-10* *5.79E-09 8.57E-08

ORALREFERENCEDOSE

(mg/kg/day)-l



AVERAGECASE

8.10E-032.29E-062.97E-047.97E-046.27E-035.34E-04*****

3.48E-04A

4.07E-05


8.38E-011.82E-051.01E-032.28E-031.79E-024.95E-03*

*

*

*

*

9.96E-04*

1.16E-04


(nig/kg/day)-!

**»*

9.0E-02l.OOE-01**

********

l.OOE+00**3.00E-014.00E-01**

COMBINED CDI

AVERAGECASE

2.4E-071.3E-063.3E-038.0E-034.2E-082.5E-08*****1.2E-03*

1.4E-08

1.2E-02

:RfO RATIO


2.9E-051.3E-051. IE-022.3E-021.4E-072.6E-07*****3.3E-03*

2. IE-07

3.7E-02

= Inhalation toxicity criteria were not available.

* - Chemical not detected in this area.

TABLE 5-7

POTENTIAL EXPOSURES AND RISKS FROM DERMAL ABSORPTION. INCIDENTAL INGESTION.AND INHALATION OF VOLATILES - FUTURE CONSTRUCTION SCENARIO



BenzeneBis 2 (ethyl hexyl) phthalate1,1-Dlchloroethane1 . l-D1chloroethy lenePCBsTetrachloroethylene1.1.2, 2-TetracnloroethaneTrichloroethyleneCarcinogenic PAHs




* *

3.71E-10 1.53E-082.93E-10 1.22E-091.22E-11 3.27E-111.22E-10 3.60E-094.89E-12 1.31E-11* *

3.27E-10 5.66E-09* *

ORALCANCERPOTENCYFACTOR(mg/kg/day)-l

2.9E-021.4E-029. IE-026.0E-017.7E4005. IE-022.0E-011. IE-021.2E401



* *1.81E-08 8.42E-073.17E-04 1.41E-031.39E-04 3.98E-041.75E-07 5.48E-062.29E-06 6.54E-06* *1.53E-04 2.83E-03* *

INHALATIONCANCERPOTENCYFACTOR(mg/kg/day) -1

2.9E-02****

1.2E+00**3.30E-032.0E-014.6E-036.1E+00

TOTAL:


AVERAGECASE

*

5.2E-122.7E-111.7E-049.4E-107.6E-09*

7. IE-07*

2E-04


*

2. IE-101. IE-104.8E-042.8E-082.2E-08*

1.3E-05*

5E-04


AcetoneBis 2 (ethyl hexyl) phthalate2-Butanone1.1-Dlchloroethane1,1-Dlchloroethylene1,2-Dlchloroethylene (trans)Di-n-butyl phthalateEthyl BenzeneTetrachloroethyleneTolueneTr ich loroethy lene1.1, 1-Tr ichloroethaneXyleneNoncarclnogenic PAHs




2.42E-07 5.99E-062.69E-08 1.10E-06* *2.10E-08 8.67E-088.75E-10 2.33E-09* ** , ** *

3.50E-10 9.32E-10* *2.34E-08 4.03E-072.76E-08 1.01E-07* *3.62E-09 6.16E-08

ORALREFERENCEDOSE

(mg/kg/day)-l


CHRONIC DAILY INTAKEFOR INHALATION(mg/kg/dayj


5.72E-02 1.52E4001.36E-06 6.32E-05* *2.38E-02 1.06E-011.04E-02 2.98E-02* ** ** *

1.72E-04 4.91E-04* *1.15E-02 2.12E-012.75E-02 1.08E-01

it *

2.54E-05 8.36E-05


(tng/kg/day)-l

****

9.0E-02l.OOE-01**

********

l.OOE+00**

3.00E-014.00E-01**

HAZARD INDEX:

COMBINED CDI

AVERAGECASE

2.4E-061.3E-06*2.4E-019.7E-08***3.5E-08*

3.2E-069.2E-02*

9. IE-09

3.3E-01

:RfD RATIO


6.0E-055;5E-05

1.1 £4002.6E-07***9.3E-08*

5.5E-053.6E-01*

1.5E-07

1.4E400

« Inhalation toxicHy criteria were not available.= Chemical not detected i* this area.

L(J(j

1,1-dichloroethylene (DCE), 1,1,2,2-tetrachloroethane and carcinogenic PAHsunder both average and plausible maximum cases and tetrachloroethylene andtrichloroethylene (TCE) for the plausible maximum case only. DCE contributesto a greater than 10"6 risk for both average and plausible maximum cases inArea 3 (Table 5-6) and in Area 4 (Table 5-7). The greater than 10-6 risk forthe plausible maximum case in Area 4 is also associated with TCE. Hazardindices exceed one (for the pausible maximum case) in Areas 2 and 4. In Area2, a CDI:RfD ratio of one is not exceeded by any specific chemical, but thehazard index exceeds one due to the combination of the CDIrRfD ratios of1,1,1-trichloroethane and xylene. In Area 4, the greater than one hazardindex is associated with the CDI:RfD ratio of 1,1-dichloroethane (1,1-DCA).

In all areas the cancer risks are driven by the inhalation exposure.Chronic daily intakes for inhalation exposure are up to 5 orders of magnitudegreater than those for dermal and incidental ingestion exposure. Inevaluating the risk attributable to 1,1-DCE it is important to note that thischemical was detected infrequently in soils (2 of 17 samples in Area 2, 1 of11 in Area 3, and 2 of 28 in Area 3) and at levels normally below ContractRequired detection limits, between 3 and 15 jig/kg. In Area 2, the twodetected values were from only one boring at depths of 4 to 6 feet and 14 to16 feet. Consequently, there is significant uncertainty as to theconcentration level present on site. 1,1-DCE is a highly volatile compoundwith a relatively high inhalation cancer potency. This results in arelatively high risk level at low soil concentration under the particularconditions of exposure evaluated in this PHE. It is also noted that 1,1-DCEhas been assigned a carcinogenicity weight-of-evidence of Level C, indicatingonly limited evidence of carcinogenicity in animals and no evidence from humanstudies. This lends additional uncertainty to the assessment.

5.4 POTENTIAL EXPOSURES AND RISKS FROM GENERATION OF DUST DURING CONSTRUCTIONA similar construction scenario as described above is used for the

evaluation of exposures and risks due to dust emissions. It is assumed thatconstruction involving soil disturbance will occur over a 6 week period.

89 »\5

Therefore, an on-site future construction worker potentially would be exposedvia inhalation of fugitive dust over 30 work days for 8 hours a day, for oneyear, for both the average and maximum plausible cases. The ventilation ratesfor workers were assumed to be 7 m3/day and 20 m3/day for the average andplausible maximum cases, respectively (EFA 1988). Quantitative information isnot available concerning the inhalation absorption of the chemicals detectedon-site; therefore, a value of 100 percent was used to represent theinhalation absorption factor for these chemicals. GDIs are calculated usingthe equation given for the GDI for inhalation exposure from volatilespresented in Section 5.3.3.

Tables 5-8 through 5-11 summarize the results of the potential exposureand risks due to inhalation of dust. Excess lifetime cancer risks range from2xlO"16 to 2xlO~19 under the average case and 3xlO"12 to IxlO"18 under theplausible maximum case; several orders of magnitude below the 10~6 target risklevel. Hazard indices are less than one for all areas and both exposurecases .

5.5 POTENTIAL EXPOSURES AND RISKS FROM FUTURE USE OF GROUNDWATERPotential risks from future use of groundwater are based on ingestion and

inhalation of volatiles released while showering as the primary routes ofexposure. The duration of this potential future exposure is based on theanalysis given in the EPA Exposure Factors Handbook (1988b) . EPA reviewedhousing census data to estimate the average and upper-bound length of timethat individuals live at a particular residence. They estimate an average(50th percentile) residence time of 9 years, and an upper -bound (90thpercentile) of 30 years. These values are taken as the length of potentialfuture exposure to contaminated groundwater at the Vestal site for the averageand plausible maximum cases. In order to provide a conservative estimate ofrisk, the 9 and 30 year periods are taken as the first 9 and 30 years of life.The average body weight for ages 0 to 9 is taken as 18 kg, and for ages 0 to30 the average is 48 kg (EPA 1988b) . Drinking water ingestion rates are

90

VO

I ABU li -8

P01FN1IAI ESIIMAIf l ) EXPOSURES AND Rl'.icsFROM INHALATION Of DUST BY ON-SI1F WORKERS

ARFA IWELL 1-1 SITE

CHEMICALS fXHlBITINGPOTENTIAL CARCINOGENICEFFECTS

BenzeneBis 2 (ethyl hexyl) phthalate1. 1-Dichloroethane1,1-DichloroethenePCBs (124.')Tetrachlomethene1 . 1 , 2 . 2 - 1 e t rach loroet haneTrichloro.-lheneCarcinogtnic PAHs

TOTAL :

CHEMICALS IXHIBITINGPOTENTIAL H(;!ICARCINOGEN1CEFfECIS

AcetoneBis 2 (elliyl hexyl) phthalate2-Butanom-I.l-Oichloroethane1 ,1-Oichli.roethenel.2-0ichl..roethene (trans)Oi-n-butyl phthalateEthyl ben/enelet rach lui oet hy leneTolueneT richloi oft hy lene1.1, 1 TnUiloethaneXylenesNoncarc iiiri.jenic PAHs

HAZARD INDU

CONCENTRATION

GeometricMean

9.78E-16 9

3.S9E-13 1

CONCENTRATION

GeometricMean

**

I . I IE-14 1t

*

9./8E-16 9ft

I.63E-15 3

I.63E-15 3*

2 28E-I5 11.27E-I2 3

(mg/m3)

Max imiim

.78E-16

.79E-12

(mg/m3)

Max imum

*

ft

.UE-14ft

ft

.78E-16

.26E-15

.26E-I5*

.76E-14

. I2E- I1

' TllRTirC DATlT TNIAKF(CDI) (mq/kq/day)

Average

1 .07E 19

3.93E-I7

CHRONIC 1

PlausibleMax i mum

3.0GF 19

b .6H- l ( j

iAllTTHTAKr

CANCI RPOIENCrt AC TOR

(mg/ky/day) 1

? !1[-0?A *

I .?E»00A A

3.3E--032. OF 014 t>r <n6 1(»00

- •-— - - - - - - --- -(COI) (mg/kg/day)

Average

«tA

9 IIE-17A

ft

B 04E-18

1.34E-17

1 34E-I7ft

1 88E-171.04E 14

PtaiibihleMax iininn

A

A

?. f>OE- l f i**

2 30E 17

7.66E-I7

7 .66F-17A

4.13E If,7 . 3 3 E - B

Rl 1 1 Rf NtlOOSI

(imj/ky/ddy)

A A

* *

H OE-0?1 .01 01

* t

* A

1.0E*00

3 OF -014 OF 01

EXfiSi UPPfR fiOIIND1 IFfllHl ( ANI1R Hl:,K

l'l,iu% ihleAvt*r<i(je Max imum

3. I I -21 M . - J I - 2 I

2.4M6 3.41-l ' j

2f 16 JE-15

... ....... ... ... . . ..... ...

Cl) l :RfO R A T I O

Ptdu-jihleAverage MaMimim

>

* *

1.01. -I1.- 2.91 I1'* A

A t

A *

* *

1.3F 17 7 7 1 - 1 7

' '4 / 1 1 7 1 .01 1'.

11 I1, 41 l'>

~s InhaTdt ion toxicity criteria "were not avaiTabTe"* - Chemii..il not detected in this area.

vO

TABIE 5 M

POTENTIAl ESTIMATED FXI'OSURES AND RISKSFROM INHALA1ION OF OUS1 BY ON-SI1E WORKI MS

ARfA ?WELL 1 I SHE

CHEMICALS EXHIBITINGP01FNTIAL CAKCINOGfNICEFTICTS,

BenzeneBis 2 (elliyl hexyl) phthalate1,1 Oichlni oothane1,1-OtchluioethenePCBsletrachloroethene1.1.2.2-lf trathloroethaneIrichlorot IheneCarcinogenic PAHs

TOIAL:

CONCENIRAIION (mq/m!)

GeometricMean

9.78E-161 30E-I32.93E-1S9.78E-164 89E-142.18E-141.30E-145 58E-142.61E-13

Max imum

3.26E 07? 38E-132.93E-159.78E-161.23E-139 71E-141 30E-I41.6SE-124.89E-13

CONCENTRATION (mg/m3)CHEMICALS EXHIBITINGPOTENTIAL NOHCARCINOGENICEFFEC1S

AcetoneBis 2 (etltyl hexyl) phthalate2-Butanom:1.1 Oichl(,roethane1,1 -Oichlnroethene1,2-Oichloroethene (trans)Di-n-butyl phthalateEthyl ben/imeTetrachloroethy leneTolueneTrichloroethylene1.1, l-TricliloroethaneXylenesNoncarcinogenic PAHs

HAZARD INDEX:

GeometricMean

*

*

8.48E-I52.93E-159.78E-163.85E-142 12E-I42.84E 142.18E-141 70E-I4S.57E-142.25E-146.42E-141.11E-12

Max imum

*2 38E-138 48E-152.93E-I59.78E-161.02E-I3? 12E-145.18E-149.71E-141 08E-131.64E-I23.31E-136.64E-I31 68E-12

CHRONIC DAltY INTAKC(CDI) (imj/kij/.ldy)

Average

1 071 191 . 4 2 E - 1 73 22E-191 07E-19S.36E-I8?.39E 181 43E-186 HE-18? .86E- I /

Pl.HISlblfMax iniiiin

1 0?1 107. 4M I/9 . I9E- I93 . 0 6 E - 1 93.86E- I/3.041 I/4.08E 18S.16E 161 V3E 1 6

" " " THROW CATTY "1 NTAKr "~

CANCERPOUNCY(ALtOR

(mq/ky/day) 1

? 9E-02A A

* 4

1 ? f»00* *

3 3E-03? Of 014 61-036.1E«00

(CDI) (mg/kq/day)

Average

A

A

6 .97E-! /

2 4 IE-178 04E-I83 16E-16I.74E-162.33E-I61 80E-I61 39E-164.58E-161.85E-165.28E-169 HE 15

Pldusih It-Max imum

*5.591 ISI .99E- I66.89E-172 30f - 1 72 39E 1 54 .98E-161.22t IS2.28E 152 53E IS3.86f 147 77t 15I.56E- 143 9SE 14

REFERENCEDOSE

(mg/kg/day)

A A

A ft

9.0E-021 OE-01

A *

A A

1 OE+00* A

3.0E 014.0E-01

• TKCTSS oprrR flOONfr • •i irniMi tANnn RISK

Averriqe

3 11 V\*

A

1.3f -19It

JM-2\2 9E-I92.81 201 . 7 E - I 6

2f 16

CDI:RfO- - - - - -

Averaqe

AA

;. / i - i e2 .4E 10

A

*

*

1 4f 16. *

6 2F ir,1 . 3t IS

.« IS

Pl.iusibleMrix iimim

:r oi - 1 21

*:)./[ -19

*

1 .O t -19H.2E-I9? 4 E - 1 H9.31-16

3t \2

RA110... . . . .Plans ihle

Max imum

A

*

<• ?E i sH.9E-16

*

•

A

2 SI 1 «.

? . (if -14-<.9l 11

/t 1-1

"TTieni i i :al not detected in this areeT= No iiihdlation toxicity criteria were available.

T.iu

TABLE S-IO

POTENTIAL ESTIMATED fXPOSURES AND RISKSFROM INITIATION OF DUST BY ON-S ITE WORKERS

AREA 3WELL l-l SHE


BenzeneBis 2 (ethyl hexyl) phthalate1.1-DichKiroethane1.1-DichluroethenePCBsTetrachloioethene1. t,2,2-IfIrachloroethaneTrichTorot-theneCare inogeti ic PAHs

TOTAL:

CONCENTRATION (mg/m3)

GeometricMean

1 27E- I31.30E-159.78E-16

1.63E-U

Max imum

3 S9E-131.30E 159.78E-16

1.63E-N

CFeiiticaT not detecfecT in"sdfTsT** - No inhalation toxicity criteria were available.NC = Not calculated.

CHRWOATnifiTAkT(COI) (rog/ku/Uay)

P Idiis ibleAverage Maximum

I . 3 9 E - 1 71.43E--191.07E-I9

4 08E3.06E

1919

1 . 7 9 E - I 8 S . I O F 18


AcetoneBis 2 (ethyl hexyl) phthalate2-Butanone1,1-DichloroethaneI.l-Dichloroethenel.2-0ichlnroethene (trans)Di-n-butyl phthalateEthyl ben/eneTetrachloi oethy leneTolueneIrichloincthylene1,1. 1-Tr KhloethaneXylenesNoncarciiMMjenic PAHs

HAZARD INOIX


GeometricMean

6.36E-141.27E-133.26E-151.30E-159.78E-161.30E-15

6.52E-16ft

I.04E-13

Maximum

2.3IE-123 59E-133.91E-151.30E-159 78E-164.24E-15

6.52E-16ft

1 04E-13

CHRONIC DAIIY INTAKE(COI) (mg/kg/day)

Average

5 22E-161 04E-152.68E-171.07E-178.04E-I8I.07E-17

S.36E 18ft

s . s / E - t e

PlausibleMaximum

5.42E-148.42E-159 I9E-173 . 06E 1 72 30E 1 79.95E-17

1 . 5 3 E - I 7A

2 4SI- IS

Fxms UPPflTBOliNDCANItRPOIENC.YFACTOR

(mg/kg/ddy)- 1

?.9f 02A A

I .2F tOOA A

3 3E-032 OE-OI4 6E 036 IE+00

REFERENCEDOSE

(mg/kg/day)

A ft

ft A

9 OE-02l.OE-01

A A

ft ft

ft*

ft A

A*

1 Of +00A A

3.01-014. OF -01

1 IM IIMt (.ANCIR RISK

PlausibleAveiagf MdKimum

1.3 -19

l . l f 17

IE-17

C O I : R f O

Average

A

A

3 OE-161. IE-16

*

A

A

A

A

A

1 . Ht 17A

3 .7 -19

J. I t - 1 7

3E-17

RATIO

PlausibleMaximum

*

A

I .OE-153. If 16

A

A

A

A

A

A

*

41-11)

TABLE 5-11

POTENTIAL ESTIMATED EXPOSURES AMD RISKSFROM INHALATION OF OUST BY ON-SITE UORKIRS

AREA 4WfIL 1-1 SITE

vo


BenzeneBis 2 (ethyl hexyl) phthalate1, 1-0 ich loroe thane1 , 1 -0 ich luroethenePCBsTetrach loroethene1 . 1 ,2.2-TetrachloroethaneTr ich loroetheneCarcinogenic PAHs

TOTAL :


GeometricMean

*

7.50E-143.91E-141.63E-151.63E-I46.52E-I6

*

4.37E-14*

Maximum

*1.23E-I26.06E-141.63E-I51.79E-136.52E-16

ft

2.82E-13*

CHRONIC DAILY INTAKE(CDI) (mg/kg/day)

PlausibleAverage Maximum

* *8.22E-I8 3.86E 164.29E-18 1.90E 171.79E-19 5. IDE 191 79E-I8 5.61E 177.I5E-20 2.04E-19

ft *

4.79E-18 8 82E-17* «

CANCERPOTENCYFACTOR

(mg/kg/day) 1

2.9E 02**

* ft .-

1.2E+00ft*

3.3E 032.0E-014.6E-036.1E+00

EXCESS UPPER BOUND "LIFfTIMf CANCIR RISK


A A

* A

2. IE-19 6. It-19* ft

2 4E-22 6.7E-22* ft

2.2E-20 4. IE-19ft *

2E-19 IE-18


AcetoneBis 2 (ethyl hexyl) phthalate2-Butanone1,1-Oichloroethane1,1-Dichloroethene1,2-D ich loroethene (trans)Di-n-butyl phthalateEthyl ben/eneTet rach loroethy leneTolueneTrich loroethy lene1 , 1 , 1 -Tr ichloethaneXylenesNoncarcinogenic PAHs

HAZARD INDEX:


GeometricMean

4.51E-137.50E-14

*

3.9IE-141.63E-15*

**

6.52E-16*4.37E-145.I5E-14*6.52E-14

Maximum

4.I9E-I21.23E-12

*

6.06E-I41.63E-I5* ,

**

6.52E-16*

2.B2E-137.04E-14

•*

7.50E-14

CHRONIC DAILY INTAKE(COI) (mg/kg/day)

PlausibleAverage Max imum

3.70E-15 9.84E-146.16E-16 2.90E-14* *3.22E-16 I.42E 151.34E-17 3.83E-17

ft *

* ft

* *

5.36E-18 1.53E 17ft *

3.59E-16 6.61E-I54.23E-16 1.65C-15

ft ft

5.36E-I6 1.76E-15

REFERENCEDOSE

(mg/kg/day)

ft*

ft*

9.0E-02l.OE 01ft*

**

* ft

ftft

ftft

l.OC+00

3 OE-014.0E-01**

CDI:RfD RATIO


3.2 -15 14 -14

1.4 15 5.5 15

bt-l1! 21-14

Inhalalion toxicity criteria Mere not available.* Chemical not detected in this area.

Uttt LUU

assumed to be 1.4 liters/day and 2 liters/day (average and plausible maximum)as given in EPA (1988b).

The chronic daily intake for ingestion of groundwater is given by

(CwUIRUEWYR)CDIinMStion - (BW)(DY)(AVG)

where

CD1ing««tion " chronic daily intake (mg/kg/day)',

Cw - concentration of chemical in groundwater (mg/liter);

IR - drinking water ingestion rate (liters/day);

E - frequency of exposure (days/year);

YR - duration of exposure (years).

The remaining terms are as defined in previous equations. In evaluatingnoncarcinogens, the averaging periods (AVG) are 9 and 30 years. This resultsin the greater exposure during the 9-year period when the ratio of ingestionrate to body weight is highest; i.e., (1.4 liters/day)/(18 kg) is greater than(2 liters per day)/(48 kg). Therefore, the 9-year exposure period representsthe plausible maximum case and the 30-year exposure represents the averagecase. However, in evaluating carcinogens the exposures are averaged over afull 75-year lifetime. This results in a lower CDI for the 9-year exposure.Therefore, the 9-year exposure represents the average case and the 30-yearexposure represents the plausible maximum case for carcinogens.

A model developed by Foster and Chrostowski (1987) was used to estimateinhalation exposure from showering. Inhalation exposures to volatile organicchemicals (VOCs) are modeled by estimating the rate of chemical release intothe air (generation rate), the buildup (shower on) and decay (shower off) ofVOCs in shower room air, and the quantity of airborne VOCs inhaled while theshower is both on and off.

95

U^ " Estimation of the VOC release into the air is based upon Liss andSlater's (1974) adaptation of the two-film gas-liquid mass transfer theory,

s The two-film boundary theory provides the basis for estimating the overallmass transfer coefficient (KL) for each VOC according to the followingequation:

KL - (1/ki + RT/Hkg)'1

where -KL - overall mass transfer coefficient (cm/hr);H - Henry's Law constant (atm-m3/>aol-K);RT - 2.4xlO"2 atm-m3/niole (gas constant of 8.2xlO~5 atm-m3/n»ol-K times

absolute temperature of 293 K)

kg - gas-film mass transfer coefficient (cm/hr); and

ki - liquid-film mass transfer coefficient (cm/hr).

The above equation describes the mass transfer rate of a compound at andair-water interface where diffusion may be limited by both liquid- and gas-phase resistances. Typical values of kL (20 cm/hr) and kg (3,000 cm/hr),

<-̂ which have been measured for C02 and H20, respectively, were used to estimateVOC-specific values for these parameters:

kg(VOC) - kg(H20)(18/MWvoe)°-5

kx(VOC) - k1(C02)(44/MWvoc)°'5

where Mtf - molecular weight (g/mol).

The mass transfer coefficient, KL, is adjusted to the shower watertemperature, T,, according to a semi-imperical equation developed to estimatethe effect of temperature on oxygen mass-transfer rate (0'Connor and Dobbins1956):

K.L -

'.OSJ

96

whereK^ - adjusted overall mass transfer coefficient (cm/hr) ;Tx - calibration water temperature pf KL (K) ;Ts - shower water temperature (K) ;ux - water viscosity at Tx (cp) ; andus - water viscosity at T, (cp) .The concentration leaving the shower droplet, C,̂ , is obtained from an

integrated rate equation based on a mass -balance approach: ...Cwd - CHO(l-exp[-K.It§/60d])

whereC^ - concentration leaving shower droplet after time t, (/ig/liter) ;Cw0 — shower water concentration (/jg/liter) ;d - shower droplet diameter (mm) ; andts - shower droplet time (sec) .The term K^/eOd combines both the rate transfer and the available

interfacial area across which volatilization can occur. The value l/60dequals the specific interfacial area, 6/d, for a spherical shower droplet ofdiameter d multiplied by conversion factors (hr/3600 sec and 10 mm/cm) .

The VOC generation rate in the shower room, S, can then be calculated bythe equation

S - Cwd(Fr)/SVwhere

S - indoor VOC generation rate (/*g/m3-min) ;Fr - shower water flow rate (liter/min) ; andSV - shower room air volume (m3).A one -box indoor air pollution model was used to estimate VOC air

concentrations in the shower room. This model can be expressed as adifferential equation describing the rate of change of the indoor pollutantconcentration with time:

dC./dt - RC. + S

97

whereCa - indoor VOC air concentration (/ig/m3) ; andR - air exchange rate (min"1) .When the above equation is integrated, the time dependent indoor

concentration can be estimated as follows:Ca(t) - (S/R)(1 - exp[-Rt]) for t < Ds

andCa(t) - (S/R(exp[RDJ -l)exp(-Rt) for t > D,

whereCa(t) - indoor air VOC concentration at time t (/jg/m3) ;D8 - shower duration (min) ; andt - time (min) .The inhalation exposure per shower can then be calculated according to

the equation

Einh - [VR/(BW)(106)] / C,(t)dt0

whereEinh — inhalation exposure per shower (mg/kg/shower) ;VR - ventilation rate (liter/min);BW - body weight (kg) ; andDt - total duration in shower room (min) .This equation can be solved as:

E«h - (Vr)(S)/[(BW)(R)(106)][D, + exp(-RDt)/R - exp[R(D. - Dt)]/R]

For both the duration of the shower and the duration in the room after theshower is turned off. Assuming one shower per day, the inhalation exposure ^per shower (Einh) is equal to the chronic daily intake for showering. r*

Although children ages 0 to 9 are likely to shower less than adults, the -,shower model is used to represent inhalation exposures from bathing. -*

98

Table 5-12 lists the input parameters to the shower model.Table 5-13 to 5-16 give the GDIs and combined excess lifetime cancer

risks and Hazard Indices for exposure via ingestion and showering for theestimated groundwater concentrations for each of the four source areas. Thetables show that the upper-bound excess lifetime cancer risks for exposuredirectly below the source areas range from 8xlO~6 to 4xlO~8 for the averagecases and 4xlO~4 to 2xlO~6 for the plausible maximum cases.

Chemicals contributing to the risk levels greater than 10"6 for exposuredirectly below the source area are carcinogenic FAHs in Area 1, chloroform,1,1-DCA, 1,1-DCE, PCBs, 1,1,2,2-tetrachloroethane (PCA) tetrachloroethylene(PCE), and trichloroethylene (TCE) in Area 2, 1,1-DCA and 1,1-DCE in Area 3,and 1,1-DCA, 1,1-DCE, TCE, and PCBs in Area 4. The uncertainties noted inSection 5.3 with respect to 1,1-DCE apply to 1,1-DCE, 1,1-DCA, PCBs, and PCAunder these exposures as well. All of the chemicals were detectedinfrequently. Therefore, there is significant uncertainty as to theconcentrations present. As noted in Section 3.0, the shape and size chosenfor the source areas also effects the predicted groundwater concentrations andrisks. The volatiles 1,1-DCE, 1,1-DCA, PCA, PCE, TCE are highly mobile andhave relatively high cancer potency factors. This results in relatively highrisk under the assumed conditions of exposure.

For source areas 2 and 4 and under the plausible maximum case only excesslifetime cancer risks for exposure at the well field exceed the 10*6 level.Two exposure cases—the plausible maximum case for exposure to groundwaterdirectly below Areas 2 and 4—result in hazard indices greater than one. Theindividual CDI:RfD ratio for TCE exceeds one in Area 2 as do the individualCDI:RfD ratios for acetone and TCE in Area 4.

5.6 EVALUATION OF INORGANICS DETECTED IN MONITORING WELLSTable 5-17 presents a quantitative assessment of the geometric mean and

maximum concentrations of inorganics detected in the monitoring wells. Theconcentrations are evaluated in terms of a drinking water exposure using thesame assumptions presented in Section 5.5. The table shows that the excess

99

TABLE 5-12

PARAMETERS USED IN THE SHOWER MODEL

PARAMETER

Snowe" flow rate, liters/mm

Shower 'oom air volume. m3

Mass transfer coefficient calibrationtemperature. (T1). K

Shower water temperature (Ts), K

Water viscosity at Tl, cp

Water viscosity at Ts. cpShower droplet diameter, im

Shower droplet time, sec

Shower duration, min

Total duration in shower room, mm

Body weight. Kg0 - 9 years0-30 years

Breathing rate. m3/day0 - 9 years0 - 3 0 years

(a) EPA (1988).

(b) Default values.

VALUE

38 (a)

6 (b)

298 (b)

319 (b)

0.898 (b)

0.602 (b)

1 (b)2 (b)

10 (b)

15 (b)

18 (a)48 (a)

24 (a)14 (a)

y\

100

lABIt 5-1.1POttNttAL EXPOSURES AND RISKS FROM FIIIUHE U5t OF GROUNDWAItR

AREA IVEStAI. WELL 1-1 SHE


BenzeneChloroforml.l-OlchloroethaneI.l-Dlchloroethylene1 . 1 .2, 2-TetrachloroethaneTetrachloroethyleneTrlchloroethyleneBls(2-ethylhexyl)phthalateCarcinogenic PAHsPCB

CHRONIC DAILY INTAKE FROM INGEST IONEXPOSURE DIRECTLY EXPOSURE ATBELOW SOURCE AREA THE WELL FIELDAverage Case

(mg/kg/d)

3.03E-07

I.68E-09ft

PlausibleMaximum Case(mg/kg/d)

S.35E-06

I.48E-07*

Average Case(mg/kg/d)

3.03E 09

1.68E 11ft


5.35E-08

I.48E-09ft

CHRONIC DAILY INTAKE FROM INGEST IONEXPOSURE DIRECTLY


M ——————————————————O Acetone" 2-Butanone

Chloroforml.l-OlchloroethaneI.l-Slchloroethylenetrans-1 ,2-DlchloroethyteneEthyl benzenetetrachloroethyleneTolueneI.l.l-TrlchloroethaneTr IchtoroethyleneXyleneBls(2-ethylhexyl)Dhtha1ateDl-n-butylphthalateNoncarclnogenlc PAHsChromiumCopper

BELOW SOURCE

Average Case

(mg/kg/d)

*

2.62E-04***

1.90E-068.50E-07*6.25E-07

•ft

*

1.09E-06*

*

1.55E-043.65E-05*

AREA


ft

S.21E-03**

*

3.52E-056.9U-05*2.30E-05

ft

*

1.56E-04**

7.04E-02S.72E-04

ft

EXPOSURE ATTHE WELL


*

2.82E-06*

*

*

I.90E-088.SOE-09*6.25E-09

ft

ft

1.09E-08**

l.SSE-063.65E-07*

FIELD


,5.2IE-05

ft

*

*

3.52E-076.91E-07*2.30E-07«*

1.56E-06**

7.04E-046.72E-06*

CHRONIC DAILY INTAKE FROM SHOWERINGEXPOSURE DIRECTLY EXPOSURE AT

ORAL BEIOV SOURCE AREA THE WELL MHOCANCER - - - - •POTENCY Average CaseFACTOR(nx,/kg/d) (mg/kg/d)

2.90E-02 3.57E-076.IOE 039 IOE-026.00E-012.00E-015 IOE-021.10E-021 .40E-021.1SE»OI 2.78E-157.70E*00 *

PlausibleMaximum Case

(mq/kg/d)

6 40E Ofi

2.49F-I.1•

Average Case

(mq/kg/d)

3.57E-09

2.78E-17ft

PlausibleMax imum Case(mq/kg/d)

6. JOE -08

2.49E-1Sft

ORAL CHRONIC DAILY INTAKE FROM SHOWERINGREFERENCE EXPOSURE DIRECTLYDOSE BELOW SOURCE

(mg/kg/d)-lAverage Case(mg/kg/d)

I.OOE-01 •5.00E-OZ 5.02E-OS1. OOE-02 'I.OOE-01 *9.00E-03 *2 OOE-02 5.01E-07l.OOE-01 2.23E-071. OOE-02 *3.00E-01 I.64E-079. OOE-02 "7.35C-03 *2.00E»00 2.87E-072. OOE-02 *l.OOE-01 •4.00E-01 4.05E-05S.OOE-03 NA3.70E-02 NA

AREA


*2.29E-06***

2.28E-084.48E-08

ft

1.50E-Q8**

l.OIE-07ft

ft

4.S3E-05NANA

EXPOSURE ATTHE WELL

Average Case

(mg/kg/d)

ft

5.02E-07ft

ft

ft

5.01E 092.Z3E-09tI.64E-09*

ft

2.87E-09ft

ft

4.05E-07NANA

FIELD


*2.29E-08***

2.28E-IO4.48E-10*1.50E-IO**

1.01E-09*

ft

4.53E-07NANA

COMBINED EXCESS UPPER-BOUND LIFETIME CANCER RISK

INHALATION EXPOSURE DIRECTLY EXPOSURE ATraurro nrtnu cnmrf ADtA Tur uri i cirinLKnLtK BllUW ;»UUKLt W(tRPOTENCY —----...-.-.---- —— ---FACTOR Average Case Plausible(mg/kg/d) Maximum Case

2.90E-02 I.9IE-OB 3 4 IE -078. IDE -02**I.20E»002.00E-013.30E-03.4.60E-03

A*

6.IOE«00 1.93E-08 1.70E-06** * *

TOTAL: 4E-08 2E-OB

Average Case

1 9IE-IO

1 93E-10ft

4E-10


3.41E-09

I.JOE -08*2E-08

INHALATION COMBINED COI:RFD RATIOREFERENCEDOSE EXPOSURE DIRECTLY

(mg/kg/d) -1 BELOW SOURCE AREA


** * *9. OOE-02 6.21E-03 I.04E-01** * *l.OOE-01 * *ft* * ft

** 9.52E-OS 1.76E-03*» 8.50E-OS 6.9IE-04ft* ft ft

1 OOE*00 2.2SE-06 7.68E-OS3.00E-OI « *ft* * ft

4.00E-0! I.26E-06 7.80E-05ft* • ••* * *" 3.89E-04 I.76E-01NA 7.29E-03 1.34E-OINA

HAZARD INDEX: 1.4E-02 4.2E-01

EXPOSURE ATTHE WELL FIELD

Average Case

«6.21E-05

ft

*

*

9.52E-078.SOE-08

ft

2.25E-08ft

ft

1.26E-08ft

ft

3.89E-067.29E-05

ft

1.4E-04


*1.04E-03

Aftft

I.76E-056.9IE-06

ft

7.68E-07ft

ft

7.80E-07*

I.76E 03I.34E-03

ft

4 2E-03

** No Inhalation criteria available for this chemical.NA - Showering exposure not applicable for Inorganics.

LOO

OrO

TABLE 5-14POTENTIAL EXPOSURES AND RISKS FROM FUTURE USE OF GROUNDWATER


CHRONIC DAILY INTAKE FROM INGESTIONEXPOSURE OIRECILY

CHEMICALS EXHIBITINGPOIENTIAL CARCINOGENICEFPfCIS

BenzeneChloroform1.1-Olchloroethane1,1-0 ten loroethyleneI , I . 2. 2-TetrachloroethaneTetrachloroethyleneTrtch loroethylene6ls(2-ethylhexyl)phthalateCarcinogenic PAHsPCS

BELOW SOURCE

Average Case

(mg/kg/d)

3.03E-07I.33E-062.52E-OS3.87E-072.85E-06I.54E-061.14E-053.84E-08I.22E-092.00E-07

AREA

PlaustbleMaximum Case(mj/kg/d)

5.35E-062.35E-054.43E-056.83E-065.02E-05I.2IE-04S.93E-031.24E-064.03E-088.8BE-06



(mg/kg/d) (mg/kg/d>

3.03E-09 5.35E-08I.33E-08 2.3SE-072.52E-08 4.43E-073.87E-09 6.83E-082.85E-08 5.02E-07I.S4E-08 I.21E-06I.14E-07 5.93E-053.84E-10 1.24E-081.22E-11 4.03E-102.00E-09 8.88E-08

CHRONIC DAILY INTAKE FROM INGESTIONEXPOSURE DIRECTLY

CHEH1CALS EXHIBITINGPOTENTIAL NONCARC1NOGEN1CEFFECTS

Acetone2-ButanoneChloroform1,1-Otchloroethanel.l-Dtchloroethylenetr«nj-l.2-DlchloroethyleneEthyl benzeneTet r«ch loroet hy leneToluenel.l.l-THchloroethantTrtch loroethyleneXyTeneBis(2-ethylhexyl)phthalateOI-n-butyTphthatateNoncarctnogentc PAHsChromiumCopper

BELOW SOURCE


•2.I6E-04S.96E-06I.12E-05I.73E-OB7.SOE-OSI.48E-056.87E-06S.50E-061.8SE-OS5.06E-053.08E-OS1.71E-071.7SE-06I.35€-M7.I2E-OS3.69E-05

AREA

PlausibleMaxim*! Case(mg/kg/d)

*3.98E-031. IDE -042.07E-043.19E-053.66E-034.99E-04S.6SE-047.60E-041.93E-032.77E-02S.86E-03S.77E-063.23E-OS3.80E-03I.3IE-036.8IE-04


Average CASH PlAusiblcMaxima* Case

(mg/kg/d) (mg/kg/d)

* *2.16EO6 3.96E-055.96E-08 1. IDE -061.12E-07 2.07E-061.73E-08 3.19E-077.SOE-07 3.66E-OSI.48E-07 4.99E-066.88E-OR S.6SE-066.50E-08 7.60E-061.85E-07 I.93E-OS5.08E-07 2.77E-043.0BE-07 S.86E-OSI.7IE-09 5.77E-08I.7SE-08 3.23E-07I.35E-06 3.80E-OS7.I2E-07 1.3IE-053.69E-07 6.81E-06

CHRONIC DAILY INTAKE FROM SHOWERINGEXPOSURE DIRECUY

ORALCANCERPOTENCYFACTOR(mg/kg/d)

2.90E-026.IOE-039.10E-026.00E-012.00E-015.IOE-021.10E-02I.40E-021.15E+017.70E«00

ORALREFERENCEDOSE

(mg/kg/dH

l.OOE-Ot5.00E-02l.OOE-02l.OOE-019.00E-032.00E-02l.OOE-01l.OOE-023. ODE -019.00E-027.35E-032. ODE tOO2.00E-02l.OOE-014.00E-015.00E-033.70E-02

BEIOW SOURCE

Average Case

(mg/kg/d)

3.57E-071.56E-062.96E-064.55E-073.10E-06I.79E-061.33E-052.23E-102.02E-15I.89E-07

ARFA


6.40E-062.80E-055.29E-058.17E-065.57E-OS1.43E-047.06E-037.32E-096.79E-148.54E-06

COMBINED EXCESS UPPER-BOUND LIFETIME CANCER RISKEXPOSURE AT

THE WELL

Average Case

(mg/kg/d)

3.57E-091.56E-082.96E-084.55E-093.10E-Q81.79E-081.33E-072.23E-122.02E-17I.89E-09

FIELD


6.40E-082.80E-075.29E-078.17E-085.57E-071.43E-067.06E-057.32E-116.79E-168.54E-08

CHRONIC DAILY INTAKE FROM SHOWERINGEXPOSURE DIRECTLYBELOW SOURCE

AvsrflQQ Cflse

(mg/kg/d)

ft

3.84E-OS1.S6E-062.96E-064.55E-071.97E-053.88E-06I.79E-06I.7IE-064.84E-061.33E-058.07E-062.23E-107.91E-093.53E-05NANA

AREA


«6.90E-042.80E-OS5.30E-058.17E-069.36E-04.28E-04.43E-04.9SE-04.92E-04.06E-031.50E-037.32E-091.42E-079.64E-04NANA

EXPOSURE ATTHE WELL


«3.84E-071.S6E-OB2.96E-084.SSE-091.97E-073.88E-081.79E-081.71E-084.84E-OB1.33E-078.07E-082.23E-127.9IE-1I3.53E-07NANA

FIELD

PlaustbleMaximum Case(mg/kg/d)

*6.90E-062.80E-07S.30E-078.17E-089.36E-061.28E-061.43E-OB1.9SE-064.92E-OS7.06E-OSi.SOE-OS7.32E-111.42E-099.64E-06NANA

INHALATIONCANCERPOTENCYFACTOR(mg/kg/d)

2.90E-028.10E-02ft*

I.20E+002.00E-013.30E-034.60E-03ft*

6.10E+00**

TOTAL:


(mg/kg/d)-!

•»9.00E-02

l!JoE-01•ft

ft*

ft*

l.OOt+003.00E-01**4.00E-01**••*•NANA

HAZARD INDEX

EXPOSURE DIRECTLYBELOW SOURCE AREA

Average Case PlausibleMax imum Case

I.9IE 08 3.4IE-071.34E-07 2.41E-062.29E-07 4 03E-OB7.78E-07 I.39E-OS1.19E-06 2.12E-058.44E-OB 6.6SE-061.86E-07 9.77E-055.37E-IO 1.73E-081.41E-08 4.64E-071.S4E-06 6.84E-OS

4E-OS 2E-04



I.91E-10 3.41E-09I.34E-09 2.41E-082.29E-09 4.03E-087.78E-09 1.391 O/1.19E-08 2.IZE-078.44E-10 6.6SE-081.86E-09 9.7/E 075.37E-I2 1 73E-10I.41E-10 4.64E-091.S4E-OB 6.84E 07

4E-08 2E-06

COMBINED COIiRFO RATIO


Average Case PlausibleMax imum Case

* *4.74E-03 B.73E-025.96E-04 1 10E-021.42E-04 2.60E-031.92E-04 3.S4E-033.75E-03 I.B3E-011.48E-04 4.99E-036 87E-04 S.6SE-022.34E-05 2.73E-032.22E-04 2.31E-02G.92E-03 3.77E«003.S6E-OS 6.68E-038.56E-06 2.89E-041.75E-05 3.23E-043.39E-04 9.49E-03I.42E-02 2.63E-OI9.98E-04 1.84E-02

: 3.3E-02 4.4E»00



* •4.74E-05 8.73E 045.96E-06 I.IOE-041.42E-06 2.60E-051.92E-06 3 54E-053.75E-05 1 83E-031.48E-06 4.99E-056.88E-OB 5.65E 042.34E-07 2 73E-052.22E-06 2.3IE 046.92E-OS 3.77E 02.56E-07 6.68E 05.S6E-OB i .89E-OB.75E-07 3.23E-06.39E-06 9 49E-05.42E-04 2.63E-0.1

9.98E-06 1.84E-04

3.3E-04 4.4E-0?

Chemical not detected In this area." No Inhalation criteria available for this chemical.NA - Shmering exposure not applicable for inorganics.

LUU

TABLE 5-15POTENTIAL EXPOSURES AND RISKS FROM FUTURE USE Ul GROUNOWATtR

AREA 3VESTAL Will l-l SHE

CHEMICALS EXHIBITINGPdfl NI IJtl rioriMfyitmrrun. n i int. LWiLf nuutniLtFFtCIS

BenreneChloroforml.l-0lchloroeth«ne1.1-Oichloroekhylene1 , 1 ,2.2-TetrachloroethaneTet rach toroethy teneTrichloroethyleneB!s(2-ethylhexyl)phthatateCarcinogenic PAHsPCB

CHRONIC DAILY INTAKE FROM INGESTIONEXPOSURE DIRECTLY EXPOSURE ATBELOW SOURCE AREA THE WELL FIELD


(mg/kg/d) (mg/kg/d)

* ** «

1.54E-06 2.70E-OS5.33E-07 9.35E-06* «

• ** «

5.15E-08 2.SSE-061.05E-IO 1.85E-09* *

Average Case

(mg/kg/d)

*

*

1.54E-085.33E-09A

**

5.ISE-IO1.05E-1Z

*


(i»g/kg/d)

*

*

^.70E-079.35E-08«

**

2.55E-08I.85E-11*

CHRONIC DAILY INTAKE FROM INGESTION


Acetone2-ButanoneChloroformI.l-Olchloroethanel.l-Oichloroethylenetrans-l,Z-Olch loroethy leneEthyl benieneTet rach loroethy leneToluenel.l.l-TrlchloroethaneI r Ich loroethy ternXyleneBls(2-ethylhexyl)phthalateDl-n-butylphthalateNoncarclnogenlc PAHsChromiumCopper



(mg/kg/d) (ng/kg/d)

4.S8E-03 3.ME-021. HE-04 2.5ZE-03

* *

6.87E-06 I.26E-042.3BE-06 4.36E-OS3.49E-06 2.08E-04

6. 9E-07 1. 4E-OS

Z.30E-07 1.J9E-OS* *

I.75E-05 3.22E-041.92E-05 S.44E-041.70E-OS 3.12E-04

EXPOSURE ATTHE WELL

Average Case

(mg/kg/d)

4.58E-051.14E-06

*

6.88E-OB2.38E-083.49E-OB

6. 9E-09

Z.30E-09*

I.7SE-071.92E-071.70E-07

FIELD

PlausibleMaxim* Case

(ng/kg/d)

3.04E-042.52E-05

ft

1.26E-064.36E-072.08E-06

1. 4E-07

1.I9E-07*

3.22C-OBS.44E-063.12E-06

CHRONIC DAILY INTAKE FROM SHOWERINGEXPOSURE DIRfCtLY EXPOSURE AT

ORAL BELOW SOURCf AREA THE WELL FIELDCANCER --- - ----..._ , . - - -POIENCY Average Case PlausibleFACIOR H.i«\mm Case

(mq/kg/d) (moA<)/H) (mq/kq/ri)

2.90E-02 • *6.IOE-03 * *9.IOE-02 I.8IE-06 3.22E-056.00E-OI 6.26E-07 I.I2E-052.00E-OI * '5. IDE -02I.IOE-021.40E-02 3.00E-10 1.5IE-08I.15E»01 1.73E-I6 3.11E-157.70E+00 * *

Average Case

(mg/kg/d)

ft

ft

1.81E-086.Z6E-09

**A

3.00E-I21.73E-18*


<m,/kg/d)

ft

ft

3.??E-071.12E-07

***

1.5IE-103.IIE-17

ft

ORAL CHRONIC DAILY INTAKE FROM SHOWERINGREFERENCE EXPOSURE DIRECTLY

DOSE BELOW SOURCE AREA(mg/kg/dH --—— — ——-— —


(mg/kg/d) (mg/kg/d)

l.OOE-OI 7.35E-04 4.75E-035. DOE-02 2.03E-OS 4.36E-04I.OOE-02 * *I.OOE-01 l.BIE-06 3.22E-OS9.00E-03 6.26E-07 1.12E-052.00E-02 9.I8E-07 5.34E-051. OOE -01l.OOE-023. OOE -019.00E-02 1. 8E-07 3. 7E-067.35E-032. OOE +002. OOE -02 3 OOE -10 1.51E-08I.OOE-OI O.OOEiOO 0. OOE tOO4. OOE -01 4.57E-06 8.18E-OS5. OOE -03 NA NA3.70E-02 NA NA

EXPOSURE ATTHE WELL

Average Case

(mg/kg/d)

7.35E-062.03E-07

ft

1.8IE-086.26E-099.18E-09

1. 8E-09

3.00E-120. OOE tOO4.57E-08

NANA

FIELD


(mg/kg/d)

4.75E-054.36E-06

*

3.22E-071.12E-075.34E-07

3. 7E-08

1.51E-10O.OOE'OO8.I8E-07

NAHA

INHALATIONCANCERPOTENCYFACTOR

(mg/kg/d)

2.90E-028.IOE-02

ftft

I.20E4002.00E-013.30E-034.60E-03»*6.IO£«00

ft*

TOTAL:

INHALATIONREFERENCE

DOSE{•xj/kg/d)-I

**

9. DOE-0?**i.ooe-oi********

1. OOE tOO3.00E-01ft*

4.00E-01*•**••MANA

HAZARD INDEX

COMBINED EXCESS UPPER-BOUND LIFETIME CANCFR RISK

EXPOSURE DIRECTLY EXPOSURE ATBELOW SOURCE *°e* Tuf ufii nrin

Average Case

**

1.40E-071.07E-06*

**

7.21E-101.20E-09

ft

IE-06

nni.rt


ft

*

2.46E-061.90E-OS

ft

ft

*

3.57E-082.I3E-08«

2E-05

COMBINED CD!

EXPOSURE DIRECTLYBELOW SOURCE ™"

Average Case

4.58E-022.51E-03

*

8 68E-052.64E-041.7SE-04

8. 4E-06

1.15E-05*4.39E-OS3.84E-034.S9E-04

S.3E-02

nnt.n


3.04E-015.52E-02

ft

1.58E-034.8SE-031.04E-02

1. 9E-04

S.9SE-04*

8.0SE-041.09E-018.43E-03

5.0E-01

Average Case

*•

I.40E-091.07E-08

*

*

*

7.2IE-I21.20E-1I*

IE-08

RFD RATIO


•*

2.46E-08I.90E-07

*ft

ft

3 57E-IO2.13E-IO

ft

2E-07


Average Case

4.SSE-042.51E-05

ft

8.68E-072.64E-061.75E-06

8. 4E-08

I.15E-07*

4.39E-073.84E-054.59E-D6

5.3E-04


3.04E-035.52E-04*1.S8E-054.85E-051.04E-04

1. 9E-06

5.95E-06ft

8.05E-06I.09E-038.43E-OS

5.0E-03

" No Inhalation criteria available for this chemical.NA - Showering exposure not applicable for Inorganics.

ott't

TABLE 5-16POItNTIAL EXPOSURES AND RISKS FROM FUTURF USE OF GROUNDWATER

AREA 4VESTAL WflL 1-1 SHE

CHRONIC DAILY INTAKE FROM INGES1ION


BenzeneCh lorof orm1,1-Dichloroethane1,1-DlchloroethyleneI,l.2.2-TetrachloroethaneTe t rach loroethy leneTrichloroethyleneBts(2-ethylhexyl)phthalateCarcinogenic PAHsPCB

EXPOSURE DIRECTLYBELOW SOURCE

Average Case

(mg/kg/d)

*

*

5.60E-05I.07E-06*7.69E-081.49E-053.69E-08

*

I.I IE-07

AREA


(mg/kg/d)

ft

*

.52E-03

.88E-05*

.35E-06

.68E-03

.06E-05ft

2.13E-05

EXPOSURE ATTHE WELL

Average Case

(mg/kg/d)

ft

*

5.60E-071.07E-08*7.69E-101.49E-073.69E-IO

*

I.IIE-09

FIELD


(mg/kg/d)

ft

*

.52E-05

.SSE-O;*

.35E-08

.68E-OS.OGE-O;ft

2.13E-07

CHRONIC DART INTAKE FROM IN6ESTIONEXPOSURE DIRECTLT


Acetone2-ButanoneCh lorof or*I.l-Dlchloroethane1,1-Olch loroethy lenetrans-1. 2-0 leh loroethy teneEthyl benzeneTetrachloroethyleneToluene1 , 1 . l-Tr IchtoroethaneTrtchloroethyleneXylene8is(2-ethylhexy Mphtha lateOt-n-butylphthalateNoncarclnogenlc PAHsChromiumCopper

BELOW SOURCE

Average Case

(mg/kg/d)

3.92E-02*

*

2.50E-M4.79E-Q6*

*3.43E-0;*6.50C-OS6.6/E-05*I.6SC-0?*1.33E-OSS.08E-051.23E-04

AREA


tmg/kg/d)

6.68E*00**

7.09E-038.79E-OS*

*6.2SE-06

•

I.63E-037.86E-03

•

4.9SE-OS*

2.80E 049.26E-042.26E-03

EXPOSURE ATTHE WELL

Average Case

(•n/kg/d)

3.92E-04*

*

?.5W-064.79E-08*

*3.43E-09*6.SOE-076.67E-07

ft

I.6SE-09ft

I.33E-07S.08E-07I.23E-06

FIELD


(•9/kg/d)

6.68E-02**

7.09E-058.79E-07«

*6.28E-08

ft

1.63E-OS7.86E-OS

ft

4.9SE-07ft

2.80E-069.26E-062.26E-05

ORALCANCFRPOTENCYFAC10R

(mg/kg/d)

2.90E-026. IDE -039.10E-026.00E 012 OOE 015.IOE-021.10E 02I.40E 02I.I5E40I7.70E«00

ORALREFERENCE

DOSE(mg/kg/d) -I

I.OOE-015.00E-021. OOE -021. OOE 019.00E-032.00E-02I.OOE-OI1 OOE-0?3.00E-OI9.00E-027.35E-032.00E«-002.00E-02t.OOE-OI4.00E-01S.OOE-033.70E-02

CHRONIC DAILY INIAKF FROM SHOWERINGEXPOSURE OIRECILYBELOW SOURCE

Average Case

(mg/kq/il)

**

6 57E-05I.26E-06

«8.94E-081.74E-052.14E-IO* .I.05E-07

AREA


(mg/kg/d)

*

ft

I.81E-032.25E-05

1.59E-OBZ.OOE-036.28E-08*? 05E-05



(mg/kq/d) (mg/kg/d)

ft ft

ft ft

6.S7E-07 I.8IE-OS1.26E-08 Z 25E-07

ft ft

8.94E-IO 1.S9E-081.74E-07 2.00E-052.14E-I2 6.28E-IO* *I.05E-09 2.05E-07

CHRONIC DAILY INTAKE FROM SHOWERINGEXPOSURE DIRECTLYBELOW SOURCE

Average Case

H/kg/d)

6.30E-03ft

ft

6.57E-05I.26E-06

ft

ft

8.94E-08ft

I.70E-051.74E-05

ft

2.I4E-IO*3.46E-06

NANA

AREA


(mg/kg/d)

1.04E«00ft

ft

I.81E-032.25E-05

ft

ft

I.59E-06*4.14E-042.00E-03

ft

6.28E-08ft

7.I1E-05NANA


Average Case PlauslbteMaximum Case

(mg/kg/d) (mg/kg/d)

6.30E-OS 1.04E-02* A« *

6.S7E-07 I.8IE-05I.26E-08 2.2SE-07* *

* *B.94E-10 1.S9E-OB

ft ft

I.70E-07 4.14E-06I.74E-07 2. DOE -05

ft ft

2.14E-12 6.28E-10ft ft

3.46E-08 7.IIE-07NA NANA NA

INHALATIONCANCERPOTENCYFACTOR

(mg/kg/d)

Z.90E-028.10E-02•*1.20E»002.00E-013.30E-034.6M-03•ft6.IOE400**

TOTAL:

INHALATIONREFERENCE

DOSE(mg/kg/d)-I

4*

9.00C-02ft*l.OOE-OIft*•*•*•*

1.00E«003. ODE -01**4.00E-01***«•«NANA

HAZARD INDEX

COMBINED EXCESS UPPER-BOUND LIFETIME CANCER RISK

EXPOSURE DIRECTLYnri fiu CfilDiT ADFAOClUw aUUKLt flKtU

Average Case PlausibleHflximura Case

* ** *

S.iOC-06 1.38E-042.16E-06 3.83E-OS

ft 4

4.22E-09 7.39E-082.45E-07 2.77E-05S.16E-10 I.48E-07

ft ft

8.SSE-07 I.64E-04

8E-06 4E-04

EXPOSURE AtTHE WELL MELD


* •* *

5.IOE-08 1 38E-062.I6E-08 3.83E-07* *4.22E-I1 7.39E-102.45E-09 2 JJl-Ql5.I6E-12 I.48E-09

ft *

8.55E-09 I.64E-06

8E-08 4E-06

COMBINED CDI :RFO RATIO



3.92E-OI 6 $8E«OI* ft

* *

3.16E-03 8.91E-025.32E-04 9.77E-03* ** *3.43E-OS 6.28E-04* •7.79E-04 I.94E-029.07E-03 I.07E*00• •8.23E-06 2.47E-03* •3.32E-OS 7.00E-04I.02E-02 I.8SE-OI3.33E-03 6.10E-02

4.2E-OI 6.8E»OI


Average Case PlauslbteMaximum Case

3.92E-03 6.68E-OI• ** >

3.I6E-05 8 9IE-04S.32E-06 9.77E-05• •

* *3.43E-07 6.28E-06* *7.79E-06 1.94E 049 07E-05 I.07E-02« *8.23E-08 2.47E-05* ft3.32E-07 7.00E-061.02E-04 1.85E-033.33E-05 6.10E-04

4.2E-03 6.8E 01

' Chemical not detected in this area.** No Inhalation criteria available for this chemical.

NA <* Showering exposure not applicable for Inorganics.

too

TABLE 5-17POTENTIAL EXPOSURES AND RISKS FROM INGESTION OF GROUNOWATER AT CONCENTRATIONS DECTECTED IN MONITORING WELLS



CHRONIC DAILY INTAKE FROM INGESTION

TOTAL DISSOLVED

EXCESS UPPER-BOUND LIFETIME CANCER RISK

TOTAL DISSOLVEDORAL—— CANCER

Average Case Plausible Average Case Plausible POTENCY ———————————————— ————————————————Maximum Case Maximum Case FACTOR Average Case Plausible Average Case Plausible

(mg/kg/d) (mg/kg/d) (mg/kg/d) (mg/kg/d) (mg/kg/d) Maximum Case Maximum Case

Arsenic 6.51E-05 4.82E-04 4.51E-05 2.03E-04 1.75E+00 IE-04 8E-04 8E-05 4E-04

o01


AntimonyArsenicBariumBerylliumChromiumLeadManganeseMercuryNickelThalliumVanadiumZinc

12711483111

.27E-03

.91E-04

.32E-03

.09E-04

.1 IE-03*

.98E-02

.72E-05

.15E-03

.64E-04

.52E-03

.28E-02

4.94E-032.25E-032.59E-011.77E-031.17E-02*

4.00E+001.59E-024.81E-013.89E-045.36E-025.19E-01

1.28E-032.01E-042.57E-033.54E-051.86E-04*9.37E-033.21E-OS9.12E-041.65E-047.49E-044.96E-04

49214

314312

ORALREFERENCEDOSE

(mg/kg/d)-lTOTAL

CDI:RFD RATIO

DISSOLVED


.62E-03

.49E-04

.34E-02

.94E-04

.67E-04*

.22E-01

.65E-02

.S8E-02

.89E-04

.94E-03

.71E-02

4.00E-04l.OOE-035.00E-025.00E-045.00E-03*2.00E-013.00E-042.00E-027.00E-057.00E-032.00E-01

3.18E+002.91E-011.46E-012.18E-012.23E-01*

2.49E-012.91E-011.58E-012.34E+002.18E-016.42E-02

7.4E+00

1.23E+012.25E+005.18E+003.55E+002.33E+00*2.00E+015.29E+012.41E+015.56E+007.66E+002.59E+00

1.4E+02


3.19E+002.01E-015.14E-027.08E-023.72E-02*4.69E-021.07E-014.56E-022.36E+001.07E-012.48E-03

6.2E+00

1.15E+019.49E-014.68E-013.89E-019.33E-02*

1.61E+005.50E+012.29E+005.56E+002.78E-011.35E-01

7.8E+01

See report text for assessment of lead via uptake blokinetic model.

tUU

"% " lifetime cancer risk from exposure to arsenic at the listed concentrationsranges from 8x10"* to 8xlO~5. Hazard indices for all cases (average andplausible maximum for total and dissolved concentrations) are greater thanone. For the geometric mean total concentrations, antimony and thallium showCDl:RfD ratios greater than one. All of the inorganics have CDI:RfD ratiosgreater than one under the plausible maximum case for total concentrations.For the dissolved concentrations, the geometric mean concentrations ofantimony and thallium result in GDI:RfD ratios greater than one. Exposure atlevels corresponding to the maximum dissolved concentrations results inCDI:RfD ratios greater than one for antimony, manganese, mercury, nickel andthallium.

The average case results presented for this exposure are based on thegeometric mean concentrations of all samples. Since the inorganiccontamination is widely scattered throughout the site and does not show anydiscernable pattern, no adjustments have been made based on known or potentialsource areas.

5.6.1 Risk Evaluation for Lead Exposure to Young ChildrenThe CDI:RfD ratio approach used above may not provide the most accurate

assessment of potential risks associated with exposure to lead. Chronichealth effects associated with lead exposure have been related to elevatedlead concentrations in the blood. As a result of recent toxicological and

1epidemiologic research, the blood lead concentrations considered to pose apublic health risk have been decreased substantially, a fact that is not yetreflected in the RfD values published by EPA. For these reasons risksassociated specifically with lead have been analyzed based on subchronic(i.e., less than lifetime) exposures to young children. This lead assessmentshould provide a more accurate characterization of risks from lead. Anotherlimitation to the GDI:RfD approach used in Section 5.6 is that it does notconsider background contributions to blood lead levels. Furtherinvestigations have indicated that the adverse effects of lead are dependentupon the age of the exposed individual. Since background exposures to lead

106

are highly variable, the same daily dose in mg/kg/day may have differenteffects on individuals of different ages. Therefore, measures of total leadin the body (via blood lead levels [PbBJ) are believed to be more accuratecorrelates of the potential effects of lead than are average daily exposure .levels (in mgAg/day) (EPA 1989d).

The Centers for Disease Control (CDC 1985) considers a blood lead levelof 25 pg/dl to represent toxic levels. However, several more recent studiessuggest that much lower levels, in the 10-15 pg/dl range, may be of publichealth concern (EPA 1986k). Some of the most recent research results(Eellinger et al. 1987) indicate that umbilical blood lead levels >10 Mg/dlmay be associated with an adverse impact on cognitive development in infants.Because lead levels, particularly in urban environments or in rural areas nearmining or smelting operations, may approach this level, it appears that anyincrease in blood lead levels could be of concern. CDC (1985) noted thatlevels of lead in soil of from 500 to 1,000 rag/kg may lead to increases inblood lead levels in children. These soil levels are consistent with datafrom EPA (1986k), which suggest that in urban areas the slope of the linerelating blood lead levels to soil lead levels ranges from 0.6 to 2.2 pg/dlper 1,000 mg/kg. In other words, the EPA data suggest that a soil leadconcentration of 500 mg/kg above background would be associated with anincrease in blood lead of from 0.3 to 1.1 pg/dl. Because of statisticalvariations and uncertainties in measurement, it would be difficult todefinitively attribute an increase of less than 1 Mg/dl in blood lead to aspecific source.

The approach used to evaluate lead exposures to young children is basedon a model used by EPA (1989d) to evaluate the lead national ambient airquality standard (NAAQS). The Integrated Uptake/Biokinetic model takes intoaccount the total intake of lead from all sources (in pg/day) and convertsintake to a blood lead concentration. The calculated blood lead levels arecompared with the 10-15 pg/dl blood lead range considered to be associatedwith significant health effects EPA 1988c). A 2-year-old child is evaluated

107

because the impacts of lead intake on blood lead are estimated to be greatestfor this age period.

For each source of lead exposure (including potential ingestion ofcontaminated groundwater), lead intakes are estimated. Then the intakes fromall sources are combined to provide a total intake estimate.

Lead Intake from Inhalation. Airborne lead levels for the average casewere taken to be 0.10 /ug/m3. This is the 50th percentile annual averageconcentration as measured at Endicott, New York (EPA 19861). Theconcentration of lead in indoor air was taken as 0.55 times the concentrationin outdoor air. This is the midpoint of the indoor-outdoor ratio recommendedby EPA (1989d). These two air concentrations (indoor and outdoor) yield anintake of lead for the average case due to inhalation of 0.665 jig/day as shownbelow:

Pblinh - [Cout*0.25)-H(Cin*0.75)]*IR*ABSi

where

Cout -outdoor lead level in air (0.10 pg/m3),

0.25 -fraction of time spent outdoors (EPA 1989b),

Cin -indoor lead level in air (0.16 pg/m3*0.55), where 0.55 is indoor-outdoor ratio (EPA 1989d), and

0.75 -fraction of time spent indoors (EPA 1989d).

IR - inhalation rate for young child 24 m3/day (EPA 1988a), and

ABSi -inhalation absorption fraction (0.42) (EPA 1989d).

This equation was also applied to estimate lead intake for a plausiblemaximum case. For this case, the maximum lead concentration of 0.21 iig/m3

measured in outdoor air (95th percentile) (EPA 19861) was used. Applying thesame assumptions as above resulted in a lead intake of 1.4 pg/day frominhalation.

108

*"v\ Lead Intake from Diet. The child's dietary exposure is taken from EPA(1989d) to be 5.5 jig lead/day. This value is used for the average and

I plausible maximum exposure conditions.Lead Intake from Soil and Dust. The intake from outdoor soil and indoor

dust ingestion was calculated assuming a child spends 75% of the time indoorsand 25% outdoors and that indoor dust concentrations are 0.55 times outdoorsoil concentrations (EPA 1989d). The equation used to estimate intake is asfollows:

0

Pblin8 - [(C.oil*0.25)+(CdMt*0.75)3*IR*ABS,*CV

where

Cgoil - outdoor soil lead concentration (mg/kg),

0.25 - fraction of time spent outdoors (EPA 1989d),

Cdust " In(*oor dust lead concentration (mg/kg),

0.75 - fraction of time spent indoors (EPA 1989d),

IR - soil ingestion rate (200 mg/day) (EPA 1988a),'***IK

ABSS - absorption from ingested soil (0.7), and

i CV - conversion factor (kg/10*103 Mg/™g)•

, Soil concentrations were taken from the supplemental RI subsurfacesampling (Table 2-2). Surface and subsurface lead concentrations are assua*dto be equal. The resulting lead intakes from soil and dust ingestion are1.11 A»g/day for the average case and 23.2 pg/day for the plausible maximumcase.

Lead Intake from Drinking Water. The lead intake from drinking water wasestimated assuming an ingestion rate of 1 liter of water per day (EPA 1988a)and an oral absorption factor of 0.5. Concentrations of lead in the waterwere taken as the geometric mean and maximum concentrations for both total anddissolved samples as given in Table 2-4.

109

Lead Intake from All Sources. The total lead intake for all of theexposure sources listed above are listed in Table 5-18 for average andplausible maximum cases using total and dissolved concentrations.

Blood Lead Levels. These lead intake values can be converted to a bloodlead level by multiplying by the EPA (1989d) slope factor of 0.404 /zg/dl perHg/day and adjusting for contribution from maternal blood. The contributionfrom maternal blood to a 2-year-old is calculated to be 0.71 /ig/dl based onEPA (1989d). The resulting blood lead levels are shown in Table 5-18. Underthe plausible maximum case, blood lead levels are greater than the 10-15 /ig/dlrange. Average case exposures are below 10 /ig/dl.

6.0 DEVELOPMENT OF TARGET CLEANUP LEVELS

In this section, health-based target cleanup levels are developed forsoils at the Vestal site. For the purpose of developing target cleanup levelsthe target risk level for chemicals exhibiting carcinogenic effects was takenas an excess upper-bound lifetime cancer risk of lxlO"fi. EPA guidancerecommends development of risk goals in the range of IxlO"4 to IxlO"7. Toobtain a IxlO"7 goal, the numbers presented below can be divided by ten. Toobtain cleanup concentrations associated with IxlO"5 to 1x10"* risks, theIxlO"6 cleanup level can be multiplied by 10 and 100, respectively. Fornoncarcinogens, the cleanup goals correspond to a CDI:RfD ratio of one.

It is emphasized that these are target cleanup levels based on healthconsiderations only; i.e., the concentration in soil corresponds to the givenhealth risk level for the specific conditions of a particular exposurescenario. Other factors may also be considered in developing cleanup levels.These include practical limitations of analytical quantification, relevant andappropriate requirements under state or federal regulations, and the technicalfeasibility of achieving a given cleanup level.

Health-based cleanup levels were developed only for those chemicals andexposure pathways that, in the risk assessment showed either an excess upper-bound lifetime cancer risk greater than IxlO"6 or a CDI:RfD ratio greater thanone. Cleanup levels are not required for chemicals and exposure pathways with

•ji

110

/•"•s

TABLE 5-18ESTIMATED BLOOD LEAD CONCENTRATIONS FOR 2-YEAR OLDS

EXPOSED TO LEAD IN DRINKING WATERAT CONCENTRATIONS EQUAL TO LEVELS DETECTED IN MONITORING WELLS


GROUNDWATERSAMPLE TYPE

Total (UnfHtered)

Geometric mean

Maximum

Dissolved (Filtered)

Geometric mean

Maximum

LEADCONCENTRATION

(mg/liter)

0.0257

0.191

0.0024

0.0138

ESTIMATEDBLOOD LEAD

CONCENTRATION (a)(ug/dl)

8.8

51.4

4.2

15.7

(a) Based on the biokinetic/uptake model presented in Section 5.6.1.

111

risks less than those stated above, as the concentrations present already meetthe target risk levels.

Since under EPA guidance for risk assessments the toxic effects ofchemicals are considered additive, this methodology may result in an•underestimation of risk. For example, if two chemicals are remediated to aIxlCT6 risk level, then the actual remaining risk (summing both chemicals) is2xlO"6. In addition, risks may be additive across exposure pathways. Thismethodology was used in order to simplify the calculations, since in the caseof multiple chemicals , there is an infinite number of possible combinations ofcleanup levels to achieve a given total target risk level. However, in manycases, when soil is remediated, exposure to all chemicals is reduced so thatcleanup goals for one chemical may be protective of risks from other

chemicals .All of the exposure models described in the previous sections develop a

linear relationship between risk and contaminant concentration; i.e., a two-fold increase in contaminant concentration results in a two -fold increase inrisk. In this situation, a mathematical ratio can be used to derive hecleanup levels as follows:

Concentration of chemical in PHE — Concentration at target cleanup levelRisk level in PHE Risk at target cleanup level

Table 6-1 presents the target cleanup levels for the Vestal site derivedas described above. Calculated cleanup levels of several chemicals, inparticular 1,1-DCE, 1,1-DCA, PCBs, and 1,1,2,2-PCA, are significantly lowerthan the mean concentrations of the chemicals in the various source areas .However, as noted in previous sections of this report, many of these chemicalswere detected at low frequency (one or two samples per area) and at levelsnormally below contract required detection limits. Therefore, there issignificant uncertainty as to the actual levels present. It is also notedthat most of the cleanup levels apply to the plausible maximum exposure case.As noted above, the plausible maximum case is designed to represent an upper-bound to possible exposures and risks. As such, use of the plausible maximum

112

TABLE 6-1HEALTH-BASED TARGET CLEANUP LEVELS


EXPOSURE PATHWAY

HEALTH-BASEDTARGET CLEANUP LEVEL (a)

AVERAGECASE (b)(mg/kg)

PLAUSIBLEMAXIMUMCASE (c)(mg/kg)

Potential exposure toconstruction workers via soilcontact (dermal absorptionand ingestion) and inhalationof volatiles.

Area 1Carcinogenic PAHs

Area 21,1-DichloroethyleneTetrachloroethylene1,1,2,2-TetrachloroethaneTrichloroethyleneCarcinogenic PAHs

Area 31,1-Dichloroethylene

Area 41,1-Dichloroethane (d)1,1-DichloroethyleneTrichloroethylene

Potential exposure toconstruction workers viainhalation of contaminateddust.

Area 1Area 2Area 3Area 4

0.7860.00003

0.025

0.8

0.00003

0.00003

0.275

0.000010.0930.0090.0660.273

0.00001

0.0050.000010.066

Leaching of contaminants togroundwater with exposuredirectly below the sourcearea.

Area 1Carcinogenic PAHs

Area 2Chloroform1,1-Dichloroethane1,1-Dichloroethylene1.1.2,2-TetrachloroethaneTetrachloroethyleneTrichloroethylenePCBTrichloroethylene (d)

Area 31.1-Dlchloroethane1,1-Dlchloroethylene

Area 41,1-Dichloroethane1,1-DichloroethyleneTrichloroethylenePCBAcetone (d)Trichloroethylene (d)

0.034

0.097

0.003

0.0240.0023

3.24

0.0030.0020.00020.0020.0450.0520.0051.34

0.0020.00020.00140.00010.0310.0034

0.190.81

113

TABLE 6-1 (continued)HEALTH-BASED TARGET CLEANUP LEVELS


HEALTH-BASEDTARGET CLEANUP LEVEL (a)

EXPOSURE PATHWAY ———————————————————————————————————-AVERAGE PLAUSIBLECASE (b) MAXIMUM

CASE (c)(mg/kg) (nig/kg)

Leaching of contaminants to «groundwater with exposureat the well field.

. .Area 1Area 2Area 3Area 4

1.1-Dichloroethane — 0.135PCB — 0.335

(a) Concentration resulting in an excess lifetime cancer risk of IE-06 or aCDIrRfD ratio of one under the specific conditions of the exposure scenario.

(b) Average case risks are based on average (but conservative) conditions of exposure andthe geometric mean soil concentration.

(c) Plausible maximum case risks are based on upper-bound conditions of exposure and thegeometric mean concentration of detected values.

(d) Based on noncarcinogenic effects.— = No individual chemicals exceeding 10-6 excess lifetime cancer risk or CDI:RfD ratio

of one; therefore, no cleanup levels calculated.

.sf

114

case in setting remedial goals likely will result in an extremely conservativecleanup level.

7.0 UNCERTAINTIES

The procedures and inputs used to assess risks in this evaluation, as inall such assessments, are subject to a wide variety of uncertainties. Ingeneral, there are the following main sources of uncertainty:

• Environmental chemistry sampling and analysis• Environmental parameter measurement• Fate and transport modeling• Exposure parameter estimation• Toxicological data

Uncertainty in environmental sampling arises in part from the potentiallyuneven distributions of chemicals in the media sampled. Typically, thisproblem is encountered more frequently in soil than in water. The collectionof grab samples allows an estimate to be made of the variation in the chemicalconcentration in the area. As noted in previous sections of this report, manyof the chemicals detected at the site were detected at low frequency (one ortwo samples per area) and at levels normally below contract required detectionlimits. Consequently, there is significant uncertainty as to the actuallevels present. Several chemicals, in particular 1,1-DCE, 1,1-DCA, PCBs, and1,1,2,2-PCA, contribute to excess lifetime cancer risks greater than 10~*under the specific conditions of exposure addressed in this PHE, although theywere detected infrequently and at low concentrations. In particular, 1,1-DCEwas detected in only one boring in Area 2 at depths of 4 to 6 feet and 14 to16 feet. However, the conservative models used assume the contaminant to bepresent at the mean concentration throughout the volume of soil in Area 2.

Environmental chemistry analysis error can stem from several sources 3including the errors inherent in the analytical methods, chain of custody r*problems, to the characteristics of the matrix being sampled. For this RI, =>

115

the analytical methods were all methods approved by EPA. Procedural orsystematic error was minimized by subjecting the data to a strict laboratoryquality control review and data validation process.

Environmental parameter measurements primarily contribute to uncertaintybecause little verified information is available. Lack of site-specificmeasurements requires that estimates be made on the basis of literaturevalues, extrapolations from regression equations, and/or best professionaljudgment. Transport models used in this assessment required literature valuesfor soil porosity and bulk density, and hydraulic conductivity.

In the Vestal PHE there are uncertainties regarding the estimates of howoften, if at all, an individual would come in contact with the chemicals ofconcern and the period of time over which such exposures would occur. Inparticular, this applies to the future construction exposures. The length ofexposure was taken as 30 days; although longer or shorter periods of exposuremay result in greater or less risk. In addition, many of the standardassumptions used throughout this assessment are assumed to represent upperbounds of potential exposure and have been used when site-specific data arenot available. Risks for certain individuals within an exposed populationwill be higher or lower depending on their actual drinking water intakes, bodyweights, etc. In the Vestal PHE, estimates of soil ingestion rates, dermalcontact rates, and absorption factors contribute significantly to uncertaintyin the assessment since site-specific and literature data on these values are,in many cases lacking.

There is also significant uncertainty in the models used to estimateexposure point concentrations. The model used to estimate air concentrationswithin a trench uses concepts from indoor air pollution to estimate the airchanges per hours in a trench. Actual air changes nay be greater. Theestimate of the flux of chemical from the soil will vary with the specificconfiguration of the trench, its depth, the presence of groundwater, or theuse of shoring in the trench. The groundwater leaching model is sensitive tothe area and volume of the source areas, which have been defined for thisassessment from the locations of the soil borings.

Jl

116

I/**•"»•,, Toxicological data error is also a large source of error in this risk

assessment. As EPA notes in its Guidelines for Carcinogenic Risk Assessment

\ (EPA 1986b):

There are major uncertainties in extrapolating both from animals tohumans and from high to low doses. There are important speciesdifferences in uptake, metabolism, and organ distribution of carcinogens,as well as species and strain differences in target site susceptibility.Huiran populations are variable with respect to genetic construction,diet, occupational and home environment, activity patterns and othercultural factors.

A particular problem is also presented by PAHs. PAHs occur in theenvironment as complex mixtures of may components with widely varying toxicpotencies. Only a few components of theses mixtures have been adequatelycharacterized, and only limited information is available on potentialsynergistic effects of the PAH mixture. The approach adopted by EPA (1980,1984) and used in this report as the basis for risk assessment is to dividethe PAHs into two subclasses, "carcinogenic" PAHs and "noncarcinogenic" PAHs,and to apply a cancer potency factor derived from oral bioassays on

/*«-̂ ,benzo(a)pyrene to the subclass of carcinogenic PAHs. Most evidence indicatesthat benzo(a)pyrene is more potent than most of the other carcinogenic PAHs

I and a mixture of carcinogenic PAHs (Schmahl 1955, Pfeiffer 1977); therefore,Ithis technique will overestimate risk.

There is also a great deal of uncertainty in assessing the toxicity of amixture of chemicals. In this assessment, the effects of exposure to each ofthe contaminants present in the environmental media have initially beenconsidered separately. However, these substances occur together at the site,and individuals may be exposed to mixtures of the chemicals. Predictions ofhow these mixtures of toxicants will interact must be based on anunderstanding of the mechanisms of such interactions. The interactions of theindividual components of chemical mixtures may occur during absorption,distribution, metabolism, excretion, or activity at the receptor site.Individual compounds may interact chemically, yielding a new existingcomponent, or may interact by causing different effects at different receptor

117

sites. Suitable data are not currently available to rigorously characterizethe effects of chemical mixtures similar to those present at the Vestal site.Consequently, as recommended in EPA's Superfund Public Health EvaluationManual (EPA 1986a) and in EPA's Guidelines for Health Risk Assessment ofChemical Mixtures (EPA 1986c), chemicals present at the Vestal site wereassumed to act addictively, and potential health risks were evaluated bysumming excess cancer risks and calculating hazard indices for chemicalsexhibiting carcinogenic and noncarcinogenie effects, respectively. Thisapproach to assessing the risk associated with mixtures of chemicals assumesthat there are no synergistic or antagonistic interactions among the chemicalsconsidered and that all chemicals have the same toxic end points andmechanisms of action. To the extent that these assumptions are incorrect, theactual risk could be under- or overestimated.

8.0 SUMMARY AND CONCLUSIONS

The Public Health Evaluation (PHE) has addressed the potential impacts tohuman health associated with the Vestal Well 1-1 site in the absence ofremedial (corrective) action. This fulfills the requirement of the NationalContingency Plan for an evaluation of the "no-action" remedial alternative,and helps to identify the extent of any remedial actions that may be required.The assessment has been limited to an evaluation of soils in four identifiedsource areas and to inorganic contaminants in groundwater. Since manychemicals were detected in these media, the sampling and analysis results havebeen evaluated to identify a subset of these chemicals for detailed evaluationin the public health evaluation (referred to as chemicals of potentialconcern). In selecting chemicals of potential concern, factors that wereconsidered included frequency of detection, relationship of the chemical toknown site activities, or, in the case of inorganics, presence at levels abovenaturally occurring background. Nineteen organic and thirteen inorganicchemicals were selected as chemicals of potential concern.

Exposure pathways whereby various populations could come in contact withcontaminated media were selected for evaluation. These were as follows:

118

1 . Potential exposure to future construction workers engaged inexcavation or other subsurface activities . Exposure may occurthrough direct contact with soil resulting in incidental ingestionand dermal absorption of soil contaminants , and inhalation ofvolatiles released from excavated soils.

2. Potential exposure to construction workers engaged in above groundactivities. Exposure may occur as a result of inhalation ofcontaminated dusts generated from loading or grading of excavatedsoils.

3. Potential indirect exposure to contaminants in soil through exposureto groundwater to which soil contaminants have leached.- Potentialexposures are considered to groundwater directly below the site andat the well field. Routes of exposure considered are ingestion ofwater and inhalation of volatiles released from water whileshowering.

The sampling of monitoring wells during the supplemental RI revealed thepresence of inorganics that appear to significantly exceed backgroundconcentrations . As a means of determining if these contaminants represent apotential risk to public health such that additional investigation or otheractions may be warranted, the PHE contains a screening analysis of thesesampling results. In the screening analysis, the detected levels are comparedto drinking water standards and health criteria. This represents an upper-bound exposure in which it is assumed that a drinking water well would beplaced at the location of the monitoring wells. Since drinking water iscurrently supplied by the town of Vestal, this analysis does not evaluateactual exposures, but rather the value of the groundwater in the monitoredarea as a potable water resource.

Concentrations of contaminants of concern at the exposure pointsidentified above were estimated in order to assess risk. For the exposurepathway involving direct contact with soils by future construction workers,exposure point concentrations were taken directly from the sampling results.However, three exposure pathways required that models be developed to estimatethe release of contaminants from soil. Release of volatiles to the air withinan area of soil excavation was estimated based on equilibrium partitioningbetween soil, water, and air; estimating diffusivity through the soil column;

119

and using an indoor air model to estimate concentrations within the area ofexcavation. Release of dust from the excavation and loading of contaminatedsoils was estimated using a construction site dust emission factor developedby EPA, and an air dispersion box model to estimate on-site airconcentrations. Leaching of contaminants from soil to groundwater wasestimated assuming equilibrium partitioning of contaminants between soil andinfiltrating rainwater, and then estimating the mixing of infiltration withgroundwater. Concentrations of contaminants in groundwater resulting fromleaching were estimated directly below the source areas, and at the Vestalwell field taking into account dilution.

Potential risks were assessed by two methods. First, exposure pointconcentrations were compared to applicable or relevant and appropriaterequirements (ARARs). Second, since ARARs do not exist for all chemicals andexposure pathways at this site, a quantitative risk assessment was performed.

The results of the comparison of groundwater concentrations predicted bythe leaching model with ARARs are as follows:

• Maximum concentrations of TCE below the source in Areas 2 and 4 exceedthe MCL and the New York standard.

• Maximum concentrations of PCBs below the source in Areas 2 and 4exceed the New York standard.

With respect to the inorganics analyzed for in monitoring wellgroundwater the following exceedances of potential ARARs are noted:

V

• Maximum total (unfiltered) concentrations of barium, chromium and leadexceed both MCLs and New York standards and the geometric meanconcentration of total lead exceeds the New York standard.

• For mercury the maximum total concentration, geometric mean totalconcentration, and maximum dissolved concentrations exceed MCLs andNew York standards.

• The maximum and geometric mean total concentrations of manganese• exceed the New York standards as does the maximum dissolvedconcentration of manganese.

-FT120 *

""N • The maximum total concentrations of arsenic, copper and zinc exceedthe New York standard.

Comparison of soil concentrations with the only available potential soilARAR (TSCA soil cleanup limits for PCBs), indicates that PCB concentrations insoils (PCBs were detected in Areas 2 and 4 only) were well below the TSCAlimits of 10 ppm for unlimited access sites and 25 ppm for sites withrestricted access.i

Comparison of estimated air concentrations from excavated soils to NYAALs indicate the following:

• In Area 1, the maximum case concentration of noncarcinogenic PAHs isgreater than the AAL.

• In Area 2, AALs are exceeded by the average case and maximum caseconcentrations of 1,1-dichloroethylene, 1,1,2,2-tetrachloroethane,trichloroethylene, and PCBs and by the maximum case concentrations oftetrachoroethylene and xylene.

• In Area 3, AALS are exceeded by the average case and maximum caseconcentrations of 1,1-dichloroethylene and by the maximum case

""*v concentration of acetone.

• In Area 4, AALs are exceeded by the average case and maximum caseconcentrations of 1,1-dichloroethylene and trichloroethylene, and bythe maximum case concentration of PCB's.

1 All estimated air concentrations due to fugitive dust generation (Table3-6) are well below AALs.

In the quantitative risk assessment, exposure point concentrations areconverted to chronic daily intakes (CDIs). A GDI is the amount of a substancetaken into the body per unit body weight per unit time, or mg/kg/day. CDIsare developed from the exposure point concentrations and assumptions about thefrequency of contact with the contaminated media, breathing rates, drinkingwater ingestion rates, metabolic absorption factors, and other parameters.Two exposure cases are considered—an average case based on average (butconservative) conditions of exposure, and a plausible maximum case based onupper-bound conditions of exposure. For chemicals exhibiting potential

ft

121

carcinogenic effects the CDI is averaged over the lifetime of the potentiallyexposed individual and multiplied by the cancer potency factor to give theupper-bound excess lifetime cancer risk for the specific conditions ofexposure. A risk level of 10~6, representing a probability of one in1,000,000 that an individual could contract cancer due to exposure to thepotential carcinogen, is often used as a benchmark by regulatory agencies,although EPA has implemented actions under Superfund associated with totalcancer risks ranging from 10"* to 10~7. Potential risks from chemicalsexhibiting potential noncarcinogenic effects are presented as the ratio of theCDI to the reference dose (RfD) also expressed as mg/kg/day. The sum of theCDI:RfD ratios is called the hazard index. In general, hazard indices whichare less than one are not likely to be associated with any health risk, andare therefore less likely to be of concern than hazard indices greater thanone.

Table 8-1 summarizes the results of the quantitative risk assessment.Major conclusions of the quantitative risk assessment are as follows:

• The combined excess lifetime cancer risks from potential exposure toconstruction workers (via dermal absorption, incidental ingestion andinhalation of volatiles) range from 5x10"* to IxlO"6 for the foursource areas.

• Hazard indices for the noncarcinogenic exposures of constructionworkers (via dermal absorption, incidental ingestion, and inhalationof volatiles) exceeded one only for the plausible maximum cases inAreas 2 and 4. The hazard index for both of the cases is 1.4.

• The combined excess lifetime cancer risks from potential exposure toconstruction workers via inhalation of contaminated dust range from3x1 0"12 to 2xlO"19 for the four source areas.

• Hazard indices for the exposure to construction workers via inhalationof contaminated dust are less than one for both average and plausiblemaximum cases and for all source areas.

• The combined excess lifetime cancer risks from exposure to groundwaterdirectly below the source areas (using estimated groundwaterconcentrations based on leaching from soils) via ingestion andinhalation while showering, range from 8xlO"6 to 4xlO~8 for the averagecases and 4xlO"4 to 2xlO~6 for the plausible maximum cases for each of

122

TABLE 8-1RISK ASSESSMENT SUMMARYVESTAL WELL 1-1 SITE

EXPOSURE

TOTAL EXCESSUPPER BOUND LIFETIME

CANCER RISK

PLAUSIBLEAVERAGE MAXIMUM

PATHWAY CASE (a) CASE (b)

HAZARD INDEX

PLAUSIBLEAVERAGE MAXIMUM

CASE (a) CASE (b)

CHEMICALSCONTRIBUTING

TO THERISK (c)

Potential exposure to construction workersvia soil contact (dermal absorption and Ingest Ion)and inhalation of vo la tiles.


IE-06 2E-05IE-04 4E-04IE-04 3E-042E-04 5E-04

IE-02 Kl'i 5E-02 l'<9E-02 Kl 1E+00 >IE-02 Kl' 4E-02 <3E-01 KI' 1E+00 >

1 Carcinogenic PAHs1 (d) 1.1-DCE. PCE, TCE. 1.1.2,2-PCA, cPAHs1 1.1-DCE1 1.1-DCE. TCE. 1.1-DCA

Potential exposure to construction workersvia inhalation of contaminated dust.

Area 1,_, Area 2to Area 3w Area 4

2E-16 3E-152E-16 3E-12IE-17 3E-173E-19 9E-19

IE-15 Kl; 6E-15 <3E-15 Kl 7E-14 <4E-16 Kl IE-15 <5E-15 Kl 2E-14 <1 =

Leaching of contaminants to groundwaterwith exposure directly below the source area.


4E-08 2E-064E-06 2E-04IE-06 2E-058E-06 4E-04

IE-02 I<1 4E-01 K3E-02 Kl 4E+00 >5E-02 Kl 5E-01 K4E-01 <1 7E+01 >

1 Carcinogenic PAHs1 Chloroform. 1.1-DCA, 1,1-OCE, 1.1.2.2-PCA. PCE. TCE. PCB1 1,1-DCA, 1,1-OCE1 1,1-DCA, 1.1-DCE. TCE. PCB, Acetone

Leaching of contaminants to groundwaterwith exposure at the well field.Area 1Area 2Area 3Area 4

4E-104E-08IE-088E-08

2E-082E-06 (d)2E-074E-06

IE-043E-045E-044E-03 (

4E-034E-025E-037E-01 1.1-DCA, Carcinogenic PAHs

luu

CO

TABLE 8-1 (continued)

RISK ASSESSMENT SUMMARYVESTAL WELL 1-1 SITE

! '

EXPOSURE PATHWAY

TOTAL EXCESSUPPER BOUND LIFETIME

CANCER RISK

PLAUSIBLEAVERAGE MAXIMUMCASE (a) CASE (b)

HAZARD INDEX

PLAUSIBLEAVERAGE MAXIMUMCASE (a) CASE (b)

/*UCUff*AI C

CONTRIBUTINGTO THE

RISK (c)

Potential exposures and risks from ingest Ionof groundwater at concentrations detected inmonitoring wells.

Total Concentrations IE-04 8E-04 7.4 (>1) 140 (>1) Arsenic, antimony, barium, beryllium, chromium,manganese, mercury, nickel, thallium,vanadium, zinc

Dissolved Concentrations 8E-05 4E-04 6.2 {>!) 78 (>1) Arsenic.mercury,

antimony, manganese,nickel, thallium

(a) Average case risks are based on average (but conservative) conditions of exposure and the geometric mean soil concentration.(b) Plausible maximum case risks are based on upper-bound conditions of exposure and the geometric mean concentration of detected

values where, except for inorganics in groundwater. maximum detected value is used.(c) Chemicals resulting in an excess lifetime cancer risk of greater than IE-06 or a COI:RfO ratio greater than one.(d) An excess lifetime cancer risk of greater than IE-06 or a CDI:RfO ratio greater than one is due only to the summation of two or more

chemicals (I.e., no Individual chemical results in an exceedance).— «= Hot relevant.NOTE: 1,1-OCE • 1,1-Dlchloroethylene; 1.1,2.2-PCA » 1.1,2,2-Tetrachloroethane; 1.1-DCA = 1.1-Dichloroethane.

LUU

the four source areas. Only the plausible maximum cases associatedwith concentrations in Areas 2 and 4 resulted in excess lifetimecancer risks of greater than 10"6 <2xlO"6 and 4xlO"6, respectively),from exposure at the wellfield.

• Two exposure cases—the plausible maximum cases for exposure togroundwater directly below Areas 2, and 4—result in hazard indices ofgreater than one. All of the other hazard indices for drinking waterexposure below the source areas and at the well field are less thanone.

• The excess lifetime cancer risk from exposure to arsenic at the listedconcentrations detected in the monitoring wells ranges from 8x10"* to8xlO"5.

• Hazard indices for exposure to noncarcinogens at the levels detectedin the monitoring wells are greater than one for all cases. For thegeometric mean, the total concentration of antimony and thallium showa CDI:RfD ratio greater than one. All of the inorganics exceptselenium have CDI:RfD ratios greater than one under the plausiblemaximum case for total concentration. For the dissolvedconcentrations, the geometric mean concentration of antimony andthallium result in a CDI:RfD ratio greater than one. Exposure atlevels corresponding to the maximum dissolved concentration results inCDI:RfD ratios greater than one for antimony, manganese, mercury,nickel, and thallium.

• An evaluation of a hypothetical exposure to lead to 2-year-olds basedon the concentrations of lead observed in monitoring wells suggestspotential adverse effects from the maximum concentrations detected,although average levels result in estimated blood-lead levels belowthe EPA target range.

Health-based target cleanup levels developed for soils at the Vestalsite have been presented in Table 6-1. For the purpose of developing targetcleanup levels the target risk level for chemicals exhibiting carcinogeniceffects was taken as an excess upper-bound lifetime cancer risk of IxlO"6.EPA guidance recommends development of risk goals in the range of 1x10"* toIxlO"7. To obtain a IxlO"7 goal, the numbers given in Table 6-1 can be dividedby ten. To obtain cleanup concentrations associated with IxlO"5 to IxlO'4

risks, the IxlO"6 cleanup level can be multiplied by 10 and 100, respectively.-4

For noncarcinogens, the cleanup goals correspond to a CDI:RfD ratio of one. 1

125

It is emphasized that these are target cleanup levels based on healthconsiderations only; i.e., the concentration in soil corresponds to the givenhealth risk level for the specific conditions of a particular exposurescenario. Other factors may also be considered in developing cleanup levels.These include practical limitations of analytical quantification (for exampleseveral of the target cleanup levels in soil are at levels below the ContractRequired Quantitation Limit (CRQL), relevant and appropriate requirementsunder state or federal regulations (ARARs), and the technical feasibility ofachieving a given cleanup level.

Health-based cleanup levels were developed only for those chemicals andexposure pathways that, in the risk assessment showed either an excess upper-bound lifetime cancer risk greater than IxlO"6 or a CDI:RfD ratio greater thanone under the maximum exposure case or under both average and maximum exposurecases. Cleanup levels are not required for chemicals and exposure pathwayswith risks less than those stated above, as the concentrations present alreadymeet the target risk levels.

Since under EPA guidance for risk assessments the toxic effects ofchemicals are considered additive, this methodology may result in anunderestimation of risk. For example, if two chemicals are remediated to a1x10"6 risk level, then the actual remaining risk (summing both chemicals) is2x1O"6. In addition, risks may be additive across exposure pathways. Thismethodology was used in order to simplify the calculations, since in the caseof multiple chemicals, there is an infinite number of possible combinations ofcleanup levels to achieve a given total target risk level. However, in manycases, when soil is remediated, exposure to all chemicals is reduced so thatcleanup goals for one chemical should be protective of risks from otherchemicals.

All of the exposure models described in the previous sections develop alinear relationship between risk and contaminant concentration; i.e., a two-fold increase in contaminant concentration results in a two-fold increase inrisk. t In this situation, a mathematical ratio can be used to derive thecleanup levels as follows:

\>126

Concentration of chemical in PHE - Concentration at target cleanup levelRisk level in PHE Risk at target cleanup level

Calculated cleanup levels of several chemicals, in particular 1,1-DCE,1,1-DCA, PCBs, and 1,1,2,2-PCA, are significantly lower than the meanconcentrations of the chemicals in the various source areas. However, asnoted in previous sections of this report, many of these chemicals weredetected at low frequency (one or two samples per area) and at levels normallybelow contract required detection limits. Therefore, there is significantuncertainty as to the actual levels present. It is also noted that most ofthe cleanup levels apply to the plausible maximum exposure case. As notedabove, the plausible maximum case is designed to represent an upper-bound topossible exposures and risks. As such, use of the plausible maximum case insetting remedial goals will likely result in an extremely conservative cleanuplevel.

127

/ — v 9 . 0 REFERENCES

i AGENCY FOR TOXIC SUBSTANCES AND DISEASE REGISTRY (ATSDR) . 1987. Draft! Toxicological Profile for Benzo[a]pyrene. October 1987

AMBROSE, A.M., LARSON, P.S., BORZELLECA, J.R. , and HENNIGAR, G.R. 1976.Long-term toxicologic assessment of nickel in dogs and rats. J. FoodSci. Technol. 13:181-187

, AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH) . 1986.Documentation of the Threshold Limit Values and Biological ExposureIndices. 5th ed. ACGIH, Cincinnati, Ohio

BALYAEVA, A. P. 1967. The effects of antimony on reproduction. Gig. TrudaProf. Zabol. 11:32

BAES, C.F., III SHARP, R.D. 1983. A proposal for estimation of soil leachingand leaching constants for use in assessment models. J. Environ. Qual.12:17-28

BAES, C.F., III, SHARP, R.D. , SJOREEN, A.L. , SHOR, R.W. 1984. A Review andAnalysis of Parameters for Assessing Transport of EnvironmentallyReleased Radionuclides through Agriculture. Prepared for the U.S.Department of Energy. ORNL-5786. September 1984.

/*"*"" BANK, W.J. 1980. Thallium. In Spencer, P.S., and Schaumberg, H.H. , eds.Experimental and Clinical Neurotoxicology. Williams and Vilkins,Baltimore. P. 571

j BARDODEJ, Z., and BARDODEJOVA, E. 1970. Biotransformation of ethylbenzene ,styrene, and alpha -me thy Istyrene in man. Am. Ind. Hyg. Assoc. J. 31:206-209

BARNES, D.W., SANDERS, V.M. , WHITE, K.L. , Jr., et al. 1985. Toxicology oftrans-l,2-dichloroethylene in the mouse. Drug Chem. Toxicol. 8:373-392

BOERNGEN, J.G., and SHACHLETTE, H.T. 1981. Chemical Analyses of Soils andOther Surficial Materials of the conterminous United States. USGS Open-File Report 81-197

BOWERS, D.E., Jr., CANNON, M.S., and JONES, D.H. 1982. Ultrastructuralchanges in livers of young and aging rats exposed to methylated benzenes.Am. J. Vet. Res. 43:679-683

BROWNING, E. 1969. Toxicity of Industrial Metal. 2nd ed. Appleton-Century- |Crofts, New York r<

128

/—x BUBEN, J.A., and O'FLAHERTY, E.J. 1985. Delineation of the role ofmetabolism in the hepatotoxicity of trichloroethylene andperchloroethylene: A dose-effect study. Toxicol. Appl. Pharmacol.78:105-122

CARPENTER, C.P., VEIL, C.S., and SMYTH, H.F. 1953. Chronic oral toxicity ofdi(2-ethylhexyl)phthalate for rats, guinea pigs, and dogs. Arch. Indust.Hyg. Occup. Med. 8:219-226

CARPENTER, C.P., KINKEAD, E.R., GEARY, D.L., Jr., SULLIVAN, L.J., and KING,J.M. 1975. Petroleum hydrocarbon toxicity studies: V. Animal andhuman response to vapors and mixed xylenes. Toxicol. Appl. Pharmacol.33:543-558

CAVENDER, F.L., CASEY, H.W., SALEM, H., SWENBERG, J.A. , and GARALLA, E.J.1983. A 90-day vapor inhalation toxicity study of methyl ethyl ketone.Fund. Appl. Toxicol. 3:264-270

CENTERS FOR DISEASE CONTROL (CDC). 1985. Preventing Lead Poisoning in YoungChildren. Public Health Services, Chronic Diseases Division, Atlanta,Georgia. July 1985

CHEMICAL INDUSTRY INSTITUTE OF TOXICOLOGY (CUT). 1980. A Twenty-Four MonthInhalation Toxicology Study in Fischer 344 Rats Exposed to AtmosphericToluene. Executive Summary and Data Tables. October 15, 1980

/*"**• CHEN, C., CHUANG, Y., YOU, S., LIN, T., and VU, H. 1986. A retrospectivestudy on malignant neoplasms of bladder, lung, and liver in blackfootdisease endemic area in Taiwan. Br. J. Cancer 53:399-405

CHIN, B.H., McKELVEY, J.A. , TYLER, T.R., CALISTI, L.J., KOZBELT, S.J., andSULLIVAN, L.J. 1980. Absorption, distribution and excretion ofethylbenzene, ethylcyclohexane and methyl ethylbenzene isomers in rats.Bull. Environ. Contain. Toxicol. 24:477-483

jCLAYTON, G.D., and CLAYTON, F.E., eds. 1984. Patty's Industrial Hygiene and

Toxicology. 3rd ed. John Wiley and Sons, New York. P. 1916

COULSON, E.J., REMINGTON, R.E., and LYNCH, K.M. 1935. Metabolism in the ratof the naturally occurring arsenic of shrimp as compared with arsenictrioxide. J. Nutr. 10:255-270

DEAN, R.B. 1981. Use of log-normal statistics in environmental monitoring.In Cooper, W.J., ed. Chemistry in Water Reuse. Ann Arbor Science, AnnArbor, Michigan. Vol. 1

DRUET, P., DRUET, E., POTDEVIN, F., and SAPIN, C. 1978. Immune typeglomerulonephritis induced by HgCl2 in the brown Norway rat. Ann.Immunol. 129C:777-792

^j*

129

EBASCO. 1988. Final Work Plan. Supplemental RemedialInvestigation/Feasibility Study. Vestal Well 1-1 Site, Vestal, New York.April 1988

EBASCO. 1990. Final Work Plan. Final Supplemental RemedialInvestigation/Feasibility Study. Vestal Well 1-1 Site, Vestal, New York.May 1990 .

ECOLOGY AND ENVIRONMENT (E&E). 1986. Remedial Investigation Report on Water1 Supply Well 1-1 Site, Vestal, New York. Prepared for New York State

Department of Environmental Conservation

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1980a. Ambient Water Quality Criteriafor Antimony. Office of Water Regulations and Standards, Washington,D.C. EPA 440/5-80-020

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1980b. Ambient Water Quality Criteriafor Phthalate Esters. Office of Water Regulations and Standards,Washington, D.C. October 1980. EPA 440/5-80-067

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1980c. Ambient Water Quality Criteriafor Chromium. Office of Water Regulations and Standards. Washington,D.C. EPA 440/5-80-035

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1980d. Ambient Water Quality Criteriafor 1,1-Dichloroethane. Office of Water Regulations and Standards,

: Washington, D.C. EPA 440/5-80-029

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1980f. Ambient Water Quality CriteriaDocument for Mercury. Prepared by the Office of Health and EnvironmentalAssessment, Environmental Criteria and Assessment Office, Cincinnati,Ohio for the Office of Water Regulation and Standards, Washington, D.C.EPA 440/5-80-058. NTIS PB 81-117699

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984a. Health Effects Assessment forAcetone. Environmental Assessment Office, Cincinnati, Ohio, EPA 504/1-86-016

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984b. Health Assessment Document forInorganic Arsenic. Office of Health and Environmental Assessment,Washington D.C. EPA 600/8-83-021F

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984c. Health Effects Assessment forBarium. Environmental Criteria and Assessment Office, Cincinnati, Ohio. |September 1984. EPA 540/1-86-021 . *

'.A!

130

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984d. Health Effects Assessment forChloroform. Environmental Criteria and Assessment Office, Cincinnati,Ohio. September 1984. EPA 540/1-86-010

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984e. Health Assessment Document forChromium. Environmental Criteria and Assessment Office, ResearchTriangle Park, N.C. EPA 600/8-83-014F

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984f. Health Effects Assessment forCopper. Environmental Criteria and Assessment Office, Cincinnati, Ohio.EPA/540-1-86-025

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984g. Health Effects Assessment for1,1-Dichloroethylene. Environmental Criteria and Assessment Office,Cincinnati, Ohio. September 1984. EPA 540/1-86-051

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984h. Health Assessment Document forManganese. Final Report. Environmental Criteria and Assessment Office,Environmental Protection Agency, Cincinnati, Ohio. August 1984.EPA 600/8-83-013F

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984i. Health Effects Assessment forManganese (and compounds). Environmental Criteria and Assessment Office,Washington, D.C. EPA 540/1-86-057

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984J. Health Effects Assessment forMercury. Environmental Criteria and Assessment Office, Cincinnati, Ohio.EPA 540/1-86-042

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984k. Health Effects Assessment forPolycyclic Aromatic Hydrocarbons (PAHs). Environmental Criteria andAssessment Office, Cincinnati, Ohio. September 1984. EPA 540/1-86-013

ENVIRONMENTAL PROTECTION AGENCY (EPA). 19841. Health Effects Assessment forNaphthalene. Environmental Criteria and Assessment Office, Cincinnati,Ohio. September 1984. EPA 540/1-86-014

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984m. Health Effects Assessment forBenzo[a]pyrene. Environmental Criteria and Assessment Office,Cincinnati, Ohio. September 1984. EPA 540/1-86-022

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984n. Health Effects Assessment forPolychlorinated Biphenyls. Environmental Criteria and Assessment Office,Cincinnati, Ohio. September 1984. EPA 540/1-86-004

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984o. Health Effects Assessment forSelenium (and Compounds). Office of Emergency and Remedial Response,Washington, D.C. EPA 540/1-86-058. September 1984

131

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984p. Health Effects Assessment for1,1,2,2-Tetrachloroethane. Environmental Criteria Assessment Office,Cincinnati, Ohio. September 1984. EPA 540/1-86-032

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984q. Health Effects Assessment for1,1,1-Trichloroethane. Final Draft. Environmental Criteria andAssessment Office, Cincinnati, Ohio. September 1984. ECAO-CIN-H005

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984r. Health Effects Assessment forZinc (and Compounds). Office of Emergency and Remedial Response,Washington, D.C. EPA 540/1-86-048. September 1984

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985a. Compilation of Air PollutantEmission Factors. Office of Air, Noise, and Radiation, Office of AirQuality Planning and Standards, Research Triangle Park, North Carolina.AP-42

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985b. Drinking Water Criteriadocument for Benzene (Final Draft). Office of Drinking Water,Washington, D.C. April 1985

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985c. Health Assessment Document forChloroform. Environmental Criteria and Assessment Office, ResearchTriangle Park, North Carolina. September 1985. EPA 600/8-84-004F

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985d. National primary drinkingwater regulations; synthetic organic chemicals, inorganic chemicals andmicroorganisms. Fed. Reg. 50:46937-47025 (November 13, 1985)

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985e. Health Assessment Document forVinylidene Chloride. Final Report. Environmental Criteria andAssessment Office, Research Triangle Park, North Carolina. August 1985.EPA 600/8-83/031F

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985f. Health Effects CriteriaDocument on Polychlorinated Biphenyls. Final Draft. Office of DrinkingWater, Washington

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985g. Health Assessment Document forTetrachloroethylene (Perchloroethylene). Office of Health andEnvironmental Assessment, Washington, D.C. July 1985. EPA 600/8-82-005F

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985h. Drinking Water CriteriaDocument for Tetrachloroethylene. Office of Drinking Water, Criteria andStandards Division, Washington, D.C. April 1985

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985i. Drinking Water Criteria.Document for Toluene. Final Draft. Office of Drinking Water,Washington, D.C. March 1985

-»132

ENVIRONMENTAL PROTECTION AGENCY (EPA) . 1985J . Drinking Water Criteria for1,1,1 -Trichloroethane (Draft). Office of Drinking Water, Criteria andStandards Division, Washington, D.C. January 1985

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985k. Health Assessment Document forTrichloroethylene. Environmental Criteria an- Assessment Office.Research Triangle Park, North Carolina. EPA/600/8-82/006F

ENVIRONMENTAL PROTECTION AGENCY (EPA). 19851. Drinking Water CriteriaDocument for Xylenes (Final Draft) . Environmental Criteria andAssessment Office, Cincinnati, Ohio. March 1985. ECAO-CIN-416.EPA 600/X-84-185-1

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1986a. Superfund Public HealthEvaluation Manual. Prepared by ICF, Inc., for Office of Emergency andRemedial Response, Washington, D.C. October 1986. EPA 400/168-060

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1986b. Guidelines for carcinogen riskassessment. Fed. Reg. 51:33992-34002 (September 25, 1986)

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1986c. Guidelines for the health riskassessment of chemical mixtures. Fed. Reg. 51:34014-34023 (September 24,1986)

ENVIRONMENTAL PROTECTION AGENCY (EPA) . 1986d. RCRA Groundwater MonitoringTechnical Enforcement Guidance Document. OSWER-9950.1. September 1986

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1986e. Ninety-Day Gavage Study inAlbino Rats Using Acetone. Office of Solid Waste, Washington, DC. Ascited in EPA 1988

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1986f. Health Assessment Document forBeryllium. Review Draft. Office of Health and Environmental Assessment,Washington, D.C. EPA 600/8-84-026B. April 1986

ENVIRONMENTAL PROTECTION AGENCY (EPA) . 1986g. Superfund Public HealthEvaluation Manual. Office of Emergency and Remedial Response,Washington, D.C. EPA 540/1-86-060

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1986h. Health Assessment Document forNickel and Nickel compounds. Office of Health and EnvironmentalAssessment, Research Triangle Park, North Carolina. EPA 600/8- 83 -012FF

ENVIRONMENTAL PROTECTION AGENCY (EPA). 19861. Health and EnvironmentalEffects Profile for Naphthalene. Environmental Criteria and AssessmentOffice, Cincinnati, Ohio

133

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1986J. Subchronic (90-day) toxicityof thallium (I) sulfate in Sprague-Dawley rats. Final Report. Preparedfor the Office of Solid Waste, U.S. EPA, Washington, D.C. Project

} No. 8702-1(18)<

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1986k. Air Quality Criteria for Lead.Office of Resarch and Development, Environmental Criteria and AssessmentOffice. Research Triangle Park, North Carolina. June 1986.EPA 600/8-83/023cF

ENVIRONMENTAL PROTECTION AGENCY (EPA). 19861. Air Quality Data—1985 AnnualStatistics. EPA 450/4-86-008

*

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987a. Draft Health Advisory forChromium. Office of Drinking Water, Washington, D.C. March 31, 1987

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987b. Drinking Water CriteriaDocument for Copper. Prepared by the Office of Health and EnvironmentalAssessment. Environmental Criteria and Assessment Office, Cincinnati,Ohio, for the Office of Drinking Water, Washington, D.C.

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987c. Health Advisory for1,1-Dichloroethene. Office of Drinking Water, Washington, D.C. March31, 1987.

*-*,< ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987d. Health Advisory forEthylbenzene. Office of Drinking Water, Washington, D.C. March 1987

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987e. Health Advisory for Nickel.| Office for Drinking Water, Washington, D.C. March 31, 1987

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987f. Health Advisory for Toluene.Office of Drinking Water, Washington, D.C. March 1987

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987g. Health Advisory forTrichloroethylene. Office of Drinking Water, Washington, D.C. March 31,1987

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987h. Health Advisory for Xylenes.Office of Drinking Water, Washington, D.C. March 1987

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1988a. Proposed guidelines forexposure-related measurements. Fed. Reg. 53:48830-48853 (December 2,1988)

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1988b. Exposure Factors Handbook.Office of Health and Environmental Assessment, Office of Research andDevelopment. September 1988

134

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989a. Integrated Risk InformationSystem (IRIS). Environmental Criteria and Assessment Office, Cincinnati,Ohio. Revised May 1, 1989

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989b. Health Effects AssessmentSummary Tables. Prepared by Office of Health and EnvironmentalAssessment, Environmental Assessment and Criteria Office, Cincinnati,Ohio, for the Office of Solid Waste and Emergency Response, Office ofEmergency and Remedial Response, Washington, D.C. March 1989

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989c. Personal communication withHerman Gibb of the Carcinogen Assessment Group (CAG). May 3, 1989

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989d. Review of the National AmbientAir Quality Standards for Lead: Exposure Analysis Methodology andValidation. Air Quality Management Division, Office of Air QualityPlanning and Standards. Research Triangle Park, NC 27711

FITZHUGH, O.G., NELSON, A.A., LAUG, E.P., and KUNZE, F.M. 1950. Chronic oraltoxicities of mercury-phenyl and mercuric salts. Arch. Ind. Hyg. Occup.Med 2:433-441

FOSTER, S.A., and CHROSTOWSKI, P.C. 1987. Inhalation exposures to volatileorganic contaminants in the shower. Presented at the 80th Annual Meetingof the Air Pollution Control Association, New York, June 21-26, 1987

FREUNDT, K.J., LIEBALDT, G.P., and LIEBERWIRTH, E. 1977. Toxicity studies ontrans-l,2-dichloroethylene. Toxicology 7:141-153

FUKUDA, K., TAKEMOTO, K., and TSURUTA, H. 1983. Inhalation carcinogenicityof trichloroethylene in mice and rats. Ind. Health 21:243-254

GERRITSE, K.G., VRIESEMA, R., DALENBERG, J.W. and DeROSS, H.P. 1982. Effectof sewage sludge on trace metal mobility in soils. J. Environ. Qual.11:359-364

GIBSON, J.E., and BECKER, B.A. 1970. Placental transfer, embryo toxicity,and teratogenicity of thallium sulfate in normal and potassium-deficientrats. Toxicol. Appl. Pharmacol. 16:120-132

GLOVER, J.R. 1967. Selenium in human urine: A tentative maximum allowableconcentration for industrial and rural populations. Ann. Occup. Hyg.10:3-10

GOYER, R.A. 1986. Toxic effects of metals. In Klaasen, C.D., Andur, M.D.,and Doull, J., eds. Casarett and Doull's Toxicology: The Basic Scienceof Poisons. 3rd ed. Macmillan Publishing Co., New York. Pp. 623-624

135

GREIM, H., BIMBOES, D., EGERT, G., GIGGELMANN, W., and KRAMER, M. 1977.Mutagenicity and chromosomal aberrations as an analytical tool for invitro detection of mammalian enzyme-mediated formation of reactivemetabolites. Arch. Toxicol. 39:159

HAMMOND, P.B., and BELILES, R.P. 1980. Metals. In Doull, J., Klaassen,C.D., and Amdur, M.O., eds. Casarett and Doull1s Toxicology: The BasicScience of Poisons. 2nd ed. Macmillan Publishing Co., New York.Pp. 409-467

HANNINEN, H., ESKELININ, L., HUSMAN, K., and NURMINEEN, M. 1976. Behavioraleffects of long-term exposure to a mixture of organic solvents. Scand.J. Work Environ. Health 2:240-255 (As cited in EPA 1987)

HARDIN, B.D., BOND, G.P., SIKOV, M.R., ANDREW, F.D., BELILES, R.P., andNIEMEIER, R.W. 1981. Testing of selected workplace chemicals forteratogenic potential. Scand. J. Work Environ. Health 7:66-75

HEYWOOD, R., SORTWELL, R.J. NOEL, P.R.B., et al. 1979. Safety evaluation oftoothpaste containing chloroform. III. Long-term study in beagle dogs.J. Environ. Pathol. Toxicol. 2:835-851

HOFMANN, H.T., BIRNSTIEL, H., and JOBST, P. 1971. The inhalation toxicity of1,1- and 1,2-dichloroethane. Arch. Toxikol. 27:248-265

HOLLAND, R.H., McCALL, M.S., and LANZ, H.C. 1959. A study of inhaledarsenic-74 in man. Cancer Res. 19:1154-1156

HORIUCHI, K., HORIGUCHI, K., KADOWAKI, K., and ARATAKE, K. 1962. Studies onthe industrial tetrachloroethane poisoning. Osaka City Med. J. 8:29-38

HUDAK, A., and UNGVARY, G. 1978. Embryotoxic effects of benzene and itsmethyl derivatives: Toluene, xylene. Toxicology 11:55-63

HWANG, S.T. 1986. Models Used in Air Release Rate Calculations inDevelopment of Advisory Levels for Polychlorinated Biphenyls (PCBs)Cleanup. U.S. Environmental Protection Agency, Office of Health andEnvironmental Assessment. OHEA-E-187

INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (IARC). 1979. IARC Monographs onthe evaluation of the carcinogenic risks of chemicals to humans.Vol. 20: Some Halogenated Hydrocarbons. World Health Organization, LyonFrance

INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (IARC). 1980. Some Metals andMetallic Compounds. IARC Monographs on the Evaluation of theCarcinogenic Risk of Chemicals to Humans. World Health Organization,Lyon, France. Vol. 23, pp. 143-204

136

INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (IARC). 1982. IARC Monographs onthe Evaluation of the Carcinogenic Risk of Chemicals to Humans. Volume27: Some Aromatic Amines, Anthraquinones and Nitroso Compounds, andInorganic Fluorides Used in Drinking-Water and Dental Preparations.World Health Organization, Lyon, France

IRISH, D.D. 1963. Vinylidene chloride. In Patty, F.A., ed. IndustrialHygiene and Toxicology. 2nd ed. John Wiley and Sons, New York.Vol. II, pp. 1305-1309

IVANKOVIC, S., and PREUSSMAN, R. 1975. Absence of toxic and carcinogeniceffects after administration of high doses of chronic oxide pigment insubacute and long-term feeding experiments in rats. Fd. Cosmet. Toxicol.13:347-351

JORGENSON, T.A., MEIERHENRY, E.F., RUSHBROOK, C.J., et al. 1985.Carcinogenicity of chloroform in drinking water to male Osborne-Mendelrats and female B6C3F1 mice. Fund. Appl. Toxicol. 5:760-769

KAO, J.K., PATTERSON, F.K., and HALL, J. 1985. Skin penetration andmetabolism of topically applied chemicals in six mammalian speciesincluding man: An in vitro study with benzo[a]pyrene and testosterone.Toxicol. Appl. Pharmacol. 81:502-516 (As cited in ATSDR 1987)

KARNOFSKY, D.A., RIDGWAY, L.P., and PATTERSON, P.A. 1950. Production ofachondroplasia in the chick embryo with thallium. Proc. Soc. Exp. fiiol.Med. 73:255-259

KAWAMURA, R., IKUTA, H., FUKUZUMI, S., et al. 1941. Intoxication bymanganese in well water. Kitasato Arch. Exp. Med. 18:145-149

KIMBROUGH, R.D., SQUIRE, R.A., LINDER, R.E., STRANDBERG, J.D., MONTALI, R.J.and BURSE, V.W. 1975. Induction of liver tumors in Sherman strainfemale rats by polychlorinated biphenyl Aroclor 1260. J. Natl. CancerInst. 55:1453

KIMMERLEE, G., and EBEN, A. 1973. Metabolism, excretion and toxicology oftrichloroethylene after inhalation. 1. Experimental exposure on rat.Arch. Toxicol. 30:115

KIMURA, E.T., EBERT, D.M., and DODGE, P.W. 1971. Acute toxicity and limitsof solvent residue for sixteen organic solvents. Toxicol. Appl.Pharmacol. 19:699-704

KJELLSTRAND.P., HOLQUIST.B., AIM,P., KANJE, M., ROMARE, S., JONSSON, I.,MANNSON, L., and BJERKEMO, M. 1983. Trichloroethylene: Further studiesof the effects on body and organ weights and plasma butyl cholinesteraseactivity in mice. Acta. Pharmacol. Toxicol. 53:375-384 (As cited in EPA1985)

137

LABELLE, C.W., and BRIEGER, H. 1955. Vapor toxicity of a composite solventand its principal components. Arch. Ind. Health 12:623-627

1AGOY, P.K. 1987. Estimated soil ingestion rates for use in risk assessment.Risk Anal., February 1987

LAI, J.C.K., LEUNG, T.K.C., and LIM, L. 1982 Activities of the mitochondrialNAD-linked isocitric dehydrogenase in different regions of the rat brain.Changes in aging and the effect of chronic manganese chlorideadministration. Gerontology 28:81-85

LANDE, S.S., DURKIN, F.R., CHRISTOPHER, D.H., HOWARD, P.H., and SAXENA, J.1976. Investigation of Selected Potential Environmental Contaminants:Ketonic Solvents. Environmental Protection Agency, Washington, D.C. EPA560/2-76-003

LEONARD, A., GERBER, G.B., JACQUET, P., andLAUWERYS, R.R. 1984.Mutagenicity, carcinogenicity, and teratogenicity of industrially usedmetals. In Kirsch-Volders, M., ed. Mutagenicity, Carcinogenicity andTeratogenicity of Industrial Pollutants. Plenum Press, New York.Pp. 59-126

LEUNG, T.K.C., LAI, J.C.K., and LIM, L. 1981. The regional distribution ofmonoamine oxidase activities towards different substrates: Effects inrat brain of chronic administration of manganese chloride and of aging.J. Neurochem. 36:2037-2043

LISS, P.S., and SLATER, P.G. 1974. Flux of gases across the air-seainterface. Nature 247:181-184

MACKENZIE, R.D., BYERRUM, R.V., DECKER, C.F., HOPPERT, C.A., AND LONGHAM, F.L.1958. Chronic toxicity studies II. Hexavalent and trivalent chromiumadministered in drinking water to rats. Arch. Ind. Health 18:232-234

MALTONI, C., LEFEMINE, G., COTTI, G., CHIECO, P., and PATELLA, V. 1985b.Experimental Research on Vinylidine Chloride Carcinogenesis. In Archivesof Research on Industrial Carcinogenesis. Princeton ScientificPublishers, Princeton, New Jersey. 3 vols.

MALTONI, C., CONTI, B., COTTI, G., and BELPOGGI, F. 1985a. Experimentalstudies on benzene carcinogenicity at the Bologna Institute of Oncology:Current results and ongoing research. Am. J. Ind. Med. 7:415-446

MANCUSO, T.F. 1975. International Conference on Heavy Metals in theEnvironment. Toronto, Canada

MIDWEST RESEARCH INSTITUTE (MRI). 1986. Subchronic (90-day) toxicity studyof thallium sulfate in Sprague-Dawley rats. Office of Solid Waste. U.S.EPA Washington, D.C

'

138

MILLS, W.B., PORCELLA, D.B., UNGS, M.K. , GHERINI, S.A. , SUMMERS, K.V. , MOK,L. , RUPP, G.L. , and BOWIE, G.L. 1985. Water Quality Assessment: AScreening Procedure of Toxic and Conventional Pollutants in Surface andGround Water. Center for Water Quality Modeling, Environmental ResearchLaboratory, Athens, Georgia. EPA 600/6-85-002a

MIRKOVA, E., ANTON, G., MIKHAILOVA, A., KHINKOVA, L. , and BENCHEV, I.V. 1983.Prenatal toxicity to xylene. J. Hyg. Epidemiol. Microbiol. Imnunol.27:337-343

NATIONAL ACADEMY OF SCIENCES (HAS). 1974. Vanadium. Committee on BiologicalEffects of Atmospheric Pollutants, Division of Medical Sciences, NationalResearch Council, Washington, D.C.

NATIONAL ACADEMY OF SCIENCE (NAS). 1976. Health Effects of Benzene: AReview Committee on Toxicology, Assembly of Life Sciences. NationalResearch Council, Washington, D.C.

NATIONAL ACADEMY OF SCIENCES (NAS). 1980. Drinking Water and Health.National Academy Press, Washington, D.C. Vol. 3

NATIONAL CANCER INSTITUTE (NCI) . 1976a. Carcinogenesis Bioassay ofChloroform. CAS No. 67-66-3. NCI Carcinogenesis Technical Report SeriesNo. 0. Bethesda, M.D. DHEW (NIH) Publication No. 76

NATIONAL CANCER INSTITUTE (NCI). 1976b. Carcinogenesis Bioassay ofTrichloroethylene . CAS No. 79-01-6. Carcinogenesis Technical ReportSeries No. 2. PB-264 122

NATIONAL CANCER INSTITUTE (NCI). 1977. Bioassay of Tetrachloroethylene forPossible Carcinogenicity. CAS No. 127-18-4. NCI CarcinogenesisTechnical Report Series No. 13, Washington, D.C. DHEW (NIH) PublicationNo. 77-813

NATIONAL CANCER INSTITUTE (NCI). 1978a. Bioassay of 1,1-Dichloroethane forPossible Carcinogenicity. CAS No. 75-34-3. NCI Carcinogenesis TechnicalReport Series No. 66, Washington, D.C. DHEW Publication No. (NIH)78-1316

NATIONAL CANCER INSTITUTE (NCI). 1978b. Bioassay of Aroclor 1254 forPossible Carcinogenicity. Cas. No. 27323-18-8. NCI CarcinogenesisTechnical Report Series No. 38. DHEW (NIH) Publication No. 78-838

NATIONAL CANCER INSTITUTE (NCI). 1978c. Bioassay of1,1,2,2-Tetrachloroethane for Possible Carcinogenicity. NCI Tech. Rep.Ser. No. 27 "

139

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH). 1977a.Criteria for a Recommended Standard—Occupational Exposure to Coal TarProducts. DHEW (NIOSH) 78-107

NATIONAL INSTITUTE OF OCCUPATIONAL SAFETY AND HEALTH (NIOSH). 1977b.Criteria for a Recommended Standard--Occupational Exposure to Vanadium.DHEW (NIOSH) Publication No. 77-222

LNATIONAL TOXICOLOGY PROGRAM (NTP). 1982. Carcinogenesis Bioassay of Di(2-

ethylhexyl)phthalate in F344 Rats and B6C3Fi Mice. Feed Study. NTPTechnical Report Series No. 217, U.S. Department of Health and HumanServices. NIH Publication No. 82-1773. NTP-80-37

NATIONAL TOXICOLOGY PROGRAM (NTP). 1983. Carclnogenesis Studies ofTrichloroethylene (Without Epichlorohydrin), GAS No. 79-01-6, in F344/Nrats and B6C3F! mice (Gavage Studies). Draft. August 1983. NTP 81-84,NTP TR 243.

NATIONAL TOXICOLOGY PROGRAM (NTP). 1984. Annual Plan for Fiscal Year 1984.DHHS, Public Health Service, Research Triangle Park, North Carolina.NTP-84-023

NATIONAL TOXICOLOGY PROGRAM (NTP). 1986a. Toxicology and CarcinogenesisStudies of Tetrachloroethylene (Perchloroethylene) (GAS No. 127-18-4) inF344/N Rats and B6C3F1 Mice (Inhalation Studies). NTP Technical ReportSeries No. 311, Research Triangle Park, North Carolina. DHEW (NIH)Publication No. 86-2567

NATIONAL TOXICOLOGY PROGRAM (NTP). 1986b. Toxicology and CarcinogenesisStudies of Xylenes (Mixed) [60X m-Xylene; 14X p-Xylene; 9X o-Xylene; 17ZEthylbenzene] in F344/N Rats and B6C3F! Mice (Gavage Studies). December1986. NTP TR 327

NAVROTSKIY, V.K., KASHIN, L.M., KULINSKAYA, I.L., ET AL. 1971. Comparativeassessment of the toxicity of a number of industrial poisons when inhaledin low concentrations for prolonged periods. Trudy S'ezda GigenistovUkranisoi 8:224-226 (Russian)

NAWROT, P.S., and STAPLES, R.E. 1979. Embryo-fetal toxicity andteratogenicity of benzene and toluene in the mouse. Teratology 19:41A

NEAL, J., and RIGDON, R.H. 1967. Gastric tumors in mice fed benzo(a)pyrene:A quantitative study. Tex. Rep. Biol. Med. 25:553-557

NEW YORK STATE DEPARTMENT OF ENVIRONMENTAL CONSERVATION (NYSDEC). 1986. NewYork State Air Guide. 1. Guidelines for the Control of Toxic AmbientAir Contaminants

140

NORBACK, D.H., and WELTMAN, R.H. 1985. Polychlorinated biphenyl induction ofhepatocellular carcinoma in the Sprague-Dawley rat. Environ. HealthPerspect. 1:134-143

NY SOIL SURVEY. 1989. Personal communication

; O'CONOR, D.J., and DOBBINS, W. 1956. The mechanics of aeration in natural'• streams. J. Sanit. Eng. Div. ASCE 82:SA6

OTT, M.G., TOWNSEND, J.C., FISHBECK, W.A., and LANGNER, R.A. 1978. Mortalityamong individuals occupationally exposed to benzene. Arch. Environ.Health 33:3-10

OTT, W.R. 1988. A Physical Explanation of the Lognormallity of PollutantConcentrations. Presented at the 81st Annual Meeting APCA June 19-24,1988

PARKER, J.C., CASEY, G.E., and BAHLNON, L.J. 1979. NIOSH currentintelligence bulletin No. 27. Chloroethanes: Review of toxicity. Am.Ind. Hyg. Assoc. J. 40:A46-A60

PERRY, H.M., KOPP, S.J., ERLANGER, M.W., and PERRY, E.G. 1983.XVII. Cardiovascular effects of chronic barium ingestion. In Hemphill,D.D. , ed. Proceedings of the University of Missouri's 17th AnnualConference of Trace Substances in Environmental Health. University of

x—s Missouri Press, Columbia, Missouri (As cited in EPA 1984)

PFEIFFER, E.H. 1977. Oncogenic interaction of carcinogenic andnoncarcinogenic polycyclic aromatic hydrocarbons. In Mohr, V., Schamhl,D., and Tomatic, L., eds. Air Pollution and Cancer in Man. IARC

4 Scientific Publication No. 16. World Health Organization, Lyon, France

POIGER, H., and SCHLATTER, C. 1980. Influence of solvents and absorbents ondermal and intestinal absorption of 2,3,7,8-TCDD. Food Cosmet. Toxciol.18:477-481

PORIES, W.J., HENZEL, J.H., ROB, C.G., and STRAIN, W.H. 1967. Accelerationof wound healing in man with zinc sulfate given by mouth. Lancet.1:121-124

PRASAD, A.S., SCHOOMAKER, E.B., ORTEGA, J., et al. 1975. Zinc deficiency insickle cell disease. Clin. Chem. 21:582-587

QUAST, J.F., HUMISTON, C.G., WADE, C.E., BALLARD, J., BEYER, J.E., SCHWETZ,R.W., and NORRIS, J.M. 1983. A chronic toxicity and oncogenicity study 3in rats and subchronic toxicity study in dogs on ingested vinylidene 4chloride. Fund. Appl. Toxicol. 3:55-62

141

RAHOLA, T., HATTULA, T., KORLAINEN, A., AND MIETTINEN, J.K. 1971. Thebiological halftime of inorganic mercury (Kg2*) in man. Scand. J. Clin.Invest. 27(suppl. 116):77 (Abstract)

RAY-BETTLEY, F., and O'SHEA, J.A. 1975. The absorption of arsenic and itsrelation to carcinoma. Br. J. Dermatol. 92:563-568

RINSKY, R.A., YOUNG, R.J., and SMITH, A.B. 1981. Leukemia in benzeneworkers. Am. J. Ind. Med. 3:217-245

RUMACK, B.H., ed. 1986. Poisindex. Microfiche ed. Micromedix, Inc.,Denver, Colorado, in association with the National Center for PoisonInformation, with updates, 1975-present

SANTODONATO, J., HOWARD, P., and BASU, D. 1981. Health and ecologicalassessment of polynuclear aromatic hydrocarbons. J. Environ. Pathol.Toxicol. 5:1-364

SARIC, M., MARKICEVIC, S., and HRUSTIC, 0. 1977. Occupational exposure tomanganese. Br. J. Ind. Med. 34:114-118

SAVOLAINEN, K. , RIIHIMAKI, V., SEPPALAINEN, A.M., and LINNOILA, M. 1980.Effects of short-term m-xylene exposure and physical exercise on thecentral nervous system. Int. Arch. Occup. Environ. Health 37:205-217

SCHAEFER, H., ZESCH, A., and STUTTGEN, G. 1983. Skin Permeability.Springer-Verlag, New York

SCHAEFFER, E., GREIM, H., and GOESSNER, W. 1984. Pathology of chronicpolychlorinated biphenyl (PCB) feeding in rats. Toxicol. Appl.Pharmacol. 75:278-288

SCHAUM, J.L. 1984. Risk Analysis of TCDD Contaminated Soil. U.S.Environmental Protection Agency, Office of Health and EnvironmentalAssessment, Washington, D.C. November 1984. EPA 600/8-84-031

SCHMAHL, D. 1955. Testing of naphthalene and anthracene as carcinogenicagents in the rat. 2. Krebsforsch. 60:697-710 (German with Englishtranslation)

SCHMIDT, P., BINNEWIES, S., GOHLKE, R., and ROTHE, R. 1972. Subacute actionof low concentrations of chlorinated ethanes on rats with and withoutadditional ethanol treatment. I. Biochemical and toxicometric aspects,especially results in subacute and chronic toxicity studies with1,1,2,2-tetrachloroethane. Int. Arch. Arbeitsmed. 30:283-298 (German)

SCHROEDER, H.A., AND MITCHNER, M. 1975. Life-term studies in rats: Effectsof aluminum, barium, beryllium, and tungsten. J. Nutr. 105:421-421

142

SCHROEDER, H.A., MITCHNER, M., and NASOR, A.P. 1970. Zirconium, niobium,antimony, vanadium, and lead in rats: Life term studies. J. Nutr.100:59-66

SCHWETZ, B.A., LEONG, B.K.J., and GEHRING, P.J. 1975. The effect ofmaternally inhaled trichloroethylene, perchloroethylene, methylchloroform, and methylene chloride on embryonal and fetal development inmice and rats. Toxicol. Appl. Pharmacol. 55:207-219

SCHWETZ, B.A., LEONG, B.K.J., and GEHRING, P.J. 1974. Embryo- and feto-toxicity of inhaled carbon tetrachloride, 1,1-dichloroethane and methylethyl ketone in rats. Toxicol. Appl. Pharmacol. 28:452-464

SHIOTA, K., and NISHIMURA, H. 1982. Teratogenicity of di(2-ethylhexyl)phthalate (DEHP) and di-n.-butyl phthalate (DBP) in mice. Environ. HealthPerspect. 45:65-70

SKOG, E., and WAHLBERG, J.E. 1964. A comparative investigation of thepercutaneous absorption of metal compounds in the guinea pig by means ofthe radioactive isotopes: 51Cr, 58Co, "Zn, 110mAg, "̂ Cd, 203Hg. J.Investigative Dermatol. 36:187-200

SMITH, C.C. 1953. Toxicity of butyl stearate, dibutyl sebacate, dibutylphthalate, and methoxyethyl oleate. Arch. Ind. Hyg. 7:310

STEPHENS, C-. 1945. Poisoning by accidental drinking of trichloroethylene.Br. Med. J. 2:218

STEWART, R.D., HAKE, C.L., FORSTER, H.V., LEBRUN, A.J., PETERSON, J.F., andWU, A. 1974. Tetrachloroethylene: Development of a biologic standardfor the industrial worker by breath analysis. Medical College ofWisconsin, Milwaukee, Wisconsin. NIOSH-MCOW-ENUM-PCE-74-6

STOKINGER, H.E., WAGNER, W.E., MOUTA1N, J.T., STACKSILL, F.R., DOBROGORSKI,O.J., and KEENAN, R.G. 1953. Unpublished Results. National Institutefor Occupational Safety and Health, Division of Occupational Health,Cincinnati, Ohio

TAKEUCHI, Y., ONO, Y., HISANAGA, N., et al. 1983. An experimental study ofthe combined effects of n-hexane and methyl ethyl ketone. Br. J. Ind.Med. 40:199-203

TARASENKO, M., PROMIN, 0., and SILAYEV, A. 1977. Barium compounds asindustrial poisons (an experimental study). J. Hyg. Epiderm. Microbial.Immunol. 21:361 (As cited in EPA 1984) |

^TASK GROUP ON METAL ACCUMULATION. 1973. Accumulation of toxic metals with

special reference to their absorption, excretion and biological ^half times. Environ. Phys. Biochem. 3:65-67 :-»

143

TATRAI, E.t TJNGVARY, G., and CSEH, I.R. 1981. The effect of long-terminhalation of o-xylene on the liver. Ind. Environ. Xenobiotics Proc.Int. Conf. Pp. 293-300

THYSSEN, J., ALTHOFF, J., KIMMERLE, G., and MOHR, U. 1981. Inhalationstudies with benzo(a)pyrene in Syrian golden hamsters. J. Natl. CancerInt. 66:575-577

TORKELSON, T.R., OYEN, F., McCOLLISTER, D.D., and ROWE, V.K. 1958. Toxicityof 1,1,1-trichloroethane as determined on laboratory animals and humansubjects. Am. Ind. Hyg. Assoc. J. 19:353-362

«

TORKELSON, T.R., and ROWE, V.K. 1981. Halogenated aliphatic hydrocarbons.In Clayton, G.D., and Clayton, P.B., eds. Patty's Industrial Hygiene andToxicology. 3rd ed. John Wiley and Sons, New York. Vol. 2B,pp. 3550-3559

TSENG, W.P. 1977. Effects and dose-response relationships of skin cancer andblackfoot disease with arsenic. Environ. Health Perspect. 19:109-119

TSENG, W.P., CHU, H.M., HOW, S.W., FONG, J.M., LIN, C.S., and YEH, S. 1968.Prevalence of skin cancer in an endemic area of chronic arsenicism inTaiwan. J. Natl. Cancer Inst. 40:453-463

U.S. WEATHER BUREAU. 1966. Evaporation Maps for the United States

VON OETTINGEN, W.F., NEAL, P.A., DONAHUE, D.D., et al. 1942b. The toxicityand potential dangers of toluene—preliminary report. J. Am. Med. Assoc.118:579-584 (As cited in EPA 1987)

VON OETTINGEN, W.F., NEAL, P.A., DONAHUE, D.D., et al. 1942a. The Toxicityand Potential Dangers of Toluene, with Special Reference to its MaximalPermissible Concentration. PHS Publication No. 279. P. 50 (As cited inEPA 1987)

WADDEN, R.A., and SCHEFF, P.A. 1983. Indoor Air Pollution. John Wiley &Sons, Inc.

WAGONER, J.K. , INFANTE, P.F., and BAYLISS, D.L. 1980. Beryllium: Anetiologic agent in the induction of lung cancer, nonneoplasticrespiratory disease, and heart disease among industrially exposedworkers. Environ. Res. 21:15-34

WOLF, M.A., ROWE, V.K., McCOLLISTER, D.D., HOLLINGSWORTH, R.L., and OYEN, F.1£56. Toxicological studies of certain alkylated benzenes and benzene.Arch. Ind. Health 14:387-398

144

WONG, 0., MORGAN, R.W., AND WHORTON, M.D. 1983. Comments on the NIOSH Studyof Leukemia in Benzene Workers. Technical report submitted to GulfCanada, Ltd. by Environmental Health Associates

WORLD HEALTH ORGANIZATION (WHO). 1976. Environmental Health Criteria,Mercury. Geneva

YANG, G., WANG, S., ZHOU, R., and SUN, S. 1983. Endemic seleniumintoxication of humans in China. Am. J. Clin. Nutr. 37:872-881

145

; remedial planning activities at selected … · the recommendation, currently being implemented,...

Documents