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APPENDIX G

AIR QUALITY ASSESSMENT RELATED TO AIR STRIPPER EMISSIONS

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APPENDIX G

AIR QUALITY ASSESSMENT RELATED TO AIR STRIPPER EMISSIONS

G.1 BACKGROUND

This appendix provides the basis for the ambient air quality modeling approach used toassess the impact of air emissions from air stripper towers located near the CSG facility.

The air strippers are being used to remove volatile organic compounds (VOCs) fromgroundwater wells in the area near the CSG facility. Operation of the air strippers releasesVOCs to the air from stacks positioned at various heights above the ground. An air qualitymodeling analysis was performed to estimate the impacts of VOCs released to theatmosphere from the air strippers. The air quality modeling analysis estimates ambientconcentrations of selected pollutants at various locations in the CSG facility area. Thepredicted ambient concentrations were used to assess the health risk posed to current andhypothetical future receptors through the inhalation of outdoor air, as described in Section6 of this report.

G.2 MODELING APPROACHG.2.1 Introduction

This section describes the air quality modeling approach utilized in this analysis to estimateambient concentrations of selected pollutants. The modeling approach required selectionof the most appropriate model for this analysis, dependent upon the following factors:

• Emissions inventory/stack characteristics.• Land use.• Stack height relative to Good Engineering Practice (GEP).• Terrain influences.

Each of these are described in the following subsections.

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G22 Emission Inventory

The emissions modeling analyzed existing air strippers. Table G-l presents the compoundsof concern and estimated emission rates of each pollutant. The estimated emission ratesare based on an assumed 100% removal of the contaminants from the groundwater and thatthe emission rates remain constant over time. Table G-2 provides stack characteristics foreach air stripper. Source combination ATJD3-5, VFCC-2, VFCC-3 and the French drainwere evaluated in the current use scenarios and source combinations AUD3-5, VFCC-2,VFCC-3 and VFCC-4 were evaluated in the future use scenarios.

G.2.3 Land Use Determination

Among the air quality models readily available and generally acceptable to EPA, theenvironmental setting must be specified as either urban or rural. This is because the airover an urban area disperses air pollutant emissions much differently than does air overrural areas. As a result, different sets of dispersion coefficients must be used.

According to EPA modeling guidance (1986a, 1987) an analysis of land use according to theclassification method of Auer (1978) is the best way to make this determination. If morethan 50% of the area within 3 km of the source can be classified as urban, then urbandispersion coefficients should be used; othei'wise it is classified as rural, and rural dispersioncoefficients should be used. Based on a review of Norristown geographical setting andreview of the land use pattern near CSG, the area is classified as rural. Therefore, modelsthat include rural dispersion coefficients were used to assess the air quality impact of theair strippers.

G2A Good Engineering Practice Stack Height Analysis for the French Drain

With respect to stack heights, Section 123 of the Clean Air Act defines Good EngineeringPractice (GEP), as "the height necessary to ensure that emissions from the stack do notresult in excessive concentrations of any pollutant in the immediate vicinity of the source

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i as a result of atmospheric downwash, eddies or wakes which may be created by me sourceitself, nearby structures or nearby terrain obstacles." For this analysis, 40 CFR 51.1(ii)

I defines nearby structure as "that distance up to five times the lesser of the height or theii (projected) width dimension of a structure, but not greater than 0.8 km...".i

i According to 40 CFR 51.1(ii), GEP stack height means the greater of:i!] . •i

I • 65 meters, measured from the ground-level elevation at the base of the stack:!i| • For stacks in existence after January 12, 1979,I

Hg = H + 1.5 Li ' f\

\ ' Where:

\ Hg = GEP stack height

H = height of nearby structure(s) measured from the ground levelI elevation at the base of the stack.ii ' • L = lesser of height or projected width of nearby structures; or

• The height demonstrated by fluid model or field study that satisfies thedefinition of GEP in Section 123 of the Clean Air Act,

| The GEP stack height analysis for the French drain air stripper was based upon the! appropriate EPA (1985) guidance document. The GEP determination was made for eachbuilding at the CSG facility, and then the air stripper stack was associated with the nearbybuilding that would result in the greatest GEP. The only building at the CSG facility thatis close enough to the French drain air stripper to cause wake-effect downwash is the airstripper building. The GEP stack height based on the air stripper building is 22.5 ft whichis slightly greater than the stack height of the stripper, 20 ft.

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Though the potential for downwash effects was not evaluated for any of the air strippers,no receptors evaluated in the risk assessment were located close enough to any stack to beinfluenced by downwash. If individual receptors near the AUD3-5 air stripper are to beevaluated, accurate data for building heights and locations will be required because theproximity of the stack to potential receptors may result in downwash effects.

G.2.5 Terrain Influences

Terrain within one mile of the air strippers varies from 75 feet mean sea level (msl) to 300feet msl, with the base elevation of the air strippers ranging between 190 and 220 feet msl.Because of the large variation in terrain elevation in proximity to the strippers, terrainelevations were used in the receptor grid. Terrain, directions were identified from USGStopographic maps of the area.

G.2.6 Model Selected

The models utilized in the analysis were the EPA Industrial Source Complex Short Term(ISCST) model and WESTON's Intermediate Terrain Model (ITM). The ITM is a hybridversion of the EPA ISCST and COMPLEX I models. The ITM model was utilized becauseintermediate and complex terrain exists within 1 km of the facility. The EPA guidance onair quality modeling requires intermediate terrain be evaluated when there are terrainelevations nearby that are above stack height and below plume height.

Stack-tip downwash.Final plume rise.Buoyancy-induced dispersion (BID).No pollutant decay.Default wind profile exponents. "Default vertical temperature profile gradients.

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. IG.2.7 Meteorological Input

The meteorological database used to model the air quality impacts of the air strippersconsisted of the data set of hourly wind speed, wind direction, ambient temperature, andwind tower description recorded at Philadelphia International Airport. The airport isapproximately 21 miles southeast of Norristown and is the nearest first order NationalWeather Service Station. This station is considered representative of the wind patterns overthe CSG facility area following EPA Modeling Guidance. Hourly observations over a 5-yearperiod (1986-1990) were combined with current upper air observations from Sterling, VA,and preprocessed with the USEPA RAMMET program to create an input file from theISCST model.

G.2.8 Receptor Network

A polar coordinate receptor grid was established for the air quality impact analysis. Thepolar grid was centered upon the French drain air stripper which is located on the CSGfacility. The receptor grid was set up with the French drain at the origin. The gridconsisted of 36 radials beginning with north and spaced 10 degrees apart; and the followingdistances (in meters) were evaluated along each radial: 100, 200, 300, 400, 500, 600, 700,800, 900, 1000, 1250, 1500, 1750, 2000, 2500, 3000, 3500, 4000, 4500, and 5000. Maximumterrain elevations between the receptor in question and all surrounding receptors were used.Discrete receptors were established at locations that correspond to the current and futureuse exposure scenarios described in Section 6, and include:

Residential private well location.Residential public well location.GWCC member and worker.GWCC future resident.VFCC current and future worker.

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G.3 AIR QUALITY IMPACTS FOR AIR STRIPPERS

GJ.l Introduction

Five-year annual average VOC concentrations at selected discrete receptors over the period1986-1990 were calculated based on a 1 gram/second emission rate for individual airstrippers. The overall maximum and 5-year annual concentrations were calculated using acombination of the sources. Emissions from air strippers AUD3-5, VFCC-2, VFCC-3 andthe French drain were evaluated as one combination for the current use exposure scenarios.AUD3-5, VFCC-2, VFCC-3, and VFCC-4 emissions were evaluated as the future usescenario source combination. The resulting concentrations based on 1 gram/second weremultiplied by the emission rate for each compound to obtain compound-specific ambientconcentration. The resulting concentrations at each receptor from each source for eachcompound were combined for each exposure scenario.

G.3.2 Air Quality Impacts for Air Strippers

Two scenarios were used in determining the potential impact of air strippers in the vicinityof the French drain air stripper. Discrete receptors were located in both residential andindustrial areas. Figure G-l shows the location of each receptor. The golf course receptorconcentration was based on combining the highest concentrations caused by each air stripperwhich occurred on the golf course. The maximum golf course concentrations from eachsource may not occur at the same location and this resulted in an extremely conservativeapproach (i.e., estimates higher concentrations) and slight overestimation of the actualconcentration impact. The overall maximum concentration was also determined for eachscenario based upon the polar grid.

Two of the air strippers, VFCC-2 and VFCC-3, have side exhaust vents. As a result, theeffective plume height would be reduced. To compensate for the inability of the ISC modelto properly simulate side exhaust vents, the ISCST model was run for VFCC-2 and VFCC-3at an exit velocity of 0.5 meter/second to simulate the reduced exit velocity.

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The location of the maximum overall concentration was located at 010°, 300 meters fromthe French drain on the golf course for the present use scenario. The golf course receptorvalue is greater than the maximum value which is also located on the course due to theconservative nature in which concentrations were calculated for golf course receptor. Forthe future use scenario, the maximum concentration occurred at 130°, 100 meters from theFrench drain which is near receptor 2. Table G-3 presents the two source combinations forboth current and future use exposure scenarios. All concentrations are in micrograms per

| cubic meter (yug/m3) and represent 5-year annual averages.iiG.4 SUMMARY

1 '

j An air quality modeling analysis was conducted for emissions from several air strippers inj the vicinity of the CSG facility. The modified ISCST model was used to calculate ambientI pollutant concentrations because of air stripper emissions. A 5-year meteorological data setI was used to estimate average annual concentrations. Emissions rates were used based onconservative calculations of pollutant emissions from groundwater measurements and

t assumed 100% removal of the contaminant to the atmosphere as a result of the airI stripping. It was also assumed that the pollutant emission rates remain constant during thei ''} operation of the air strippers.

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** m TJ- en n- Tf ino o o o o o oI I I I I I IM W Ld Ld til U UJCN in p- oo r~ vo men in •** vo CN o\ -in tf CN CN CN oo o\

S S 8 § S S Stil W Id U til til UdOO T— 00 O\ OO O VOen i* «-< CN •rr H ost~ •<-* CN VO rf t- CN

s s s § s si iw w u at— -i CNCJ <-< en en r-Oin p~ CN n- en »-< CN

Page 45: u'. ~ O C < -*§: *S ( • ta U.U.U: i. tw · O CUIU O O • Sg** **** S o o o v u 5s£§uP •S'S'S'S'S'S oooooo ib ^»-.-,~^^. d o. dodo A §ooo§S N e o O">o»-«so«- x

REFERENCES

I Auer, AH. Jr., 1978. "Correlation of Land Use and Cover with Meteorological Anomalies."i Journal of Applied Meteorology. 17:636-643.\l *

i Environmental Protection Agency (EPA). 1977. Guidelines for Air Quality Maintenance1 Planning and Analysis. Volume 10R: Procedures for Evaluating Air Quality Impact of NewI Stationary Sources. EPA Publication No. EPA 450/4-77-001. U.S. Environmental| Protection Agency, Research Triangle Park, NC. (NTIS NO. PB 274087).

EPA 1985. Guideline for Determination of Good Engineering Practice Stack Heighti (Technical Support Document for the Stack Height Regulations) (Revised). U.S.| Environmental Protection Agency, Research Triangle Park, NC. (NTIS No. PB 85-225241).

I EPA 1986a. Guideline on Air Quality Models (Revised). EPA Publication No. EPA-450/2-78-027R. U.S. Environmental Protection Agency, Research Triangle Park, NC.

EPA, 1986b. User's Network for Applied Modeling of Air Pollution (UNAMAP). Version6 (Computer Programs on Tape). National Technical Information Sendee, Springfield, VANTIS No. PB 86-222361.

EPA. 1987. Supplemental A to the Guideline on Air Quality Models (Revised). EPAPublication No. EPA-450/2-78-037R Supplement A

j MK01\RPT:28550303\commodor.apg G-13 • 02/11/92

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••'

APPENDIX H

MOS WASTE DISPOSAL RECORDS AND CSG WASTE ANALYSIS PLAN

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MONTHLY MAX TO SOLVENT TANK

Acetone 70 gallons

Freon 10 gallons

ISO Alcohol 170 gallons

Methanol Alcohol 105 gallons

Xylene , 120 gallons

J-100 Stripper 160 gallons

1112 Shipley Remover 60 gallons

A2351 Developer . 80 gallons

Starlith Developer A § B 10 gallons

DI Water . " . 1215 gallons

TOTAL makeup of tank per month 2000*gallons approx.for removal

H-l /IR3033M

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e

TANKER TRUCK

Acetone . ' - 7 0 gallons

Freon 10 gallons

ISO Alcohol 170 gallons

Methanol Alcohol 105 gallons

Xylene • 120 gallons

J-100 Stripper 160 gallons

1112 Shipley Remover 60 gallons

A2351 Developer 80 gallons

Starlith Developer A § B 10 gallons

TCE 50 gallons

DI Water 1165 gallons

TOTAL makeup of tank per monthfor removal 2000 gallons approx.

H"2 flR3033if5

Page 49: u'. ~ O C < -*§: *S ( • ta U.U.U: i. tw · O CUIU O O • Sg** **** S o o o v u 5s£§uP •S'S'S'S'S'S oooooo ib ^»-.-,~^^. d o. dodo A §ooo§S N e o O">o»-«so«- x

! • January 2, 1980

j .. 800 GALLONS PER 'MONTH*

XYLENE 120 gallons

ACE-TONE 90 gallonsj

FRE^N - 30 gallonsJi

ISO|-ALCOHOL 200 gallons

METHAL ALCOHOL • 125 gallons

111J2 SHIPLEY REMOVER 60 gallons

A2351 DEVELOPER 80 gallonsI

STAkLITH DEVELOPER A-B 10 gallons

DI WATER 85 gallonsj| TOTAL 800 gallons

- L&VLW+TJ -

H-3

Page 50: u'. ~ O C < -*§: *S ( • ta U.U.U: i. tw · O CUIU O O • Sg** **** S o o o v u 5s£§uP •S'S'S'S'S'S oooooo ib ^»-.-,~^^. d o. dodo A §ooo§S N e o O">o»-«so«- x

1tfOSTECHNOlOGYlNc: ''•' 'MLIEY FOHSE COBWRATE CENTER «« RITTEHHOUS€ ROAD NOfimSTOWII,P*.H4t1 Bt5)liM»M ORIGINAL PURCHASE ORDER «fe~— ,

/ - . 4feJ ' | Furnish all items in accordance with terms and conditions specified here and °' ^H

T0 Ashland Chemical r*y'rie lid* h<trtef- ' ^PP 0 BOX 35 Q Thil Purchot* Order shall only become effective, if the attached acknowledgement_ * * » A. J 3 U copy is signed and returned by you within 10 days from the above date.

' .LoU*t« Refcir to this Purchase Order on all packages, invoices, shipping documents andothiir correspondence related to this order.Ship prepaid and include transportation charges on invoice as a separate item andattach supporting receipts.

1 _ 1 Forward invoice in duplicate to Accounts Payable Department.

TERMS >v . F.O.8. SHtP VIA BUYER

ITEM

BLA

QUANTITY

KET

. ••'

_

\. DESCRIPTION

This order, to be in effect for one yearfros AugusV 1. 1979 to Jiily 30, 19»0.

Material will\be released as required.

Aano. Hydroxide N,Acetic Acid \Acetone N,Amaouiuo Fluoride-HF Mixhydrochloric Acid \Hydrofluoric Acid \Metiiaael \Hydrogen Peroxide— v r-. -S\ x\vi JJNitric Acid \Phosphoric Acid \ sSal f uric Acid aj\ 4Trichloroetkylane ^Xylene !•$'•'Isopropyl AlctkrholCfaroaium TrioxideCaustic Soda 50* Liquid i dr«« dep»sit

Hydrochloric Acid § drua .Lepos'lt

Sodium Hezamet&phospbateFreon TF S gal./60 lb.Vv o^s vS l0 -Sv- \ * •-

DELIVERYSCHEDULE

Si

6

/////

•>

— N.

UNITPRICE

I A*^ 4?f/ "/ .66

.-83-3.36.664iJ!S9*3.2C4. SO.48.44.565.933.443/368.55.091

.29

.362

^<— a** \

TOTAL

,

J^

,na \.-? :_, \,3,\ ^n * ' ^BP.-i."?, <«, \t -e \•H$ i. '_. S i<• •• Si. j

3> • "3 (. ia, . -> a. /

is <=} . 3-r /=7jr

,lax hX*ftpt L&rt./46-3«7I»«l ^ A J S ~>

( .J A£©S TKH{>l6-OGY, INC.PURCHASING * Z ' -J &~&

f J PURCHASING AGENT

p.R. NO. ACCOUNT NO. REQUESTED. BY DEPARTMENT INSPECTION ^ ^^

2m n=; c nnr REQUIRED n NOT REQUIRED g^^

H"4 HR30331.7

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i —r"

RECEIVEDDEC 1***GEOSC1ENCES DEPT

\o c/€3v/i -He

5

W exi; i LuwAA /^-^C1 S/-n////>A

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H-7 RR303350

Page 54: u'. ~ O C < -*§: *S ( • ta U.U.U: i. tw · O CUIU O O • Sg** **** S o o o v u 5s£§uP •S'S'S'S'S'S oooooo ib ^»-.-,~^^. d o. dodo A §ooo§S N e o O">o»-«so«- x

C—«Aem tea/

__Manufacturers of Reagent and Allied Chemicals

Office and PlantTyburn Road and Cedar Lane • Fairless Hills, Pa. 19030

215 CY 5-5006

March 21, 1980

Mr. Sully Gil lets-Materials ManagerMOS TechnologyValley Forge Corporate Center950 Rittenhouse RoadNorristown, Penna. 19401

Dear Sully:ii Shown below are our revised prices, for the chemicals that you purchase:j

! Product Package/Size Price

Sulfuric Acid, ACS 6x9#/cs. $0.38/lb.Acetic Acid, ACS 6x5#/cs. 0.85/lb.Ammonium Hydroxide, ACS 6x4*705. 0.65/lb.

; Hydrochloric Acid, ACS 4xlOVcs. 0.46/lb.Hydroflouric Acid, ACS 4xlO#/cs. . . 1.50/lb.Nitric Acid, ACS 4x7#/cs. 0.52/lb.Phosphoric Acid, ACS 6x8*705. 0.48/lb.Acetone 4x1 gal./cs. 3.70/gal.Hydrogen Peroxide 4x1 gal./cs. 5.25/gal.Methanol 4 x 1 gal ./cs . 3 .50/gal .Trichloroethylene 4x1 gal./cs. 6.30/gaI.Xylene 4x1 gal./cs. 3.75/gal.Isopropyl Alcohol 4x1 gal./cs. 3.75/gal.Hydrochloric Acid 500* Drum 0.3l/lb.

Dr. deposit 25.00/ea.Methylene Chloride 4x1 gal./cs. 4.95/gal.Methyl Ethyl Ketone 4x 1 gal./cs. 5.20/gal.

We will continue to meet your quality and delivery requirements as in the past,

Very truly yours,

£?& —— yEdmund J.Bogddn H_8Sales Representative

Page 55: u'. ~ O C < -*§: *S ( • ta U.U.U: i. tw · O CUIU O O • Sg** **** S o o o v u 5s£§uP •S'S'S'S'S'S oooooo ib ^»-.-,~^^. d o. dodo A §ooo§S N e o O">o»-«so«- x

An American NuKEM CompanyAnalytiKEM Inc.28 Springdale Road

Cherry Hill. NJ 08003609/751-1122215/923-2068

TEST REPORT NO. A17182

September 30, 1988

Prepared for:

Commodore Semi-Conductor Group950 Rittenhouse RoadNorristown, PA 19403

Attention: Debbie Edmond

Project: Wastewater and Waste Analysis

Date of Sample Receipt: September 7, 1988

Sampled by: AnalytiKEM

Sample Quantity: Four (4)

NJ Certification No. NJ 04012 " Reviewed &———————— Approved by:

NY Certification No. NY 10815Name Michael Shmookler. Ph.D.

SC Certification No. SC 94004 *'" Title Technical Director

NC Certification No. NC 258

ftR303352

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AnalytiKEM

TABLE OF CONTENTS

Page

I. Definition of Terms 1

II. Sample Designation 2

III. Methodology 3-7

IV. Analytical Results 8-16

V. Quality Control Data 17 - 24

H-10 AR3Q3353

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! Test Report No. A17182 ' , -; Page i AnalytiKEMii I. Definition of Terms

Term Definition

D Detected; result must be greater than zero.

I DI Deionized Water!

| J Compound was detected at levels below the practical• quantitation limit. The level reported is approximate.

I MS/MSD Matrix Spike/Matrix Spike Duplicateii • '" •! NA Analysis not applicable to the sample matrix.

l ND Not Detected!3

\ NR Not Requestedii NTU Nephelometric Turbidity Units

; RPD Relative Percent Difference

i RSD Relative Standard Deviationj'' TON Threshold Odor Number

U Compound was analyzed for but not detected. The preceding; number is the practical quantitation limit for the compound.

i ppb Parts-per-billion; may be converted to ppm by dividing; ' by 1,000.

i ppm Parts-per-million; may be converted to ppb by multiplying1 by 1,000.j| ug/1 Micrograms of constituent per liter of sample; equivalent

to parts-per-billion.

ug/kg Micrograms of constituent per kilogram of sample; equivalentto parts-per-billion.

ug/kg dw Micrograms of constituent per kilogram of sample reportedon a dry weight basis.

CCC Calibration Check Compound; used to verify the precision ofa GC/MS calibration curve.

SPCC System Performance Check Compound; used to verify the correctoperation of a GC/MS instrument.

•PQL Practical Quantitation Limit; the minimum level at whichcompounds can be dependably quantitated.

H-ll AR30335U

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AnalytiKEM

Test Report No. A17182Page 3

III. Methodology

Volatiles

Aqueous

. Method 624. Purgeables, Federal Register, Vol 49, No. 209,October 26, 1984.

Polychlorinated Biphenyls

Aqueous

Method 608, Organochlorine Pesticides and PCBs. Federal Register,,Vol. 49, No. 209, October 26, 1984.

Nonaqueous

. Method 3550, Sonication Extraction, Test Methods for EvaluatingSolid Waste, Physical/Chemical Methods, SW-846, Second Edition,USEPA.

. Method 8080, Organochlorine Pesticides and PCBs, Test Methodsfor Evaluating Solid Waste, Physical/Chemical Methods, SW846,Second Edition, USEPA.

H-12 AR303355

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AnalytiKEM

Test Report No. A17182Page 2

II. Sample Designation

AnalytiKEM Client DateDesignation Designation Matrix Sampled

A17182-1 Neutralization Process Aqueous 9/7/88A17182-2 - Waste Solvent Aqueous 9/7/88A17182-3 Spent Oil Nonaqueous 9/7/88A17182-4 Photoresist Nonaqueous 9/7/88

Note: Samples will be retained for 30 days beyond the test reportdate unless otherwise requested.

H-13 AR3Q3356

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AnalytiKEM

Test.Report No. A17182Page 4

III. Methodology (Cont'd)

Metals

Aqueous

Sample Preparation Methods

Test Methods for Evaluating Solid Waste, Physical/Chemical Methods,SW846, Second Edition, USEPA.

. Method 3010: Acid Digestion of Aqueous Samples and Extracts forTotal Metals for Analysis by Flame Atomic AbsorptionSpectroscopy or Inductively Coupled Plasma Spectroscopy.

. Method 3020: Acid Digestion of Aqueous Samples and Extracts forTotal Metals for Analysis by Furnace Atomic AbsorptionSpectroscopy.

Sample Analysis Methods

Methods for Chemical Analysis of Water and Wastes, EPA 600/4-79-020,USEPA, March 1983.

. Method 206.2: Arsenic (Atomic Absorption, Furnace Technique).

. Method 245.1: Mercury (Manual Cold Vapor Technique).

. Method 270.2: Selenium (Atomic Absorption, Furnace Technique).

Method 200.7: Inductively Coupleid Plasma-Atomic EmissionSpectrometric Method for Trace Element Analysisof Water and Wastes.

H~14 AR303357

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AnalytiKEMTest Report No. A17182Page 5

III. Methodology (Cont'd)i

General Chemistry

Acidity

. Methods for Chemical Analysis of Water and Wastes, EPA-600/4-79-020,USEPA, Method 305.1, March 1983.

Alkalinity

. Methods for Chemical Analysis of Water and Wastes, EPA-600/4-79-020,USEPA, Method 310.1, March 1983.

Heat of Combustion

. 1980 Annual Book of ASTM Standards, Method D3176-74, 1980.

Chloride

. Methods for Chemical Analysis of Water and Wastes, EPA-600/4-79-020,USEPA, Method 300.0, January 1984.

Cyanide, total and amenable

. Test Methods for Evaluating Solid Waste, USEPA, SW-846, SecondEdition, Method 9012.

,EP Toxicity Procedure

. Test Methods for Evaluating Solid Waste, USEPA, SW-846, SecondEdition, Method 1310.

Flashpoint

Test Methods for Evaluating Solid Waste, USEPA, SW-846, SecondEdition, Method 1010.

Isopropyl Alcohol by GC

. 2-Propanol was analyzed by direct inject chromatography using a6 ft. by 4 mm id column packed with 1% SP1000 on 60/80 meshCarbopack B and an FID detector.

H-15 AR303358

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AnalytiKEM

Test Report No. A17182Page 6

III- Methodology (Cont'd)

General Chemistry

Nitrogen, Ammonia

. Standard Methods for the Examination of Water and Wastewater, AmericanPublic Health Association, 16th Edition, Method 417, 1985.

Nitrogen. Nitrate

. Methods for Chemical Analysis of Water and Wastes, EPA-600/4-79-020,USEPA, Method 300.0, January 1984.

. Methods for Chemical Analysis of Water and Wastes, EPA-600/4-79-020,USEPA, Method 150.1, March 1983.

. Test Methods for Evaluating Solid Waste, USEPA, SW-846, SecondEdition, Method 9045.

Phosphorus

. Methods for Chemical Analysis of Water and Wastes, EPA-600/4-79-020,USEPA, Method 365.2, March 1983.

Phenolics, total

. Methods for Chemical Analysis of Water and Wastes, EPA-600/4-79-020,USEPA, Method 420.2, March 1983.

Reactivity

. Test Methods for Evaluating Solid Waste, USEPA, SW-846, SecondEdition, Method 1110.

Residue, total (TS)

. Standard Methods for Examination of Water and Wastewater, AmericanPublic Health Association, 16th Edition, Method 209A, 1985.

H-16 _^^AR303359

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AnalytiKEM

Test Report No. A17182Page 7

Ii::. Methodology (Cont'd)

General Chemistry

Residue, total volatile (TVS)

. Standard Methods for Examination of Water and Wastewater, AmericanPublic Health Association, 16th Edition, Method 209D, 1985.

Specific Gravity

. 1980 Annual Book of ASTM Standards, Method 1480-62, 1980.

i Sulfatei * ~i —•—jI . Methods for Chemical Analysis of Water and Wastes, EPA-600/4-79-020,! USEPA, Method 300.0, January 1984.i ')

Waterj

. 1980 Annual Book of ASTM Standards, Method D1744-64, 1980.

i Fluoride

. Methods for Chemical Analysis of Water and Wastes, EPA-600/4-79-020,1 USEPA. Method 300.0, January 1984.

j Surfactants (MBAS)

| . Standard Methods for the Examination of Water and Wastewater,I American Public Health Association, 16th Edition, Method 512B, 1985.

H"17 AR303360

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AnalytiKEM

Test Report No. A17182Page 8

IV. Analytical Results

Volatile Organics

Sample Designation '

A17182-1 A17182-2Method Neutralization Method Waste

Constituent Blank 1 Process Blank 2 Solvent

Chloromethane 1 U 1 U 10 U 1,000,000 U-Bromomethane 1 U 1 U 10 U 1,000,000 UVinyl Chloride 1 U 1 U 10 U 1,000,000 UChloroethane 1 U. 1 U 10 U 1,000,000 U

Methylene Chloride 1 U 4.0 10 U 1,000,000 U1,1-Dichloroethene 1 U 1 U 10 U 1,000,000 U1,1-Dichloroethane 1 U 1 U 10 U 1,000,000 U

trans-l,2-Dichloroethene 1 U 7.6 10 U 1,000,000 UChloroform 1 U 1 U 10 U 1,000,0001,2-Dichloroethane 1 U 1 U 10 U 1,000,0001,1,1-Trichloroethane 1 U 1 U 10 U 1,000,000 U

Carbon Tetrachloride 1 U 1 U 10 U 1,000,000 UBromodichloromethane 1 U 1 U 10 U 1,000,000 U1,2-Dichloropropane 1 U 1 U 10 U 1,000,000 Utrans-l,3-Dichloropropene 1 U 1 U 10 U 1,000,000 U

Trichloroethene 0.8 J 4.2 10 U 1,000,000 UDibromochloromethane • 1 U 1 U 10 U 1,000,000 U1,1,2-Trichloroethane 1 U 1 U 10 U 1,000,000 UBenzene 1 U 1 U 10 U 1,000,000 Ucis-l,3-Dichloropropene 1 U 1 U 10 U 1,000,000 U

2-Chloroethyl Vinyl Ether 1 U 1 U 10 U 1,000,000 UBromoform 1 U 1 U 10 U 1,000,000 UTetrachloroethene 1 U 1 U 10 U 1,000,000 U

1,1,2,2-Tetrachloroethane 1 U 1 U 10 U 1,000,000 UToluene 1 U 1.4 10 U 1,000,000 UChlorobenzene 1 U 1 U 10 U 1,000,000 UEthylbenzene 1 U 0.7 J 10 U 1,000,000 U

m-Xylene 1 U 3.3 10 U 1,000,000 Uo,p-Xylene 1 U 3.3 10 U 1,000,000

Units (ug/1) (ug/1) • (ug/1) (ug/1)

H"18 AR30336I

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AnalytiKEM

Test Report No. A17182Page 9

IV. Analytical Results (Cont'd)

EPA/NIH/NBS Nontargetted Library Search

No nontargetted compounds were detected in the following samples:

Method Blank 1Method Blank 2

AnalytiKEM Designation A17 182-1Neutralization

Client Designation Process

CAS Number

67-64-1

. '

76-13-1

j

109-99-9

Compound Name

2-Propanone (Acetone)

Unknown Compound1,1,2-Trichloro-1,2,2-trifluoroethane

Unknown Compound

Tetrahydrofuran

Fraction

VOA

VOA

VOA

VOA

VOA

ScanNumber

216

253

363

63 '

317

EstimatedConcentration(ug/1)

7.5

3.5

27

3.2

1.3

AnalytiKEM Designation Al7182-2Waste

Client Designation Solvent

GAS Number

67-64-1

,,

^ 76-13-1

Compound Name

2-Propanone (Acetone)

Unknown Compound1,1,2-Trichloro-1 , 2 , 2-trif luoroethane

Fraction

VOA

VOA

VOA

ScanNumber

216

254

364

EstimatedConcentration(ug/1)

12,000,000

1,100,000

1,400,000

Note: Estimated concentration is calculated against «-v,i standard. e tne nearest eluting internal

i H-19 AR303362

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AnalytiKEM

Test Report No. A17182Page 10

IV. Analytical Results (Cont'd)

Polychlorinated Biphenyls

Sample Designation

Aqueous A171'82-1 A17182-2Method Neutralization Waste

Constituent Blank Process Solvent

Aroclor 1016 1.0 U 1.0 U 1.0 UAroclor 1221 1.0 U 1.0 U 1.0 UAroclor 1232 1.0 U 1.0 U 1.0 UAroclor 1242 1.0 U 1.0 U 1.0 UAroclor 1248 1.0 U '1.0 U 1.0 UAroclor 1254 1.0 U 1.0 U 1.0 UAroclor 1260 1.0 U 1.0 U 1.0 U

Units (ug/1) (ug/1) (ug/1)

Sample Designation

Nonaqueous Al 7182-3Method Spent A17182-4

Constituent Blank _0il_____ Photoresist

Aroclor 1016 330 U ' 3,300 U 3,300 UAroclor 1221 330 U 3,300 U 3,300 UAroclor 1232 330 U 3,300 U 3,300 UAroclor 1242 330 U 3,300 U 3,300 UAroclor 1248 330 U 3,300 U 3,300 UAroclor 1254 330 U 3,300 U 3,300 UAroclor 1260 330 U 3,300 U 3,300 U

Units (ug/kg) (ug/kg) (ug/kg)

•prpfl

AR303363

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AnalytiKEM

Test Report No. A17182Page 11

IV. Analytical Results (Cont'd)

Metals

Sample Designation

A17182-1 A17182-2Method - Neutralization Waste

Parameter ' Blank Process Solvent

Arsenic, total 10 U 10 U 82Barium, total 200 U 200 U 78 JCadmium, total 10 U 10 U 10 UChromium, total 50 U 50 U 50 U

Copper, total 50 U 50 U 150Iron, total . 100 U 61 J 290Lead, total 50 U 50 U 50 UMercury, total 2.0 U 2.0 U 1.5 JNickel, total 40 U 40 U 40 USelenium, total 10 U 10 U 10 U

Silver, total 50 U 50 U 50 USodium, total 5,000 U 3,200 J 3,000 JZinc, total 20 U 53 620Boron, total 50 U 72 540Silicon, total 50 U 3,400 640

Units (ug/1) (ug/1) (ug/1)

H-21 AR303361*

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AnalytiKEM

Test Report No. A17182Page 12

III. Analytical Results (Cont'd)

EP Toxicity Procedures

Sample Designation

A17182-3Method Spent A17182-4 ' EP Toxicity

Parameter • Blank Oil Photoresist Limits

Arsenic 500 U 500 U 500 U 5,000Barium 2,000 U 2,000 U 2,000 U 100,000Cadmium 100 U 100 U 100 U 1,000Chromium 500 U 500 U 500 U 5,000

Lead 500 U 500 U 500 U 5,000-Mercury 2.0 U 2.0 U 2.0 U 200Selenium 300 U 300 U 300 U 1,000Silver 500 U 500 U 500 U 5,000

Units (ug/1) (ug/1) (ug/1) (ug/1)

H-22 AR303365

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AnalytiKEM

. Test Report No. A17182Page 13

IV. Analytical Results (Cont'd)

Reactivity

The observations for Reactivity were as follows:

. The sample(s) did not undergo violent changes under normal conditions.

The sample(s) did not react violently or form a potentially explosivemixture with water.

. The sample(s) did not appear readily capable of detonation, explosivedecomposition or reaction at standard temperature or pressure.

. The sample(s) did not generate toxic gases, vapors or fumes when exposedto pH conditions between 2 and 12.5.

The results for reactive sulfide and cyanide are as follows:

Sample Designation

Method A17182-3 A17182-4Parameter Blank Spent Oil Photoresist -

Sulfide 50,000 U 50,000 U 50,000 UCyanide 50,000 U 50,000 U 50,000 U

Units (ug/kg) (ug/kg) (ug/kg)

H"23 AR303366

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AnalytiKEM

Test Report No. A17182Page 14

IV. Analytical Results (Cont'd)

General Chemistry

Sample Designation

A17182-1Method Neutralization

Parameter Blank Process

Cyanide, total 25 U 25 UPhenolics, total, as phenol 25 U 850Flashpoint, closed cup, °F — >180pH, units — <2.0

Acidity, as CaC03 — 1,400,000Heat of Combustion, BTU/lb. — <1,000Water, % 1.0 U 87

Residue, total -10,000 U 1,800,000Total Volatile Residue 10,000 • U 20,000Ammonia-N 170 1,400Nitrate-N 500 U 4,800Phosphorus, total 50 U 600

Sulfate 1,000 U 1,800,000Chloride ' 500 U 86,000Fluoride 500 ' U 30,000Surfactants (MBAS) 100 U 2002-Propanol 150 U 560

Units (ug/1) (ug/1)

H-24 AR303367

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AnalytiKEM

Test Report No. A17182Page 15

IV. Analytical Results (Cont'd)

General Chemistry

Sample Designation

A17182-2Method Waste

Parameter Blank Solvent

Cyanide, total 25 U 25 UPhenolics, total, as phenol 25 U 10,000Flashpoint, closed cup, °F — <70pH, units . — 2.5

Acidity, as CaC03 — 470,000Heat of Combustion, BTU/lb. '— 3,100Water, % 1.0 U 39

Residue, total 10,000 U 1,300,000Total Volatile Residue 10,000 U 31,000Ammonia-N 170 13,000Nitrate-N 500 U 1,300Phosphorus, total 50 U 330

Sulfate 1,000 U 110,000Chloride ' 500 U 3,300Fluoride 500 U 11,000Surfactants. (MBAS) 100 U 100 U*2-Propanol 150 U 110,000,000

Units (ug/1) (ug/1)

* MBAS not applicable due to background color of sample.

H-25 AR303368

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AnalytiKEM

Test Report No. A17182Page 16

IV. Analytical Results (Cont'd)

General Chemistry

Sample Designation

A17182-3 A17182-4Parameter ' Spent Oil Photoresist

Flashpoint, closed cup, °F >180 >180pH, units 4.4 5.1Heat of Combustion, BTU/lb. 19,000 12,000Specific Gravity 0.9 1.0

H-26 AR303369

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AnalytiKEM

Test Report No. A17182Page 17

V. Quality Control Data

Volatile Organics

Aqueous Matrix Spike/Matrix Spike Duplicate Recovery Data

Sample Spiked A17230-1

Amount RecoveryConstituent of Spike MS MSP RPD

Chloromethane 0.25 99 107 8Bromomethane 0.25 . 89 105 17Vinyl Chloride 0.25 95 107 13Chloroethane 0.25 95 107 12Methylene Chloride 0.25 99 106 6

1,1-Dichloroethene 0.25 100 108 71,1-Dichloroethane 0.25 99 106 7trans-l,2-Dichloroethene 0.25 106 106 0Chloroform 0.25 104 111 71,2-Dichloroethane 0.25 95 101 6

1,1,1-Trichloroethane 0.25 101 106 5Carbon Tetrachloride 0.25 100 106 5Bromodichloromethane 0.25 98 100 21,2-Dichloropropane 0.25 100 104 4trans-l,3-Dichloropropene 0.25 99 92 7

Trichloroethene (TCE) 0.25 173 171 TDibromochloromethane 0.25 101 103 21,1,2-Trichloroethane 0.25 99 100 1Benzene 0.25 100 105 5cis-l,3-Dichloropropene 0.25 101 87 16

2-Chloroethyl Vinyl Ether 0.25 103 105 3Bromoform 0.25 97 103 6Tetrachloroethene 0.25 96 104 8Toluene 0.25 96 105. 9

Chlorobenzene 0.25 . 98 102 4Ethylbenzene 0.25 100 110 9o-Xylene 0.25 96 114 17

Units (ug) (%) (%) (%)

H-27 AR303370

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AnalytiKEM

Test Report No. A17182Page 18

V. Quality Control Data (Cont'd)

Volatile Organics

Aqueous Matrix Spike/Matrix Spike Duplicate Recovery Data

Sample Spiked PI Water

Amount RecoveryConstituent of Spike MS

Chloromethane 0.25 105Bromomethane 0.25 98Vinyl Chloride 0.25 100Chloroethane 0.25 100Methylene Chloride 0.25 107

1,1-Dichloroethene 0.25 1071,1-Dichloroethane 0.25 100trans-l,2-Dichloroethene 0.25 113Chloroform 0.25 1021,2-Dichloroethane 0.25 94

1,1,1-Trichloroethane 0.25 98Carbon Tetrachloride 0.25 100Bromodichloromethane 0.25 1041,2-Dichloropropane 0.25 99trans-l,3-Dichloropropene 0.25 98

Trichlbroethene (TCE) 0.25 109Dibromochloromethane 0.25 1091,1,2-Trichloroethane 0.25 108Benzene 0.25 105cis-l,3-Dichloropropene 0.25 95

2-Chloroethyl Vinyl Ether 0.25 101Bromoform 0.25 109Tetrachloroethene 0.25 1021,1,2,2-Tetrachloroethane 107Toluene 0.25 101

Chlorobenzene 0.25 102Ethylbenzene 0.25 102o-Xylene 0.25 100

Units (ug) (%)

H-28 AR3Q337!

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AnalytiKEM

Test Report No. A17182Page 19

V. Quality Control Data (Cont'd)

Volatile Organics

Aqueous Surrogate Recovery Data

Surrogate Recovery

Sample l,2-Dichloroethane-d4 Toluene-dg 4-BromofluorobenzeneDesignation (0.25 ug Added)____ (0.25 ug Added) (0.25 ug Added)

Method Blank 1 91 100 101Method Blank 2 94 99 98A17230-1 Spike 98 100 102A17230-1 Spike Dup. 103 101 105DI Water Spike 88 98 95A17182-1 92 105 92A17182-2 96 98 99

Units (%) U) (%)

H-29 AR303372

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AnalytiKEM

Test Report No. A17182Page 20

V. Quality Control Data (Cont'd)

Polychlorinated Biphenyls

Aqueous Matrix Spike/Matrix Spike Duplicate Recovery Data

PCB Sample Spiked A17175-6

Amount RecoveryConstituent of Spike MS_ MSP RPD

Aroclor 1254 20 63 47 29

Units (ug) (%) (%) (%)

Nonaqueous Matrix Spike/Matrix Spike Duplicate Recovery Data

PCB Sample Spiked A17194-4

Amount RecoveryConstituent of Spike MS MSP RPD

Aroclor 1254 20 73 75 3

Units (ug) (%) (%) (%)

H-30 AR303373

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AnalytiKEM

Test Report No. A17182Page 21

V. Quality Control Data (Cont'd)

Polychlorinated Biphenyls

Aqueous Surrogate Recovery Data and Retention Time Shift

Dibutylchlorendate(1.0 ug Added)

Sample RetentionDesignation Recovery Time Shift

Method Blank 88 0A17175-6 Spike 25 0.5A17175-6 Spike Dup. 44 0.5A17182-1 103 0.4A17182-2 86 2.6

Units (%) (%)

Nonaqueous Surrogate Recovery Data and Retention Time Shift

Dibutylchlorendate(1.0 ug Added)

Sample RetentionDesignation . Recovery Time Shift

Method Blank 98 0.3A17194-4 Spike 95 1.3A17194-4 Spike Dup. 98 1.0Dl Water Spike 83 1.3A17182-3 ' 85 0.6A17182-4 55 1.4

Units (%) (%)

AR30337I+

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AnalytiKEM

Test Report No. A17182Page 22

V. Quality Control Data (Cont'd)

Metals

Aqueous Matrix Spike/Matrix Spike Duplicate Recovery Data

Sample Amount RecoveryConstituent Spiked of Spike MS MSP RPD

Arsenic A17197-1 100 81 85 5Barium Al7197-1 300 76 77 1Boron A17197-1 1,000 81 80 1Cadmium A17197-1 300 88 88 0Chromium A17197-1 300 90 89 1

Copper A17197-1 300 92 91 1Iron A17185-3 300 70 78 11Iron DI Water 300 80Lead A17197-1 300 91 91 0Mercury A17197-1 20 121 117 3

Nickel A17197-1 300 89 90 1Selenium A17197-1 100 87 96 10Silicon A17197-1 1,000 76 66 14Silicon DI Water 1,000 82

Silver A17197-1 300 81 61 28Silver DI Water 300 88Sodium A17185-3 1,000 * *Sodium DI Water 1,000 79Zinc A17197-1 300 87 87 0

Units (ug) (%) (%) (%)

* Not recovered due to high amount of analyte in sample.

H-32 AR303375

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AnalytiKEM

Test Report No. A17182Page 23

V. Quality Control Data (Cont'd)

EP Toxicity Procedure

Matrix Spike/Matrix Spike Duplicate Recovery Data

Sample Amount RecoveryConstituent Spiked of Spike MS MSP RPD

Arsenic A17223-1 100 87 93 7Barium Al 7223-1 300 89 93 4Cadmium A17223-1 300 87 91 4Chromium A17223-1 300 86 90 5

Lead A17223-1 300 85 90 6Mercury A17232-1 20 101 100 1Selenium A17223-1 100 82 86 5Silver A17223-1 300 16 21 27Silver DI Water 300 13

Units (ug) (%) (%) (%)

H-33AR303376

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AnalytiKEM

Test Report No. A17182Page 24

V. Quality Control Data (Cont'd)

General Chemistry

Aqueous Matrix Spike/Matrix Spike Duplicate Recovery Data

Sample Amount RecoveryConstituent Spiked of Spike MS MSP RPP

Cyanide A17184-2 30 95 99 4Phenolics A17172-1 10 101 101 0Ammonia-N A17039-1 1,000 83 83 0Nitrate-N A17182-2 50 94 98 4Phosphorus A17182-2 1,000 69 68 1Sulfate A17182-2 200 103 103 0

Chloride A17182-2 50 94 119 23Fluoride A17182-2 12.5 104 104 0Surfactants A17182-2 • 50 77 79 3Water A17182-2 15,000 100 100 02-Propanol PI Water 4 97 102 5

Units (ug) (%) (%) (%)

rr_ 04

flR303377

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An American NuKEM Company

AnalytiKEM Inc.28 Springdale Road

Cherry Hill, NJ 08003609/751-1122215/923-2068

CHAIN OF CUSTODY RECORD

Name of Unit and Address

Number Item ' Description of Samples

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H-35

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SH303380

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H-38 AR303381

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COMMODORE SEMICONDUCTOR GROUP

WASTE ANALYSIS PLAN

AS REQUIRED UNDER RCRA40CFR 265.200, 265.13

COMMODORE SEMICONDUCTOR GROUP950 RITTENHOUJ5E ROADNORRISTOWN, PA 19403

APRIL 22, 1988REV. MAY 4, 1988

H-39 fl8303382

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1.0 COMMODORE WASTE STREAMS

Commodore generates six waste streams on a regular-basis:

(1) Elementary Neutralization System

Process wastewater containing mixtures of acids and caustics, andeffluent .water from wet impingment fume exhaust scrubbers arepiped to an elementary neutralization system. In theneutralization system, the waste is pH adjusted to neutral (6.0to 9.0) and discharged to the POTW.

Analytical testing helps to ensure that the neutralizationsystem's effluent meets all federal, state, and local parameters.

(2) Solvent

A mixture of solvents, mainly consisting of acetone, isopropylalcohol and freons, are piped or manually dumped into anunderground storage tank.

Waste analytical results determine how and where the waste streamcan be disposed of.

(3) Spent Photo Resist

Photo Resist is accumulated in 55 gallon drums. Chemicalconstituents are xylene, n-butyl acetate, mineral spirits, and 2ethoxyethyl acetate.

Analytical results determine how and where the waste stream canbe disposed of.

(4) Used Oil

Used oil is not regulated as a hazardous waste by federal orPennsylvania state law. «

However, analytical testing is still performed to ensure that theoil does not contain any metals or other hazardouscharacteristics.

H-40 AR303383

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1.0 COMMODORE WASTE STREAMS (cont'd.)

(5) Arsenic tyaste

Manufacturing uses arsenic in its process. Arsenic waste isgenerated when preventive maintenance is performed on the processequipment. The waste is mainly comprised of rags, gloves, paper,and other debris contaminated . with a small amount of arsenicaldust.

Analytical testing is necessary to determine how much arsenic isin the waste; thereby determining disposal method and location.

(6) Carbon

Waste carbon is generated from three sources:

There is an activated carbon filtration system incorporatedin the potable water system. This is to eliminate solventcontaminents in the drinking water.

Deionized water system utilizes carbon filtration toinhibit solvent contaminents from entering the process waterand contaminating the product.

Outside air intake on HVA/C #1 uses a carbon filtrationsystem to control the quality of air entering the building.

Waste analysis is necessary to determine what contaminents havebeen absorbed by the carbon, and how much. This will determinethe method of disposal and the disposal facility for the waste.

H-41 AR30338**

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2.0 ANALYTICAL PARAMETERS

Commodore's waste streams are comprised of mixtures -of manychemical constituents; therefore, analytical parameters are basedupon the need to identify the waste stream characteristics(corrosivity, ignitability, reactivity, toxicity). Additionalanalytical parameters (heat of combustion, percentage of water,specific gravity, etc.) are vital for establishing the disposalmethod and for completing the waste profiles required by thedisposal facility.

All analytical work is performed by a certified, independant,EPA approved, laboratory.

Laboratories used by Commodore:

AnalytiKEM Inc.128 Springdale RoadCherry Hill, NJ 08003

AGES1151 South Trooper RoadNorristown, PA 19403

H-42 AR303385

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H-43 AR303386

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3.0 TEST METHODOLOGY

VOLATILESAqueous

Method 624, Purceables. Federal Register, Vol. 49, No. 209,October 26, 1984.

PESTICIDES AND POLYCHLQRINATED BIPHENYLSAqueous

Method 608, Organochlorine Pesticides and PCB'e. FederalRegister, Vol. 49, No. 209, October 26, 1984.

NonaqueousMethod 3550, Sonication Extraction. Test Methods forEvaluationg Solid Waste, Physical/Chemical Methods, SW-846,Third Edition, USEPA, November 1986.

- Method 8080, Organochlorine Pesticides and PCB'e, TestMethods for Evaluating Solid Waste, Physical/ChemicalMethods, SW-846, Third Edition, USEPA, November 1986.

METALSAqueous

Sample Preparation MethodsTest Method for Evaluation Solid Waste, Physical/ChemicalMethods, SW-846, Third Edition, USEPA, November 1986.

Method 3010: Acid Digestion of Aqueous Samples and Extractsfor Total Metals for Analysis by Flame Atomic AbsorptionSpectroscopy of Inductively Coupled Plasma Spectroscopy.

Method 3020: Acid Digestion of Aqueous Samples and Extractsfor Total Metals for Analysis by Furnace Atomic AbsorptionSpectroscopy.

Sample Analysis MethodsMethods for Chemical Analysis of Water and Wastes, EPA 600/4-79-020, OSEPA, March 1983.

Method 206.2: Arsenic (Atomic Absorption, FurnaceTechnique).

Method 239.2: Lead (Atomic Absorption, 'Furnace Technique).

Method 245.1: Mercury Manual Cold Vapor Technique).

Method 270.2: Selenium (Atomic Absorption, Furnace. Furnace Technique)

H-44 AR3Q3387

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3.0 TEST METHODOLOGY (cont'd)

Method 200.7: Inductively Coupled Plasma-Atomic EmissionSpectrometric Method for Trace Element Analysis of Water andWastes .

GENERAL CHEMISTRYAcidity- Methods for Chemical Analysis of Water and Wastes, EPA-

600/4-79-020, USEFA, Method 305.1, March 1983.

AlkalinityMethods for Chemical Analysis of Water and Wastes, EPA-600/4-79-020, DSEPA, Method 310.1, March 1983.

Heat of Combustion1980 Annual Book of ASTM Standards, Method D3 176-74, 1980.

ChlorideMethods for Chemical Analysis of Water and Wastes, EPA-600/4-79-020, USEPA, Method 300.0, January 1984.

Cyanid^. total and amenableTest Methods for Evaluating Solid Waste, USEPA, SW-846,Third Edition, Method 9012, November 1986.

EP Toxicity ProcedureTest Methods for Evaluating Solid Waste, USEPA, SW-846,Third Edition, Method 1310, November 1986.

FlashpointTest Methods for Evaluating Solid Waste, USEPA, SW-846,third Edition, Method 1010, November 1986.

F \uprjdeMethods for Chemical Analysis of Water and Wastes, EPA-600/4-79-020, USEPA, Method 300.0, January 1984.

en . AmmoniaStandard Methods for the Examination of Water andWastewater, American Public Health Association, 16thEdition, Method 417, 1985.

NitrateMethods for Chemical Analysis of Water and Wastes, EPA-600/4-79-020, USEPA, Method 300.0, January 1984.

H-45 flR303388

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3.0 TEST METHODOLOGY (cont'd)

EttMethods for Chemical Analysis of Water and Wastes, EPA-600/4-79-020, USEPA, Method 150.1, March 1983.

Test Methods for Evaluating Solid Waste, USEPA, SW-846,Third Edition, Method 9045, November 1986.

Phenolics. totalMethods for Chemical Analysis of Water and Wastes, EPA-600/4-79-020, USEPA, Method 420.2, March 1983.

PhosphorusMethods for Chemical Analysis of Water and Wastes, EPA-600/4-79-020, USEPA, Method 420.2, March 1983.

ReactivityTest Methods for Evaluating Solid Waste, USEPA, SW-846,Third Edition, Method 1110, November 1986.

SoJ.ids. totalStandard Methods for Examination of Water and Wastewater,American Public Health Association, 16th Edition, Method209A, 1985.

Solids, total volatileStandard Methods for Examination of Water and Wastewater,American Public Health Association, 16th Edition, Method209A, 1985.

SulfateMethods for Chemical Analysis of Water and Wastes, EPA-600/4-79-020, USEPA, Method 300.0, January 1984.

Surfactants .( MBAS 1Standard Methods for Examination of Water and Wastewater,American Public Health Association, 16th Edition, Method512B, 1985.

Water1980 Annual Book of ASTM Standards, Method D1744-64, 1980.

Specific Gravity1980 Annual Book of ASTM Standards, Method 1480-62, 1980.

IsopropanolIsopropanol is analyzed by temperature programmed gaschromatography using a 6 ft. by 2 mm. id column packed with1% SP1000 on 60180 mesh Carbopack B and an FID dectector.

H-46 AR3Q3389

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4.0 SAMPLING METHODOLOGY

SAMPLING EQUIPMENT

WEIGHTED LARGEWASTE COLIWASA BOTTLE TRIER DIPPER

Neutralization SystemSolvent XSpent Photo Resist XDsed Oil XArsenic Waste XCarbon w/TCE X

Composite samples are obtained when possible.

Sampling of waste streams for analysis is performed by fieldtechnicians of a certified, EPA approved, independantlaboratory. Proper sampling and analysis protocols are inaccordance with SW-846, "Test Methods for Evaluating SolidWaste".

H-47 AR303390

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5.0 FREQUENCY OF ANALYSIS

Waste streams are analyzed on a routine basis to ensure that allanalysis are accurate and up-to-date. Frequency is alsodependant upon process and/or constituent changes.

• . . FREQUENCY OF ANALYSIS

WASTE STREAM fill SA A.

Neutralization System X

Solvent ' X

Spent Photo Resist X

Used Oil . X

Arsenic Waste X

Carbon w/TCE X

QU = QuarterlySA = Semi-annualA = Annual

AR30339I

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_: '*£-'•& •"'.•:.' '-/.'•'"•:

APPENDIX I

TOXICITY PROFILES

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WESTON WAYWEST CHESTER, PA 19380PHONE: 215-692-3030TELEX: 83-5348

MANAGERS X -X DESOeRS/CONSUUANTS

Ms. Ruth Rzepski 10 June, 1992U.S.EPA Region III, (3HW12)841 Chestnut BuildingPhiladelphia, PA 19107

Dear Ms. Rzepski:

Attached are the Toxicity Profiles requested which will be included in the Commodore RIReport. Also attached are the short-term pumping test results.

Both of these will be included as appendices in the final report.

If you have any questions, please call me at (215)430-7254.

Very truly yoursRoy F. Weston, In

Steven E. JakaProject Site Manager

cc: Olsen, J.Ng, R.

AR303393

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TOXICOLOGY PROFILES

INTRODUCTION

The following toxicology profiles present an overview of the health effects associated withchronic exposure to the chemicals found in the vicinity of the CSG site. The profiles wereprepared in order to support the chronic reference doses and cancer slope factors used inthe risk assessment. When information concerning chronic toxicity was not found in theavailable literature, subchronic toxicity data were used to identify potential target organs andother health effects.

The profiles address human health effects. Each profile is introduced with a summary ofoverall effects. The human health section is subdivided into noncarcinogenic toxicity andcarcinogenicity for those compounds classified as carcinogens. Human evidence fromavailable epidemiological studies is discussed first. This is followed by chronic or subchronicanimal studies describing the effects from inhalation, oral, and dermal administration of thechemical. Information from long term reproductive studies is included but informationfrom short term teratogenicity studies is not. No-observed-effect levels (NOELs) andlowest-observed-effect levels (LOELs) are presented when available. Evidence for thecarcinogenic potential of each chemical from epidemiologic and animal studies is discussedand EPA's cancer classification is presented when available. Genotoxicity information,where available, is presented as a separate subsection due to the probable mechanisticrelationship between mutagenicity and the expression of some tumors. If nothing ismentioned in the profile about a particular toxic endpoint, this means that no data orstudies were found covering that particular toxic endpoint.

The information presented in the toxicology profiles is based on:

Toxicological Profiles prepared for the Agency for Toxic Substances and

toxproco.602 J S Juoe 1992

AR303391*

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Disease Registry (ATSDR).

Toxicity profiles in The Installation Restoration Program Toxicology Guideprepared by Oak Ridge National Laboratory.

An on-line search of EPA's Integrated Risk Information System (IRIS).

If a Toxicological Profile prepared for the Agency for Toxic Substances and Disease Registrywas available for a chemical, it was used as the primary reference for describing humanhealth and ecological effects; the lexicological profile is not cited in the text but appears inthe references.

toxproco.602 2 *Juoe I992

AR303395

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BROMODICHLOROMETHANE (BDCM)

SUMMARY

Oral toxicity studies in animals indicate the liver, kidney, and intestine as the principal targetorgans. BDCM causes the widest spectrum of liver and kidney tumors in rats and mice andis the only trichloromethane observed to cause intestinal tumors. There is some evidencethat BDCM is a genotoxin. No information was found on the effects of BDCM in man.

HUMAN HEALTH

Noncarcinogenic Effects - subchronic and chronic oral toxicity studies, indicateadverse effects on the liver and kidneys, which include increased organ weight, focalareas of inflammation and degeneration, and decreased function. These effects tendto appear in both tissues at roughly similar doses, usually between 25 and 100mg/kg/day. These findings indicate that both tissues are approximately equallysusceptible to BDCM. The doses which lead to renal and hepatic injury followingintermediate or chronic exposure are generally similar to those causing acute effects,suggesting that there is a relatively low tendency toward cumulative injury for thesenoncarcinogenic endpoints.

Carcinogenicity - No studies were found on the potential carcinogenic effects ofBDCM in man. However, chronic oral studies in animals provide convincingevidence that BDCM is carcinogenic. In rats, increased frequency of liver tumorswas observed in females exposed to 150 mg/kg/day for 180 weeks, and kidney tumorswere observed in both males and females exposed to 100 mg/kg/day. Incidences ofrenal tumors were 13/50 and 15/50 in males and females, respectively. Tumors ofthe large intestine were also observed in rats, at incidences of 13/50 and 45/50 inmales exposed to 50 and 100 mg/kg/day, and at an incidence of 12/47 in femalesdosed at 100 mg/kg/day. In mice, renal tumors were observed in males dosed with

h»j034.ipt f June 1992

AR303396

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50 mg/kg/day, and hepatic tumors were observed in females dosed with 75 or 150mg/kg/day. Increased intestinal tumors were not observed in mice.

EPA has classified BDCM as a probable human carcinogen (i.e., Group B2) whichdenotes sufficient evidence of carcinogenicity in animals and inadequate evidence inhumans (EPA, 1992).

Genotoxicitv - BCDM was negative in 4 Salmonella strains with and withoutmetabolic activation. Weak genotoxic effects were noted in two studies withSaccharomyces cerevisiae without metabolic activation; no effects were noted in thepresence of an activating system. Gene mutations were reported in a mouselymphoma assay. BDCM did not cause chromosomal aberrations in Chinese hamsterovary cells and was negative in 2 of 4 sister chromatid exchange assays. These resultssuggest that BDCM is a potential mutagen.

REFERENCES

ATSDR (Agency for Toxic Substances and Disease Registry), 1989. Toxicological Profilefor Bromodichloromethene. Final Report dated December 1989.

EPA, 1992. The Integrated Risk Information System (IRIS), On-line. EnvironmentalCriteria and Assessment Office, Cincinnati, OH.

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AR303397

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CHLOROFORM

SUMMARY

Chloroform induces effects on the central nervous system, liver, and kidneys of human oranimal species following acute or chronic oral and inhalation exposure. Chronic oral toxicitystudies indicate increased incidences of liver and kidney tumors in mice and rats; however,the data for mice are conflicting. There is some evidence that chloroform is a weakmutagen.

HUMAN HEALTH

Noncarcinogenic Effects - The liver is a primary target organ of chloroform toxicityin humans and animals following acute and chronic inhalation or oral exposures.Impaired liver function as manifested by increased sulfobromophthalein retention hasbeen reported in some patients exposed to chloroform via anesthesia. Case reportsof intentional and accidental ingestion of high doses (>, 2.5 g/kg) indicate severeclinical and biochemical effects of the liver. Occupational exposure to 14-400 ppmchloroform resulted in jaundice in one study and exposures to 2-205 ppm resulted inadverse effects on the liver as indicated by hepatomegaly, enhanced serum glutamic-pyruvic transaminase (SGPT) and serum glutamic-oxaloacetic transaminase (SGOT)activities, and hypergammaglobulinemia in another study. In contrast, no clinicalevidence of liver toxicity was found among chloroform workers exposed to <. 237ppm. Liver damage was induced by chronic use of a cough medicine containingchloroform, but not in individuals chronically exposed to chloroform in mouthwash.

Adverse effects in the liver have been reported in chronic oral toxicity studies withrats, mice, and dogs. The effects included nodular hyperplasia and fibrosis of theliver and increased SGPT activities at concentration >, 15 mg/kg/day.

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Case studies of individuals who intentionally or accidentally ingested high doses ofchloroform report biochemical changes indicative of kidney damage, as well as fattydegeneration at autopsy. Albuminuria and casts were also reported in case ofchronic use of a cough medicine containing chloroform; however, no renal effectswere observed in individuals chronically exposed to chloroform in a mouthwash.

In animals, studies indicate increased kidney weights and cloudy swelling in rats anddogs following subchronic inhalation of chloroform at concentration .>. 25 ppm.Several subchronic oral toxicity studies indicate increased relative kidney weights,tubular necrosis, and chronic inflammation. It has been demonstrated that kidneydamage is related to the ability of the kidney to metabolize chloroform to phosgene.No definite renal effects were observed in rats or mice dosed orally with chloroformat concentrations of <. 200 and < 477 mg/kg/day, respectively. However, fatdeposition in renal glomeruli was reported in dogs dosed orally at 30 mg/kg/day for7.5 years.

Neurological effects in humans and animals after acute or chronic exposure are welldocumented. Central nervous system toxicity following acute inhalation or oralexposure appear to be similar. Chronic inhalation exposure to chloroform resultedin exhaustion, lack of concentration, depression, and irritability in occupationallyexposed people. In a case study, chloroform inhalation for 12 years resulted inpsychotic episodes, hallucinations, and convulsions.

garcinogenicity - Epidemiology studies suggest an association between chronicexposure to chloroform from chlorinated drinking water sources and increasedincidences of gastrointestinal cancer, urinary tract cancer, brain cancer, andHodgkin's lymphoma. However, chloroform is one of many organic contaminantsfound in chlorinated drinking water, many of which are considered to havecarcinogenic potential. No studies were available regarding cancer in humans oranimals after inhalation exposure to chloroform.

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The carcinogenic potential of chloroform has been tested in animal studies. A dose-related increase in the incidence of liver tumors was observed in mice exposed tochloroform for intermediate durations. Chronic exposure induced an increasedincidence of renal adenoma and carcinoma in rats exposed to chloroform in drinkingwater and in rats treated by gavage with chloroform in oil. Hepatic neoplasticnodules were observed in female rats, and lymphosarcoma was observed in male ratsexposed to chloroform in drinking water. In addition, hepatocellular carcinoma wasobserved in mice given chloroform in oil by gavage and kidney rumors were observedin ICI mice exposed by gavage to chloroform in toothpaste.

The data concerning mouse liver tumors are conflicting. In contrast to the increasedincidence of liver tumors observed in mice exposed by gavage to chloroform in oil,no increased incidence of liver tumors was observed in female mice exposed tochloroform in drinking water. This result is consistent with the absence of livertumor effects in four other strains of mice exposed by gavage to chloroform intoothpaste.

EPA has classified chloroform as a probable human carcinogen (i.e., Group B2)which denotes the presence of sufficient evidence of carcinogenicity in animals andinadequate evidence in humans (EPA, 1992).

Genotoxicity - In general, most of the assays for chloroform genotoxicity are negative.Therefore, it seems that chloroform is a weak mutagen and that its potential tointeract with DNA is low. In in vitro experiments, chloroform did not cause reversemutations in Salmonella typhimurium or in Escherichia coli with or withoutmetabolic activitation. Inconclusive results were obtained in Saccharomycescerevisiae and Schistozosaccharomyces pombe: however, chloroform inducedaneuplodia in Aspergillus nidulans. Chloroform caused forward mutations in L5178Ymouse lymphoma cells after metabolic activation, but did not cause mutations at 8-azaguanine locus in Chinese hamster lung fibroblasts or sister chromatid exchangein Chinese hamster ovary cells. In human lymphocytes, chloroform did not induce

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unscheduled DNA synthesis and did not increase the frequency of sister chromatidexchange and chromosome aberrations. In contrast, increases in sister chromatidexchange were reported after metabolic activation in another study.

REFERENCES

ATSDR (Agency for Toxic Substances and Disease Registry), 1991. Toxicological Profilefor Chloroform. Draft Report dated October 1991.

EPA, 1992. The Integrated Risk Information System (IRIS), On line. EnvironmentalCriteria and Assessment Office, Cincinnati, OH.

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1.2-DICHLOROBENZENE (12-DCB)

SUMMARY

The major target organs for 1,2-DCB are the liver, kidneys and central nervous system. The1,2-DCB-isomer appears to have a low toxicity to humans. Case reports have linked chronicinhalation exposure to various forms of leukemia, but no conclusions can be drawn from theavailable information. A lifetime feeding study with rats and mice gave no evidence ofcarcinogenicity. Possible evidence of mutagenic activity was reported in a group of workersaccidentally exposed to 1,2-DCB.

jHUMAN HEALTH

Noncarcinogenic Toxicity - Most cases of human poisoning from 1,2-DCB haveresulted from chronic inhalation of vapors. Six months of industrial exposure to aproduct containing a mixture of 1,2-DCB (95%) and the 1,4-isomer (5%) resulted inpallor, exhaustion, vomiting, intense abdominal pain, headache and hemolytic anemiain one worker. Complete recovery followed after cessation of exposure. Thirteensimilarly exposed coworkers were unaffected.

Analyses of workroom air and medical evaluations of workers associated with 1,2-DCB manufacture and handling operations at the Dow Chemical Company revealedno evidence of organic injury or adverse hematologic effects attributable to 1,2-DCBexposure (NLM, 1991). The average air concentrations were 15 ppm, but the lengthof exposure was not reported. Chronic skin contact with a 1,2-DCB solution hasbeen reported to cause eczematoid dermatitis. Liver necrosis was reported in ratsand mice dosed orally by gavage at 250 mg/kg/days, 5 days per week for 13 weeks.Treatment-related liver effects were also noted in rats at doses > 125 mg/kg/day.

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Rats given 1,2-DCB by gavage, 5 days per week for 28 weeks, exhibited minimal liverand kidney damage at 188 and 376 mg/kg/day, but no adverse effects at 18.8mg/kg/day. However, no evidence of treatment-related effects on the liver wasnoted in rats and mice given orally 60 or 120 mg/kg/day 1,2-DCB, 5 days per weekfor 103 weeks.

In a two-year study, groups of male and female mice were given 1,2-DCB in com oilby gavage at doses of 0, 60, and 120 mg/kg/day, 5days/week for 103 weeks. Theonly nonneoplastic effect noted in the study was an increase in tubular regenerationof the kidney in the high-dose male mice. However, this effect was not consideredcompound related.

No adverse effects were observed in mice, guinea pigs, rabbits and monkeys after 6to 7 months of exposure to 93 ppm 1,2-DCB, 7 hours/day, 5 days/week; however,rats exposed to 93 ppm had reduced, body weights.

Carcinogenicitv - Three cases of leukemia have been reported which involved chronicexposure to DCE mixtures. However, no definitive conclusions can be drawn aboutthe causes of these leukemias.

The carcinogenicity of 1,2-DCB has been evaluated by the National ToxicologyProgram. Groups of rats and mice were administered 1,2-DCB in corn oil by oralgavage, 5 times per week in doses of 60 or 120 mg/kg body weight for 103 weeks.Increased incidences of malignant histiocytic lymphomas were observed in male andfemale mice at the high dose levels, but the incidence of all types of lymphomas inmale and female mice was not increased. Therefore, the increase in histiocyticlymphomas was discounted (ORNL» 1989). In the rat study no compound relatedtumors were detected. However, EPA (1992) concluded that a maximum tolerated

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. dose (MTD) had not been achieve. 1-2-DCB has been placed in group D (i.e., notclassifiable as to human carcinogencity).

Genotoxicity - Chromosomal analysis of white blood cells in laboratory workersexposed to 1,2-DCB during pest control revealed the presence of a significantnumber of altered cells. These were identified as having clastogenic chromosomalalterations (NLM, 1991).

1,2 DCB was not found to be mutagenic in three studies involving 8 bacterial strains(histidine-requiring mutants of Salmonella typhimurium) tested with and withoutmetabolic activation (ORNL, 1989). In an in vivo micronucleus assay, 8-week oldmale mice were injected intraperitoneally with 187, 375, 562, or 750 mg of 1,2-DCB/kg body weight. A statistically significant, dose-related increase in micronucleiwas observed in the bone marrow cells.

REFERENCES

NLM (National Library of Medicine), 1991. Hazardous Substance Databank, on line.

EPA 1992. The Integrated Risk Information System (IRIS), on line. EnvironmentalCriteria and Assessment Office, Cincinnati, OH.

ORNL, 1989. The Installation Restoration Program Toxicology Guide. Prepared for HarryG. Armstrong Aerospace Medical Research Laboratory, Wright-Patterson Air Force Base,Ohio, dated July 1989.

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1.1-DICHLOROETHANE (1.1.DCA>

SUMMARY

1,1-DCA exhibits anaesthetic properties in humans at high concentrations. In experimentalanimals, 1,1-DCA exhibits adverse effects on the liver and kidneys. Chronic exposure of ratsand mice resulted in increased incidences of adenocarcinomas and hemangiosarcomasamong female rats and increased incidences of benign tumors in female mice. 1,1-DCA islisted as a possible carcinogen (Group C). Data on the genotoxicity of 1,1-DCA areconflicting.

HUMAN HEALTH

Noncarcinogenic Toxicity - 1,1-DCA was used in the past as an anesthetic at aconcentration of approximately 26,000 ppm. This use was discontinued when it wasdiscovered that this compound induced cardiac arrhythmias.

Subchronic intermittent inhalation exposure to 500 ppm of 1,1-DCA for 13 weeksfollowed by 1,000 ppm for an additional 13 weeks did not produce any adverseclinical effects in rats, rabbits, or guinea pigs. However this study was limited by aninadequate number of test animals. Histological examination of the liver and kidneysafter 26 weeks revealed no treatment-related lesions. Six days after the tenth andlast daily exposure to 6,000 ppm 1,1-DCA, female rats exhibited a slight, butstatistically significant, increase in relative liver weight.

Renal injuries were apparent in cats intermittently exposed to 1,000 ppm 1,1-DCAfor 13 weeks following 13 weeks of intermittent exposure to 500 ppm 1,1-DCA.Histological lesions of the kidney tubules was noted. The ill health of these animals

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was also manifested by a progressive decrease in body weight. The lexicologicalsignificance of these findings is unclear.

Carcinogenicity - There are no reports of cancer causation in humans. An oralcarcinogenicity bioassay was performed by the National Cancer Institute (NCI) withrats receiving dosages ranging from 382 lo 950 mg/kg/day and mice receivingdosages ranging from 1442 to 3331 mg/kg/day. A marginal dose-related increase inthe incidence of mammary adenocarcinomas and hemangiosarcomas among femalerats and an increase in the incidence of benign tumors in female mice wereidentified. This study provided only limited evidence thai the compound wascarcinogenic because of the high mortality in the treatment groups (EPA, 1991).

In a follow-up study with mice, a two-stage carcinogenesis protocol was used to assessthe ability of 1,1-DCA to act as a promoter. Mice were exposed to 1,1-DCA indrinking water (0 to 534 mg/kg/day). Neither 1,1-DCA treated animals initiatedwith diethylnitrosamine (DENA), or animals trealed wilh 1,1-DCA without initiationshowed a significant increase in the incidence of lung or liver tumors over controls.A shortcoming of this study is that the exposure duration to DENA was for 4-weeksand exposure to 1,1-DCA lasted for only 52 weeks for both groups (EPA, 1991).

1,1-DCA is classified by EPA as a possible human carcinogen (i.e., Group C). Thisclassification is based on the similarity in struclure and toxicity endpoints of 1,1-DCAto its isomer 1,2-dichloroethane which is considered to be a probable humancarcinogen by EPA (EPA, 1991).

Genotoxicity - No studies were located regarding in vivo genotoxic effects in humans.Resulls from ihree sludies conducled in Salmonella typhimurium tesler strains wereconflicting. 1,1-DCA was nonmutagenic in yeast cells even in the presence of a

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metabolic activation system. Because of insufficient reporting of data, no assessmentof the genoloxic polenlial of 1,1-DCA in Saccharomyces cerevisiae can be made.The available dala from Ihe remaining sludies indicate that, although 1,1-DCE didnot induce cell transformation in BALB/C-3T3 cells, it increased the frequency oftransformations induced by Simian adenovirus (SA7) in hamster embryo cells.

jREFERENCES

ATSDR (Agency for Toxic Substances and Disease Registry), 1989. Toxicological Profilefor 1.1-Dichloroethane. Draft dated October 1989.

EPA, 1991. The Integrated Risk Information System (IRIS), on line. EnvironmentalCriteria and Assessment Office, Cincinnati, OH.

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M-PICHLOROETHYLENE (Ll-DCE)

SUMMARY

Limited evidence suggests that repealed exposure lo 1,1-DCE is associated wilh liverdamage in humans. The major largel organs of 1,1-DCE loxicity in animals appear to bethe liver, kidneys and lungs. Short-term exposure in both humans and animals has beenassociated with effecls on ihe central nervous system. Available dala were inadequate loevaluate the relationship between the occurrence of cancer and occupational exposure to1,1,-DCE. Of various carcinogenicity studies conducted wilh a number of animal species,only one chronic inhalation sludy provides clear evidence of a positive carcinogenic effect1,1-DCE is mutagenic, and a metabolite is known to alkylate and bind covalently lo DNA

HUMAN HEALTH

Noncarcinogenic Effects - A high incidence of hepaloloxicity was reported in apreliminary clinical study of workers exposed lo 1,1-DCE for up lo 6 years in a 1,1-DCE polymerization plant. Marked liver dysfunction was found in 27 of 46 workers.No other studies were found. In animals, hepatoloxicity is evident by bothbiochemical and histopathological changes. These effecls appear lo follow a dose-response relationship that may also be influenced by the duration of exposure. Ratsexposed by inhalation to Si 24 ppm 1,1-DCE, 6 hours/day, 5 days/week for 18 monthsexhibited fairy changes in the liver. Chronic oral toxicity studies with rats indicatefew trealmenl-related changes in the liver at low doses ranging from 9-20 mg/kg/day.

Renal effects have been reported in animal studies primarily following acuteexposures. Severe nephrotoxicity occurred in male mice exposed lo 25 ppm 1,1-DCE,4 hours/day, 4 lo 5 days/week for one year. However, no treatmenl-relaled effeclswere noted following chronic inhalation (24 or 72 ppm, 5 hours/day, 5 days/week,for 18 monlhs) or oral (25 lo 200 mg/kg/day) exposures.

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Subchronic inhalation exposure lo 1,1-DCE is also associated with adverse respiratoryeffects. Inflammation of Ihe trachea of rats exposed to 72 ppm for 6 monlhs hasbeen reported. Olher pulmonary effecls seen in rals, guinea pigs, and dogs exposedlo 48 lo 189 mg/m3 for 90 days include discoloration and morphologic changes in thelungs.

Carcinogenicitv - Available data were inadequate to evaluate the carcinogenicpotential of 1,1-DCE to humans. The carcinogenicity of 1,1-DCE followinginhalation, oral, or dermal exposure has been evaluated in several animal species.However, only one inhalation study with mice provided clear evidence of a positivecarcinogenic effect. In this study increases in renal adenocarcinomas were notedin male mice exposed to 25 ppm 1,1-DCE, 4 hours/day, 4-5 days/week for 1 yearand then observed for one year. Results from a dermal initiation-promotion studywith mice indicated thai 1,1-DCE is an active lumor-iniliating agent. EPA hasclassified 1,1-DCE as a possible human carcinogen (i.e., Group C) which denotesinadequate evidence in humans and limited evidence in animals (EPA, 1992).

Genotoxicitv - Available studies suggest thai 1,1-DCE is genotoxic in a number oftest systems. The results of in vitro and in-vivo studies indicate that 1,1-DCE ismutagenic in bacteria and yeast in the presence of a mammalian metabolicsystem. It also induces gene conversion in yeast, chromosome aberrations and sisterchromatid exchanges in cultured mammalian cells in vitro and DNA damage in micein vivo. These results indicate thai DCE is mutagenic.

REFERENCES

ATSDR (Agency for Toxic Substances and Disease Registry), 1988, Toxicological Profile for1.1-Dichloroethene. Draft Report dated December, 1988.

EPA, 1992. The Integrated Risk Information Syslem (IRIS), on line. EnvironmentalCriteria and Assessmenl Office, Cincinnati, OH.

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CIS- AND TRANS-O-DICHLOROETHENE (DCE>

SUMMARY

No chronic human health effects data were available; however, DCE is a central nervoussystem depressant following acute exposures. Exposure of experimenlal animals lo DCEresulted in liver and kidney damage. No dala were found on ihe carcinogenic potential ofeilher isomer in humans or experimenlal animals, cjs-DCE is apparently genotoxic.

HUMAN HEALTH

Noncarcinogenic Toxicity - There is no information available concerning the relativeloxicilies of the cis- and trans-isomers. Most of the available toxicity information isfor trans-DCE. The lowesl-observed-adverse-effecl level (LOAEL) for irans-DCEbased on a 16 week inhalation study in rals was 200 ppm; bolh respiratory and liverfunction effecls were reported. Dogs and cals exposed lo cjs-DCE concenlrations of1,000 and 1,900 ppm for an unspecified duration exhibited loss of appetite, decreasedbody weighl, and pathological changes in the liver, kidney and lungs (ATSDR, 1989).

Male mice receiving 385 mg/kg/day trans-DCE in drinking water for 90 daysexhibited increased hepatic glulalhione levels compared to controls. Female micereceiving 224 mg/kg/day trans-DCE exhibited elevated SGOT and SGPT activities.A significant increase in hepatic microsomal aniline hydroxylase activity was alsonoted in female mice receiving 23 mg/kg/day.

In a 90-day study with rats, administration of trans-1.2-DCE in drinking water at353, mg/kg/day resulted in a dose-related increase in absolute and relative kidney

weighls of female rals. A dose-relaled increase in absolute and relative liver weighlwas also observed in rals exposed to cjs-DCE at concentration S:97 mg/kg/day.However, no histopalhologic lesions were noted in eilher organ.

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Carcinogenicity - No information assessing carcinogenicity in humans or animals byeilher isomer is available. EPA (1992) has Iherefore classified bolh isomers asGroup D compounds.

Genotoxicity - No dala are available on Ihe genoloxic effecls of eilher isomer inhumans. In vilro sludies using Escherichia coli K12, several strains of Salmonellatyphimurium, and Saccharomyces cerevisiae were negative for bolh cjg and irans-DCE. In vivo lesls indicate lhal cjs-DCE is a genoloxin. cjs-DCE was shown lo bemulagenic in vivo in Ihe mouse bone marrow assay and hosl mediated (mice) studieswith Salmonella tester slrains.

REFERENCES

ATSDR (Agency for Toxic Subslances and Disease Regislry), 1990. Toxicity Profile for cis-1,2-Dichloroelhene. lrans-lT2-Dichloroelhene. 1.2-Dichloroelhene. Draft dated October,1989.

EPA, 1992. The Integrated Risk Information Systems (IRIS), on line. EnvironmentalCriteria and Assessmenl Office, Cincinnati, OH.

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TETRACHLOROETHYLENE (Tetra-CE.-

SUMMARY

Humans exposed to Telra-CE by inhalation or oral exposure showed liver, kidney, andcenlral nervous system disfunction. Evidence of carcinogenicity in humans is inconclusive.Test mammals exposed lo Tetra-CE through oral or inhalation routes developed livercarcinoma and mononuclear cell leukemia. Toxicity to test mammals occurred followingoral or inhalation exposure with the main target organs being the liver and kidney. Tetra-CE is not a genotoxin.

HUMAN HEALTH

Noncarcinogenic Toxicity - Telra-CE is a commercially importanl solvenl widely usedin dry-cleaning, textile processing and metal degreasing. Humans are exposed toTetra-CE primarily ihrough inhalation and il is readily absorbed Ihrough Ihe lungsand into Ihe blood. Information on Ihe chronic toxicity of Tetra-CE in humans waslimited. Groups of workers occupationally exposed to 60 ppm Tetra-CE for up to15 years complained of headaches, fatigue, and dizziness (ORNL, 1989). Similarsymptoms were found for subjects exposed to 25 or 100 ppm for 5.5 hours daily for55 days. Hepatoloxic effecls (i.e. hepalilis, cirrhosis, liver-cell necrosis and enlargedliver) resulting from long-term exposure has been documented al concentrationsgreater than 100 ppm.

Rals and mice exposed Ihrough inhalation of Telra-CE (e.g. 200 or 400 ppm or 100or 200 ppm respectively for 6 hours daily, 5 days weekly for 103 weeks) showedincreased mortality for male and female mice and male rals. Key findings in exposedrats included nephropathy, wb«reas mice exhibited both liver and kidney damage.

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In another trial, liver and kidney pathology was observed in rats exposed to 230 ppmfor 8 hours daily, 5 days weekly for up lo 7 monlhs (ORNL, 1989).

Increased mortality occurred in mice and rals following exposure lo Tetra-CE (e.g.administered in corn oil by gavage to male rats al 471 and 941 mg/kg/day, femalerats at 474 and 949 mg/kg/day, male mice at 536 and 1072 mg/kg/day, and femalemice at 386 and 772 mg/kg/day as a time weighted average for 5 days/week for 78weeks). Death was due to toxic nephropalhy.

*

Carcinogenicity - Epidemiological studies of dry-cleaning and laundry workers havelinked Telra-CE exposure wilh cancers of the lung, cervix, kidney, skin and/or colon(ORNjL, 1989). However, these studies are regarded inconclusive because ofnumerous confounding factors.

Male and female rats exposed lo 200 or 400 ppm Telra-CE Ihrough inhalation 6hours per day, 5 days per week for 103 weeks showed a significanl increase in Iheincidence of mononuclear cell leukemia when compared to controls. Mice exposedto 100 or 200 ppm Telra-CE 6 hours per day, 5 days per week for 103 weeks showedsignificantly increased incidences .of hepatocellular adenomas and carcinomas inmales and hepatocellular carcinomas in females.

In a second study, rals and mice were exposed lo Telra-CE administered in corn oilby gavage (male rats: 471 and 941 mg/kg/day; female rats: 474 and 949 mg/kg/day;male mice: 536 and 1072 mg/kg/day; and female mice: 386 and 772 mg/kg/day asa time weighted average for 5 days/week) for 78 weeks. Increased incidences ofhepalocellular carcinomas (40 lo 65%) were noted in treated male and female micecompared to controls. In rats a high incidence of early deaths due to toxicnephropathy rendered Ihe bioassay inconclusive.

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EPA (1992) has classified Telra-CE as a probable human carcinogen (i.e. Group B2which signifies inadequate human evidence for carcinogenicity and sufficient animalevidence).

Genotoxicitv - A large number of studies of the in vitro genotoxicity of Tetra-CEhave been performed using prokaryotic, eukaryolic and mammalian cells. Responseswere weak and required high concenlralions of Ihe chemical and no clear dose-response relationships were eslablished. Therefore, Telra-CE has nol been clearlyshown to be a mutagen.

REFERENCES

ATSDR (Agency for Toxic Subslances and Disease Regislry), 1990. Toxicological profile forTelrachloroethvlene. Draft dated January 1990.

EPA, 1992. The Integrated Risk Information System (IRIS), On line. EnvironmentalCriteria and Assessment Office, Cincinnati, OH.

ORNL (Oak Ridge National Laboratory), 1989. The Inslallarion Restoration ProgramToxicity Guide. Prepared for Harry G. Armstrong Aerospace Medical Research Laboratory,Wright-Patlerson Air Force Base, Ohio, dated July 1989.

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1.14-TRlCHLOROETHANE (TCA)

SUMMARY

Neurological effects are Ihe preeminenl symptoms of acute inhalation exposure lo TCA.Long-term oral, dermal and respiratory exposure lo TCA in animal studies has resulted inmild liver effecls. There is no experimental evidence suggesting lhal TCA is a human oranimal carcinogen or genotoxin.

HUMAN HEALTH

Noncarcinogenic Toxicity - The chronic inhalation NOAEL (no-observed-adverse-effect level) developed for the cardiovascular, hematopoietic, hepatic, and renalsystems in Ihe workplace is 150 ppm and Ihe NOAEL for Ihe cenlral nervous systemis 200 ppm. Inhalation exposure of rals to 1,500 ppm of TCA, 6 hours/day, 5days/week, for 2 years resulted in a significant decrease in body weight of femalesand very slight hepatic effecls in bolh sexes.

A chronic (78 weeks, 5 days per week) oral LOAEL (lowesl-observed-adverse effecllevel) for rals was determined to be 750 mg/kg/day. Rats exposed to moderatelevels of TCA via ingestion also had elevated levels of SGOT (serum glulamicoxidase Iransferase) indicating hepatic (liver) damage.

Results from a subchronic dermal toxicity study with rals indicated a NOAEL of 240mg/kg/day. Levels of SGOT and serum ornilhine carbamyllransferase (enzymesreleased into Ihe blood from damaged liver tissue) were significantly higher in ratsdermally exposed to low levels of TCA.

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Carcinogenicity - No information was found on Ihe carcinogenic potential of TCAin humans. No effecls were found in rats and mice exposed to 1,500 ppm TCA,6 hours/day, 5 days/week for 2 years. In a 78-week oral toxicity study with rats andmice no evidence was found of neoplaslic lesions al 750 and 2,807 mg/kg/day,respectively. However, ihis study was not considered to be adequate to evaluateTCA carcinogenicity. A second chronic toxicity study with rats dosed orally with 500'mg/kg/day TCA, 4 to 5 days/week for 2 years, similarly failed to identify positive ornegative association between oral exposure and cancer incidence. TCA is listed inGroup D of EPA's Weighl-of-Evidence classification system for carcinogenicity (i.e.nol classifiable as to human carcinogenicity), (EPA, 1991).

, Genotoxicitv - Technical grade TCA has been shown to be weakly mutagenic, in vitrowhen assays were conducted in a desiccator lo minimize evaporation. However, aconlaminanl, para-dioxane, a known carcinogen, may be responsible for ihis reaction(EPA, 1991). No studies are available which indicate Ihere are genoloxic effecls tohumans or animals from TCA through the oral, dermal, or inhalation routes ofexposure.

REFERENCES

ATSDR (Agency for Toxic Substances and Disease Registry), 1990. Toxicological Profilefor 1.1.1-Trichloroethane. Draft dated February 16, 1990.

EPA, 1991. The Integrated Risk Information System (IRIS), on line. EnvironmenlalCriteria and Assessmehl Office, Cincinnati, OH.

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TRICHLOROETHENE (TCE)

SUMMARY

The principal largel organs for chronic inhalation exposure to TCE are Ihe cenlral nervoussystem, liver and kidney. Animal studies indicate thai Ihe liver, kidney and immunologicalsystem are Ihe principal largel organs following oral adminislralion of TCE. Availableepidemiological studies are limited and a definite conclusion cannot be drawn concerningTCE exposure and cancer risk in humans. Chronic oral toxicity studies with mice and ratsindicate increased incidences of hepatocellular carcinomas and renal tubular cell adenomas.Studies wilh occupationally exposed workers are inconclusive regarding genotoxicity. In vivoand in vitro assays are suggestive of a genotoxic effect.

HUMAN HEALTH

Noncarcinogenic Toxicity - Results from a study of CNS effects of workers exposedto TCE for an average of 3.75 years indicated vertigo, headache, short-term memoryloss, and fewer word associations in workers exposed to 85 ppm TCE as comparedto 14 or 34 ppm. The lowest-observed-adverse-effect level for CNS effecls in animalsfor subchronic inhalation exposure is 100 ppm.

Information on hepatic and renal toxicity in humans following inhalation exposureis derived primarily from cases of acute overexposure. No studies were available fororal exposure. Results from three subchronic inhalation studies with mice and ratsindicate increased liver weighls and histopathological alterations of Ihe liver al aconcenlration of .37 ppm. Increased kidney weights and renal dysfunction have alsobeen reported in mice and rals exposed lo TCE by inhalation. The LOAEL andNOAEL for subchronic exposure lo TCE are 75 and 35 ppm, respectively.

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Subchronic and chronic oral toxicity studies also indicate adverse hepatic and renaleffects associated with TCE exposure. The LOAEL for hepatic effects followingsubchronic exposure lo TCE is 250 mg/kg. The LOAEL for renal effecls followingchronic exposure lo TCE is 500 mg/kg/day. NOAELs were not achieved.

The immunological system is also a principal target organ in animals following oralexposure. Depressed cell-mediated immunity to sheep erylhrocytes and inhibitedbone marrow stem cell colonization has been reported in mice receiving .18mg/kg/day TCE in drinking water for 6 months (the lowest dose tested).

In a 2 generation reproductive toxicity study no effects were noted on fertility andreproductive performance in rals and mice fed diels containing 75, 150 or 300mg/kg/day and 195, 390 or 780 mg/kg/day, respectively. However, increased liverand kidney weighls were noted in rals exposed lo _>:75 mg/kg/day.

Dogs exposed to 500 or 750 ppm TCE vapor for up lo 8 hours daily, up to 6 daysweekly, for up to 8 weeks showed toxicity symptoms including lethargy, anorexia,nausea, vomiting, weighl loss, and liver disfunction (NLM, 1991). Cals and guineapigs exposed lo 1000 ppm TCE for 1.5 hours daily for up lo 10 months showed livercirrhosis and biliary hyperplasia.

Carcinogenicity - A number of epidemiological studies have been conducted toinvestigate adverse health effects in humans following exposure to TCE in theworkplace. Results of these studies were conflicting and confounded by exposure loolher compounds, unknown duration of exposure, and/or small sample size.

Available evidence indicates lhai exposure lo TCE vapor is carcinogenic inlaboratory animals. Increased incidences of hepatocellular carcinomas were notedin male and female mice exposed lo 100,300 or 600 ppm technical grade TCE vaporfor 6 hours/day, 5 days/week, for 24 months. No carcinogenic effects were observed

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in rats exposed to the same regimen. Two strains of mice exposed to TCE at 0,100,300, or 600 ppm, 7 hours/day, 5 days/week for 78 weeks showed an increasedincidence of liver and lung tumors at Ihe two highest dose levels. Rats exposed tothe same dosing regimen for 24 monlhs exhibited increased incidences of leslicularLeydig cell lumors al all conceniralions and renal adenomas and carcinomascombined in Ihe high dose group. Increased incidences of lung adenocarcinomaswere also noted in mice exposed lo 150 or 450 ppm TCE, 7 hours/day, 5 days/weekfor 104 weeks; no tumors were noted in mice exposed lo 50 ppm or rals exposed toall three conceniralions.

Mice and rals were exposed orally to 99% pure TCE in corn oil by gavage 5 daysweekly for 78 weeks and were sacrificed after 90 and 110 weeks, respectively. Thetime weighted average exposures were 0,1169 or 2339 mg/kg/day for male mice; 0,869 or 1739 for female mice; and 0, 549, or 1097 for male and female rats. Nocompound-related carcinogenic effects were seen in rats, bul high mortality ralesconfounded Ihe results. There was a significant increase in Ihe incidence ofhepatocellular carcinomas in male mice al bolh dose levels and in female mice al Ihehighest dose level.

EPA classifies TCE as a probable human carcinogen i.e. B2, indicating lhat there issufficient evidence of carcinogenicity in animals and inadequate or no evidence inhumans (EPA, 1991).

Genotoxicity - A large number of in vivo and in vilro genotoxicity studies of TCEhave been conducted, bul resulls have been inconclusive. IB vitro tests on bacterial,fungal, animal hepatocyle, and embryo and human lymphocyte cells wilh and wilhoulmelabolic activation had a more or less equal distribution of positive and negativeresulls. In vivo studies on mice, rals, fruit fly and human occupational exposureshowed bolh positive and negative resulls. Melaboliles of TCE may also be in rats

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exposed potentially genoloxic. Il is concluded lhal available dala suggesl lhalcommercial-grade TCE is a weakly active indirecl mulagen.

REFERENCES

ATSDR (Agency for Toxic Substances and Disease Registry), 1989. Toxicological profilefor Trichloroelhylene. Draft dated January 1988.

EPA, 1991. The Integrated Risk Information System (IRIS), on line. EnvironmentalCriteria and Assessment Office, Cincinnati, OH.

NLM (National Library of Medicine), 1991. Hazardous Substance Databank, on line.

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VINYL CHLORIDE (VO

SUMMARYThe liver is the primary targel organ for bolh Ihe noncarcinogenic and carcinogenic effeclsof VC in humans and animals. VC has been shown to be genotoxic to humans and il ismutagenic and genoloxic in a variety of in vivo and in vitro assay systems.

HUMAN HjEALTH

Noncarcinogenic Effects - Chronic occupational exposure of humans lo VC hasproduced "vinyl chloride disease." This disease is characterized by severe damage lothe liver, effects on the lungs, poor circulation in Ihe fingers, changes in Ihe bonesal Ihe end of Ihe fingers, ihickening of Ihe skin, and changes in Ihe blood. While Ihelevels of exposure required to cause Ihese effecls have nol been quantified, they arecertainly far above levels expected lo be encountered in Ihe environment.

Effects on the liver have been documented in rodenls after chronic exposure lo VCIhrough ingeslion (levels as low as 0.1 mg/kg/day) or inhalation (levels as low as 10ppm). Chronic inhalation studies with rodenls have demonstrated testicular effeclsand reduced body weighl gain al levels in Ihe range of 10 lo 100 ppm, whereas,kidney effecls have been observed at levels over 1,000 ppm. Chronic oral toxicitystudies in rodents have resulted in blood effecls al levels around 10 mg/kg/day.

Carcinogenicity - Vinyl Chloride is regarded worldwide as a chemical that causescancer in humans, but exposure levels necessary to cause cancer in humans are notknown. To date, only workers exposed to very high levels of VC have shown anincreased incidence of liver cancer.

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In inhalation studies with laboratory animals, lung cancer has been observed in miceat levels as low as 10 ppm and liver cancer has been observed in mice, rats, andhamsters al levels between 10 and 100 ppm. Cancer has also been reported in ratsexposed orally to VC al levels between 1 and 10 mg/kg/day. The carcinogenicpotential of vinyl chloride is currently under review (EPA, 1991).

Genotoxicity - A no-observed-adverse-effecl level for chromosomal aberrations inperipheral lymphocytes of occupaliorially exposed workers was found lo be 1 ppm forinhalation exposures.

VC tested positive for recessive lethal effects but negative for dominant lethal effecls,chromosomal iranslocalion, and sex chromosome loss in Drosophila melanogaster.Negative results were also obtained for the dominant lethal tesl in mice. Positiveresulls were oblained in mutation and cell Iransformalion lesls and in chromosomalaberration lesls in in vivo and in vilro in mammalian systems. Positive resulls werealso reported for DNA alkylalion lesls in rals and mice and for RNA alkylation inrat liver microsomes. VC has been found lo be mutagenic to bacteria and yeasts.

REFERENCES

ATSDR (Agency for Toxic Substances and Disease Registry), 1989. Toxicological Profilefor Vinyl Chloride. Final report dated August, 1989.

EPA, 1991. The Integrated Risk Information System (IRIS), on line. Environmental Criteriaand Assessment Office, Cincinnati, OH.

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WESTON WAYWEST CHESTER, PA 19380PHONE: 215-692-3030TELEX: 83-5348

MANAGERS \> S DESIGNERS/CONSULTANTS

US. EPA Region III, (3HW12) 13 July, 1992841 Chestnut BuildingPhiladelphia, PA 19107

Attn:Ms. Ruth Rzepski

I have received two (2) copies of the Commodore Semiconductor RI/FS Report dated July,1992.

'Signature (for ,U$ 'EPA)

Name (printed)

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