Well No. MP-75 Boring No. X-Ref: sp-2 MONITOR WELL ... · _ 0-10-20 30 50 Well No. MP-75 Boring No. X-Ref: sp-2 MONITOR WELL CONSTRUCTION SUMMARY Survay Coords: N22992611724_____

_ 0

-10

-20

30

50

Well No. MP-75Boring No. X-Ref: sp-2

MONITOR WELL CONSTRUCTION SUMMARYSurvay Coords: N22992611724________ Elavatlon Ground i «v«i 581.8_____________E2322871.4907_________ Top of C«l»« 585.48

Drilling Summary:

Total Dwth 60.Q1Borahol* Diameter 8" to 16.5'; 3" to 60.0'Casing Stick-up Height: PVC to 1.14'; Al-3.68"DrlBar KitlinsXi Drilling Associates______Harrisbura, Pennsylvania____

Rig ___Tnicj mounted auger/coreBtt (s) S" Q._P, ngj.low stem auc er and

Drtlfrio Fluid . Potable watercore______________________ _ ____________ _____ _____ _____ _____

< Q2 <UJ C£ cProtactlva C««tno 4" aluminum

Watl Design It Specifications

Basis: Oaologtc Log X Geophysical Log _Casing String (•): C • Casing S » Scraan.

Dapth . String f«) EfavatlonM -.

- +1.14

4 -

Screen (SI)Casing (CD

527.8 ,556.8556.8 -.584.34

Casing (C31577.3 .585.48

Tima3/4" PVC Schedule 40 solid

C2 4". Aluminum casing

Ser«an:-S1 3/4" PVC schedule 40 - handslotted Raeovary Data:

\S ~ ——————————————————h 60

82 ________________________Q>

Paefc: Grad^ i; 55 to 22*.

Filter sand: 55 to 56; 21! to 22'Grout S««I: glnrrv; 171 to 3*

Cement-seal 0' to 3'Sintontt* S««i: Pellets: 59' to 56'

17' to 21'

Centering Dicks:

Construction Tim* Log:

TackDrDIing8" hollow stem

coringG*ophyt.LoggingCasing:4" Aluminum

FUtar Piacanrwnt:Camvntlng:Davelopmant:

StartData Tim*

_6-13

6-13

6-17

6-166-17

PM

PM

1300PM .

FW*hDat* Time

6-13

6-16

6-17

6-176-17

PH

AM

PM

PMPM

Wtll Dtv«lopm»nt:

Stabilization T«at Data:

p H Sp*c. Cond. Tamp ( C )

100 __•0

•0

v«R 20Y

20 40 «0 »0 100

TIME ( )

No centering disks caved hole 59' to 60* screen slotted with hack saw;Piezometer locfced with E21 Master lock - HMI loefc. ______

•£

o &C £

Iff C

u1 Ol

2trUJQ.

AR30349I

FIELD LOG - SOIL BOREHOLE•SITE NAME AND LOCATION

West of existing milking barn and north « • , „ „ . _ , , ,. .of the northern most •»"-*="••> *«<«>— 8" P.P. hollow stem auoerina and/or.diversion swale (grid coordinates:

DATUM ___ ELEVATION

ORBJJNG METHOD:

drivin of NX casino.SAMPLE METHOD; 2» spU(. spQon

(unconsolidated) and NX coring(consolidated)

WATER LEVEL

TTME

DATECASING DEPTH

28.710386-1615.0

28.612156-1715.0

SCfllNG NO.

SHEET

DRILLJMGSTART

TTME

DATE6-13

FMSH

DATE

6-19

uTIME °

Dam. RIG True* mounted auger/core rig SURFACE eoNpmoNS vegetated pasture: soil coatedANQLE vertical BEARING with cow manureJL rotten potato residue.SAMPLE HAMMER TORQUE 140 FT.HBS

CAMPLE NUMBERAND

DESCRIPTION OF MATERIAL OWS /

FN CASI

DEPTHN

PEET DESCRIPTION OP OPERATIONOOO

AND jg

REMARKS Wo:O

— 2H-

•rilb

•H. s

~ lo

rr_ 14€ ...... ..._™_ „»«- — ~-™^ . «""" "" o _

— 16

- 18

I

543366912121213S14IS1215

16

ML-dark yellowish-brown silt,loose, dry.ML/CL-strong brown silt, friabledry. KH-yellotfisb-reTTTo redmicaceous gilt.ML/MH-strong brown to yellowish-red micaceous silty clay to MH-olive-green to~Brovm~quartz.Saprolite. _; J:___-__ -----_

Very fissle phyllitic saprolitepyrite plus limoniteSaprolite . MH-rMnQ +_ FeOz alongfoliationSaprolite, dry * foliation = 70

= 450 ... 4,Very fissile, phylliticsjiprolite, HnO * t~&J2

Weathered pyrite to limonitegreenish-gray to yellowish-brownsaprolite *cl * 3G-45O to 16.3*

. o(continued on Page 2)

£

16.3 split spoon refusal, 8" augerto 16.5'

CO'aiui

LOGGED 8Y

ROCK BOREHOLE LOGSTTI NAME ANO LOCATION

H«t of existing milking barn and northof the northern aost surface drainagediversion swale (grid coordinates:

DATUM ELEVATIONDRILL wo Truck mounted auger/core rig

DRILLING METHOD:

8" O.D. hollow cttam anfi&rinn »nrt/nr-

drivlno of NTT rmqirifiSAMPLING METHOD' •}«split spoon(unconsolidated) and NX coring(consolidated)

WATES LEVEL

TIME

DATECASING DEPTH

ANGLE vertical BEARING —SAMPLI HAMMER TORQUE 140 FT.-LBS

06PTH WPEET

CeLEVATIOM)

IT" 2

6

E" s

ZL.10

— 12

~14

~™— 16

-20

E~24

E~28

WLOWS' f M.

^MBAMPitff

iHecoveHY)

100/.3

13.520

26

29.3

CORES

'ON NOW

16.

1

2

3

4

i §< HJg §

3

% RECOVERY j

2.52.5

1.5

6.06.0

3. ~3

|

0

o.c

0

0

SCO. DESCR**nONOR

ROCK UTHOLOGY

(See page 1)

Greenish-blue to greenphyllite heavy weathereI*U2 * flnu coatings onfoliation planes ** 70as/ab. $ foliation * 70°broken up, very soft*

as/ob; pyrite alteredto limonite alongfoliation and cleavageplanes, rock verymicaceous. Drillingwater lost at 25. Qf

Pnyllit*, FeOj + HnOcoatings along foliatiodrilling water recoversat 27*.

28.710386-1615.0

28.612156-1715.0

SORING NO.

MP-7s/S?-2SHEET

2" OF 3DR8JJNG

START FINISH

TIME TWE

DATE DATE

6-13 6-19SURFACE CONDITIONS Vegetated pasture: soil coated

with cow manure; rotten potato residue-

SYMBOL

V7//////////////7/

ROCK

STRUCTURE

^foliation s 700, ol.br. silty clay coatingson foliation.

Cl. *=60o overprinted by foliation

*«70o.

*foliation«70o, gradesto ^ 800 at 29.37limonite xtals ori«ntealong foliation and200 obtuse to foliatic

SAMPLER ANO BIT

SOu

11

CASINO TYPE

inVDr-l

Q*J

C— itna)U

OLOWS/FOOT

ON, CASINO

f* —

-i """•~4 ~~(0 —«3 _Jj —~

TEST RESULTSDEPTH

INFEET

£O

PERMAE ABILITY

CM. /SEC

NG CO'NTR

KitH

nsfc

l Associates

_io:D

enc"s—46-

*Z

CJ•s.M*Ji— 1

Iw(U.*-J

CDOUJC3ao

•c«:>->~VIc

1tru

"nuLIfS

COm

_jcc

2-S

r-1

*i

U

>CDako-XIi\ooJ->Cl—4

<c

UJ•Prin»«d on raycfed p«p«r

ROCK BOREHOLE LOGSITE NAME ANO LOCATION

i . West of existing milking barn and north| of the northern most surface drainage

diversion swale (grid coordinates:

DATUM ELEVATIONDRILL RIG Truck mounted auger/core rig~

DRR-UNG METHOD:

8' O.D- hn?l«w cfom jti.fjarfnn »r,A/nr

drivinc nf NX racfnnSAMPUNGMSTHOD: 2" Split Spoon

(unconsolidated) and NX coring{consolidated)

WATER LEVEL 28.7 28.6TIME 1038 1215DATE 6-16 6-17

CASING DEPTH 15.0 15.0

ANGLE vertical BEARING . —SAMPLE HAMMER TORQUE 140 FT.-LBS

u.g

BLOWS/

BIN.

ON SAMPLER

(RECOVERY)

CORES

C

Stn_ UJ

< 01

I i

AU3A003U •*

Sff

SOIL DESCRIPTION

ORROCKUTHOLOGY

BORNG NO.

MP-7S/SP-2SHEET

3 OP 3DfllLUNG

START FINISH

TIME TTME

DATE DATE

6-13 6-19SURFACE CONDITIONS Vegetated pasture: soil coated

with cow manure; rotten potato residue.

SYMBOL ROCK _

STRUCTURE

CD

ccUl

m

3d/UONISV3

BLOWS/FOOT

ON CASINO

TEST RESULTSDEPTH

INFEET

£ P

g.

P

—— 32

Z_ 34

F-.36

Z_ 38

— 40

~ 42

~ 44

~ 46

— 48

~ 50

r" 52— 54

|T- 56

—— 58

— 60

32.5

35.4

39,2

41.7

45.3

48.7

54.5

60-9

5

6

7

6

9

10

11

3.23.2

2.92.9

3-83.8

2.52.5

3.63.6

2.83.0

4.86.2

5.4S.5

l.C3.;

3.52,c

1.93.8

1.02.5

2.23.6

03.C

6.2

05.5

Bl. gr. grn wthrd phylldisplays porphyroblastitexture: feldspar x-tal

as/ob, qtz veins withweathered limonitex-tals.as ab; porphyroblastictexture at 38-39 CaCOsinclusions in qtz veinsdiscordant to foliation

as/ab; fol * changes t_c850 at 41-0', . ..--

as/ob; qtz veins f--8Q°qtz veins have pyrite/limonite x-tals, MnO,Fe02 staining on fol,planes.

Bluish-gray siltymicaceous phyllite* £ol.«8So/ - = ,- - = : •

as/ob; £fol=SQo morecnToTitic more graphictexture very micaceous,very fissile, wthrdfyrlte x-tals alongoliatlon planes.

as/ob; wthring alongcontacts of qtz veinsand host rocks.*fol=60o

Total Depth=60.0'

L

^

Xs

X

1

*fol U) = 45°f|jl-<300* 75-80° (micaIcintz bond with vert.fold axis?fol (2) = 80o fwthrdfractures cl=45o=350

*toU2) = 800^cl a 800-over printedCaC03 stringers parellfto foliation (2).5fol= fcls80°, CaC03stringers absent

filled with qtz withlimonite x-talsas/ab at 42.3'45-45.5 qtz vein46.0 reworked zone;possible shear zone

46.8-47.8 qtz vein f =75-80048.5 CaCOs stringers* fol*80o50.1 broken up softzone _ .

*fol=80°

*fol=85o, qtz vein53.6

54.0-54.3 qtz vein-as/ab

*=35o, «n + FeOj ctgs.

B" «5' qtz veins9" * hor.2"

I

OcIoU

i

in*

to4

O4->

uutr-iomV*jtos<-**4Offi

£3OsCO

Of —1—t m.

y —————

•H ——-^ ——Q. —Of __<___*J —O —2 _

Well NO. _____ MP-8d/MP-8i— u

;o

- 30

- 30

- 40

- 60

- 70

yu

- 110

-130

-140

1 </////////////////////////////////////////, 8& :.*;&

8ew

'*.

'*".:1*? -'", -,' —

KMON1TC

Survay Coordt:

Boring No. X-Rel)R WELL CONSTRUCTION SUMM,

H229896.5859 Etavatlen Sro xS Lt

E2323003.2SS2

• Driiling Summary:

• Total D«>th ISO*• Sorthott Di«m«t«r 8" to 321 :

Casing Sttek-up HI Dr*«r Mvers

•loht: Steelfi" to 15iV3' PVC 2.5'

Brothers Drilling*• SalungaP PA:H BJQ T4H - 900 - Inqerso• Rlt(«1 10" Haamer Sit; 6"

11 RandHanuner Bit

• Drmna Fkjid Potable water

Protactfw Casing 6" carbon steel casing

• We!! Design & Specifications

H aas c: o*wogic Log X Mopnystcai Log _^H Casing String (*): C - Gating S « Seraan.

§ Deoth Strinofs) Elevation

= *= -.-

I •

•c,V1"

JU9 -133.3133 -3 _+2.2

115.3 -10Q.3100-3 _+2. 2

32 -+3

Casino;: CT ,„ 3;

S£K£flJ£i)Casing CC1)

Screen [S?]Casing (C2)

Casing (C5)

'4" Sch 40 PV

435.4 - 451.1

451-1 _586.69

469,1 - 484.2484.1 _586.67

552.4 .587.49

C solid -MP-8d

C2 3/4" Sch 40 PVC solid- MP-8!C3 §" Ca pon steel

Sera«n:S1 3/4" Sch 40 PVC Hacksaw slotsevery 6M alternate sides

S2 3/4" Sch 40 PVC Hacksaw slotsevery 6" alternate sides

Fft*rPack: SI - 149.7 to i?o« - H«TH»S3 - n? ,tfl 55.-;• - Gr*rfP 1

Grout Saaf;

Conrrctc 0-*

83f to 31

3' .. ._

SentonKa ftaaf: P*H*!-« 0 - 15Q fn M7-1 - 95.5 to S31

Cantering Disks:

Top of Cai

Construction T

TaskDrilling

8" drill6" drill

Otophy*. Logging :Gating:fi" r»<;in<7

FKar Placarrwnt;

D«v*lopmant:by Rig

:; DP-2d/DP-2i

fi RYw«l 584 . 4

Inn 587-49

[me Lofit

Data

6-8

6-8

6-9-886-10-8S

0:irtTlma

1350.

1330

12001145

Fh-D>t«

6-8

fi-fl

6-9-86-10-

ilthTImt

13201430

1350

! 1630!8 1230

Walt Development:

Stabilization Test Data:

Tim* PH SP»c. Cond. T»mp i C )

Recovery Data:Q, S0-

%"~

C ao0E *°R »Y

0

Comments: Centering aisks not used due to bridging

10 «o ao ao 100TIME ( )

problems. 6" casing to berasroved upon piezometer decooissioning.

.... .. . .._......_.. . . . . .

f

flR303t;95

ROCK BOREHOLE LOG Pi_ter Mp.8d/Mp.8iSfTE NAM£ AND LOCATION

Modern Landfill .Southwest Expansion

. R. D. #9Yorfc, Pennsylvania

DATUM _______'___ELEVATION

QfltLL*JS METHOD: Air rotary percussion

drillinordrill 8'* hole to 32* intocompetent rock; set 6" casino; 6" hole to TD

METHOD: .Grab samples of _sirrotary cutting.

WATER LEVEL

TIME

DATECASING DEPTH

39.-85'

1138

6-9-8832

MP-8d HP-81 (elev.)540.61 541 04

7-13-8E 7-13-8832

SORING NO.

DP-2SHEET1

DRILLING

START

TIME

1200DATE

6-8

FINISH

TWE

1430DATE

6-8DRILL RIG T4H . 9 - inqersbll "Rand SURFACE CONDITIONS Tm<Bd gQrffitno fieldr dr? _

ANGLE Vertical BEARING — vegetated with timothy clover, ryeSAMPLE HAMMER TORQUE FT.-LBS

- 0

10

— 30

— 35

— 40

— 50

CORES

OSOIL DESCRIPTION

ORSOCK LfTHOLOGY

Topsail, tilled field.dry light yellow-browrand 2.5Y 6/4 Fine Saricand Gravel to'lUJKb/4ngnt yellow-brownVery Fine Sandy SmallGravel, slight5* to 20*AS"acove - more sTltyclay, decrease sand,very powdery, slightlymoist to dry,20'Etlht.gray dry to v -slightly moist ^ \

•' -'T.

Phyllite --powderyretansr"*ery mica-ceous

Phyllite; light grayvery powdery, occa-sional unpulverizedfragments indicatemicaceous partings, ^

Q

At 70-72' brown coarsesandy zone - No waterevident - quartztitic.

BOCKSTRUCTURE

Very little structureleft.

OSto

II

TEST RESULTSDEPTHrjFEET

5

OO

ELO

aUJ

»«Mdon*eyt»dM»r (©) SR303U96

ROCK BOREHOLE LOG P1_ter Hp.8d/MP.8I«TE NAME AND LOCATION

Hoderan LandfillSouthwest ExpansionR. D. *SYorX, Pennsylvania

DATUM ELEVATION

DRILL *KS T4H - 9 - Ingersoll Hand

ORtLNG METHOD: Air rotarv percussiondrilling; drill 8" hole to 32' intocoapetent rocX; set 6" casing; 6" hole to TSAMPLING METHOD: Grab samples of airRotary Cuttings

WATER LEVELTTME

DATE

CASING DEPTH

ANGLE Vcrtial ICARjNO ——

SAMPLE HAMMER TORQUE FT. -LSS

e|

i -t

E"?5

— 95

—100

Z-125

ZU30

—— '40

.145

CL

W.OWB/ ttL.

OM&AMPllft

([Rccovenvi CORES

RUN MO.

^ Ul» O

if!

i I % RlECOVBRY 1

X.

»0t DCSCRiPnONOR

HOCK UTHOCOGY

As above; Phyllite -light gray powderyreturns.

100-105' - sandy-coarser textureslightly noist; nowater evident.

125-135 - sandy - Veryslightly moistPhyllite - No waterevdient, large to•edium grained - Lightgray to white -Phyllite continues toTb.Light gray powderysmall, sandy tjuartzitizonesTD - 150'Hashed hole at- bottomfor 3/4 hour - Con-tinued washing wtiileslowly pulling rods.No icasurable ground-water yield.

39.8511386-9-8832

I

BORIMG NO.DP-2

•HEET

2 OF 2ORLUNG

START FINISH

TME TIME

1200 1430DATE DATE

i-8 6-8SURFACE GONomoNS Tilled forming field; dry -vegetated with timothy clover, rye

1

'//////////////////////////////////////

ROCK

BTHUCTURE

SAMPLER ANO BIT

I BLOWa/FOOT

ONCASVstQ

<*4

L.

to

UC

t\o

ajr- "O

uo1-c<uoo

M

TEST RESULTSDEPTH

fvjFEET

§ o

5iu

IIJ

NG CONTR

Myers

Brothers

Dri

llin

g-

R. E. W

righ

t As

soci

ates

, Inc.

LOGGED

BY

Carl c,.

Buyer

DRILL

AR3031+97

— 15

-20•— 25

— 35

— 40

XN' Drffllng Fluid Potable water

XXXXXXXXX.N,

____-_pH- SPBC. Cond. Tamp ( C )_ ',•- <-.d.w . f* */a» PVT cfh^vftiie an tnTiA

1—30 V X >XXXNXXXXXXXNXNXXXNXNXN..-

Well No. MP-9SBoring No. X-Ref: SP-I

MONITOR WELL CONSTRUCTION SUMMARY 5mcSurvay Coord«: N230308.9334______' Etovation Ground Laval 531.5 '____' _ &

E23'23352,8767.; ._______^ Top of Casing 533.84

Drilling Summary:

Total Dapth 37.0'Borahofa Dlamater 3.5" to 13', NX core to 37'Casing Stlck-up Halght: pvc 0.64-"A1 2.34Dria«r F-_T- Kitlinsky Associates

Harrisbura, Pennsylvania

Rig Truck mounted auger/core rigBit(t) 3-7/8..ID Auger, NX core bit, 2"

split spoon______________

Protactfva C*«ing 4" aluminum casingFKtar Placamant:Camantlng:Davalopmant:

Wafl D«»!gn A Specifications b? Rl9Not applicable

e»ft: Gaotogic Log Jt_ Gaophylcal Log —— Wt,, D.v.Jopm.nt:Gating String (»); C « Casing S * Scraan.

D«Dth34.75 - 19.7519.75 - 0.64

-4.66 _ *2.34

String fcl , ElavatlonScreen (SI) I 496.75-511.7Casing (CD, 511.7 .532.14

JCasing_tC2: 526.9 _533,8

Tim*3/4" PVC schedule .40 solid

C2 —4" Aluminum casing

Scraan: SI 3/4" PVC schedule 40 hand slotevery 6" - alternate sides

Fttar Pack: Grade 1 - Horie_s_and_15' - 35' R

Efilter nacX: IB* to 12.5'Grout Saal: slurry - 9.5 to 4'

Cement seal - 0 to 41 'B*ntonfta Saah Pellet 12.5 to 9.5'

Caved Formation 35' to 37.0'Centering Dicks:

Construction Tim* Log:

TatkDrilling2" split spoonXX. core.

Gt.ophyt.teggfngCasing;3-7/8 ID Auger4" Al casina

Start

Data TJm»

6-158-3

8-4

8-4g-1

430400

240

1205

FinishData Time

6-168-9

8-4

8-48-4

1215-1130

305

240"330

Not developed

Stabilization T»tt Data:

R*eov*ry Data:

co 40 to ao tooTIME ( )

Comments:

AR3D3^98

RELD LOG - SOIL BOREHOLEtlTi NAMS ANO LOCATION

Modern Landfill - Southwest ExpansionNo'rtheast and downgradient of existingailKing barn in existing pasture, west ofstrcan.

OATLW _________ ELEVATION

DRILLING METHOD: Drive NX casing,clean out with 3" .split spoon

METHOD; 3" sput spoon, NX coresampling method

WATER LEVEL

TMEDATE

CASING DEPTH

Dry8306-1613.0

20-5'12308-213,0

27.0'

16301-325.0 removed

SORING NO.

MP-9S/SP-1SHEET

1DRILLING

START

TME

1630DATE

6-15-8

PMSH

TIME

1205DATE

5-9-88DWU.RK3 SHid rig SURFACE cONorroNS Non vegetated

vertical cow pastureSAMPLE HAMMER TORQUE 140 FT.-LSS

•AMPLE NUMBER

J2 ANO§• OeSCRJPTJON OF MATEWALW

81t*

DEPTHIsJ

FEET OESCRIPDON OF OPERATKDN

ANDREMARKS

Ooe

HL-daric yellow brovn siltr dry,loose, firm, very frlSBTe, veryaiffsf^ntts

10

.12

3-20

—.22

-28

:39-30

1014

16

** ' XXXN2 ML-yellow brown to olive brown14 21

48

484226152050

38

5240253555

80

"NXXN2b.XXXN 3XXXN 3a.XXXN 35

4a,xxx>

.XXXN

.XXXN

.XXXN

.XXXN Sa6b

150i5012 J3

Saatpli,, Pale_olive tp_olive green

to 24'

24

.XXX'NXXVNXXV

NXXX'XXXVXXXX1

clay silt to green grey sapro-——— — ——lite

MH-green gray to olive brownpoyllitic japrolita, foliation80* to 90*— —————HL/HH-olive brown phyllitic"tff very micaceous, wea-

ITong foliation planes.dryHL;HH-olive brown phylliticfaprolite, very raicaceous, very

Ilaonite x-tals commondryML/HH olive brown to yellowbrown sap_rollte, very fissi.dry

issile,

fm^J-j-yg. V + W-1.J J i BED111' "Ci jsuiL,ruiiatlon < * o5 ,highly weathered phyllite withvuggy quartz veins/lensesparellel to foliation

vuggy quartz vein, weatheredout pyrite/liaonite x-talsbrokan up - 19* to 20' .

No saaple recovered from 20'

ML-olive brown fine sandvfirm, moist to wet

So sa*ple - 29* to 30'

Split spoon refusal at 12.3'

NX coring from 13f to 27'

=1C=6C=2C

1515.316.216.7

NX Casing advanced to 25'

Split spoon to 29"

No sample

FIELD LOG - SOIL BOREHOLESITE NAME AND LOCATlOr-

Modern Landfill --. Northeast and dow^B milXing barn in e

stream.

DATUM

J DRILLING METHOD: Drive NX casing, BORING NOSouthwest Expansion ——————————— • —————————————————— - MP-9s/S?-l

•ngradient of existing clean out with 3" split spoonxisting pasture, west of SHEET

SAMPUNG METHOD: 2"splitSpOOn 2 OF 2

sampling method .— - - DRJLUJGSTART FINISH

WATER LEVELTIME

DATE "

ELEVATION CASING DEPTH

TIME TIME

1630 1205DATE DATE6-15-88 8-4-SS

DRILL RIG skid rig - - - - - — - SURFACE coNDfnoNS MOn vegetatedANGLE vertical BEARING — cow pastureSAMPLE HAMMER TORQUE 140 ~ ~ ~ FT.-LBS

DEPTH IN FEET

(EteVATION)

~ 30

——32

— 34

f

»

*

P V

.

BLOWS/ AJU.

DESAMPLER

(RECOVERY)

15253550.2

I

C

XXXXxxxxxxxxxxxxxxxxXXXNNXXXxxxxxxxxXXXNXXXNxxxxxxxxxxxx

o* CAMPLE NUMBER<£•

Q, AND

=}• DESCRJFTtON OF MATERIAL

CO '- - - SAMPLER AND BtT

CASWOTYPE

BLOWS/FOOT

ON CASINO

DEPTHIN

FEET

Cu.O

DESCRIPTION OF OPERATION

AND

REMARKS

31ML-light olive brown fine

7 sandy saprolite, very soft.loose, dry

Vuggy quartz vein fragmentsrecovered, olive brown togreen gray phyllite host rock* foliation = 80°High rate of Fe02 stainingmaterial very fine to finesandy texture

Total cored depth = 37.0'

UCH O-* OQ.O.W 10

Q)t-.Oo

< H

*PBI

t*PB

•

«

4MH

«P*B

M

^ ^

^

•1

fm

H

•1

» *"

H

«••

Split spoon refusal at 31.7';NX cored to 37' , 0.4* recoveredover 5.3'; sample very soft,washed out by coring operation

&^ HHOUJOUU

F.T.

Ki

tlln

ski

Associates

DRILLING CONTH

LOGGED BY

Luke Smeltz/Steve MltcneU

-1Q

- 20

- 30

40

50

-70

Well No. HP-IPSBoring No. X-Ref: SP-S

MONITOR WELL CONSTRUCTION SUMMARYN229174.7368_________ _ Eltvatten Ground L.v«t 619-7£2323843.0059________ T»p 6f C lna 622.36

Drilling Summary:

TotaJ Dtoth 73.2Sor«hota DUm«ttr 8" tP §' 2-1/4" to 73.2'Gating Stlck-up Htfght: AL 2.66'; PVC 2.47'Dr»«r Kitlinski Drilling Associates______Harrisburo. Pennsylvania

Rig ___TrjJcX-jgunted_auger/coresooonr NX ggre_

DriMng pud Potssle water

frotact » Ca«tng 4" aluminumFHUr Plactmant:Ctmantlng:D»v«lopm«frt:

W«H D»«icn ft Sp«ciflcatlont by Ri9_No_fcL_ applicable

Batii: G*otag)c Log I Oaophytlcaf Leg _Caiing String (t): C * Gating S « Scr**n.

D«pth67.3 -* 16,316.3, -1-2.47

4 ^ -t-2.66

String (t)

Cl

C2

Eftva'.Ion552.4 - 603.4

603.4 _ 622.1:615.7 622.3<

Tim« p H Sptc. Cond. T»mp ( C JGating: Cl 3/4" solid PVC

Scra»n:S1 3/4" PVC with hacKsaw slots

C2Heo ^ - K, F|tw. fmek: 67>3, tQ 13>0. qrade x sand

n" t-n I?.*;1 f^^J*^ «:«nd

Qrout Saal:

Saneonit. S«Bl: Pellet seal 12.5' to 10'B*Dtonite slurry 10' to 3'concr*te 3'Omt«ring Disks:

Conctruction Tfm* Log:

Drilling2" S.S./NX core

Qvophys. Logging:Casing:

StartData

6-1-88

6-7-88

6~7-8S5-8-88

Tlm«

1515

1500

1545"1100-

FW«h

Date

6- 7 -83

6-8-886-9-88

TFme

1430

1545

11001030

W«H Oavaiopm«nt:

Not applicable

Stabilization T*tt Data:

ucC2 4" aluminum protector Pipe

Rtcovtry Data:Q-

to

ER 20Y

0 20 40 W « 100

TIME ( )

Ccmm«nt»: Hole caved in from 73,2' back to 67.3' well construction started at 67.3*

(§) AR30350

Ponn

Etr«£atS ^S |Pf C^ s

CV

«E

OUJCO

UJ UJo. t-

ROCK BOREHOLE LOGSrtE NAME A«) LOCATION

> Modern Landfill•reposed Southwest Exparyorfc. Pennsylvania

DATUM

sion

ELEVATIONDRtL Rio Truck Mounted Auger /Core Rig

DRJLLJNG METHOD:

Split suoon fo11nwi»rt hv auaers to refusaLNX core to required depth.•AMPLJNG METHOD:

Split spoons

WATER LEVEL

TM€

DATE

CASING DEPTH

ANGLE Vertical BEARINGCAMPLE HAMMER TORQUE 30/140 FT.-tBS

(NOI1VA313)XBUNIHidW

»<o£«wfgl

—— 1

i— 4

H- 6

^- 7

— 10

— 11

kL-T14

F 15

33

23

35

911

916

16" 33

16

1037

10C

CORES

{11A

IB

22A2B2C

33A

3B

3C

44A4B4C

1

2

3

tfw ^M» o

< IU. IT0 0

LU

SUUJE

1.32,0

2.C

2.0

LSi2.0

2.22.3

8C

1.=2.2

•Oft. DESCWPTIONOR

ROCK LJTHOLOCY

Brown-gray brown, silt,micaceous, dry brittle,some root materialBrown to red brown siltclayey, micaceous,moist . -Brown red silt, claymoist . r- — . - :.-Phyllite with quartsfragments, weatheredrock, saprolite, incasing siltrahd moremicaceous with depthdry.As Above, increasinaroc*, decreasing cia;Olive-gray to brown-:Saprolite micaceous.Eraaiag to wnite, ar^rittle, micaceous,graphitic texture,weathered.Pnyllite/Saprolite,

*?,

re-

r

.ed

increasing quartz,decreasing oica/ highlyweathered sandy seams,becoming olive-gray.Auger refusal at 7*.Split-spoon refusal at 8'8-9 ' NX core - no recoveryPhyllite, grayish-brownweathered trace to 15%liraonite crystalsalong foliation planesjoints show manganeseiron coatings.

Phyllite, as aboverlay weathering andinfilling along joints.

, continuous core

12.6PM6-68.0'

21.0 29.61439 15306-7 6-78.0' 8.0'

1OR*4C* NO.

MP-lOs/SP-5BHEET1 OF 5

DSLJJNGBTART RMSH

TTMS TME

1515 1430DATE DATEfi-1 6-7

CURPACE CONOmohis Tilled field; reseeded with corn.

tf

«o

-

'\\'\\x\.\\!\\.\\\\

HOCK

£

S

•>109

U

§i1<p

Joints at 9.75 '-63-6-5'10.81 -63-65°

Smooth joints, wellweathered.Foliations 2° to 5"

Jointing at 3" 'to 6"intervals ranging from35° to 50°. All jointplanes show weatheringor clay infilling.

og.0)•U—I"S.m

£oug

V

|

O

35

OU

I

Mm

•M

<BIHl

'•M

^ M

Q, —Q. ——

O "•

3zy •-

TEST RESULTSD€PTHFEET

IE £

Cis1"if

Assoc

oooIjcco

t Associates,

Inc

z/E. A

. Timmins)

R E. H

r{Luke

Sm

>- -7*= iOUJO UJo bS §

flR303502

ROCK BOREHOLE LOG«TC NAME AND LOCATION

' Modern Landfill'reposed Southwest Expansiontorfc. Pennsylvania

DATUM ELEVATIONDRtL Rio Truck Mounted Auger/Core Rig

DRILLING METHOD:

Sol it SDoon followed hv aimers to refusalNX core to required depth.CAMPLMC METHOD: ......

Split spoons

WATER LEVEL

TTME

DATECASING DEPTH

ANGLE Vertical IEARJNG•AMPLE HAMMER TORQUE 30/140 FT.-LSS

Z| ifCORES

RUM NO.

N u3 u

2 P

>

8•Of. DESCftPTTON

ORROCK UTHOLOGY

, continuous core

12.6PM6-68.0'

21.0 29.61439 15306-7 6-78.0' 8.0'

•QR1SH3 NO.MP-lOs/SP-5«H6ET

2 or 5DRJLUNG

•TART FMSH

1515 1430DATE DATE

6-1 6-7SURFACE CONDITIONS Tilled field; reseeded with corn.

SYMBOL

E16-3

3

— 19~19.5

:z. 20

E" 21— 22

Z23.S— 24

— 26

H 27

Z. 28

.29

£ so

4

5

6

7

2.43.2

3.33.5

1.91.9

9*. 4

2.43.2

3.33.5

1821.5

l.C9.4

Phyllite, as above.

Phyllite, gray-greenthinly bedded,weathered micaceous,quartz veining withcommon weatheringfroa 21 to 23.9slightly vuggy.

Phyllite, as above.with abundant oijartzveins, some pitting,abundant limoniteinclusions.

Phyllite, as above.abundant quartz veinswith vuggy texture,numerous pits withmanganese/ ironoxide inclusions.

7////////////////////////////////////1

ROCKSTRUCTURE

SAMPLER AND BIT

CASINO TYPE

BLOWS/FOOT

OM CASJNO

TEST RESULTSD€PTHFEET

Io

5UJ*"H

lo

Joints, weathered 6"spacing with 35° to 40°orientation, Joint .planes have clayinfilling and manganeseoxide coatings.

Jointing at 6" to 9V .intervals with orienta-tion of 65°.

Jointing at 5" to 12Hintervals trending 30°to 55°. Weatheringand clay infillingalong joints.

C

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£o(J

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R. E.

Wrt

qht Associates. Inc.

LOGGED

BY

(Luke Smltz/E. A.

Tlmmins)

DRILL

f

COCOCOCM

>-tn

XO-

LUf-O

AR303503

ROCK BOREHOLE LOGTE NAME AND LOCATION

Modem Landfill— . .__._-Proposed Southwest ExpansionforX, Pennsylvania - - - - -

DATUM

DRlLLISTG METHOD:

Split spoon followed bv auo*r< t-oNX core to required depth.

METHOD:

Split spoons, continuous core

WATER LEVEL

DATECASING DEPTH

12.6PM6-68.0'

21.014396-78.0'

29.615306-78.0'

•ORtsK! NO.MP-10s/SP-56KET

3 OP 5

•TART

T-ME

1515DATE

6-1

FINISH

1TME

1430DATE6-7

OWu. RIG True* Mounted* Auger/Core Rig SURFACE CONDITONS Tilled field; reseeded with com. &

CC

O

tcO

ANGLE Vertical SEARINGSAMPLE HAMMER TORQUE 30/140 FT.-LBS

CORES

10

11

12

•OS. DESCRIPTIONOR

ROOK UTHOLOGY

RC-CX

TEST RESULTSDEPTH

•SiFEET II

1.52.0

2.02.0

4.C1.J4.:

3.4

2.4

abundant quartz veins*9 with manganese iron2.C oxide stains.

.42.

4.:

3.4

0

Phyllite, as above.

Phyllite, as above. _quartz vein 33' to 33,2Manganese iron oxidecoatings.

Phyllite - Grayish-green

Phyllite, as.above.thin easily identifiedfoliations, moderate

3.41.1 weathering, quartz veins.125" to *50".

ghyllite, as abovequartz veining asindicated above.

2.42.<

$"

Fracture at 32.7'(25-30°).

Fractures at 25-30*very brown.with abundant mica,

and abundant quartzveins - .125" to ..500" L \| o.w oFoliation becoming les,distinct.Entire rock weathered,iron/manganese oxidecoatings, liinonitecrystals.

1Jointing at 38.75' to39.75 with orientation65-70°.

Jointing at 42.4 and42.6 with orientation35-40°.

«c.

inv m

OS— '

enOLU

fittmaantt

ROCK BOREHOLE LOG•m NAMC AND LOCATION

Modern LandfillProposed Southwest ExpaiYorK, Pennsylvania

DRJLLWG METHOD; -

SDlit.sDoen followed hv a.iaers to refusalis*°n NX core to required depth.

•AMPUstC METHOD:

Split spopns , continuous core

DATUM

WATER LEVEL

TIME

DATE

BJFVATIOM CASING DEPTHORU. R*o TrucX Mounted Auger/Core RigANGLE Vertical SCARINGSAMPU KAMMCR TORQUE 30/140 FT.-LSS

Z<

(AH3AOO3elWiIWSHO

iMT /IMOIS

CORES

RON NO.

i W LLI

9 x % RECOVERY

S£

ORMOCK LTTHOLOGY

12.6PH6-68.0'

21.0 29.61439 15306-7 6-78.0' 8.0'

SORING NO

MPlOs/SP-5SHEET

4 OP 5DRlLJJslG

START

TIME

3515DATE6-1

RN1SH

TWE

2430DATE

6-7SURFACE CONDITIONS Tilled field; reseeded with com.

SYMBOL MOCK

STRUCTURE

1

1fjg

BdAAONlBVO

OT4SVONO

lOOd<KMO>a

TEST RESULTSDEPTH

IMFEET

|e

ti65S

PCRMAE

CM./

~ 46

Z. 47

43

i~* *9«' SO

E" 51ZL. 52—52.3

z_ 54E. 55

Z_ 56

Z. 57

7" 58

- SSI"59'3— 60

13

14

8.03.0

S.67.0

2.18.C

837.C

;

Phyllite, grayish-green Micaceous thinfoliations apparentmoderately weathered.

Manganese and ironoxide coatings andstaining.

Phyllite, as above.

^

Jointing at 45' to49'. 1-foot intervalat 40° to 45° orienta-tion.

Joints at 52.5-40-45°59.0 - 40e59.3-30°

All joints showmoderate weatheringand limonite andpyrite along jointplanes.

OawJ-J— 11— «oE(N

£ou

m

o1-4-H

O

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3T.Z

PrMHf M MBMM BBtMT fW

<7)OjJ—4

OUIU5•C

JCW

*jS

IT

r>

D'RtLLfNG C

.„„„_„„.,

R- E

. Hright Associates, Inc.

LOGGED BY

(Luke

Sraeltz/E. A.

Tlronlns)

•arrlsbnrq, PennslyvanTTT

COCOOJCO

iV)

—41-

•c

u

CDOkoCD0)r-t

O

1

UJ

o

AR303505

({

ROCK BOREHOLE LOGSrn NAME AMD LOCATION

» 'odern Landfillroposed Southwest E.YorX, Pennsylvania

DPJUJNG METHOD:

. - " . .".:: ."- - _SpU.t sooonfollowed bv auoers to r*»fM<:*lxpansion NX core to required depth.

SAMPLING METHOD:

Split spoons, continuous core

DATUM

WATER LEVEL

TWE

DATE

- ELEVATION CAStNG DEPTH

DRILL RIG True* Mounted Auger/Core RigANGLE Vertical - BEARINGSAMPLE HAMMER TORQUE 30/140 FT.-LSS

DOTH IN FEET

(ELEVATKJNl

BLOWS/ AM

ONSAMPteTT

(RECOVERY]

CORES

RUN NO,

1

UJ ns W& V

f1z u !%

RECOVERY

8cSOB. DESCRIPTION

ORROCK UTHOLOGY

12.6PM6-68.0'

SURFACE CONDITIONS

21.0 29.61439 15306-7 6-78.01 8.0'

SORING NO,MP-lOs/SP-5SHEET

5 OF 5DRJLUNG

START

TIME

1515DATE6-1

FMSH

TME

1430DATE

6-7'Tilled field; reseeded with corn.

SYMBOL

ROCKSTRUCTURE

SAMPLER AND BIT

I **1 S«

TEST RESULTSDEPTH

INFEET

1 o

ABILITY

SEC.

ÊRMAE

CM /

Z_61

Z-62

i— 64

Z64.9— 65

Z"66

E" 67

— 68

_-69

Z"70

r*72Z.73

JHL74

15

16

4.64.6

3.3).3

2.C4.e

D.S8.3

Phyllite orav-oreen toblue-gray, foliated,micaceous, iron oxidestaining, alongfoliation and jointplanes.

Phyllite, tjray-creenthinly foliatedmanganese/ iron oxidealong joints.

Becoming highlyweathered at base,black staining.

Total depth at 73.2'.

^

|

Joints from 60.7'to 62.8'. Increasingorientation from 20"to .55".

Joints and weatheredsurfaces have pyriteand limonite.

Joints at 65.2* andand 66.1' orientationat 60°.

c9am+J— HrHO,w

r»

£ou£

014Jw

of*ôa:Qc!CO

««45£8e

+ +m j Not applicable

Not Applicable

^lll

llll

llll

Mlll

llll

llll

llll

llll

llll

llll

mill

Mlll

llll

imll

llll

llll

lim

"T&T 51-6-1

elates

TR

KHll

nskl

Asso

0O

i_jCCO

R. E

. Hrighb Associates. Inc.

LOGGED BY

(Luke

Sraeltz/E. A.

Timrains)

WELL DECOMMISIONING FORMWELL NO. 306_______

WELL INFORMATION

WELL INSTALLED BY SHM______________ DATE INSTALLED 2/25/89DESIGN WELL DEPTH 132.5____________ MEASURED DEPTH 132.5DEPTH TO WATER 11.91'B.G-S._________ WELL CASING TYPE NAINSIDE CASING DIA. "M______________ INSIDE,. .CASING DEPTH NASCREEN TYPE NA_____________________ SCREEN.LENGTH NA _____SURFACE CASING TYPE ££_____________ SURFACE CASING DIA. NABOREHOLE DIA. 2,75!l/_______________(KNOWN 0_R ASSUMED)

DECOMMISSIONING INFORMATION

DECOMMISSIONING SUPERVISED BY SHM ________________ DATE 3/1/89SURFACE CASING REMOVED?SELL CASING REMOVED? NA ______________________ .(PULLED OUT-DRILLED OUT)OVERDRILLING METHOD m ______________ DRILL RIG Acker Soil SentryOVERDRILL DEPTH NA ____________________ OVERDRILL DIA. NA _____________GROUT TYPE Volclav ___________________ _ GROUT? , MIX. RATIO 1.5 Baas/40Gallonss . : - - -CALCULATED VOLUME REQUIRED 96 Gallons ________________________________VOLUME TAKEN 110

COMMENTS 6Q.Q7 of drilling- rods were left in hole whendecommissioning * _________________________________ ___ __

JOB NUMBER IJS3-6158

PROJECT WMI/RIFS /MODERN

COLDER ASSOCIATES

MADE BY AMT

DATE 3/1/89

flR303507

WELL DECOMMISIONING FORMWELL NO. 306AB_____

WELL INFORMATION

WELL INSTALLED BY SHM _: DATE . INS.TALLEE) 2/15/8 9_.DESIGN WELL DEPTH 50.O7 _________ MEASURED DEPTH 50.0'DEPTH TO WATER NA _______ WELL CASING TYPE "NAINSIDE CASING DIA. NA___________INSIDE CASING DEPTH NA_SCREEN TYPE NA "" " ' " """' SCREEN "LENGTH NA______SURFACE CASING TYPE KA_____" SUgE&CE CASING DIA, NABOREHOLE DIA. 8^___________________(KNOWN OR ASSUMED)

DECOMMISSIONING INFORMATION

DECOMMISSIONING SUPERVISED BY SHM________~________ DATE_ 2-17-89SURFACE CASING REMOVED? NA -: - •_____ "______________

WELL CASING REMOVED? NA______________________ (PULLED OUT-DRILLED OUT)OVERDRILLING METHOD NA________________...DRILL BIG Acker Soil SentrvOVERDRILL DEPTH NA__________' ' •" OVERDRILL DIA.1 NA ___________GROUT TYPE. Volclav________ '• • •'_________,GBOUT_ MIX RATIO 1.5 BAGS/40GALLONS , ...-.-.-.. : \ .'..-:.- •-•-. -.-.-- : . - - - _ . . _ . . - -

CALCULATED VOLUME REQUIRED 130 Gallons________________________________VOLUME TAKEN 140 Gallons_________' ______________

COMMENTS No veil was installed. Only saprolite was incountered whiledrilling. "' " —-—-----— ___ -- ______________

i JOB NUMBER ________________ . _ . ........ -;._ ..MADE BY AMT

COLDER ASSOCIATES

PROJECT WMI/RIFS/MODERN —DATE 3/1/89________———————————————————:——————————flR3035Q8

WELL DECOMMISIONING FORMWELL NO. MU319_____

WELL INFORMATION

WELL INSTATED BY &M£______________ DATE INSTALLED 12/9/88DESIGN WELL DEPTH 150______________ MEASURED DEPTH 150,0DEPTH TO WATER 16.Q________________.WELL CASING TYPE NA

INSIDE CASING DIA. KA______________ INSIDE CASING DEPTH NASCREEN TYPE NA_____________________ SCREEN LENGTH NA______SURFACE CASING TYPE NA_____________ SURFACE CASING DIA. _____BOREHOLE DIA. 2.75"________________(KNOWN OR ASSUMED)

_____________________DECOMMISSIONING INFORMATION______________

DECOMMISSIONING SUPERVISED BY AMT________________ DATE 12/13/88SURFACE CASING REMOVED? NA____________________________________

WELL CASING REMOVED? HO______________________.(PULLED OUT-DRILLED OUT)

OVERDRILLING METHOD ffl________________ .DRILL £IG CHE_____OVERDRILL DEPTH NA____________________ OVERDRILL DIA...NAGROUT TYPE Volclav___________________ GROUT MIX RATIO 1.5 bags/

40 gal,CALCULATED VOLUME REQUIRED 263 Gallons______;___________________VOLUME TAKEN 3QQ Gallons_______________________________________COMMENTS National Foundation Engineering lost their NO drill stringin hole MU319. it broke off approximately 50.0 ft down. 90 ft ofrods and a 10 ft core barrel were grouted in the hole. Attemptswere made for four davs to retrieve their rods and equipment_____unsuccessfully,_________________________"______________

JOB NUMBER BS3-6158_____ .MADE BY A. Templeton

GOLDER ASSOCIATES

PROJECT WMI/RIFS/MODERN DATE 1/15/89_______

AR303509

o3Q.X

flR3035IO

APPENDIX I

GLOSSARY OF GEOLOGIC TERMS

4R3035]i

GLOSSARY OF GEOLOGIC TERMS

Acadian orogeny: A middle Paleozoic. deformation,especially in the northern Appalachians. In Gaspeand adj acent areas. its climax is dated as early inthe Late Devonian, but deformational, plutonic, andmetamorphic events were prolonged over a moreextended period. The Acadian had best be regarded,not as a single orogenic episode, but as erogenicera.

Alluvium: A general term for detrital deposits made bystreams on river beds, flood plains, and alluvialfans; esp. a deposit of silt or silty clay laid downduring time of flood. The term appl ies to streamdeposits of recent time. It does not includesubaqueous sediments of seas and lakes.

Azimuth: The direction of a horizontal line as a measuredon an imaginary horizontal circle. It is thehorizontal direction expressed as the angulardistance between the vertical plane passing throughthe observer and the poles of the earth and thevertical plane passing through the observer and theobject under observation. Azimuths are measuredclockwise from north or clockwise from south.

Boudinage: A structure common in strongly deformedsedimentary and metamorphic rocks, in which anoriginal continuous competent layer or bed betweenless competent layers has been stretched, thinned,and broken at regular intervals into bodiesresembling boudins or sausages.

Breccia: A coarse-grained clastic rock, composed ofangular broken rock fragments held together by amineral cement or a fine-grained matrix, e.g. acollapse breccia, fault breccia, or volcanic breccia.

Brittle: Said of a rock that fractures at less than 3-5%deformation or strain.

Cambrian: The earliest period of the Paleozoic era,thought to have covered the span of time between 570and 500 million years ago; also, the correspondingsystem of rocks. It is named after Cambria, theRoman name for Wales, where rocks of this age werefirst studied.

Gower Associates flR303512

Glossary o.f Geologic Terras (continued)

Clastr. An individual constituent, grain, or -fragment of adetfital sediment or sedimentary rock, produced bythe physical disintegration of a larger rock mass.

Cleavage: , The property or tendency of a rock to splitalong parallel, closely spaced planar surfaces. Itis independent; of bedding and i s produced bydeformation or metamdrphism.

Colluvium: A general ternT applied to loose and incoherentdeposits, usually at the foot of a slope or cliff andbrought there chiefly by gravity. Talus and cliffdebris are included in such deposits.

Concordant: 1. Said of a contact between an igneousintrusion and the country rock, which parallels thefoliation or bedding of the latter. 2. Structurallycomformable; said of strata displaying parallelism ofbedding or .structure. 3. , Said of radiometric ages,determined by more than one method or by the samemethod or by the . same method from moire than onemineral, that are in agreement.

Dip: The angle that a stratum or any planar feature makeswith __the horizontal, measured perpendicular to thestrike and in the.vertical plane.

Discordant: 1. Said of a- contact between an igneousintrusion and the country rock that is not parallelto the foliation or bedding of the latter. 2.Structurally uncoraformable; said of strata lackingparallelism of bedding or structure. 3. Said ofradiometric ages, determined by more than one methodfor the same sample or for coexisting minerals, thatare in disagreement beyond experimental error. 4.Said of topographic features that do not have thesame or nearly the same elevation, e.g. a valleywhose stream enters the main stream by a waterfall.

Ductile: Said of a rock that is able to sustain, under agiven set... of conditions, 5-10% deformation beforefracturing or faulting.

Fault: A fracture or fracture zone along which there hasbeen displacement of the sides relative to oneanother parallel to the fracture.

AR3035I3Colder Associates

Glossary of Geologic Terms ("continued^

Fault breccia: Angular fragments resulting from the crush-ing, shattering, or shearing of rocks during movementon a fault or in a fault zone.

Fault gouge: Pulverized claylike material, commonly amixture of minerals, found along some faults; aslippery mud that coats the fault surface or cementsthe fault breccia. It is formed by decompositioncaused by circulating solutions.

Fault set: A group of faults that are parallel or nearlyso, and that are related to a particular deform-ational episode.

Fault system: 1. Two or more interconnecting fault sets.2. A syn. of fault set.

Foliation: 1. A planar arrangement of textural orstructural features in any type of rock; esp. theplanar structure that results from flattening of -theconstituent grains of a metamorphic rock. 2. Thelayered structure produced in the ice of a glacier byplastic deformation.

Formation: 1. A body of rock strata that consists domi-nantly of a certain lithologic type or combination oftypes. It is fundamental lithostratigraphic unit.Formations may be combined into groups or subdividedinto members. 2. A lithologically distinct, rnappablebody of igneous or metamorphic rock.

Fracture: A crack, joint, fault, or other break in rocks.

Fracture cleavage: A type of cleavage that occurs indeformed but only slightly metamorphosed rocks andthat is based on closely spaced, parallel joints andfractures.

Granoblastic: Pertaining to a homeoblastic type oftexture in a nonschistose metamorphic rock in whichrecrystallization formed essentially equidimensionalcrystals with normally well sutured boundaries.

Hinge: The locus of maximum curvature or bending in afolded surface, usually a line.

Isoclinal fold: isocline

Isocline: A fold whose limbs are parallel

AR3035Colder Associates

Glossarv of Geologic Terms (continued)

Isograd: V"A~.~ line on a map joining points at whichmetamorphism proceeded at similar values of pressureand temperature", as indicated by rocks belonging tothe same metamorphic facies. Such a~ line representsthe intersection of an inclined surface with theearth's surface corresponding to the boundary betweentwo contiguous facies or zones of metamorphic grade,as defined, by the appearance of specific indexminerals, e.g. garnet isograd, staurolite isograd.

Joint:. _A surface of fracture or parting in a rock,without displacement; the surface is often plane andmay occur with parallel joints to form a joint set.

Joint set: A group of more or less parallel joints.

Joint system: . Two or more j oint sets that intersect.They may be of the same age or of different ages.

Kink fold: A fold with planar limbs and sharp angularhinge.

Lithology: 1. The description of rocks, esp. in handspecimen and - in outcrop, on the basis of suchcharacteristics as color, mineralogic composition,and grain size.. 2. The physical character of arock - - - - -

Marker bedt 1. A geologic formation serving as a marker.2. Key bed.

Marker horizon: A marker represented by a rock surface orstratigraphic level, such as a boundary based onelectric or other mechanically recorded logs, thatmay serve, to delineate lithostratigraphic units.

Massive: 1. Said of rocks of any origin that are more orless homogeneous in texture or fabric, displaying anabsence of flow layering, foliation, cleavage,j bints, f issility, or thin bedding. 2. In rockmechanics, said of durable rock that is essentiallyisotropic and homogeneous and is free of fissures,bedding, and other planar discontinuities.

Metamorphic facies: A set of metamorphic rocks character-ized by particular mineral associations, indicatingorigin under restricted temperature-pressureconditions.

SR3035I5Colder Associates

Glossary of. Geologic Terms (continued)

Metamorphic grade: The intensity of metamorphism, measuredby the degree of difference between the parent rockand the metamorphic rock. It indicates in a generalway the P-T environment or facies in which themetarnorphism took place. For example, conversion _ofshale to slate or phyllite would be low-grademetamorphism, whereas its continued alternation to agarnet-sillimanite schist would be highgrademetamorphism.

Metamorphic rock: Any rock derived from pre-existingrocks by mineralogical, chemical, and/or structuralchanges, essentially in the solid state, in responseto marked changes in temperature, pressure, shearingstress, and chemical environment, general at depth inthe earth's crust.

Metamorphism: The mineralogical, chemical, and structuraladjustment of solid rocks to physical and chemicalconditions imposed at depth below the surface zonesof weathering and cementation, which differ from theconditions under which the rocks originated.

Ordovician: The second earliest period of the Paleozoicera (after the Cambrian and before the Silurian),thought to have covered the span of the time between500 and 440 million years ago; also, thecorresponding system of rocks. It is named after aCeltic tribe called the Ordovices.

Paleogeography: The study of the physical geography ofall or a part of the earth's surface at some time inthe geologic past.

Physiographic province: A region of which all parts aresimilar in geologic structure and climate and whichhas had a unified geomorphic history; its relieffeatures differ significantly from those of adjacentregions.

Porphyroblast: A large crystal developed in a metamorphicrock by recrystallization, such as garnet orstaurolite in mica schist.

Recumbent fold: An overturned fold in which the axialsurface is more or less horizontal.

Colder AssociatesRR303516

Glossary of" Geologic Terms (continued)

Regional metamorphism: A general.term for metamorphismaffecting an extensive ..region.,., as opposed to localmetamorphism. It is used almost synonymously withdynamothermal metamorphism.

Rheology: The study of the deformation and flow ofmatter. . . . . . . . . . .

Rose diagram: A .circular or semicircular graph indicatingvalues in several directions of bearing, consistingof radiating rays drawn proportional in~length to thevalue, e.g. for wind currents or joint directions.

Saprolite:- A soft, earthy, clay-rich thoroughlydecomposed rock .formed in. place by . chemicalweathering of igneous or metamorphic rocks. Thecolor is commonly red or - brown, Saprolite ischaracterized by preservation of structures that werepresent in the unweathered rock.

Shear: - A- deformation resulting from stresses that causecontiguous parts of- a body to slide relatively toeach other in a direction parallel to their plane ofcontact. It is the mode of failure in which theportion of a mass on one side of the plane or surfaceslides past the. portion on the opposite side. Ingeological literature the_ .term.... refers .almostinvariably to strain rather than to stress. It isalso used to refer to surfaces and zones of failureby shear, and to surfaces along which differentialmovement has taken place. - --

Shear fold: A fold model of which the mechanism isshearing or slipping along closely spaced planesparallel to the fold's axial surface. The resultantstructure is a similar fold. _

Shear, -fracture: Â fracture that results from stressesthat tend to shear one part of a rock past theadjacent part.

Shear zone: A tabular zone of rock that has been crushedand brecciated by many parallel fractures due toshear strain. Such an area is often mineralized byore-forming solutions.

AR3035I7Colder Associates

Glossary of Geologic Terms (continued)

Slaty cleavage: A parallel foliation of fine-grained,platy minerals, mainly chlorite and sericite, in adirection perpendicular to the direction of maximumfinite shortening, developed in slate or otherhomogeneous rock by deformation and low-grademetamorphism. Most slay cleavage is also axial-planecleavage.

Stress ellipsoid: A geometric representation of the stateof stress at a point that is defined by threemutually perpendicular principal stresses and theirintensities.

Strike: The direction taken by a structural surface, e.g.a bedding or fault plane, as it intersects thehorizontal.

Synform: A fold whose limbs close downward in strata forwhich the stratigraphic sequence is unknown.

Taconic orogeny: An orogeny in the latter part of theOrdovician period, named for the Taconic Range ofeastern New York State, well developed through mostof the northern Appalachians in the U.S. and Canada.In places it can be strictly defined as LateOrdovician by limiting fossiliferous strata, butelsewhere it can be extended to include manypulsations that occurred from place to place fromearly in the Ordovician to early in the Silurian.

Thrust fault: A fault with a dip of 45° or less over mushof its extent, on which the hanging wall ; appears _tohave moved upward relative to the footwall.Horizontal compression rather than verticaldisplacement is its characteristic feature.

Vug: A small cavity in a vein or in rock, usually linedwith crystals of a different mineral composition fromthe enclosing rock.

A:6158GLOS

Colder Associates AR3035I8

a=3O_Xc-

58303519

APPENDIX J

PACKER TEST RESULTS

RR303520

RECOVERY TEST (RISING HEAD METHOD)

COREHOLE # MD317

WELL ANGLE - .-,.. ._ ,._ . 90.0 (DEGREE)CASTING DIAMETER 2.0 (INCH)SAND PACK DIAMETER 6.0 (INCH)SATURATED PACK LENGTH 31.0 (INCH)

TESTED LENGTH OF KINTERVAL TESTED

INTERVAL(FEET) (FEET) (CM/S)

119.0150.0 31.0 3.8E-07

COREHOLE # MD319R

WELL ANGLE 90.0 (DEGREE)CASTING DIAMETER 2.0 (INCH)SAND PACK DIAMETER 6.0 (INCH)SATURATED PACK LENGTH 43.0 (INCH)

TESTED LENGTH OF KINTERVAL TESTED


110.0153.0 43.0 5.9E-08

flR30352I

MD317 RECOVERY TEST"

9 -O.O016 -u)X -0,0013 -

* -O.OO2 -

-O.O022

-O.O02* -

-0,0026 -

-0.0023 -

-Q.O03 -

-O.OO32O.-* 0.8 1.2 1.6 2 2.4 2-8

(Thousands)TIME (seconds)

MD319R RECOVERY TEST:

2CThousands)

TIME (seconds)

HR303522

PACKER TEST (FALLING HEAD METHOD)

COREHOLE |306

WELLINSIIRODSWELL

1

ANGLEDE DRILLINGRADIUSRADIUS

TEST -JUMBER

1

2

3

4

5 .

60.003.02

3.79

- - - . TESTED

(FEET ALONGDRILL. RODS)

- - - 27.5051.5051.5072.5071.5092.5091.50112.50111.50132.50

INTERVAL

(FEET BELOWGROUND SRF.)

23.8244.6044.6062.7961.9280.1179.2497.4396.56114.75

<

LENGTH OF

INTERVAL(FEET)

24.00

21.00

21.00

21.00

21.00

[DEGREE)(CM)

(CM)

K

(CM/S)

8.2E-04

1.6E-03

5.7E-06

3. IE-04

5.2E-05

RR303523

1=5

PACKER TEST:- ALL DATA 'RECORDEDCOREHOLE 3 0 6 TEST # 1 . . .

MAXMUM EXCESS HEAD

DECAY OF EXCESS HEAD

07 -J-O,8

O -c

PACKER TEST - FALLING HEAD METHODCOREHOLE 306 TEST #1

-0,3 -

-1,5-1

-2.5-

-J 5 -

-4,5 -

-5 i t 1 1 j i t i i t2 * 5 . - a 10

TIME (Minutes) ' " "D Recorded values

GoMwAuociaiM

PACKER" TEST TALUDATA: RECORDEDCOREHOLE -306 TEST 02 -

1.56 -

1.54 -

1,52 -

1.5 -

C:. -1-48- ~

£ -- 1.46 -Z.. .. _-_ . .:..S 1.44 -Oo - . . -S 1 .42 -s .o .-r:A _oo-J 1.38 -

1.36 -

1.34 -

1.32 -

1.3 --C

-:-

-

:,- . - - . : _ .

- , - . . -

--- -~ — — — - - --

& —— , — y { n p rHj.a •_._ -0:4 ^ '. .c

I

t

I

a - - -

i T

1atT ^ _^ ^ ETHtiQ o -s ogniJ i

LB,,k!Spr —— —— f^ — — = —— j^ —— -~f- —— , —— «-; — = —— ip ———!_,.. 0.4__ _.. OB-. . _. . JJ2_ . t.6 2

LOG TIME (Minutes) "

PACKER TEST; --FALLING. HEAD METHOD _o -

-1 -

g -^--^-cr _ .o5x .--•--- :-i-,_. — _3 .

f „

_4 -

-5 -

COREHOLE 306 TEST #2

"o =" " -'-]--' - ~~ : """"• -•--.'---——.- — :- ;•D • " _ : . . * _ . _ : = - - - - - - ' - _ _ : - - - - - - .

D " '- - - - .- _ ,-.- - . _, ,_ -... - - - = - - -D .-•-..-. --..:-—. ±±rf.=. ...... .:_~-^n_:._=--_- -• -:._- : ...n - -- ..=. '^. ... . . . - _ . - _ ; - - . . . . . ^ __ .: _^ . _..: _. ....a .. ~:T " : ; ~ . ; ~ -- ";rr -.-"a , . - . : : : - . : . : = " - -, -=; _; ; ••-•-•..:-: .==•:.:-.-. .".•.,.._

a ; = "- ; - - '- _ . . _ , . . . .

_ _.. . Qaa = .: - - ----- -a ... ", , . .

a . . . . .a n ' - - • - ' : • "

DOan_ "--. . -. ' - -:

- -- . - - .. D-nDDD.Q::!DD.aoaaDnDaaaDa

— ————— I ——— —— —— 1 ——————— 1 ——————— | ——————— I ——————— r- ----- —— ] ———— - T ,

3 1 2 .3 . 4 S

TIME (Minutes)D Recorded values

AR303525

PACKER TEST - ALL DATA""RECQRDEDCOREHOLE 306 TEST #3 " ~

£u.

ifEC^

§

i«ao -1.SS -1.54 -1,53 -1.52 -1.31 -1,5 -1,49"-1.48 -

1.47 -1.46 -

1.45 -1.44 -

1.43 -

1,42 -1,41 -14 -

1.39 -1.38 -1.37 -1.35 -1.35 -

-C

3 —————— B ——— m —— B—S-i

_

c a- ra HHOM a i i H ^

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II

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C lI

I I

1 1

C l

/ i i1 1 1 T 1 L 1 1 1 1 1 1 I

.8 -0.4 0 0.4 0.8 . -1.2 1.6 2

LOG TIME (Minutes)

PACKER TEST --FALLING HEAD METHOD. .

9i3is

o -

-0.01 -

-0=02 -

-O.O3 -

-0.04 -

-O.05 -

-0.06 -

-0.07 -

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aa

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20 - 40 . , . _ _ _ . _ 50


GoM* AttociatM AR303526

PACKER" TEST: —ALL: DATA RECORDED"COREHOLE 306 TEST #4

0 -i-B

.Q... . _ . .0,4 . _..0.8

LOG'TIME (Minutes)

PACKER TEST;-" FALLING HEAD METHODCO.REHOLE 306 TEST #4 " ~

-2 -

-6 -

-7

D .

D

DD

i i i i i i r f i i.2 . . . : . _ * . 6 8. 10

TIME (Minutes) .O Recorded values

ftR303527

1,6

PACKER TEST —ALL .DATA RECORDEDCOREHOLE 306 TEST #5

1,15-O.5 -0.4 0 0.4 0.3 1.2 1.6

LOG TIME (Minutes)


-0,2 --0,3 --0,4 --0.5 --as --0,7 --O,8 -

-0.9 -—* 1 *•

-1.1 --1-2 -

\

14-

1,5 -1.6 -1.7 -1.S -1,9 -

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VI -1-2 H DLD

a

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2 0 - - 4 0 . . 6 0


AR303528Goktor AuodatM


COREHOLE |306R

WELL ANGLE 60.00 (DEGREE)INSIDE DRILLING 3.02 (CM)RODS RADIUSWELL RADIUS 3.79 (CM)

TEST TESTED INTERVAL LENGTH OF KNUMBER .---—.— ——i.—•-——,.,.«-.-_«..*-. TESTED

(FEET ALONG (FEET BELOW INTERVALDRILL.RODS) GROUND SRF.) (FEET) (CM/S)

1 101.50 87.90118.80 102.88 17.30 2.7E-05

2 115.00 99.59138.00 119.51 23.00 3.7E-04

3 135.00 116.91158.80 137.52 23.80 4.0E-05

RR303529

1.54

PACKER TEST - ALL DATA RECORDEDCOREHOLE 306R TEST #1

1.52 -

1.5 -

1.43 -

1.46 -

1*44 -

1-42 ~*** ~1.3* -

1.34-

1.32 -

1.3 -

1.2B -

1,26 -

1.24

1.22

11 D Q D BOD1

-O.8 -O,4 0 0.4 O.8 , 1 . 2 1.5

LOG TIME (Minutes)

PACKER TEST --FALLING HEAD METHODCOREHOUE 3O6R TEST #1

-0.2 H Do a a a a a o

-0-3 -

-0.4 -

-O.5 -

-O.S -

-0,9 -

-1 -

-1,1 -

-1,2

DD

-0.6 H

12 16 20 24 26 32

TIME (Minutes)O Recorded values

AR303530

PACKER TEST - ALLiXJATA"'RECORD EDCOREHOLE 306R' TEST #2

I .30 —

1.56 -

1,54 -

1.52 -

1.5 -

1 " 1.48 -u.z -.- 1.46 -

g 1.44 -

£ 1.42 -Q .__. ——— _ ——

0 1.4 -

" 1 .38 -

1.36 -

1,34 -

1,32,

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0 -

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D ———— : ——— B ———— S —— S — O— {

1 1 1.8 - -o."4 • ; c

PACKER.JESTc

V " ' : ;\ '- ;

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LOG 'TIME .CMInutes}"

—-FALLING. HEAD METHOD". . .".OREHOLE =3O6R TEST #2

- -

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. --_^-r~-- -• _;.v;'T "->:- .-: .

--— - . . _ . . -.— - - . . -— -— . -- - ----" - - -

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D -_.__; .-,. .. i .. .._ __ . . Q

aQ

TIME (Minutes)a Recorded values

AR30353I

1,33

PACKER TEST -"ALL DATA RECORDEDCOREHOLE 306R TEST #3

1.56 -

1.54 -

1.52 -

O !•* -•>_, 1.48 -

I 1.46 -

| 1.44-

* 1.42 -

8J 1.4 -

1,38 -

1,36 -

1,34 -

1,32-O,S -0.4 0. 0.4 0,8. : - 1.2 1.6

LOG TIME (Minutes)

PACKER TEST - FALLING" HEAD .METHOD.COREHOLE 30S#R TEST #3

-O.1 --O,2 --0=3 --0,4 --0,5 --0.6 --0,7 --0.8 --0.9 --i -

-1.1 --1.2 --1J --1.4 -

-1,5 --1,5 --1.7 --1,8 --1.9 --2-

-2,1 -

ao a

aoao a

QD

12 16 20 . 24 28

TIME (Minutes)Recorded values

AR303532


COREHOLE #307


TEST TESTED INTERVAL LENGTH OF KNUMBER - -——————.------.=_-_==_-— TESTED


70.00 60.62-91.00 78.81 21.00 2.3E-0390.00 77.94111.00 96,13 21.00 2.3E-03110.00 95.26131.00 113.45 21.00 8.5E-05

AR3G3533

1.551.541,531,521.3.1.5

1-49

I'+a1.471.46

1.45

PACKER TEST - ALL DATA RECORDEDCOREHOLE 307 TEST #1

C 1.

1.4 -

1.39 -1 -38 -1,37 -1.36 i i ) r

e—B—i i—o- g s o-g> i \ \

-O.8 -O,6 -0.4 -0.2 0 0.2 0.4 ,0.6 0,8

LOG TIME (Mtnutes)

PACKER TEST - FALLING HEAD METHODCOREHOLE 307 TEST #1 - - --

T1ME (Minutes)Q Recorded values

^303531+

PACKER TEST -"ALL .DATA RECORDEDCOREHOLE 307 TEST #2 "~ - •- - - --

-O..4 .. - 0 ' ..-'" XJ.4

LOG TIME " (Minutes)

PACKER TEST .-FALLING HEAD: METHODCOREHOLE 3O3 TEST #2 ------—--- -------

3Daa

-i -| oan..aDo

I"

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2~- :—•••- 4--- --6 ' "8 10 12 14 16 18


flR303535

PACKER TEST -~7\LL DATA RECORDEDCOREHOLE 307 TEST *3

1.4 -

1.3S -

1.36 -1.34 -

? 1,32 -

£ 1,3-2i ii2s~| 1-2S -

a t.24 -§ 1.22 -

1.2 -

1.13 -

MS -

1.14 -

1.12 --C

-

3 —————— B ——— 3 —— D>-B-i

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irTE/&e """""•"'"Hi i ^ ssgaa

f1 1 i 1 1 1 ) 1 1 1 1 1

)8 -0.4 0 0.4 0.8 - 1.2 1.6 . .2

LOG TIME (Minutes)

PACKER TEST - FALLING HEAD METHOD0 -1

9iX

— * -

-5 -


>V\ : :D • - - - - - - -

a T- :: :. =--

D

a

a

a

Q k i i i i i i i0 10 20 --. . 3D . ._. . .40

TIME (Minutes)Q Recorded values

RR303536


COREHOLE #311


TEST TESTED INTERVAL LENGTH OF KNUMBER -———————————————————— TESTED


22.50 19.4940.50 35.07 18.00 7.2E-0639.50 34.2160.50 52.39 21.00 1.5E-0359.50 51.5380.50 69.72 21.00 8.2E-0679.50 68.85100.50 87.04 21.00 4.IE-0489.50 77.51110.50 95.70 21.00 2.2E-04109.50 94.83130.50 113.02 21.00 5.3E-05129.50 112.15150.50 130.34 21.00 6.6E-06149.50 129.47170.50 147.66 21.00 3.IE-07

AR303537

PACKER TES"T--"ALL DATA RECORDEDCOREHOLE 31 1 TEST #1

1 1 -

1 -

0.9 -f~t% o.a -u.z

i 0-5 ~

8 0,4 -

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LOG TIME Canutes) " . . _. ". 'IJ.~~~~ '._

0 T

-0:1 -

-0-.3 -

8 -0,4 -S9 _o,5 -£5 -0.6 -

-0.7 -

-O.S -

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PACKER TEST -'FALLING HEAD METHOD":; 'COREHOLE 31 1 TEST- #1

t— —————————— rrn-m a i n er n S .a _ B , D . D - a

, --- ". - -- ' . .--. : .--,..-.

————————————— [ ————————————— 1 ————————————— I ————————————— 1 ————————————— I ————————————— 1 —————————————

3 20 40 , . 50

TIME (Minutes)D Recorded volues

Gold«r Associates AR303538

1.5

PACKER. TEST -—-ALL' DATA RECO-R-DEDCOREHOLE -311 ;TEST #2 "

1.4 -

1 -3,-

!- - ,, HQ -^-oo

1 -

0.9 -

o.s i i i i i r i '-0.3 --Q.6 -0.4 . T-Q.2 - - 0 - -" 0.2 : . 0.4 0,6 0.8

LOG.TIME (Minutes)

PACKER. TEST ..-'FALLING HEAD-METHODCOREHOLE 312 TEST #2 -

____v-2 -

TIME (Minutes)O. - Recorded votues

ftR303539

PACKER TEST - -ALL DATA RECORDEDCOREHOLE 311 TEST #3

*liz

11

I

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1.5 -

1.45 -

1.4 -

1 .35 -

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1,2 -

1.15 --C

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lsx.XL

7

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,! ——— [1 1 1 1 1 1 1 1 1 1 1 1 1

>.S -CL4. . 0 0.4 0.8 12 1-6.-.. :2

LOG TIME (Minutes)

PACKER TEST - FALLING HEAD METHOD .... ...0 -i

-o.i -

-0,2 -

-O-3 -

-O.4 -

-OJ5 -

-0,6 -

-0.7 -

-0.8 -

-0.9 -

(

COREHOLE "311 TEST #3

^ fcrj

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1.55

PACKEE"TEST .--ALL" DATA RECORDED_ ._ ..COREHOLE 311 'TEST #4

1.15-0,3 - :-O.4. .' __.... Q .:___ _.~-._Q;4- ' ' - CL8.

LOG TfME. (Minutes)

PACKER, TEST; — FALLING/HEAD; METHODCOREHOLE 31 1 .TEST #4

-5

TIME (Minutes)O Recorded values .

Goldw Associates AR3035UI

1,55


1.15-O.S -O.4 O 0.4 0.3 : 1.2

LOG TiME .(Minutes) _ _ .. . _ ;

PACKER TEST - FALLING HEAD METHODCOREHOLE 3T1 TEST #5

-6

oa

aa ---

aa ~

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-3 Ha u a

n aG

j I 1 t I I 1 T 1 I I 1 I I t I t I I I

0 2-4 6 8 10 12 14 16 18 20

TIME (Minutes)a Recorded values

GoM«r AssoctetM AR3035^2

PACKER. TEST. — .ALC DATA" RECORDEDCORO-tOLE 311. TEST #S - "

PACKER TEST"- FALLOW HEAD. .METHODCOREHCLE. 311. TEST #6

-0.5 -| — yn .nD

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••°a

x. : ....Z - Daa

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D""aD"aa

i i i i i i i.10 . 20 : ! .. ... 30 . . 40

TIME (Minutes)n Recorded values

Gotdw Associates

1.56

PACKER TEST --ALL DATA RECORDEDCOREHOLE 311 TEST #7

1.54 -

1,52 -

1.48 -^ 1.46 -1 1,44 -

. -H6 1.4 -

1 tjft -§ 1-36 -g 1-34 -

1,32 -1.3 -

1-28 -

1.26 -1,24

1.22

-S—B--B-O

-0,8 -0.4 0 0.4 0.8 1.2 - 1.6

LOG TIME (Minutes)

PACKER TEST -STALLING HEAD .METHODCOREHOLE 311 TEST #7 -

9 _o.* H£§ -O-5 ~

Z -O.S -

-0,7 -

-0,3 -

oa

a

aa .. . .. - -

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20 40 60


Ooldsr AssodalM /IR3Q35H

LOG DRAWDOWN (Feet)

Q_*<

o

Z.•z.

PACKER TEST -" ALL-DATA RECORDED1.56 -

1.54 -

1.52 -

1.5 -

1.48 -

1.46 -

1.42 -

. 1.4 -

. - 1 .38 -

-_- .1-36.-

1.34 -

1.32 -

1.3 -

1.28 -

1.26 --C

COREHOLE. 31 1 TEST #S

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Goldcr Associates AR3035^5


COREHOLE #312


TEST TESTED INTERVAL LENGTH OF KNUMBER ————————————————————— TESTED


14 27.50 23.8238.17 33.06 10.67 5.3E-07

13 29.50 25.5540.17 34.79 10,67 3.7E-07

12 39.50 34.2150.00 43.30 10.50 5.9E-04

11 49.50 42.8760.00 51.96 10.50 1.IE-03

10 59.50 51.5370.00 60.62 10.50 4.8E-04

9 69.50 60.1990.50 78.38 21.00 1.IE-06

1 89.50 77.51110.50 95.70 21,00 8.0E-07

2 109.50 94.83130.50 113.02 21.00 1.IE-06

3 129.50 112.15150.50 130.34 21.00 8.5E-08

4 149.50 129.47170.50 147.66 21.00 1.7E-06

5 169.50 146.79 f190.50 164.98 21.00 5.8E-08

6 189.50 164.11210.50 182.30 21.00 1.3E-08

7 209.50 181.43230.50 199.62 21.00 7.9E-04

8 229.50 198.75250.50 216.94 21.00 5.8E-04

PACKER TEST - ALL.,DATA RECORDED. COREHOLE- 312 TEST_jjf1

0.9-0.8 -O.4

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PACKER TEST*- "FALLING:,HEAD METHODCOREHOLE 312 TEST #1 = - ; ; ' _ _ _ _ _ _ _

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PACKER":TEST -:JALL' DATA 'RECORDEDCOREHOLE 312 TEST #3

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&R3035U9Qoldw Assodtrtss

PACKER TEST —ALL DATA RECORDEDCOREHOLE 312 TEST #4

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PACKER TEST - FALLING HEAD "METHODCOREHOLE 312 TEST #4

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PACKEK-'TEST" ---ALL. DATA "RECO'RDEDCOREHOLE.312TEST #5

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PACKER "TEST :- TALLlRG HEAD: .METHODCOREHOLE~-312"TEST #5 ~

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SR303551


1,5 -

1.45 -

14 -

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PACKER TEST --FALLING" HEAD METHODCOREHOLE 312 TEST #6 " '

I Srar5——5———n—rn:——u .D. " 5 n^LJ n ~ - -™ - .

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Qoid«r Assodstss AR303552

PACKER" TEST ---ALL 1'DATA "RECORDED. . COREHOLE 312' TEST #7c _ _" _v

0.9-2 r -.——— - -i " 0

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PACKER7TEST"- -FALLING "HEAD METHODCOREHOLE 312 TEST #7 - - -

TIME (Minute*)Recorded values

AR303553QoWsf Assodslvs

1,55

PACKER TEST -"ALL DATA RECORDED"COREHOLE 312 TEST #8

1.3 -

1.45 -

1.4 -

1.35 -

1,3 -

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PACKER TEST - FALLING HEAD METHODCOREHOLE 312 TEST


A_t AR30355lfGoMw Associates

PACKER -TEST" - 'ALL.JD'ATA" RECORDED'COREHOLE'312 TEST #9

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PACKER TEST.:-. FALLING. HEAD METHODo -i:

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flR303555

1,5

PACKER TEST - ALL DATA'RECORDEDCOREHOLE 312 TEST #10

1.5 -

1.4 -

1.3 -

I.I -

0 0.4 .- _0,8

LOG TIME (MTnutes)

PACKER TEST --FALLING "HEAD METHODCOREHOLE 312 TEST #10

10 12- 14 , 16

TIME (Minutes) -O Recorded values

GoMtr Associates AR303556

PACKER. TEST. —ALL,DATA RECORDEDCOREHOLE 3"! 2 TEST #11 _ i.

-0,8 - -Q.4 . .0 _ -. .0-4.. . -" ' O.S

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PACKER-TEST -'FALLING.HEAD .METHODCOREHOLE 312 TEST #n' " = "~''

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QoMsr Assodatss AR303557


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PACKER TEST --FALLING HEAD METHODCOREHOLE 312 TEST #12

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Gotdtr Associates AR303558

PACKER. TEST. -.ALL - DATA RECORDEDCOREHOLE 312 TEST #13

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PACKER TEST -FALLING HEAD METHOD'COREHOLE 312 TEST #14

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QoMar Associate* flR303560


COREHOLE #313


TEST TESTED LENGTH OF KNUMBER --———--—— TESTED

(FEET ALONG INTERVALDRILL.RODS) (FEET) (CM/S)

8 39.0061.80 22.80 1.6E-06

7 59.0081.80 22.80 8.4E-04

6 79.00101.80 22.80 9.0E-04

5 99.00121.80 22.80 2.2E-04

4 119.00141.80 22.80 2.2E-06

3 139.00161.80 22.80 1.2E-06

2 159.00181.80 22.80 8.2E-07

1 179.00200.00 21.00 5.0E-06

AR30356

PACKER TEST"-" ALL DATA RECORDEDCOREHOLE 313 TEST #1

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-0,01 -

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flR303562

PACKER TEST - ALL DATA RECORDEDCQREHOLE 313 TEST #2 ~ ^

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Qold«rA«.wei.rtot ftR303563

PACKER TEST - ALL. DATA RECORDEDCOREHOLE 313 TEST #3

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-O.O01 --0,002 --0,003 --O.OO4 --O.OO5 --0,006 --O.O07 --o,oo« --0.009 --0.01 --O.O11 --O.O12 --aoi3 --O.O14 --0.015 --O.O16 --O.O17 --0.013 --0.019 --O.02 -

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PACKER:TEST::—"FALLING HEAD METHODCOREHOLE-..313 TEST #4 -

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ftR3Q3565

1.421.61 -1.6 -


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-0,8 -O.4 0 0.4 0.8

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PACKER TEST - FALLING HEAD METHODCOREHOLE 313 TEST #5 ._ '.

-1 -

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Gofetor AuodatM AR303566

PACKER.. TEST ---ALL'DATA RECORDEDCOREHOLE":313 TEST #6' ' "^ '

1.43

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PACKER TEST - PALLING HEAD. .METHODCOREHOLE ,313 .TEST #6 . " '

-4-O 0.4 0.8 . 1.2

TIME (Minutes)D" Recorded values

GoMw Associates RR303567

1.61

PACKER TEST - ALL DATA "RECORDEDCOREHOLE 313 TEST #7

1,6 -1.53 -1-58 -1,57 -1,56 -1.35 -1-54 -

1,5-1.49 -1.43 -1,47 -1.46 -1.45 -1.44 -

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PACKER TEST - FALLING HEAD" METHODCOREHOLE 313 TEST #7

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Qotdw Associates flR303568

PACKER:TEST~--"ALL:DATA RECORDED"COREHOLE-313 TEST_#3

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PACKER TEST::.-,. FALLING HEAD METHOD" ..COREHOLE 313 TEST #8

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Ooidsr Associates RR3Q35S9


COREHOLE #314


TEST TESTED LENGTH OF KNUMBER INTERVAL TESTED


6 50.0072.20 22.20 1.4E-03

5 60.0082.20 22.20 3.8E-04

4 80.00102.20 22.20 6.3E-04

3 100.00122.20 22.20 6.OE-04

2 120.00139.00 19.00 9.4E-06

1 138.00158.00 20.00 3.0E-05

AR303570

PACKER" -TEST —-ALLi DATA RECORDEDCOREHOLE 314 TEST #1

tl.z5oQS

aoo_).. .

O1

X .z-J

1 ./ —

1.6 -

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LOG. TIME T (Minutes)

PACKER TESTV-TALUNG HEAD METHOD"COREHOLE 314 TEST #1

0 -i —————————————— : ———————— = ————————————————— : ————— : ———— : ————————————— : ————————— : ————

-0.1 -

-0.2 -

-0.3 -

-0.4 -

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- =. a" : - " " - . . -- • . . 7 -

. _ . . a_ _ . ._.._. — _ ——— . . .. . —— _ . .._ _. —— . — . . _ . . _ _ . ._ _..

a : - __ .___ ._. _ ._. _ ... ... ....a

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a .. ... .. ....D

D._ . :. .-..= :- --=. -.-- .... - - -

D

20 - -— 40 . - 6O

TIME (MinutesJ ' "I 7D Recorded values

Debtor AciecM*. ftR30357i

PACKER TEST - ALL DATA'RECORDEDCOREHOLE 314 TEST #2

I,/ —

1.6 -

1.5 -

i2 1-4 -

1 -*-

§

1.2 -

1,1 -

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I

0.2 0.6 ... . -=1 . 1.4 . 1.8

LOG TIME (Minutes)

PACKER TEST - FALLING. HEAD METHOD . .0 -

-0,1 -

-0,2 -

0 -0.3 -

19 -0.4 -XZ-» -o.s -

-0.6 -

-0,7 -

-n s -


V*

aD ' ' -

a -•-• :--:- --- -----a -

D : - -

a - - - - - , ,D

aa

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20 40 60


&R303572

PACKER TEST' -"ALL 'DATA RETCORDED."1 ,1.7 -

1.6 -

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Z 1.4 -

OQ .

ao

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1.1 -

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. _ _COREHOL£.314:T£ST #3". .. ~. "

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cbliib

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LOG TfME (Minutes)

PACKER TEST;- FALLING HEAD: METHOD . .o -

-1 -

-2 ~O

te

_. ... _ _ . _ . _ .

-4 -

-5 -

COREHOLE 31 4 TEST #3 ' '— —"

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— - - - -— --- ----------- - ~ - n- Q c

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- • • • - • - . a

24 2S


AR303573


1 ,f

1.6 -

1-5 -

u.

I 1.3 -a

1.2 -

1.1 -

1 --C

—— -

B— ————————— e —— m — m—i

I\1

"11

1 1 1 i I 1 I I 1 I 1 1 1 1 1 1 1 1 1

).8 -0.6 -0.4 -0.2 0 0.2 0.4 0.6 . 0.8 1 1.2

LOG TIME (MTnutesy " " - ---

PACKER TEST - FALLING" HEAD METHOD..: .,0 -j

-0,3 -

-1 -

0 -1,5-

3

1 ~2 ~X . _z_J _ t « _— •£*&

-3 -

-3.3 -

—A. —

COREHOLE 31 4 TEST #4

n _aoanD

a

o

a

a - ' . -. ; . . .

D - - - .

aaa ....

a n a a D am adanaaa'm


AR30357U

1.7

PACKER TEST"-—-ALL "DATA =RE<JORDEDCOREHOLE 314 TEST #5

0 . 9 . . .1.4

LOG TIME (Minutes)

PACKER TESr— FALLING-.-HEAD' METHOD^CDREHOLE 314 TEST #5

-40 0.4 0.8 1.2 1,6 2 2-4 2.8


AR303575

1.5

1.4 -

1.3 -

PACKER TEST - ALL-DATA RECORDEDCOREHOLE 314 TEST #6

1.2

PACKER TEST --FALLING "HEAD'METHODCOREHOLE 314 TEST #6

Oa

-0,5 -1

-1.3 J

-3,5 -

-4,5 H

-3


GoktorAMoeMM flR303576

1.5

PACKER'TESTl-r-ALL. DATA RECORDEDCQREHOLE 31.6,. TEST

-0.3 -. - 0.4 . ,. Q.._-. . ._. .. ;.0_4 . . ... 0-3 -

LOG-TIME (Minutes)

PACKER TEST_--FALLING HEAD' METHODCOREHOLE 316 TEST #1 - '

DODao

~2-| aa

g| -3HQ25.

-5 Ha _ . . - . - .

a _. .:-6 -\ --- a ^.. .

D a D a

-7 i i i \ t i i \ > i n "12 16 ' 20 - 24 28 32


{\R3Q3577

PACKER TEST —ALL DATA RECORDEDCOREHOLE 316 TEST #2

_

iL.

2

§

S

I

_i

i.o -

1.4 -

1.3 -

1.2-

1.1 -

1 -

09 --C

3 —————— m — — &— .g — g-i

i

t

' "V3B]3l9 m

E

C

i

1

!

k

.8 -O.4 0 0.4 . 0.8... . .1.2 1,6"

LOG TIME (Minutes) 7 . ----- - - -

PACKER TEST --FALLING HEAD METHOD ."o -

-0,002 --O.O04 -

-O.OO6 --O.OO8 -

-0.01 --O.012 --O.014 -

-O.016 -

-O.01S -

-0.02 --0.022 --O.O24 -

-O.026 -

-0.028 -

-O.03--

-0,032 -_n mti _

COREHOLE 316 TEST #2 " .

V1 "

1a o . : :•; -

a -. ' - : La . - -- -a . - - .n - .....a -o .._, - - -. .. ,a - . _ _ , = _ .a .a

a a a " -O -a o a

5 12 16 20 . 24 28 32

TIME (Minutes) '. .O Recorded values . . . . .

GoktorAuod-rtM AR303578

"eu.

_OG DRAWDOWN i

OP

Ou .

z-I

1.6 -

1.5 --

1.4 -

1.3 -

1.2 -

1.1 -

1 -

0.9 -

0 -i

-0.02 -

-0.04 -

-0.05- -

-0.08 -

-0.1. -

-0.12 -

-0.14 -

-0.16 -

-d;i8 --0.2 --O-22 -

-0-24 -

-0.26 -

-0.28 -

-0.3 -

-0.32 -C

PACKER: TE<

. .. .,„ ... ^ .,_ .- . . _ . . _

.... _. — . _

3 ——————— D-" " -O —— B — B-f

t i i>.3. - ..-0.4 ... - __C

PACKER TEST

\, "

V^

- - - - - - - — =-=-

. ,--.., -

) 4 __ _8

5-T -::ALL,DATA RECORDED-COREH-OLE,:M6't_ST #3 _ .. •

'X.E l

n

(i

(i

nn

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1 1

y-i"«l'MllllimiHIIIIIIIIWl||||.dl ^

. .I t 1 1 1 1 1 I

i - .-'-':.-... 0.4. ".::..: as... ,..._. 1.2 . 1.5LOG TIME (Minutes)

r— FALLING "HEAD "METHODCOREHpLE/316 TEST #3 ~ ' "

.

....

X,a -- - -

— — a t-_ •; L ~ . ~ .-.-•_-. "" " . ""ao

- .._ , ..,,... aa

-_,_, - - .,--. .- . — -- --..aa

- -- - -- - nna

a12 -- - 16 .-." 20 24 2

TIME (Minutes)D - Recorded values

Qoktor Associates AR303579

PACKER TEST -"ALL DATA RECORDEDCOREHOLE 316 TEST #4

u.2

I

i§

QXz

i 10 -

1.3 -

1.4 -

1.3 -

1.2 -

1.1 -

0.9 -»*c

-

3 —— = ——— g--*--=g —— 0 D-E

!n

E l

n

C l

11 u

/ I>,S -O=4 0 0.4 0,8 , 1 . 2 1.6

LOG TIME .(Minutes) ; .

PACKER TEST -"FALLING" HEAD METHOD.:o -

-0,02 --O.04 -

-O.O6 -

-O.Q8 --0,1 -

-O,12 --O.14 -

-0.16 -

-0,18 --0.2 -

-0.22 --0.24 -

-0.28 -

-0.2S -

-0,3 -

-Q.32 -

-0.34 -(

COREHOL£316 TEST #4

V^

O :O a " _a a

a :a - - --- - ...a " . :a - - - . _ _ _ _ :o - -.- - -

a : _ " " - •

a ; . ..

n

oi i i i i i < i i i i i i i i i

D 4 S 12 16 20 24 28 32 -


Qokter Assodatss flR303580

1.6 -

1.S -

1.4 -

oo

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< i •»Q: 1.2 -a :- — ..-OO

1.1 -

1 -

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o:

5 ~3~x. .:"-: :-.= -Z -

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PACKER TESTCOR

- -

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... . .

G ———— — B —— 3 — a- n -E

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PACKER "TEST5-COF

a - _. , - _ - - -a - ----- -----~-r-.O - - ~, . .

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------:— —

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I -1"I

1I1 £D

/ ^ . , 1K -win. ——— ^—— y

J O.4 .,.0,8- , 1.2

OG T[ME (Minutes)

—FALLING," HEAD METHOD?EHOI_E 316 TEST #5

; -'=-•:---.".:." ;': - : " - — "

1 : _ . . . -D -

a . "-r_-j _ __.._ -_' - '

a .n

D : - -

n .-- - - - - - D

aa

aa

TiME "(Minutes?"D . Recorded volues

AR30358


39

-i

9iIB3

U 1

-O.O1 -

-0.02 -

-O.O3 -

-O.Q4 -

-0,05 -

-O.O6 -

-0.07 -

C

SJjaoo

a . - . ... io a o - .

n

D

n- .

D

Q

1 t 1 1 1 j 1 1 1 1 1 1 1 1 ) 1) 4 8 12 16 20 24 r 28 32

TIME (Minutes)D Recorded vclues

PACKER TEST -.FALLING HEAD METHOD... : Vo -s

-0.01 -

-0.02 -

-0.03 -

-0.04 -

-0,05 -

-O.06 -

-0,07 -

COREHOLE 316 TEST #6s; —————" Ba a

na _ ._ .D a . .a o

n . _ ; . . .

D

D

a


AR303582


COREHOLE |316


TEST TESTED INTERVAL LENGTH OF KNUMBER —————•-—————————.^-^^-.^ TESTED


1 39.50 34.2156.00 48.50 16.50 1.5E-03

2 49.50 42.8776.50 66.25 27.00 6.6E-07

3 68.50 59.3295.50 82.71 27.00 6.7E-06

4 88.50 76.64115.50 100.03 27.00 5.8E-05

5 108.50 93.96135.50 13-7-35 27.00 1.IE-03

6 128.50 111.28155.50 134.67 27.00 1.8E-06

AR303583


COREHOLE #318


TEST TESTED INTERVAL LENGTH OF KNUMBER ———————————————————— TESTED


1 52.00 45.0369.00 59.76 17.00 6.7E-05

2 68.00 58.8989.00 77.08 21.00 3.3E-05

3 88.00 76.21109.00 94.40 21.00 9.3E-06

4 108.00 93.53129.00 111.72 21.00 2.8E-05

AR30358U

1.58

PACKER TEST:- ALLJDATA RECORDEDCOREHOLE .3i_e:_TE5T #i -~ ~ :. •-" --'.

1.56 -

1.54 -

1.52 -

5— -1.46 -OQ£ . 1,44 -20 1.42O-> 1.4 -

1.38 -

1.3.6 -

1.34 -

1.32-O.S . __ -O.4 . .__. .0 " ." O.4 " G.3.. ."" .. 1.2 1.6

LOG TIME (Minutes) '

PACKER TEST:-.FALLING HEAD METHODCOREHOLE"318 TEST #1

-1.6 -

-1.8 -

-2.2-

-2.4 -

-2.6

a • • . . -•a ,_ - .. .--"-•- - - - - a

a an " . ".:

O --:--- -- a . -" -an

i i i i i i i i i i i r r t i4 8 12 16 .20 24 28 32

TIME (Minutes)a -.Recorded voiues

AR303585

g

1.58

PACKER TEST - ALL DATA RECORDEDCOREHOLE 318 TEST #2 - - - ~~

-0,8 -O.4 0 0.4 0.8 -1.2

LOG TIME (Minutes)

PACKER TEST - FALLING HEAD METHODCOREHOLE 318 TEST #2 :

-O.I -

-0,2 -

-O J --Q4 -

-O.S -

-0,6 -

| ---0.7-

* -0-8-3 -0.9 -Sz -1

-1.1 -

-1,2 -

-1.3 --1.4 -

-1,5 -

-1.6 -

-1.7-12 16 2O 24 2S

TIME Canutes)Recorded values

RR303586

PACKER TE T:"-.ALL DATA RECORDEDCOREHOLE 318 TEST #3

^-"Se

ZJ

OQ.Sa:O -oo

o.1oUJIz_l

1 .30 -

1.56 -

1.54 -

1.52 -

1.5 -

1.48 -

1.46 -

1 .44 -

1..42 -

1.4 -.

1.38 -

1.36 -

1.34 -

1.32 -

1.3 -

1.28 -

. ..= =..

- - —

- - - - — ---- -

. .- -

—— - ..=—— -.-. -._ -. -:^-

___ _ __ —— .. __

- -- - ------

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- a a a- [f *" '"" '- i

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T ^^ ^ ^

^ T3

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'

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£ lIQ - - - . " .

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nn.i.n-m,,,..' ' C!""•nnni i n 1 1 iiininiiiniiiim L

1..0 i i i i - - - - - — — i — — i — — i ————— i ————— i ————— i ————— \ — — — — \ — — — —-o.s -o;4 . .a. __ 0.4 '"'I' o.s ..1.2 1.6

LOG. TIME (Minutes)

PACKER,TESTJ- FALLING "'HEAD"1i1"ETHOD.COREHOLE'318 TEST #3 .;.

-0.05 -

-0.1 -

-0,15 -

_ -0-2. -'-

-0.25 -:--0.3 -

-0.35 -

-0.4 -

"o -:" : --- "~':"- ' :-- ::~ ""•""•a - . ... .- . -n . . . . - - . . .____ _ . . .___._._ _ .n " " . . . . • _ _._. . .

D.. "-a- ,,,. ,- -...-- ....... , -.--.. .._,n . - . . .

a - ,__._ . . . . . ._D ; : " " . - " - -"--'-' -- - -.

... —— .. _ . _ . — .. ._..... _ . . . _ .... __-. _ _ _ _ _ _a - --..-

.... _._...._.. — .... ...... . . . . . . .

D. . . . .

,.._.. T_ . _ ._ . . _ _ _ . . . . ^. .._ _ . .a

-•*'•••' r i i i i i i ——— f ——— i ——— [ ——— i ——— i ——— i ——— i ——— j ——— | ——— | ——— i04 8 12 16 20 24 28 32

TIME (Minutes)Q " Recorded values

AR303587

PACKER TEST. - ALL DATA RECORDEDCOREHOLE 318 TEST #4

1,2-O.8 -O.4 0 0.4 0,8 1.2 1-6

LOG TIME (Minutes)

PACKER TEST - FALLJNG HEAD METHODCOREHOLE 318 TEST #4 - - -

-0,2 -r

-0.4

O -0,5

* -"0,8

| -O.T

3 -0.8

-0.9

-1

-1.1

-1-2

-1.3

OD

O a ooDD

| ———— i ———— | ———— I ————— I ———— I ———— I ————— I ——12 16 2O. 24 28


QoU*r Associate* AR303588

•o

flR303589

APPENDIX K

SUMMARY_OF RESULTS FROM FIELD, TRIP, AND LABORATORY BLANKS

RR3Q3590

12-D*c-89>

Summary of Chemicals Detected itvJTrip angiJ.ieldBlank Samples at Modern Land?if r

Frequency of Geometric. MaximumChemical Detection (a) Mean (b) Detected

Qrganics (ug/1):

acetone 1/19 5.1 6.0carbon disulflde 1/19 NR .. .1.9di-n-butylphthalate 1/6 4.2 , . 4.2methylene chloride 1/14 NR 2.0total dichlorobenzenes 1/13 MR 4.0trichloroethene 1/19 2.5 .. 3.0trtchlorofluoromethane 3/13 MR 4.0'

Inorganics (ug/1):aluminum (total) 9/18 17.4 130.0antimony (total) 7/18 1.9 - 75.0arsenic [total) 6/18 1.0 1.0barium (total) 7/18 0.6 . 7.8beryllium (total) 6/18 -, 0.5 1.0cadniua (total) 8/18 .1.6 2.9calcium (dissolved) 1/1 HA • 15.6calcium (total) 13/18 11.4 550.0chromium (total) 6/18 1.7 41.0cobalt ftotal) 6/18 1.6 2.3copper (dissolved) 1/1 HA 6.4copper (total) 8/18 1.8 5.4cyanide (total) 6/8 10.0 10.0Iron (total) 14/18 7.6 . 215.0lead (dissolved) 1/1 HA 5.8lead (total) 9/18 1.0 10.6magnesium (dissolved) 1/1 HA 1.4magnesium (total! 16/18 6.2 52.0manganese (total) 9/18 0.8 25.0mercury (total) 7/18 0.1 0.2molybdenum (total) 6/6 8.3 6.3nickel (total} 6/18 8.3 - 34.0potassium (total) 7/18 40.1 . .. _ 151.0selenium (total) 6/18 0.6 . 2.7silver (total) 6/18 1.7 12.0aodiura (total) 17/18 91.2 781.0thallium (total) 6/18 1.0 1.5vanadium (total) 6/18 -2.7 2.7zinc (dissolved) 1/1 NA 22.0zinc (total) 18/18 - 10.3 - 166.0

Radioactive Compounds (pCi/1):

gross alpha 3/6 0.6 . 1.5gross beta 5/6 0.8 2.6r*d1ura 228 1/6 NR 0.3thorium 230 6/6 0.4 1.9uraniua 2/6 0.2 1.8

Note*: - - •(a) The number of samples In which the contaminant was detected divided by the total number of

samples analyzed.(bj Non-detected sawlea were set to one-half the detection limit for calculating geometric means. Samples in

which the contaminant was not detected at a detection limit at least two times greater than the maximum detectedconcentration were not included In estimating geometric mean concentrations.

NA " Hot applicable since there was only one sample.NR « The geometric mean was not reported (MR), as this concentrations was greater than the maximum detected

value (as a result of including detection limits that exceeded two times the maximum detected valueIn calculating the geometric mean).

AR3Q359I

Summary of Chemicals Detected, in Lab Blank Samplesat Modern Landf iH-

Phase IA (Sumner 1988)

ChemicalRange of

Water . SoilDetected Values Range of Detected Valuesfrg/U ' - - [ug/kg)

Organics '-- -" " ~ ; ~

No Chemicals of Concern Detected

Inorganics

AluminumAntimonyArsenicBariumCalciumCopper

k IronB Magnesium

SeleniumS i TverSodiumThalliumZinc

._..__ _._. , . .

........ ...--,- . -.-.__. . =_._ 34

- - - , 1• - ND

NDHONOND_ .. H.fi

-. —.. •--.--. " TT. ~2.5" ND

•- - ——- ^——— ------ •" - --fJQ

- -' -- i 3.5

...= ...,__..,.

^ - ~ - • ' " - '.- 48.7. .-4 '- 1- 7.3'- 26.2- 7- 23.?- 2.3' "-9-~42.5-'2.2- 8.3, .

ND -58.1 -1

HD -ND -ND -ND -1.3 -—15....

6 -

47.412

21.74.28.716.61.7

_. . .

_.11.7

Hotes:

—= Chemical not detected in any lab blank samples

ND - Sot Detected -

RR303592

Summary of Chemicals Detected in Lab Blank Samplesat Modern Landfill

Phase IB (Spring 1989)

Chemical

Organ Ics:

Bichlorobenzene

Inorganics:

AluminumAntimonyBariumCalciumCopperIronLeadMagnesiumPotassiumSeleniumSilverSodiumThalliumZinc

Water SoilRange of Detected Values Range of Detected Values

(ufl/L) (ug/kg)

3

ND

NDNDND

8.1

NDND1.1.3.8NO2.3

_ 7 - —

- r- -

- 130.4ND —— -~- 1- 2.2- 14.9ND-32.5 . - _._.__—.1.2- 18.3- 170.3 —— -- 1.6 '. — - - -

E O "__-__ - - -^ O,Q *•- - - ——

- 73.1 . . _... . —- 2,910

Motes:

-— • Chemical not detected in any lab blank samples

ND « Not Detected

ftR303593

OTPA . CLP

COVER"~PA.C.-; - LNOUGANtC, ANALYSES.. .DATA PACKAGE

Lab Name-:

Lab Code::1' -..;_--:--_-_: ~~_ . ciiScf No::;r ~-~433~8 . ... SAS .Np_.__:.._._ . ... SDG

SOW" No. :-_-._ . - --Q~r

EPA Sample .No. •-. -.it- :— - - -- . Lab Sample ID-. . . .. ,_. _ . . - . , , L, • • <ya,3fl-ot _____ _.

6 1471 /WO-TMSQR473W05DUP

~ Cff

4 33-

Were ICP interelement corrections applied? " - Yes/No VE5

Were XCP background corrections applied? - - Yes/No .If yes— were, raw data generated beforeapplication of background corrections? - Yes/No

Comments:

roHCU gfimsnt>.J e gp fey rpg flumwrf mm<fci.ic/g.tj

Release of the data contained in this hardcopy data package and in thecomputer-readable data submitted b! a ..floppy diskette has been authorized bythe laboratory Manager or _the Mjanager1 s_designee, asfollowing signatureT ~ :r r: ": . -;-."" - . "- " = ..

• - . : " . ; -'Date:COVER PAGE - IN 7/B"7

*

4338 2001AR303591*

U-S- EPA -VCLP t _ . . . . .

COVER PAGE - INORGANIC'ANALYSES DATA PACKAGE

Lab Name: erOAoX N ___ Contract: ;;. _.

Lab Code: _____ ...___ Case No-j gg , . ,. J° - - f .^

SOW No.:

EPA Sample No. . Lab Sample ID.4338- 2.

-2.4

- 314518 -

8P 1566/a IPS433* -4334-33

Were ICP interelement corrections applied? ... _„ . _. _ .. Yes/No

W re IC3? baclcgfround corrections applied? Yes/No Y££Xf yes-were raw data generated beforeapplication of background corrections? Yes/No NO

Comments:

Release of the data contained in this hardcopy data package and in thecomputer-readable data submitted on floppy diskette has been aut ior/zed bytlie Laboratory Manager or the Manager's designee, asfollowing signature.

Lab Manager:

) " ' Date:

COVER PAGE - IN 7/87

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APPENDIX L

TOXICITY SUMMARIES FOR CHEMICALS OF POTENTIAL CONCERN

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TOXICITY SUMMARIES

A-l QSSAHICS

ACETONE

Acetone is absorbed in humans and animals following oral orinhalation exposure (EPA 1984). Approximately 75 percent ofinhaled vapor is absorbed by the pulmonary route (Kagan 1924).Acute exposure to acetone vapors of 500 ppm produce irritation ofthe mucosal membranes in humans (EPA 1984, Nelson et al. 1945).Prolonged or repeated dermal contact may defect the skin andproduce dermatitis (Krasavage et al. 1981). Rats acutely exposedto acetone vapors showed behavioral changes as demonstrated by aninability to pole climb following stimulation (Goldberg etal. 1964). In rats, slight increases in organ weights, decreasesin body weights and nephrotoxicity have been observed followinglong-term oral exposure to acetone (EPA 1986). Humanschronically exposed to atmospheric concentrations in excess of10,000 ppm are likely to experience central nervous systemdepression and narcotic effects (Krasavage et al. 1981).

EPA (1989) derived an oral reference dose (RfD) for acetone of0.1 mg/kg/day based on a study sponsored by the EPA Office ofSolid Waste (EPA 1986) in which increased liver and kidneyweights and nephrotoxicity were observed in rats exposed orallyto acetone; an uncertainty factor of 1,000 was used to derive theRfD.

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BENZENE - .;,

Benzene is readily absorbed following oral and inhalationexposure (EPA 1985). The toxic effects of benzene in humans andother animals following exposure by inhalation include centralnervous system effects, hematological effects, and immune systemdepression. In humans, acute exposures to high concentrations ofbenzene vapors have been associated with dizziness, nausea,vomiting, headache, drowsiness, narcosis, coma, and death (NAS1976). Chronic exposure to benzene vapors can produce reducedleukocyte, platelet, and red blood cell counts (EPA 1985).Benzene induced both solid tumors and leukemias in rats exposedby gavage (Maltoni et al. 1985). Many studies have alsodescribed a causal relationship between exposure to benzene byinhalation (either alone or in combination with other chemicals)and leukemia in humans (IARC 1982).

Applying EPA's criteria for evaluating the overall evidence ofcarcinogenicity to humans, benzene is classified in Group A(Human Carcinogen) based on adequate evidence of carcinogenicityfrom epidemiological studies. EPA (1989) derived both an oraland an inhalation cancer potency factor for benzene of 2-9X10"2(mg/Kg/day) "1. This value was based on several studies in whichincreased incidences of nonlymphocytic leukemia were observed inhumans occupationally exposed to benzene principally byinhalation (Rinsky 1981, Ott 1978, Wong 1983). EPA (1989) iscurrently reviewing an oral RfD for benzene, and its status ispending. :

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BIS(2-ETHYLHEXYL)PHTHALATE

Bis(2-ethylhexyl)phthalate, also known as di-ethylhexyl phthalate(DEHP), is readily absorbed following oral or inhalation exposure(EPA 1980). Chronic exposure to relatively high concentrationsof DEHP in the diet can cause retardation of growth and increasedliver and kidney weights in laboratory animals (NTP 1982,EPA 1980, Carpenter et al. 1953). Reduced fetal weight andincreased number of resorptions have been observed in ratsexposed orally to DEHP (EPA 1980). DEHP is reported to becarcinogenic in rats and mice, causing increased incidences ofhepatocellular carcinomas or neoplastic nodules following oraladministration (NTP 1982).

DEHP has been classified in Group B2—Probable Human Carcinogen(EPA 1986, 1989). EPA (1989) calculated an oral cancer potency

—2 —1factor for DEHP of 1.4x10 (mo;/kg/day) based on data from theNTP (1982) study. EPA has recommended an oral reference dose(RfD) for DEHP of 0.02 mg/kg/day based on a study by Carpenter etal. (1953) In which increased liver weight was observed in femaleguinea pigs exposed to 19 mg/kg bw/day in the diet for 1 year(EPA 1989); an uncertainty factor.of 1,000 was used to developthe RfD.

CARBON TETRACHLORIDE

Carbon tetrachloride (CC1J is readily absorbed following oraland inhalation exposure. About 60% of an oral dose was absorbedby 6 hours, and up to 86% was absorbed by 24 hours. Absorptionfrom the lung has been estimated at about 30% (EPA 1984). CC14/like many other chlorinated hydrocarbons, acts as a centralnervous system depressant (ACGIH 1986). The toxic effects of

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oral and inhalation exposure to CC14 in humans and animalsinclude damage to the liver, kidney and Iiing, although the liveris the most sensitive tissue (EPA 1985, Bruckner et al 1986). Inanimals, acute oral administration produces fatty infiltrationand histological alterations in the liver. High doses produceirreversible liver damage and necrosis while the effects observedfollowing lower doses are largely reversible (EPA 1985). Humansoccupationally exposed to 5-15 ppm of CC14 experience biochemical.alterations, nausea, headaches and in more severe cases, liverdysfunction (jaundice, enlargement and fatty infiltration) (ACGIH1986, EPA 1984). Animals chronically exposed to CC14 exhibiteffects similar to those observed following acute exposure.Prenatal toxicity has been demonstrated in mammalian fetuses andneonates after inhalation exposure in pregnant rats (EPA 1984),although CC14 has not been shown to be teratogenic (EPA 1985) .Carbon tetrachloride is a carcinogen in animals producing mainlyhepatic neoplasms. Oral administration of 30 mg/kg/day or higherfor 6 months has been found to produce an increased frequency ofhepatomas, hepatocellular adenomas and hepatocellular carcinomasin mice, rats and hamsters (EPA 1985).

EPA (1989) has classified CC14 as a B2 agent (probable humancarcinogen) . The cancer potency factor for both oral andinhalation exposure is l,3xlOM (mg/kg/day)"1. EPA (1989)established the cancer potency factor based on several gavagestudies in which hepatocellular carcinomas and hepatomas wereobserved in rats, mice and hamsters (Delia Porta et al. 1961,Edwards et al. 1942, NCI 1976a, 1976b, 1977). EPA (1989) hasderived an oral reference dose (RfD) of 7xlO"4 mg/kg/day based ona subchronic rat gavage study in which liver lesions were themost sensitive effect (Bruckner et al. 1986). A no observed

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adverse effect level (NOAEL) of 0.71 mg/kg/day and an uncertaintyfactor of 1,000 were used to derive the RfD.

CHLOROETHANE (ETHYL CHLORIDE)

Chloroethane is primarily absorbed through the lungs, althoughsome dermal absorption may occur. Absorption and excretion ofChloroethane occurs rapidly via the lungs; it is not metabolizedto a significant degree (Clayton and Clayton 1981). Severe acuteinhalation of Chloroethane by humans produces minor neurologicaleffects that are manifested as stupor and lack of coordination,and in some incidences as cardiac arrhythmia produced by thepotantiation of adrenalin (Clayton and Clayton 1981). Acuteinhalation of Chloroethane by animals has produced histologicalor pathological changes in the liver, brain, and lungs (Troshina1964). Chronic exposure of animals to Chloroethane producedkidney damage and fatty changes in the liver, and at high levelshas upset cardiac rhythm (EPA 1985). Studies assessing themutagenicity and carcinogenicity of Chloroethane are currentlybeing conducted (EPA 1985). No health based criteria numbershave been established by EPA.

CHLOROFORM

Chloroform, a trihalomethane, is rapidly absorbed through therespiratory and gastrointestinal tracts in humans andexperimental animals; dermal absorption from contact of the skinwith liquid chloroform can also occur (EPA 1985) . In humans,acute exposures to chloroform may result in depression of thecentral nervous system, hepatic and renal damage and death causedby ventricular fibrillation following an acute ingested dose of10 ml (EPA 1984). Acute exposure to chloroform may also cause

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irritation to the skin, eyes, and gastrointestinal tract (EPA1984, 1985). In experimental animals, chronic exposure may leadto fatty cyst formation in the liver (Heywdod et al. 1979),renal, and cardiac effects and central nervous system depression(EPA 1985) . Chloroform has been reported to induce renalepithelial tumors in rats (Jorgenson et_al. 1985) andhepatocellular carcinbma$ in mice (NCI 1976). Suggestiveevidence from7 human epidemiological studies indicates that long-term exposure to chloroform and other trihalomethanes incontaminated water supplies may be associated with an increasedincidence of bladder tumors (EPA 1985). Chloroform isembryotoxic in pregnant rats and has retarded fetal developmentand increased the incidences of fetal resorption, acadia (absenceof tail), imperforate anus, missing ribs and delayed ossificationof sternebrae (Schwetz et al. 1974).

Chloroform has been classified by EPA as a Group B2 Carcinogen(Probable Human Carcinogen) (EPA 1989). EPA (1989) developed anoral cancer potency factor for chloroform of 6.1xlO"3 (mg/kg/day)"1 based on a study in which kidney tumors were observed in ratsexposed to chloroform in drinking watery (Jorgenson et al. 1985) .An inhalation cancer potency factor of S.lxio"2 (mg/kg/day)"1 hasbeen developed by EPA (1989) based on an NCI (1976) bioassay inwhich liver tumors were observed in mice. EPA (1989) alsoderived an oral reference dose (RfD) of 0.01 mg/kg/day forchloroform based on ~a chronic bioassay in dogs in which livereffects were observed at 12.9 mg/kg/day (Heywood et al. 1979); anuncertainty factor of 1,000 was used to derive the RfD.

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DICHLOROBENZENES

1,4-dichlorobenzene (1,4 DCB) is a solid used as an air deodorantand as an insecticide. EPA (1987) reports that 100% of an oraldose and 60% of an inhalation dose of 1,4-DCB are absorbed whenexposure persists for longer than one to three hours (Astrand1975, Dallas et al. 1983). 1,2-DCB and 1,3-DCB are also readilyabsorbed through the lungs, skin and gastrointestinal tract (EPA1987, EPA 1985). The principal toxic effects of 1,2-DCB and1,4-DCB in humans and experimental animals from acute and longer-term exposure include central nervous system depression, blooddyscrasias, and lung, kidney, and liver damage (EPA 1985, NTP1985, Riley et al. 1980). Although no studies were available onthe acute or chronic effects of 1,3-DCB-exposure, these effectsare expected to be similar to those associated with 1,2-DCB or1,4-DCB. In humans, pigmentation and allergic dermatitis havebeen reported after dermal contact to 1,2-DCB and 1,4-DCB (EPA1987, NTP 1985). Chromosome breaks also have been observed inexposed humans to 1,2- and 1,4-DCB (EPA 1987). 1,4-DCB was foundto cause renal adenocarcinomas in male rats and carcinomas andadenocarcinomas of the liver in female mice in a 10 3-week gavagestudy (NTP 1986).

EPA classified 1,4-DCB in Group B2—Probable Human Carcinogenbased on adequate evidence of carcinogenicity in animals (EPA19.87}. An oral cancer potency factor of 2.4xlO"2 (mg/kg/day)"1has been reported by EPA (EPA 1989b). EPA (1987) also derived anoral reference dose (RfD) for 1,4-DCB of 0.1 mg/kg/day based onthe NTP (1986) rat study in which a no-observed-adverse-effectlevel (HOAEL) of 150 mg/kg/day for renal lesions was identified.An uncertainty factor of 1,000 was used to derive the RfD. EPA(1989b) has developed an inhalation RfD for 1,4-DCB of 0.7 mg/m3

A-7

based on liver and kidney effects in rats (Riley et al. 1980). Asafety factor of 100 was used to derive the RfD. EPA (1989a) hasreported an oral RfD for 1,2-DCB of 9xlO"2 mg/kg/day based _on anNTP (1985) study in which liver effects were observed in ratsexposed to l,2-pCB_for 11, weeks; an uncertainty factor of 1,000was used to develop the RfD. EPA (1989b) has also derived aninhalation RfD of 0.04 mg/kg/day for 1,2-DCB based on a study inwhich decreased body weight gain was observed in ratsadministered 1,2-DCB for up to 7 months (Hollingsworth et al.1958); an uncertainty factor of 1,000 was used to derive the RfD.EPA (1987) calculated an oral RfD for 1,3-DCB based on subchronicdata for 1,2-DCB. In two separate unpublished studies (Battelle-Columbus 1978a,b), rats and mice were administered 1,2-DCB incorn oil by gavage for 13 weeks. A NOAEL of 125 mg/kg/day wasidentified from these studies; at higher doses (188 mg/kg/day)increased kidney and liver weights were noted in rats. Applyinga safety factor of 1,000 to the NOAEL, EPA (1987) derived an oralRfD for 1,3-DCB of 8.9xlO"2 mg/kg/day.

1,4-DICHLOROBENZENE

1,4-dichlorobenzene is a_solid used as an air deodorant and as aninsecticide. EPA (1987) reports that 100% of an oral dose and60% of an inhalation dose are absorbed when exposure persists forlonger than one to three hours (Astrand 1975, Dallas etal. 1983). The principal toxic effects of this compound inhumans and experimental animals from acute and longer-termexposure include central nervous system depression, blooddyscrasias, and lung, kidney, and liver damage (EPA 1985). Inhumans, pigmentation and allergic dermatitis have been reportedafter dermal contact (EPA 1987). Chromosome breaks also havebeen observed in exposed humans (EPA 1987). 1,4-Dichlorobenzene

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was found to cause renal adenocarcinomas in male rats andcarcinomas and adenocarcinomas of the liver in female mice in a103-week gavage study (NTP 1986).

EPA classified 1,4-dichlorobenzene in Group B2—Probable HumanCarcinogen based on adequate evidence of carcinogenicity inanimals (EPA 1987). An oral cancer potency factor of 2.4xlO"2(mg/kg/day)"1 has been reported by EPA (EPA 1989). EPA (1987)also derived an oral reference dose (RfD) for 1,4-dichlorobenzeneof 0.1 mg/kg/day based on the NTP (1986) rat study in which a no-observed-adverse-effect level (NOAEL) of 150 mg/kg/day for renallesions was identified. An uncertainty factor of 1,000 was usedto derive the RfD. This RfD was used to develop a lifetimehealth advisory for 1,4-dichlorobenzene.

1,1-DICHLOROETHANE -

1,1-DCA is probably less toxic than the 1,2-isomer (EPA 1980).At one time, the compound was used as an anesthetic, but itinduced cardiac arrhythmias and its use was discontinued. It isprobable that human exposure to sufficiently high levels of1,1-DCA would cause central nervous system depression andrespiratory tract and skin irritation, since many of thechlorinated aliphatics cause these effects (Parker at al. 1979).However, no dose-response data concerning these effects areavailable. Renal damage was observed in cats exposed byinhalation in a subchronic study (Hofmann et al. 1971).Inhalation exposure of pregnant rats to high doses of 1,1-DCA(6,000 ppm) retarded fetal development (Schwetz et al. 1974). Acarcinogenicity bioassay of 1,1-DCA was limited by poor survivalof both treatment and control groups, and the physical conditionsof the treated animals were markedly stressed. Dose-related

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marginal increases in mammary gland adenocarcinomas and inhemangiosarcomas were seen.in female rats, and a statisticallysignificant increase in endometrial stromal polyps was seen infemale mice; however, these "data were not interpreted asproviding conclusive evidence for the carcinogenicity of 1,l-DCAbecause of the previously mentioned limitations of the bioassay(NCI 1978).

EPA (1989) has classified 1,1-DCA as a Group B2 agent (ProbableHuman Carcinogen) and reported an oral cancer potency factor of9. IxlO"2(mg/kg/day)"1. This potency factor is based on structure-activity relationship to the isomer 1,2-dichloroethane, aGroup B2 carcinogen and on the increased incidence ofhemangiosarcomas observed in rats administered 1,1-DCA via gavage(NCI 1978). EPA (1989) developed an oral and inhalationreference dose of 0.1 mg/kg/day based on adverse renal effectsseen in cats following subchronic inhalation exposure (Hofmann etal. 1971). A safety factor of 1000 was used to develop the RfD.

1,2-DICHLOROETHANE

Data on the toxicokinetics of 1,2-dichloroethane (1,2-DCA) inhumans are limited, but data from animal studies suggest that thechemical is rapidly absorbed following oral and inhalationexposure and after dermal contact with the liquid form of thecompound (EPA 1985), Effects of acute inhalation exposure inhumans include irritation of mucous membranes in the respiratorytract and central nervous system depression (EPA 1985). Deathmay occur: as a result of respiratory and circulatory failure.Pathological examinations typically show congestion,degeneration, necrosis, and hemorrhagic lesions of the

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respiratory and gastrointestinal tracts, liver, kidney, spleen,and lungs (EPA 1985). Adverse effects caused by less extremeexposures are generally associated with the gastrointestinal andnervous systems. Occupational exposures to 1,2-DCA vapors resultin anorexia, nausea, vomiting, fatigue, nervousness, epigastricpain, irritation of the eyes and respiratory tract, andgastrointestinal, liver, and gallbladder disease (EPA 1984,1985). Chronic studies in animals also have revealed toxiceffects following inhalation exposure including degeneration ofthe liver (EPA 1985). Available data suggest that 1,2-DCA doesnot adversely affect reproductive or developmental processes inexperimental animals except at maternally toxic levels (EPA1985). In long-term oral bioassays sponsored by the NationalCancer Institute (NCI 1978), increased incidences ofsquamous-cell carcinomas of_the forestomach, mammary glandadenocarcinomas, and hemangiosarcomas have been observed in ratsexposed to 1,2-DCA; pulmonary adenomas, mammary adenocarcinomas,and uterine endometrial tumors have been observed in mice exposedto this chemical.

EPA (1989) has classified 1,2-DCA in Group B2 (Probable HumanCarcinogen) based on inadequate evidence of carcinogenicity fromhuman studies and sufficient evidence of carcinogenicity fromanimal studies. EPA (1989) derived an oral and an inhalationcancer potency factor (q-j*) of 9-lxlO"2 (mg/kg/day)"1 for 1,2-DCAbased on the incidences of hemangiosarcomas in Osborne-Mendelmale rats observed in the NCI (1978) gavage study.

1,1-DICHLQROETHENE

1,1-Dichloroethene (1,1-DCE) is rapidly absorbed after oral andinhalation exposures (EPA 1984, 1987). Humans acutely exposed to

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1,1-DCE vapors exhibit central nervous system depression. Inanimals, the liver is the principal target of 1,1-DCE toxicity.Acute exposures result in liver damage which ranges from fattyinfiltration to necrosis (EPA 1987). Workers chronically exposedto 1,1-DCE in combination with other vinyl compounds exhibitliver dysfunction, headaches, vision problems, weakness, fatigueand neurological sensory disturbances (EPA 1987). Chronic oraladministration of~1,1-DCE to experimental animals results in bothhepatic and renal toxicity (EPA 1984, Quast et al. 1983).Inhalation or oral exposure of rats and rabbits has producedfetotoxicity and minor skeletal abnormalities, but only atmaternally toxic doses. 1,1-DCE vapors produced kidney tumorsand leukemia in a single study of mice exposed by inhalation, butthe results of other studies were equivocal or negative (EPA1987, Maltoni et al. 1985).

EPA has classified 1,1-DCE as a Group C agent (Possible HumanCarcinogen) and has developed inhalation and oral cancer potencyfactors of 1.2 (mg/kg/day)"1 and 0.6 (mg/kg/day)"1, respectively(EPA 1985, 1989). The inhalation potency factor was based onthe increased incidence of renal adenocarcinbmas in male miceexposed to 1,1-DCE via inhalation for 52 weeks and observed for atotal of 121 weeks (Maltoni et al. 1985). The oral potencyfactor was derived by estimating an upper-limit value fromnegative bioassay data and assuming that a carcinogenic responseoccurs via ingest ion, although there is no direct evidence thatthis is true. EPA (1989) developed an oral reference dose (RfD)of 9xlO"3 mg/kg/day based on the occurrence of hepatic lesions inrats chronically exposed to 1,1-DCE in drinking water (Quast etal. 1983). A safety factor of 1000 was applied to the lowest-observed-adverse-effect level (LOAEL) of 9 mg/kg/day to derivethe oral RfD.

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trans-1,2-DICHLOROETHENE

trans-1,2-Dichloroethene is expected to be absorbed by any routeof exposure. Information on the health effects oftrans-1.2-dichloroethene is limited. In humans, trans-1,2-dichloroethene is a central nervous system depressant, andexposure to high concentrations can result in anesthetic effects(Irish 1963). Inhalation exposure of rats to 200 ppm has beenassociated with pneumonic infiltration of the lungs andprogressive fatty degeneration of the liver (Freundt et al.1977). Acute exposure to higher dose levels can cause narcosisand death in rats (Torkelson and Rowe 1981).

EPA (1985) proposed a maximum contaminant level goal (MCLG) of70 g/liter for both cis- and trans-i,2-dichloroethene based onthe adjusted acceptable daily intake (AADI) of 350 jug/liter,assuming 20% of the exposure is via drinking water. EPA (1989)has derived an oral reference dose (RfD) of 2xlO"2 mg/kg/day fortrans-1.2-dichloroethene based on a 90-day drinking water studyconducted in mice (Barnes et al. 1985). A no-observed-adverse-effect level (NOAEL) of 17 mg/kg/day for increased serum alkalinephosphatase and an uncertainty factor of 1,000 were used toderive the RfD.

trans- and cis-1,2-DICHLOROETHENE

Both trans-1,2-Dichloroethene (1,2-DCE) and cis-1,2-DCE areexpected to be absorbed by any route of exposure (EPA 1987) .Information on the health effects of both trans-1,2-DCE and cis-1,2-DCE are limited. In humans, trans-1,2-DCE and cis-l.2-DCEare central nervous system depressants, and exposure to highconcentrations can result in anesthetic effects (Irish 1963 Acute

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exposure to higher dose levels of the trans-isomer can causenarcosis and death in rats (Torkelson and Rowe 1981). Inanimals, cis-l,2-DCE also has narcotic effects at high doses.Inhalation exposure of rats to 200 ppm trans-1,2-DCE has beenassociated with pneumonic infiltration of the lungs andprogressive fatty degeneration of the liver (Freundt et al.1977). Exposure of rats to 200 ppm trans- or cis-l,2-DCE byinhalation has been observed to result in inhibition of the mixedfunction oxidase enzyme system; the cis-isomer was more potent(Freundt and Macholz 1978) . Chronic oral exposure of rats totrans-1,2-DCE has resulted in increased serum alkalinephosphatase (Bames et al. 1985). Rats chronically administeredcls-1. 2-PCE in their diet have exhibited hepatocellular swellingand fatty changes {Quast et al. 1983). cis-1,2-DCE was reportedto induce mutations using a host-mediated assay and chromosomalaberrations in mouse bone marrow cells (Cerna and Kypenova 1977).

EPA (1985) proposed a maximum contaminant level goal (MCLG) of70 j*g/liter for both cis- and trans-1.2-dichloroethene based onthe adjusted acceptable daily intake (AADI) of 350 jug/liter,assuming 20% of the exposure is via drinking water. EPA (1989)has derived an oral reference dose (RfD) of 2xlO"2 mg/kg/day fortrans-l,2-DCE based on a 90-day drinking water study conducted inmice (Barnes et al. 1985). A no-observed-adverse-effect level(NOAEL) of 17 mg/kg/day for increased serum alkaline phosphataseand an uncertainty factor of 1,000 were used to derive the RfD.EPA (1987) has derived an oral RfD or 0.01 mg/kg/day based onresults of a 2-year chronic toxicity/ oncogenicity study in whichrats exhibited significant microscopic liver changes and minimalhepatocellular swelling and fatty changes (Quast et al. 1983).The RfD was calculated using a lowest-observed-effect level(LOAEL) of 10 mg/kg/day and an uncertainty factor of 1,000.

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DICHLOROFLUOROMETHANE

Dichlorofluoromethane is absorbed in animals following oral andinhalation exposures (ACGIH 1986) . In rats, the LC50 value for a4 hour exposure to dichlorofluoromethane is 49,900 ppm (ACGIH1986). Death was observed in rats and guinea pigs exposed to100,000 ppm for one hour (Weigand 1971). Further tests usingguinea pigs (Nuckolls 1935, Booth and Bixby 1932) and mice (Boothand Bixby 1932) acutely exposed to concentrations of 50,000 ppmhave resulted in unconsciousness or death. Rats exposedrepeatedly to 10,000 ppm dichlorofluoromethane for 6 hours perday, five days per week for two weeks (Aviado and Smith 1975)showed histopathological changes of .the liver (e.g.,centrilobular necrosis). Rats exposed to 1,000 or 5,000 ppm for90 days showed hair loss, cirrhosis, and excessive mortality(Trochinowicz et al. 1977). Studies using dogs exposed to 10,000ppm dichlorofluoromethane and intravenous epinephrine have shownevidence of serious arrhythmia (ACGIH 1986). Hypotension andtachycardia were observed in monkeys (Aviado and Smith 1975) andin dogs (Belej and Aviado 1975) exposed to concentrations rangingfrom 50,000-100,000 ppm. Reproductive effects (e.g. pre-implantation loss) in pregnant rats exposed to 10,000 ppmdichlorofluoromethane were observed (ACGIH 1986) . No informationon mutagenicity, teratogenicity, or carcinogenicity ofdichlorofluoromethane were located. EPA has not established anyhealth based criteria values for dichlorofluoromethane.

ETHYLBENZENB

Ethylbenzene is absorbed via inhalation and distributedthroughout the body in rats; the highest levels were detected in

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the kidney, lung, adipose tissue, digestive tract, and liver(Chin et al. 1980). In humans, short-term inhalation exposure to435 mg/m3 ethylbenzene for 8 hours can result in sleepiness,fatigue, headache, and mild eye and respiratory irritation(Bardodej and Bardodejova 1970); eye irritation has also beenobserved in experimental animals exposed to ethylbenzene (EPA1987). Increased weights and cloudy swelling were observed inthe liver and kidney of rats exposed to ethylbenzene by gavage ata dose of 408 mg/kg/day for 182 days. (Wolf et al. 1956). Asingle oral dose of ethylbenzene administered to male and femaleWistar-derived rats was reported to have an LD50 of 3,500 mg/kgbody weight, with systemic effects occurring primarily in theliver and kidney (Wolf et al. 1956). Maternal toxicity wasobserved in rats expo'sed by inhalation to 4,348 mg/m3ethylbenzene for 6-7 hours/day during the first 19 days ofgestation (Hardin et al. 1981).

EPA (1989) derived an oral reference dose of 0.1 mg/kg/day forethylbenzene based on the chronic study by Wolf et al. (1956) inwhich no liver or kidney effects were observed in rats exposed to136 mg/kg/day. An uncertainty factor of 1,000 was applied to theno-observed-effect-level to derive the reference dose.

4-METHYL PHENOL (P-CRESOL)

Experimental evidence indicates that 4-methyl phenol is absorbedfollowing ingestion and inhalation (EPA 1984) and also afterdermal exposure (NIOSH 1978). Effects following acute exposureto 4-methyl phenol include muscular weakness; gastroentericdisturbances; severe depression; edema of the lungs; injury tothe eyes, skin, kidneys, liver, pancreas, spleen, and vascularsystem; collapse; and death (Deichmann and Keplinger 1981, NIOSH

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1978). Effects in rats following subchronic exposure to 4-methylphenol include increased mortality; reduction in body weight;increased kidney-to-body weight and liver-to-body weight ratios;and CNS effects such as salivation, rapid respiration, lethargy,ataxia, coma, dyspnea, tremors, diarrhea, and convulsions (EPA1986, 1987). Lysol, a cresol-containing solution producesextensive hemolysis, erosion of blood vessels, kidney tubulardamage, liver necrosis, and death in humans followingintravaginal application to induce abortion (Vance 1945, Presleyand Brown 1956).

EPA (1988) derived an oral reference dose of 0.05 mg/kg/day basedon decreased body weights and neurotoxicity in rats administered4-methyl phenol by gavage (EPA 1986, 1987). A safety factor of1,000 was used to derive the RfD.

METHYLENE CHLORIDE (Dichloromethane)

Methylene chloride is absorbed following oral and inhalationexposure. The amount of airborne methylene chloride absorbedfollowing inhalation exposure increases in direct proportion toits concentration in inspired air, the duration of exposure, andphysical activity. Dermal absorption has not been accuratelymeasured (EPA 1985a). Acute human exposure to methylene chloridemay result in irritation of eyes, skin, and respiratory tract;central nervous system depression; elevated carboxyhemoglobinlevels; and circulatory disorders that may be fatal (EPA 1980).Chronic exposure of animals can produce renal and hepatic toxic-ity (NCA 1982} • Methylene chloride is mutagenic for Salmonella•tvphljOTyimn and produces mitotic recombination in yeast (EPA1989a). Several inhalation studies conducted in animals provideclear evidence of methylene chloride's carcinogenicity (NTP

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1986). There is only suggestive evidence in experimental animalsthat hepatocellular carcinomas and neoplastic nodules arise fromoral exposure (EPA 1985a,b).

EPA (1989a) classified methylene chloride in Group B2—ProbableHuman Carcinogen. It has been concluded by EPA (1985b) that theinduction of distant site tumors from inhalation exposure and theborderline significance for induction of tumors in a drinkingwater study are,an adequate basis for concluding that methylenechloride be considered a probable human carcinogen via ingestionas well as inhalation. EPA (1989a) derived an inhalation cancerpotency factorTlat 1.4x_10"_2 (mg/kg/day)"1 based on the results of aNational Toxicology Program (NTP) inhalation bioassay conductedin rats and mice (NTP 1986). Mammary tumors were noted in rats,while lung and liver tumors were observed in mice. EPA (1989a)determined an oral cancer potency factor of 7.5xlO"3 (mg/kg/day)"1based on the results of the NTP (1986) inhalation bioassay and onan ingestion bioassay conducted by the National CoffeeAssociation (NCA 1983). In the NCA study, hepatocellularadenomas and/or carcinomas were observed in male mice. An oralreference dose (RfD) of 0.06 mg/kg/day has been developed by EPA(1989a) based on a 2-year rat drinking water bioassay (NCA 1982)that identified no-observed-effect levels (NOELs) of 5.85 and6.47 mg/kg/day for-male and female rats, respectively. Livertoxicity was observed at doses of 52.58 and 58.32 mg/kg/day formales and females, respectively. An uncertainty factor of 100was used to derive the RfD. EPA (1989b) has established aninhalation RfD of 3 mg/m3 based on a study by Nitschke etal. (1988) in which rats were exposed to 200 ppm (694.8 mg/m3)for 2 years. A-safety factor of 100 was used to derive the RfD.This RfD is currently undergoing verification by EPA (1989a).

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POLYCYCLIC AROMATIC HYDROCARBONS (Noncarcinogenic)

Polycyclic aromatic hydrocarbons (PAHs) occur in the environmentas complex mixtures of which only a few components have beenadequately characterized. Only limited information is availableon the relative potencies of the "noncarcinogenic" PAHs.However, many have been shown to have some weak carcinogenicactivity, or to act as promoters or cocarcinogens.

PAH absorption following oral and inhalation exposure is inferredfrom the demonstrated toxicity of PAHs following these routes ofadministration (EPA 1984a). PAHs are also absorbed followingdermal exposure (Kao et al. 1985). Acute effects from directcontact with PAHs and related materials are limited primarily tophototoxicity; the primary effect is dermatitis (NIOSH 1977).PAHs have also been shown to cause cytotoxicity in rapidlyproliferating cells throughout the body; the hematopoieticsystem, lymphoid system, and testes are frequent targets(Santodonato et al. 1981). Some of the noncarcinogenic PAHs havebeen shown to cause systemic toxicity but these effects aregenerally seen at high doses (Santodonato et al. 1981). Slightmorphological changes in the liver and kidney of rats have beenreported following oral exposure to acenaphthene for 40 days (EPA1984a) . Subchronic oral administration of naphthalene to rabbitsand rats has resulted in cataract formation (EPA I984b).

EPA (1989) developed an oral reference dose of 0.4 mg/kg/day fornaphthalene based on the development of ocular and systemiclesions In rats (Schmahl 1955, EPA 1986) and occupational data oncoke oven workers. An uncertainty factor of 100 was applied tothe aniiaal data in the development of the reference dose.

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RADIOACTIVE COMPOUNDS

Radioactive materials undergo spontaneous disintegration (decay)and emit energetic alpha or beta particles or electromagneticradiation that can damage cells. Current scientific consensus isthat radiation can increase the probability of cancer and aconservative assumption is that no threshold dose exists belowwhich there is no additional risk of cancer. The alpha particlesare more ionizing and less penetrating than the beta particles;they can travel only very short distances in the body (about 4 or5 cell diameters) if they are emitted from within the body.Gamma radiation is more penetrating than the alpha or betaparticles, but it is also the less ionizing (Weast 1983). It ispossibile.that any amount of an alpha emitting radioactivesubstance has the potential to cause cancer. This is based onthe fact that other alpha-emitting radioactive substances such asradon, radium and plutonium are known to cause cancer fromradiation.

Thorium is found mostly (99%) as the thorium isotope-232.Thorium-232 is mildly radioactive and decays by emission of alphaparticles at a half-life of 1.41 x 1010 years (Weast 1983) .Thorium also disintegrates into other unstable radionuclides suchas radium-226, radium-228, thoron and radon-222 which decayfurther until a stable product is formed. Since thorium isradioactive and may be s_tored in bone for a long time, bonecancer is a potential concern (Lloyd et al. 1985, Mays et al.1987, Wrenn et al. 1986). Increased risks of lung, pancreaticand hematopoietic cancers were found in workers occupationallyexposed to thorium (Archer et al. 1973a, Polednak et al. 1983,Stehney et al. 1980) ; however, the workers were concomitantly

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exposed to other substances, which prevent any direct correlationof thorium exposure to cancer incidence.

Natural uranium contains more than 99% uranium-238 which decaysinto alpha particles and decay products including radium andradon and has a half-life of 4.46 x 109 years (Weast 1985) . Nohuman or animal studies have definitely linked inhalation or oralexposure to natural uranium to the development of cancer.Epidemiology studies of uranium miners have found an increase inmortality due to lung cancers (Archer et al. I973b. Gottlieb andHusen 1982, Lundin et al. 1969, Saccomanno et al. 1986, Samet etal. 1984) but this evidence is insufficient to attribute uraniumexposure to cancer since the miners were concurrently exposed toother suspected carcinogens such as tobacco smoke, radon and itsdecay products, silica and other dusts and diesel exhaust fumes.However, since uranium is radioactive, it is possible that humanscan develop cancer from uranium; the risk depends largely on theamount of radiation to which they are exposed.

Radium is formed when thorium and uranium decay. Radioactiveemissions of alpha and beta particles are considered to beresponsible for most of the biologically deleterious effectsobserved in exposed persons to radium. Radium-226 decays byemission of alpha particles with a half-life of 1600 years;radium-228 emits beta partcles and has a much shorter half-lifeof 5.7 years (Weast 1985) . In humans, radium-226 and radium-228have induced bone sarcomas, while carcinomas of bones includingthe mastoid air cells and paranasal sinuses are known to beinduced by exposure to radium-226; these carcinomas are believedto be caused by radon, a gaseous daughter of radium-226 (Rundo etal. 1986). EPA (1989) has classified radium as a group A—Human

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carcinogen based of adequate .evidence of carcinogencity inhumans.

TETRACHLOROETHENE '..

Tetrachloroethene is absorbed following inhalation (IARC 1979)and oral (EPA 1985a,b) exposure. Tetrachloroethene vapors andliquid also.can be absorbed through the skin (EPA 1985a,b). Theprincipal toxic effects of tetrachloroethlene in humans andanimals following acute and longer-term exposures include centralnervous system (CNS) depression and fatty infiltration of theliver and kidney with concomitant changes in serum enzymeactivity levels indicative of tissue damage (EPA 1985a,b).Humans exposed to doses of between 136 and 1,018 mg/m3 for 5weeks develop central nervous system effects, such as lassitudeand signs of inebriation (Stewart et al. 1974). The offspring offemale rats arid mice exposed" to high concentrations oftetrachloroethene for 7 hours daily on days 6-15 of gestationdeveloped toxic effects, including a decrease in fetal bodyweight in mice and a small but significant increase in fetalresorption in rats (Schwetz et al. 1975). Mice also exhibiteddevelopmental effects, including subcutaneous edema and delayedossification of skull bones and sternebrae (Schwetz et al. 1975).In a National Cancer Institute bioassay (NCI 1977), increasedincidences of hepatocellular carcinoma was observed in both sexesof B6C3F1 mice administered tetrachloroethene in corn oil bygavage for 78 weeks. Increased incidences of mononuclear cellleukemia and renal adenomas and carcinomas (combined) have alsobeen observed in long term bioassays in which rats were exposedto tetrachloroethene by inhalation (NTP 1986).

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

—2 —1oral cancer potency factor (q*) of 5.1x10 (mg/kg/day) basedon liver tumors observed in the NCI (1977) gavage bioassay_for _mice. The inhalation cancer potency factor for tetrachloroetheneof 3.3xlO"3 (mg/kg/day)"1 is based on an NTP (1986) bioassay inrats and mice in which leukemia and liver tumors were observed(EPA 1989b). Both cancer potency factors are currently, underreview by EPA (1989a) . EPA (1989a,b) also has derived an oralreference dose (RfD) of ixio"2 mg/kg/day for tetrachloroethenebased on a gavage study by Buben _and O_'Flaherty (1985). In thisstudy, liver weight/body weight ratios were significantlyincreased in mice and rats treated with 71 mg/kg/day tetrachloro-ethene but not in animals treated with 14 mg/kg/day. Using aNOAEL of 14 mg/kg/day and applying an uncertainty factor of1,000, the RfD was derived.

TOLUENE

Toluene is absorbed in humans following both inhalation anddermal exposure (EPA 1985). In humans, the primary acute effectsof toluene vapor are central nervous system (CNS) depression andnarcosis. These effects occur at concentrations of 200 ppm(754 mg/m3) (von Oettingen et al. 1942a,b). In experimentalanimals, acute oral and inhalation exposures to toluene canresult in central nervous system (CNS) depression and lesions ofthe lungs, liver, and kidneys (EPA 1987). The earliestobservable sign of acute oral toxicity in animals is depressionof the CNS, which becomes evident at approximately 2,000 mg/kg(Kimura et al. 1971). In humans, chronic exposure to toluenevapors at concentrations of approximately 200 and 800 ppm hasbeen associated with CNS and peripheral nervous system effects.

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hepatomegaly, and hepatic and renal function changes (EPA 1987).Toxic effects following prolonged exposure of experimentalanimals to toluene are similar to those seen following acuteexposure (Hanninen et al. 1976, von Oettingen et al. 1942a). Inrats, chronic exposure to toluene via inhalation results in CNStoxicity and a dose-related reduction in hematocrit values (CUT1980) . There is some evidence in mice that oral exposure togreater than Q.3 ml/kg toluene during gestation results inemi>ryotoxicity_(Nawrot and Staples 1979). Inhalation exposure ofup to 1,000 mg/m3 by pregnant rats during gestation has beenassociated with significant increases in skeletal retardation(Hudak and Ungvary 1978).

EPA (1989a) has derived an oral risk reference dose (RfD) of0.3 mg/kg/day for toluene based on a 24-month inhalation study inwhich rats were exposed to concentrations as high as 300 ppm(29 mg/kg/day) and hematological parameters were examined (CUT1980). No adverse effects were observed in any of the treatedanimals. Using a norobserve_d-adverse-effect level (NOAEL) of29 mg/kg/day and an uncertainty factor of 100, the oral RfD wasderived. EPA (1989b) reported an inhalation RfD for toluene of1.0 mg/kg/day also based on this CUT study in which CNS effectswere noted and an uncertainty factor of 100 was used.

1,1,1-TRICHLOROETHANE

Like other chlorinated aliphatic hydrocarbons,1,1,1-trichloroethane (1,1,1-TCA, methyl chloroform) is rapidlyand completely absorbed following both the oral and inhalationexposure. Pulmonary absorption is initially large and graduallydecreases to a steady-state condition. Absorption through theskin is slow. 1,1,1-TCA distributes throughout the body and

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readlily crosses the blood-brain barrier (EPA 1984). The mostnotable toxic effects of 1,1,1-TCA inhalation exposure in humansand animals are central nervous system depression, includinganesthesia at very high concentrations, and impairment ofcoordination, equilibrium, and judgment at lower concentrations(350 ppm and above) . In both humans and animals, cardiovasculareffects, including premature ventricular contractions, decreasedblood pressure, and sensitization to epinephrine-inducedarrhythmia can result from acute exposure to high concentrationsof 1,1,1-TCA vapor (EPA 1985). Fatty liver changes have beenreported in guinea pigs following subchronic inhalation exposure(Torkelson et al. 1958) . NTP (1984) reported preliminary resultsof bioassays in rats and mice indicating that oral administrationof 1,1,1-TCA increases the incidence of hepatocellular carcinomasin female mice but not for male rats. This study was inadequateto evaluate the carcinogenicity of 1,1,1-TCA in female rats andmale mice.

EPA (1989a) calculated an oral reference dose (RfD) for 1,1,1-trichloroethane based on an inhalation study by Torkelson etal. (1958) in which rats, rabbits, guinea pigs and monkeys wereexposed to 1,1,1-TCA vapor. A no-observed-adverse-effect (NOAEL)of 500 ppm (2,730 mg/m3, or 90 mg/kg/day) was identified fromthis study. Using the NOAEL of 90 mg/kg/day and an uncertaintyfactor of 1,000, a RfD of 9xlO"2 mg/kg/day was derived. Aninhalation RfD of 0.3 mg/kg/day for 1,1,1-TCA also has beendetermined by EPA (1989b) based on this same study, in whichhepatotoxicity was observed in guinea pigs. An uncertaintyfactor of 1,000 was used in calculating the RfD.

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TRICHLOROETHENE

Absorption of trichloroethene (TCE) from the gastrointestinaltract is virtually complete. Absorption following inhalationexposure is proportional to concentration and duration ofexposure (EPA 1985). TCE is a central nervous system depressantfollowing acute and chronic exposures. In humans, single oraldoses of 15 to 25 ml (21 to 35 grams) of TCE have resulted invomiting and abdominal pain, followed by transientunconsciousness (Stephens 1945), High-level exposure can resultin death due to respiratory and cardiac failure (EPA 1985).Hepatotoxicity has been reported in human and animal studiesfollowing acute exposure to TCE (EPA 1985). Nephrotoxicity hasbeen observed in animals following acute exposure to TCE vapors(ACGIH 1986, Torkelson and Rowe 1981). Subacute inhalationexposures of mice have resulted in transient trichloroethene-induced increased liver weights (Kjellstrand et al. 1983).Industrial use of TCE is often associated with adversedermatological effects including reddening and skin burns oncontact with the liquid form, and dermatitis resulting fromvapors. These effects are usually the result of contact withconcentrated solvent, however, and no effects have been reportedafter exposure to TCE in dilute, aqueous solutions (EPA 1985).Trichloroethene has caused significant increases in the incidenceof hepatocellular carcinomas in mice (NCI 1976) and renaltubular-cell neoplasms in rats exposed by gavage (NTP 1983), andpulmonary adenocarcinomas in mice following inhalation exposure(Fukuda et al. 1983). Trichloroethene was mutagenic inSalmonella tYph-i-nm-r-*"™ anrf -in E. coli (strain K-12), utilizingliver microsomes for activation (Greim et al. 1977).

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EPA (1989) classified trichloroethene in Group B2—Probable HumanCarcinogen based on inadequate evidence in humans and sufficientevidence of carcinogenicity from animals studies. An oral cancerpotency factor of _l.lxlO"2 (mg/kg/day)"1 and an inhalation cancer

-3 —1potency factor of 4.6x10 (mg/kg/day) (EPA 1984) have beenderived for trichloroethene based on the mouse liver tumor datain the NCI (1976) and NTP (1983) gavage studies. EPA (1987)

—3developed an oral reference dose (RfD) of 7.35x10 mg/kg/daybased on a subchronic inhalation study in rats in which elevatedliver weights were observed following exposure to 55 ppm,5 days/week for 14 weeks (Kimmerle and Eben 1973). A safetyfactor of 1,000 was used to calculate the RfD. However, this RfDis currently under review by EPA.

TRXCHIiOROFLUOROMETHANE

Trichlorofluoromethane is rapidly absorbed in humans and animalsfollowing oral and inhalation exposures (ACGIH 1986, Mergner etal. 1975, Adir et al. 1975). Oral administration of 2.5 ml/kg inrats resulted in neither death or liver toxicity (Slater 1965)and application to the eyes or skin caused only mild reversibleirritation (Scholz 1962, Quevauviller et al. 1964, Hood 1964).The LCjQ of trichlorofluoromethane in rats after a 4 hourexposure has been determined to be 26,200 ppm (ACGtlT 1986).Metabolic changes (e.g., increased blood glucose and lactic acid,decreased oxygen uptake) were reported in rats and rabbitsexposed to 50,000 ppm trichlorofluoromethane for one hour dailyfor 15 days (Paulet 1975). Dogs exposed to the sameconcentration for 20 minutes showed increases in blood glucoseand lactic acid. A subchronic study using dogs exposed totrichlorofluoromethane in the air for 90 days showed elevated BUNlevels and lung lesions (Jenkins et al. 1970). Evidence of

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cardiotoxicity (cardiac arrhythmias) in dogs exposed to 5000 ppmtrichloromethane and intravenous epinephrine _was provided byReinhardt et al. (1971). Subsequent experiments have shown theeffects to be brief with the animals recovering shortly after theend of exposure (Clark et al. 1972). Other animals exposed totrichlorofluoromethane concentrations between 5,000 to 15,00 ppmhave also been shown to exhibit cardiovascular and circulatoryabnormalities (Flowers et al. 1975, Taylor and Drew 1975, Taylor1975, Aviado 1975). The available evidence suggests thattrichlorofluoromethane is not carcinogenic (NCI 1978). Thisstudy did show an association between dose and increasedincidence of mortality in rats.

EPA (1989) has reported an inhalation RfD fortrichlorofluoromethane of 0.2 mg/kg/day based on studiesinvestigating elevated BUN levels and lung lesions in dogs(Jenkins et al. 1970); and uncertainty factor of 10,000 was usedto develop the RfD. EPA (1989) has also reported an oralreference dose of 0.3 mg/kg/day-for trichlorofluoromethane basedon a chronic rat study in which increased mortality was observed(NCI 1978) . An uncertainty factor of 1000 was used to derive theRfD.

VINYL CHLORIDE -

Vinyl chloride is rapidly absorbed in rats following oral andinhalation exposure, while dermal absorption of vinyl chloride isminor (EPA 1985). At high inhalation exposure levels, workershave experienced dizziness, headaches, euphoria, and narcosis.In experimental animals, inhalation exposure to high levels ofvinyl chloride can induce narcosis and death. Lower doses resultin ataxia, narcosis, congestion and edema of the lungs, and

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hyperemia in the liver (EPA 1985). Chronic inhalation exposureof workers to vinyl chloride is associated with hepatotoxicity,central nervous system disturbances, pulmonary insufficiency,cardiovascular toxicity, gastrointestinal toxicity, andacro-osteolysis (EPA 1985). Experimental animals chronicallyexposed via inhalation or ingestion have exhibited effectsinvolving the liver, spleen, kidneys, hematopoietic system, andskeletal system (EPA 1984). Feron et al. (1975) found thatadministration of vinyl chloride to rats by gavage.resulted inhematologic, biochemical, and organ-weight effects at doses above30 mg/kg/day. Evidence for an association between human exposureto vinyl chloride and birth defects or fetal loss is conflicting(EPA 1987). Human exposure to vinyl chloride has been associatedwith an increased incidence of hepatic angiosarcoma and brain,lung, and hemolymphopoietic cancers. In animal studies, chronicinhalation and ingestion of vinyl chloride at levels as low as1.7 and 5 mg/kg/day have induced cancer in the liver and in othertissues of rats and mice (IARC 1979; Feron et al. 1981; Maltoniet al. 1980, 1981).

EPA (1989) has classified vinyl chloride in Group A (HumanCarcinogen) based on adequate evidence of carcinogenicity fromepidemiological studies.EPA (1989) reported an oral cancer potency factor (q-*) of 2.3(mg/kg/day)-1 for vinyl chloride based on the long-term ingestionstudy in rats in which lung tumors were observed (Feron et al.1981). The inhalation cancer potency factor for vinyl chlorideis 2.95xlO"1 (mg/kg/day)"1 (EPA 1989) and is based on a chronicinhalation studies conducted by Maltoni et al. (1980, 1981) inwhich liver tumors were observed in rats.

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XYLENES

The three xylene isomers, compounds that have the same chemicalconstituents in a different configuration, have similartoxicolog;ical - properties and are discussed together. Data fromanimals and humans suggest that approximately 60% of an inhaleddose is absorbed. Inference from metabolism and excretionstudies suggests that absorption of orally administered xylene isnearly complete. Dermal absorption is reported to be minorfollowing exposure to~~xylene vapor but may be significantfollowing contact with the liquid (EPA 1985) . In humans, acuteinhalation exposures to relatively high concentrations of xyleneadversely affect the central nervous system and lungs and canirritate mucous membranes (EPA 1987). Savolainen et al. (1980)observed that body balance and manual coordination were impairedin eight male -students following inhalation exposure to m-xylene.However, tolerance against the observed effects developed duringone work week. In experimental rats, long-term inhalationexposure to o-xylene resulted in hepatomegaly (Tatrai et al.1981). Oral exposure to 200 mg/kg xylene in the diet for up to 6months was also associated with liver toxicity, specifically thedevelopment of intracellular vesicles (Bowers et al. 1982).Prolonged oral exposures in mice resulted in hyperactivity, amanifestation of CNS toxicity (NTP 1986). Xylene appears to befetotoxic and may increase the incidence of visceral and skeletalmalformations in offspring of exposed experimental animals(Mirkova et al. 1983) . There is suggestive evidence that xyleneis carcinogenic in experimental animals when exposed by oralgavage-(Maltoni et al. 1985).

EPA (1989a) calculated an oral reference dose (RfD) for mixedxylenes of 2 mg/kg/day based on an NTP (1986) study in which male

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rats given a gavage dose of 179 mg/kg/day for 103 weeks did notexhibit hyperactivity, decreased body weight or a significantincreased mortality. The oral RfD was derived using the no-observed-adverse-effect level (NOAEL) of 179 mg/kg/day and anuncertainty factor of 100. EPA (1989b) reported an inhalationRfD for mixed xylenes of 0.4 mg/kg/day based on a study in whichno effects were observed in rats exposed to 398 mg/m3 for 13weeks (Carpenter et al. 1975); an uncertainty factor of 1,000 wasused to develop the RfD.

A. 2

ALUMINUM

Little is known about the absorption of aluminum following oralexposure, although there are reports that this inorganic metal isabsorbed from the gastrointestinal tract to some extent (NAS1982) . Aluminum has low acute toxicity following oral exposure.Oral LDjQS in several animal species range from 380 to 780 mg/kg(EPA 1985) . Few data exist from subchronic or chronic phosphorusbalance (EPA 1985). Neurofibrillar degeneration has beenobserved in experimental animals given subcutaneous injections ofaluminum (NAS 1982) . Intratracheal and intraperitonealadministration of aluminum compounds have been associated inexperimental animals with pulmonary fibrosis and fibroticperitonitis, respectively (NAS 1982) . Evidence to date suggeststhat aluminum is not teratogenic or fetotoxic; however, ratsexposed by gavage to 2.5 mg/kg aluminum for 6 months had reducedsperm counts and reduced sperm motility (EPA 1985) . Studies toevaluate the potential of aluminum or its salts to inducemutagenic or carcinogenic effects have yielded negative results(EPA 1985). In humans, pulmonary fibrosis has been observed

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following inhalation of aluminum suggested as a potentialetiolbgical factor in two neurological disorders: Alzheimer'sdisease and chronic renal failure accompanied by senile dementia(EPA 1985). However, the importance of aluminum in thesedisorders had not been fully established. Because there areinadequate dose-response data from which to estimate anacceptable daily intake level for ionic aluminum, no referencesdoes (RfD) has been established.

BARIUM

Adverse effects in humans following oral exposure to solublebarium compounds include gastroenteritis/ muscular paralysis,hypertension, ventricular fibrillation, and central nervoussystem damage (EPA 1984, Perry et al. 1983). inhalation ofbarium sulfate or barium carbonate in occupationally exposedworkers has been associated with baritosis, a benignpneumoconiosis (Goyer 1986). Experimental animals exposedchronically to barium in drinking water developed increased bloodpressure (EPA 1984). Inhalation of barium carbonate dust byexperimental animals has been associated with reduced spermcount, increased fetal mortality, atresia of the ovarianfollicles, decreased body weight, and alterations in liverfunction (EPA 1984, TarasenKo et al. 1977).

EPA (1989a) derived an oral reference dose (RfD) based on achronic rat study in which a lowest-observed-adverse-effect level(LOAEL) for increased blood pressure was observed (Perry et al.1983). Using the LOAEL of 5.1 mg/kg/day and an uncertaintyfactor of 100, an oral RfD of 5xlO"2 mg/kg/day was calculated.EPA (1989b) has also developed an inhalation RfD ofl.OxlO"4 mg/kg/day for barium based on a study by Tarasenko et

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al. (1977) . In this study rats were exposed to barium carbonatedust at airborne concentrations of up to 5.2 mg/m3 for 4-6months. Adverse effects noted at this concentration includeddecreased body weight, alterations in liver function, andincreased fetal mortality. An uncertainty factor pf_1,000 wasused in developing the RfD.

CADMIUM

Gastrointestinal absorption of cadmium in humans ranges from 5-6%(EPA 19S5a). Pulmonary absorption of cadmium in humans isreported to range from 10% to 50% (CDHS 1986). Cadmiumbioaccumulates in humans, particularly in the kidney and liver(EPA 1985a,b) . Chronic oral or inhalation exposure of humans tocadmium has been associated with renal dysfunction, itai-itaidisease (bone damage), hypertension, anemia, endocrinealterations, and immunosuppression. Renal toxicity occurs inhumans at a renal cortex concentration of cadmium of 200 Mg/g(EPA 19S5b). Epidemiological studies have demonstrated a strongassociation between inhalation exposure to cadmium and cancers ofthe lungs, kidney, and prostate (EPA 1985b, Thun et al. 1985).In experimental animals, cadmium induces injection-site sarcomasand testicular tumors. When administered by inhalation, cadmiumchloride is a potent pulmonary carcinogen in rats. Cadmium is awell-documented animal teratogen (EPA 1985b).

EPA (19S9a,b) classified cadmium as a Group Bl agent (ProbableHuman Carcinogen) by inhalation. This classification applies toagents for which there is limited evidence of carcinogenicity inhumans from epidemiologic studies. EPA (1989a,b) derived aninhalation cancer potency factor of 6.1 (mg/kg/day)"1 for cadmiumbased on epidemiologic studies in which respiratory tract tumors

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were observed (Thun et al. 1985, EPA 1985b). Using renaltoxicity as an endpoint, and a safety factor of 10, EPA (1980,1987, 1989b) has derived two separate oral reference doses (RfD).The RfD associated with oral exposure to drinking water is 5xlO"4mg/kg/day, and is based upon the lowest-observed-adverse-effectlevel (LOAEL) of 0.005 mg/kg in humans (Friberg et al. 1974).The RfD associated with exposure to cadmium in food or othernonaqueous oral exposures is Ixio"3 mg/kg/day.

COBALT

Cobalt is an essential trace element in human nutrition. Cobaltis generally Well absorbed following ingestion. Acute ingestionof large doses toy huihans"produces..gastrointestinal disturbances(vomiting, diarrhea), and a sensation of warmth. Signs of acutepoisoning in animals fed cobalt salts consist of diarrhea, lossof appetite, paralysis of hind legs, cutaneous vasodilation, andreduced body temperature prior to death. Large doses producedanuria, while.smaller doses resulted in albuminuria (Stokinger1981). In animals, subchronic oral exposures result in disturbedconditioned reflexes and alterations in__hematopoiesis (NRC 1973) .In humans, chronic oral exposure to cobalt in high doses cancause goiter, decreased thyroid function, increased heart andrespiratory rates and blood lipid changes (Hammond and Beliles1980). Chronic exposure to cobalt dust has been reported toproduce respiratory disease in workers (Stokinger 1981). Cobaltsalts included in a beer formulation at concentrations 1.2 to1.5 mg/liter were reported to be responsible for a number ofdeaths due to congestive heart failure (NRC 1973). Cobaltadministered to laboratory rodents produced adverse reproductiveeffects including craniofacial developmental abnormalities inmice (Leonard et al. 1984) and decreased body weight in rats

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(Shepard 1986). Cobalt has been reported to cause sarcomas atthe site of injection in rats (Gilraan 1962, Heath 1960); however,the results of carcinogenesis studies performed by other routesof exposure have been negative. EPA has not classified cobalt onthe basis of its carcinogenicity and no health based standardshave been derived.

CYANIDES

The toxicity of cyanides is strongly dependent on their chemicalspeciation. Free cyanides are readily absorbed from thegastrointestinal tract, lungs, and skin and, once absorbed, arerapidly distributed throughout the body (EPA 1985). The toxiceffects in humans following acute oral exposure to free cyanidesinclude hyperventilation, vomiting, unconsciousness, convulsions,vascular collapse and cyanosis, and death (EPA 1985). Inhalationof high concentrations of hydrogen cyanide (HCN) gas results inalmost immediate collapse, respiratory arrest, and death withinminutes (DiPalma 1971). Airborne hydrogen cyanide concentrationsbetween 99 and 528 mg/m3 are fatal within 30-60 minutes (NIOSH1976) . There is limited data on chronic exposures of cyanide inhumans, although the following effects have been identified inchronic occupationally exposed workers in some epidemiologicstudies: neurological dysfunction, lacrimation, abdominal pain,muscular weakness, and shortness of breath (NIOSH 1976) . Cyanideappears to be less toxic to animals following chronic exposuresthan following acute exposures. In animals, chronic oralexposure has produced weight loss, thyroid effects and myelindegeneration (Howard and Hanzal 1955). Cyanide can causeteratogenic effects when subcutaneously administered to hamsters;this teratogenic effect has not been observed in other speciesalthough some reproductive toxicity has been noted (EPA 1985) .

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EPA (1989a, 1989b) calculated an oral reference dose (RfD) of0.02 mg/kg/day for cyanide based on a chronic study by Howard andHanzal (1955) in which rats were maintained on a diet fumigatedwith hydrogen cyanide and exhibited weight loss, thyroid effectsand myelin degeneration. No observed adverse effects (NOAEL)were noted at the highest dose administered (10.8 mg/kg/day). ANOAEL of 10 .8 mg/kg/day and a safety .factor of 500 were used toderive the RfD (EPA 1989a).

IRON

Gastrointestinal absorption of iron in humans ranges from 1% to25% (EPA 1984). Absorption of iron following inhalation exposurehas not been thoroughly studied. Iron is an essential elementand is therefore nontoxic at doses necessary for maintainingnormal health and nutrition (EPA 1984). However, overexposure toiron can cause adverse health effects. Gastrointestinalirritation is the primary effect observed in humans followingacute oral overexposure to iron. Chronic oral overexposure ofhumans to iron has been associated with gastrointestinalbleeding, metabolic acidosis, hepatic toxicity, hemosiderosis,and hemochromatosis (EPA 1984). Human fatalities have occurredfollowing ingestion of iron at doses of 100 mg/kg/day (Venugopaland Luckey 1978). Chronic inhalation overexposure of humans toiron-containing dusts and fumes produces respiratory irritationand various pulmonary lesions (EPA 1984). There is limitedevidence from studies with experimental animals that certainsoluble iron salts are teratogenic. Certain iron compounds arealso reported to be genotoxic. Iron oxide enhances thecarcinogenic action of various organic carcinogens(benzo[a]pyrene for example) and may act as a tumor promoter.

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Local sarcomas have been induced by subcutaneous injection ofiron-dextran (EPA 1984).

The National Research Council of the National Academy of Sciences(NRC 1980) has suggested the recommended dietary allowances(RDAs) for iron of between 10 and 60 mg. Therefore, the maximumrecommended daily intake of iron can be used as a conservativeallowable intake for chronic exposure. No health based criteriahave been derived by EPA.

LEAD

Absorption of lead from the gastrointestinal tract of adulthumans is estimated at 8%-45%. In children, absorption from non-paint sources ranges from 30% to 50% (Hammond and Beliles 1980,EPA 1986a). There are other interpretations of the data (Duggan1983) which suggest this may be as high as 70%. For adulthumans, the deposition rate of particulate airborne lead is 30%-50%, and essentially all of the lead deposited is absorbed. Leadis stored in the body in the kidney, liver and bone (EPA 1984) .The major adverse effects in humans caused by lead includealterations in the hematopoietic and nervous systems. The toxiceffects are generally related to the concentration of this metalin blood. Blood concentration levels of over 80 jug/dl inchildren and over 100 /ig/dl in sensitive adults can cause severe,irreversible brain damage, encephalopathy, and possible death.The Centers for Disease Control (CDC 1985) have used the value of25 Mq/oH as an acceptable level of blood lead. Recentinformation, however (EPA 1988), indicates that physiologicaland/or biochemical effects can occur even at lower levels. Theseinclude enzyme inhibition (16 /ig/dl) , elevated erythrocyteprotoporphyrin (15 jig/dl), interference with Vitamin D

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metabolism, cognitive dysfunction in infants (10 to 15 tg/dl) ,electrophysiological dysfunction (6 Atg/dl), and reduced childhoodgrowth (4 /ig/dl). Decreased fertility, fetotoxic effects, andskeletal malformations have been observed in experimental animalsexposed to lead (EPA 1984). Chronic oral ingestion of certainlead salts (lead-acetate, lead phosphate, lead subacetate) hasbeen associated in experimental animals with increased renaltumors. Doses of lead that induced kidney tumors were high andwere beyond the lethal dose in humans (EPA 1985).

EPA classified certain lead salts in Group B2—-Probable HumanCarcinogen, although no cancer potency factor has beenestablished (EPA 1989a). This category applies to those agentsfor which there "is sufficient evidence of carcinogenicity inanimals and inadequate evidence of carcinogenicity in humans.EPA (1988) has recently proposed a maximum contaminant level goal(MCLG) of zero for lead. EPA (1989a) considers it inappropriateto develop a reference dose (RfD) for inorganic lead and leadcompounds, since many.of the health effects associated with leadintake occur essentially without a threshold. The new proposedMCLG is based on subtle effects of lead at low blood levels, theoverall Agency goal of reducing lead exposures, and the probablecarcinogenicity of lead at very high doses. Underlying thisproposal was the -assumption that blood lead levels in the rangeof 10-15 pg/&l. are associated with serious effects. AdditionallyEPA noted that existing body burdens of lead were already in therange where adverse effects could result.

An alternative approach is used in this assessment to evaluatepotential .subchronic lead exposures to young children. Thisapproach is based on a linear pharmacokinetic model used by EPA'sOffice of Air Quality Planning and Standards (OAQPS) for lead

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standard setting (EPA 1989b). The model, based on work by Harleyand Kneip (1985), takes into account the uptake, retention andexcretion of lead. It is referred to as the "IntegratedUptake/Biokinetic Model", and it estimates blood lead levels. Inthis assessment the model will be applied to a two-year old childsince lead intake by this age category is likely to have thegreatest impact on blood lead levels. The estimated blood leadlevels can then be compared to the 10-15 Mg~/dl level of concernidentified by EPA (1986b). It should be noted that this modelcan predict blood lead levels only up to 30 jug/dl (i.e., therelationship between lead intake and blood lead levels isnonlinear at blood lead levels above 30

MANGANESE

Manganese is absorbed at low levels following oral or inhalationexposure (EPA 1984a). The effects following acute exposure tomanganese are unknown. Chronic oral and inhalation exposure ofhumans to high levels of manganese causes pneumonitis in exposedworkers and has been associated with a condition known asmanganism, a progressive neurological disease characterized byspeech disturbances, tremors, and difficulties in walking(Kawamura et al. 1941). Altered hematologic parameters(hemoglobin concentrations, erythrocyte counts) have also beenobserved in persons exposed chronically. Chronic oral exposureof rats to manganese chloride results in central nervous systemdysfunction (Leung et al. 1981, Lai et al. 1982). Manganese hasnot been reported to be teratogenic; however, this metal has beenobserved to cause depressed reproductive performance and reducedfertility in humans and experimental animals (EPA 1984a).Certain manganese compounds have been shown to be mutagenic in avariety of bacterial tests. Manganese chloride and potassiumpermanganate caused chromosomal aberrations in mouse mammarycarcinomal cells. Manganese was moderately effective in

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enhancing viral transformation of Syrian hamster embryo cells(EPA 1984a,b).

EPA (1989) established an oral reference dose (RfD) of 2.0X10"1mg/kg/day for manganese based on no observed adverse effects(NOAEL) in rats exposed chronically to manganese in drinkingwater (Leung et al. 1981, Lai et al. 1982). An uncertaintyfactor of 100 was used to derive the reference dose. EPA (1989)calculated an inhalation reference dose based upon anoccupational study conducted by Saric et al. (1977). Using aNOAEL of 2.1-mg/day and an uncertainty factor of 100, aninhalation RfD of 3,OxlO"4 mg/kg/day was derived. Both theinhalation and oral intake values are based upon central nervoussystem effects (EPA 1989).

MERCURY - - . - . , . _ _ . _ =-... ,

In humans, inorganic mercury is absorbed following inhalation andoral exposure, however only 7% to 15% of administered inorganicmercury is absorbed following oral exposure (EPA 1984, Rahola etal. 1971, Task Group on Metal Accumulation 1973). Organicmercury is almost completely absorbed from the gastrointestinaltract and is assumed to be well absorbed via inhalation in humans(EPA 1984). A primary target organ for inorganic compounds isthe kidney. Acute and chronic exposures of humans to inorganicmercury compounds have been associated with anuria, polyuria,proteinuria, and renal lesions (Hammond and Beliles 1980).Chronic occupational exposure of workers to elemental mercuryvapors (0.1 to 0.2 mg/m3) has been associated with mentaldisturbances, tremors, and gingivitis (EPA 1984). Animalsexposed to inorganic mercury for 12 weeks have exhibitedproteinuria, nephrotic syndrome and renal disease (Druet et al.1978). Rats chronically administered inorganic mercury (asmercuric acetate) in their diet have exhibited decreased body

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weights and significantly increased kidney weights (Fitzhugh etal. 1950). The central nervous system is a major target fororganic mercury compounds. Adverse effects in humans, resultingfrom subchronic and chronic oral exposures to organic mercurycompounds have included destruction of cortical cerebral neurons,damage to Purkinje cells, and lesions of the cerebellum.Clinical symptoms following exposure to organic mercury compoundshave included paresthesia, loss of sensation in extremities,ataxia, and hearing and visual impairment (WHO 1976).Embryotoxic and teratogenic effects, including malformations ofthe skeletal and genitourinary systems, have been observed inanimals exposed orally to organic mercury (EPA 1984). Bothorganic and inorganic compounds are reported to be genotoxic ineukaryotic systems (Leonard et al. 1984).

EPA (1989) has reported an oral RfD for alkyl and inorganicmercury of 3xlO"4 mg/kg/day based on studies investigatingcentral nervous system effects in humans exposed to mercury (EPA1980); an uncertainty factor of 10 was used to develop the RfD.EPA (1989) has also reported an oral reference dose of3x10"* mg/kg/day for inorganic mercury based on a chronic ratstudy in which kidney effects were observed (Fitzhugh et al.1950). An uncertainty factor of 1,000 was used to derive theRfD.

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NICKEL - —-- - ----:-—- - . . . ' . . .

Nickel compounds can be absorbed; following inhalation, ingestion,or dermal exposure. -The amount absorbed depends on the doseadministered and the chemical and physical form of the particularnickel compound (EPA 1986). Dermal exposure of humans to nickelproduces allergic contact dermatitis (EPA 1986). Adverse effectsassociated with acute exposure in animals have included depressedweight gain, altered hematological parameters, and increased irondeposition in blood, heart, liver, and testes (EPA 1987).Chronic or subchronic exposure of experimental animals to nickelhas been associated with reduced weight gain, degenerativelesions of the male reproductive tract, asthma, nasal septalperforations, rhinitis, sinusitis, hyperglycemia, decreasedprolactin levels, decreased iodine, uptake, and vasoconstrictionof the coronary vessels (EPA 1986). Teratogenic and fetotoxiceffects have been observed in the of f spring of exposed animals(EPA 1986). Inhalation exposure of experimental animals tonickel carbonyl or nickel subsulfide induces pulmonary tumors(EPA 1986). Several nickel salts cause localized tumors whenadministered by subcutane_QU_s _injection or implantation.Epidemiological evidence indicates that inhalation of nickelrefinery dust and nickeLsubsulfide is associated with cancers ofthe nasal cavity, lung, larynx, kidney, and prostate (EPA 1986).

Nickel refinery dust and nickel subsulfide are both categorizedin Group A—Human Carcinogens. These classifications are basedon an increase incidence of lung and nasal tumors observed inworkers occupationally exposed to nickel refinery dust. Thesematerials have inhalation cancer potency factors of 0.84(mg/kg/day)"1 and 1.7 (mg/kg/day)"1, respectively (EPA 1989).Nickel carbonyl is categorized in Group B2—Probable HumanCarcinogen; however, a potency factor has not been derived fornickel carbonyl (EPA 1989). EPA (1989) derived an oral reference

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dose (RfD) for nickel of 2xlO"2 mg/kg/day based on a study byAmbrose et al. (1976) in which rats administered 5 mg/kg/day(NOAEL) nickel in the diet for 2 years did not experiencedecreased weight gain observed in animals administered50 mg/kg/day (LOAEL). A safety factor of 300 was used tocalculate the RfD.

VANADIUM

Pentavalent vanadium compounds are generally considered to bemore toxic than other valence states. Many incidents of shortterm and long term occupational exposures to vanadium, mainlyvanadium pentoxide dust, have been reported. Inhalation causesrespiratory tract irritation, coughing, wheezing, laboredbreathing, bronchitis, chest pains, eye and skin irritation anddiscoloration of the tongue (NIOSH 1977, NAS 1974). Effects seenin experimental animals following chronic inhalation exposureinclude fatty degeneration of the liver and kidneys, hemorrhage,and bone marrow changes (Browning 1969).

EPA (1989b) has derived an oral reference dose (RfD) of 7xlO"3mg/kg/day based on a chronic study in which rats receivedvanadium in their drinking water (Schroeder et al. 1970) . A no-observed-adverse-effect level (NOAEL) of 0.77 mg/kg/day and anuncertainty factor of 100 were used to develop the RfD. EPA(1989a) has established an oral RfD for vanadium pentoxide of9xlO"3 mg/kg/day. This value is based on a chronic rat study inwhich a NOAEL of 0.89 mg vanadium pent oxide/kg/day was noted.The only reported effect was a decrease in the amount of cystinein the hair (Stokinger et al. 1953). An uncertainty factor of100 was used to calculate the vanadium pentoxide RfD. EPA hasnot developed inhalation criteria for vanadium.

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REFERENCES

ORGANICS

Acetone .._..__ .... _ __ "r~.....________.__._

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984. Health EffectsAssessment for Acetone. Environmental Criteria andAssessment Office, Cincinnati, Ohio. EPA 540/1-86-016

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1986. Ninety-Day GavageStudy in Albino .Rats. .Using Acetone. Off ice of Solid Waste,Washington, DC. As cited in EPA 1988

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989. Integrated RiskInformation System (IRIS). Environmental Criteria andAssessment Office, Cincinnati, Ohio. Revised May 1, 1989

GOLDBERG, M.E., JOHNSON, H.E., POZZANI, N.C., and SMYTH, H.F.1964. Effects of repeated inhalation of vapors ofindustrial solvents on animal behavior. Am. Ind. Hyg.Assoc, J. 25:369-375

KAGAN, E. 1924. Arch Hyg. 94:41 (As cited in Krasavage etal. 1981)

KRASAVAGE, W. J. , O'DONQGHUE, J.L. , and DIVENCENZO, C.D. 1981.Ketones. In Clayton, G.D., and Clayton, P.B., eds. Patty'sindustrial Hygiene and Toxicology. 3rd ed. John Wiley andSons, New York. Vol. 2B

NELSON, K.W., EGE, J.F., ROSS, N., WOODMAN, L.E., and SILVERMAN,L. 1943. Sensory response to industrial solvent vapors.J. Ind. Hyg. Toxicol- 25:282-285

Benzene ..__....__. _ _ _ _ _ _ _ _ _ _ _ .._ _____ ._.___

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985. Drinking WaterCriteria document for Benzene (Final Draft). Office ofDrinking Water, Washington, D.C. April 1985

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989. Integrated RiskInformation System (IRIS). Environmental Criteria andAssessment Office, Cincinnati, Ohio. Revised July 1, 1989

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INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (IARC) . 1982. IARCMonographs on the Evaluation of the Carcinogenic Risk ofChemicals to Humans. Some Aromatic Amines, Anthraquinonesand Nitroso Compounds, and Inorganic Fluorides Used inDrinking-Water and Dental Preparations. World HealthOrganization, Lyon, France. Vol. 27

MALTONI, C. , CONTI, B. , COTTI, G., and BELPOGGI, F. 1985.Experimental studies on benzene carcinogenicity at theBologna Institute of Oncology: Current results and ongoingresearch. Am. J. Ind. Med. 7:415-446

NATIONAL ACADEMY OF SCIENCE (NAS). 1976. Health Effects ofBenzene: A Review Committee on Toxicology, Assembly of LifeSciences. National Research Council, Washington, D.C.

OTT, M.G. , TOWNSEND, J.C., FISHBECK, W.A. , and LANGNER, R.A.1978. Mortality among individuals occupationally exposed tobenzene. Arch, Environ. Health 33:3-10

RINSKY, R.A. , YOUNG, R. J. , and SMITH, A.B. 1981. Leukemia inbenzene workers. Am. J. Ind. Med. 3:217-245

WONG, O., MORGAN, R.W. , and WHORTON, M.D. 1983. Comments on theNIOSH Study of Leukemia in Benzene Workers. Technicalreport submitted to Gulf Canada, Ltd., by EnvironmentalHealth Associates

CARPENTER, C.P. , WEIL, C.S. , and SMYTH, H.F. 1953. Chronic oraltoxicity of di(2-ethylhexyl)phthalate for rats, guinea pigs,and dogs. Arch. Indust. Hyg. occup. Med. 8:219-226

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1980. Ambient WaterQuality Criteria for Phthalate Esters. Office of WaterRegulations and Standards, Criteria and Standards Division,Washington, D.C. October 1980. EPA 40/5-80-067

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1986. Superfund PublicHealth Evaluation Manual. Office of Emergency and RemedialResponse, Washington, D.C. EPA 540/1-86-060

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989. Integrated RiskInformation System (IRIS) . Environmental Criteria andAssessment Office, Cincinnati, Ohio. Revised May 1, 1989

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NATIONAL TOXICOLOGY PROGRAM (NTP). 1982. CarcinogenesisBioassay of Di(2-ethylhexyl)phthalate in F344 Rats and B6C3F,Mice. Feed Study. __NTP Technical Report Series No. 217,U.S. Department of Health and Human Services. NIHPublication No. 82-1773. NTP-80-37

Carbon tetrachloride . : . . . . ,

AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS(ACGIH). 1986. Documentation of the Threshold Limit Valuesand Biological Exposure Indices. 5th ed. ACGIH, Inc.Cincinnati, Ohio

BRUCKNER, J.V., MACKENZIE, W.F., MURALIDHARA, S., et al. 1986.Oral toxicity of carbon tetrachloride: Acute, subacute andchronic studies in rats. Fund. Appl. Toxicol. 6(1):16-34

DELIA PORTA, G.B. , TERRACINI, B., and SHUBIK, K.P. 1961.Induction with carbon tetrachloride of liver cell carcinomasin hamsters. J. Natl. Cancer Inst. 26:855-863

EDWARDS, J., HESTON, W.E., and DALTON, H.A. 1942. Induction ofcarbon tetrachloride hepatoma in strain L mice. J. Natl.Cancer Inst. 3:297-301

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984. Health AssessmentDocument for Carbon Tetrachloride. Environmental criteriaand Assessment Office, Cincinnati, Ohio. September 1984.EPA-600/8-82-001F

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985. Drinking WaterCriteria Document for Carbon Tetrachloride (Final Draft).Office of--Drinking Water, Washington, D.C. January 1985

ENVIRONMENTAL PROTECTION AGENCY (EPA) . 1989. Integrated RiskInformation System (IRIS). Environmental Criteria andAssessment Office, Cincinnati, Ohio. Revised June 1, 1989

NATIONAL CANCER INSTITUTE (NCI). 1976a.- Report on theCarcinogenesis Bioassay of Chloroform. CarcinogenesisProgram, Division of Cancer Cause and Prevention,Washington, D.C.

NATIONAL CANCER INSTITUTE (NCI). 1976b. Carcinogenesis Bioassayof Trichloroethylene. Carcinogenesis Technical ReportSeries No. 2, Washington, D.C.

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NATIONAL CANCER INSTITUTE (NCI). 1977. Bioassay of 1,1,1-Trichloroethane for Possible Carcinogenicity.Carcinogenesis Technical Report Series No. *, Washington,D.C.

Chloroethane (Ethyl chloride^

CLAYTON, G. and CLAYTON, F. , ed. 1981. Patty's IndustrialHygiene and Toxicology: Volume 2B-Toxicology. 3rd ed.John Wiley and Sons, New York, New York

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985. Chemical,Physical, and Biological Properties of Compounds Present atHazardous Waste Sites. Final Report: Methyl Chloride.Prepared for EPA by Clement Associates, Inc., Arlington ,Va. September 27

TROSHINA, M. 1964. Toksikol. Novykk. Prom. Khim. Veshchestv. 645 (through Chem. Abstr.) (As cited in Clayton and Clayton1981)

Ch-ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984. Health Effects

Assessment for Chloroform. Environmental Criteria andAssessment Office, Cincinnati, Ohio. September 1984/ EPA540/1-86-010

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985. Health AssessmentDocument for Chloroform. Environmental Criteria andAssessment Office, Research Triangle Park, North Carolina.September 1985. EPA 600/8-84-004F


HEYWOOD, R,, SORTWELL, R.J. NOEL, P.R.B. , et al. 1979. Safetyevaluation of toothpaste containing chloroform. III.Long-term study in beagle dogs. J. Environ. Pathol.Toxicol. 2:835-851

JORGENSON, T.A. , HEIERHENRY, E.F., RUSHBROOK, C.J., et al. 1985.Carcinogenicity of chloroform in drinking water to maleOsborne-Mendel rats and female B6C3F1 mice. Fund. Appl.Toxicol. 5:760-769

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NATIONAL CANCER INSTITUTE (NCI). 1976. Carcinogenesis Bioassayof Chloroform. .GAS No. 67-66-3. NCI CarcinogenesisTechnical" Report Series No. 0. Bethesda, M.D. DHEW (NIH)Publication No. 76

SCHWETZ, B.A., LEONG, B.K.J., GEHRING, P.J. 1974. Embryo- andfetotoxicity of inhaled chloroform in rats. Toxicol. Appl.Pharmacol. 28:442-451

Dichlorobenzenes _.. _ _..„„. ., „_ „

ASTRAND, I. 1975. Uptake of Solvents in the blood and tissuesof man. Scand. J. Work Environ. Health 1:199-208 (As citedin EPA 1987)

BATELLE'S COLUMBUS LABORATORIES. 1978a. Subchronic toxicitystudy: ortho-Dichlorobenzene (C54944), B6C3F1 mice.Subcontract No. 76-34-106002. December 21, 1978(unpublished report) (As cited in EPA 1987)

BATELLE'S COLUMBUS LABORATORIES. 1978b. Subchronic toxicitystudy: ortho-Dichlorobenzene (C54944), Fisher 344 Rats.Subcontract No. 76-34-106002. (unpublished report) (Ascited in EPA 1987)

DALLAS, C.E., WEIR, F.W. , FELDMAN, S., PUTCHA, L., and BRUCKNER,J.V. 1983. The uptake and distribution of1,1-dichloroethylene in rats during inhalation exposure.Toxicol. Appl. Pharmacol. 68:140-151 (As cited in EPA 1987)

ENVIRONMENTAL PROTECTION AGENCY (EPA) . 1985. Drinking WaterCriteria Document for ortho-Dichlorobenzene, meta-Dichlorobenzene, and para-Dichlorobenzene (Draft). Officeof Drinking Water, Washington, D.C. June 1985. PB86-117918

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987. Health Advisoryfor ortho-, meta-, and Ea arDichlorobenzene. Office of DrinkingWater, Washington, D.C. March 31, 1987

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989a. Integrated RiskInformation System (IRIS) . Environmental Criteria andAssessment Office, Cincinnati, Ohio

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989b. Health EffectsAssessment Summary Tables. Prepared by the Office of Healthand Environmental Assessment, Environmental Assessment andCriteria office, Cincinnati, Ohio, for the Office of SolidWaste and Emergency Response, Office of Emergency andRemedial Response, Washington, D.C. April 1989

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HOLLINGSWORTH, R.L. , ROWE, V.K. , OYEN, F. , TORKELSON, T.R. , andADAMS, E.M. 1958. Toxicity of 0-dichlorobenzene: studieson animals and industrial experience AMA Arch. Inc. Health17(1):130-189

NATIONAL TOXICOLOGY PROGRAM. 1986. Toxicology andCarcinogenesis studies of 1,4-dichlorobenzene in F344/N rats andB6C3F1 mice. U.S. DHHS, NIH Technical Report Series No. 319

RILEY, R.A., CHART, I.S., DOSS, A. et al. 1980. Para-dichlorobenzene: Long-term Inhalation Study in the rat.ICI Report WSO CTL/P/447. August 1980 . . . . . .

1,4-DichlQrobenssene

ASTRAND, I, 1975. Uptake of Solvents in the blood and tissuesof man, Scand. J. Work Environ. Health 1:199-208 (As citedin EPA 1987)

DALLAS, C.E., WEIR, F.W., FELDMAN, S., PUTCHA, L., and BRUCKNER,J.V. 1983. The uptake and distribution of1,1-dichloroethylene in rats during inhalation exposure.Toxicol. Appl. Pharmacol. 68:140-151 (As cited in SPA 1987)

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985. Drinking WaterCriteria Document for ortho-Dichlorobenzene, roeta-Dichlorobenzene, and para-Dichlorobenzene (Draft). Officeof Drinking Water, Washington, D.C. June 1985. PB86-117918

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987. Health Advisoryfor ortho-. meta-, and para-Dichlorobenzene. Office of DrinkingWater, Washington, D.C. March 31, 1987

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989. Health EffectsAssessment Summary Tables. Prepared by the Office of Healthand Environmental Assessment, Environmental Assessment andCriteria Office, Cincinnati, Ohio, for the Office of SolidWaste and Emergency Response, Office of Emergency andRemedial Response, Washington, D.C. April 1989

NATIONAL TOXICOLOGY PROGRAM. 1986. Toxicology andCarcinogenesis studies of 1,4-dichlorobenzene in F344/N rats andB6C3F1 mice. U.S. DHHS, NIH Technical Report Series No. 319

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1,1-Dichloroethane =-.... . ,

ENVIRONMENTAL PROTECTION "AGENCY (EPA). 1980. Ambient WaterQuality Criteria .

for l,1-Dichloroethane. Office of Water Regulations andStandards, Washington, D.C.- EPA 440/5-80-029

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989. Health EffectsAssessment Summary Tables Prepared by Office of Health andEnvironmental Assessment, Environmental criteria andAssessment Office, Cincinnati Ohio for the Office of SolidWaste and Emergency"Response, Office of Emergency andRemedial Response, Washington, D.C. April 1989

HOFMANN, H.T., BIRNSTIEL, H., and JOBST, P. 1971. Theinhalation toxicity

of 1,1- and 1,2-dichloroethane. Arch. Toxikol. 27:248-265

NATIONAL CANCER INSTITUTE (NCI). 1978. Bioassay of1,1-Dichloroethane for

Possible Carcinogenicity. CAS No. 75-34-3. NCICarcinogenesis Technical Report Series No. 66, Washington,D.C. DHEW Publication No. (NIH) 78-1316

PARKER, J.C., CASEY, G.B., and BAHLNON, L.J. 1979. NIOSHcurrent

intelligence bulletin No. 27. Chloroethanes: Review oftoxicity. ____Am. _In_d.__Hyg. Assoc. J. 40:A46-A60

SCHWETZ, B.A., LEONG, B.K.J., and GEHRING, P.J. "1974. Embryoand

fetotoxicity of inhaled carbon tetrachloride,1,1-dichloroethane, and methyl ethyl ketone. Toxicol. Appl.Pharmacol. 28:452-464

1,2-Dichloroethane _._._ .._ . _ _ . , __ .... _.

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984. Health EffectsAssessment for

1,2-Dichloroethane. Environmental Criteria and AssessmentOffice, Cincinnati, Ohio. September 1984. EPA 540/1-86-002

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985. Health AssessmentDocument f o r . _ _ . _ . _ . . . . . _ .

1,2-Dichloroethane. Office of Health and EnvironmentalAssessment, Washington, D.C. September 1985. EPA600/8-84-006F _:: _ -

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NATIONAL CANCER INSTITUTE (NCI). 1978. Bioassay of1,2-Dichloroethane for

Possible Carcinogenicity. NCI Carcinogenesis TechnicalReport Series No. 55. Washington, D.C. DHEW (NIH)Publication N o . 78-1361 _ . _ . , _

1,1-Dichloroethene . . .

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987. Health Advisoryfor 1,1-Dichloroethene. Office of Drinking Water,Washington, D.C. March 31, 1987.

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985. Health AssessmentDocument for Vinylidene Chloride. Final Report.Environmental Criteria and Assessment Office, ResearchTriangle Park, North Carolina. August 1985. EPA 600/8-83/031F

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989. Integrated RiskInformation System (IRIS). Environmental Criteria andAssessment Office. Cincinnati, Ohio. Revised May 1, 1989

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984. Health EffectsAssessment for 1,1-Dichloroethylene- Environmental Criteriaand Assessment Office, Cincinnati, Ohio. September 1984.EPA 540/1-86-051

MAI.XONI, C., LBFEMINE, G. , COTTI, G., CHIECO, P., and PATELLA, V.1985. Experimental Research on Vinyl idine ChlorideCarcinogenesis. In Archives of Research on IndustrialCarcinogenesis. Princeton Scientific Publishers, Princeton,New Jersey. 3 vols.

QUAST, J.F., HUMISTON, C.G., WADE, C.E., BALLARD, J., BEYER,J.E., SCHWETZ, R.W., and NORRIS, J.M. 1983. A chronictoxicity and oncogenicity study in rats and subchronictoxicity study in dogs on ingested vinylidene chloride.Fund. Appl. Toxicol. 3:55-62

trans- and cis—1.2-dichloroethene

BARNES, D.W., SANDERS, V.M., WHITE, K.L., Jr., et al. 1985.Toxicology of trans-l. 2-dichloroethvlene in the mouse. DrugChem. Toxicol. 8:373-392

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CERNA, M., KYPENOVA, H. 1977. Mutagenic activity ofchloroethylenes analyzed by screening system tests. Mutat.Res. 46:214-215

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985. National primarydrinking water regulations; synthetic organic chemicals,inorganic chemicals and microorganisms. Fed. Reg.50:46937-47025 (November 13, 1985)

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987. Health Advisoryfor cis-l,2-pichloroethylene. Office of Drinking Water.Washington, D.C. March 31, 1987

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989. Integrated RiskInformation System (IRIS). Environmental Criteria andAssessment Office, Cincinnati, Ohio. May 1, 1989

FREUNDT, K.J., LIEBALDT, G.P., and LIEBERWIRTH, E. 1977.Toxicity studies on trans-1,2-dichloroethvlene. Toxicology7:141-153

FREUNDT, K.J., MACHOLZ, J. 1978. Inhibition of mixed functionoxidases in rat liver by trans- and cis-l,2-Dichloroethylene. Toxicology 10:131-139. (As cited in EPA1987)

IRISH, D.D. 1963. Vinylidene chloride. In Patty, F.A., ed.Industrial Hygiene and Toxicology. 2nd ed. John Wiley andSons, New York. Vol. II, pp. 1305-1309

QUAST, J.F., HUMISTON, C.G., WADE, L.E., BALLARD, J., BEYER,J.E., SCHWETZ, R.W., and NORRIS, J.M. 1983. A chronictoxicity and pncqgenicity study in rats and subchronictoxicity study in dogs on ingested vinylidene chloride.Fund. Appl. Toxicol,. 3:55-62. (As cited in EPA 1987)

TORKELSON, T.R., and ROWE, V.K. 1981. Halogenated aliphatichydrocarbons.. In Clayton, G.D., and Clayton, P.B., eds.Patty's Industrial Hygiene and Toxicology. 3rd ed. JohnWiley and Sons, New York. Vol. 2B, pp. 3550-3555

Dichlorofluoromethane . . . . _ _ .

AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS(ACGIH). 1986. Documentation of the Threshold Limit Valuesand Biological Exposure Indices. 5th Edition. Cincinnati,Ohio

AVIADO, D.M., and SMITH, D.G. 1975. Toxicology. 3:241

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BELEJ, M.A., and AVIADO, D.M. 1975. J. Clin. Pharmacol. 15:105

BOOTH, H.S., and BIXBY, E.M. 1932. Ind. Eng. Chem. 24:637

NUCKOLLS, A.H. 1935. Miscellaneous Hazard No. 2630,Underwriters' Lab. Report

TROCHIMOWICZ, H. J. , LYON, J.P. , KELLY, D.P. , and CHIU, T. 1977.Presented at 16th Annual Meeting of the Society ofToxicology; abstr. Tox. Appl. Pharm. Pp. 200

WEIGAND, W. 1971. Zentralbl. Arbeitsmed. Arbeitsschutz . 21:149

BARDODEJ, Z., and BARDODEJOVA, E. 1970, Biotrans format ion ofethylbenzene, styrene, and alpha-methylstyrene in man. Am.Ind. Hyg. Assoc. J. 31:206-209

CHIN, B.H., McKELVEY, J.A. , TYLER, T.R, , CALISTI, L.J., KOZBELT,S,J., and SULLIVAN, L.J. 1980. Absorption, distributionand excretion of ethylbenzene, ethylcyclohexane and methylethylbenzene isomers in rats. Bull. Environ. Contam.Toxicol. 24:477-483

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987. Health Advisoryfor Ethylbenzene, Office of Drinking Water, Washington,D.C. March 1987


HARDIN, B.D., BOND, G.P., SIKOV, M.R. , ANDREW, F.D., BELILES,R.P., andNIEMEIER, R,W. 1981. Testing of selected workplacechemicals for teratogenic potential. Scand. J. WorkEnviron. Health 7:66-75

WOIiF, M.A. , ROWE, V.K. , McCOLLISTER, D.D. , HOLLINGSWORTH,and OYEN, F.

1956. Toxicological studies of certain alkylated benzenesand benzene. Arch. Ind. Health 14:387-398

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4-Methvl phenol fp-cresoli_____

DEICHMANN, W.B., and KEPLINGER, M.L. 1981. Phenols and phenoliccompounds. In Clayton, G., and Clayton, F., eds. Patty'sIndustrial Hygiene and Toxicology. 3rd ed. John Wiley andSons, New York. Vol 2A, pp. 2597-2601

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984. Health EffectsAssessment for Cresols. Environmental Criteria andAssessment Office, Cincinnati, Ohio, and Office of Emergencyand Remedial Response, Washington, D.C. September 1984.EPA/540/1-86-050

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1986. o, &, p-Cresol.90-Day Oral Subchronic Toxicity Studies in Rats. Office ofSolid Waste, Washington, D.C.

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987. o, &/ £-Cresol.90-Day Oral Subchronic Neurotoxicity Study in Rats. Officeof Solid Waste, Washington, D.C.

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1988. Integrated RiskInformation System (IRIS). Environmental Criteria andAssessment Office. Cincinnati, Ohio. Revised August 22,1988

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).1978. Criteria for a Recommended Standard—OccupationalExposure to Cresol. U.S. DHEW, PHS/CDC. U.S.GovernmentPrinting Office, Washington, D.C. February 1978

PRESLEY, J.,-and BROWN, W. 1956. Lysol-induced criminalabortion. Obstet. Gynecol. 8:368-370

VANCE, B. 1945. Intrauterine injection of Lysol as anabortifacient. Report of a fatal case complicated by oilembolism and Lysol poisoning. Arch. Pathol. 40:395-398

Methvlene Chloride fpichloromethane)

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1980. Ambient WaterQuality Criteria for Halomethanes. Office of WaterRegulations and Standards, Criteria and Standards Division,Washington, D.C. October 1980. EPA 440.5-80-051

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985a. Health AssessmentDocument for Dichloromethane. Office of Health and

. Environmental Assessment, Washington, D.C. February 1985.EPA/600/8-82004F - . . . . . .

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ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985b. Addendum to theHealth

Assessment Document for Dichloromethane. Office of Healthand Environmental Assessment, Washington, D.C. September1985. EPA/600/8-82-004F ... - _

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989a. Integrated RiskInformation System (IRIS). Environmental Criteria andAssessment Office, Cincinnati, Ohio. Revised May 1, 1989

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989b. Health EffectsAssessment Summary Tables. Prepared by Office of Health andEnvironmental Assessment. Environmental Assessment andCriteria Office, Cincinnati, Ohio, for the Office of SolidWaste and Emergency Response, Office of Emergency andRemedial Response, Washington, D.C. March 1989

NATIONAL COFFEE ASSOCIATION (NCA). 1982. Twenty-four MonthChronic Toxicity and Oncogenicity Study of MethyleneChloride in Rats. Final Report. Prepared by HazeltonLaboratories America, Inc., Vienna, Virginia. August 11,1982

NATIONAL COFFEE ASSOCIATION (NCA). 1983. Twenty-fourth-MonthOncogenicity

Study of Methylene Chloride in Mice. Unpublished reportprepared by Hazelton Laboratories, Inc., Vienna, Virginia

NATIONAL TOXICOLOGY PROGRAM (NTP). 1986. NTP Technical Reporton the

Toxicology and Carcinogenesis Studies of Dichloromethane inF344/N Rats and B6C3F1 Mice (Inhalation Studies). NTP TR306

NITSCHKE, K.D., BURED, J.D., BELL, T.J., et al. 1988. MethyleneChloride: A 2 year inhalation toxicity and Oncogenicitystudy in rats. Fund. Appl. Toxicology (in press) (as citedby EPA 1989b)

Polvcyclic Aromatic Hydrocarbons fNoncarcinogenic)

ENVIRONMENTAL PROTECTION AGENCY (EPA). 19$4a. Health EffectsAssessment for Polycyclic Aromatic Hydrocarbons (PAHs).Environmental Criteria and Assessment Office, Cincinnati,Ohio. September 1984. EPA 540/1-86-013

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984b. Health EffectsAssessment for Naphthalene. Environmental Criteria andAssessment Office, Cincinnati, Ohio. September 1984. EPA540/1-86-014

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ENVIRONMENTAL PROTECTION AGENCY (EPAJ . 1986. _ Health andEnvironmental Effects Profile for Naphthalene,Environmental Criteria and Assessment Office, Cincinnati,Ohio

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989. Health EffectsAssessment Summary Tables, Prepared by Office of Health andEnvironmental Assessment, Environmental Assessment andCriteria Office, Cincinnati, Ohio, for the Office of Solid -Waste and Emergency Response, Office of Emergency andRemedial Response, Washington, D.C. March 1989

KAO, J.K., PATTERSON, F.K., and HALL, J. 1985. Skin penetrationand metabolism of topically applied chemicals in sixmammalian species including man: An in vitro study withbenzo[a]pyrene and testosterone. Toxicol. Appl. Pharmacol.81:502-516 (As cited in ATSDR 1987)

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).1977. Criteria for a Recommended Standard—OccupationalExposure to Coal Tar Products.. DHEW (NIOSH) 78-107

SCHMAHL, D. 1955. Testing of naphthalene and anthracene ascarcinogenic agents in the rat. Z. Krebsforsch. 60:697-710(German with English translation)

SANTODONATO, J., HOWARD, P., and BASU, D. 1981. Health andecological assessment of polynuclear aromatic hydrocarbons.J. Environ. Pathol. Toxicol. 5:1-3 64

Radioactive Compounds

ARCHER, V.E., WAGONER, J.K., LUNDIN, F.E. 1973. Cancer mortalityamong uranium mill workers. J Occup Med 15:11-14

ARCHER, V.E., WAGONER, J.K., LUNDIN, F.E. 1973b. Lung Canceramong uranium miners in the United States. Health Phys25:351-371.

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989. Integrated RiskInformation System. U.S. Environmental Protection Agency.Washington DC, January 1989.

GOTTLIEB, L.S., HUSEN, L.A. 1982. Lung cancer among Navajouranium miners. Chest 81:449-452. i

LUNDIN, F.E., LLOYD, W., SMITH, E.M,, et al. 1969. Mortality ofuranium miners in relation to ratiation exposure, hard rockmining and cigarette smoking 1950 through September 1967.Health Phys 16:571-578.

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LLOYD, g-D., WRENN, M.E., TAYLOR, G.N., et al. 1985. Toxicityof Ra and Z2STh relative to 226Ra for bone sarcoma inductionin beagles. Strahlentherapie [Sonderb] 80:65-69.

MAYS, C.W., LLOYD, R.D., TAYLOR, G.N., et al. 1987. Cancerincidence and lifespan vs. alpha-particle dose in beagles.Health Phys 52:617-624.

POLEDNAK, A.P., STEHNEY, A.F., LUCAS, H.F. 1983. Mortalityamong male workers at a thorium-processing plant. HealthPhys 44(Suppl 1):239-251.

RUNDO, J., KEANE, A.T., LUCAS, H.F.. et al. 1986. Current(1984) status of the study of 6RA in humans at the centerfor Human Radiobiology. Strahlentherapie [Sonderb] 80:14-21.

SACCOMANNO, G., YALE, C., DIXON, W. , et al. 1986. Anepidemiology analysis of the relationship between exposureto radon progeny, smoking and bronchogenic carcinoma in theuranium-mining population of the Colorado Plateau (USA) :1960-1980. Health Phys 50:605-618.

SAMET, J.M. , KUTVIRT, D.M. , WAXWEILER, R. J. , et al. 1984.Uranium mining and lung cancer in Navaho men. N Eng J Med310:1481-1484.

STEHNEY, A.F., POLEDNAK, A.P., RUNDO, J., et al. 1980 Healthstatus and body radioactivity of former thorium workers.Argonne, IL, Argonne Natl. Laboratory Anl. 80:37-44.

WEAST, R.C., ed. 1983. CRC handbook of chemistry and physics.64th ed. Boca Raton, FL: CRC Press, Inc., B149-B150.

WEAST, R., ed. 1985. CRC handbook of chemistry and physics.66th ed. Boca Raton, FL: CRC Press, B-146; B-440 to B-441,

WRENN, M.E., TAYLOR, G.N., STEVENS, W., et al. 1986. DOE life-span radiation effects studies in experimental animals atUniversity of Utah, Division of Radiobiology. In: Life-spanradiation effects in animals: What can they tell us?Conference: U.S. Department of Energy, 830951.

T trachloroethene

BUBEN, J.A., and O'FLAHERTY, E.J. 1985. Delineation of the roleof metabolism in the hepatotoxicity of trichloroethylene andperchloroethylene: A dose-effect study. Toxicol. Appl.Pharmacol. 78:105-122

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ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985b. Drinking WaterCriteria Document for Tetrachloroethylene. Office ofDrinking Water, Criteria and Standards Division, Washington,D.C. April 1985


ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989b. Health EffectsAssessment Summary Tables. Prepared by Office of Health andEnvironmental Assessment, Environmental Assessment andCriteria Office, Cincinnati, Ohio, for the Office of SolidWaste and Emergency Response, Office of Remedial Response,Washington, D.C. April 1989

INTERNATIONAL AGENCY FOR RESAERCH ON CANCER (IARC). 1979. IARCMonographs on the evaluation of the carcinogenic risks ofchemicals to humans. Vol. 20: Some HalogenatedHydrocarbons. World Health Organization, Lyon France

NATIONAL CANCER INSTITUTE (NCI). 1977. Bioassay ofTetrachloroethylene for

Possible Carcinogenicity. CAS No. 127-18-4. NCICarcinogenesis Technical Report Series No. 13, Washington,D.C. DHEW (NIH) Publication No. 77-813

NATIONAL TOXICOLOGY PROGRAM (NTP). 1986. Toxicology andCarcinogenesis

Studies of Tetrachloroethylene (Perchloroethylene) (CASNo. 127-18-4) in F344/N Rats and B6C3F1 Mice (InhalationStudies). NTP Technical Report Series No. 311, ResearchTriangle Park, North Carolina. DHEW (NIH) PublicationNo. 86-2567

SCHWETZ, B.A., LEONG, B.K.J., and GEHRING, P.J. 1975. Theeffect of maternally inhaled trichloroethylene,perchloroethylene, methyl chloroform, and methylene chlorideon embryonal and fetal development in mice and rats.Toxicol. Appl. Pharmacol. 55:207-219

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STEWART, R.D., HAKE, C.L., FORSTER, H.V., LEBRUN, A.J., PETERSON,J.F., and WU, A. 1974. Tetrachloroethylene: Developmentof a biologic standard for the industrial worker by breathanalysis. Medical College of Wisconsin, Milwaukee,Wisconsin. NIOSH-MCOW-ENUM-PCE-74-6

Toluene

CHEMICAL INDUSTRY INSTITUTE OF TOXICOLOGY (CUT). 1980. ATwenty-Four Month Inhalation Toxicology Study in Fischer 344Rats Exposed to Atmospheric Toluene. Executive Summary andData Tables. October 15, 1980

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985. Drinking WaterCriteria Document for Toluene, Final Draft. Office ofDrinking Water, Washington, D.C. March 1985

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987. Health Advisoryfor Toluene. Office of Drinking Water, Washington, D.C.March 1987


ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989b. Health EffectsAssessment Summary Tables. Prepared by Office of Health andEnvironmental Assessment, Environmental Assessment andCriteria Office, Cincinnati, Ohio, for the Office of SolidWaste and Emergency Response, Office of Emergency andRemedial Response, Washington, D.C. April 1989

E&NNINEN, H., ESKELININ, L., HUSMAN, K., and NURMINEEN, M. 1976.Behavioral effects of long-term exposure to a mixture oforganic solvents. Scand. J. Work Environ. Health 2:240-255(As cited in EPA 1987)

HUDAK, A., and UNGVARY, G. 1978. Embryotoxic effects of benzeneand its methyl derivatives: Toluene, xylene. Toxicology11:55-63

KIMURA, E.T., SBERT, D.M., and DODGE, P.W. 1971. Acute toxicityand limits of solvent residue for sixteen organic solvents.Toxicol. Appl. Pharmacol. 19:699-704

NAWROT, P.S., and STAPLES, R.E. 1979. Embryo-fetal toxicity andteratogenicity of benzene and toluene in the mouse.Teratology 19:41A

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VON OETTINGEN, W.F., NEAL, P.A., DQNAHUE, D.D., et al. 1942a.The Toxicity and Potential Dangers of Toluene, with SpecialReference to its Maximal Permissible Concentration. PHSPublication No. 279. P. 50 (As cited in EPA 1987)

VON OETTINGEN, W.F., NEAL, P.A., DONAHUE, D.D., et al. 1942b.The toxicity and potential dangers of toluene—preliminaryreport. J. Am- Med. Assoc. 118:579-584 (As cited in EPA1987)

1,1.1-Trichloroethane _ . . . . . , . _ . . . . . . . . . . .

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984, Health EffectsAssessment for 1,1,1-Trichloroethane. Final Draft.Environmental Criteria and Assessment Office, Cincinnati,Ohio. Septe_aber 1984. ECAO-CIN-H005

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985. Drinking WaterCriteria for 1,1,1-Trichloroethane (Draft). Office ofDrinking Water, Criteria and Standards Division, Washington,D.C. January 1985

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989a. Integrated RiskInformation System (IRIS). Environmental Criteria andAssessment Office, Cincinnati, Ohio. Revised July l, 1989

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989b. Health EffectsAssessment Summary Tables. Prepared by the Office of Healthand Environmental Assessment, Environmental Assessment andCriteria Office, Cincinnati, Ohio for the Office of SolidWaste and Remedial Response, Office of-Emergency andRemedial Response, Washington, D.C, April 1989

NATIONAL TOXICOLOGY PROGRAM (NTP). 1984. Annual Plan for FiscalYear 1984. DHHS, Public Health Service, Research TrianglePark, North Carolina. NTP-84-Q23

TORKELSON, T.R., OYEN, F., McCOI<LISTER, D.D., and ROWE, V.K.1958. Toxicity of 1,1,1-trichloroethane as determined onlaboratory animals and human subjects. Am. Ind. Hyg. Assoc.J. 19:353-362

Trichloroethene .„ ......... .....__ - .

AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS(ACGIH). 1986. Documentation of the Threshold Limit Valuesand Biological Exposure indices. 5th ed. ACGIH,Cincinnati, Ohio

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ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984. Health EffectsAssessment for Trichloroethylene. Environmental Criteriaand Assessment Office, Cincinnati, Ohio. EPA 540/1-86-046

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985. Health AssessmentDocument for Trichloroethylene. Environmental Criteria andAssessment Office. Research Triangle Park, North Carolina.EPA/600/8-82/006F

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987. Health Advisoryfor Trichloroethylene. Office of Drinking Water,Washington, D.C. March 31, 1987

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989. Integrated RiskInformation System (IRIS). Environmental Criteria andAssessment Office, Cincinnati, Ohio. Revised May 1, 1989

FUKUDA, K., TAKEMOTO, K., and TSURUTA, H. 1983. Inhalationcarcinogenicity of trichloroethylene in mice and rats. Ind.Health 21:243-254

GREIM, H., BIMBOES, D., EGERT, G., GIGGELMANN, W., and KRAMER, M.1977. Mutagenicity and chromosomal aberrations as ananalytical tool for in vitro detection of mammalian enzyme-mediated formation of reactive metabolites. Arch. Toxicol.39:159

KIMMERLE, G., and EBEN, A. 1973. Metabolism, excretion andtoxicology of trichloroethylene after inhalation. 1.Experimental exposure on rat. Arch. Toxicol. 30:115

KJELLSTRAND, P., HOLQUIST, B. , ALM, P., KANJE, M. , ROMARE, S.,JONSSON, I., MANNSON, L. , and BJERKEMO, M. 1983.Trichloroethylene: Further studies of the effects on bodyand organ weights and plasma butyl cholinesterase activity _in mice. Acta. Pharmacol. Toxicol. 53:375-384 (As cited inEPA 1985)

NATIONAL CANCER INSTITUTE (NCI). 1976. Carcinogenesis Bioassayof Trichloroethylene. CAS No. 79-01-6. CarcinogenesisTechnical Report Series No. 2. PB-264 122

NATIONAL TOXICOLOGY PROGRAM (NTP). 1983. Carcinogenesis Studiesof Trichloroethylene (Without Epichlorohydrin), CASNo. 79-01-6, in F344/N rats and B6C3F- mice (GavageStudies). Draft. August 1983. NTP 51-84, NTP TR 243.

STEPHENS, C. 1945. Poisoning by accidental drinking oftrichloroethylene. Br. Med. J. 2:218

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AMERICAN CONFERENCE .OF GOVERNMENTAL INDUSTRIAL HYGIENISTS(ACGIH). 1986. Documentation of the Threshold Limit Valuesand Biological Exposure Indices. 5th Edition. Cincinnati,Ohio - -— -— ---------- - —-——

ADIR, J., BLAKE, D.A., and MERGNER, G.M. 1975. J. Clin.Pharmacol. 15:760

AVIADO, D.M. 1975. Toxicology 3:311

BARRAS, C.E. 1974. Unpublished data. Haskell Laboratory,DuPont Co., Wilmingtbn, DE. October 1974

CLARKE, D.G., and TINSTON, D.J. 1972. Proc. Eur. Soc. DrugToxicity 13:212 .._.._ _ .._ . ______ _ _

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989. Health EffectsAssessment Summary Tables. Prepared by Office of Health andEnvironmental Assessment, Environmental Assessment andCriteria Office, Cincinnati, Ohio, for the Office of SolidWaste and Emergency Response, Office of Emergency andRemedial Response, Washington, D.C. April 1989

FLOWERS, N.C., HAND, R.C., and HORAN, L.G. 1975. Arch. Env.Health- 30:353_ ..... .. . : : . . - . : : . ,/.-.:.

HOOD, D.B. 1964. Unpublished data. Haskell Laboratory, DuPontCo., Wilmington, DE. September 1964

JENKINS, L.J., JONES, R.A., COON, R.A., and SIEGEL, J. 1970.Tox. Appl. Pharm. 16:133

LESTER, D., and GREENBERG, L*A. 1950. Arch. Ind. Hyg. Occup.Med. 2:335

MERGNER, G.W., BLAKE, D.A., and HELRICH, M. 1975.Anesthesiology 42:345

NATIONAL CANCER INSTITUTE (NCI). 1978. Bioassay ofTrichlorofluoromethane for Possible Carcinogenicity. NCICarcinogenesis Tech. Rep. Ser. No. 106. (Also publ as DHEW(NIH) 78-1356)

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PAULET, G., RONCIN, G., and VIDAL, E., et al. 1975. Tox. Apl.Pharm. 34:197

QUEVAUVILLER, A., SCHRENZEL, M., and HUYEN, V.N. 1964. Therapie19:247

REINHARDT, C.F., AZAR, A., and MAXFIELD, ME., et al. 1971.Arch. Env. Health. 22:265

SCHOLZ, J. 1962. Fortschr. Biol. Aerosolforsch. Jahren1957-1961. Ber. Aerosol-Kongr. 4:420

SLATER, T.F. 1965. Biochem. Pharmacol. 14:178

TAYLOR, G.J. 1975. Arch. Env. Health. 30:349

TAYLOR, G.J., and DREW, R.T. 1975. Tox. Appl. Pharm. 32:177

Vinyl Chloride

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984. Health EffectsAssessment for Vinyl Chloride. Environmental Criteria andAssessment Office, Cincinnati, Ohio. September 1984. EPA540/1-86-036

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985. Drinking WaterCriteria Document on Vinyl Chloride. Final-Draft. Officeof Drinking Water, Washington, D.C. January 1985

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987. Memo from SandraLee (Program Manager, Regional Support Team, ToxicsIntegration Branch) to Addresses, Subject: UpdatedReference Dose and Cancer Potency Numbers for Use in RiskAssessments. Office of Solid Waste and Emergency Response,Washington, D.C. October 1984. 19 pp.

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989. Health EffectsAssessment Summary Tables. Prepared by the Office of Healthand Environmental Assessment, Environmental Assessment andCriteria Office, Cincinnati, Ohio, for the Office of SolidWast© and Remedial Response, Office of Emergency andRemedial Response, Washington, D.C. April 1989

FERON, V.J., SPEEK, A.J., WILLIAMS, M.I., VAN BATTUM, D., and DEGROOT, A.F. 1975. Observations on the oral administrationand toxicity of vinyl chloride in rats. Food. Cosmet.Toxicol. 13:633-638

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FERON, V.J., HENDRIKSEN, C.F.M., SPEEK, A.J., TIL, H.P., andSPIT, B.J. 1981. Lifespan oral toxicity study of vinylchloride in rats. Food Cosmet. Toxicol. 19:317-333

INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (IARC). 1979. IARCMonographs on the Evaluation of the Carcinogenic Risks ofChemicals to Humans. Some Halogenated Hydrocarbons. WorldHealth Organization, Lyon, France. " Vol. 20

MALTONI, C., G. LEFEMINE, A. CILIBERTI, et al. 1980. Vinylchloride carcinogenicity bioassays (BT project) as anexperimental model for risk identification and assessmentin environmental and occupational Carcinogenesis.Epidemiol. Anim. Epidemiol. Hum: Cas Chlorure VinyleMonomere. Reun Club Cancerog. Chim. 20th, Meeting Date1979. Publ Essent, Paris, France. Pp. 11-112

MALTONI, C., G. LEFEMINE, A. CILIBERTI, et al. 1981.Carcinogenicity bioassays of vinyl chloride monomer: Amodel of risk assessment on an experimental basis. Environ.Health-Perspect. 41:329

Xylenes - , -,'.:..; —.,:- --

BOWERS, D.E., Jr., CANNON, M.S., and JONES, D.H. 1982.Ultrastructural changes in livers of young and aging ratsexposed to methylated benzenes. Am. J. Vet. Res. 43:679-683

CARPENTER, C.P., KINKEAD, E.R. , GEARY, D.L. , Jr., SULLIVAN, L.J.,and KING, J.M. 1975. Petroleum hydrocarbon toxicitystudies: V. Animal and human response to vapors and mixedxylenes. Toxicol, Appl. Pharmacol. 33:543-558

ENVIRONMENTAL PROTECTION AGENCY (EPA) . 1985. Drinking WaterCriteria Document for Xylenes (Final Draft). EnvironmentalCriteria and Assessment Office, Cincinnati, Ohio. March1985. ECAO-CIN-416. EPA 600/X-84-185-1

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987. Health Advisoryfor Xylenes. Office of Drinking Water, Washington, D.C.March 1987

ENVIRONMENTAL PROTECTION AGENCY (EPA) . 1989a. Integrated RiskInformation System (IRIS). Environmental Criteria andAssessment Office, Cincinnati, Ohio. Revised May 1, 1989

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ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989b. Health EffectsAssessment Summary Tables. Prepared by Office of Health andEnvironmental Assessment, Environmental Assessment andCriteria Office, Cincinnati, Ohio, for the Office of SolidWaste and Emergency Response, Office of Emergency andRemedial Response, Washington, D.C. April 1989

MALTONI, C., CONTI, B., COTTI, G., and BELPOGGI, F. 1985.Experimental studies on benzene carcinogenicity at theBologna Institute of Oncology: Current results and ongoingresearch. Am. J. Ind. Med. 7:415-416

MIRKOVA, E,, ANTON, G., MIKHAILOVA, A., KHINKOVA, L., andBENCHEV, I.V,

1983. Prenatal toxicity to xylene. J. Hyg. Epidemiol.Microbiol. Immunol. 27:337-343

NATIONAL TOXICOLOGY PROGRAM (NTP). 1986. Toxicology andCarcinogenesis Studies of Xylenes (Mixed) [60% s-Xylene; 14%£-Xylene; 9% o-Xylene; 17% Ethylbenzene] in F344/N Rats andB6C3F. Mice (Gavage Studies). December 1986. NTP TR 327

SAVOLAINEN, K., RIIHIMAKI, V., SEPPALAINEN, A.M., and LINNOILA,M. 1980. Effects of short-term s-xylene exposure andphysical exercise on the central nervous system. Int. Arch.Occup. Environ. Health 37:205-217

TATRAI, E., UNGVARY, G., and CSEH, I.R. 1981. The effect oflong-term inhalation of o-xylene on the liver. Ind.Environ. Xenobiotics Proc. Int. Conf. Pp. 293-300

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INORGANICS

Aluminum __._._...__ __ ,..__ ,„_,_...„..... , ..„..._ -..-. -. —.

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985. National primarydrinking water regulation; synthetic organic chemicals,inorganic chemicals and microorganisms. Fed. Reg.50:46937-47025 (November 13, 1985)

GOYER, R.A. 1986. Toxic effects of metals. In Classen, C.D.,Amdur, M.D., and Doull, J., eds. Casarett and Doull'sToxicology. 3rd ed. MacMillan Publishing Co., New York

NATIONAL ACADEMY OF SCIENCE (NAS) . 1982. Drinking Water andHealth." 4 vols. National Academy Press, Washington, D.C.

Barium . _.._ . . . . . . . . . .

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984. Health EffectsAssessment for Barium. Environmental Criteria andAssessment Office, Cincinnati, Ohio, September 1984.EPA 540/1-86-021

ENVIRONMENTAL PROTECTION AGENCY" (EPA) . 1989a. Integrated RiskInformation System (IRIS). Environmental Criteria andAssessment Office. Cincinnati, Ohio. Revised July 1, 1989

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989b. Health EffectsAssessment Summary Tables. Prepared by Office of Health andEnvironmental Assessment, Environmental Assessment aridCriteria Office, Cincinnati, OH, for the Office of SolidWaste and Emergency Response, Office of Emergency andRemedial Response, Washington, D.C. April 1989.

GOYER, R.A. 1986. Toxic effects of metals. In Klaasen, C.D.,Amdur, M.D., and Doull, J., eds. Casarett and Doull'sToxicology: The Basic Science of Poisons. 3rd ed.Macmillan Publishing Co., New York. Pp. 623-624

PERRY, H.M., KOPP, S. J., ERLANGER, M.W., and PERRY, E.G. 1983.XVII. Cardiovascular effects of chronic barium ingestion.In Hemphill, D.D., ed. Proceedings of lie University ofMissouri's 17th Annual Conference of Trace Substances inEnvironmental Health. University of Missouri Press,Columbia, Missouri (As cited in EPA 1984)

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' AR303663

iSENKO, M., PROMIN, O., and SILAYEV, A. 1977. Bariumcompounds as industrial poisons (an experimental study).J. Hyg. Epiderm. Microbial. Immunol. 21:361 (As cited in EPA1984)

CALIFORNIA DEPARTMENT OF HEALTH SERVICES (CDHS). 1986. Reportto the Scientific Review Panel on Cadmium. Part B. HealthEffects of Cadmium. Revised. Prepared by theEpidemiological Studies and Surveillance Section, Berkeley,California. September 19, 1986

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1980. Ambient WaterQuality Criteria Document for Cadmium. Prepared by theOffice of Health and Environmental Assessment, EnvironmentalCriteria and Assessment Office, Cincinnati, Ohio for theOffice of Water Regulations and Standards, Washington, D.C.EPA 440/5-80-025

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985a, Drinking WaterCriteria Document for Cadmium. Final Draft. Office ofDrinking Water, Washington, D.C. April 1985. PB86-117934

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985b. UpdatedMutagenicity and Carcinogenicity Assessment of .Cadmium.Addendum to the Health Assessment Document for Cadmium (May1981; EPA/600/8-81/023). Office of Health and EnvironmentalAssessment, Washington, D.C. June 1985. EPA 600/8-83-025F

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987. Health Advisoryfor Cadmium. Office of Drinking Water, Washington, D.C.March 31, 1987

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989a. Integrated RiskInformation System (IRIS). Environmental Criteria andAssessment Office, Cincinnati, Ohio. August l, 1989

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989b. Health EffectsAssessment Summary Tables. Prepared by Office of Health andEnvironmental Assessment, Environmental Assessment andCriteria Office, Cincinnati, Ohio for the Office of SolidWaste and Emergency Response, Office of Emergency andRemedial Response, Washington, D.C. April 1989

FRIBERG, L. , PISCATOR, M., NORDBERG, G.F., and KJELLSTROM, T.1974. Cadmium in the Environment. 2nd ed. CRC Press,Inc., Boca Raton, Florida

A-67

AR30366t*

THUN, M.J., SCHNORR, T.M., SMITH, A.B., HALPERIN, W.E. , andLEMEN, B.A. 1985. Mortality among a cohort of U.S. cadmiumproduction workers—an update. JNCI 74:325-333

Cobalt

GILMAN, J.P.W. 1962. Metal Carcinogenesis: II. A study oncarcinogenic activity of cobalt, copper, iron, and nickelcompounds. Cancer Res. 22:158-165

HAMMOND, P.B., and BELILES, R,P, 1980. Metals. In Doull, J.,Klassen, C.D., and Amdur, M.O., eds. Casarett and Doull'sToxicology: The Basic Science of Poisons. 2nd ed.Macmillian Publishing Co., New York

HEATH, J.C. 1960. The histogenesis of malignant tumors inducedby cobalt in the rat. Br. J. Cancer 14:478-482

LEONARD, P., GERBER, G.B, , JACQUET, P. , and LAUWERYS, R.R. 1984,Mutagenicity, Carcinogenicity and Teratogenicity ofIndustrially Used Metals. In Kirsch-Volders, M., ed.Mutagenicity, Carcinogenicity and Teratogenicity ofIndustrial Pollutants. Plenum Press, New York. Pp. 59-126

NATIONAL RESEARCH COUNCIL (NRC) . 1977 Drinking Water andHealth. National Academy of Sciences, Washington, D.C.

SHEPARD, T.H. 1986. Catalog of Teratogenic Agents. 5th ed.Johns Hopkihs University Press, Baltimore. P. 380

STOKINGER, H.E. 1981. The Metals. In Clayton, C.P., andClayton, P.B., eds. Patty's Industrial Hygiene andToxicology. 3rd_ed, John Wiley and Sons, New York. Vol.2A •" "-"-

Cyanides , 7 ;

DIPALMA, J.R., ed. 1971. Noxious gases and vapors: I. Carbonmonoxide, cyanides, methemoglobin, and sulfhemoglobin. InDrill's Pharmacology in Medicine. McGraw-Hill Book Co., NewYork. Pp. 1189-1205

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985. Drinking WaterCriteria Document for Cyanide (Final Draft). EnvironmentalCriteria and Assessment Office, Cincinnati, Ohio. EPA600/X-84-192-1. PB86-117793

A-68

AR303665

ENVIRONMENTAL PROTECTION AGENCY (EPA) . 1989a. Integrated RiskInformation System (IRIS). Environmental Criteria andAssessment Office, Cincinnati, Ohio. Revised June 1, 1989

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989b. Health EffectsAssessment Summary Tables. Prepared by Office of Health andEnvironmental Assessment, Environmental Assessment andCriteria Office, Cincinnati, Ohio for the Office of SolidWaste and Emergency Response, Office of Emergency andRemedial Response, Washington, D,C. March 1989

HOWARD, J.W. and HANZAL, R.F. 1955. Chronic toxicity for ratsof food treated with hydrogen cyanide. J. Agric. Food Chem.3:325-329

NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH (NIOSH).1976. Criteria for a Recommended Standard—OccupationalExposure to Hydrogen Cyanide and Cyanide Salts (NsCN, KCN,and Ca(CN)2). Washington, D.C. DHEW (NIOSH) Publication No.77-108

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984. Health, EffectsAssessment for Iron. Environmental Criteria and AssessmentOffice, Cincinnati, Ohio. September 1984. ECAO-CIN-H054(Final Draft)

NATIONAL RESEARCH COUNCIL (NRC). 1980. Drinking Water andHealth. Safe Drinking Water Committee. National AcademyPress, Washington, D.C. Vol. 3, 415 pp.

VENUGOPAL, B. and LUCKEY, T.D. 1978. Metal Toxicity in MammalsIn Chemical Toxicity of Metals and Metalloids. PlenumPress, New York.

CENTERS FOR DISEASE CONTROL (CDC) . 1985. Preventing LeadPoisoning in Young Children. U.S. Department of Health andHuman Services. Atlanta, GA

DUGGAN, M.J. 1983. The uptake and excretion of lead by youngchildren. Arch. Env. Health 38147:246-247

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984. Health EffectsAssessment for Lead. Environmental Criteria and AssessmentOffice, Cincinnati, Ohio. EPA/540/1-86-055

A-69

RR303666

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985. National primarydrinking water regulations; synthetic.organic chemicals,inorganic chemicals and microorganisms. Fed. Reg. 50:46937-47025 (November 13, 1985)

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1986a. Guidelines forcarcinogenic risk assessment of chemical mixtures. Fed.Reg. 51:34014-34025 (September 24, 1986)

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1986b. Air QualityCriteria for Lead, office of Research and Development,Environmental Criteria and Assessment Office. ResearchTriangle Park, North Carolina. June 1986.EPA/600/8-83/023CF

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1988. Drinking WaterRegulations Maximum Contaminant Levels Goals and NationalPrimary Prinking Water Regulations for Lead and Copper;Proposed Rule. August 18, 1988. 53 FR 31516-31578

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989a. Integrated RiskInformation System (IRIS). Environmental Criteria andAssessment Office, Cincinnati, Ohio. Revised June 1, 1989

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989b. Review of theNational Ambient Air Quality Standards for Lead: ExposureAnalysis Methodology and Validation. Air Quality ManagementDivision, Office of Air Quality Planning and Standards,Research Triangle Park, NC 27711

HAMMOND, P.B., and BELILES, R.P. 1980. Metals. In: Casarettand Doull's Toxicology: The Basic Science of Poisons, 2ndEd., Doull, J., Klaassen, C.D., Amdur, M.O. (eds).MacMillan Publishing Co., New York, Toronto, and London.Pp. 421-428

Manganese

ENVIRONMENTAL PROTECTION AGENCY (EPA) . 1984a. Health AssessmentDocument for Manganese. Final Report. EnvironmentalCriteria and Assessment Office, Environmental ProtectionAgency, Cincinnati, Ohio. August 1984. EPA 600/8-83-013F

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984b. Health EffectsAssessment for Manganese (and compounds). EnvironmentalCriteria and Assessment Office, Washington, D.C.EPA 540/1-86-057

A-70

AR303667

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1986. Guidelines forcarcinogen risk assessment. Fed. Reg. 51:33992-34003(September 24, 1986)

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989. Health EffectsAssessment Summary Tables. Prepared by Office of Health andEnvironmental Assessment, Environmental Assessment andCriteria Office, Cincinnati, Ohio, for the Office of SolidWaste and Emergency Response, Office of Emergency andRemedial Response, Washignton, D.C. March 1989

KAWAMURA, R., IKUTA, H. , FUKUZUMI, S., et al. 1941.Intoxication by manganese in well water. Kitasato Arch.Exp. Med. 18:145-149

LAI, J.C.K,, LEUNG, T.K.C., and LIM, L. 1982 Activities of themitochondrial NAD-linked isocitric dehydrogenase indifferent regions of the rat brain. Changes in aging andthe effect of chronic manganese chloride administration.Gerontology 28:81-85

LEUNG, T.K.C., LAI, J.C.K., and LIM, L. 1981. The regionaldistribution of monoamine oxidase activities towardsdifferent substrates: Effects in rat brain of chronicadministration of manganese chloride and of aging.J. Neurochem. 36:2037-2043

SARIC, M., MARKICEVIC, S., and HRUSTIC, O. 1977. Occupationalexposure to manganese. Br. J. Ind. Med. 34:114-118

Mercury

DRUET, P., DRUET, E., POTDEVIN, F., and SAPIN, C. 1978. Immunetype glomerulonephritis induced by HgCl2 in the brown Norwayrat. Ann. Immunol. 129C:777-792

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1980. Ambient WaterQuality Criteria Document for Mercury. Prepared by theOffice of Health and Environmental Assessment, EnvironmentalCriteria and Assessment Office, Cincinnati, Ohio for theOffice of Water Regulation and Standards, Washington, D.C.SPA 440/5-80-058. NTIS PB 81-117699

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984. Health EffectsAssessment for Mercury. Environmental Criteria andAssessment Office, Cincinnati, Ohio. EPA 540/1-86-042

A-71

AR303668

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989. Health EffectsAssessment Summary Tables. Prepared by Office of Health andEnvironmental Assessment "Environmental Assessment andCriteria Office, Cincinnati, Ohio, for the Office of SolidWaste and Emergency Resposne, Office of Emergency andRemedial Response, Washington, D.C. March 1989

FITZHUGH, O.G., NELSON, A.A., LAUG, E.P., and .KUNZE, F.M. 1950.Chronic oral toxicities of mercury-phenyl and mercuricsalts. Arch. Ind. Hyg. Occup. Med 2:433-441

HAMMOND, P.B., and BELILES, R.P. 1980. Metals. In Doull, J.,Klaassen, C.D., and Amdur, M.O., eds. Casarett and Doull'sToxicology: The Basic Science of Poisons. 2nd ed.Macmillan Publishing Co., New York. Pp. 421-428

LEONARD, A., GERBER, G.B., JACQUET, P., and LAUWERYS, R.R. 1984.Mutagenicity, carcinogenicity, and teratogenicity ofindustrially used metals. In Kirsch-Volders, M., ed.Mutagenicity, Carcinogenicity and Teratogenicity ofIndustrial Pollutants. Plenum Press, New York. Pp. 59-126

RAHOLA, T., HATTULA, T. , KORLAINEN, A., AND MIETTINEN, J.K.1971, The biological half time of inorganic mercury (Hg ) inman. Scand. J. Clin. Invest. 27(suppl. 116):77 (Abstract)

TASK GROUP ON METAL ACCUMULATION. 1973. Accumulation of toxicmetals with special reference to their absorption, excretionand biological halftimes. Environ. Phys. Biochem. 3:65-67

WORLD HEALTH ORGANIZATION (WHO). 1976. Environmental HealthCriteria, Mercury, Geneva

Nickel " " " ;."""

AMBROSE, A.M., LARSON, P.S., BORZELLECA, J.R., and HENNIGAR, G.R.1976. Long-term toxicologic assessment of nickel in dogsand rats. J. Food Sci, Technol. 13:181-187

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1986, Health AssessmentDocument for Nickel and Nickel compounds. Office of Healthand Environmental Assessment, Research Triangle Park, NorthCarolina. EPA 600/8-83-012FF

ENVIRONMENT.. PROTECTION AGENCY (EPA) . 1987. Health Advisoryfor Nickel. Office for Drinking Water, Washington, D.C.March 31, 1987

A-72

AR303669

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989. Integrated RiskInformation system (IRIS). Environmental Criteria andAssessment Office, Cincinnati, Ohio. August 1, 1989

Vanadium

BROWNING, E. 1969. Toxicity of Industrial Metal. 2nd ed.Appleton-Century-Crofts, New York

ENVIRONMENTAL PROTECTION AGENCY (EPA). 1989a. Integrated RiskInformation System (IRIS). Health Criteria and AssessmentOffice, Cincinnati, Ohio. Revised May 1, 1989

ENVIRONMENTAL PROTECTION AGENCY (EPA) . 1989b. Health EffectsAssessment Summary Tables. Prepared by Office of Health andEnvironmental Assessment, Environmental Assessment andCriteria Office, Cincinnati, Ohio, for the Office of SolidWaste and Emergency Response, Office of Emergency andRemedial Response, Washington, D.C. March 1989

NATIONAL ACADEMY OF SCIENCES (NAS). 1974. Vanadium. Committeeon Biological Effects of Atmospheric Pollutants, Division ofMedical Sciences, National Research Council, Washington,D.C.

NATIONAL INSTITUTE OF OCCUPATIONAL SAFETY AND HEALTH (NIOSH).1977. Criteria for a Recommended Standard—OccupationalExposure to Vanadium. DHEW (NIOSH) Publication No. 77-222

SCHROEDER, J.A., MITCHNER, M., and NASON, A.P. 1970. Zirconium,niobium, antium, antimony, vanadium and lead in rats: Lifeterm studies. J. Nutr. 100(1):59-68

STOKINGER, H.E., WAGNER, W.E., MOUTAIN, J.T. , STACKSILL, F.R.,DOBROGORSKI, O.J., and KEENAN, R.G. 1953. UnpublishedResults. National Institute for Occupational Safety andHealth, Division of Occupational Health, Cincinnati, Ohio

A-73 *

flR303670

•o

a.ic

AR30367I

APPENDIX M

PLOTS OF RELATIVE CONCENTRATION VERSUS DISTANCE FOR THEMODERN LANDFILL-REMEDIAL INVESTIGATION

RR303672

RELATJVE-CONCENTFATfDN VS.'. DISTANCETRiCHLOROETHYLEÊ" .." " ":

0.9 -

O.S -

0.7.-

0.5 -oU\ 0.5 .-O

0.4 -

0.3 -

0.2 -

0,1 -

,, oar;• 1.2 ",. . i.e ._.,-" 2 2.4

(Thousands)DISTANCE (Feet)

D . 1987 - . . - - > • .--1958 - - .-" o ;_: 1939 .

NOTES 1) C/Co HAS BEEN CALCULATED USING THE AVERAGE OF FOURSAMPLING EVENTS DURING ONE YEAR AT EACH WELL, DIVIDEDBY THE HIGHEST OF THE YEARLY AVERAGES CALCULATEDFOR THE WELLS UNDER CONSIDERATION,

2) DISTANCE HAS BEEN MEASURED FROM THE LANDFILL BOUNDARYALONG THE INTERPRETED FLOW LINES. THE ESTIMATEDDISTANCES ARE LISTED BELOW :

MD120 300 Ft.

W60A 400 Ft.

W60 500 Ft.

MD119 550 Ft.

JOBNO 883-6158 SCALE NADRAWN pQ OATE 11/16/89

CHECKED 7,-ax D*° NC

Golder Associates

MD1 14S 1600 Ft.

MD115D 1610 Ft.

MD113S 2200 Ft.

MD114D 2210 Ft.

RELATIVE CONCENTRATION VERSUSDISTANCE

TRICHLOROETHYLENEMODERN LflMfly P^M-1

RELATIVE CONCENTRATION :VS DISTANCE. „ ~L

C-9 - 1

0.3 -

Qt -

0.6 -aux 0,5 -

0 a -

03 -

0-2 -

0 i -

o -J ——— . ——0

im^

C A 05

i

l

——————— l ————— * ————— i —————— : ————— tf ——————————— '

\.2 . T - s.-S . . ,— _.l- . .. _. 2.-

j

.. : ~ "

DISTANCE: crest) ' . . _ _ . _ .Q 1S3T •-

NOTES 1} C/Co HAS BEEN CALCULATED USING THE AVERAGE OF FSAMPLING EVENTS DURING ONE YEAR AT EACH WELL, Dl

J

OURVIDEO

BY THE HIGHEST OF THE YEARLY AVERAGES CALCULATEDFOR THE WELLS UNDER CONSIDERATION.

2} DISTANCE HAS BEEN MEASURED FROM THE LANDFILL BOUNDARYALONG THE INTERPRETED FLOW LINES. THE ESTIMATEDDISTANCES ARE LISTED BELOW :

MD120

W60A

W60

MD119

-OINO gg3.ei58 S

D**WM pQ C

CHCCKEC £#%, C

300 Ft.

400 Ft.

500 Ft.

550 Ft.

CAJ NA*'f 11/16/89WO NO

Golder Associates

MD1 14S 1600 Ft.

MD115D 1610 Ft.

MD113S 2200 Ft.

MD114D 2210 Ft.

RELATIVE CONCENTRATIONDISTANCE

VERÊ

1 , 1-DICHLOROETHANEMODERN LANDFILL lr:

fittJUJD/H-^ M-2

R E CAT! VETCaNCENJ RAT IQ N... V S. • D1STANf C E..._.1.1,1-TRlCHLORQETHANE ". .

O

0.4 -^— -0.8 , ..- 1,2 . -1.6 2 2.4(Thousands.) . . . . .

DISTANCE treefl " " ..a 1937" . .:".: -jr.. n- .1983 ..,:,.., .0../.1989.

NOTES 1) C/Co HAS BEEN CALCULATED USING THE AVERAGE OF FOURSAMPLING. EVENTS DURING ONE YEAR AT EACH WELL, DIVIDEDBY THE HIGHEST OF THE YEARLY AVERAGES CALCULATEDFOR THE WELLS UNDER CONSIDERATION.


MD120 300 Ft. MD114S 1600 Ft.

W60A 400 Ft. MD115D 1610 Ft.

W60 500 Ft. MD113S 2200 Ft.

MD119 550 Ft. MD114D 2210 Ft.

.oe NO 883-6 1 58DSAW" FGCHECKED

5CALE NAOATE 11/16/890*G N0

Golder Associates


1 , 1 , 1-TRICHLOROETHANE

RELATIVE CONCENT• i0-9 -

OS -

07 -

06 - *0 \u »

^ ° S " \0* - v

0 3 - \

02-j ^ ^

0-1 -I 0In I

RATION; vs" DISTANCE::

i

!

D _ . - -

i - m ~~ —

,'

; -

i

0 C * OS -e 1 -2 '4-s ' -& .„ . 2_ r _ 2~* . -_(Thcusahas;

D'ST nCE têei) \ ._!." . . . . . "a '-9ETV ... - " -*• ;. 1988 . , ._ . .^^

NOTES 1) C/Co HAS BEEN CALCULATED USING THE AVERAGE OF FOURSAMPLING EVENTS DURING ONE YEAR AT EACH WELL, DIVIDEDBY THE HIGHEST OF THE YEARLY AVERAGES CALCULATEDFOR THE WELLS UNDER CONSIDERATION.


MD120 300 Ft.

W60A 400 Ft.

W60 500 Ft.

MD119 550 Ft.

J0i*c 883-6158 SCA-E NA°**WN FG DiT£ 11/16/89CHECKED ffi*'Jt& Dws N°

Golder Associates

MD1 14S 1600 Ft.

MD115D 1610 Ft.

MD113S 2200 Ft.

MD114D 2210 Ft.

——— -RELATIVE CONCENTRATION VERS^

DISTANCE1 ,2-TR ANS-DICHLOROETHYLENE

MODERN LANDFILL 1 '-'= M-4flR303676

RE!1 ———————— \

0.9" - - - -- -

O.S - -

0.7 -

O.S - -— --oO -x 0.5 -U

0.4 - — - - -----

0,3 -

0.2 - - - -

0.1--

0 -| ————— i ——0

NOTES 1) C/Co HASAMPLIN

.AnVETCUNCE3\rrRATR2N. V5- DISTANCE _: T ~VINYL CHLQRIQE" ' ' . '

•

-,

— g om ; ———— , ———— ,— —— H ———— i ——— P ——— i ———— i ——— w ——— i ———— t0.4 -. . . 0.3_..._. ... .=__; _ ..1-2 ._ .".~_T_~__:; 1.5 , - . 2 2.4

(Thausarrcfs.) ~~ "DISTANCf (Feet) ~ ~ "

n; 19-87 _. ,+ ;1988.-=, _ --, - 9.-.. - 1989

S BEEN CALCULATED USING THE AVERAGE OF FOURG EVENTS DURING ONE YEAR AT EACH WELL, DIVIDED

BY THE HIGHEST OF THE YEARLY AVERAGES CALCULATEDFOR THE WELLS UNDER CONSIDERATION.


MD120

W60A

W60

MD119

JOBNO 883-6158 sDRAWN pQ 0

CHECKED 3s £S D

300 Ft.

400 Ft.

500 Ft.

550 Ft.

CALE NA

&TE 11/16/89WC NO

Colder Associates

MD1 14S 1600 Ft.

MD1 15D 1610 Ft.

MD1 13S 2200 Ft.

MD114D 2210 Ft.


VINYL CHLORIDEMODERN L^y I F l ; 7 -j"3""" M-5

e

RELATIVE ..CONCENTRATION VS DISJANCMETHYLENE CHLORIDE ~~ ~ ~.

X

0=4 0,6 1.2 " , 1.6 - .2-. - 2.4.(TFiouânds

DISTANCE (Feet)O 1987 _ * 1933. , _o 1989.

NOTES 1) C/Co HAS BEEN CALCULATED USING THE AVERAGE OF FOURSAMPLING EVENTS DURING ONE YEAR AT EACH WELL. DIVIDEDBY THE HIGHEST OF THE YEARLY AVERAGES CALCULATEDFOR THE WELLS UNDER CONSIDERATION.

2} DISTANCE HAS BEEN MEASURED FROM THE LANDFILL BOUNDARYALONG THE INTERPRETED FLOW LINES. THE ESTIMATEDDISTANCES ARE LISTED BELOW :

MD120 300 Ft. MD114S 1600 Ft.

W60A 400 Ft. MD115D 1610 Ft.

W60 500 Ft. MD113S 2200 Ft.

MD119 550 Ft. MD114D 2210 Ft.

JOBNO 883-6153FG

CHECKED

SC4..E NA11/16/89

OWC NO

RELATIVE CONCENTRATION VER!DISTANCE

METHYLENE CHLORIDEGolder Associates MODERN UWBRHit 7R!r:""r M-6

RE

0.9 - --- ---

0,8 - =--- ---

0.7 -| -

0.6 •- ... -.-.

o\ 0.5 r -O- - — --

0.4 - -

03-

H0 - ———— r—0

, — e- —— •• ——— " ' " - - • •-

- - -,----- --, -^- -_.=

\\

n

f?ATlS2N&VS. DISTANCE" " ; '.'..

i

.- - -.--. ,--;_ ._ . - . . . - . ; ,.--.

j

,

,

C-~ - - - O.S -_- ..« -, .l-2_ 1.6 - 2 2,4. . -("thousands"";? - -

D 19"S_7 "•" ".;-•1935,- . ,".; ' - . . . < > - .1989

NOTES 1) C/Co HAS BEEN CALCULATED USING THE AVERAGE OF FOURSAMPLING EVENTS DURING ONE YEAR AT EACH WELL. DIVIDEDBY THE HIGHEST OF THE YEARLY AVERAGES CALCULATEDFOR THE WELLS UNDER CONSIDERATION.


MD120

W60A

W60

MD119

.OB NO 883-6158MM* FGCHECK EC /-.pi/

300 Ft.

400 Ft.

500 Ft.

550 Ft.

SCAÊ NA

OATE 11/16/890*C NO

Golder Associates

MD1 14S 1600 Ft.

MD115D 1610 Ft.

MD113S 2200 Ft.

MD114D 2210 Ft.


TRICHLOROFLUOROMETHANEMODERN LAND U . "''* M-7

RELATIVE CONCENTRATION, VS DISTANCE"-.; :-:_ . . .£ALUMINUM

\ '09 - \

0=3 - o \\o

\o.& - \

0 \O x.\ o.s - \O " N.

0.4 - - ^

0.3 -

0,2 -

0=1 -

\' o ^ -^

0 . 0.4 0.8 -1-2 . 1 . 6 . . 2 2.4.(Thousands)

DISTANCE: (Feet) .. . ; _.3 1939 : '_. . • - -



MD120 300 Ft.

W60A 400 Ft.

W60 500 Ft.

MD119 550 Ft.

J°*N° 883-6158 SCAUE NAOT1W* FG DATE 11/16/89CHECKED fff/ S*G NO :

Golder Associates

MD1 14S 1600 Ft.

MD1 15D 1610 Ft.

MD113S 2200 Ft.

MD114D 2210 Ft.

RELATIVE CONCENTRATION VER ADISTANCEALUMINUM

MODERN fefttSRfSL SO FS-"E M-8

RELATTVE:rCON.C:E;NTRATLON""yS .DISTANCE.BARIUM . . ... .. '..

1

0.9 -

0.8 -

0.7 -

0.6" -

0.5--

0.4 -

-9—B

C;4~ . . ;- 0.5 ._ ' 1,2 " :.."-_. .1.6 . 2 2.4(Thousands)

DISTANCE T et)D- -19.37 -— .. - . 19,88 .,_.,... _ -i>_... ... 1989



MD120 300 Ft. MD1 14S 1600 Ft.

W60A 400 Ft. MD115D 1610 Ft.

W60 500 Ft. MD113S 2200 Ft.

MD119 550 Ft. MD114D 2210 Ft.

JOBNO 883-6158DR..WN

CHECKED tttftf

SCALE NADATE 1i/16/69

Dws N0

RELATIVE CONCENTRATION VERSUSDISTANCEBARIUM

Golder Associates MODERN LA$B6iQl3&8 t5" M-9

RELATIVE CONCENTRATION VS DISTANCEBARIUM

0,9 -

0,3 -

0=7

CJ

0 Q.* 0,8 1.2 ..=... 1.6 - Z „ - ' . . . 2.4(Thousands)

DISTANCE (FeeO . 1 " " ~_3 '937 - + 7988 . . ; O,.. .1939" " ... ",. -". " _ _ . „ . :

NOTES 1)THE GEOMETRIC MEAN OF THE BACKGROUND SAMPLES (35 >UQ/|) HAS BEENSUBTRACTED FROM ALL THE CONSIDERED CONCENTRATIONS.

2>C/Co HAS BEEN CALCULATED USING THE AVERAGE OF FOURSAMPLING EVENTS DURING ONE YEAR AT EACH WELL, DIVIDEDBY THE HIGHEST OF THE YEARLY AVERAGES CALCULATEDFOR THE WELLS UNDER CONSIDERATION.


MD120 300 Ft. MD114S 1600 Ft.

W60A 400 Ft. MD115D 1610 Ft.

W60 500 Ft. . MD113S 2200 Ft.

MD119 550 Ft. MD114D 2210 Ft.

Mti

J0i"° 883-6158MAWN —Q

CHcaccD fagg

»C*L6 NA

MTE 11/16/89owe NO

Colder Associates

RELATIVE CONCENTRATION VERSUSDISTANCEBARIUM

MODERN LAfttfrf.J--} & Q2ou"EM-10

•oT3O3Q.XZ

BR303683

APPENDIX N

EXPOSURE ASSESSMENT METHODOLOGY

AR30368U

. . EXPOSURE ESTIMATION METHODOLOGY

The purpose of this appendix is to present the methodology

used to estimate exposures in the risk assessment for the ModernLandfill site. - - - - - - _...—.-. - ._ ,_._,____.

B.I INGESTXON OF GROUNDWATER

The GDI estimates for ingestion of groundwater were calculatedas follows: - -- - . - ; _ _ _ _ . - . - _ - -•--.;

GDI = (Cw)(I)(P)(YR)

(BW) (DY) (YL)

where: — _ r

GDI = chronic daily intake (ing/kg/day);

CH - chemical concentration in groundwater (mg/liter);

I = amount of water ingested (liter/day);

F = frequency of exposure (days/yr);

YR = years of exposure (year);

BW = average body weight (kg) ;

DY......= —days in a year (365 days/year); and

YL = - -years in lifetime or in the period over which riskis being assessed (70 year lifetime for carcinogens,less than lifetime for noncarcinogens).

flR303685

B.2 DIRECT CONTACT WITH CONTAMINANTS IN SEDIMENTS

Chronic daily intake (GDI) estimates for incidental sediment

ingestion are calculated as follows:

GDI - « (YR)(BW) (DY) (YL)

where:

GDI « chronic daily intake (mg/kg/day) ;

Cs «• chemical concentration in sediment (mg/kg) ;

I « amount of sediment ingested (rag/day) ;

Al « relative oral absorption factor;

F — frequency of exposure (days/yr);

YR « years of exposure (years) ;

X « conversion factor (kg/106 mg) ;

Bff « average body weight (kg);

DY « days in a year (365 days/year); and

YL = years in lifetime or in the period over which riskis being estimated (70 year lifetime forcarcinogens, period of exposure for noncarcinogens).

•-2

AR303686

GDIs for dermal absorption of chemicals of potential concern

are calculated as follows:

_ (Cs) (CD) (F) (YR) (Z) (ABS)V_*J-/-i ' "~~ " - - -- ' . . _ - , . - - r_. - -

(BW) (DY) (YL)

where:

GDI ~ chronic daily intake (mg/kg/day);

Cs - chemical concentration in sediment (mg/kg);

CD = contact rate for sediment (ing/day) ;

F = "frequency of exposure (days/year);

YR = years of exposure;

Z - conversion factor (kg/106 mg) ;

ABS = dermal absorption factor;

BW ss - ' average body weight (kg) ;

DY = days in a year (365 days/year); and

YL = years in lifetime or in the period over which riskis being estimated (70 year lifetime forcarcinogens, period of exposure for noncarcinogens).

The total GDI associated with direct contact with sediments

is the sum of the GDIs from incidental ingestion and dermal

absorption.

flR303687

B.3 DIRECT CONTACT WITH CONTAMINANTS IN SURFACE WATER

Chronic daily intakes (GDIs) for direct surface water contact

are calculated as follows:

. (Csw) (Q) (SA) (P) (HRS) (F) (YR)

(BW) (DY) (YL)

wher©:

GDI •« chronic daily intake (mg/kg/day) ;

CSH » chemical concentration in surface water (ug/1) ;

Q — conversion factor (1/103 cm3) ;

SA » skin surface area exposed (cm2) ;

P •« water permeability rate constant (cm/hr) ;

HRS » hours exposed per day (hrs/day) ;

F =* frequency of exposure (days/year) ;

YR » years of exposure;

BW = average body weight (kg) ;

DY « days in a year (365 days /year) ; and

YL « years in lifetime or in the period over which riskis being estimated (70 year lifetime forcarcinogens, period of exposure for noncarcinogens) .

flR303688

Documents

Well No. MP-75 Boring No. X-Ref: sp-2 MONITOR WELL ... · _ 0-10-20 30 50 Well No. MP-75 Boring No. X-Ref: sp-2 MONITOR WELL CONSTRUCTION SUMMARY Survay Coords: N22992611724_____