plant site appendices b - l vineland, nj - records collections
TRANSCRIPT
PROGRAM
REMEDIAL PLANNING ACTIVITIES AT SELECTED UNCONTROLLED
HAZARDOUS SUBSTANCE DISPOSAL SITES
EPA CONTRACT 68-01-7250
EBASCO SERVICES INCORPORATED
EPA WORK ASSIGNMENT NUMBER: 37-2LB8 EPA CONTRACT NUMBER: 68-01-7250 EBASCO SERVICES INCORPORATED
VINELAND CHEMICAL COMPANY SITE FINAL DRAFT
REMEDIAL INVESTIGATION REPORT PLANT SITE
VINELAND, NEW JERSEY APPENDICES B - L
JUNE 1989
C??ED OR QUOTED Sf«D ' X S "BEING SLATED® OMTCOS "" '
8118b
APPENDICES B - L
B. Boring Logs - Monitoring Wells C. Boring Logs - Soil Borings
D. Monitoring Well Construction Sheets E. MW-10 Pumping Test Analysis
F* Groundwater Velocity Calculations For One-Dimensional Model
G. Laboratory Analysis For Chemical Extraction of Soils
H. Laboratory Analysis For Chemical Fixation of Soils I. Laboratory Analysis For Groundwater J. Toxicological Profiles
K* Water Balance Calculations
L. Vineland Chemical Company Monitoring Well Boring Logs
8118b
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VIN 001
1686
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BOAIHO HO. .
APPEND
IX C
IN 001
1740
APPENDIX C
BORING LOGS - SOIL BORINGS
6835b
»c«» LOG OF BORING
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LOG OF BORING / • «t|t
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M A O J T C T _
elevation ^- ' OIL C M*». N A S .
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LOG OF BORING t »wtft c
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C L C V A T I O N
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cut-m (c**> - q»0enn0.^-=36 ? • omimc i—5
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re«M •»« ca*»co stavicti log of boring i«cn
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ONOIN NO. 56 J'. • ONIN6 NO. J&IHS ^
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AP
PE
ND
IX D
VIN
0
01
1
77
1
APPENDIX D
MONITORING WELL CONSTRUCTION SHEETS
c VINE LAND CHEMICAL COMPANY SITE
IO*'NC NO'
OVERBURDEN MONITORING WEll SHEET
.EW ' I d
•ift.trr
(
r
MOJlCtiift 42*,.. ELEVATION. MELD GFOlOGf$T_T^ZjdaulCa
location iomng— date l- 'ir-fl
~ 1 a
GROUND IKVATlON - - TTRI 01 luiuci MAI' T
I-
I:
OiiUd OlilllNG METHOD•
j. /wz C--U*.
u!swjssi£ satut
IlIVATtON 0' TOR0' Su»'ACl CASING : IKVATlON Of TOR 0« UUI URt:
STiCK. UR TOR 0* SUifACI CASING: STICK- URiiSttRiRI: 5-'
ID ofsutricrCASING _ TtRi of SUK'ACI casing. r^t'lfel
3%' KiStRRiRllO , , , „ TTRI 0' KiSliRiRI Sl-U pv/>-
12zl •OKEHOLI DiAMITii
TTRt Of IACKRIU'.
IKVAT0N f DtRTH TO* OR HAL:
' TtRI Of SlAt: ggmraro-rc pl »(,
8Z '
• OiRTH TOR Of SAND RACK:
HtVATlON/DtRTHTOROfSCAIIN
TTRi Of SCAIIN scft fe 9vc bozo
93'
MOT SWiKNCTH
ID Of SCUtN __2J4
• TTRI Of UNO RACK •
IK VAT0N f DIRTH IOTTOM Of SCAKN.
Ill VAT0NI Of *TH iOTTOM 0» SAND *ACA: itri 0* iackini iiioaioastavai0n mi*... f-<lkj>c. *( eptjk
- |KvATlON'Ot**NOf NOll
icfr'
-
ips' < m z o o
-4 oj
<r £~0j- /a7
OVCRBUKDIN MONITORING WELL SHEET
|»»f\itrr ^?36. 3/3 IrAOJf CT Mft V<OHr-M I HE VATlON. iliiVAiiun • A - v 1 he 10 gf ologlst-^h^d &
location IQAING—•£ ^ , j— ia7s-ZZ^2$]55Z
C*OUNO IKVATlON
r ••
n
L i
~4
r*t . • •
wuii tt/^afcwi Sg EX£I ^_
III VAT ion 0» TO» or SUM ACE CASING: litVATlON or tor 0» mu r#t: stick, ur tor or sumacicasmg: stick .vnuuim:
tyre or sumact ual: c^aotat
3'
10 or sumact casing _ t«» or sukiaci casing. 6"
Rtsis riM i o — mi 01 ftlSUWt: 5 »0M«0K DiAMITI*
mtor iackhu.:— Q/Z0t< T
IK VATION / OirtH TOR or sua.:
miOTUAi:
-3/
DIRTH TOR Or UNO RACK:
IK VATlON / OirtH TOR or SCUIN:
TTRI orSCUIN , 5C/*'
SLOT S>ZC • LINGTH:
• D OT SCUIN:
-27'
2.c
4"
• mi or unorack: ^ t Anv2/£"_
_ HE VATlON / OIRTH BOTTOM 0* SCUIN.
_ (K VATQN r OIRTn tOTTOM 0» UNO RACK: TvRl o* |ACKf til ttlOW OlSt*VATlON WE IT .
- ikvationrqlhwotmoil
3*7
37
< h 2 o o
-j -j 4*.
|0«ing«o £ujis_
overburden f^nwitorlng well sheet — r»m«th.
project 4?- ftjf'zfl - rtlqn -c /a PROJECT NO. tOKING--^^
iifvatlon iffliirt ft f l ^t" hudgtologlst— rff^
SB ssgrgwp >&j<£
IilvAfiOW Of 10* Of WWACI CASWG: tltvAliON OHO»W Mtt Ml:
(TICK • U*10* Of WWACtCASM6: VTtC* • U* tiMAMI:
T**l Of WWACI MAI: ,
3'
3E
• I D Of WWACI CASIWC . t**j O' WW ACICASING j£.
77"
*rrr*l-
• tiSltMtlD SY*l Of wit Ml:
4'
itgt a-lOWHOll DiAMITIt;
tx« Of lactfiu-—
7/ t»y
umofuatt - " DlfTH TO* Of WWPACK:
Jl,tVATlONfDttTHWOftCtIW: • orm ' 40 WC
TT*t Of SCtCIN' -^£lI — j?c stct kof »'« • tlfctm: •
ID Of tCtUN:
r/z'
j*'
__ -t i qia)f - lt*t Of SAWDtAC*: !—Z -*—
UtVATON ' Dlf* tOIIOMOf KMIN.
ssnss -'ssssar' will
_ iitviiiioiii'pif,|<p,l,^l
JlL mll
/* '
<j1
VINELAND CHEMICAL COMPANY SITE
|0*tNGN0 '
OVERBURDEN MONITORING WELL SHEET
yw km , £>v<ty _ I *0jictn0._£12lu-ii3. rowing—mttnqp 4*^7
. . . . ( r - „ . v 7
-mix*
r
III VATlON 0' t0»0» tUK'ACI CASING : ik valton 0110» 0' tisu w: STICK • g» T0» 0» SUft'AM CAUNG: SUCK-ur kittftfttt:
_2l j2=z.
-- TtH 01 IWK'ACI SIAl*
to o' sumac! casing--irrio* sumaci cajimft- 2ZML ftttlt»i»|id t*h of kistthh
37/*
he
iokimok diamitik TvT TT« 0' SACK Kill" hr*)1 kufotik
: cfic r |KVATt0N/DtKTHl0»0»SlAI:
tth 0» SIAl: pLiJtj tE
DIKTH TO* 0' SANOAACK « 4 iii vatton / otrtm 10» or icgiin imoncuiN —
uouaitungtm 10 otkuin
il
~$7% fii.0
Wl or SANOMCI- C^ADz. ^
lllVATCN/OirtH I0110M 0» kCWIM.
Ill VATlON / 0tn« SO"OV 01 SANO »ACK
— lilvatiqmpi>rwornol!
31
il_ < m z o o
-j on
VINELAND CHEMICAL CCMPANY SITE
io«<n6«o _£"±£: OVERIURDCN
MONITORING WELL SHEET
PROJECT. PROJECT NO IICVATION
•0rlnc-^sz2mi FlilDCEOlOGtST.
i f f jm r -n -• DATI P7 j u)cTi,Z '
CtOUND IllVATlON
k «"
I
III vAliON ©I TO» 0' SU*r ACt CASING : IllVAIiON 0* 10*01 RiSU W:
STICC -U»T0»0» SUMACI CASING: IHCCUM4IIW:
- - tT« orsumaciMai* £ C<MgiJr
I l.
!
/« • • 7 • • • • • «
f ruf ©ftllllNG MIYNOO *w iz+jfcy
SSSBzam
ID 01 SUtiAClCASING _ 1t« 0'SuMACI UHNG-
lal
2SE ftisu*i*ito i/ft 1**1 01 """*»• ' 'j s rpvi-
iounOii diamltl* ait T**l 0' SACCIIU- 6»<2»o r
- illvaylon / dl*ln 10* 01hal: • 1**1 0* slal* 6^mt*>ajvt%. <vo (y DIMN10* 01SANDRACC:
• III VATCN / Dt*1H 10* Or SCRMN:
• 1**1 or SCRIIN ^ U py C-
U01 sot • ungtm . &*0>Q
10 or SMIIN __3_/^
•1**10* SAND PACT
lit VAliON / DI*1N S0110M or SCMIN.
• |UVAT«X*W*1N»0"0V0»SAND*AC* 1**l or SACclAI RUO* OtSltvAION «i«n- x**i4
- uivaion >0t*rm0r MOLL
r
zc
a±_ 21'
(?£*oc 41 acj?
37' 3>7'
3T
VINELAND CHEMICAL COMPANY SITE
|0«IN6 NO {IO'-2 3
MOJICT pro if ct mft 373 hi id 61 ologht eh*lam
OVERBURDEN MONITORING WELL SHEET
orialrjtf*^ ORUlfNG MITHOD —Mm**
SSSSfetWI IOCATION boring
ilo'jis
m0$i -2
( '
n
UfVATiON 0» TO*0* SURfACICASWC: HtvAliON Of TOR0» MIR plh-.
STICK <U>TO* Of SURfACI CASING: ST*K -UR RiSIRRiRI:
c i2&a r TTRI Of SURfACI MAI- >V ty&Hret)
10 Of SURfACI CASING -TTRi 0'SURfACI CASING.
RiSlRRiRHO TtRlOf RiSIRRiRI
IOR(«OLI DAMITIR
TYRI 0»l*«flU — 7
III VATlON IOIRTN TOR 01 UAL:
OIRT* TOR 0'UNO PACK: £L /
HIVATlONf OIRTM TOR Of SCRIIN: tmoncmw uoiwiauncvm: —— tc?r~
-f 10 Of SCRIIN
mi Of SAND RACK'. * t
LT-J< HlvATiON f OCRTM BOTTOM Of SCRIIN. _ (itvATON 10(RTM BOTTOM Of UNO RACK l»Ri Of lACKlm BllO*OBSIRlfAT«N
Wlu__—
V*
- tLlvATQNlOIRTNOfWOll " & < H 3 o o
00
VINELAND CHEMICAL C (MP ANY SITE
IQtlWCWO
OVERIURDIN MONITORING WELL SHEET
< m 2 o o
-j -j *£>
b0«in6 MO £ U1-4M
OVERBURDEN MONITORING WELL SHEET
»rrntrr l///u£(-/hud pro ject mq +136-373 ELEVATION held geologist ei
r-
LOCATION BORING . uj-4s1
GROUND IllVATiON
I
!«-
£•-;«
• ' • **• •
DRiLtfRiTi
zss ii&jsatx
zsssffiee m
IKVATION or TO* 0' SURiACE CASING: IKVATiON Of TO* 0* ROER *#i:
STICK • U* TO* 0» SUREACI CASING: STICK >U* RISER PtPI:
3 ' 2:*
TYPE OrSURTACI SEAL:
i d or sutrac! casing:-tt*x or suwaci casing. 6 "
3 tl RiltR *i*E ID TT*1 or mil»!»»• X /lL so At
•oremole diameter TFT
type 0' iacktill: :— wt
ELEVATION / DEPTH TO* 0* SEAL:
tt*e 0* seal: Ltr A^AJTfcA*
ftfj iivi re DEPTH TO* or SAND PACK:
ELEVATION / DEPTH TO* 0* SCREEN:
- TYPE OT SCREEN '
:JV* 3-V
SLOT SIZE i LENGTH . c -020
ID Of SCREEN: sn
- ttpe or sand pack: t>£ * /-&wd
ELtVATiON / depth IOTTOM 0* SCREEN.
ELEVATION IDEPSH BOTTOM 0* UND PACK:
*3 /
TtPL well - IKvATiONiDiP'HOr HOLE
4 S < m 2 o o
-j 00 o
!
VINELAND CHEMICAL COMPANY SITE
|0»IMG«0 fu>-&
mojict mojict no ikvatlon
OVEKIUKDEN MONITORING WELL SHEET
piuuu. v gfttssi ioc atlon -^lk^zsi iqmnq , 6 i~2
mp mod vr-* avy* £',»2m£±^£
G«OUND lllvatton
1 ^ « -4 —
« —
1 f 1 |«
1 f 4 -
III VAIiON 01 tO» 0' SUUACl CASING : IllVAHON Or WOr ftiStt Ml:
$TtCK -U»TO»Or SUt'ACt CASMG: sttcc.ur ahum!: - - TYUOISUMACISIAI• _jCJLfi&£eOX-
f t
m xtr. VM
>* ' • • ' '
_2l 2..'
ID ortutrACfCASING ItPi O' SUWACI CASING; hit. *l
ftrttmitlld 1*»l 0» »««m| L/. /' c, u<k f *v t
tl »Ott«OllOiAM|T|R
Trfi or lACcriu-—£gge°r
III VATONI OirtN W 0» MAI:
WlorSIAlr Bg<oTo»Jirt flq(a_
DI'TH 10* or SANO DACK:
utwATCN / ocriM io» or iouin:
t*« or KfttiN KH *(-
uonaitunctm: . 0-o2q j."
ID OTKMIN —
•1r«
• til VAUON /OiriM »0"0M or SOU*.
• htv*'l0n'd("*t0t10v0' sand pack: Itli or |ack*hi ill©* OtSttvAlON
mu' l2*de 'i it**
- titvasonrotmnqrwoa
2al
4.s"
Or SAND MCN: 2Ao €. SAriQ
z r
22* < m 2 o o
-j CO
VINE1AND CHEMICAL CCMPANY SITE
IO«inC NO -
OVERBURDEN MONITORING WEIL SHEET
(
n
iqzavon h+'r iohing—£l±^2-DATE */i/n
etiuia BKIUMO-l.0 mtmo&a£l- rt 1sll
UIVAT©* or TO* 0' IU*'ACI CAHWO: IllVAT©* O' 10* Of ftAlft MH:
riCK • W» TO* or tUtrACI CAS*©: liCK.u>
mionvwactmai-enmi*sr
S-TA*R/*NR
• 10 0' Ul*'ACf CAt(M6- £ mi or iumaci omnfc irret
3 v *r>|ft riri i i • mi or rlmawf: fg f* <-
• I0«l«0ll ©lAMITH , 7
• mi o» i*c<riu-. (?****-
- lit VAT©* / ©inn TO* or MAl
mi or MAI-. rs.l~-.4t p/fk + i »lhmlo»ortandmcx: lit VAT©* / OtftH TO* 0» ftCRttN:
TvrtortCUlN —90 Puc
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/p?
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MOTim• UWCTW* , 1° '
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APPENDIX E
VIN 00 J
1809
s
APPENDIX E MW-10 PUMPING TEST ANALYSIS
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APPENDIX F n
VIN 001
1819
APPENDIX F GROUNDWATER FLOW CALCULATIONS
Q = KIA* where K = 294 Ft = 2199 gpd/ft2 day
10/19/R7 Area^, = 36.5' x 1100* . = 40,150 ft2, 11 = 2 = .0018
(1000 "4— 0.90) = .0018
Area2, = 39' x 550 1 = 21,450 ft2
1-2 - / = .0015 (600 H- 0.90)
= .0015
Area3' = 54 ' x 440 ' = 23,760 ft2, I3 - o, s = .005
(90 -r- 0.90) = .005
ql - (2199 gpd/ft2)(.0018) (40,150 ft2) = 158,922 gpd q2 - (2199 gpd/ft2)(.0015) (21,450 ft2) = 70,753 gpd q3 = (2199 gpd/ft2) ( .005) (23,760 ft2) = 261.241 anrl
Q Total 490,916 gpd 11/2/87 Areaji = 36.5' x 1100' = 40,150 ft2
11 - 1 = .0017 (1030 -f- 0.90)
Area2 = 39' x 550' = 21,450 ft2 1 2 = 1 = .0015
(600 -7— 0.90) Area3 = 5 4 ' " x 440* = 23,760 ft2
J 3 - £L_5 = .0028 (160 -f- 0.90)
< i«n!?fhAr-eaS may -bS S6en °n the three figures in Appendix F. The * iTdth ^1S4-haSS°Cia^e Wlth the area in each direction and the "f1S the associate width of each flow path such that it does ° not overlap with the flow path from the other 2 areas. °
co nj o 8118b
Ql = (2199 gpd/ft2)(.0017)(40,150 ft2) = 150,093 gpd Q2 = (2199 gpd/ft2)(.0015)(21,450 ft2) = 70,753 gpd Q3 = (2199 gpd/ft2)(.0028)(23,760 ft2) = 146,295 gpd
Q TOTAL 367,141 gpd 1/27/88 Area^ = 36.5' x 1100' = 40,150 ft2 X1 = 2.5 = .0018
( 1260-r 0.90) Area2 = 39' x 550' 1 2 = 2 (900-f- 0.90) Area3 = 54' x 440' Il= 1.5
(190 -7- 0.90)
= 21,450 ft2 = .002
= 23,760 ft2 = .007
Q1 = (2199 gpd/ft2)(.0018)(40,150 ft2) = 158,922 gpd
Q2 = (2194 gpd/ft2)(.002)(21,450 ft2) = 94,337 gpd
Q3 = (2199 gpd/ft2)(.007)(23,760 ft2) = 365,738 gpd
Q TOTAL 618,997 gpd
Date 10/19/87
11/2/87
1/27/88
Total q (gpd )
490,916 367,141
618,997
AVERAGE Q = 492,351 gpd
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APPENDIX G LABORATORY ANALYSIS FOR CHEMICAL EXTRACTION OF SOILS
6835b
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REM III PROGRAM
EPA CONTRACT NO. 68-01-7250
TREATABILITY STUDIES FOR EXTRACTION OF ARSENIC FROM SOIL COLLECTED FROM
THE VINELAND CHEMICAL SITE
FINAL REPORT
DECEMBER 9, 1987
H1TTMAN EBASCO ASSOCIATES INC.
t J
. T
r •
.9..
- *i •
TABLE OF CONTENTS
PAGE
I. INTRODUCTION 1
II. SUMMARY OF ANALYTICAL METHODS 2
III. SUMMARY OF RESULTS: SOIL TESTS 3
IV. DESCRIPTION OF EXPERIMENTS PERFORMED 5
V. DISCUSSION OF RESULTS 6
VI. APPENDIX OF LABORATORY DATA 8
< z o o
CP
CP
INTRODUCTION
Field personnel from Ebasco Services Incorporated collected soil samples
from numerous unspecified locations within the 54-acre 'Vineland Chemical
Company (ViChem) Site located in Cumberland County, New Jersey. Samples
were combined in a 5 gallon plastic bucket and delivered to the Hittman
Ebasco Laboratory in Columbia, Maryland on'july 20, 1987. The composite
sample was stored in a walk-in cold room at approximately 4°C.
After an initial chemical and physical characterization, bench-scale
treatability tests were performed to determine the feasibility of
removing arsenic from the solid phase. A number of batch extraction'
experiments were conducted at room temperature (22-23°C) using tap
water, with and without chelating compounds added, at acid, alkali and neutral pH.
During the treatability work, the scope of the original project was
changed. The inability of the batch treatments to consistently produce
solids containing less than 20 mg/Kg total arsenic, and the production
of relatively large volumes of non-filterable aqueous waste with high
suspended solids and arsenic content, made further investigations
unwarranted. Therefore, many of the experiments described in the
Base-Bid Technical Specifications were eliminated.
This report summarizes the experimental methods, analytical protocols
and results of the treatability study performed by personnel from Hittman Ebasco Associates Inc. under the direction of Ebasco Services
Incorporated. The results of the sample characterization analyses, a
comparison of the efficacy of the extraction agents and an evaluation of
the effects of pH on arsenic removal from the ViChem soil are presented.
<C, £.
i —d
II. SUMMARY OF ANALYTICAL METHODS
Analyte Method •
• Aluminum 200.7 (Ref. 2J
Arsenic 7060 (Ref. 1)
Calcium 215.1 (Ref. 2)
Ir°n 236.1 (Ref. 2)
Total Organic Carbon 9060 (Ref. 1)
% Solids 160.1 (Ref. 2)
Particle Size ASTM D422
t
REFERENCES
1. "Test Methods for Evaluating Solid Wastes", EPA SW-846, 3rd Edition, 1986.
2. "Methods for Chemical Analysis of Water and Wastes", EPA-600/4- 79-020, 1979.
o o
2
SUMMARY OF RESULTS: SOIL TESTS
A. INITIAL CHARACTERIZATION (Total ng/Kg) • '
Aluminum _ Arsenic Calcium Iron 138 Total Organic Carbon f ?,ft % Solids J;730
97% B. ROOM TEMPERATURE EXTRACTIONS WITHOUT CHELATORS
soil at pH = 3 38 • * , soil at pH = 7 17 tota' arsenic (mg/Kg soil at ph = 7 4i soil at pH = 12 17
ROOK TEMPERATURE EXTRACTIONS AT PH - 7 WITH CHELATORS
;.°!i ti ttoiaiarsenic
soil with oxalate 44 arsenic (mg/Kg soil with EDTA
C.
35-
* average (mean) of three separate digestions and analyses
1 » i t H , • i r
l9 - tz-t. flAlfO NOUVOVM <X O*0«O«
fir
una. «* V VM I«M NOUOIftfl) MUM <o AT* O* TMMN
iiiiwomth OOt 0»l 001 0/ OC 0* OC Ot 91 »l Ol • * r C MM % I Ml I t 9 9 SaltKTIN lAK OOVOMVIf t n IIU3M M 9NINUO lAIS OaVOMVIf t n
001
• i,_ I
t/) m
8 p
t^q\ \oo a
IV. DESCRIPTION OF EXPERIMENTS PERFORMED
Simple batch extraction experiments performed on the ViChem soil sample
at room temperature (Section III. A-C) were carried' out by combining
200 grams of undried sample with 200 ml of tap water in a 1L pyrex
griffin beaker. When chelating agents were added, the following
compounds were'used in the amounts given below:
These additions 'resulted in a final concentration of the chelating agent
of approximately 0.01 molar. Next, the pH of the solution was adjusted
as necessary with 1 + 1 hydrochloric acid or 5N sodium hydroxide.
Solutions were stirred on a Phipps and Bird paddle stirrer at 30-40 rpm
for two hours with periodic monitoring and adjustment of pH. After two
hours of continous stirring, the solids were allowed to settle for 30
minutes and the supernatant decanted. Retained solids were washed three
times with tap water to remove any .residual reagent and submitted to the lab for analysis.
Chelator Grams Added per Beaker sodium citrate
sodium oxalate 1.03
1.13
0.46 tetrasodium EDTA
2. o o
5
DISCUSSION OF RESULTS
The composite soil sample is a dark brownish-grey, medium grained sand
with visible organic matter present. One problem, typical of such sandy
soils, was in obtaining a representative homogeneous subsample from a 5
gallon bucked filled with many Individual soil samples.collected from
the ViChem Site. Once recognized, this problem was minimized by
repeated manual mixing followed by collection of a large (2 Kg)
subsample which was thoroughly mixed again and used as the source of
subsequent aliquots for experimentation.
Results of the treatability testing indicate that the arsenic contained
in the soil is associated with both the organic material and the
inorganic sand fraction. The nature of this association, such as
chemical bonding or absorption, was 'not investigated and any comments
would be speculative. Extraction treatments that removed much of the
organic material such as solubilization by addition of NaOH followed try
decantation and thorough washing, removed between 50 and 80% of the
total arsenic. Neither the chelating agents nor the pH adjustments
employed in this emperical study were effective in producing post
treatment solids that met the target criterion of less than 20 mg total
arsenic per kg of dry solids (all arsenic values are expressed on a dry
weight basis).
In addition to the inability of batch extraction techniques studied
herein to meet the 20 mg/kg target, large amounts of aqueous, black,
organic-rich," arsenic wastes were produced from decantation of the
extract supernatant solutions and multiple washings of the retained
solids. This aqueous waste would have to be treated and disposed of, a
senario not investigated in this study. Reduction of volume by
dewatering may prove to be the most difficult step. The very fine
organic suspensions do not readily settle out.
In summary, the batch extraction experiments conducted on the- ViChem
soil samples supplied by Ebasco were not effective in lowering their
arsenic content to a level that would comply with disposal protocols.
Another serious drawback was the generation of relatively large volumes
of aqueous wastes containing leached arsenic and f.infe suspended
particulates that will be difficult to treat by conventional methods.
Thus, simple batch extraction treatments using citrate, oxalate or EDTA
chelators in combination with solution pH adjustments between 5 and 12
did not provide conditions favorable for treatment of these contaminated
wastes.
APPENDIX OF LABORATORY DATA
<
o o
cp v*
8
. !
QA/QC DATA SUMMARY LAB CONTROL RESULTS
CLIENT: VINELAND CHEMICAL/SOILS
CONTRACT NO: ESI -1002-101
UNITS: ARSENIC, ug/L TOTAL ORGANIC CARBON, mg/L
PARAMETER QC RESULT QC TRUE VALUE % RECOVERY
TOC 1140 1160 98
ARSENIC 82 80 103
TOC 1020 1160 88
ARSENIC 84 80 105
TOC 1020 1160 88
B1ank*nWer? ^9®sted and analyzed during each sample preparation Arsenic^S ug/L) values were below instrumental detection limits for
*
9 -41
.A.:
QA/QC DATA SUMMARY DUPLICATE RESULTS
CLIENT: VINELAND CHEMICAL/SOILS «
f • I w"
fe. " CONTRACT NO: ESI -1002-101
UNITS: ARSENIC, ug/L W"~~ TOC mg/kg
w. —- SAMPLE SAMPLE DUPLICATE % Si IS
PARAMETER ID RESULT RESULT DIFFERENCE
ARSENIC 4767 7.3 <5 NON CALCULABLE -1 . TOTAL ORGANIC CARBON 4767 2700 8750 106 *
1" ARSENIC 4908 564 407 32 J r
ARSENIC 5031 70 64 9.4 — TOTAL ORGANIC CARBON 5030 <90 <93 NON-CALCULABLE
• i . ARSENIC 5830 53 68 25
* AVERAGE OF DUPLICATES WAS REPORTED DUE TO POOR PRECISION.
z.
10
8$
QA/QC DATA SUMMARY SPIKE RESULTS
CLIENT:
CONTRACT NO:
UNITS:
VINELAND CHEMICAL/SOILS
ESI-1002-101
ARSENIC ug/L TOTAL ORGANIC mg/L
t • i
PARAMETER SAMPLE
ID SAMPLE RESULT
SPIKE RESULT
SPIKE ADDED
% RECOVERY
ARSENIC 4767 7.3 45 40 94
ARSENIC 4908 564 426 40 0
ARSENIC 5030 73 127 40 135
TOC 5030 <100 675 1000 68
ARSENIC 5829 37 63 . 40 65
N = SPIKE RECOVERY OUT OF CONTROL WINDOW OF 75 - 125%. MATRIX INTERFERENCE IS INDICATED.
* = SPIKE ADDED WAS TOO LOW FOR THE SAMPLE LEVEL. CONTROL LIMITS ON PERCENT RECOVERY NOT APPLICABLE.
11
APPEND
IX H
VIN
0
01
1
84
0
APPENDIX H LABORATORY ANALYSIS FOR CHEMICAL FIXATION OF SOILS
6835b
TREATABILITY STUDIES FOR CHEMICAL FIXATION OF ARSENIC AND SOLIDIFICATION OF SOIL
VINELAND CHEMICAL COMPANY SITE PROJECT VINELAND, NEW JERSEY
TASK II FINAL REPORT
December 11,1987
Report Prepared For: KBASCO SERVICBS INCOPORATED REM III PROGRAM U.S. ENVIRONMENTAL PROTECTION AGENCY Task Leader: M. Kuo Site Manager: W. Colvin Project Identification No. WA-37.2LB8
Report Prepared By: LOPAT ENTERPRISES INCORPORATED Wanaaassa, New Jersey 07712 Project Supervisor: C. Falk Project Manager: G. Gironda
Proj. I.D. No. WA-37.2LB8 Ebasco: M. Kuo, W. Colvin
Lopat Ent. Inc. Task II Report December 11, 1987
SOIL SAMPLER
Untreated Log 87-63
Color
Physical Characteristics
Grey, Brown, Orange
Sandy
Treatment 1106-83-1
Treatment 1106-83-2
Concrete -like
Concrete -like
Treatment 1106-84-1
Cement Grey Cement Grey Dark Grey
Hard Dry Mud
Density, g/cc 1.37
Unconfined ©8h: 0 Compressive S24h: 0 Strength® ©32h: 0 lbs/f>* ©48h: 0
^ Increase in Volume due to '1 reatment
Increase in ••jgh' Due to
. • • -if •
2.07
6180 >9000 >9000 >9000
17
1.94
4100 >9000 >9000 >9000
24.7
2.13
0 3200 4800 5800
16
77 76 81
U.C.S. was done with aSoiltest Pocket Penetrometer Model CL-700 having a ,.c between 0 9000 lb/ft2 in 500 lb. increments. Each reported number is
the average of 10 determinations.
Soil Page 1
Proj. I.D. No. WA-37.2LB8 Ebaaco: M. Kuo, W. Colvin
Lopat Bnt. Inc. Task II Report Decenber 11, 1987
TREATBD SOIL SAMPLES
EP TOXICITY TEST RESULTS (in mg/1)
1106-83-1 1106-83-2 1106-84-1 1106-91-1 (repeat of 1106-83-1)
0.24 0.36 0.22 0.27
0.6 0.7 0.6 0.5
<0.005 <0.005 <0.005 <0.005
0.09 0.05 0.01 0.06
<0.005 <0.005 <0.005 <0.005
0.0004 <0.0002 <0.0002 <0.0002
<0.005 <0.005 <0.005 0.008
<0.01 <0.01 <0.01 <0.01
Soil Page 2
Proj. I.D. No. HA-37.21B8 Ebasco: N. Kuo, N. Colvin
Lopat Ent. Inc. Task II Report Oeceaber 11, 1967
TREATED SOTL SWLfS Test Results of 1106-83-1
fn Tor 1 2 3 4 5 6 7 8 9 10
A: r " 0.20 0.20 0.21 0.15 0.15 0.17 0.07 0.13 0.17 0.14
6a O.t. <0.1 <0.1 <0.1 <0.1 <0.1 <0.1 <0.1 <0.1 <0.1 <0.1
M (1.005 <0.005 <0.005 <0.005 <0.005 <0.005 <0.005 <0.005 <0.005 <0.005 <0.005
- 0 03 <0.01. <0.01 <0.01 <0.01 (0.01 (0.01 (0.01 <0.01 <0.01
Pt J05 < 0.005 < 0.005 (0.005 <0.005 <0.005 <0.005 <0.005 <0.005 <0.005 <0.005
He 0.2X4 <0.0002 <0.0002 <0.0002 <0.0002 (0.0002 <0.0002 (0.0002 <0.0002 '0.0002 <0.0002
Se xCi.005 <0.005 <0.005 <0.005 <0.005 <0.005 <0.005 <0.005 <0.005 <0.005 <0.005
As <0.01 <0.01 <0.01 <0.01 <0.01 <0.01 (0.01 <0.01 <0.01 <0.01 <0.01
KP Test Results for 1106-91-1 (Treataent the saae as 1106-81-1)
1 2 3 4 5 6 7 8 9
0.14 0.10 0.12 . 0.10 0.08 0.07 0.07 0.08 0.11
(0.1 <0.1 (0.1 <0.1 <0.1 <0.1 <0.1 <0.1 <0.1
Cd <0.005 <0.005 <0.005 <0.005 <0.005 <0.005 <0.005 <0.005 <0.005 <0.005
Cr 0.06 0.02 0.02 <0.01 0.04 0.02 <0.01 <0.01 <0.01 <0.01
ft <ii. 005 '0.005 <0.005 <0.005 0.007 <0.005 <0.005 <0.005 <0.005 <0.005
«g <0.0002 (0.0002 <0.0002 <0.0002 <0.0002 <0.0002 <0.0002 <0.0002 <0.0002 (0.0002
Se 0.008 <0.005 <0.005 <0.005 <0.005 <0.005 (0.005 <0.005 <0.005 (0.005
*9 <0.01 <0.01 <0.01 <0.01 <0.01 <0.01 <0.01 <0.01 <0.01 <0.01
ALL RESULTS REPORTED IN MILLIGRAMS PER LITER.
Soil Page 3
00 in
Proj. T.D. No. WA-37.2LB8 Bbasco: M. Kuo, W. Colvin
Lopat Bnt. Inc. Task II Report December 11, 1987
LABORATORY TRBATXENT OF SOIL
ID*
Treatment
W:.of Soil
K-20 LS Part A
K-20 LS Part B
Tap Water
Fixative
1106-83-1 (and 1106-91-1)
*1
400g
1.16g
. 84g
103g
8g Darco Gro-safe
+ 80g
Class F Fly Ash + 160g
Portland Cement Type I
1106-83-2
#2 400g
1.16g
. 84 g
112g
8g Darco Gro-safe
+ 60g
Class F Fly Ash +
80g Lime Type SA
80g Portland Cement Type I
1106-84-1
*3
400g
1.16g
. 84 g
134g
8g Darco Gro-safe
+ 80g
Class F Fly Ash + 160g
Lime Type SA
Soil Page 4
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00 o>
Proj. I.D. No. WA-37.2LB8 Ebasco: M. Kuo, W. Colvin
Lopat Bnt. Inc. Task II Report December II, 1987
LABORATORY AND SCALB-UP PROCEDURES AND RAW MATERIALS
COSTS FOR TREATED SOIL SAMPLE 1106-83-1 or 1106-91-1
! K.iortitory Scale Scale-up (per ton of noil) Quantity (coat)
Scale-up (per yd3 of soil) (1 yd3 of soil=2310 lb) Quantity (coat)
400i: Toil ap Water
2g K-20 LSC* 8.0g Darco Gro-safe" 80.Og Class F Fly Ashc 160.0>? Portland Cement,
1 gal ($40.00) 40 lb ($15.60) 400 lb ($ 2.10) 800 lb ($26,80) TOTAL $84.50
2000 lb 515 lb
1.16 gal ($46.20) 46.2 lb ($18.02) 462 lb ($ 2.43) 924 lb ($30.95) TOTAL $97.60
1 yd3 soil 595 lb
Type I*
Ingredients were added and nixed in the sane order as listed.
a) Lopat Enterprises K-20 LSC, $40.00 per gal. FOB Wanamassa7~NJi b) Darco Gro-safe activated carbon, Anerican Norit Co., $0.39 per lb.
FOB Marshall, TX. c) Class F Fly Ash, Ash Management Corp., $10.50 per ton,(bulk)
FOB Trenton,NJ d) Portland Cement, Saylor's Type I, Coplay Cement Co., $67.00 per ton.(bulk)
FOB Nazareth, PA.
NOTE. The above raw materials costs are approximate, as they are determined by a laboratory screening treatment process. In most cases, pilot studies show that site treatment costs will be lower.
< H 2
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Proj. I.D. No. WA-37.2LB8 Bbasco: M. Kuo, W. Colvin
Lopat Bnt. Inc. Task II Report December 11, 1987
SAMPLE PREPARATION
Log 87-63:The soil sample was essentially a sand, brown and orange, s-.tirring and raking the soil, the material became fairly homogeneous, plastic scoop was used to remove 400g of soil for each experiment.
Soil Page 6
Proj. I. D. No. WA-37.2I.Hft Ebasco: M. Kuo, W. Colvin
Lopat Ent. Inc. Task II Report December 11, 1987
Unconfined compressive strength vs. time
Treated Sample://0*-83"'
10000
Time, Hours 3
o NOTE: Each plotted point Is the average of 10 U.C.S. deten ® on(
03 VO
..\ $5ASK$
Proj. I.D. No. WA-37.2l.nR Ebaaco: M. Kuo, W. Colvin
Lopat Ent. Inc. Task II Report December 11, 1987
llneonfined compressive strength vs. time
Treated Sample : 1106-?3" "^rt
10000 j
< M Time, Hours z
o NOTE: Each plotted point Is the average of 10 U.C.S. deter* o ona
CO ui o
Proj. I. D. No. WA-37. 2I.IUI Ebasco: M. Kuo, W. Colvin
Lopat Ent. Inc. Task II Report December 11, 1987
Unconfined compressive strength vs . t ime
Treated Sample
2 Time, Hours
o o NOTE: Each plotted point Is the average of 10 U.C.S. determir M
oo ui M
Proj. I. D. No. WA-37. 2I,I)P Ebnsco: M. Kuo, W. Colvin
Lopat Ent. Inc. Task II Report. December 11, 1987
Unconflned compressive strength vs. time
rested Sample: Soil (Same Treatment as 1106-83-1)
?ooc
"Of'-! :
1 v 'Q0
7 000 Minimum acceptable UCS (1500 lb/f t ) after 68 hr curing.
10001 I 16 26 32 60 68
Time, Hours < M 3
NOTE: Each plotted point is the average of 10 U.C.S. del o atlor
oo en to
00 U1 U)
APPENDIX I
LABORATORY ANALYSIS FOR GROUNDWATER
HITTMAN EBASCO ASSOCIATES INC.
REM III PROGRAM
EPA CONTRACT NO. 68-01-7250
VINELAND CHEMICAL COMPANY SITE PROJECT
TREATABILITY STUDIES FOR REMOVAL OF ARSENIC BY REVERSE OSMOSIS, ION
EXCHANGE AND ADSORPTION
FINAL REPORT
December 28, 1987
ESI-1002-602
TABLE OF CONTENTS
PAGE
I. INTRODUCTION j
II. SUMMARY OF ANALYTICAL METHODS 2
III. SUMMARY OF RESULTS: INITIAL CHARACTERIZATION 3
IV. SUMMARY OF RESULTS: REVERSE OSMOSIS 4
V. SUMMARY OF RESULTS: ION EXCHANGE 5
VI. SUMMARY OF RESULTS: ADSORPTION 7
VII. DESCRIPTION OF EXPERIMENTS PERFORMED 9
A. Reverse Osmosis B. Ion Exchange C. Adsorption
VIII. DISCUSSION OF RESULTS
A. Reverse Osmosis B. Ion Exchange C. Adsorption
IX. APPENDIX: QUALITY CONTROL DATA 22
< H 2
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I. INTRODUCTION
A water sample was collected on July 29, 1987, from Monitoring Well
Number 1 at the Vine!and Chemical Company (ViChem) Site located in
Cumberland County, New Jersey. The sample was shipped 1n eight,
5-gallon cubitainers and arrived at the Hittman Ebasco laboratory on
August 1, 1987. This 40 gallon water sample was used as the feed stock
for all subsequent treatability experiments. The original containers
were stored in a walk-in cold room at 4°C until a subsample was required
for experimentation. Equal volumes were then withdrawn from each of the
eight cubitainers. No chemical preservatives were added to the original
feed stock sample in order to avoid altering pH values representative of
conditions at the ViChem Site.
After an initial chemical characterization (see Section III.) which
confirmed a significant level of arsenic contamination, bench-scale;
treatability tests were performed to determine the feasibility of
arsenic removal by reverse osmosis, ion exchange and activated
adsorption.
This report summarizes the analytical protocols, experimental methods
and results of technology-specific Investigations conducted by Hittman
Ebasco scientists under the direction of Ebasco Services Incorporated.
For each of the three treatment technologies, data were generated to
assess the feasibility and economics of each type of treatment in terms
of the potential to achieve a final effluent that meets the Federal and
State of New Jersey criterion of less than 0.05 mg/L total arsenic
content. A discussion of the results compares the efficacy of each
treatment process at removing arsenic from wastewater generated at the
ViChem Site. < H 2
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00 m -J
1
II. SUMMARY OF ANALYTICAL METHODS
Analyte Method*
Alkalinity 310.1
Arsenic 206.2
Calcium 200.7
Chloride 325.3
Cyanide 335.2
Iron 200.7
Oil and Grease 413.1
pH 150.1
Sulfate 375.3
Total Hardness 130.2
Total Organic Carbon 415.1
Total Suspended Solids 160.2
Turbidity 180.1
* All methods are taken from "Methods for Chemical Analysis of Water and Wastes," EPA-600/4-79-020, 1979.
2
III. SUHMARY OF RESULTS: INITIAL CHARACTERIZATION
Parameter
AT kalinity
Chloride
Cyanide
Oil and Grease
Sulfate
Total Organic Carbon
Total Suspended Solids
Total Hardness (EDTA)
Turbidity
Arsenic
Calcium
Iron
pH
Detection Limit Result Units
1 5 mg CaC03/L
1 24 mg/L
10 <10 ug/L
5 <5 mg/L
1 13 mg/L
1 <1 mg/L
1 4 mg/L
] 11 mg CaC03/L
1 25 NTU
• 0.010 ' 1.6 mg/L
0.045 1.9 mg/L
0.010 5.2 mg/L
2-12 6.34
IV. SUMMARY OF RESULTS: REVERSE OSMOSIS
EXPERIMENT #1 - Membrane ST-10: spiral wound, cellulose acetate
Operating Pressure (psi)
400 500 700
Concentrate Flow (qph)
250 84
120*
Permeate Flow (qph)
8.7 10 15
Arsenic Content of Permeate (uq/LV
<5 <5 <5
*Arsenic content of concentrate stream - 47 ug/L, pH - 5.3
EXPERIMENT #2 - Membrane MS-02: spiral wound, thin film poly amide
Operating Pressure (psi)
400 500 700
Concentrate Flow (qph)
250 84
102*
Permeate Flow (qph)
33 38 54
Arsenic Content of Permeate (uq/L)
<5 <5 <5
kArsenic content of concentrate stream = 54 ug/L.
CHEMICAL CHARACTERIZATION OF REJECT STREAM: Membrane MS-02 at 700 psi (After a 60-705. volume reduction of the waste)
Alkalinity: 52 mg CaC03/L Chloride: 58 mg/L Cyanide: <10 ug/L Oil and Grease: <5 mg/L Sulfate: 61 mg/L TOC: 440 mg/L
TSS <1 mg/L Hardness: 36 mg CaC03/L Turbidity: 1.0 NTU Arsenic: Calcium: Iron: pH:
0.089 mg/L 4.8 mg/L 0.035 ng/L 5.7
SUMMARY OF RESULTS: ION EXCHANGE
EXPERIMENT #1: RESIN - Amber!ite IRA-400 (Cl)/L
ANALYTICAL DATA
RUN #1: Arsenic Content of ViChem Feedstock: 400 ug/L
Sample Identification
836-011-01 836-011-02 836-011-03 836-011-04 836-011-05 836-011-06
Time of Collection
+ 7 min. + 1 hr.
.+ 4 hrs. + 8 hrs. +16.75 hrs, +24 hrs.
Arsenic Content (m/i)
1 1
7 7
12 33 27
Arsenic Content of Bulk Regenerant: 3,420 ug/L
RUN #2:
Sample Identification
836-012-02 836-012-03 836-012-04 836-012-05 836-012-06 836-012-07
Time of Collection
+ 7 min. + 1 hr. + 4 hrs. + 8 hrs. +16.75 hrs. +24 hrs.
Arsenic Content (ug/L)
65 35 25 39 19 23
PRODUCTION DATA
Production Volume: Run Time: Average Flow Rate: Bed Volume (void): Empty Bed Contact Time (EBCT): Regenerant Volume:
2000 ml (27C bed volumes) per run 1440 minutes (24 hours) per run 2.8 ml/minute 7.4 ml 2.7 minutes 145 ml
ION EXCHANGE EXPERIMENT #2: RESIN - Bio-Rad AG1-X8
ANALYTICAL DATA
RUN #1: Arsenic Content of Vichem Feedstock: 400 ug/L
Sample Identification
Time of Collection
Arsenic Content (uq/L)
836-013-01 + 7 min. <5 836-013-02 + 1 hr. <5 836-013-03 + 4 hrs. <5 836-013-04 + 8 hrs. <5 836-013-05 +15.75 hrs. 6 836-013-06 +24 hrs. 10
Arsenic Content of Bulk Regenerant: 8,860 ug/L
RUN #2:
Sample Time of Arsenic Content Identification Collection (uq/L)
836-016-01 + 7 min. 38 836-016-02 + 1 hr. 13 836-016-04 + 8 hrs~. 13 836-016-05 + 17.5 hrs. 8 836-016-06 + 24 hrs. 10 836-016-03 + 29.5 hrs. 10
PRODUCTION DATA
Production Volume: 3350 ml Run Time: Run #1 Average Flow Rate: Run #1 Bed Volume (void) 6.6 ml Contact Time (EBCT): Run #1 Regenerant Volume: 140 ml
(508 bed volumes) per run ' 1440 min.; Run #2 - 1770 min. » 2.3 ml/min.; Run #2 « 1.9 ml/min
• 2. 8 min.; Run #2 • 3.5 min.
SUMMARY OF RESULTS: BATCH ADSORPTION
EXPERIMENT #1: ADSORBENT - ALCOA F-l Alumina
FLASK M (mq) C (uq/L) X (uq) X/M (mq/q)
A 0 188 ... ...
B 5.1 178 2.5 0.49 C 11.0 143 11.25 1.02 D 22.1 101 21.75 0.98 E 43.0 52 34.0 0.79 F 82.1 33 38.75 0.47 G 103 36 38.0 0.37
EXPERIMENT #2: ADSORBENT - Titanium Oxide
FLASK M (mo) C (uq/L) * (ug ) . X/M (mq/q)
A 0 65 ... ...
B 10.0 97 -8.0 -0.80 C 20 .0 148 -20.75 -1.04 D 40.0 196 -32.75 -0.82 E 80.0 160 -23.75 -0.30 F 160 256 -47.75 -0.30 G 400 266 -50.25 -0.13
EXPERIMENT #3: ADSORBENT - ALCOA F-l Alumina
BOTTLE M (mq) C (uq/L) x ("9) X/M (mq/q)
A 0 191 ... • . .
B 20 98 23.25 1.16. C 50 50 35.25 0.70 D 100 15 44.0 0.44 E 500 11 45.0 0.09
M » Adsorbent added to flask C « Aqueous As concentration after 5 days X » Total As removed from solution by adsorbent X/M « Solid phase loading capacity
+0.10 -Plot of Log X/M - Log K + (l/n)Log C Data from Section
0 -
ISOTHERM CONSTANTS
FOR ARSENIC ADSORPTION ONTO AULUMINA i: AT pH - 6.1 AND TEMPERATURE - 32°C "
-0.10 -o
I s -0.20 -
-0.30
o
I _J
Log C °-8
J I 1.0
FREUNDLICH MODEL ISOTHERM CONSTANTS FOR ARSENIC ADSORPTION ONTO AULUMINA
AT pH - 6.1 AND TEMPERATURE • 32°C
Log X/M - Log K + 1/n Log C (see previous tabular data summary and graph).
Isotherm constants were derived by the slope-intercept method regression
ISOTHERM CONSTANTS
K - 0.117 1/n - 0.46
(correlation coefficient • 0.934)
EQUATION: X/M - 0.117 C°-*6
UNITS: C (ug/L) X/M (mg/g)
NOTE: The data from the batch adsorption experiment using TiO? (Experiment #2) do not fit the Freundlich Isotherm Model
< H 2
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8 00 <31 U1
DESCRIPTION OF EXPERIMENTS PERFORMED
A. Reverse Osmosi s
Two experiments were performed in order to evaluate two different
RO membranes. Process evaluation data were generated with the use
of a PES/0SM0-19T-80 reverse osmosis machine supplied by Osmonics,
Inc., Minnetonka, MN. This unit featured dual, multi-stage
centrifugal stainless steel pumps, flow and pressure gages,
stainless steel and nylon tubing, polypropylene and PVC fittings,
and a styrene acrylonitrile 5 micron prefilter cartridge unit.
For Experiment #1, a spiral wound cellulose acetate membrane
designated ST-10 was installed by the manufacturer (both membranes
were supplied by Osmonics, Inc.). This membrane is relatively
thick, durable and resistant to damage by oxidizing agents and pH
extremes. The ST-10 membrane was replaced by one designated MS - 02
for Experiment #2. The MS-02 membrane, a spiral wound polyamide
type, is thinner and allows greater flow rates but is more
susceptible to clogging and chemical damage by corrosive or
oxidizing feedstocks.
Each membrane was evaluated at pressures of 400, 500 and 700 psi.
A 10-gallon polyethylene tank was filled with the ViChem composite
groundwater which had a pH of 5.3 after reaching room
temperature. The Qsmo RO machine was energized and purged with 10
gallons of deionized water. The first four gallons of ViChem
feedstock were run through the machine and disgarded after which
the reject and permeate streams were directed back into the
10-gallon feed tank. The four gallons of feedstock lost during
this initial purge were replaced so that the total volume of ViChem
feedstock was 10 gallons. At the 400 end 500 psi pressure
regimes, only one of the centrifugal pumps was energized. The
reject and permeate flows were recirculated back into the feed
tank for a period of 30 minutes after which a 100 ml sample of the
permeate was collected for arsenic analysis and all machine
parameters recorded. Both pumps were energized to maintain 700
psi and samples of the permeate (100 ml) were collected after five
minutes of stable operation at this pressure. A sample of the
reject (concentrate) stream was also collected at this time to
determine the arsenic content of the filtered feedstock just prior
to membrane filtration. In addition, a 4-l1ter sample of the
reject stream from the MS-02 membrane at 700 psi was collected and
analyzed for an expanded list of water quality parameters (see
Section IV.). This final sample from the reject stream was
collected after the volume of feedstock had been reduced from 10
to approximately three gallons by withdrawing the permeate flow
tube from the feed tank and disgarding all permeate generated
while only the reject stream was recirculated.
Ion.Exchange
The ion exchange resin used in Experiment #1 (see Section V.) was
Amberlite IRA-400 (CI), a Rohm and Haas Company product. It was
purchased from Aldrich Chemical Company (catalog no. 24, 766-9) in
the chloride form and used as received without further
preparation. Although no sizing data were supplied, it appeared
to be approximately 50-100 mesh. The resin was packed as a slurry
in deionized water into 20 mm (1.d.) Pyrex columns to a depth of
100 mm at a flow rate of 2-4 nl/m1nute. The resin bed was
supported by a integral coarse fritted disc. A small plug of
10
glass wool was carefully placed on top of the bed so that addition
of the ViChem feedstock would not disturb the resin material. The
column was filled completely with the ViChem feedstock and a
single-hole silicone stopper was placed in the top opening. Tygon
tubing was used to connect a 20-liter polyethylene feed tank to a
glass tube inserted through the stopper in the top of the column.
Flow through the column was controlled by the adjustment of a
rotaflow-type stopcock attached to the bottom of the column with a short length of Tygon tubing.
The feedstock was prepared by mixing equal volumes from each of
the eight, 5-gallon cubitainers sent to Hittman Ebasco from the
ViChem site and adjusting the pH to 9.2 with 5 N sodium
hydroxide. It was found that approximately 6 ml of aqueous sodium
hydorxide at this normality was sufficient to maintain a pH of 9.2
for each 10 liters of ViChem feedstock. An aliquot of this
feedstock was analyzed and found to contain 0.40 mg arsenic per 1 iter.
Elution runs were performed over two 24-hour periods. Times were
recorded at the beginning of sample collection. Each 100 ml
sample took about 36 minutes to collect. Immediately after each
sample was collected, a few drops of 50% (v/v) nitric acid were
added to reduce the pH below 2. Arsenic concentrations were
determined by graphite furnace AAS. The first 24-hour elution
(Run #1, Section V) was followed by a regeneration step using 10%
(w/v) sodium chloride in deionized water as the regenerant. The
resin bed was allowed to soak for 24 hours in this reagent, then
rinsed with several bed volumes of deionized water. Another
24-hour elution was repeated as described above (Run #2) to
complete one entire cycle of ion exchange operation.
11
The 1on exchange resin used 1n Experiment #2 was AG 1-X8, a
cleaned and sized Dowex 1-X8 resin purchased from Bio-Rad
Laboratories (catalog No. 140-1441). The resin was of mesh size
100-200 and obtained in the chloride form. Column packing and
experimental design details were as previously described for
Experiment #1. The same ViChem feedstock with pH adjusted to 9.2
was eluted through the resin bed. Run #1 lasted 24 hours and was
followed by a regeneration step using 10% sodium chloride and
column rinsing as before. Run #2 lasted almost 30 hours with six
aliquots of column elutriate collected at the times Indicated in
Section V, Experiment #2, Run #2. Times were recorded at the
beginning of sample collection. Each 100 ml sample took about 48
minutes to collect. Preservation and analysis of sample aliouots
were performed as described above.
C. Adsorption
Two different adsorbents were tested to determine their
effectiveness in removing arsenic from the ViChem aqueous
feedstock. Activated alumina (A12O3) was obtained from ALCOA
(F-l), and reagent grade titanic oxide (Ti02) purchased from
Fisher Chemical Company (T-315). Both adsorbents were used just
as they were received from the manufacturer without any further
purification or pretreatment.
For Experiments #1 and #2 (see Section VI), carefully weighed
portions of the adsorbent of interest were added to a series of
seven, 500 ml Pyrex Erlenmeyer flasks containing 250 ml of the
composited ViChem groundwater sample (pH>6.1). Procedures for
Experiment #3 were the same except that five 500 ml Teflon bottles < H 25
O o
w OO <js V£>
12
were used instead of Pyrex flasks. One flask or bottle in each
experiment contained feedstock but no adsorbent and served as the
control. The containers were capped and continuously agitated on
an Eberbach shaker table. After five days, 125 ml aliquots were
filtered through 0.45 micron filter discs and analyzed for arsenic
by graphite furnace AAS. One analysis was performed on each flask.
13
DISCUSSION OF RESULTS
A. Reverse Osmosis
Results of arsenic analyses on the permeate samples (Section IV)
Indicate that both the ST-10 and the MS-02 membranes were
effective in reducing arsenic levels not only below the discharge
limit of 50 ug/L, but to levels below the detection limit of the
graphite furnace AAS. The only problem encountered in operating
the RO machine was the rapid clogging of the prefilter cartridge.
During the several months that the original VIChem water samples
have reamined in cold storage, a fine rust-colored precipitate has
formed in each container. The precipitate settles to the bottom
of the containers, but when portions of the sample are removed for
experimentation, the resulting agitation resuspends the
precipitate. We have had good success in vaccuum filtering the
sample through 15 cm diameter glass fiber filters (Watman GF/F),
and reductions in flow rates across either RO membrane were not
noted during machine operation. However, the prefilter cartridge
clogged within minutes of the start of the RO process and was
automatically bypassed. The ST-10 membrane did an excellent job
of removing the reamining precipitate without signs of clogging.
With the much larger volumes of waste to process in the field,
however, treatment to remove suspended solids, although not
difficult, will have to be addressed 1n planning field-scale
treatment activities using reverse osmosis. As to the nature of
the precipitate, the large reductions 1n Iron and arsenic content
evident when comparing results of Initial characterization
(Section III) with values for the filtered reject strearil after
concentration by a factor of three, and pH values that decrease
from 6.3 to 5.3 during storage of the feedstock, indicate that
14
Iron and arsenic are co-prec1pitat1ng as hydroxides. Iron
oxy-hydroxides typically exhibit the light reddish-brown color
noted in this case. As Indicated by the arsenic content of the
concentrate stream during Experiments #1 and #2, precipitation
followed by filtration of the Fe/As hydroxides removed almost 97%
of the total arsenic from the sample and resulted In dissolved
arsenic values very close to the target concentration.
Due to relatively low arsenic content of the filtered feedstock,
the lack of a large volume of sample with which to experiment and
project time constraints, the point at which the arsenic content
of the concentrated reject stream reaches a level that results in
breakthrough into the permeate stream at detectable levels was
never determined. In evaluating these two membranes, the
capability of the MS-02 thin film polyamide unit to produce higher
flow rates by about four times that of the ST-10 cellulose acetate
unit at the same operating pressures appears to be the most
significant advantage. The purported durability of the ST-10
membrane is not a significant advantage due to the benign chemical
characteristics of the ViChem groundwater. If a simple
prefiltration procedure is developed, then the ability of the
MS-02 membrane to operate at lower pressures and still provide
satisfactory permeate flow rates makes this membrane the clear
choice assuming premature breakthrough . does not occur as the
arsenic associated with the reject stream is concentrated.
< H 2
o o
15 00 -vl NJ
Ion Exchange
The Amberlite IRA-400 (CI) strong base anion exchange resin used
1n Experiment #1 (see Section V) worked well 1n removing dissolved
arsenic from the ViChem wastewater. It should be noted that the
arsenic content of a composite of the waste had fallen from 1.61
ppm to 0.40 ppm since the sample was received. This is probably
due to precipitation during storage at 4°C (the raw feedstock had
not been preserved with nitric acid 1n order to avoid large
changes in pH), or by some combination of adsorption and
precipitation mechanisms when the pH was adjusted to 9.2 in
preparation for the column study. Throughout Experiment #1, the
average arsenic concentration of the column elutriate was less
than 6% of the feedstock and only one sample, taken immediately
after the regeneration step, was above the 50 ppb target value.
The elevated arsenic concentration of this sample was probably the
result of incomplete washing of residual regeneration reagent from the resin bed.
After column regeneration and during Experiment 11, Run #2, air
bubbles were noted within the resin bed. Efforts to eliminate
these bubbles proved fruitless and they probably affected the flow
characteristics of the column leading to more erratic arsenic data
from Run #2. Nevertheless, after one complete cycle of operation,
the column continued to remove 94% of the arsenic from the ViChem
feedstock. Because column breakthrough was never observed,
ultimate column capacity could not be determined.
If one assumes constant flow over the first 24-hour elution -period
(Experiment #1, Run #1) and average arsenic values as follows:
0 0 - 8 h o u r s « 1 0 u g / L a r s e n i c
8-16 hours • 22 ug/L arsenic
16 - 24 hours • 30 ug/L arsenic
16
Then, with a. feedstock arsenic concentration of 0.40 mg/L and 2
liters production volume, a total of 0.80 mg arsenic went in the
column of which (10 ug/L x 0.67 L) + (22 ug/L x 0.67 L) + (30 ug/L
x 0.67 L) - 0.04 mg arsenic passed through. Thus, the Amberlite
resin trapped 0.80 - 0.40 • 0.76 mg or 95% of the total arsenic.
Upon regeneration, a total of 3.42 mg/L x 0.145 L - 0.496 mg
arsenic was recovered in the bulk regenerant solution, roughly 65?*
of the total amount trapped. This figure is lower than expected
and should be considered when estimating the useful life of the
resin. However, during the second 24-hour elution period
(Experiment #1, Run #2) the arsenic data from elutriate samples do not indicate any loss of column efficiency.
The AG 1-X8 strong base anion exchange resin used in Experiment #2
proved to be an excellent substrate for removing dissolved arsenic
from the ViChem groundwater at a pH of 9.2. Throughout most of
the study, the arsenic concentrations of the column elutriates
were at or just slightly above instrumental detection limits. In
every case, the arsenic concentrations were well below the 50 ppb target value.
If one assumes a constant flow rate over the first 24-hour elution
period (Experiment #2, Run #1) and average arsenic concentrations as follows:
Then, as a mass balance exercise, with a feedstock arsenic concentration of 0.40 mg/L and 3.35 liters production volume, a total of 1.34 mg arsenic went in the column of which (3 ug/L x 1.12 I) + 6 ug/L x 1.12 L) + 8 ug/L x 1.12 L) - 0.02 mg arsenic passed through. Thus, the AG 1-X8 resin trapped 1.34 - 0.02 -
1.32 mg or greater than 98% of the total arsenic.
00 - 8 hours
8-16 hours
16 - 24 hours 6 ug/L arsenic 8 ug/L arsenic
3 ug/L arsenic
17
Upon regeneration, a total of 8.86 mg/L x 0.140 L - 1.24 mg
arsenic was recovered in the bulk regenerant solution, roughly 95%
of the total amount trapped. This figure is in line with typical regeneration efficiencies for Ion exchange resins.
In summary, either ion exchange resin would be effective in
polishing the ViChem groundwater in order to reduce total arsenic
content to below 50 ug/L. More consistent results were obtained
with the AG 1-X8 resin probably because 1t was precleaned and
sized by Bio-Rad Laboratories for research use. The Dowex 1-X8
equivalent would probably be more cost effective for larger scale pilot studies.
C. Activated Adsorption
Experiments #] and *3 - Alumina Adsorption Isotherm Test:
Alumina proved to be an effective adsorbent for removing arsenic
from the ViChem feedstock to concentrations below the target value
of 50 ug/L. Reaction flasks with at least 50 mg of added alumina
exhibited equilibrium arsenic concentrations (C) that achieved or
surpassed this target. Total arsenic removed from solution by the
alumina (X) was calculated by subtracting the arsenic
concentration (C 1n ug/L) of each flask after five days from that
of the control, then multiplying the result by the volume of
feedstock used (0.25 L). Solid phase loading was determined by
dividing arsenic removed (X) by the amount of adsorbent added
(M). Loading capacities thus obtained (X/M) are expressed as mg
As adsorbed per gram of alumina added. Figure I (page 7a) presents
< H
O O
00 •VJ cn
18
the combined data from both alumina batch adsorption tests
(Section VI - Experiments #1 and #3) plotted according to the
linerized form of the Freundlich Equilibrium Isotherm Model. .
Constants derived from this plot by the slope-intercept method are
presented on page 8. Data from Experiment #1 - Flasks A (the
control) B and G ; and Experiment #3 - Bottle A (the control) and
E were not included in the calculation of isotherm constants. In
the case of Experiment #1 - Flask B, the small amount of alumina
added was not enough to significantly alter the arsenic content
relative to the control. In the case of Experiment #1 - Flask G
and Experiment #3 - Bottle E, the equilibrium concentrations were
so low that adding more alumina had little effect.
Experiment #2 - Titanium Oxide Isotherm Test:
The titanic oxide adsorbent was found to be unsuitable for use ir
removing arsenic from the ViChem feedstock. As shown in Section
VI - Experiment #2, adding this adsorbent actually increased
arsenic concentrations relative to the control. , After a
discussion with representatives of Fisher Chemical Company, it was
learned that laboratory grade TiO? contains approximately 2.4 ppm
arsenic as a contaminant. However, this amount is much less than
the increase in arsenic concentration 1n the aqueous phase if all
arsenic in excess of that found in the control is assumed to come
from the Ti02- Instead, the presence of the Ti02 seems in some
way to alter the partitioning of arsenic between solid and. liquid
phases within the reaction flasks. The nature of this observed
interaction is unknown. Because of the apparent leaching of
arsenic from the solid phase, meaningful isotherm adsorption
constants could not be calculated for the Ti(>2 experiment.
Using the emperical values for K and 1/n presented on page 8, the
Freundlich Isotherm Model for adsorption of arsenic by alumina
from the ViChem groundwater at pH • 6.1 and temperature of 32° C,
predicts for an equilibrium arsenic concentration of 50 ug/L,
adsorbent loading would be approximately 0.71 mg arsenic per gram
of alumina. In order to reduce the Initial arsenic concentration
from 1610 ug/L to the 50 ug/L target value, about 2.3 g of alumina
would have to be added to each liter of ViChem groundwater.
However, upon close examination of the experimental data in
Section VI, Experiment #1 - Flask E and Experiment #2 - Bottle C
obtained equilibrium arsenic concentrations of 52 and 50 ug/L
using only 43 and 50 mg of alumina respectively. These data imply
that the addition of only about 0.2 g of alumina per liter of
ViChem groundwater would result 1n the necessary arsenic
reduction. The order of magnitude discrepancy can be explained bv
noting that the experimental controls (Flask/Bottle A) had
approximately 190 ug/L of arsenic, about 88% less than the
original feedstock. In order to determine whether the loss of
aqueous arsenic was due to precipitation or adsorption onto the
walls of the borosilicate glass flasks used in Experiment #1, a
second alumina adsorption study.(Experiment #3) was conducted
using Teflon bottles. Because the results of these two
experiments are almost Identical, the precipitation mechanism is
most likely the cause for the shift in the distribution
coefficient of arsenic from the aqueous to a solid phase prior to the addition of the alumina adsorbent.
From previous studies, solid phase alumina loading capacity for
the experimental conditions of these tests was expected to be
20
about 3 to 4 mg of arsenic per gram of alumina at 50 ug/L final
dissolved arsenic concentration; It has been shown that adsorbent
loading capacity is directly proportional to concentration,
especially at low concentrations. Binding and removal of most of
the arsenic by precipitation would lower the aqueous equilibrium
arsenic concentration and therefore the loading capacity of the
alumina. Another possible explanation for low capacity might
Involve the lack of any pretreatment of the adsorbent prior to
use. In this case, ALCOA research chemists suggest that the F-l
alumina be conditioned by preparing a slurry of the product in
water with sufficient hydrochloric acid to maintain the pH at or
below 5.5 units. Solid and liquid phases would then be separated
and the alumina washed with deionized water prior to use. It is
estimated that such preconditioning would result in a 2 to 3-fold
increase in the effective loading capacity by removing impurities
and increasing the number of active sites per gram of adsorbent.
21
APPENDIX OF LABORATORY DATA
22
QUALITY CONTROL: LAB CONTROL RESULTS
CLIENT: VINELAND CHEMICAL/WATERS
UNITS: ARSENIC, ug/L TOTAL ORGANIC CARBON, mg/L
MMHETER QC RESULT Qc TRUE VALUE , RECOVERY
T0C ' 30.0
ARSENIC 73
TOC 498
ARSENIC 72
TOC 37
ARSENIC 7]
29
80
459
80 37
80
103
91
108
90
100
89
23
< M 2
o o
M OO 00 o
QUALITY CONTROL: DUPLICATE RESULTS
CLIENT: VINELAND CHEMICAL/WATERS
UNITS:. ARSENIC ug/L TOC mg/L
PARAMETER SAMPLE ID SAMPLE RESULT
DUPLICATE RESULT XDIFFERENCE
TOC ARSENIC
ARSENIC
ARSENIC
4918 4922
5498
5802
1 1610
3420
8880
1 1610
-3470 8840
NON-CALCULABLE 0
1.5 0.5
24
QUALITY CONTROL: SPIKE RESULTS
CLIENT: VINELAND CHEMICAL/WATERS
UNITS: ARSENIC ug/L TOTAL ORGANIC mg/L
PARAMETER SAMPLE ID SAMPLE RESULT SPIKE RESULT SPIKE ADDED * RECOVERY
TOC 4918 1 43.8 50 88
ARSENIC 4922 1610 1600 20 0*
ARSENIC 5498 3420 4760 1200 112
ARSENIC 5803 399 448 20 245*
25
AP
PE
ND
IX J
VIN 001
1882
APPENDIX J TOXICOLOGICAL PROFILES
APPENDIX J TOXICOLOGICAL PROFILES
ARSENIC
INTRODUCTION
Arsenic is a naturally occurring metalloid which can be present in a number of different valence states and as a constituent in both inorganic and organic compounds. Elemental arsenic is used in industry as an alloying agent; both inorganic and organic arsenical compounds have been used as pesticides.
QUALITATIVE DESCRIPTION OF HEALTH EFFECTS
Toxicological information on arsenic has been reviewed by EPA in its Ambient Water Quality Criteria Document (EPA 1980) and Health Assessment Document -(EPA 1984). Acute poisoning of humans with arsenic may result in gastrointestinal effects, hemolysis, and neuropathy. Chronic exposure has characteristic toxic effects on the peripheral nervous system and, in children, on the central nervous system. In humans, keratosis, hyperpigmentation, precancerous dermal lesions, and cardiovascular injury frequently follow chronic exposure to arsenic. Arsenic has been found to be embryotoxic, fetotoxic, and teratogenic in several animal species.
Arsenic induces chromosomal aberrations and impairs DNA repair but has not been shown to be a point mutagen. Epidemiological studies have shown that inhalation of arsenic is strongly associated with lung cancer and perhaps with hepatic angiosarcoma; ingestion of arsenic has been linked to a form of skin cancer and more recently to bladder, liver, and lung cancer (Tseng et al. 1968, Chen et al. 1986). Although arsenic's potential as a human carcinogen has long been recognised, it is only recently that its carcinogenicity has been demonstrated in animal models.
•EPA is currently reevaluating the toxicity data base for the health effects of ingested arsenic (EPA 1986).
QUANTITATIVE DESCRIPTION OF HEALTH EFFECTS
The EPA (1984) has classified arsenic in Group A--Human Carcinogen. This category applies to chemical agents for which there is sufficient evidence of carcinogenicity from animal and human studies.
INGESTION TOXICITY
To estimate the risks posed by ingestion of arsenic, EPA (1984) used the data that Tseng et al. (1968) obtained in Taiwan. Tseng et al. used the Weibull model to relate skin cancer incidence, age, and level of exposure via drinking water. In 37 villages that had obtained drinking water from artesian wells with various elevated levels of arsenic for 45 years, 40,421 individuals were examined for hyperpigmentation, keratosis, skin cancer, and blackfoot disease (in which impaired peripheral circulation leads to gangrene). The local well waters were analyzed for arsenic, and age-specific cancer prevalence rates were found to be correlated with both local arsenic concentrations and age (duration of exposure). Extrapolation to low dose levels yielded a risk of 4.3x10*^ associated with lifetime exposure to 1 /ig/liter of arsenic in drinking water (EPA 1984). In the same area, Chen et al. (1986) reported an association between bladder, lung, and liver tumors and ingestion of arsenic-contaminated drinking water. EPA (1986) reevaluated the carcinogenic potency of arsenic because results indicated that the risk of skin cancer was about an order of magnitude lower than originally predicted. However, the possibility that various internal tumors may be associated with arsenic exposure was not factored in (EPA 1986). EPA (1987) currently is recommending a cancer potency factor for oral exposure to arsenic of 1.5 (mgAg/day) "l.
Another study (Astolfi et al. 1981) has shown an association between the ingestion of arsenic in drinking water (at concentrations around 1 ppm) and skin cancer. Epidemiological studies conducted in the United States have not yet shown such an association, but the reported studies were generally too insensitive to have shown such an association if it had existed at the predicted magnitude (Andelman and Barnett 1983, EPA 1984).
—Hg
The EPA primary drinking water standard for arsenic is 50 #ig/liter (CFR 1984). This value was established as a maximum allowable level for arsenic in drinking water by the U.S. Public Health Service in 1942, and it continues to be used in the current EPA regulations (EPA 1985). EPA's Office of Drinking Water is considering maintaining the present maximum contaminant level for arsenic in municipal drinking water supplies (EPA 1985), and has proposed a maximum contaminant level goal (MCLG) of 50 jig/liter.
One factor complicating risk assessments for ingested arsenic is possible variation in carcinogenic potency according to the chemical form of arsenic. Trivalent inorganic arsenic compounds are generally more toxic than pentavalent inorganic arsenic compounds or organic arsenic compounds (EPA 1980, 1984). Epidemiological studies of copper smelter workers have often reported that increased lung cancer incidences were associated with exposure to trivalent inorganic arsenic (see below). For this reason, it has been speculated that the CAG unit risk for ingested arsenic may be applicable only to trivalent inorganic arsenic (EPA 1980). However, recent studies have shown that water samples from the area of Taiwan where Tseng et al.'s studies were carried out contain primarily pentavalent inorganic arsenic and no organic arsenicals (EPA 1984). The CAG unit risk is therefore applicable to other circumstances in which pentavalent arsenic compounds are ingested.
INHALATION TOXICITY
The health risks posed by airborne arsenic compounds have been reviewed in considerable detail by EPA (1984), and studies on the carcinogenicity of arsenic compounds were reviewed by the International Agency for Research on Cancer (IARC) in 1980. Risk assessments for exposure to airborne arsenic were presented by the Occupational Safety and Health Administration OSHA (1983) and EPA (1984). The following summary is based on these reviews and risk assessments and on an extensive review of the primary literature.
< M It is well established that inhalation of certain arsenic compounds can cause ^ cancer in humans. Several studies of workers in smelters and plants § manufacturing arsenical pesticides have shown significant excess rates of death 1-1
from lung cancer (EPA 1984). The carcinogenic effects of inhaled arsenic have ^ CO o*
only recently been demonstrated in experimental animals, using a model that enhanced.retention of arsenic in the lung (Ishinishi et al. 1983, Pershagen et al. 1983).
EPA (1984) based its quantitative risk assessment for inhaled arsenic on five studies of three exposed worker populations (Higgins et al. 1982, Lee-Feldstein 1983, Brown and Chu 1982, 1983a,b, Enterline and Marsh 1980, Ott et al. 1974). All five studies showed excess risks of lung cancer that were related to the intensity and duration of exposure and the duration of follow-up (latency). The estimates of unit risk1 obtained from the five studies were in reasonably good agreement, ranging from 1.25xlO*3 to 1.36xl0*2 (Mg/m3)*1. EPA omitted the highest value, derived from the study of Ott et al. which was considered least reliable, and calculated the geometric mean for each of the two remaining populations and then an overall geometric mean to obtain a best estimate of 4.3x10 (ng/m )" for the unit risk. This unit risk estimate corresponds to an inhalation cancer potency factor of 50.1 (mgAg/day)'1 (EPA 1984).
Given the limitations of the available data on exposure and risk, EPA's procedures appear reasonable, and the consistency of results among the studies is impressive. The figure of 4.3xl0"3 (jig/m3)*1 is thus an estimate of the unit risk for exposure to the high levels characteristic of the three work environments where the data were obtained. This value is intended to be an upper-limit estimate of risk, and actual risks are unlikely to be higher.
The American Conference of Governmental Industrial Hygienists (ACGIH 1986) recommends a time-weighted average threshold limit value (TLV) of 0.2 mg/m3 for arsenic and soluble compounds of arsenic.
SUMMARY
Arsenic's carcinogenic potential in humans has been amply demonstrated. The quantitative estimates of oral dose-response relationships derived from Tseng et al. (1968) upon which the EPA assessment was based are concordant with other estimates of arsenic's carcinogenic potency based on inhalation exposure (EPA
1 The unit risk is the risk associated with lifetime exposure to 1 unit
(generally 1 mg/kg/day, 1 mg/liter, or 1 ng/m ) of a substance.
1984). EPA is currently reevaluating the toxicity data base for the health effects of ingested arsenic (EPA 1986).
/ I J
Both unit risks were derived from epidemiological studies and are appropriate for application to human populations exposed to arsenic under comparable circumstances. Neither unit risk is based on a calculation that incorporates important conservative assumptions, except for the assumption of a linear dose-response relationship, which is supported by the data from the occupational studies.
SUMMARY OF ARSENIC CRTTF.RTA
EPA carcinogen classification
Oral carcinogenic potency (q^*)
Inhalation carcinogenic potency (q^*)
Maximum Contaminant Level (MCL)
Proposed Maximum Contaminant Level Goal (MCLG)
AWQC (cogcentration associated with a 10 excess lifetime cancer risk)
Ingestion of water only Ingestion of water and aquatic
organisms Ingestion of aquatic organisms
Group A
1.5 (mg/kg/day) -1
50.1 (mg/kg/day)
50 Mg/liter
50 Mg/liter
2.5 ng/liter 2.2 ng/liter
17.5 ng/liter
-1
REFERENCES
AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH). 1986. Documentation of the Threshold Limit Values and Biological Exposure Indices. 5th ed. Cincinnati, Ohio
ANDELMAN, J.B., and BARNETT, M. 1985. Feasibility Study to Resolve Questions on the Relationship of Arsenic in Drinking Water to Skin Cancer. U.S. Environmental Protection Agency. Cooperative Agreement No. CR-806815-02-1
ASTOLFI, E., MACCAGNO, A., GARCIA-FERNANDEZ, J.C., VACCARO, R., and STIM0LA,|R. 1981. Relation between arsenic in drinking water and skin cancer. Biol. Trace Elem. Res. 3:133-143
BROWN, C.C., and CHU, K.C. 1982. Approaches to epidemiologic analysis of prospective and retrospective studies: Example of lung cancer and exposure to arsenic. In Prentice, R.L., and Whittemore, A.S., eds. Environmental Epidemiology: Risk Assessment. SIAM, Philadelphia
BROWN, C.C., and CHU, K.C. 1983a. A new method for the analyses of cohort studies: Implications of the multistage theory of carcinogenesis applied to occupational arsenic exposure. Environ. Health Perspect 50:293-308
BROWN, C.C.,.and CHU, K.C. 1983b. Implications of the multistage theory of carcinogenesis applied to occupational arsenic exposure. JNCI 70:455-463
CHEN. C., CHUANG, Y., YOU, S., LIN, T., and WU, H. 1986. A retrospective study on malignant neoplasms of bladder, lung and liver in blackfoot disease endemic area in Taiwan. Brit. J. Cancer 53:399-405
CODE OF FEDERAL REGULATIONS (CFR). 1984. 40 CFR 141, Environmental Protection Agency, National Interim Primary Drinking Water Regulations. U.S. Government Printing Office, Washington, D.C.
ENTERLINE, P.E., and MARSH, G.M. 1980. Mortality studies on smelter workers. J. Ind. Med. 1:251-259
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1980. Ambient Water Quality Criteria for Arsenic. Office of Water Regulations and Standards, Criteria and Standards Division, Washington, D.C. October 1980. EPA 440/5-80-021
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984. Health Assessment Document for Inorganic Arsenic. Office of Health and Environmental Assessment, Washington, D.C. March 1984. EPA 600/8-83-021F
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985. National primary drinking water regulations; synthetic organic chemicals, inorganic chemicals and microorganisms; proposed rule. 40 CFR Part 141. (Fed. Reg. 50(219):46936-47025 (November 13, 1985)
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1986. Special Report on Ingested Inorganic Arsenic and Certain Human Health Effects. Risk Assessment Forum, Washington, D.C. October 1986. External Review Draft
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987. Memo from Sandra Lee (Program Manager, Regional Support Team, Toxics Integration Branch) to Addresses. Subject: Updated Reference Dose and Cancer Potency Numbers for Use in Risk Assessments. Office of Solid Waste and Emergency Response. Washington, D.C. October 1987. 19 pp. (Sandra Lee: (202)382-4307)
HIGGINS, I., WELCH, K., and BURCHFIELD, C. 1982. Mortality of Anaconda smelter workers in relation to arsenic and other exposures. Dept. of Epidemiology, University of Michigan, Ann Arbor, Michigan (As cited in EPA 1984a)
INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (IARC). 1980. IARC Monographs on the Evaluation of Carcinogenic Risk of Chemicals to Humans. Vol. 23: Some Metals and Metallic Compounds. World Health Organization Lyon France. Pp. 39-324 ' '
ISHINISHI, N.. YAMAMOTO, A., HISANAGA, A., and INAMASU, T. 1983. Tumorigenicity of arsenic trioxide to the lung in Syrian golden hamsters by intermittent instillations. Cancer Lett. 21:141-147
LEE-FELDSTEIN, A. 1983. Arsenic and respiratory cancer in man: Follow-up of an occupational study. In Lederer, W., and Fensterheim, R., eds. Arsenic: Industrial, Biomedical and Environmental Perspectives. Van Nostrand Reinhold, New York
OCCUPATIONAL SAFETY AND HEALTH ADMINISTRATION (OSHA). 1983. Occupational exposure to inorganic arsenic. Fed. Reg. 48:1864-1903
OTT, M.G., HOLDER, B.B., and GORDON, H.L. 1974. Respiratory cancer and occupational exposure to arsenicals. Arch. Environ. Health 29:250-255
PERSHAGEN, G., NORDBERG, G., and BJORKLUND, N.E. 1983. Carcinomas of the respiratory tract in hamsters given arsenic trioxide and/or benzo(a)pyrene by the pulmonary route. Environ. Res. (In Press). (As cited in EPA 1984)
TSENG, V.P., CHU, H.M., HOW, S.W., FONG, J.M., LIN, C.S., and YEH, S. 1968. Prevalence of skin cancer in an endemic area of chronic arsenicism in Taiwan. J. Natl. Cancer Inst. 40:453-463
APPENDIX J (con't)
CADMIUM
INTRODUCTION
Cadmium is an element of the transitional metal series that occurs widely in nature, usually in lead or zinc ores. Elemental cadmium is insoluble in water, although many cadmium salts are quite soluble (EPA 1985 a,b). The general human population is exposed to cadmium in drinking water and food; cigarette smoke also contains high levels of cadmium. Additional inhalation exposure occurs in industrial settings (EPA 1985a,b).
QUALITATIVE DESCRIPTION OF HEALTH EFFECTS
The toxicology of cadmium has been reviewed by Friberg et al. (1974), IARC (1976), and EPA (19S0, 1981, 1985b,c). Injection of cadmium into laboratory animals results in injection-site sarcomas and testicular tumors of the Leydig cells (EPA 1981) . A relationship between human exposure to cadmium and cancer of the prostate, lung, or kidney has been suggested by several epidemiological studies (Thun et al. 1985, EPA 1985b). Cadmium may impair DNA repair but has not been shown to be mutagenic. It is a well-documented animal teratogen.
Cadmium bioaccumulates in mammals, particularly in the kidney and liver (EPA 1981, 1985c). Epidemiological studies have revealed an association between nonmalignant pulmonary diseases and inhalation of cadmium. Renal tubular dysfunction, of which the first sign is proteinuria, occurs at lower levels of oral or inhalation exposure to cadmium and may be the primary defect responsible for the bone damage characteristic of Itai-Itai disease. It is also suspected that chronic exposure to cadmium produces hypertension, anemia, sensory loss (particularly smell), endocrine alterations, and immunosuppression in humans.
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QUANTITATIVE DESCRIPTION OF HEALTH EFFECTS
INGESTION TOXICITY
The maximum contaminant level (MCL) established for cadmium by EPA in its national interim primary drinking water standards and the Ambient Water Quality-Criterion for the protection of human health are both 10 Mg/liter (EPA 1980, CFR 1984). EPA established the standard for cadmium on the basis of the "generally accepted" estimate of 200 Mg/g-wet weight of cadmium in the renal cortex as the critical concentration for renal toxicity. Friberg et al. (1974) estimated that daily ingestion of 250-350 jig cadmium over 50 years would result in such renal concentrations. Other more recent reviews suggest that 200 4g/day is an acceptable daily limit for cadmium intake.
A provisional AADI for cadmium was calculated by EPA (1985a) using the data by Friberg et al. (1974) and renal dysfunction as an endpoint. A daily cadmium of intake of 0.352 mg/day was identified as the LOAEL for renal effects in humans. This LOAEL corresponds to a renal cortex concentration of cadmium of 200 /ig/g. Assuming consumption of 2 liters of water per day and applying an uncertainty factor of 10, an AADI for cadmium of 0.018 mg/liter was derived (EPA 1985a).
The EPA Office of Drinking Water (EPA 1985a) has promulgated a proposed maximum contaminant level goal (MCLG) for cadmium of 0.005 mg/liter. The proposed MCLG is based on the estimate of 200 Mg/g wet weight of cadmium in the renal cortex as the critical concentration for renal toxicity (Friberg et al. 1974) and a 25% contribution to daily exposure from drinking water (AADI of 0.18 mg/liter x 0-25 - .005 mg/liter). The proposed MCLG is comparable to the NAS and WHO guidelines of 0.005 mg/liter (EPA 1985a).
A risk reference dose (RfD) of 5x10 mg/kg/day can be derived from the EPA Office of Drinking Water (ODW) analysis. Using the AADI (adjusted acceptable daily intake) of 0.18 mg/liter and assuming a person weighs 70 kg and consumes 2 liters of water per day, an oral RfD for cadmium of .0005 mg/kg/day can be calculated (.018 mg/liter x 1/70 kg x 2 liters - 0.0005 mg/kg/day).
EPA (1984) recommended that 20 /ig/liter be applied as the maximum additional increment from drinking water sources based on the drinking water criterion level of 10 /ig/liter cadmium proposed by EPA (1980) and assuming that an adult consumes 2 liters of water per day. The resulting acceptable intake chronic (AIC*) is 5.7x10 ^ mg/kg/day (assuming that an individual weighs 70 kg).
Aughey et al. (1984) reported that treatment of male Wistar rats for only 24 weeks with 50 mg/liter cadmium in their drinking water produced clear symptoms of nephritis when the accumulated renal concentration of cadmium was 60 /ig/g wet weight. This last concentration is less than one-third the 200 Mg/g wet weight identified as the critical level in humans.
Cadmium and some of its compounds are known to be carcinogenic in experimental animals exposed by injection or inhalation, but the carcinogenic effects are absent when cadmium is administered orally (EPA 1985b). It is not known which cadmium compounds are responsible for the inhalation carcinogenic effects in humans.
INHALATION TOXICITY
EPA (1981) has reviewed the health risks posed by airborne cadmium compounds in considerable detail, while studies on the carcinogenicity of cadmium compounds have been reviewed by the IARC (1976). Both reviews were updated by EPA (1985b), which also presented a risk assessment for exposure to airborne cadmium.
Applying the criteria described in EPA's Guidelines for Assessment of Carcinogenic Risk (EPA 1986), cadmium has been classified by EPA (1985a, 1987) on the basis of inhalation data in Group Bl--Probable Human Carcinogen. This category applies to agents for which there is limited evidence from human studies and sufficient evidence from animal studies (EPA 1984).
The evidence that exposure to airborne cadmium compounds increases the risk of cancer in humans is characterized as limited (IARC 1982, EPA 1985b). Although several studies of exposed workers have suggested that airborne cadmium increases the risk of cancer of the lung or prostate, most of the results have
been inconclusive because of small sample sizes, lack of statistical significance, confounding effects of other exposures, or other factors. The most recent study (Thun et al. 1985), however, showed a significant increase in the number of lung cancer deaths (16 observed versus 6.99 expected) among a group of cadmium smelter workers. Although this finding may be somewhat confounded by the effects of smoking and exposure to arsenic, EPA (1985b) concluded that neither of the latter was sufficient to explain the observed effect.
EPA (1985b) based its quantitative risk assessment for inhaled cadmium on the study by Thun et al. (1985). Very scanty information on exposure levels and incomplete information on exposure duration were used to compile a single average measure of cumulative exposure of the exposed workers. This was converted to a lifetime average exposure level. The extent of the deviations of the exposure estimates from the actual exposure is unknown. Use of the lifetime average exposure level in the risk calculations incorporates the questionable assumption that exposure to cadmium at any time during life would lead to the same increase in lifetime risk of lung cancer. The data were then fitted to a model which assumed that the effect of exposure to cadmium would be to increase the background rate of lung cancer by a factor proportional to the lifetime average exposure level. The selection of this model was arbitrary, in that no information on the dose-response relationship was provided between exposure and induction of lung cancers, and excess risk is likely to be very conservative. The best estimate of the exposure and response of the exposed
- 3 3 - 1 population gave rise to a "unit risk" estimate of 1.6x10 (Mg/m ) For a 70 kg person breathing a volume of air of 20 m3/day, this unit risk estimate corresponds to a cancer potency factor of approximately 6.1 (mg/kg/day). However, because of uncertainties in the estimates of both exposure and response, the range of uncertainties in the unit risk estimate was very wide, ranging from 4.3x10*6 to 3.8x10*2 (/ig/m3)'1. The last figure was obtained by combining "worst case" estimates of all exposure and risk parameters, and probably represents a "worse than worst case" calculation.
Given the severe limitations of the available data, this quantitative risk assessment appears as reasonable as could be achieved. However, the estimate of "unit risk" is extremely uncertain and probably extremely conservative. The
study itself is not regarded as fully conclusive in showing any increased cancer risk and at least part of this is attributable to confounding factors. The exposure estimates are very uncertain, the assumption of a linear exposure response relationship is arbitrary, and the extrapolation over a range of 5 ordets of magnitude in dose is very tenuous. Thus, the estimate of "unit risk" presented by EPA (1985b) could be inaccurate and is likely to be conservative when applied to general population exposure.
Recent studies have firmly associated inhalation of airborne cadmium with lung cancer in animals. In a bioassay in which male Wistar rats were administered cadmium chloride aerosols 23 hours/day for 18 months at concentrations of 0
3 12.5, 25, and 50 /jg/m , Takenaka et al. (1983) found a highly significant dose-response relationship. The incidence of lung carcinomas was 0/38, 6/39, 20/38, and 25/35 in the four treatment groups. This marked response adds further support to the evidence on the carcinogenicity of inhaled cadmium and justifies the use of Thun et al.'s (1985) data as the basis for risk assessments of airborne cadmium. Like the injection-site sarcomas and Leydigomas reported in animals (EPA 1985b), these lung carcinomas might be interpreted as carcinogenic responses in the directly exposed tissue only.
The American Conference of Governmental Industrial Hygienists (ACGIH 1986) recommends a time-weighted average Threshold Limit Value (TLV) of 0.05 mg/m3 for all forms of cadmium dusts and salts and a ceiling limit of 0.05 mg/m3 for cadmium oxide fume.
SUMMARY
Cadmium has not been demonstrated to be a systemic carcinogen, but it has been shown to be a highly potent pulmonary carcinogen (see Takenaka et al. 1983) and renal effects are associated with ingestion. For inhalation, the unit risk
- 3 3 - 1 value of 1.8x10 (ng/a ) (which corresponds to a cancer potency factor of 6.1 (mg/kg/day)**) is an appropriate basis for risk assessment. This unit risk was derived from epidemiological data and does not incorporate any conservative assumptions (except that the dose-response relationship is linear), but it is subject to a wide range of uncertainty. For ingestion, the calculations upon which the MCL and ambient water quality criterion are based are equally
applicable to ingestion via soil or other media. Based on the assessment of Friberg et al. (1974), daily ingestion of 20 cadmium (in addition to background exposure via food) would contribute between 6% and 8% of the estimated critical daily intake of cadmium. This intake of 20 pg/day from other than normal dietary sources was intended to provide an ample margin of safety, but Aughey et al.'s (1984) study suggests that it may not be as conservative as originally intended.
SUMMARY OF CADMIUM CRITERIA
EPA carcinogen classification (inhalation only)
Oral chronic allowable intake (AIC)
Inhalation carcinogenic potency (q^*)
Maximum Contaminant Level (MCL)
Proposed MCLG
RfD (ingestion, based on ODW analysis)
Group B1
,-4 5.7x10 mg/kg/day
6.1 (mg/kg/day)
10 g/liter
5 jig/liter -4 5x10 mg/kg/day
REFERENCES
AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH). 1986. Documentation of the Threshold Limit Values and Biological Exposure Indices. 5th ed. Cincinnati, Ohio
AUGHEY, E., FELL, G.S., SCOTT, R., and BLACK, M. 1984. Histopathology of early effects of oral cadmium in the rat kidney. Environ. Health Perspect. 54:153-161
CODE OF FEDERAL REGULATIONS (CFR). 1984. 40 CFR 141, Environmental Protection Agency, National Interim Primary Drinking Water Regulations. U.S. Government Printing Office, Washington, D.C.
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1980. Ambient Water Quality Criteria for Cadmium. Environmental Criteria and Assessment Office, Cincinnati, Ohio. EPA 440/5-80-025
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1981. Health Assessment Document for Cadmium. Research Triangle Park, North Carolina. EPA 600/8-81-023.
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984. Health Effects Assessment for Cadmium. Environmental Criteria and Assessment Office, Cincinnati, Ohio September 1984. EPA 540/1-86-038
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985a. National primary drinking water regulations; synthetic organic chemicals, inorganic chemicals and microorganisms; proposed rule. 40 CFR Part 141. Fed. Reg. 50(219):46936-47025 (November 13, 1985)
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985b. Updated Mutagenicity and Carcinogenicity Assessment of Cadmium. Addendum to the Health Assessment Document for Cadmium (May 1981; EPA/600/8-81/023). Office of Health and Environmental Assessment, Washington, D.C. June 1985. EPA 600/8-83-025F
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985c. Drinking Water Criteria Document for Cadmium (Final Draft). Office of Drinking Water, Washington D.C. April 1985. PB86 117934/AS
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985d. Water quality criteria; notice of final ambient water quality criteria documents. Fed Reg. 50:30784-30796. (July 29, 1985)
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1986. Guidelines for carcinogenic risk assessment. Fed. Reg. 51:33992-34003. (September 24)
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987. Integrated Risk Information System (IRIS). Environmental Criteria and Assessment Office. Cincinnati, Ohio. Revised September 30, 1987
FRIBERG, L.T., PISCATOR, M., and N0RDBERG, G. 1974. Cadmium in the Environment. 2nd ed. CRC Press, Cleveland
INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (IARC). 1976. IARC Monographs on the Carcinogenic Risk of Chemicals to Man. Vol. 11: Cadmium, Nickel, Some Epoxides, Miscellaneous Industrial Chemicals, and General Considerations on Volatile Anaesthetics. World Health Organization, Lyon France. Pp. 39-74
INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (IARC). 1982. IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Vol. 29: Some Industrial Chemicals and Dyestuffs. World Health Organization, Lyon, France
TAKENAKA, S., OLDIGES, H., KOENIG, H., HOCHRAINER, D., and OBERDOERSTER, G. 1983. Carcinogenicity of cadmium chloride aerosols in W rats. JNCI 70:367-373
THUN, M.J., SCHNORR, T.M., SMITH, A.B., HALPERIN, W.E., and LEMEN, B.A. 1985. Mortality among a cohort of U.S. Cadmium production workers - An update JNCI 74:325-333
APPENDIX J (con't)
LEAD
INTRODUCTION
Elemental lead is heavy, ductile, and bluish-white in color, with the atomic number 82 and an atomic weight of 207 g/mole. It is used widely in industry because of its softness, resistance to corrosion and radiation, and high density. Lead is also used as a paint pigment, in solders, and in storage batteries.
TOXICOKINETICS
Absorption of lead from the gastrointestinal tract is estimated at 10-15%. For adult humans, the deposition rate of particulate airborne lead is 30-50%, and essentially all of the lead deposited is. absorbed. Respiratory uptake by children appears to be greater on a body weight basis. More than 99% of blood lead in humans is associated with the erythrocytes, but it is the very small fraction of lead transported in plasma and extracellular fluid that provides lead to the various body organs. Lead is stored in the body in bone, kidney, and liver, where it may remain for long periods of time. Lead is primarily excreted by the kidneys into the urine, and lesser amounts are eliminated by biliary excretion (EPA 1984a).
QUALITATIVE DESCRIPTION OF HEALTH EFFECTS
The following Information has been summarized from EPA (1984a). Lead has diverse biological effects in humans and animals. Its effects are seen at the subcellular level of structures and processes as well as at the overall level of general functioning of the body. Considerable data exist on the effects of lead exposure in humans, but the effects are generally related to blood lead levels rather than to estimated exposure.
A major problem associated with lead exposure is the ublquitbus nature of the compound. Unlike most other contaminants for which exposure may be related to a specific route or situation, substantial background lead exposure occurs,
primarily through food. This background exposure must be considered when additional significant exposure routes are identified.
The major toxic effects caused by exposure to lead are alterations in the hematopoietic and nervous systems. Anemia caused by lead exposure has the following pathogenesis. Heme synthesis is inhibited by the effects of lead on a number of steps in the biosynthetic pathway. Specifically, lead stimulates delta-aminolevulinic acid synthetase (ALA-S) and therefore increases the production of delta-aminolevulinic acid dehydrase (ALA-D) and therefore decreases the production of porphyrobilinogen from ALA; and finally, lead inhibits the incorporation of iron into protoporphyrin to form heme. No threshold has been identified for this effect on heme production. Decreased heme production results in decreased hemoglobin production and anemia. Decreased heme production can also have deleterious effects on other heme-containing proteins, such as cytochrome P450, which detoxify certain chemicals in the body. Impaired heme synthesis has been reported in adults at levels of less than 30 Mg/dl lead in the blood (EPA 1984a).
Two types of neurotoxic effects are associated with exposure to lead. Levels of lead in the blood (PbB) of over 80 g/dl in children and over 100 Mg/dl in sensitive adults can cause severe, irreversible brain damage, encephalopathy, and possibly death. Persons with these high levels may be asymptomatic or show only slight signs of intoxication, but rapid deterioration can occur. In children, permanent learning disabilities are seen at these levels, even if there are no overt signs of lead poisoning (EPA 1984a).
Other adverse effects are associated with exposure to low levels of lead. Slow nerve conduction in peripheral nerves has been seen in adults at 30-40 jig/dl blood lead level (PbB); altered testicular function was observed in men with PbB levels as low as 40-50 g/dl; and renal dysfunction has been associated with PbB levels as low as 40 pg/dl (EPA 1984a).
Conflicting evidence is available for the genotoxicity of lead and lead compounds. Lead salts have not been shown to be mutagenic in bacteria or fungi, but they have been reported to induce mutations in vascular plants. Certain compounds induce chromosome abnormalities in plants but not in cultured
mammalian cells. Positive results have bee'obtained in a cell transformation assay. In vivo studies of lead salts produce conflicting results. Chromosomal aberrations have been induced in bone marrow of rats and mice and in cultured peripheral lymphocytes obtained from monkeys. Cytogenetic studies with people exposed to lead have produced positive results in approximately half the reports (IARC 1982).
Decreased fertility and fetotoxic effects have been reported in laboratory rodents exposed to lead, but these effects may have been related to deficiencies of other trace metals in these studies. Lead exposure has been associated with spontaneous abortions, premature delivery, and early membrane rupture in humans; however, reliable exposure estimates are lacking in most cases (EPA 1984b). Skeletal malformations after lead injection have been reported in rats, mice and hamsters (Leonard et al. 1984).
QUANTITATIVE DESCRIPTION OF HEALTH EFFECTS
Oral ingestion of certain lead salts (lead acetate, lead phosphate, lead subacetate) have been associated with increased renal tumor frequency in rats (EPA 1985a), but no quantitative estimate of excess cancer risk has been performed by the Carcinogen Assessment Group of EPA. Applying the criteria described in EPA's Guidelines for Carcinogenic Risk Assessment (EPA 1986), these lead salts have been classified by EPA (1985b) in Group B2--Probable Human Carcinogen. This category applies to agents for which there is inadequate evidence from human studies and sufficient evidence from animal studies. However. EPA (1985b) also has noted that the available data provide an insufficient basis on which to regulate lead acetate, lead phosphate, and lead subacetate as human carcinogens. Dosages that induced kidney tumors in rats were very high (beyond the lethal dose in humans), and several extensive epidemiology studies have not shown an association between lead exposure and increased incidences of tumors in occupationally exposed workers (EPA 1985b).
The interim maximum contaminant level (MCL) for drinking water and the ambient water quality criterion are both 50 Mg/liter (EPA 1980, CFR 1984). In deriving the ambient water quality criterion, EPA determined that consumption of water
contaminated with 50 jig/liter would increase PbB levels to around 15 Mg/dl in children. If the population average was 15 Mg/dl, the Centers for Disease Control (CDC) calculated that 99% of all children would have a PbB level of
\
less than 30 ng/dl. This was based on a CDC definition of "lead toxicity" in a child as a PbB level greater than or equal to 30 pg/dl and an erythrocyte protoporphyrin (EP) level greater than or equal to 50 Mg/dl. Based on this calculation, EPA determined that the present drinking water standard was acceptable as an upper limit. However, based primarily on the new information suggesting that neurological impairment may occur in children at PbB levels of less than 30 Mg/dl, CDC has revised its criteria for lead toxicity to PbB levels greater than or equal to 25 ng/dl and EP levels greater than or equal to 35 Mg/dl (CDC 1985).
A drinking water maximum contaminant level goal (MCLG) of 20 Mg/liter (.02 mg/liter) has been proposed by the EPA Office of Drinking Water (ODW). The proposed MCLG is based upon the health effects of lead in infants and pregnant women as a sensitive subpopulation (EPA 1985b). Blood levels above 15 ng/dl were identified as the level of concern, and fetuses and infants under 2 years of age are the sensitive subpopulation. In order to protect the fetus, it was considered advisable to limit the blood lead level in women of child-bearing age to between 15 and 20 ng/dl since studies indicate that the ratio of fetal/maternal blood lead values in close to 1:1 (Hubermont et al. 1978 as cited in EPA 1985a). An absorption constant of 0.16 was identified as the ratio of blood lead in infants to lead Intake in the diet (Ryu et al. 1983 as cited in EPA 1985b). An oral risk reference dose (RfD) of
-4 6x10 mg/kg/day can be derived based on the ODW analysis (0.02 mg/liter x 2 liter/day x 1/70 kg).
The Clean Air Act National Ambient Air Quality Standard for lead is 1.5 fig/a^. This standard is currently being evaluated for revision (EPA 1985c).
Acceptable intakes for chronic or subchronlc periods of exposure were not calculated for either inhalation or oral ingestion in the Health Effects Assessment Document (EPA 1984b) because the general population is already accruing unavoidable background exposures through food, water, and dust. Any
significant increase above background exposure would represent a cause for concern.
At present, human health criteria for lead in soil have not been established in the United States. The United Kingdom Directorate of the Environment has developed a tentative guideline of 550 ppm for lead in soil in residential areas (Smith 1981). Vernon Houk of the Centers for Disease Control has been quoted as indicating that levels of lead in soil of 300-400 ppm are acceptable based on studies of childhood lead poisoning (Mielke et al. 1984).
The American Conference of Governmental Industrial Hygienists (ACGIH 1986) recommends a time-weighted average Threshold Limit Value (TLV) of 0.15 mg/m3 lead in air.
SUMMARY OF LEAD CRITERIA
Interim MCL 50 Mg/liter Proposed MCLG 20 g/liter Oral RfD (based on ODW analysis) 6xl0*4 mg/kg/day
National Ambient Air Quality Standard 1.5 >ig/m3
REFERENCES
AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH). 1986. Documentation of the Threshold Limit Values and Biological Exposure Indices. 5th ed. Cincinnati, Ohio
CENTERS FOR DISEASE CONTROL (CDC). 1985. Preventing Lead Poisoning in Young Children. Public Health Service, Chronic Disease Division, Atlanta, Georgia. July 1985
CODE OF FEDERAL REGULATIONS (CFR). 1984. 40 CFR 141, Environmental Protection Agency. National Interim Primary Drinking Water Regulations. U.S. Government Printing Office, Washington, D.C.
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984a. Air Quality Criteria for Lead. Environmental Criteria and Assessment Office, Research Triangle Park, North Carolina. External Review Draft. September 1984. EPA 600/8-83-028B
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984b. Health Effects Assessment for Lead. Environmental Criteria and Assessment Office. Cincinnati. Ohio. EPA 540/1-86-055
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985a. Draft Health Advisory for Lead. Office of Drinking Water. Washington, D.C. September 30, 1985
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985b. National primary drinking water regulation; synthetic organic chemicals, inorganic chemicals and microorganisms; proposed rule. Fed. Reg. 50:46936-47025 (November 13 1985) . '
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985c. Draft air quality criteria document for lead: Notice of a corrigendum to the second external review draft. Fed. Reg. 50:14289-14294 (April 11, 1985)
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985d. Water quality criteria; notice of final ambient water quality criteria documents. Fed. Reg. 50:30784-30796 (July 29, 1985)
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1986. Guidelines for carcinogenic risk assessment. Fed. Reg. 51:33992-34003 (September 24, 1986)
HUBERMONT, G., BUCHET, J.P., R0ELS, H., and LAUWERYS, R. 1978. Placental transfer of lead, mercury and cadmium in women living in a rural area: importance of drinking water in lead exposure. Int. Occup. Environ. Health 41:117-124 (As cited in EPA 1984b)
INTERNATIONAL AGENCY FOR RESEARCH ON CANCER (IARC). 1982. IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Supplement 4: Chemicals, Industrial Processes and Industries Associated with Cancer in Humans. World Health Organization, Lyon, France. Pp 149-150
LEONARD, A., GERBER, G.B., JACQUET, P., and LAUWERYS, R.R. 1984. Mutagenicity, Carcinogenicity, and Teratogenicity of Industrially Used Metals. In Kirsch-Volders, M., ed. Mutagenicity, Carcinogenicity, and Teratogenicity of Industrial Pollutants. Plenum Press, New York. Pp. 59-126
MIELKE, H.W., BLAKE, B., BURROUGHS, S., and HASSINGER, N. 1984. Urban lead levels in Minneapolis: The case of the Hmong children. Environ. Rev. 34:64-76 (As cited in EPA 1984b)
RYU, J.E., ZXECLER, E.E., NELSON, F.E., and FOMON, S.J. 1983. Dietary intake of lead and blood lead concentration in early infancy. Am. J. Dis. Child. 137:886-891 (As cited in EPA 1984b)
SMITH, M.A. 1981. Tentative Guidelines for Acceptable Concentrations of Contaminants in Soils. Department of the Environment, United Kingdom Z
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APPENDIX K (con't)
MERCURY
INTRODUCTION
Elemental mercury is a silvery, heavy liquid with atomic number 80 and an atomic weight of 200.6 g/mole. It is present in the environment in its elemental form, in univalent (mercurous) and divalent (mercuric) inorganic states, and in numerous organic forms. Mercury has many industrial uses because of its unique properties as the only heavy metal in the liquid state. Metallic mercury is used as a cathode in the electrolytic preparation of chlorine and caustic soda, in electrical appliances, dental amalgams, catalysts, and in pulp and paper manufacture (EPA 1987a).
PHARMACOKINETICS
Elemental and inorganic mercury are poorly absorbed from the gastrointestinal tract (less than 15%) and easily absorbed by inhalation (approximately 80%) in
r humans. Organic mercury is almost completely absorbed from the gut and is assumed to be well absorbed via inhalation (EPA 1984). The extent of dermal absorption is not precisely known, but alkyl mercury is probably well absorbed. Organic mercury is metabolized to inorganic mercury in human tissues. Distribution of organic mercury is primarily to the kidney. Elimination is by biliary excretion and in the urine (EPA 1980).
QUALITATIVE DESCRIPTION OF HEALTH EFFECTS
Mercury has long been recognized as one of the more toxic metals. The toxicity of mercury depends to some extent on its form. Irrespective of the chemical form, the major target organs for mercury toxicity are the central nervous system (CNS) and the kidney. Mercury has been shown to have adverse neurological effects in humans. Organic mercury compounds are generally more neurotoxic than inorganic mercury. In addition, the different forms of mercury can cause somewhat different neurotoxic effects initially, although both will elicit the same effects at higher doses (Hammond and Bellies 1980).
Classical symptoms of elemental mercury vapor Intoxication are mental disturbances, objective tremors, and gingivitis, which have been observed following chronic occupational exposure to average air concentrations of
3 0.1-0.2 mg/m mercury (EPA 1984). The CNS appears to be the primary target of organic mercury intoxication. Primary lesions include destruction of cortical cerebral neurons and damage to the Purkinje cells and granular layer of the cerebellum. Clinical symptoms suggest damage to peripheral nerves, but histopathological documentation is lacking. Clinical symptoms include paresthesia, loss of sensation in the extremities, ataxia, constriction of the visual field, and hearing impairment (WHO 1976). CNS lesions similar to those in humans, proteinuria and morphological kidney changes have been reported in animals exposed to mercury (Roller 1979, EPA 1987a).
The kidney is the primary target organ for inorganic divalent mercury. Massive oral doses in humans lead to anuria followed by polyuria and finally to a recovery of normal renal function. Chronic low dose industrial exposure has been shown to result in proteinuria which, if severe, can lead to hypoproteinemia with edema. Methyl mercury does not appear to be nephrotoxic (Hammond and Beliles 1980).
Me thylme rcury chloride fed in the diet at 15 ppm induced renal adenomas and adenocarcinomas in male mice after 53 weeks of exposure. No tumors were induced in female mice at this dose level or in males or females fed at a 30 ppm dose level. However, the authors of this report noted that all animals receiving the high dose died due to neurotoxicity by week 26 (Mitsumori et al. 1981). Mercuric chloride and methylmercury chloride administered to mice in the drinking water did not induce tumors over a lifetime, but the doses used in these tests were very low and did not approach maximally tolerated doses (Schroeder and Mitchener 1975). Phenylmercuric acetate administered to mice by gavage early in life followed by administration in the diet for the next 18 months did not result in tumor formation (Innes et al. 1969).
Both Inorganic and organic mercury compounds have been reported to be genotoxic in eukaryotic systems. In all test systems, organic mercury compounds appear to be more potent than inorganic compounds. The most notable effect is the production of C-mitosis which can result in aneuploidy and polyploidy.
Observations on plants suggest that organic mercury may also act directly on genetic material producing chromosome fragmentation and somatic mutations. Evidence for the production of structural chromosomal anomalies in mammalian systems is not conclusive. Elevated levels of chromosomal abnormalities in lymphocytes of occupationally exposed people have been reported, but the authors have noted that the effects seen may have been due to other chemicals to which the workers were concomitantly exposed (Leonard et al. 1984).
Several investigators have reported embryotoxic and teratogenic effects in experimental animals treated with organic mercury. The most common findings are neurological effects, but skeletal malformations including cleft palate and jaw and facial defects have been reported in mice, hamsters and dogs. 1 Genitourinary malformations have been reported in rats (Leonard et al. 1984). Brain damage, but not anatomical defects, has been reported in humans exposed prenatally to organic mercury. These epidemiological studies may not have been sensitive enough to detect possible teratogenic effects of organic mercury in human populations (EPA 1984).
QUANTITATIVE DESCRIPTION OF HEALTH EFFECTS
Limited data are available regarding the carcinogenic potential of mercury in humans or animals. Applying the criteria for evaluation of the overall weight of evidence of carcinogenicity to humans proposed by the Carcinogen Assessment Group (EPA 1986a), the EPA (1984) has determined that mercury is most appropriately classified in Group D--Not Classified.
The interim drinking water maximum contaminant level (MCL) for mercury is 2 Mg/liter. A maximum contaminant level goal (MCLG) of 3 /ig/liter has been proposed (EPA 1985a).
EPA (1986b) has previously derived an oral reference dose (RfD) for inorganic mercury of 0.002 mg/kg/day based on a study in which rats were exposed to mercury (as mercuric acetate) in the diet (Fitzhugh et al. 1950). A lowest-observed-adverse-effect level (LOAEL) of 2 mgAg/d*y identified based on the presence of morphological changes in the kidney (EPA 1986b). EPA
(1987b) has since revised the oral RfD; the revised value is 1.4xl0*3 mgAg/day. The basis for this change was not reported (EPA 1987b).
A reference dose for methyl mercury of 0.0003 mg/kg/day was developed by EPA based on several studies reporting human poisonings. A blood level of 200 ng mercury/ml of blood, equivalent to 3 MgAg/day, was identified as the LOAEL from these studies. The earliest detected effects were CNS effects such as ataxia and paresthesia (EPA 1986b).
EPA's Office of Drinking Water has developed a draft lifetime health advisory of 1.1 fig/liter. The advisory is based on a study by Druet et al. (1978) that reported proteinuria in rats exposed to 0.1 mgAg/day mercuric chloride by subcutaneous injection for 12 weeks. A no-observed-adverse-effect level (NOAEL) of 0.05 mg/kg/day was identified, from which a human allowable intake of 11 Mg/day was derived. Factoring in the assumed daily relative source contribution from water of 20% results in a safe drinking water concentration of 2.2 jig/day, or 1.1 /ig/liter for an adult consuming 2 liters of water per day. The health advisory assumes that most of the mercury in drinking water is in the inorganic form (EPA 1987a).
The EPA Environmental Criteria and Assessment Office (EPA 1984) calculated oral and inhalation allowable intakes for organic and inorganic forms of mercury. For inorganic mercury, the oral allowable intakes are derived from the study by Fitzhugh et al. (1950) discussed previously. For both the oral subchronic allowable intake (AIS) and the oral chronic allowable intake (AIC), the animal LOAEL of 2 mgAg/day was extrapolated to 2 MgAg/day for humans by using a safety factor of 1000. The inhalation AIS of 0.51 MgAg/day was extrapolated from the threshold limit value (TLV) for mercury vapor. The inhalation AIC of 0.051 MgAg/day was derived by applying an additional safety factor of 10 to the AIS (EPA 1984).
For organic mercury, both the oral AIS and the oral AIC of 0.28 MgAg/day were based on data from an outbreak of mercury poisoning in Niigata, Japan. Niettinen (1973) estimated that an intake of 200 Mg/day of organic mercury corresponded to a blood level of 200 ng/ml blood, which was estimated to be a
threshold level for the development of neurological symptoms (EPA 1984). The Inhalation AIS and AIC of 0.1 MgAg/day were derived from the TLV (EPA 1984).
The EPA Office of Water Regulations and Standards has developed an Ambient Water Quality Criterion (AWQC) for the protection of human health from the toxic effects of mercury ingested through consumption of contaminated water and aquatic organisms of 144 ng/liter and a criterion of 146 ng/liter for the effects of mercury ingested through consumption of aquatic organisms alone (EPA 1985b). EPA has also derived an adjusted criterion of 10 g/liter based on the effects of mercury ingested through drinking water alone (EPA 1986c).
The American Conference of Governmental Industrial Hygienists (ACGIH 1986) recommends a time-weighted average Threshold Limit Value (TLV) of 0.01 mg mercury based on the severity of the CNS effects from absorption of alkyl mercury compounds.
SUMMARY OF INORGANIC MERCURY CRITERIA
EPA carcinogen classification Group D
Interim MCL 2 /ig/liter
3 /ig/liter .3 1.4x10 mgAg/day
1.1 jig/liter
2 pgAg/day
0.51 pgAg/day
0.051 pgAg/day
Proposed MCLG
Oral RfD
Lifetime HA (draft)
AIS and AIC (oral)
AIS (inhalation)
AIC (inhalation)
Ambieng Water Quality Criteria (AWQC) (10 estimated lifetime cancer risk)
Ingestion of water and aquatic organisms Ingestion of aquatic organisms Ingestion of water
144 ng/liter 146 ng/liter 10 pg/liter
SUMMARY OF ORGANIC MERCURY CRITERIA
EPA Carcinogen classification
RfD, verified
AIS and AIC (oral)
AIS and AIC (inhalation)
REFERENCES
AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH). 1986. Documentation of the Threshold Limit Values and Biological Exposure Indices. 5th ed. Cincinnati, Ohio
DRUET, P., DRUET, E., POTDEVIN, F., and SAPIN, C. 1978. Immune type glomerulonephritis induced by HgCl. in the Brown-Norway rat. Ann. Immunol. 129:777-792 1
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1980. Ambient Water Quality Criteria for Mercury. Office of Water Regulations and Standards. Washington, D.C. EPA 440/5-80-053
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984. Health Effects Assessment for Mercury. Environmental Criteria and Assessment Office. Cincinnati, Ohio. EPA 540/1-86-042
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985a. National Primary Drinking Water Regulations; Synthetic Organic Chemicals, Inorganic Chemicals, and Microorganisms; Proposed Rule. Fed. Reg. 50:46936-47025
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985b. Water quality criteria; notice of final ambient water quality criteria documents. Fed. Reg. 50:30784-30796. (July 29, 1985)
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1986a. Guidelines for carcinogenic risk assessment. Fed. Reg. 51:33992-34003, September 24, 1986
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1986b. Integrated Risk Information System (IRIS) Chemical Files. November 1986
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1986c. Superfund Public Health Evaluation Manual. Office of Emergency and Remedial Response, Washington, D.C. EPA 540/1-86-060. October 1986
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987a. Draft Health Advisory for Mercury. Office of Drinking Water. Washington, D.C. September 30, Draft
Group D
0.3 /igAg/day
0.28 pgAg/day
0.1 /igAg/day
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987b. Memo from Sandra Lee (Program Manager, Regional Support Team, Toxics Integration Branch) to Addresses. Subject: Updated Reference Dose and Cancer Potency Numbers for Use in Risk Assessments. Office of Solid Waste and Emergency Response. Washington, D.C. October 1987. 19pp. (Sandra Lee: (202) 382-4307
FITZHUGH, 0., NELSON, A., LAUG, E., and KUNZE, F. 1950. Chronic oral • toxicities of mercuric-phenyl and mercuric salts. Arch. Ind. Hya Occup Med. 2:433-441
HAMMOND, P.B., and BELILES, R.P. 1980. Metals. In: Casarett and Doull's Toxicology: The Basic Science of Poisons, 2nd Ed., Doull, J., Klaassen, C.D., and Amdur, M.O. (eds.), Macmillan Publishing Co., New York, Toronto, and London, pp. 421-428
INNES, J.R.M., ULLAND, B.M., VALERIO, M.G., PETRUCELLI, L., FISHBEIN, L HART E.R., PALLOTA, A.J., BATES, R.R., FALK, H.L., GART, J.J., KLEIN, M., MITCHELL, I., and PETERS, J. 1969. Bioassay of pesticides and industrial chemicals for tumorigenicity in mice: A preliminary note. J. Natl. Cancer Inst. 42:1101-1114
ROLLER, L. 1979. Methylmercury toxicity, model no. 158. In: Jones, T.C., Hackel, D.B., andMigaki, G., eds. Handbook: Animal Models of Human Disease. Registry of Comparative Pathology, Armed Forces Institute of Pathology, Washington, D.C.
LEONARD, A., GERBER, G.B., JACQUET, P., and LAUWERYS, R.R 1984. Mutagenicity, Carcinogenicity and Teratogenicity of Industrially Used Metals. In: Mutagenicity, Carcinogenicity and Teratogenicity of Industrial Pollutants. Kirsch-Volders, M. (eds.), Plenum Press, New York and London, pp. 59-126
MIETTINEl^ J.K. 1973. Absorption and elimination of dietary mercury (Hg ) and methylmercury in man. In Miller, M., and Clarkson, T., eds. Mercury, Mercurials and Mercaptans. , Charles C. Thomas, Springfield, Illinois
SCHROEDER, H.A., and MITCHENER, M. 1975. Life-term effects of mercury, methylmercury and nine other trace metals on mice. J. Nutr. 105:452-458
WORLD HEALTH ORGANIZATION (WHO). 1976. Environmental Health Criteria, Mercury. Geneva
APPENDIX K (con't)
TRICHLOROETHYLENE (TRICHLOROETHENE)
Trichloroethylene is a colorless, highly volatile liquid widely used as a metal degreaser. Since it is not consumed as a result of this use, trichloroethylene occurs widely in the environment. It is a common contaminant in air, soil, groundwater, and surface water (EPA 1985a).
TOXICOKINETICS
The toxicokinetics and metabolism of trichloroethylene have been studied in man as well as in laboratory animals. Absorption after oral ingestion is virtually complete. With inhalation exposure, absorption is proportional to concentration and duration of exposure. Trichloroethylene distributes widely into body tissues; metabolism occurs primarily in the liver. Elimination is by urinary excretion of liver metabolites and by pulmonary excretion of unchanged trichloroethylenes (EPA 1985a).
QUALITATIVE DESCRIPTION OF HEALTH EFFECTS
CARCINOGENICITY
Several studies investigating the carcinogenic potential of trichloroethylene have been conducted. Two of these studies, one with technical-grade trichloroethylene containing epichlorohydrin and the second with epichlorohydrin-free trichloroethylene, revealed significant increases in the incidence of liver tumors among both sexes of B6C3F1 mice exposed by gavage (NCI 1976, NTP 1983). A third study indicated an increased incidence of pulmonary adenocarcinomas in female ICR mice after inhalation exposure (Fukuda et al. 1983).
Gavage exposure to epichlorohydrin-free trichloroethylene caused renal tubular-cell neoplasms in male F344/N rats and produced toxic nephrosis in both sexes. No evidence of carcinogenicity was observed in female F344/N rats. Trichloroethylene (without epichlorohydrin) was carcinogenic for B6C3F^ mice, causing an Increased incidence of hepatocellular carcinomas in both sexes and hepatocellular adenomas in female mice (NTP 1983).
There is disagreement in the scientific community about the relevance of mouse liver tumors as indicators of human cancer risk. Several strains of laboratory mice, including the B6C3F1 hybrid, appear to develop a high and variable proportion of liver tumors in one or both sexes with or without exposure to carcinogenic chemicals. Certain scientists believe that the increased incidence of mouse liver tumors should be treated in the same manner as the increased incidence of tumors at other rodent organ sites, while others believe that mouse liver tumors are an experimental artifact which is not relevant to human hazard (EPA 1985b).
MUTAGENICITY
Mutagenic effects have been associated with commercial-grade trichloroethylene, suggesting that it may be a weakly active indirect mutagen (EPA 1985a).
TERATOGENICITY/REPRODUCTIVE EFFECTS
Teratogenic effects have not been observed in rats, mice, or rabbits exposed to high doses of trichloroethylene.
ACUTE/CHRONIC EFFECTS
Trichloroethylene is a central nervous system depressant from acute and chronic exposure. High level exposure can result in death due to respiratory and cardiac failure. Trichloroethylene was once used as a general anesthetic, but its use was discontinued due to longer-term CNS effects. The longer-term effects may have been due to impurities introduced by soda lime used to remove carbon dioxide (EPA 1980).
The hepatotoxic potential of trichloroethylene has been evaluated in human and animal studies. Animal studies have revealed transient increased liver weights with relative liver weights decreasing post-exposure (Kjellstrand et al. 1983). Observations of liver or renal dysfunction in workers have been Infrequent, and factors other than trichloroethylene probably were more causally related to the hepatorenal disturbances noted (EPA 1985a).
Industrial use of trichloroethylene is often associated with dermatological problems including reddening and skin burns on contact and dermatitis resulting from,vapors. These effects are usually the result of contact with concentrated solvent, however, and no effects have been reported after exposure to trichloroethylene in dilute, aqueous solutions (EPA 1985a).
QUANTITATIVE DESCRIPTION OF HEALTH EFFECTS
EPA (1987) has classified trichloroethylene as a Group B2 carcinogen. This classification is for those chemical agents for which there is sufficient evidence of carcinogenicity in animals and inadequate evidence of carcinogenicity in humans.
Because of its classification as a carcinogen, neither a subchronic acceptable intake nor a chronic acceptable intake for trichloroethylene was calculated by EPA in its Health Effects Assessment (HEA) for this compound (EPA 1984a). EPA
-2 1 (1987) has derived carcinogenic potencies (q.*) of 1.1x10 (mg/kg/<*ay) for ~ 2 -1 oral exposure and 1.3x10* (mgAg/day)" for inhalation exposure. These
estimates are based on the mouse liver tumor data in the NCI (1976) and NTP (1983) gavage studies.
A drinking water maximum contaminant level (MCL) of 5 pg/liter and a Maximum ? Contaminant Level Goal of 0 /ig/liter have been promulgated for trichloroethylene by EPA (1987). \ -
The Office of Drinking Water (EPA 1984b) issued a draft lifetime health advisory for the noncarclnogenic effects of trichloroethylene. A relative source contribution factor was not Included. The advisory of 260 pg/liter was based on a study by Kimmerle and Eben (1973) that reported increased liver weights when rats were administered 55 ppm trichloroethylene for 14 weeks. The estimated excess cancer risk associated with lifetime exposure to drinking water containing 260 jig/liter of trichloroethylene is 8.2x10 .
An oral risk reference dose (RfD) for trichloroethylene is under review by an EPA work group (EPA 1987).
SUMMARY OF TRICHLOROETHYLENE CRITERIA
EPA classification Group B2
Oral carcinogenic potency (q^*)
Inhalation carcinogenic potency (q^*)
l.lxlO"2 (mg/kg/day)
1.3x10"2 (mg/kg/day)"*
MCL 5 /ig/liter
MCLG 0 Mg/liter
Lifetime HA (for noncarcinogenic effects only)
260 pg/llter
Oral RfD Under Review
REFERENCES
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1980. Ambient Water Quality Criteria for Trichloroethylene. Office of Water Planning and Standards. Washington, D.C. EPA 440/5-80-077
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984a. Health Effects Assessment for Trichloroethylene. Environmental Criteria and Assessment Office. Cincinnati, Ohio. EPA 540/1-86-046
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1984b. Draft Health Advisory for Trichloroethylene. Office of Drinking Water. Washington, D.C. September 30, 1984
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985a. Health Assessment Document for Trichloroethylene. Environmental Criteria and Assessment Office. Research Triangle Park, North Carolina. EPA/600/8-82/006F
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985b. National primary drinking water regulations; volatile synthetic organic chemicals; final rule. Fed. Reg. 50:46880-46901 (November 13, 1985)
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1985c. National primary drinking water regulations; volatile synthetic organic chemicals, proposed rule. Fed. Reg. 50:46902-46933 (November 13, 1985)
ENVIRONMENTAL PROTECTION AGENCY (EPA). 1987. Integrated Risk Information System (IRIS). Environmental Criteria and Assessment Office. Cincinnati, Ohio. Revised September 30, 1987
FUKUDA, K., TAKEMOTO, K., AND TSURUTA, H. 1983. Inhalation carcinogenicity of trichloroethylene in mice and rats. Ind. Health 21:243-254
KJELLSTRAND, P., HOLMQUIST, B., ALM, P., KANJE, M., ROMARE, S., JONSSON, I., MANNSON, L., and BJERKEMO. M. 1983. Trichloroethylene: further studies of the effects on body and organ weights and plasma butytyl cholinesterase activity in mice. Acta. Pharmacol. Toxicol. 53:375-384 (As cited in EPA 1985a)
NATIONAL CANCER INSTITUTE (NCI). 1976. Carcinogenesis Bioassay of . Trichloroethylene. CAS No. 79-01-6. Carcinogenesis Technical Report
Series No. 2. PB-264 122
NATIONAL TOXICOLOGY PROGRAM (NTP). 1983. Carcinogenesis Studies of Trichloroethylene (Without Epichlorohydrin), CAS No. 79-01-6, in F344/N rats and B6C3F. mice* (Gavage Studies). Draft. August 1983. NTP 81-84 NTP TR 243.
APPENDIX K
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APPENDIX L
VIN 001
1932
APPENDIX L
VINELAND CHEMICAL COMPANY MONITORING WELL BORING LOGS
M O N I T O R I N G W E L L S f N U N C O N S O L I D A T E D F O R M A T I O N S BUREAU OF GROUND WATER MANAGEMENT . DATE:|-|,-o
REVISION NO." STEEL CAP WITH PADLOCK-TT-
LENGTH OP STEEL CASING SECURELY SET IN CONCRETE" PAD
L—>=—PVC SCREW CAP • TT
—,VruCA^l4-|NCH PVC CASING -^SCH.40 EOUIV. OR GREATER) \ \ \\ wvcx^wwl'
> CASING SEAL- CEMENT GROUT, BENTONITE, OR NEAT CEMENT (&2 «ol./94 lb. boo)
l-E FEET
1-FOOT BENTONITE GRANULAR OR PELLET SEAL
PVC COUPLING
-INCH 0R4HNCH PVC WELL SCREEN NO. 20 SLOT SIZE IN MOST CASES)"
6-INCH OR eHNCH BORE HOLE' '•'•SSv
PVC CAP
>FIELD OETERl
GRAVEL PACK
C'JESSE MORIE *1 OIS7-.OS9 *nt IN MOST CASES 0
REQUIREMENTS:
1. Notification to the Division is required two C2) weeks prior to drilling.
2. Driller is required to obtain a State-Well Permit for each monitor well.
3* hM«.dri1-leT/U?J ®aintain an '"urate written log of all materials penetrated in ea< , eeord all construction details for each well, and record static, water le"**
*' t o k e "<• « « « » « j o i « f are acceptable (no glue joints). <
5" dilJh.™" J® IT"1 Packe* [when necessary) and developed to yieia a 'aand-fre 3 " least two (2) gallons per minute where possible.
f~ /-U 6. A length of steel casing with a locking cap must be securely set in dement an £ ><
7. Top of the PVC casing (excluding ca^) nsjst be surveyed to the nearest bundret c (0.01) by a licensed surveyor.
128 Edwards Drive Gloucester. N. j . 0803C 609 -456-6318 'DATE- l-l l RC 565 E. Herd ing H ighway Mays Land ing. N . j . 083, 60g . 625.170£) ^ Q
Testing ..- inspection ,- Asphalt ,- Chemical Analysis -.- Test Borinis -.- renditions ,- So,Is wtttfr ... Sleel
Vineland Chcaieal Co., Inc. DAT; ~ ~~ : * DATc January 10, 1977
1OJECT Plant Control — Koaitoring Veils LAB. v 2G24* iring No. J-Hv-X Sheet No. of
Ground Water Date A - Method of Advancing Borina Grounr -jr!aee Elev.
I »-X=,
30-
35-
04-CD S - 2" 0. D. Split Spoon Sample Q U - Undisturbed Simple. 3" Oiemetir
Core Drilling
Hater first encountered at 15.0 Auger Boring Coepleted at 25.0 Veil Point set at 25.0'. Pusplng Eate 30 gallons per Bin Jhrev l)owa 3.0*. Static Vater Level 12'2n.
ate.
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CRAIG TESTING LABORATORIES, INC. Date, Hi.M
128 Edwards Drive Gloucester, N. J. 08030 609.456-6318 REVISION MA "r 565 E. Harding Highway Mays Landing, N. J. 0S330 609 - 625-1700 '
T"'ing Inspection -:• • Asphalt -;- Chanical Anclyiis Test Boring: Foundations .;. Soils H'o/er S/f*/
-•« C Vineland Chemical Co., Inc. DATE January 10, 1977 OJECT Plant Control - Monitoring Wells LAB. NO. 20246 ring No. KW-2- Sheet No. 1 of 1 Ground Surface Elev. —
Ground Water Data A - Method of Advancing Baring Depth Depth Hour Date Hrs. After
Completion 8" Drilled in Cesing CM o
o Hrs. After
Completion to
.2.0' 1-9477 24 hours to
Depth
Sample
No. Depth Soil Clasification Remarks
10-
15-
20-
25-
0'-2*
2'-5'
5'-12'
12'-15'
15'-20'
20'-25*
Danp,Brown Fine Sand
Da»p,Org-Brn Fine Sand 2.0'
5.0'
Danp,Tan Fine Sand
Hoist,Tan Fine to Medium Sand
12.0'
15.0'
Wet,Tan Fine to Medium Sand
Wet,Tan Fine to Coarse Sand
20.0' J
25.0*
30-
35-
<0-
Water first encountered at 15. ( Auger Boring Completed at 25.0 Well Point set at 25.0'• Pumping Bate 30 gallons per nix Draw Down 4.0*• Static Water Level 12.0*.
ute.
< M 2
o o
us u> OD S - 2" 0. 0. Split Spoon Sample p U - Undisturbed Sample, 3" Diameter &. Harrison
12S Edwards Drive 565 E. Harding Highway
Gloucester, N. J. 08030 Mays Landing, N. J. 08330
609.456-6318 D A T E : M l -609-625-1700 REVISION NO
10-
20-
0 ' -3*
3 ' -14 '
14 ' -24 '
Damp,Bra. Fine to Med Sand
Damp,Tan Fine Sand
Wet,Tan Fine to Coarse Sand
3.0 '
14.0'
2 4 . 0 1
25-
30-
35-
40-03 S - 2" 0. D. Split Spoon Sample CU-Undisturbed Sample. 3" Diameter
Water first encountered at 14. { Auger Boring Completed at 24.0' Well Point set at 24.0'. Pumping Rate 30 gallons per Blifcte. Draw Down 3.0'. Static Water Level 11*2".
R. Harrison
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(JKA1C* TiSSTiWU mL.. 128 Edwards Drive Gloucester, N.J. 08030 609 . <56-0318 DATE: Ml- C -565 E. Harding Highway Mays Landing, N. J. 08330 509 -625-1700 REVIS'?'1 II0.
Tes:ing Inspection Asphalt »;. Chemical Analysis Test Borings -> Foundations ... 0jjs ... wBier Sicel
Vinelaad Chemical Company, Inc. ROJECT plant Control - Monitoring Wells oring No. Sheet.No. of i
DATE January 10, 1977 LAB. NO. 28246 Ground Surface Elev.
Groun d Water Data
£.
A - Method of Advancing Boring Depth Depth Hour Date Hrs. Alter
Completion
£.
R" Drf11r»d -fn C.pjiAn£ n» 1o o/c« Depth Hour Date Hrs. Alter
Completion
£. to
1?'V 1-R. .?• "n~7t, nf.,hnl £. to Depth No. Depth Soil Classification Remarks
10-
20-
25-
O'-S'
8'-13'
i3'-i6'
le'^o1
2o,-26l
Damp,Brown Fine to Medium Sand
8.0'
Damp,Tan Fine to Medium Sand
Moist,Tan F/M Send
Wet,Tan F/M Sand
13.0'
16.0'
20.0*
Wet,Tan Fine to Coarse Sand some Medium to Fine Gravel 26.0'
30-
35-
40-
CDS-2" 0 . D . Sp l i t Spoon Sample C U - Undisturbed Sample. 3" Diameter
V?ater first encountered at 16.( Anger Boring Completed at 26.0 Well Point set at 26.0'. Pumping Rate 12 gallons per mi4ute. Draw Down 12.0*. Static Water Level 12*3".
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R. Harrison
^'•R- 138 •• ••'"s 5 l . i.J STATE OF NEW JERSEY
- t -1 DEPARTMENT OF ENVIRONMENTAL PROTECTION ZJ L'-JL/ DIVISION OF WATER RESOURCES
WELL RECORD
DATE: 1-II-&4-R E yj s i ° • ? r~ • PERMIT NO^ r _>• - L f
APPLICATION NO.
COUNTV-'TVC • w
OWNER Vlr.elcng Clerical Owner's Well No.
LOCATION
ADDRESS 1611 'freet .~c., Vlnslana, ::.j.
SURFACE ELEVATION Feet <AO°w mu/1 Ml /. rf/;
DATE COMPLETED / -/l2-/ei DIAMETER: Top7_3VZLipeh£ CASING: Type TVr
SCREEN: Type" ^ Size of Opening _Q20 Diameter
driller V?rr e svim^ c^.r Trr<
Bottom7 •'/it inches
Diar* »ter TOTAL DEPTH
L" + 2 Ebv. E.l." .Feet
B . w f T°P T? Range in Depth / / Bottom ~ ?
. Inches
. Inches Length, \ g.
Feet Feet
Length _2£L
Geologic Formation cat-san^i/
Tailpiece: Diameter. — '"Che's Length.
WELL FLOWS NATURALLY , n/a Ga„ons minute „ __
W8Ierrisejt0 — - Feetabovesurf.ee
-Feet
Feetabovesurf.ee '
RECORD OF TEST: Date Yield. Static water level before pumping __
Pumping level 1- feet below surface after __
Drawdown __ Feet Specific Capacity.
Gallons per minute
How pumped
- Feet below surface
• hours pumping Gals, per min. per ft. of drawdown
Observed effect on nearby wells How measured
PERMANENT PUMPING EQUIPMENT: T v ° * - T/A
Mfrs. Name Capacity Depth of Pump in well
H.P. G.P.M. HOW Driven "
Feet Depth of Footpiece in well D.pth ol Air Lin. in w.,1 F,„ Typt o( M,,„ „„ Pump
R.P.M.
Size. USED FOR
QUALITY OF WATER 1 Taste
ftaeir^Aan v.-en r.nl y
ZA
f Average
- Feet —Inches
Gallons Daily Gallons Daily
Feet
Feet
o o
i-* «J0 OJ VO
. DATE: |-ii-£4 WELL tt5 REVISION NO. :
ft! to iVft. v;ifcr=, or?n:r* '..and, ft, to 1=ft. ''6d* "RH N •M1~VF>RC' j1?"*1 IN C0^:>r. ft. to 20 ft. I'sd! rr,jJ Gni'nr"?? ifh!nClni t0 *€llow sand ct 1~ 't V ft. to 25 ft. " n bnii°r= li-£ht brown sand. " " **•>. ll 1° 11: 4"ht =*«• cram uniform sand. .
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•' '•.T'nr"iDEPARTMENTOf: environmental protection permitno DIVISION OF WATER RESOURCES PERMIT NO. J / APPLICATION NO. * V ^ • - • • «» _ W -» »•* « FCJ A FC
WELL RECORD county r''—v«~i .... J
vfvER V'nc- land Chemical i f . . . . . . . . z =- ADDRESS 1611 -fr-eat :-.c», vtnelanfl, ??, j. Owner's Well N'o
— SURFACE ELEVATION , LOCATION (Abort metn sti hrtl)
DATE COMPLETED DRILIE-V.AA. n, m.., ,
DIAMETER. TopJ£_5/£mches Bottom inches TOTAL DEPTH T1
CASING: Type --r» DlimM,r iH , . + 2 ft. efcv. H, L. ." Diameter _A Inches Length_U Feet
SCREEN: Type _E1£ Size of Opening 0 Di.meter inches Length __£Q_Feet
D ^ f Top U peet engem ep j- ^^ Geologic Formation 1 '
Tail Piece: Diameter . |nche, Length ___Feet
WELL FLOWS NATURALLY j/£_ Gollon, p., minu,. „ _ F.„ lbo>, Wjlerrije$t0 - Feet above surface
RECORD OF TEST: Date •• /A • v. ,. ' Yield - Gallons per minute
static water level before pumping Feet below surface '
Pumping level ; i'feet below surface efter^ . hours pumping
d0Wn " Feet Specific Capacity Gals, per min. per ft. of drawdown How pumped „
' How measured Observed effect, on neerbv well.
PERMANENT PUMPING EQUIPMENT: ._ • '
Type ^ .' Mfrs. Name —
Cip.eity CAM. HwDrl>„._ HJ> B p M D.pth .1 Pump In well pm D«pm p, Footpi.= TO ortt F,„
Dtpth of Air Lin. in well F« Typt of Mm, on Pump
USED FOR Observation veil ortlv • (*•«?• Gallons Daily
• Maximum Gallons Daily QUALITY OF WATER -/.
" "•/•'- ' Sample: Y«t No___ T"te — Odor C-,.. M — uolor • Tamp. °F. 3
LOG _ — b r » r V ,1 tlnric /o, *«, p/.m ,V,n,b,e? °
•SOURCE OF DATA Vrmr.t r->. Tnc.' vre-p rcrf>W»e ' M
QATA 03TAINED BY ''nnee T*»p» T ^ / /«. 1-1
—— " r^> i Thr.—tT» -'fn*on d... r/ir/"i vo " ' —• £*
MI-64 Vi^LL #6 ptvisign tv
R\ S t. to " ft. •*. 2 't. to 10 ft. 10 ft..to 1-} ft. i- ft. to 20 ft. 20 ft. to 20ft. r • CO ft. to 30 ft. 30 ft. to 33 ft.
red. -rein uniforrr. li:*ht sand. « cd. * rein inifom li.~ht send — crenrlnt* to v;ht. at * "r* red. rrain unlfors lirht brov/n cr .nd. i'ed. rrain - uniform lighter in color. Yc-llov; rcea. (sore pine ) Vroin sand. it • M •i it
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••'.V. • D£?ART :; ENVIRONMENTAL PROTECTION PERMIT NO 3£-£ 93A , D.iv ' N OF WATER RESOURCES 1
.-> rrw\7 *7 UJR-LL. ;.a application no.
> t/ELL RECORD * COUNTY- — , •
'• OWNER. VlDBlsnd ChEr.lccl address v. t -a.. vir,f1M V T
w,n No— surface elevation r I. LOCATION • Vabo*» mttn «e« seTj eel
i. DATE COMPLETED r/l R/R, _ _ DRtLLER V,... — -T~ T_, , , „ I. DIAMETER: Top J2_5/ii„ches Bo-:om7 j/l, inch., TOTAL DEPTH ,, F<(t
5. CASINO: Type Dl,m„„ _a lp^ ? ?,!-• .... SCREEN: Type" IXC SIP. ofOp.pin.X12Q Di.rn.Mp_t; L.p„K On .•••
. - f Top 3J Feet
" ( Bonon, _XJ p.., Ge°'0"C ' '
TailPiece: Diameter. inches Lenoth Feet
7. WELL FLOWS NATURALLY _n/2_ Gallons per minute at , __ Feet above surface
Water rises to . . Feet above surface
8. RECORD OF TEST: Dare n /p ' ~ Tieid _______— Gallons per minute
^ Static water level before pumping ^_1_ __ Feet below surface
Pumping level : 1- feet be|ow surface after . heim pufnpinfl
D awdown . Feet Specific Capacity Gals, per min. per ft. of drawdown
H0W Pumped How measured Observed effect on nearby wells
9. PERMANENT PUMPING EQUIPMENT:
Type a/e / Mfrs. Name _____ Capacity _ GtP.M> How Driven ' H.p. . ' R p M
Depth of Pump in well Feet Depth of Footpieee in well peet
D.P* .1 Al, Lin, Fm Typt „( M,„r „„ Pumt, Si„
10. USED FOR ChrcnrnM n wrU inly AMOUNT J Avera;°e Gallons Daily \ Maximum Gallons Daily
11. QUALITY OF WATER . s.mp,.: <
T"'e — : C0,n,__ T.mp of. 2 12. LOG — o
""" " •» «<>""» '""vie io, w mac w fu£,™£?j" mi',b,e? — 2
^OURCE OF DATA "ir.re- •VInnar rn. . -rvn| •••ell r€fir-in '
.14. DATA OBTAINED BY "r>-\rr r<-> r _ _ ... . SP 1 'NR« <L £N®2N DATE C/1-/^1 £
TOLL #7 DATE: 1-11-6^ REVISIT! t"_
- it" ir/^ Hark trn# =e<3' rrain S2nd tuminrr orange at * ft ; ' 5 « - t o 1 5 ' k . S g T 4 & i n ^ ' , ^ n s i n e s l o r " • « •
23 ft' o? ._c-a. jrain unifora licit color sane. 25 A', to 30 n! " t0 =,a- IF®1? OTOitnM. non-uniforo 20 ft. to 33 ft. " •• 11 „ 1 40 ' fine)
\
m < M a o o
vo
f
i
> Owp. :3s . ^ATE: 1 -11-6-3 3 • . STATE OF NEW JERSEY REVISION • 0
( T.-R~L DEPARTMENT OF ENVIRONMENTAL PROTECTION PERMIT NO 35--DC3, Q . L J DIVISION OF WATER RESOURCES PERM7NO. _J j nV Y .7 7
' • " - * « lOfUL-— ' I'i -l x / APPLICATION NO. ! ' : " " ~ - = - i .
WELL RECORD countyCur->-«twi
OWNER Vlnelana Chezlcal IF:'11 rV,a* ... ' • • ; ; • ADDRESS ./heau Mnelang, ".J. Owner'* Well No _ ' •
SURFACE ELEVATION ' f LOCATION ' Z255« mttn tu level) ee*
DATE COMPLETED =ZlV|1 ^ DRILLER v.... ,v, p. MM — /, P 111 I I ,'CTie Psn
DIAMETER: fUA*. Bott*7 V*_ inch,, TQTAI OFPTu 89 ft. 6 lh-CASING: Typei^ D,.m„er ' '^£2^
SCREEN: Type TV£ Sia of 0penin»02ft Diemeter J±1 lndl„ Un(th2a Fm
B • rr w f T°P P"t ' " anse in ep ^ g o t f „ . ^ G e o l o g i c F o r m a t i o n . C g W v s ^ •
Tailpiece: Diameter |nchei Lenfftf) ^
WELL FLOWS NATURALLY _JZs, G.llon, pe, minute „ F.„ lto„ • W"crfi,es t0— : — Feet above surface
• RECORDOFTEST: Pat, n/a ' ' r. Y,eld Gallons per minute
jtatic water level before DumDino _ . . . — Feet below surface
. PumpinB level . V feet beIow Jurf,ce after ' ^
d°Wn^ —Feet Specific Capacity, Gals, per min. per ft. of drawdown How pumped ..
————— How measured
C'bst^ed e.Sect on nearby welis
. PERMANENT PUMPING EQUIPMENT:
Type : . Mfn. Name
Capacity , ^ G.P.M. How Driven * un R.P.M.
Depth of PumD in well c . . _ ' Feet Depth of Footpiece in well
Depth of Air Line in well Fee, Type M„e,, Pump ^ Sii, ^
' USED F0R CfcrsrrHpTj veil nrO v AMOUNT j 6,Ilo,u D,il*
• , I Maximum Gallons Daily . QUALITY OF WATER n/a y ~ Sample: Yes No $
Tertt °d0r Color Temp. __ oF 2
-JPG— IwCn back 0
rn " "" """" " » """ wC;'," s SOURCE of DATA Vance .Skinner Co. t Inc.' V/e 11 records
V DATA OBTAINED BY VP^n -Innrr V. T„„ , tef—- f/m./nt 2 ' ' U1
WELL £8 DATE: 1-11-54 REV'S iC'1 t:c. • 3
-t. 3RN--t "(J • sr-: ornr.-s -??. ~rrl: -od, t?.1? r!:* Li*; lit in color ced. try. ;.n sane.
8: to Is n: *l52st <"ellow ^ * VS:
rV i! ?r 2" * i;:c<2« t0 coarse prain sand. 11. 10 ~0 ft. " " '« ii ft. to 31 ft. 6 in. " it -
Lost circulation at 30 ft. ver? coarse sa^erial 1/4" to peerravel in sarnie
< H 3
<44/ • o
Water 'Allocation CN-029 Trenton, N. J. 0862S
ERMIT TO DRILL WELL
DEPARTMENT or ENVIRON ME NT aj. PROTECTION DIVISION OP WATER RESOURCES TRENTON. N. J. -
; Hermit Mo
VALID ONLY AFTER APPROVAL BY THE D.E.P.' •--' RtYlSKW;
'dress Address *.0._te £ Tin*! bM jl • _._ OgggQ
- - -• . • . y -ijr • z sg-. "' ".'•Vic • "S6
lite Atlas Map No_-Jj>__0
j Draw sketch showing distance and relations ol wefl site to ^ nearest public tcaos, streets, septic systems, etc.
.27 * \
•k* C-- i*:-
iL-w-.r ful (~'A —
I 3/ .
North .,.,,. N i
' '*'. '.' "j T: V •.'•.AKt'Tr*- N. "-••• » • • --'.TOv*. A'lW'f/! .• —>v
C\! . : : '.west - ' . •/'
East
South
™EA"lnvA^E^r,JMP0RTANT PR0V,SI0NS AND Regulations penaining to this w?,^-^i Anrv,- «Dermi15 rnaoc SUBJECT to acceptance ot and compliance witn :r.e loliowmg ADDITIONAL CONDITIONS v
Q Permit issued m accordance with provisions ol 'cue: ot transmittal oatefl
LlneCeS Geophysical Logs ot this well be/node by the Division ot Water !eQU',e me 0«,t€r ,0 oli ,he Dw®ion ** RnGNE
wn, 2232) when drilling is completed. Permanent pumping equipment SHALL" NO. oe installed until such logs are made 1
U Samotes ol cuttings required everv •O -
t
TTW IO*CC to> Affve**! Sirry
vvr.il .'LH .ViT a p p r o v e d
• JCN 21 ,Jk*
oBPT. env. f noncrcN; «£S0U*Ct2
|j5SI
" -, •
R> "£L
In compliance wnn R. S. 58:<A.t4. epplication ts maoe for a permit to drill a well as described sbq*. » ' A. .
A £ § -i~1
&• is -J ^
Y I k U ka ivita V rv Vance Skinner Company, Inc.
P.O. Box 2,931 W. Sherman Avenue, Vineland, New Jersey 0S360 692-S439
0
FK$ 11rA11 an nrnnarKf * Location of well onDroperty .. Well Dia. ^GZLS.Q^.UWJLQJI. Quantity of water desired _..7 Date well started
Surface Election „ County _
Date well completed — First water line Water line in well _ Screen—Length & Material Permit No. 35- 3D SO Type of Seal—Top & Bottom . Electric Log Pump used with well _ Water Analysis
.Municipality -Block ljf.3 ±ot ...Index
CATE: l - i i -REVISION ti'o :&U
"h'ru, hzfrrvd.. yllpJd: ct>/<n
120 180
-j'.y
x\
_ • H n-crnji - ynxJt .QOacn
— > LbJutL a j- jrrnr -— I C I < ^ c u i l & -r-
I ~i~trr\JU. tjJmxl . 'J):iJ.r^,CniK'TpjJL;—
80 W 11
t\ II
3^ " \ ^r~ II kjm&l .an ami — nHam sJxrrcf' —-JUjrufLJha UJLI£I_CCI— — ( r + m C Q.*uVv*S> z/&sg£\
40>Wte rmcA. Tno" — y Arrv, cnar .,
130
140
150
160
190
200
210
220
< H 2 o o M
VO CO
CN-029 Trenton, N. J. 08625
PERMIT TO DRILL WELL
D;V;S'ON' OC WATE3 RESOURCES . . TRENTON. N. J. .
• . _ Permit No
VALID ONLY AFTER APPROVAL BY THE D.E.P." DATE: T-H-84* REVISION NO. • o
> _ 5S3j!Hi.SSJ5l
JJ!!J3»*-5®5S. ..... iai„ss _?.p.._Barf t J
_08j6p_ _vi l an <3 L _ 5. J._ _ _08 560 ;
diameter of well
A inches
LOCATION OF WELL
proposed depth of well
AO feet method of drilling Rotary use of well
proposed capacity of pump
M/A G.P.M. Observation veil'* }()
^ f*rhHpu&lie, dom«nc. indunriil. eut>le-*uoo»y. iej!."etc") )—
lot * block #• 173
municipality Yinelend
State Atlas Map N0
county . 1 Draw sketch showing distance and relalions of well site to maserlang nearest public roads, streets, septic systems, etc.
North ~
A-r-rAenrQ — .
p!t ' U'
3</. 30
South
?r ,MP0RTANT PROVISIONS AND REGULATIONS pertaining to this ' .. T0
I Q Permit issued in accordance with provisions of letter of transmittal
dated
- Re1o?fre S Th.,h!L£!°PK Car 1098 of ,his we" P«» e by the Division of Water ~ ( 2 23 wh rtr-tf -,equire ,he driller ,0 no,rfy ,he Division by PHONE * _ NOT be installed until tjch k>J?s ST55d?.' SHALL Q Samples of cuttings required every
This toice lor Approval Si»me WELL a>ERM! T
A P P P 0 V E D JUN 21 lStt
In compliance with R. S 58 4A.U. application is made for a permit to drill a well as described abgve.^ / , ) AA-, v s'S/fr/f .. ..,/// /
I above , x? /
< H 5!
o o
vo ihk vo
ame Address Location of well on property Well Dia. Quantity of water desired
WELL, RECORD Vance Skinner Company, Inc.
P.O. Box 2, 931 W. Sherman Avenue, Vineland, New Jersey 08360 . 692-5439
LLL
Date well started ted Date well completed
First water line Water line in well Screen—Length & Material &O..EL. Type of Seal—Top & Bottom Pump used with well..
60
— — — AkJTcW/v lia-Kx — — SOrrA . x —
C\ anv ) ~
..Surface Elevation JDounty ..Municipality ..Block L?Ji _Lot 7. Index
>„ Permit No. ~.J35 Electric Log _
—Water Analysis
120
frftoru ULT
70 130
— > W ii
J -Lirrv\W2jro_> md-:
2Q 80
1 0 rirtiTQi- .5! ZI — //ITiXil - <«V\ OA.ro -• JCrrtL.TY Sard. —
H |4vn4 W. rfTtacl. ZI lOinv /MOfOOfij—
140
*• /U
DATE: \-tt:.E4 REVISION NO. : 0.
30 90 150
Z SET loe.lt.- 3d ft-. C.L. -
dLl
180
190
200
210
3
o o
40 100 160 220 <J1 O
Water Allocation CN-029
Irenton, N. J. 06625- ' ",
" r\f *'P VIRONMENT*1 PROTECTION DIVISION OP WATER RESOURCES
TRENTON. N.J. Permit No._
ERMITTO DRILL WELL VALID ONLY AFTER APPROVAL BY THE D.E.P. • *'64 ' REVrsiO'fl i;o.c
Driiier"— JaBc® _§ Wimjor _ Co. *__In d*
Address
'ner, C2s_< i c al
dress -!f-J__
Vance Skinner Company, Inc. P .O. Box 2, 931 W. Sherman Avenue, Vineland. New Jersey 08360
• • 692-5439
Name .dress —
Location of well on property T__ Well Dia. Quantity of water desired ! Date well started fa]J?.J..* Date well completed _..6., First water line _../-2...£c Water line in well Screen—Length & Material c2Q
Type of Seal—Top & Bottom Pump used with well
60 Z > ImeJo rnvJL. ~
Z
¥~
Municipality ~.4 .-.Block Z?3 —Lot ...index ...Permit No. -JSL.l3o!2eL ...Electric Log
L'AT£: |-i|-£j< RE VIS'Oh' r . 'C 'V '
..Water Analysis
120 180
I t
70 Z \ ILnV-^L/rfL JUjijdi Z — nicrJ^orar-
~ (fc> r , ~ .. ya.'Yij.vu- iiaAvb — jxaTT i
20 V I L 80" — (Yttid tr i im<L x — — /tnca^.^od ~
130
140
190
200
— V tl \ \ —
30 fx 90 150
;rrix*LE»FkC.L. Z 210
3
40 100 160
o o 220
Vo Cn NJ