Public Health Evaluation
Transcript of Public Health Evaluation
8.0 PUBLIC HEALTH EVALUATION
8.1 Introduction
The public health evaluation conducted for the Toms River Chemical Company
(TRC) RI provides a qualitative assessment of the nature of chemical
contamination at the site, contaminant release pathways that could lead to human
exposure and the potential health effects that could.be associated, under certain
conditions, with that exposure. The evaluation is based on physical, chemical, and
other data obtained during the RI and presented in previous chapters. Conclusions
from the evaluation will aid in determining the degree of remedial action needed at
the site to protect the public health and environment.
The draft Superfund Public Health Evaluation Manual (ICF Incorporated, 1985) and
the final draft Superfund Exposure Assessment Manual (Versar Inc., 198*0 were
consulted for guidance on the process and the level of detail required to conduct
such an evaluation. The public health evaluation of TRC addresses:
o the selection of indicator chemicals for the public health evaluation,
o the environmental fate and transport of the indicator chemicals,
o the toxicity of the indicator chemicals,
o the routes of human exposure to the indicator chemicals, and
o the qualitative characterization of potential health risks that could be
seen under certain conditions
This evaluation is limited by the quality of chemical analytical data, the
availability of toxicologic data on the compounds detected, the relevance of the
toxicologic data to site-specific conditions and the degree to which human
exposure scenarios can be accurately defined. The evaluation presents the
speculative risks to humans from the TRC site since human contact is extremely
minimial gross asusmptions of chemical ingestion were necessary.
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i iiiiiwiiiiiin
8-1
CIB 006 1789
8.2 Selection of Indicator Chemicals
The following subsections describe the process used to select indicator chemicals
for the TRC public health evaluation. Unless indicated, the worksheets used in the
process are similar to those described in the draft Superfund Public Health
Evaluation Manual (ICF Incorporated, 1985).
The indicator chemical selection process evaluates each chemical detected on the
basis of concentration in various media, toxicity, mobility and persistence in the
environment. Those compounds that pose the greatest potential for human
exposure are then chosen as indicator chemicals.
Since the public health evaluation becomes a factor in the determination of
remedial alternatives, i t is important to separate any possible background
contaminants from those contaminants attributable to the site. Hydrogeologic
studies at TRC during the RI investigation have concluded that groundwater and
soil samples collected from the following areas represent local background:
o Upgradient wells in the Cohansey Formation
o Wells in the confined Kirkwood Formation
o Soil from an undisturbed area northwest of the TRC plant; 500-900 feet
east of well #502
Compounds detected in background samples and common laboratory contaminants,
including methylene chloride and acetone, unless detected in gross amounts, were
excluded from the initial list of compounds to be evaluated through the selection
process. Every result from each samplng activity was thoroughly evaluated before
inclusion in the main data bank.
8-2
C I B 006 1790
The indicator chemical selection process is organized into the following tables:
o Concentrations and Koc Values in Various Environmental Media
Table 8-1 lists the compounds detected in each medium sampled during the RI
and provides the Chemical Abstract Service (CAS) number and the organic
carbon partition coefficients (Koc) for each compound. In general,
compounds with Koc values greater than 1000 would be tightly bound to
organic matter in soils and considered to be immobile. Compounds with Koc
values of 100 or less are believed to be moderately to highly mobile (Kenaga,
1980), having a higher potential to leach through soil to the groundwater or
be incorporated in runoff to surface waters.
The minimum, maximum and representative contaminant concentrations are
reported in mg/1 for aqueous (groundwater and surface water) samples and
mg/kg for solid (sediment, surface soil and subsurface soil) samples. The
representative concentration is the arithmetic mean of all samples within a
media. A zero value was used for each compound reported either below the
analytical laboratory's quantitation limit or below the instrument detection
l imit .
The frequency of detection versus the total number of samples that passed
EPA QA/QC requirements is also listed for each chemical within a medium.
o Toxicity Information - Oral Route
Table 8-2 groups the initial list of compounds into two toxicological classes:
potential carcinogens (PC) and/or non-carcinogens (NC). An EPA weight-of-
evidence rating for potential carcinogens or a severity of effect rating value
for non-carcinogens are listed for each chemical.
The non-carcinogen severity of effect ratings are derived using the minimum
effective dose (MED) for chronic effects and standard factors for oral or
inhalation intake (e.g., 70 kg body weight, 2 liters/day drinking water, 20
cubic meters/day of air).
8-3
C I B 006 1791
IULE t - l
BCORINB FOR INDICMM OCRIC*. KUCtlONl CtjtraiMIIONI MO Koc VM.UEI III VMIOUS miR0M«TM. RHI*
Sfoantt Syrlici lUitr »«r«i" Soil lu i - lu r l i t t toll h l l n i t
1,,/H ( i i / l l l H " | l »•»'»•.> • • ! " •»
ttE'fa.l Wu t R,n,t Rtprtok Fr i , c Kwti Rt i r i i • f « l t Rt-lt «•»«•» f " i c Rinii Room • Frii c Rinit 1 ^
VOIMIUO t n i t f i t 03 NO-0.010 0.0003 3717
71-41-2 ttlsrokniint 310 RI1.10 0.123 1/37
101-10-7 CMofolari I I WO. 017 0.002 3/37
17-M-I 1,2-ticklorottkiiit 14 ND-0.70 0.012 1/57
••1-04-02 lr«ii-l,2-DlchlorMtktM 50 W-0.31 0.012 1/37
MO-M-0 1,2-llckloretroitiit SI 7R-R7-S Elkf l iMimt 1100
R1-0.71 0.007V 2/100 RD-2.10 0.120 17)3
Nl-O.OOtl 0.00023 2/33 • - / • • i r B i n r u r B B M i B a i
OO
t 1 1 M RO-O.IO 0.001 27100 RI-11.0 1.110 10/33
IOO-4I-4 2 * . . . « . . - M-0.0107 0.000*1 1/12
S1I-7R-1
i 0 4 " " ! ' . RI-0.03 0.0014 U/J3
RI-0.043 0.00041 2/17
1,1,2,2-Ttlricklorotthcnt I IB
]t4 MD-2.60 0.041 5/37 •» - • • • ! V10O
{ J j ^ J j ' . . . u. . «« ««•» , „ i i>.ii M i i o.Mtu l / l l n-0.01 0.00031 3/100 RO-74.10 1.JM27/J3 M-0.021 — 1/01 300 HO-0.33 0.010 3/57 W-0.O0II 0.0001 l / l l RVO.OJ 0.00031 3/100
RI-0.0072 0.0*007 2/100 101-N-J 1,1,1 Irlcklorottkint 132 7I-J3-1 Irlcklorottkttil 121 M-17.00 0.471 12/37 R0-O.0031 0.00041 3/11
° i ' , ; " ; ' , 240 NO-0.017 0.0003 1/37 «M. I7 1.0*17 1/100 MSS.O 1.110 11/13
01 1110-20-7
Q KHI-VOLRIIIEI g RatkrKlM (J) 120-12-7
NuillKUtkficKH 34-33-1 ImolklFUoriotkni 203-11-2
M I m o l i l H i t r M l k t i i i 207-W-1 H i i o l i l r y i M
14000 M)-IEt07 127.100 It/14
13*0000 •-24.0 0.2M 1/14
330000 »-3*.0 •.177 7/14
330000 m-u.o 0.171 9/14
9300000 RI-21.0 0.117 3/14
IMU l-l com d
BCOtlHB FOR IKIICMOR CKHICM. SEUCtlDNi imFJIRtllOMS MO Hoc VM.UES IN VMIDUS tWIROIKNIRl REIIt
ChMlCll ICU Ro.l
Koc Vilni
Broond katir
(•0/11
Ranat Rtorti • Frio, c
tardea Nittr RVIict loll luk-fcirlici toll Ml tMi
laf/tl <aa/ial Ua/kcjl IMJ/I|I
Rin|i Riarn k Frag c Rmaa Riarn k Froa, c Rw|i Rtarei k Fraa, t R«i|t Riarn k Frig c
SO-H-R
1
O M to
«9 8
tn
UJ
*taio(|hll»ir»lnii 1400000 NO-0.34 o.oost 1/94 1*1-24-2 fcni,l Alcodnl — HO-I.O 0.0447 1/37 IM-91-i ••tilknirlRktkiltti — m-4.1 0.240 4/44 IS-41-7 CaryiiM ,00000 Rt-JS.O 0.1*4 7/»4 2 I I -»M 1,1 llcklorknum 1700 Mt-0.13 0.003 2/57 m-3.1 0.121 7/*4 H-» - l ll-n-htrlafcthiloti 170000 RD-4.3 0.123 IR/»4 •4-74-2 Fliorntkiio J8000 RO-77.0 1.170 l»/*2 204-44-* U<i«oM,2,)-c4ir,>ri«i 1400000 RV0.S2 0.0033 l/»4 W-H-3 Riptkilmi — m-4.2 0.072 »/»4 »l-2*-l RI trot Mint 54 NO-II 0.113 1/57 »-o.i» 0.004 t/44 »-»5-! Fkntiitkrini 14000 •1-43.0 0.39* 17/M
is-ei-i F i r m J00OO MM.* O.fOO 11/44
in-»o-« 1,2,4 Iricklorokifltni T200 ND-I./0 0.031 2/37 M-4.3 0.212 1/14 I2M2-I 2,4,1 Trlcklsroaktaal 2000 RR-M-2
KltlCIRC/Ftl'i Cklorfim 140000 RR-0.0I 0.0*014 tin 37-74-* 4,4-1(1 4400000 RI-0.010 •.0*037 »/*l 72-33-t l l i l tr la 1700 H-t.004 0.00004 l/fl **-S7-l frtoulfut II — »-*.» 0.113 3/43 1)213-43 » Htatacklor tan III 220 R*-*.)4 0.0073 3/4) 1*24-37-1 •ti l lal i i i l 33OO0O n-o.N 0.000*4 1/43
Kt-7*.* 4.030 2/2*
RO-44.* 2.100 4/20
Kt-l.l O.ltO 2/20
IMXt I-1 cont'd
SCOFIllll FM IMOICAIOf) CHERICM. SEUCtlONi CMCHTRRTIOM MS Koc VALUES IN VMIOW EWIItOIMUTM. HEIIA
Cknic i l ICM No.)
Hoc Vi l l i !
Bfount Hilar
taa/ll
Rin| i R tpm b frt% c
b r l i c t Nitor
U | / l l
Rin|i Riarn • Frio, t
l a r f ic i t i l l
(0|/k|l
Rin| i R iarn • f r i i c
tok-turlui lol l
Ranai Rtfr i i I Fr i t c
t i l l MOt <••/••> Rinii Riarn k frti c
oo i
ON
O M 00
«9
VJO
H0-0.0I4 0.0OOJ7 1/41
KO-0.20 0.0014 22/SR
RI-0.02 0.0013 1/13
0)4-34 J
INORMNICS Alaalaaa
7429-90-5 tr i tnlc
7440-11-2 lar iat 7440-14-1 Ckri i l ta 7440-47-1 Cofiif 7M0-30-I I I I *
7414-92-1 RiMi i iot 7419-93-4 R M I M M I
7419-94-3 Rtrctrt
7419-97-4 Rlc l i l 7440-02-0 III>tr
7440-22-4 I I I 7440- 31-3 Vl lM' lu
7441- 42-2 Hie 7441-44-4
Ht - Nat l i t K t i i t - Ottotir 1983 dita
I - Nun ol riaortM' »•!«•• and n n i r r i t n t i t i vi concin(ritlon| l i ro i l l * lor i l l « i l « u r •aortal t i kiloa l i lact io* h a l t or ki lo* liberator, o,uaatltatlM Halt
t - Freqaiact ol coalnnd ditictid ailthin neb atdl i | chini i i In InooUatir v i l l i r i l l K l a t a i l i i tbil I K aot ana OA/OC r i q i l r m n t t
M.MK SPACE - Coaaouali i n i l r n d (or kit not d i t i c l i l - Not avall<bI• or not calculated
NI-4170 2)6.31 92/94
ND-142 3.220 22/38
ND-0.IB9 0.019 11/31
ND-0.03 0.001) 1/33
Nl -U* 23.20 43/94
RR-1770 140.44 94/94
303-SI4M NM.9 32/32
NI-I4I 4.030 17/12
NI-II39 333.000 30/32
M-30400 4040.300 29/37
NI-474 74.330 29/32
Nt-240 14.110 J0/32
N0-J7 1.140 1/32
M-210 21.440 22/32
Nt-144 44.130 23/12
RI-30 — 1/04
NO-ISO 29.02 1/04
NI-230 1/01
TABLE 6-2
SCORING FOR INDICATOR CHEMICAL SELECTION: TOXICITY INFORMATION - ORAL ROUTE
Tox icolooic Toxicity Constants
Tox icolooic Rating Value/EPA w 2 s 2 CIass' Category 1 T T
PC A 7. 43E-03 3. 17E-07 NC 5 1.17E-01 5.5BE-06 NC 4 1.43E-01 7.41E-06 PC B2 5.17E-.02 2.B6E-06 PC B2 6.57E-03 3.29E-07 NC .10 1.76E-02 B.80E-07 NC 5 5.29E-02 2.65E-06 NC 10 1.00E-01 5.00E-06 NC 4 1. 10E-02 5.52E-07 PC C 4.B6E-02 2.43E-06 NC 5 4.55E-01 2.27E-05 PC C 5.14E-03 2.57E-07 NC 7 9.62E-03 4.B1E-07 NC 7 5.20E-03 2.60E-07 NC 2 7.33E-04 3.67E-08 PC B2 5.14E-03 2.57E-07 NC 5 1.05E-00 5.26E-05
i nsufiic i ent data i nsuf f i ci ent data insufficient data
PC B2 6.00E-01 3.00E-05 PC B2 4.29E+00 2.14E-04 PC B2 1.43E + 0.1 7. 14E-04 NC 8 2.67E+01 1.33E-03 PC B2 1.43E-01 7. 14E-06 NC A 5.19E-02 2.60E-06 NC 8 3.B1E-02 1.90E-06 NC A • 2.14E-01 1.07E-05 PC B2 2.29E-03 1. 14E-07
i nsuffi c i ent data in s u f f i cient data insufficient data • insufficient data insufficient data i nsuf f icient data insufficient data insufficient data i nsuf f i cient data i nsuf f i c i e n t data i nsuf f i cient data
Chemical
VOLATILES Benzene
Chlorobenzene Chl or of or m 1,2-Dichloroethane
Trans-l,2-Dichloroethene 1 i2-Dichloropropane Ethylbenz ene
1 , 1 ,2,2-Tetrachloroethane
Tetrachloroethene
Toluene 1,1,1 Tri chloroethane Tr i ch1oroethene
2-Hex anone Styrene Xylenes
SEMI-VOLATILES Benz(a)Anthracene Benzo(b)Fluoranthene Benzo(a)Pyrene
Chrysene 1,2 Dichlorbenzene Di-n-Butylphthalate 1,2,4 Trichlorobenzene 2,4,6 Trichlorophenol Anthracene Benzo(k)Fluoranthene Benzo(ohi)perylene Benzyl Alcohol Butylbenzylphthalate Fluoranthene Indeno(1,2,3-cd)Pyrene Napthalene Ni trobenzene Phenanthrene Pyrene
8-7
CIB 006 1795
TABLE 8-2 cont'd
SCORING FOR INDICATOR CHEMICAL SELECTION: TOXICITY INFORMATION - ORAL ROUTE
Cheini cal Toxicologic
Class Rating Value/EPA
Category 1
Toxi ci ty w 2 T
Constants s 2 T
PESTICIDE/PCB's Chlordane PC il 2. 37E + 00 1.19E-04 4,4'-DDE PC B2 1.09E-01 5.43E-06 Di eldri n PC B2 3.71E+00 1.B6E-04 Heptachlor Epoxide PC B2 1.03E+00 5.14E-05 PCB's (mixed) PC B2 1.06E+00 5.29E-05 Endosulfan I I insufficient data
INORGANICS Arseni c PC A 3.71E+00 1.86E-04
NC 9 1.80E-01 9.00E-04 Barium NC 10 4.0BE+00 2.04E-04 Copper NC 5 7.14E-01 3.57E-05 Lead (inorganic) NC 10 8.93E-01 4.46E-05 Mercury (inorganic) NC 7 1.B4E+01 9.21E-04 Nickel NC 10 4.26E+00 2.13E-04 Silver NC 1 2.00E+01 1.00E-03 Vanadi urn NC 1 1.43E-01 7.14E-06 Zinc NC B 1.07E-01 5.33E-06 Aluminun i nsuf f icient data Magnesium insufficient data Manaoanese i nsuf f i ci ent data Tin insuf f i cient data
1 - Rating volume is for severity of effect for noncarcinogens, range in l(low) to lO(high)} EPA carcinogenic category is a Qualitative weight-of-evidence designation for potential carcinogens; A is a proven human carcinogen and B2 is a probable human carcinogen. Information taken from Appendix D, Superfund Public Health Evaluation manual, December 1.985
2 - Data taken from Appendix C, Superfund Public Health Evaluation manual, December 1965
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CIB 006 1796
The oral toxicity constants ( T for water and T for soil) listed are medium-
specific and are derived from both carcinogenic and other chronic effects.
The non-carcinogenic toxicity constants for inhalation are not presented,
since inhalation was not determined to be a route of ingestion. All potential
carcinogens are also classified as having non-carcinogenic effects although
toxicity constants associated with these effects were often not available.
Compounds that had insufficient data for indicator scoring were classified as
such and were not evaluated further in the selection process.
Calculation of CT and IS Values for Carcinogenic and Noncarcinogenic
Effects
Contaminant concentration/toxicity (CT) values were calculated for each
compound by multiplying the toxicity constants from Table 8-2 by their
maximum and representative concentrations from Table 8-1 within each
media. The CT values for potential carcinogens and non-carcinogens are
listed on Tables 8-3 and 8-4 respectively. The indicator score (IS) value is the
sum of all the CT values for each chemical, keeping maximum and
representative values separate. The higher CT value of either groundwater
or surface water was used in the calculations.
The IS values were then ranked separately for the potential carcinogens and
non-carcinogens. The rank provides a relative indicator of the potential
health risk posed by each compound.
Final Chemical Selection
Table 8-5, developed for the TRC public health evaluation presents the top
ranking potential carcinogens and non-carcinogens in terms of site-specific
conditions at TRC. Eighteen compounds, including both organic and inorganic
potential carcinogens and non-carcinogens were evaluated.
8-9
C I B 0®6 1 7 9 7
1MVIE I-)
ICUIW F« IUICRTW CKh-ICAL KlECtlOMi CM.CU.«IIWI Of C! MR II VM.UEI FOR CMCIROKNIC EFFEC1I
00 I
O M 00
<9
00
Srouii litor CT
Bur Iict tutor CI
turlict loll CI
M-lorlKO loll CT
MtltRt CI
Cknlctl Nil ••pm loom Flu Rtproi Nil Mini Nil Rtprii
II Viloti
Hoi Room
VOLATILE!
Itoitni 7.4JE-03 2.21E-01
Ckloroloro 4.47E-01 I.I4E-04
1,2-llcMoroitkMt 4.40E-O3 7.18E-OS
1,1,2,2-IitricilorooUiii
MricktorottkMO I.J4E-02 2.32E-04
trickier oitkini
Hm-VOUTIIEI
Imi ItlRotkricom
ItiiolblFWoriitkiM
tOIIOlll'irOM
Cfcryiiii
2,1,1 IrlckloroikoMl
KITICIK/PU'i
Cklorltnt
1,4'-lit
l lol lr l i
HtfUcklor Epoilii
FCI'i ItUtll
IkWSMIICt
ftrmlc
I.74E-I2 2.44E-0) 2.88E-04 2.2IE-M
3.44E-02 .17E-0J
4.IIE-M I.74E-I0
7.20E-O4 7.I0E-M
I.24E-42 1.431-44
2.07E-42 2.2tl-04
2.34E-0I 2.IIE-04
1.S2E-M I.I2M7
S.41E-H 2.IIE-4W
I.I2E-M I.I2E-M
I.7SE-M 1.R3E-47
4.2K-M 4.33E-44)
I.2IE-47 J.47E-II
S.40E-04 l.HE-07
4.JJE-47 2.I4E-M
2.41E-I2 I .HEH
7.4 JEM 2.2IE-M
4.47E-01 I.I4E-04
4.I0E-0) 7.HE-03
I.2IE-07 J.47E-04
I.J4E-02 2.S2E-04
I.74E-02 2.4W-0J
7.20E-04 7.IOE-04
I.241-02 I.I3E-04
2.07E-02 2.24E-04
2.30E-04 2.IIE-04
4.JJE-07 2.IIE-M
4.37E-0* I.02E-07
3.4JE-OI 2.0IE04
I.I2E-M I.I2E-0I
I.73E-03 J.I3E-07
4.2K-M 4.33E-M
I.IK-02 J.03E-0J
ToolitI«• RMI
In Roorit
10
4
7
It
4
2
10
t
7
It
I
2
I I
3 3
J 4
» 1
13 14
12 12
17 17
14 13
II II
IJ I)
ft
IULE 1-4
BCMIM FOR IMICRTOR CKMCM. KUCIIONi CW.Cli.MIOR OF CI RM) II VM.UEI FOR INOXIKIIIORniC EFFECTI
Braunl Nitir CI
Clinical *•« **prii
turlici Nttir CI
turfici t i l l CI
Ri> Riirii Nil Rtirn
M- lv f ic i loll CI
IUI
Itilont CI
Riirii Nil Rtirn
II Vtlmt
Nil Riirii
ImUtl i i Riot
Nil l i i r n
00 I
VOUIILEI
••••Mi I.I7E-01 Chlwootiuni 4.72E-0I 1,2-llchlorottkiM I.2X-02 !riM-l,2-0lc»loroiUni 2.70E-02 1,2-llckloroirooini EtkvllMIIM 1,1,2,2-lftrKkloroothiM IitrickloroitkNi llWtM 1,1,1 IrlcklorwtkiM IrUkiorottkont
2.SOE-02 2.UE-01
3.51E-05 I.71E-02 2.IIE-04 i.lSE-04
4.7IE-04 3.20E-03
l.7BE«OI S.02E-0I
4.2IE-03 1.I2E-03
S.I8E-01 4.S2E-04
S.t4E-0i S.44E-0B
S.S2E-M S.52E-I0
7.tTE-0R 7.I0E-01 2.ME-I0
l.»JE-04 I.SIE-IO 2.S71-I2
I.SOE-03 I.14E-07
4.4SE-N I.OSE-OS I.IX-M I.01E-03 I. MI-OS
1.2SE-04 7.2K-07 J.IOE-OI S.7IE-07 I.7RE-07 S.tK-Of
I.I7E-0I 4.72E-OI 1.211-02 2.70E-02 4.4X01 1.031-OS I.IX-Ot 2.301-02 2.NE-I) 2.I4E-I0 l.70E»OI
3.5IE-OS I.74E-02 2.IIE-04 t.lSE-04 1.7X04 7.2JE-07 J.IOE-OI 4.7IE-04 S.20E-0S 2.37E-I2 J.02E-OI
It S
IJ 10 21 20 22 II It 24 I
II 4
II II 22 If 21 12 17 21 I
KD
KHI-VOUIILEI
BMiotilPyriM
1,2 lUkltrlmiMt I.73E-01 l l -«-Kt»l iMki l i l i 1,2,1 IrlcklorokMiiM 1.I4E-0I
I.36E-04
t.tlE-01
l.ltE-02 I. IK-OS I.JS-Ot 4.4X-45
4.22E-04 1.I4E07 4.I7E-07 2.4OE-04 4.42E-04 2.44E-OS
l.ltE-02 t.741-01 1.3X04 1.44E0I
4.22E-04 I.34E-04 4.I7E-07 t.tlE-01
I 14 21 7
II It 20 7
O 1-4 03
Q 8 CP
IMrMICI
t/ttilc b r i l l Cniir I I I ! Rtruri Nlckil II Ivor ViMllaa Hoc
2.IBE-0I 1.141-01
4 HE-03 l iK -02
8.0SE-0I 8.0tt-02
2.74E0I 2.I4E-02
4.4JE-0J S.471-04
1.431-01 I.IX-01
2.2IE-0I I.SX02
1.7OE-02 I.ME-U 1.441-01
I.I4E-0J I.J7E-04 2.44E-04
I.70E-01 t.trE-01 I.24E-0J
.1X-01
4.1H-0I B.ltE-OI I.JRE-ll 4.44E-01 4.47E-II I.4X-0I 1.7IE-02 I.ME-01 I.421-02
I.4K-I2 I.J4E-02
l.2tE-01 l.ttt-02 R.Off-02 I.I4E-01 I.37E04 1.1X04
t 2
17 13 4 I •
II 12
3 t
I 1 2 4
IS 10
TABLE 8-3
6C0RIN8 FOR INDICATOR CHEMICAL SELECT I(Wi FINAL CHEMICAL SELECTION
EPA TOX. RATING/ TRC USE/ PRESENCE IN FREO. PRESENI COMPOUND PC NC NT. OF EVIDENCE NABTE . 0NS1TE 6N IN 6H • HEDIA OFFSITE
VOLATILES
Benz trie 10 IB 3/A I I 5/57 I I Chlarobanztne - 4 4 I I 9/57 3 1 Chlorofora a - B2 I 5/57 1 I 1,2 Dichloroethane 7 14 10/12 I 1/57 1 Trtni-I,2-dichlorotthini - II S I 8/57 1 Totrachlorotthtnt 3 12 7/C I I 5/57 3 I Tolumi - 17 7 1 I 5/57 4 I Trichloroflthint 2 1 S/B2 I 12/57 2 I
BEMl-VOLATILES
Itnz <«)mthricini B - B2 1 Bantolblfluorinthana S - B2 1 Itniodlpyreni 4 13 B/B2 I Chryiana 9 - B2 I 1,2 Dichlorobmzini - 16 4 I I 2/87 2 I 1,2,4 Trichloroteniena - 7 4 1 I 2/57 2 I
1N0R8ANICB
Artinic t S 9/A I I 1/43 2 Biriua - A 10 I 22/38 1 Htrcury - 3 7 1 2 I Nicktl - 2 10 1 la/SB 1
NO^B. • • final l i l t of Indicator cheaicali
The primary concern at TRC is the threat of groundwater contamination from
improper containment of wastes therefore final selection was not based solely on
indicator scores. The indicator chemicals selected focused on those compounds
which appeared in groundwater, have a history of use and disposal at the site, and
had been found in private wells irrigation off site. There is no evidence that the
private drinking water of the area residents have any chemical contamination.
The final list of indicator chemicals are:
Potential Carcinogens: Non-Carcinogens:
o Arsenic
o Benzene
o Chloroform
o Tetrachloroethene
o Trichloroethene
o Barium
o Chlorobenzene
o 1,2-Dichlorobenzene
o Mercury
o Nickel
o Toluene
o Trans-1,2-Dichlorobenzene
o 1,2,4-Trichlorobenzene
The remaining compounds were excluded on the basis that they did not appear in
any groundwater samples and their chemical-physical characteristics indicate they
were not likely to. volatilize or migrate offsite in an aqueous medium:
o Benz(a)anthracene
o Benzo(a)pyrene
o Benzo(b)fluoranthene
o Chrysene
1,2 Dichloroethane was excluded due to infrequency of detection and no past
history of use or disposal at TRC.
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8.3 Environmental Fate and Transport of Indicator Chemicals
The fate of chemicals released into the environment will be determined by a
number of factors including volatility, solubility, reactivity, sorption capacity,
bioaccumulation and biotransformation. Table 8-6 lists the indicator chemicals for
the TRC site and some of the chemical/physical constants that will aid in
predicting their environmental fate and transport. The table was compiled from
data presented in Clement Associates, Inc. (1985) and ICF Incorporated (1985).
8.3.1 Organic Indicator Chemicals
8.3.1.1 Volatilization
Vapor pressures and Henry's Law constants are indicators of a compound's volatility
which can help to predict the migration of contaminants from chemical spills or
contaminated surface waters (e.g. lagoons and ponds). Although these constants
suggest that volatilization would be a significant transport mechanism for the
organic indicator chemicals, sampling results from the RI show minimal
contamination of the surface soils and surface water. Therefore, this process does
not appear to be a major concern at the TRC site.
8.3.1.2 Transport
Once contaminants are, dissolved in the groundwater, transport is determined by
the factors of advection, dispersion, sorption and biochemical transformation
(Mackay et al., 1985). Sampling results show the potential for the indicator
chemicals to be dissolved in groundwater but some compounds may not completely
dissolve and, depending on their specific gravity, can travel at the top or bottom of
the water table as a non-aqueous-phase-liquid. However, the concentrations of
contaminants detected at TRC are far below their maximum solubilities which
indicates that there would not be a significant non-aqueous phase and any
contamination would be found evenly throughout the groundwater.
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TABLE 8-6
CHEMICAL AMD PHYSICAL PROPERTIES OF INDICATOR CHEMICALS
ChMicii
Henry a L M Constant (atB-a3/aolal
Vapor Prntura (at Hq)
Natar Solubility (•o/U
Specific 6revity
K K
(ei/qi loa Km
Benzene 5.39E-03 9.52E+01 1.73E+03 0
0.879 (20/4 0 83 2.12
CMorobenzene 3.72E-03 1.17E+01 4.66E+02 0
1.103 (23/23 C) 330 2.84
Chlorofore 2.87E-03 1.31E+02 8.20E+03 0
1.489 (20/20 0 31 1.97
Trani-l,2-DichloroethMe 6.56E-03 3.24E+02 6.30E+03 1.257 59 0.48
Tetr»chl oroethene 2.39E-02 1.78E+0L 1.05E+02 0
1.423 (20/20 0 364 2.60
Tolutni 6.37E-03 2.81E+01 5.33E+02 0
0.8a* (20/4 0 300 2.73
Trlchloroethene 9.10E-03 5.79E+01 1.10E+03 0
1.460 (23 0 126 2.38
1,2 Oichlorobtnztnf 1.93E-03 1.00E+00 1.0OE+02 1.284 1700 3.60
1,2,4 Trichlorobenzene 2.31E-03 2.90E-01 3.00E+01 0
1.463 (23 0 9200 4.30
Arttnic . . . . . . —
Bariua
Mercury --- 2.00E-03
Nickel
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Advection is the passive movement of solutes along with the general flow of
groundwater. Therefore, the faster the groundwater flows, the further a
contaminant will be transported from its source.
Dispersion is the movement of solutes within a body of water. This movement is
influenced by molecular diffusion and mechanical mixing. Although dispersion
contributes to the dilution of a contaminant, i t can also increase the area which
will be affected.
Sorption refers to the interaction of dissolved contaminants with aquifer solids.
The degree of interaction, for both organics and inorganics, depends on the organic
content of the aquifer, the pH and the type and presence of other dissolved
compounds. Usually, compounds with the highest Koc values would be expected to
adsorb to organic matter, thereby reducing their rate of migration within the
aquifer. However, sorption of organics is less of a factor in aquifers composed
primarily of sand and gravel (Newsom, 1985), as is the case at TRC.
8.3.1.3 Hydrolysis and Oxidation
Hydrolysis and oxidation are the primary chemical reactions expected for organic
compounds in groundwater. Chlorinated hydrocarbons and aromatics do not readily
enter into these reactions unless there are elevated temperatures or significant
change in pH from neutral and thus these indicator organic chemicals are not
expected to be changed at the TRC site.
8.3.1.4 Degradation
Under normal conditions, it is likely that any degradation of these organic
compounds would be the result of metabolism by microorganisms in the aquifer.
Contaminant concentration, temperature, pH and the types of organisms present
will determine the extent of biodegradation and the products formed. One study
suggests that the contaminant concentration is the most important factor. Results
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showed that a contaminant must be present at parts per million concentrations in
order to be metabolized to any extent by microorganisms. The other factors will
determine the type and activity of the microorganisms present (Mackay et al.,
1985).
Halogenated aliphatics (chloroform, trans-1,2-dichloroethene, trichloroethene and
tetrachloroethene) are believed to degrade under anaerobic but not aerobic
conditions (Newsom, 1985). Although the process is extremely slow,
trihalomethanes, like chloroform, appear to degrade ten times faster than other
halogenated alipahtics (Roberts et ah, 1982). There was no specific information
regarding the degradation of trans-l,2-dichloroethene. Wood et al. (1981) suggests
that it is an intermediate in the transformation of tetrachloroethene and/or
trichloroethene to vinyl chloride under anaerobic conditions.
Alkyl benzenes (toluene and possibly benzene) are known to degrade under aerobic
conditions. A Swiss study measured the infiltration of contaminants from the Glatt
River to groundwater observation wells. Aerobic respiration and nitrification were
found to be the dominant fate processes. The decline in parent compounds was
seen throughout the year even at water temperatures near 5°C. The alkyl
benzenes were found to degrade much faster than the halogenated aromatics (e.g.
chlorobenzene, 1,2-dichlorobenzene, and 1,2,4-trichlorobenzene). However, the
same study showed that chlorobenzenes can be degraded to phenols and catechols
under aerobic conditions (Newsom, 1985).
Anaerobic degradation does not appear to be a significant fate process for
chlorinated aromatics but may be for the alkyl aromatics. A study by Wilson and
Enfield (1983) reported that toluene degraded both above and below a shallow
flood plain aquifer in Oklahoma whereas, the chlorinated aromatics decomposed
above but not below the water table (Newsom, 1985).
In some cases, groundwater contaminants can migrate through the aquifer
unchanged and outlet to a drinking water source.
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8.3..1.5 Bioaccumulation
The octanol/water part i t ion coeff icients (Kow) listed in Table 8-6 are indicators of
a compound's potential to bioaccumulate. Most of the organic indicator chemicals
are l ipid soluble and would be expected to accumulate in the fats of exposed
animals. The exceptions are trans-1,2-dichloroethene and trlchloroethene which
have not been shown to bioaccumulate in animals or food chains (EPA, 1985). Thus
any of the organic chemicals migrat ing from the TRC site would be expected to
enter the environmental food chain.
8.3.2 Inorganic Indicator Chemicals
The environmental fate of the inorganic indicator chemicals at TRC wi l l be
primari ly determined by factors including chemical speciation, volat i l i ty , sorption
capacity, bioaccumulation and biotransformation.
8.3.2.1 Arsenic
Arsenic can exist in four valence states with the +5 and +3 states predominating.
These differences in chemical speciation allow arsenic to complex with organic
matter in clays, aluminum hydroxide or, more commonly, w i th hydrous oxides of
i ron. Arsenic can also be biotransformed by microorganisms via reactions with
sulfhydryl and methyl groups. However, i t does not bioaccumulate due to i ts
toxic i ty at higher trophic levels.
8.3.2.2 Barium
Barium is a divalent metal which is not found free in nature but exists in a number
of salt forms. Barium acetate, n i t rate, chloride and hydroxide are soluble in water,
whereas barium carbonate, sulfate and flouride are nearly insoluble. Barium can
also complex with arsenate to form Ba3(AsO^)2 thereby reducing the mobil i ty of
arsenic. Barium occurs at low levels in most surface and ground waters with
reported levels less than 340 ug/l (EPA, 1985).
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8.3.2.3 Mercury
Mercury can form a variety of reversible complexes in the environment. Although
sorption to sediment may be the dominant fate, mercurials have also been found in
air and water. Since only a small fraction of mercury in groundwater or surface
water occurs as the organic form, i t has been shown to be biotransformed via
complexes with methyl, sulfhydryl and amino groups. Methyl-mercury not found at
this site is the only predominant mercurial form shown to bioaccumulate in aquatic
species.
8.3.2.4 Nickel
Nickel is probably the most mobile of the indicator compounds in an aquatic
environment. It is not likely to volatilize, adsorb to organic matter or
bioaccumulate. Nickel primarily forms complexes with sulfate, carbonate or
hydroxide which increases its solubility in water. Because nickel compounds are
relatively insoluble, the level of nickel in most surface or ground waters is less
than 100 ug/l (EPA, 1985).
8.* Toxicity Assessments
The following section presents toxicity profiles for each indicator chemical.
Unless otherwise noted, these discussions are a summary of the relevant data
available in the EPA preliminary draft "Health Effects Assessment Documents"
(EPA, 1984) and the EPA draft Health Advisories for 52 Chemicals Which Have
Been Detected in Drinking Water (EPA, 1985). Regulatory guidance are also
briefly summarized for each indicator chemical as provided in a number of sources
(EPA, 1980, 1985). Where available, Maximum Contaminant Levels and Ambient
Water Quality Criteria, as defined below, are presented.
Maximum Contaminant Levels (MCLs/RMCLs) - MCLs are enforceable standards
promulgated under the Safe Drinking Water Act and are designed solely for the
protection of human health. MCLs are based on laboratory or epidemiological
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studies and the economic and technical feasibility of achieving the guidelines in
drinking water consumed by a minimum of 25 persons. They are designed for
prevention of health effects associated with lifetime exposure (70-year lifetime) of
an average adult (70 kilograms) consuming 2 liters of water per day. These
guidelines also reflect the fraction of the toxicant expected to be absorbed by the
gastrointestinal tract. Recommended Maximum Contaminant Levels (RMCLs) are
specified as zero for carcinogenic substances, based on the assumption of
nonthreshold toxicity, and do not consider the technical feasibility of achieving
these goals. Proposed Maximum Contaminant Levels and Proposed Recommended
Maximum Contaminant Levels are MCLs and RMCLs, respectively, that have been
offered by the EPA but have not been legislatively approved to date. These
guidelines are included if MCLs or RMCLs are unavailable.
Ambient Water Quality Criteria (AWQC) - AWQCs are not enforceable regulatory
guidelines but are of primary utility in assessing acute and chronic toxic effects on
aquatic organisms. AWQCs consider acute and chronic effects in both freshwater
and saltwater aquatic l i fe , and adverse carcinogenic and noncarcinogenic health
effects in humans from ingestion of both water (2 liters/day) and aquatic organisms
(6.5 grams/day) and from ingestion of water alone (2 liters/day). The AWQCs for
protection of human health for carcinogenic substances are based on EPA's
specified incremental cancer risk of 1 additional case of cancer in an exposed
population of 1 million people (i.e., the 10"6guideline).
Carcinogenic Potency Factor (CPF) - The CPF is applicable for estimating the
lifetime probability (assumed 70-year lifespan) of human receptors contracting
cancer caused by exposure generally by the oral route to known or suspected human
carcinogens. This factor is generally reported in (kg-day/mg)~l a n d j s the slope of
the cancer risk does-response curve. This slope is determined by EPA through an
assumed low-dosage linear relationship and extrapolation from high to low dose-
responses determined from animal studies. The value used in reporting the slope
factor is the upper 95 percent confidence l imit . This factor may be used to
determine the probability that an individual could contract cancer upon lifetime
exposure.
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Arsenic
Toxicity Profile; Arsenic:, particularly the trivalent inorganic form, has been
associated with the occurrence of lung and skin cancers in humans. Although
animal studies have produced conflicting results, the EPA Carcinogen Assessment
Group determined that there was sufficient evidence to classify arsenic as a Group
A - Human Carcinogen.
Exposure to arsenic (As) can be through inhalation of contaminated dusts, volatile
arsenic trioxide or by ingestion of soluble arsenic compounds in water.
The absorption and toxic effects of arsenic depend on its form in the environment.
Arsenic trioxide can be rapidly absorbed through the alveoli of the lungs while As +3
and As + ^ are preferentially absorbed in the gastrointestinal tract. As+3 is
considered to be most toxic whereas, some methylated forms found in shrimp and
fish could be considered non-toxic.
Sub-chronic and chronic studies have shown the targets of arsenic toxicity to be
the skin, lungs, peripheral nervous system, peripheral vascular system,
gastrointestinal tract and kidneys. Rats have proved to be more susceptible than
either guinea pigs, cats, dogs or man.
A No Observed Adverse Effect Level (NOAEL) of 0.001-0.017 mg As/1 of drinking
water has been established for arsenic-related peripheral vascular disease.
Evidence of the carcinogenic effect of arsenic in humans was shown in an
investigation that followed 7k patients who used an antiasthmatic at an estimated
2.5 mg As/day as arsenic trioxide or 10.3 mg As/day as arsenic sulfide for periods
ranging from 6 months to 15 years. Five percent of the patients developed internal
malignancies including squamous cell carcinomas of the lung and gall bladder and
one hemangiosarcoma of the liver. A carcinogenic potency factor has been
calculated as 1.5 E + 01 (mg/kg/day) - 1 based on a study that linked arsenic in
drinking water with an increased incidence of skin cancer in Taiwan.
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Regulatory Requirements. Standards and Criteria: The MCL for arsenic in drinking
water is 0.05 mg/1. The AWQC for the protection of human health from the
potential carcinogenic effects due to exposure to arsenic through ingestion of
contaminated water and aquatic organisms is zero. The level which may result in
an incremental increase of cancer risk over the lifetime, estimated at 10 - 6 and
adjusted for ingestion of water only, is 0.025 ug/l.
Bari um
Toxicity Profile: The rate of absorption and toxic effects of Barium (Ba) depend on
a number of factors including age, species and dietary composition. The toxicity of
barium has not been well defined however i t appears that barium exerts its toxic
effect by replacing calcium in a number of calcium-mediated activities. There are
reports that barium exposure can lead to an increase in muscle excitability,
primarily cardiac muscle, along with effects on the hematopoietic system and
central nervous system. However, chronic and sub-chronic studies do not support
these findings.
A No Observed Effect Level (NOEL) has been set at 0.1 mg Ba/L of drinking water.
The level was set after an Illinois study showed an increase in cardiovascular
disease where a community consumed water containing 7 Ba mg/1 but no effect in a
community where the Ba level was 0.1 mg/1.
Regulatory Requirements, Standards and Criteria: An MCL of 1.0 mg/1 has been
established for Ba in drinking water. Promulgation of a proposed MCL of 1.5 mg/1
is pending.
Benzene
Toxicity Profile: Extensive case reports and epidemiologic studies define benzene
as a carcinogen in both humans and laboratory animals. Based on criteria set forth
by the EPA Carcinogen Assessment Group, benzene has been ranked as a Group A -
Human Carcinogen.
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The primary target of benzene toxicity is the hematopoietic system and is believed
to. cause pancytopenia, a reduction in the number of all types of circulating blood
cells.
In a study with female Wistar rats dosed, by gavage, with benzene at 1, 10, 50 or
100 mg/kg benzene in olive oil, 5 days/week for, 187 days adverse hematopoietic
effects were seen at all dose levels except the lowest. This study was used to
determine an NOEL of 1 mg/kg for leukopenia and/or erythrocytopenia in female
rats. Similarly, a sub-chronic inhalation study established a 31 ppm NOEL for
leukopenia in rats.
Chronic studies were not available regarding oral exposure to benzene in humans or
laboratory animals.
Chronic inhalation studies in humans are represented by several epidemiologic
reports on benzene exposure in the work place that showed a significant increase in
the incidence of leukemia among workers occupationally exposed to benzene. The
EPA Carcinogen Assessment Group used these studies to calculate a carcinogenic
potency factor of 2.59 E"02 (mg/kg/day)-l for inhalation of benzene.
A single chronic study was used to predict the carcinogenic potency factor of 4.45
E"02 (mg/kg/day)-l for oral exposure to benzene.
Studies on the teratogenic effects of benzene exposure have had conflicting
results. An oral study showed no significant fetotoxic effects in mice at 0.3, 0.5 or
1 mg/kg/day administered on day 6 through 15 of gestation. Similarly, another
study showed no treatment-related effects in the litters of rabbits exposed to 500
ppm, 7 hours/day, on days 6 through 18 of gestation. However, an inhalation study
with Sprague-Dawley rats produced fetotoxic effects at 50 ppm and 500 ppm but
none at 10 ppm. This study suggested a NOEL of 10 ppm for fetotoxic effects in
rats.
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Regulatory Requirements, Standards and Criteria: An MCL of 5 ug/l has been
proposed for benzene based, in part, on a final RMCL of zero. The AWQC for the
protection of human health from the potential carcinogenic effects due to exposure
to benzene through ingestion of contaminated water and aquatic organisms is zero.
The level which may result in an incremental increase of cancer risk over the
lifetime, estimated at 10-6 and adjusted for ingestion of water only, is 0.67 ug/l.
Chlorobenzene
Toxicity Profile: The toxic effects of chlorobenzene exposure have not been well
defined. Animal studies with rats and dogs have shown the liver and kidneys to be
the target organs of chlorobenzene toxicity.
One study showed increased liver and kidney weights in rats given 144 and 288
mg/kg/day of chlorobenzene, 5 days/week, for 192 days. No effects were seen in
rats given 14.4 to 18.8 mg/kg under the same dosing regimen.
Two studies showed NOELs to be 27.3 mg/kg/day in dogs and 50 mg/kg/day in rats
after oral dosing for 90 to 99 days. The highest dose in dogs (272.5 mg/kg/day)
produced histopathological changes in the liver, kidneys and spleen. The highest
dose in rats (250 mg/kg/day) led to increased liver and kidney weights.
There was insufficient evidence in the literature to draw conclusions on the
teratogenic or carcinogenic potential of chlorobenzene exposure.
Regulatory Requirements, Standards and Criteria: An RMCL of 60 ug/l has been
proposed for chlorobenzene. Based upon available toxicity data, the AWQC for the
protection of human health, adjusted for drinking water only, is 488 ug/l.
Chloroform
Toxicity Profile: Chloroform exposure has lead to the development of
hepatocellular carcinomas and kidney epithelial tumors in laboratory animals.
Based on criteria set forth by the EPA Carcinogen Assessment Group, chloroform
has been classified as Group B2 - Probable Human Carcinogen.
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Much of the available toxicity information has been the result of the use of
chloroform as an anesthetic. Acute exposure to high concentrations of chloroform
leads to central nervous system (CNS) depression and narcosis. In addition to its
CNS effects, chloroform has been associated with hepatic and renal toxicity. An
inhalation study resulted in cloudy swelling of the kidneys and necrosis of the liver
in rats exposed to 50 and 85 ppm, 7 hours/day, 4 days/week for 6 months.
Chronic oral studies have focused on the carcinogenic effects of chloroform.
Osborne-Mendel rats and B6C3F1 mice were administered various concentrations
of chloroform by gavage. Male rats developed kidney epithelial tumors at 90 and
180 mg/kg/day. Male mice developed hepatocellular carcinomas at 138 and 277
mg/kg/day whereas female mice developed similar carcinomas at 238 and 477
mg/kg/day. The EPA Carcinogen Assessment Group used this data to calculate a
carcinogenic potency factor of 7.0 E"02 (mg/kg/day)-1 based on animal studies.
The level which may result in ah incremental cancer risk over the lifetime,
estimated at 10"^ and adjusted for drinking water only, is 0.5 ug/l.
Teratology studies have produced conflicting results. On the whole, chloroform
appears to be more fetotoxic than teratogenic, with the inhalation route showing
more pronounced toxicity than administration by gavage.
Regulatory Requirements, Standards and Criteria: The MCL for chloroform in
drinking water (actually set for total trihalomethanes) is 100 ug/l. The AWQC for
the protection of human health from the potential carcinogenic effects due to
exposure to chlorofrom through ingestion of contaminated water and aquatic
organisms is zero. The level which may result in an incremental increase in cancer
risk over the lifetime, estimated at 10"6 and adjusted for drinking water only, is
0.19 ug/l.
1,2-Dichlorobenzene
Toxicity Profile: The toxic effects of exposure to 1,2-dichlorobenzene (1,2-DCB)
have not been well defined. Limited animal studies show the target organs of 1,2-
DCB toxicity as the liver and kidneys.
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A sub-chronic study in rats showed liver and kidney toxicity at doses of 250 and 500
mg/kg, for 5 days/week, over 13 weeks. The toxic effects included hepatic
necrosis and tubular degeneration of the kidneys. The same study showed no
treatment-related effects at doses less than 125 mg/kg under the same dosing
regimen.
A chronic inhalation study exposed various species to a range of concentrations of
1,2-DCB for 7 days/week over 6 to 7 months. No adverse effects were observed in
rats, guinea pigs or mice at 49 ppm 1,2-DCB or similarly in rats, guinea pigs,
rabbits or monkeys at 93 ppm.
No relevant data was found regarding human exposure to 1,2-DCB.
There is no evidence in the literature that shows a relationship between exposure
to 1,2-DCB and teratogenic or carcinogenic effects.
Regulatory Requirements, Standards and Criteria: An RMCL of 620 ug/l has been
proposed for 1,2,-DCB. Based upon available toxicity data, the AWQC for the
protection of human health, adjusted for drinking water only, is 470 ug/l.
Mercury (Inorganic)
Toxicity Profile: Although inorganic mercury (Hg) is poorly absorbed in the
gastrointestinal tract, i t has the potential to form organc complexes that can
bioaccumulate in the environment.
The primary target organ for inorganic mercury is the kidney. A chronic ingestion
study administered 0.1, 0.5, 2.5, 10, 40, or 160 ppb mercury acetate to male and
female rats for up to 2 years with the estimated daily mercury intake ranging from
0.05 to 8.0 mg/kg. Toxic effects at the proximal tubule of the kidneys were seen in
the 2.0 and 8.0 mg/kg groups. More severe effects were seen in females than in
males.
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Chronic ingestion of Hg leads to the synthesis of metallothionein which acts as a
scavenger of free Hg in the body, therefore decreasing its toxic effect.
There is no evidence in the literature to suggest mutagenic or carcinogenic effects
from mercury exposure.
Regulatory Requirements, Standards and Criteria: An MCL of 2 ug/l has been
established for mercury in drinking water. Promulgation of a proposed MCL of 3.0
ug/l is pending. The AWQC for the protection of human health from the toxic
properties of mercury ingested though contaminated water and aquatic organisms
is 0.144 ug/l. The AWQC adjusted for drinking water only is 10 ug/l.
Nickel
Toxicity Profile: Although inhalation of nickel compounds has been associated with
respiratory tract cancers, few toxic effects can be attributed to the ingestion of
nickel due to its poor absorption from the gastrointestinal tract. In fact, a chronic
study showed no uptake of nickel in rats exposed to 5 ppm in drinking water.
High doses of dietary nickel (1000 ppm) accumulate in the kidneys, liver, heart and
testes, therefore, toxic effects are primarily seen in these organs. For example,
daily oral doses of 25 mg/kg of nickel sulfate over 4 months in male rats caused
degenerative cellular changes in the kidneys and liver along with testicular
atrophy, interstitial cell proliferation and reduction in the number of spermatozoa
produced.
Teratogenicity studies have shown nickel to be slightly fetotoxic but not
teratogenic. There is no evidence that demonstrates the mutagenic or
carcinogenic potential of soluble nickel compounds.
Regulatory Requirements, Standards and Criteria: The AWQC for the protection
of human health from the toxic properties of nickel ingested through contaminated
water and aquatic organisms is 13.4 ug/l. The AWQC adjusted for drinking water
only is 15.4 ug/l.
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trans-l,2-Dichloroethene
Toxicity Profile: Only minimal data exists on the toxic effects of trans-1,2-
dichloroethene.
A sub-chronic oral study administered a mixture of the cis and trans isotners of
dichloroethene and found no adverse effects at doses less than 1 g/kg in female
Wistar rats. A sub-chronic inhalation study exposed six female Wistar rats to 200
ppm trans-1,2-dichloroethene for 7 hours/day, 5 days/week, for 1, 2, 8 or 16 weeks.
Results showed progressive damage to lungs and fatty changes in the liver.
No information was available regarding the chronic, carcinogenic or teratogenic
effects of trans-l,2-dichloroethene exposure.
Regulatory Requirements, Standards and Criteria: An RMCL of 70 ug/l has been
proposed for trans-1,2-dichloroethene. An AWQC for the protection of human
health has not been determined due to insufficient data.
1,2,4-Trichlorobenzene
Toxicity Profile: No relevant information was found regarding the toxic effects of
1,2,4-trichlorobenzene in humans or animals.
Regulatory Requirements, Standards and Criteria: An AWQC for the protection of
human health has not been determined due to insufficient data.
Tetrachloroethene
Toxicity Profile: Tetrachloroethene (PCE) has been classified as a possible
carcinogen. However, human studies centered on dry-cleaners who were exposed
to a number of other chemicals, including trichloroethene and carbon tetrachloride.
Animal studies have been inconclusive with results showing carcinogenic potential
in mice but not in rats.
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No information was available on the effects of sub-chronic oral exposures in
humans or laboratory animals. Similarly, no information was available on chronic
oral exposures in humans.
Sub-chronic inhalation studies showed liver and kidney toxicity in albino rats and
guinea pigs at 200 to 400 ppm PCE. However, no adverse effects were seen in
rabbits or monkeys.
A chronic oral study resulted in nephrotoxicity in rats and mice at levels ranging
from 300 to 500 mg/kg/day, 5 days/week, for 78 weeks.
The teratogenic effects of PCE inhalation were demonstrated using Sprague-
Dawley rats and Swiss-Webster mice. The subjects were exposed to 300 ppm for 7
hours per day on days 6 through 15 of gestation. Results showed an increased
number of resorptions in rats, along with subcutaneous edema, delayed ossification
of the skull and split sternebrae in mice.
The carcinogenic potential of PCE was evaluated by the increased incidence of
hepatocellular carcinoma in mice and the increased incidence of death due to
carcinomas in laundry workers exposed to PCE. Application of the criteria set
forth by the EPA Carcinogen Assessment Group has classified PCE as a Group C -
Possible Human Carcinogen. The same group has calculated a carcinogenic
potency factor of 3.98 E"02 (mg/kg/day)-l for oral exposure to PCE.
Regulatory Requirements, Standards and Criteria; The AWQC for the protection
of human health from the potential carcinogenic effects due to exposure to PCE
through ingestion of contaminated water and aquatic organisms is zero. The level
which may result in an incremental increase of cancer risk over the lifetime,
estimated at 10"^ and adjusted for ingestion of drinking water only, is 0.88 ug/l.
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Toluene
Toxicity Profile: Adverse health effects from toluene are usually associated with
prolonged exposure to concentrations greater than 200 ppm. The primary target is
the CNS and can lead to memory loss, impared speech, incoordination and ataxia.
These severe results have often been seen in chronic toluene abusers (e.g. glue
sniffers).
The extent of toxicity to other organ systems has been widely debated. A sub-
chronic oral study suggests a NOAEL greater than 590 mg/kg/day in female rats.
Similarly, a sub-chronic inhalation study showed no changes in liver or kidney
function after mice were exposed to 4000 ppm toluene at 3 hours/day for 8 weeks
(Bruckner and Peterson, 1976).
In contrast, chronic toluene abuse and prolonged occupational exposures (at levels
ranging from 200 to 800 ppm) have been associated with hepatic and renal function
changes. However, chronic toluene inhalation can not be compared to effects
which may result from low level environmental exposures.
In a single teratogenicity study, 860 mg/kg of toluene was administered to pregnant
CD-I mice three times daily on days 6 through 15 of gestation. The results showed
a significant increase in the incidence of cleft palates.
Several studies have shown no relationship between toluene exposure and increased
cancer risk in rats and mice.
Regulatory Requirements, Standards and Criteria: An RMCL of 2000 ug/l has been
proposed. The AWQC for the protection of human health from the toxic properties
of toluene ingested through contaminated water and aquatic organisms is 14,300
ug/l. The AWQC adjusted for drinking water only is 15,000 ug/l.
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T ri chl oroethene
Toxicity Profile; Based on the results of animal studies, trichloroethene <TCE) has
been ranked as a potential human carcinogen. Oral and inhalation studies in mice
have resulted in an increased incidence of hepatocellular carcinoma and lung
adenocarcinoma, respectively. Human epidemiologic studies have not shown
evidence of a relationship between TCE and increased cancer risk, nor have animal
experiments in species other than the mouse. Based on criteria set forth by the
EPA Carcinogen Assessment Group, TCE has been classified as a Group B2 -
Probable Human Carcinogen.
A 6-month sub-chronic oral study exposed male, and female mice to various
concentrations of TCE in their drinking water. The females showed an increase in
liver and kidney weights along with increased ketones and proteins in their urine at
793.3 mg/kg/day. Males appeared more susceptible in that increased liver weights
were prominent in the 216.7 mg/kg/day group and increased proteins and ketones
were measured in the urine at 393.0 mg/kg/day.
A 6-month sub-chronic inhalation study resulted in increased liver and kidney
weights in those rats exposed to 400 ppm for 7 hours/day.
No pertinent data was available on chronic effects of TCE via inhalation or oral
routes.
No pertinent data was available on the carcinogenic effects of TCE in humans.
The National Toxicology Program studied the carcinogenic effects of TCE in Fisher
344 "rats at 500 mg/kg or 1000 mg/kg, 5 days/week, for 103 weeks. Higher dose
males showed an increase in kidney tubular adenocarcinomas and a number died of
toxic nephrosis. When the high dose regimen was repeated in B6C3F1 mice, there
was an increase in hepatocellular carcinoma, hepatocellular adenoma and toxic
nephrosis. The carcinogenic potency factor has been calculated at 1.90 E _02
(mg/kg/day) - 1 for oral exposure to TCE.
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Regulatory Requirements. Standards and Criteria: An MCL of 5 ug/l has been
proposed based, in part, on a final RMCL of zero. The AWQC for the protection of
human health from the potential carcinogenic effects due to exposure to TCE
through ingestion of contaminated water and aquatic organisms is zero. The level
which may result in an incremental increase of cancer risk over the lifetime,
estimated at 10"6 and adjusted for ingestion of water only, is 2.8 ug/l.
8.5 Routes of Exposure
This section describes, for the TRC site and the nearby vicinity, the exposure
routes and completed exposure pathways whereby the public could be exposed to
migrating contaminants. The human exposure routes of inhalation, dermal
absorption and ingestion are considered and then completed exposure pathways
specific to the TRC Site are evaluated.
8.5.1 General Exposure Routes
o Inhalation: Certain compounds can be inhaled after volatilizing from surface
soils or surface water. Volatile compounds detected in groundwater can
become an exposure factor if the groundwater releases to a surface water
body or marshland.
Possible exposures that can result from domestic uses of contaminated
groundwater include inhalation of contaminants volatilized from boiling
water or soluble contaminants in the form of aerosols from showers or garden
sprayers.
Contaminants that are likely to adsorb to soils can be transported and
subsequently inhaled in the form of fugitive dusts. Once inhaled, compounds
may be absorbed through the lungs or dust particles can be trapped by mucous
and swallowed resulting in either absorption or excretion via the gastro
intestinal tract.
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o Dermal Absorption: Some compounds have the potential to be absorbed
through the skin. In this case the contaminated media, either soil or water,
must come into direct contact with the body.
Direct contact with soils usually results from children playing in a
contaminated area or, if the land is developed at a later date, workers can be
exposed to soils during construction activities. Dermal contact with
contaminated water can be from recreational (e.g. swimming or boating) or
from domestic (e.g. bathing or laundry) uses.
o Ingestion: Exposure by contaminants may result from the inadvertent
ingestion of contaminated soil or water.
There is no evidence that residents private drinking wells are contaminated.
A likely situation is the ingestion of contaminants in water either directly
from drinking and swimming or indirectly from eating plants that have been
irrigated with contaminated water.
The exposure scenarios presented are not found at the TRC site for every
chemical. The completed pathways for the chemical contaminants found at the
TRC site are presented in the next section.
8.5.2 Completed Exposure Pathways
A completed exposure pathway consists of a source and mechanism of chemical
release, an environmental transport medium, a point of potential human contact
and a human exposure route.
As determined from the RI, exposure pathways from the TRC site are complete for
inhalation and dermal contact exposures to groundwater and surface water.
Contaminated groundwater has moved off the TRC site and people living southeast
of the site who rely on private groundwater wells may be at risk of inhalation and
dermal contact exposure however, no evidence exists that contaminated
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groundwater is ingested rountinely or even used except for agricultural purposes. "
The focus of concern, then, is the possible use of contaminated groundwater for
domestic purposes including cooking, washing, bathing and irrigation of gardens.
Potential exposure scenarios include: '
o ingestion of foods processed or prepared with contaminated water
o dermal exposure during bathing
o dermal exposure during washing (laundry) activities
o inhalation of contaminated aerosols during bathing
While the surface water study detected only low, parts per billion, quantities of a
few indicator compounds in the Toms River, hydrogeologic studies show that the
groundwater outlets to the river. Therefore, all groundwater contaminants have
the potential to be released to the river and encountered by the public during
recreational use. Potential exposure scenarios include:
o incidental ingestion of contaminated water during recreation
o dermal exposure during swimming and other contact recreation
o inhalation of contaminated aerosols during recreation
Completed exposure routes to contaminated soils appears unlikely. Access to the
site is restricted and any contact with the contaminated areas would be incidental.
There is no evidence that the contaminants are being transported via fugitive dusts
since soil contaminants were detected in a few localized areas. If dust transport
was significant, contamination would be more widespread throughout the TRC site.
? / 8.6 Public Health Evaluation
Due to the limited amount of data from which to extrapolate potential exposure
point concentrations and potential human intakes, and the uncertainty normally
associated with such extrapolations, the following evaluation is a qualitative
discussion of public health concerns related to chemical contamination emanating
from the TRC site.
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As noted earlier, completed pathways exist for exposure of the public southeast of
the TRC Site utilizing groundwater for domestic purposes, including drinking,
cooking, washing, bathing and irrigation of gardens. Of concern is chemically
contaminated groundwater in the Cohansey Formation traveling under the Cardinal
Drive residential community. As can be seen from Table 8.7, chemical
contamination in groundwater from residential taps and from monitoring wells 4-D
and 1-XD (screened at the bottom of the Cohansey Formation as are many of the
private residential wells) currently exceeds appropriate regulatory standards and
criteria for many of the indicator compounds. Most notable in this regard are
concentrations of benzene, chloroform, trichloroethene, trans-1,2-dichloroethene
and chlorobenzene.
Also of concern is the potential human exposure to contaminants released to the
Toms River and the marshlands along the shoreline of the river. The potential
exists for limited dermal, inhalation and incidental ingestion exposures of
swimmers, waders and other primary contact recreational users the waterway. The
greatest potential for exposure exists in areas where groundwater is outletting to
the river or the marshlands. These exposure routes and associated semi
quantitative risk evaluations may need to be further developed in the Feasibility
Study.
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TABLE 8.7 COMPARISON OF CHEMICAL CONTAMINATION IN
GROUNDWATER VS. REGULATORY STANDARDS AND CRITERIA
Maximum R eported Groundwater Concentration Repulatorv StanHarrU nr Cr\tf>r\: Indicator Chemical
RI Monitoring W e l l 3
ug/l (Well //) Residential Well ug/l (Well //)
Well / /4-Da ug/l
Well //1-XDa ug/l
n i
ug/l Source
Benzene 10 (5D) 92 (TW-1) 3 ND 5 MCL (proposed)
Chloroform 87 (5D) 251 (TW-1) ND ND 100 MCL
Trans-1,2-Dichloroethene
510 (4D) ND 510 ND 70 RMCL (proposed)
Trlchloroethene 17000 (C115) 27 (TW-1) 45 ND 5 MCL (proposed)
Tetrachloroethene 2600 (C131) 40 (GW-14) ND ND 0.88 AWQC (adjusted)
Toluene 550 (C131) 8 (TW-4) ND 8 2000 RMCL (proposed)
Chlorobenzene 3300 (C131) 74 (TW-1) 1200 ND 60 RMCL (proposed)
1,2-Dichlorobenzene 130 (4D) 21 (TW-1) 130 ND 620 RMCL (proposed)
1,2,4-Tri chlorobenzene
1700 (C131) 3 (TW-1) 48 ND —
Arsenic 16 (9) ND ND ND 50 MCL
Barium 200 (13D) 3 (GW-6) ND ND 1000 MCL
Mercury ND 0.62 (GW-14) ND ND 2 MCL
Nickel 189 (21S) 3 (GW-1I) ND ND 632 AWQC
a = October, 1985 data MCL = Maximum Contaminant Level AWQC = Ambient Water Quality Cr i ter ia ND = Not detected RMCL = Recommended Maximum Contaminant Level