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.

.[ 235999

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

8-8

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.

8-14

CIB 006 1 8 0 2

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

8-15

CIB 0©6 1803

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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C I B 006 1804

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

8-19

C I B 006 1807

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.

8-20

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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.

8-21

C I B 006 1809

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.

8-22

C I B 006 1810

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.

8-23

C I B 006 1Q1

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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C I B 0®6 1B12

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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C I B 006 1813

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.


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.

8-26

C I B 0®6 1814

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.


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.

8-28

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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.

8-29

C I B *** 1817

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.


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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C I B 006 1818

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.

8-31

C I B 006 1819

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.

8-32

CIB 006 1 8 2 0

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

8-33

C I B 006 1821

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.

8-34

C I B 006 1822

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.

8-35

C I B 006 1823

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

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