- DEC· :,·;:~:~:;: (ti 6W-SP

19
003304 - - UNITED STATES ENVIRONMENTAL AEQION VI . ' .. , .. ,·: '-) \ ALLIED BANK TOWER AT l'OUl~TAIN PLACE HUAO$S AVENUE DALLAS. TEXAS 15202 ' , ..... \. . ' \- DEC· 21987 > ;~ :,·;:~:~:;:_ (ti DECO 2 1987 REPLY TO: 6W-SP MEMORANDUM SUBJECT: ,, L ,. H Statue of Drinking Water Maximum Contaminant Level (MCL) for Chromium Fil.OH: Myron o. Knudson. P.E. Director - Water Management-1>1.v:6ion./(6W) TO: Allyn M. Davis Director Hazardous Waste Management Division (6H) The original MCL for chromium under the Safe Drinking Water Act was promulgated as 0.05 mg/1 {total ehromium) on June 24. 1977. It was established to prevent dermal and toxic effects, particularly ln the hexavalent fon. At this time, thla is still the official EPA drinking water standard. Under the 1986 Amendments to the Safe Drinking Water Act, EPA is revleving its current Prifllary Drinking Water Regulations. A process to revise the drinking water regulations was already underway prior to the amendments. On November 13, 1985. EPA proposed a drinking water goal (RMCL) for chromium as o.12 'llf!,/l. (see attached) This goal is also supported by a Health Advisory for chromium published on March 31, 1987. In this docu- ment, a Lifetime Health Advisory for total ¢hromium is derived as 120 ug/1 (0.12 mg/1) to protect against toxic effects. There is no evidence of carcinogenic affects fro~ ingestion of chromium and, therefore, no cancer assessments for chromium were made for drinking water. The regulation development prouea for chromium under the SDWA Amendments is scheduled to be completed by June. 1988. At the present time the process is geared to propose the increase of the chromium level to 0.10 mg,/1 in early 1988 (probably February). The level was rounded off from .12 to .10 by the Work Group (according to Craig Bogt, Office of Drinking Water). Any official change will not occur until June, 1988 (likely delayed u~til September. 1988). The incorporation of a drinking water chromium level into your Odessa Chromium I and II strategy at this time h very tricky. It certainly appears that EPA may raise the drinking water MCL for chromium but it would be pre- mature for us to preempt official Agency action. Attachments i/ -.,..e-~ 'cl',~~ ,,,A.,U~-f/J /----,../1;>-v / d \' ~P-- /,~ i-tl.J- 7'~ .,/~ --"/~ cez~,;_,,,_ 0,1~-,/d (;~ - "- ... - 000007 .;

Transcript of - DEC· :,·;:~:~:;: (ti 6W-SP

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003304

- -UNITED STATES ENVIRONMENTAL AEQION VI . '

.. , .. ,·: '-) \ ~

ALLIED BANK TOWER AT l'OUl~TAIN PLACE HUAO$S AVENUE

DALLAS. TEXAS 15202 ' , .....

\. . ' \-

DEC· 21987 > ;~

:,·;:~:~:;:_ (ti DECO 2 1987

REPLY TO: 6W-SP

MEMORANDUM

SUBJECT:

,, L

,. H

Statue of Drinking Water Maximum Contaminant Level (MCL) for Chromium

Fil.OH: Myron o. Knudson. P.E. Director -~ Water Management-1>1.v:6ion./(6W)

TO: Allyn M. Davis Director Hazardous Waste Management Division (6H)

The original MCL for chromium under the Safe Drinking Water Act was promulgated as 0.05 mg/1 {total ehromium) on June 24. 1977. It was established to prevent dermal and toxic effects, particularly ln the hexavalent fon. At this time, thla is still the official EPA drinking water standard.

Under the 1986 Amendments to the Safe Drinking Water Act, EPA is revleving its current Prifllary Drinking Water Regulations. A process to revise the drinking water regulations was already underway prior to the amendments. On November 13, 1985. EPA proposed a drinking water goal (RMCL) for chromium as o.12 'llf!,/l. (see attached) This goal is also supported by a Health Advisory for chromium published on March 31, 1987. In this docu­ment, a Lifetime Health Advisory for total ¢hromium is derived as 120 ug/1 (0.12 mg/1) to protect against toxic effects. There is no evidence of carcinogenic affects fro~ ingestion of chromium and, therefore, no cancer assessments for chromium were made for drinking water.

The regulation development prouea for chromium under the SDWA Amendments is scheduled to be completed by June. 1988. At the present time the process is geared to propose the increase of the chromium level to 0.10 mg,/1 in early 1988 (probably February). The level was rounded off from .12 to .10 by the Work Group (according to Craig Bogt, Office of Drinking Water). Any official change will not occur until June, 1988 (likely delayed u~til September. 1988).

The incorporation of a drinking water chromium level into your Odessa Chromium I and II strategy at this time h very tricky. It certainly appears that EPA may raise the drinking water MCL for chromium but it would be pre­mature for us to preempt official Agency action.

Attachments i/ -.,..e-~ 'cl',~~ ,,,A.,U~-f/J /----,../1;>-v ~ / d \'

~P-- ~ /,~ i-tl.J- 7'~ .,/~ --"/~ cez~,;_,,,_ 0,1~-,/d (;~ -~ "- ~~ ... - 000007

.;

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003305

·e·· Wednesday November 13, 1985

Part IV

Environments, . Protection Agency 40 CfR Part 141 · NatlonaJ Primary Drinking Water Regutatfons; Synthetic Orlanlc Chemlcals. Inorganic Chemlcal1 and Mlcfoorpnlama; PropoeedRule

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I ,ii

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Federal Regltte, I Vol o. %10 f Wedn~sday. November H, · I Propoted ltute.

I 1' t.lO "-ffltftdff muknunl tonlamlnw :levela for o,gtnlc toft1amlna,llle,.

(a)• • • • •

(&) Acrylallde, • (7)AJaC:W.,, (I) Ollordane, (9JOBCP. (10) EDD. (11) EpicWorohydrin,

· (12) He~lor, (IS) Hep&ac:hlor epo.ldde, (l4)PCBI.. (15) Touphene. [b) •••

fll~-*'*"_,.~...,llcblll.,.. .... . IS)~.__ ______ _

tl'IVO o, f.,,OdK. ct •:.s = ~~i.. ....... =·-=~=~i.:,•;.-::.:.:.:.:.:.-:: (IOI E..,.__. ______ _

~ JM:l 111 ... uni.-.. o.ooat cu,.....,.,.,, UI ,.,, .... IOd .. (lf)fl•:lsdlla:4' .... UI ..~..,._ .... ,111,- u (IJ)U,1-TII' Ult ,, .. .,...,. ....

a. II la propoaed lbat propoMd Subpait P. I HU1 be ame.aded by

. . 1ddiq (b) table entrl .. (Z) lhtOQgh (U) to read .. rollowa:

I HUt lluo t.meoded ~ COCIIM!lnanl In.a. tor~ corilaflllnlnla

(a) (Re1ervedJ (b) •••

CllN111111C.--------'31~ ......... IN~---(419wU11..,..._ _______ _ ('>CM .. ,._ ...... _______ _

.... "·' u ·-

c-- Ma.• llogll

111°"""""1111111 .... Cl'>C:..... t.l Ill ... . ....,, ... (!Gt __ ,. ... 11,, ........ ... 1111 --·-------· 4. b .. prupoMd lo ldd • IN'W I 1'1.12 ID 40 all Put 141 to sud II follows:

f 1,t.a RecClfflfMflded lllallmlm eo.1tW1•.-i1 '""''°' IM:l'Otllll oontw.•**-

(a) Recommended maxlmlllll contammaAt level. are zero for th• followlna mic:roorsanl•ma: total colilorw. Giard/a. ud vlruaea.

(b) Recommended maximum contaminant level, for lhe following rnlaooraaal11nt parameten ere u Indicated: TW"bldlty 0-1 Nepbe1omelric Tarb!dlt, UnlL (Ftl Doc. 8$-2M17 Flied 11-~ 8.4$ ... .a.IQ~ .......

• !

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. ~

":J! ,J, .:.*'

':~

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003307

:r. JNT~:>OUCTJON

CHRClilUi -

Kealth Advisory Office of Drinking Water

u.s. fhviroMental Protection Agency

I

'nle Health Advisory (HA) Program, 1ponsoted by the Office of Drinking water (ODW), provides infomation on the health effects, analytical aethod• olo9y and t.reata1ent technology that would be u11ful in dHUng with the cont.a•ination of drinking water. Health Mvi1ories describe nonregulatory concentrations of drinking water contuinant• at w.ich advtr•• health effects would not be anticipated to occur over specific expo1ure durations. Health Advis~ri•s contain a margin of safety to protect 1ensitive aem~ers of the popt.t la ti on•

Health Advisories serve as infonal technical guidance to assist Federal, Stat~ and lo:al officials responsible for protecting public health when ':l.·Hrgency spills or contaminat.ion situations occur. '!hey are not to be construed as legally enforceable Federal standards. 'lhe HAs are subject to chan;e as new information becomes available.

Health k:!visories are developeJ for One-day, Ten-day, tonger-term (approximately 7 years, or 10\ of an individual's lifetime) and Lifetime e~posures baseJ on da~a describing noncarcinogenic end points of toxicity. Health Advisories do not· quantitatively incorporate any potential carcinogenic ris~ fr0111 such exposure. For those sUbstances that are known or probable huma~ carcinogens, according to the Agency classification ache~e (Group A or B), l.ifetime H1\.s are not recommended. 'nle chemical concentration values for Group A or B carcinogens are corr9latej with carcinogenic risk estimates by e~ploy1~~ a cancer potency (unit risk) value together with assumptions for lifeti~e exposure and the consumption of drinking water. The cancer unit ris~ is usually derivej fro~ the linear ~Jltista;e aodel with 95\ upper confidence li~its. 'Ibis provides & low•dose estimate of cancer risk to huma~s that is considered unlikely to pose a carcinogenic risk in exce$~ of the stated values. Excess cancer riak:6stimates aay also be calculatej usiAi the One-hit, Weibull, Logit or Probit IDOdels, 'lbere is no curre~t understanding of the biological 111echani1ms involved in cancer to suggest that any one of ~hese aodels is able to predict risk eore accurately than anot~~r. Because each model is based on differi119 assuaptions, the eatiaates that are derived can differ by several orders of aagnitude.

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- -Thi• H•alth Advisory ii baat4 on infonaation pr111nt~ int.he Office

of Drinking Water'• Health Effects Criteria Docwunt (CDJ for chro,aiu,a (U.S, EP~, 1985). 'nit H1' and CD toraata are •J.allar for •••Y refertnc,. lnd1vidiu!1 desirinc, further inforaation on the t.0xicol09ic&l dau 'bait or rationale Cor r11~ ch1racteri1ation 1hould con1ult the CD, Tht CD 11 availabla for rtview u ••ch £PA Regiond Office of DriMJ.n9 lfattr counterpart (1,9,, Water Bupply &ranch or Drinking Wat•r aranch), or for a f•e fran the National hchnical lnforution S.rvice, u.s, DtpartJaent of Coa111erc•, 528$ Port Royal Rd,, Sprin9• fitld, VA 22161, Pl 186•118012/AS, 'nle toll-fr•• ftWl~f 11 (800} 336•4?00, in the Washington, D,C, area, (703) 487•4650,

JJ, GENtRAL JNFORHATION AHO PROPERTJts

CU No. -• Cnr011iJ~ -- 7440•4?•3

Synony111s

Chro•ium (111) Chl~ridt •• \0025-73•7 Chr011ic A(;id, Oip-,tassium Salt -- 7789•00•6

• None

Chr0r.1iu~ an~ its salts have a variety of uses includini the followin;

. ..

1.,~

(t:,r additional information see Hartford, 1979): ,+.

• Hexavalent chrOlliu~ ccnpounds are ueed widely in industry for chroae ·· allo1 and chr011,ium •etal production, for aetal finishing and corrosi~n conttol (Love, 1941) an~ as aordants in the textile industry (Iler, 19!>4) •

• C~r01aiu~ salts are used as anticorrosive agents in cooling water,, in the leather tannini in~~stry, in the aanufacture of catalyats, in pigments anJ pai~t&, a~ in fungicides Ind "Ood preservatives (Hartford, 19'19).

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troeert1u (Ilea, _o, Weast, ,,,,, Windholi, 191'4t

• Tn• pr ope run o! chrcaiu• coapoW1d1 vary wi\h t.ht 1.s,ecif 1c c0111poun~: so .. exaapl•• are 11 follova,

Chea.icc1 l roraula A\calc/Hol•eular Weight Phrucal lt.ne 8;)iUh9 Point Mt1un9 PoiM Oen1U.y Vapor Pnuun Wu.er solubility J.ot O:t1nol/W1ttr

Partition Cod fl cie:\t. Tut• 1hreshold ruor 2brHh~l:!

Chroaiua

Cr ,, .t96 blH""lfhit.• 10U4 2, 64l•c 1,eoo•c 7, 14 9111/cal

o. i ug/1,

Cbrcniua UU) Chloride

CrCl3 122,90 •olid

Q\rod.c Acid, Dipot111iuM Silt

83 •c ,,e. l tc 2,'16 9/caa3 (U•c) 2. ,-32 9/c1113 (U•c>

inaloublt ,.2. 9 911 oo •L uo·~;

• Chrcmiu~ is a relatively rare, naturally occurring eleaent in the earth's cr~•t• ChrC>lfliwa occurs in most rocks and miMrals at levels of 200 ppc. A few aineral, contain chrcni\lll\ at levels o! 2-3,o,o ppr. •• ChrOl!liu~ is not •1ned in the U.S. COMtrcially, it 1& iMported. Chra:iiU11 11 release~ to lhe enviro11111a~l ddt\n) industrial activities, Jbwever, current data sug~est that surface and ground water levels of chroai~~ are the result of nat~rally•occurring chrcniua leaehin; fra:. aineral deposits. SolU!>le chroaiu• has been rep,rted to occur in

·surface vatera at levels up to 84 ug/L and in ground wat~r at levels of so ug/:. (u.s. EPI., 1987 >.

• .Feder&~ &Jrveys of surface an.i ground water drinking water supplies have rei\)rteJ t.hat •ost supplies contain less than S ug/L. currently,

·17 gro~n:! ~ater supplies and one._aurfact vater 1upply exce~ the · interi= aundard of so 119/L (u.s. EPA, 1981), ~

11 l , PHARHACOKJNETJCS

Absorption

ln general, "1th the exception of the Cr III glucose tolerance factor (GTF), ~r Vl ts •ore rea~i!t absorbed than Cr IlJ1

1 In bu.ans and experlaental ani•als, 91strointeatinal absorption of inorganic salts of Cr Ill ia low (frob 0,5\ to l\). H~~ever, Cr Vl

'+na or91nic cc:nplexes of Cr Ill are •ore redily 1b1orbed (approxi• mately 2, to 10\ for Cr VI and 10\ to 2S\ for organic co~plexes of

. Cr UJ) (U,S, DA, 1985) •

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Chrcai11111 - -• In hu•&na adainistered 20 ng of tr 111 as 51crC13 in v•ter, o.s, of the

dose ,i,aa recovered in the urine, indicating little lhaorp~ion (Donald• son a~ Berreru, 1966). ln rats, Menz et &1. (1965) reported 2\ to 3\ ab1orption of Cr(ltl) bated on total body counting of animals adain• htered 1tlcrc1 3 by in~ubation •t dons ranging ftCIII I.S to 100 u9/kg.

• GTF, an organic ccaplex of er III vith nicotinie acid and an uino acid that ii found in brewer's yeast, wu absorbed in nt.a at 10\ to ~~\ o( t.he td11init.\t.rt4 .4o.. (.,_.r~, 19761 Herta et. al,, t 978).

• An estimate of 2.1, abaorption of Cr VI baaed on recov•ry in urine was reported for humans ad~inistered 20 ng of Na251cro4 in water (Donald~on and Barreras, 1966),

• Rau ad:ninistered drinking vater contairling 2S 1119/L Cr III as chrOlllie chlorid~ had 12.~ times 9reater tissue levels of chromium than rats ~hose drin,ing water contained 2S •g/L Cr VI as potassiu~ chromate (Ma:ken1ie et al., 19S8l,

Dist.ributi.>n

Dependin; on the particular CCll\pound (e.g., GTF) Cr lll and Cr VI differ in their distribution within an organism, in general CT 111 crosses ae~~ranes much •ore &lowly than Cr Vl (U,S. D>A, 198~):

• Chromiwr. circulates ln the plasma primarily in a nondiffusible for~. A s~a:1 fracticn (9\ to 12\) is in a more diffusible fonn which i& filterej anj P3rtially reabsorbed in the kidney (Collins et al,, 1961), An ap~roximate plasma half-life of 6 hours for S1cr Jll in rats was reported by Hopkins (196~) ~fter intravenous administration of either 0.1 or 1,0 ug/kg,

• Cr llI has ~n affinity for iron-binding proteins (Gray and Sterlin;, 19SO, Hopkins r1nd Schwan, 1964),

• The spleen And kidneys vere shown to have the higheat concentrations of c:hroru u1:1 when rats were administered Cr JU H c:hroai WII cblori:le in intr&venous doses of 0,1 or 1.:0 ug/ki (Hoplt}u. 196$). Similar results were reported by Mackenzie et al. (1958) ~hen ~•t• received drinking vater containing 25 ag/L of either er JU as chrCMic chloride or Cr Vl as potaasiura chromate. 'lbe calculated doses were 1,87 •g/kg/day for males and 2,41 mg/kg/day for feaiales.

• 'Jbe placenta appears to be highly •electiv~ in ita permeability to the various fot'llls of chrcnium. Inorganic Cr JIJ adlllir.istared as 51 crc1 3 (chroJaiwa chloride) intravenously or by 1t011ach intubatio~ does not cross the placental barrier to an appreciable extent in rats (Heru et al,, 1969). Jiowever, Cr Ill adllliniatered by atODl&ch

_:iJlt\d>at.ion to pregnant rats in the foni of GTF (obtained frcm yeast) is recov~red readily fr011 the fet~s (Hertz and Roginski, 1971). ~he dosages ln the3e two atudies were unspecified,

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• Cr VI trav!es biological a,embranes by d1-cio~ or !ac1litatej transport, possibly via an anion transport. ayste~ (Alexander et al., 1982). Jt 1s rejuced to Cr Ill intracellularly by the eytochrcme P•4S0 syi.tem in the presence of NAOPII. Cr JU reacts vith nucleophilic ligands and cellular •acr~olecules (Gruber and Jennette, 1978),

MetaboU.s:n

• The metabolism of chrC111ium in mammalian apecies ia not well under• stood and is complicated by the preaene11 of the two oxidation atates, Cr III and Cr VI (U.S, EPA, 198S),

txcretio:,

The kidney appears to be the principal route of excretion of chrcmiWII CO'!ll>')Unds:

• Tia urinary system is the major excretory route for absorbed ehr01l',iu111, accounting for 80\ or more of chromiWII excretion (Kraintz and Talmag~, 1952). Very little is known about the form in which chr0111ium is excreted.

• After intravenous administration, chranium is also excreted in the feces, althoug!'i reports in the 1i terature vary eo,,-.iderably on the pHcent.age. Hop1<ins (196S) reported that O.S\ to 1.,, of the initial d~se of Cr III was excreted in the feces of tats eight hours after ir.travenous aJMinistration of 51 crc1 3 at 0.1 ug/100 9•

l \', HtALTH EFFECTS

In ge~eral, Cr VI compounds are more toxic than Cr III ccnpounds:

• The toxicity of chromium has been attributed primarily to er VI, \ir.iieh has bee~ shown to produce liver and kidney duiage, ihternal he~orrha;e, dermatitis and respiratory proble,s. 'lhe Ulll)ediate symptoms are caene_rally na:isea, re~ated vomiting_ and diarrhla (U. s • .tP~, t 985).

• Doses of o.s to 1.5 9 of k2Cr207 have been fatal in hWllans. ~e estillate~ LDLO for Kf::r20, in children 11 26 ag/kg (Cr VI at 9.2 ag/)t9) (NIOSH, 1983).

- Subchronic and chronic dermal exposure to er VI in the fom of chror.ic acid •ay cause contact dermatitis and ulcer,tion of the akin (BJrro~s, 1978). For example, Denton et al. (1954) re;>orte~ infonation on an individual W'!lo was patch-tested on three occasions With 0.00S\ -potassium dichrcrnate aolution and the filtr1te of two ceeent &Mples which contained o.0001\ and 0,0004\ Cr vi. 'lhe individual repeatedly showe~ a positive erythematous, edematous, p&pulovesicular pateh•te,t reaction to each test solution,

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> Chromiur.i - Harch :11, 1967

• Chronic inhalation of dust or air containing Cr VI may c•~•• res?ira­tory proble,ns includin9 perforated or ulcerated ~•sal septa and decreased apircaetric values (U.S. EPA, 198S). For axa•ple, a10011!iel~ and Blum (1928) reported perforated/ulcerated nasal aepta and in[lame! nasAl Mucosa in 1it0rkers exposed to chromic •cid (Cr VI) (1.1 to S.6 ~g/m3 air) for one veek to three years.

AnilllllS __. ........

Short•ter• Exposure

ln general, Cr VI cC111pounds are more toxic than Cr llI ccnpounds:

• The oral LDso for various salts of Cr III ruge from 600 to 2,600 •g/ki (S•yth et al., 1969),

,. ;,-,-~

• The oral LDso of er VI (as Na2Cr20,> in rats is 19.8 mg/kg CNIOSH, t9e3J.

• Jt-3 t:.. were expose;i to drinking water containing Cr VI (Kz=ro4) at. ltvels of both eo and 134 mg Cr Vl/L for 60 days (8.3 an~ 14.4 •g er Vl/ki/da1 respectively) without adverse effect (Gross and Heller, 1946).

Long•term Exposure

• In a one year rat drinking water study, consumption or water eonta!nin; 0 to 25 Dt9/:, :,f either Cr 111 (CrCl3) or Cr VI (K~ro4) (0 to 1.&7 m9/k~/day formal• rats and Oto 2.41 •;/kg/day for female rats) produced no significa~t differences in weight gain, appearance ~r path~lo~iea1 changes in the blood or ~ther tissues (Hacke~ie et al., 19~8). NOAE!o of 1,87 1119/kg/day (inales) and 2.41 111g/lt1/day (fer:ialesl can be identifiej fro~ the results of this study.

• In a rat drin.\in; water study in which S 119/L Cr 111 (about o. 42 mg/ki/day) wa~ ~ministered from the time of weaning until death, no adverse effects were observed (Schroeder et al., 1965). A HQ.\£L e! 0.42 ag/kg/day can be identified fran the results of this study.

• In a,. four year female dog drinlcin~ water 1tudy:(five dose 9roups 11·ah two ani11als per group), Cr V1 (K2'=r06) at 0.45 to 11.2 119/L (0.011 t:> 0.30 119/kg er VI) was without effect in terms of changes in physical condition, food consumption, growth rate, organ veighU, urinalysis results and hematological analyses. Therefore, a NOAtL of 0,30 ~s/\g/day can be identified from the results of this •tudy (Anwar et al,, 1961).

Reproduet~ve Effects

• No information was found in the availa~le literature on the reprodJctive effects Df chrOlliu~.

Develoeeental Effects

• No information was found in the available literature on the develCF­Mntal efhcts of chrollliWI•

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H;1u9eniei ty - -• The 9enotoxic effect• of chrcniiu~ are well do~••nted both in in vivo

and in vitro st.udiU • 'ftle pathvay by llhich Chroadum exert.I thtte­effe«s--ri"'believe~ to involve penetration of the cell 111abrane by Cr Vl, followed by intracellular reduction t.o Cr 111. l:x.t.racellular er 111 crosses the cell 111embrane, but l•,• efficiently. Once inside the cell, Cr Jll can form ti9ht COlllplexes with DNA, accounting for its 11\UUgenic p:>tent.ial (U.S. D>A, 1985) •

• C0111pounda of both er ltl and Cr VI increase non•cMple•entary nucleo• tide incorporation into DH.». (R.affetto et al,, 19171 Hajone and Rensi, 1979), with Cr VI producing effects at lower doses. Exposure of cells froo ~at liver and kidney to Cr Vl lead& to increased cross•linkin1 in DNA. Petrilli•~~ De tlora (1918) reported positive Am•s teats for Ct Vl, However, Cr 111 exerted no effect at relat~vely high concAntrations (presumably because of its inability to penetrate cells). Similar results were reporte1 by Gentile et al. (1981).

• The dtfficulty of observing muta9enic effects of Cr lll may be related to its sli.9ht \ll)U~e by cells under most conditions, Warren et. al. (\~~11, studied the mutagenicity of a series of hexacoordinate Cr lIJ cor.ipoundc and concluded that, in the proper ligand envirolVllent, t~e Metal ;»ss~sses considerable genetic toxicity.

Carcincgenicity

There is 1naje;J\t~ evidence to determine whether or not oral exp~sure to chro~iu~ ca~ lea3 to cancer:

• No increase in t~Mor rate~ ov~~ t~at of the control ani~als was obser·.-ed in ra t.s exposed rats to Cr Ul Cchr0111i WII oxide pi9111e:its) at 293, S86 or 1,466 ag/kg/day in the diet for two years (lvankovic and J>reJssmann, 1975).

• While the carcinogenicity oC inhale~ Cr Vl is well established for occupational exposJre of humans (Hayes et al., 1979), the effects are ot>served only i~ the respiratory paasa9es and in the lun9s, and ar• believed to have no bearing on carcinogenit risk following oral exposure to the metal (U.S, EP~, 1985).

v. OtJANTIFlCATION or TOXICOLOGICAL EFFECTS

Health Advisories (HAS) are generally detennined for One-day, Ten-day, Longer-t~r~ (approxi~.ately 7 years) and Lifetiae exposures if adequate data are available that identify a aensitive noncarcinogenic end J!Oint of toxicity. '!be flAs for noncarcinogenic toxicanu are derived usin9 t~~ following for•ula:

HA ~ ~i::. or LOAtL) x (8~) • _ llg/L (_ ug/L) (OF) X (_ :./day)

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003314

....

where:

Marcli 31, 1987

.. 9. -!.

NOAEL or LOA£L •No-or Loweat~Observed•Adve·· ,-tffect•Level in •9/kg bw/day.

aw• assu~•~ body weight of• child (10 kg) or t.n adult .(7Q kg).

ur • uncertainty factor (10, 100 or 1,000), in eccordance with N~S/ODW guidelines.

_ L/dar • assumed daily water conswnption of a child C 1 L/day) or_ an adult ( 2 L/day).

ln considering the toxicity of chromium compounds, it is imp->rtant to re!lii~ that chrc:nium lll is an essential nutrient re~uired in trace quantities for normal glucose metabolism - i.e. GTF. Some forms of chromium may also be ia;:,orunt in tho metabolism of lipids and other carbohydrates (u.s. !:PA, aes} ~-

1he Health Mvisories will be detemined on the basis of the effect~?~ er Vl measured as total chromium. Separate Health Advisories will ~ot be estJblishe..1 for Cr i11 for the following reasons:

,. Based on the work of Schroeder and Lee (1975), there is reason to believe that oxidizing agents <~•9• due to chlorination of water) naay accelerate the normal conversio~ of Cr 111 to er Vl at the point o{ consumption (i.e., the tap).

2, Health A1vis~ries based on total chr:xnium will allow f~r the p~ssible conversion of er Ill to Cr VI.

3. As discussed in this document, there is reason to believe that Cr Vl is 111ore toxic than Cr Ill. 'lhus Health Advisories butt\ ?"l t:·1"' effects of Cr VI vill conservatively protect against the toxic effects o! any Cr Ill not converted to Cr. VI,

One-day Health Advisory • • I •

The availablt data are insufficient to develop a One-day ~ for c'1coaiu.":I. It is recomaendej that the Tan-day HA of 1.4 mg/L be used as the One-day w. for the to kg child.

~ay Health Advi1ory

Gross an, Heller {1946) exposed both male and feaale rau for 60 days t.o drinking water cont&inihg JC~r04 at either 300 or 500 m.g/L (Cr Vl u. 80 119/L and 1 H i:,9/L, respectively). tlsin~ reported average body weights of 270 1nd 260 g, respectively, and 1sau1n9 ~ons~tlon of 28 •L water per day, the average ingeste~ doses of Cr VI are calculated t.o be 8.3 and 14.4 ~J/\i/day, respectively. After tvo 11onth1, the rats rectiving Cr VI at e. 3 11\g/k.g/day· were descr1bed ~s norMal. A •a119ht rou9hneas of coat• w~i n~tod in rats receiving 14,4 •g/ki1/day, but this ia not considered to be an adverse health effect, this observation is not associated with other advetae health effects. 'l'bere!ore, u. 4 1119/kil/day upreaents the NOA.EL for Cr Vl in this 1tui:Sy.

. ~- •1

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. . , '. . . . . : ' ' ' ', . , . ·. ' ';.' ' ' \ ' I t I •

the Ten--day HA !r a 10•k9 child la calculated - follow:;:

• 'Where:

Ten-day HA• (14.4 111g/kfday) (10 ~., 1.4 •9/l. (1400 ug/L) (100) t L/day)

- 14.4 111g/k~/day • NOAEL based on the absence of adverae effects in rats exposed to chrond\1111 in drinking water.

10 leg • assu.u~ body weight of • child. ,, ._ .. ·-·1·:·~:····· ,·,··,:,:,-;:~r= .. 'r!J;'-r:ri~~'J1if":1'~""f:,~'·"f''J :·· ·. ,11 i:'J,,f:~F~- .... ' ·: •.: -e::··.·t .-··.·:; '•!l"'d'.~!it

100 • uncertainty factor, chosen in accordance with NAS/0~ guidelines for use with a No,tu fr0111 an animal stu~y.

1 L/day • ass~~ed daily water consWl\ption of a child.

Longer-term Health Advison'.

Mackenzie et al. (1958) studie:, the effects of chronic ingestio'l ,,,. er III and Cr VI in rats. Both male and female Sprague Dawley rats (34 day~ old) vere supplie~ with drinking water containing Cr as CrCl3 (Cr Ill) or as K2cro, (Cr VI) in a series of doses up to 25 119/L for a period of one year. As~unin3 an &verage weight of 37S g for males and 290 g for fe•ales, and an average daily water intake of 28 ~L (Arrington, 1912), the av~r4~P. dose for inale; a~d females receiving 2S ~9/L is calculat~l t~ be 1.87 and 2.41 mg Cr VI/Kg/day, respectively. No significant adverse eff~cta on appearance, weight gain, food co:'lsumption or blood chemistrJ ~,ere 'lt>to.J at any of the dose levels. Hl"'~ ,er, the ani111als receiving the highest dose ( ~S 1119/:.,) o! er VI s'l·.1w1s! 1 ,. , approximate 20\ reduction in water consumption.

Cr VI at 2.41 mg/kg/day was identified as the NOAtL in this stu~y. The Longer-te~~ Hhs are calculated as follows:

ro: a 10-kg child:

where:

Longer-term AA • ' 2 141 ,ng/kg/day) (~ • 0,24 119/L (240 ug/:, J · (100)0 L/dal') ,

2.41 •;/k9/day ·• HOAEL based on the absence of adverse effects in rats expc>ud to chrOlliwn !ft drinking water.

10 kg • assumed. b.od~ W&i1Jht of_ ~ child.

100 • uncertainty f&ctor, chosen in accord&~ce with NAS/0~ guidelines for use with a NO\tL fro.~ a~ ~hiMAl study.

L/day • assumej daily water conswnption of a child.

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. :. - -10-

ror • 70-kg •dult:

Where:

Longer•ter.n w. • u.4t 1112~fday) PO k9) • o.84 119/1, (840'1g/L) (i 00 2 L/day)

2.41 m9/kg/day • NOAtL based on the &b1enca of adver•e •ffects in rats exs.oa&d to chrc,ndwa in dri.nll.i~g water.

'70 k.g • usumed body weight of an &dlllt..

100 • uncertainty factor, chosen in accordance "'1~h NAS/00,,i tJ·1\deU.ne1 for use with a llOAEL frOftl an afti11al 1t.u:!y.

2 t/day • assu111ed daily water cons11111ption of an adult..

~tl111e Health A:3visory

T'ne Lifetime W. represents that portion of an individu~1·~ total exposure that is attributed to drinking water and is consider•~ protective of ftoncar• cin~e:iic a1ver,;,• '·•'H~t'l effects over a lifet1111e exposure. The Lifetime H.t. is deriv<:1 ~-1, :;·,,cc step procesa. Step? determines the Refennc:e Dose {~!D), !or~erly eall&d the Acceptable Daily Intake (A~JJ. Tne RfO is an esti~ •ate of a daily e~posure to the huMan population that ls likely to be without appreciable ri~~ ~f l~l~terious effects over a lifetillie, and is derived fror.. the ~O\EL (or Lo.ait~l, i3~ntified fro,n a chronic (or subchr~nic) at~dy, divided by an uncertainty factor(s). tran the ~co, a Drinkin~ Water Equivalent Level (™E~) c:an be deter~ined (Step 2). A IMEL is a medium-specific (i.e., ~rinking wate:) lif~ti•e exposure level, assuming 100\ exposure ftan that aed1um, at which adverse, noncardno3--M~: ~.~-tlth effeet.s would not be expeeteJ to oc:;ur. The ~t~ is derive1 frcr., the mul tiplieation of the JlfO by the assur.ie~ bod/ 'tleight. o! an adult and divided by the asswr.ed daily vater consu'll.,ti :,·, of an a1J:~. T1~ Life~l.llle HJ. is determined in Step 3 by factoring in other sources of exposure, the nlativ~ ,s,,.,,.~"! contribution (RSC}. 'lbe RSC fro111 drinking wate~ is based on actual ex?osure_data or, if data are not available, a value o! 20\ is a.uu111e.:, for synthetic organic: cheaicah a11.\ A value of \0\ is assume~ for i~organie c:he111ic:ala. If t~e contaminant 1~ classified as a Group A or 8 carcin,J«~, according to the Agency•, clalsification acheae of carcinogenic potential (u.s. EPA, 1986}, then caution ahould be exercised in assessing the risk& associated '-'ith lifetiae expos,10:ot to t.'l\h c:he1ti1cal.

'nle study by HacKen.zie et Al, (1958) (described under th~ t.?f\•JU .. ttrm HA) is considerej 4pp~opriate to serve as the basis for the Lifetime HA. '!be Anwar et al. (1961) studf was not selected because only tvo ani•al1 per dose group were used.

UsinJ th-t- S:>A£L of 2.41 11;/kg/day, the J.ifetiae RA h derived aa followr.:

.St,,p 1, Deterr.iinat.l.on o! the Raferen~• D:>se (RfD)

Rf?• (2.41 •g/kg/day) • 0.0048 mg/kg/day ,: . (H19t (~) .

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003317

v.-iere: - -2.4t m~/>tg/day a NOA£L basej upon the absence of adverse effects in

rats exJ)Osed to chrolliWII in drinking water,

100 • uncertainty factor, chosen in accordance with NAS/0~ 9uidel1nea for uae with • NOA.EL froro .l"\ -1•1i"'al study,

S • additional uncertainty factor to canpensate for 1ess­than-lifet1~e; ,xJ)Osure,

··.··!

Step 2: Deter111ination of the Drinking Water Equivalent Level (DWEL)

D',;tL • (0 ,0048 lllg/kg) (70 k9) • \70 ug/L (2 L/day)

where:

o. 0)4'1 :--.... .-:::; = ~!:>.

70 kg • assumed body weight of a_n &dul t,

2 L/day • ass~me1 daily vater consU111ption of an ad~lt.

Step 3: Determination of Lifetiri-1 ~·•<\\tl~ A.1visory

1.ifeti.l!le HA• l110 ug/L) (11\) • 120 ug/L

wnere:

170 ug, .. ,. DWEl...

71\ • assa~e1 relative source contribution frcm water.

E\aluation of Carcinoge~~c Potential

• There is no evidence of carein<>,J~~ic ~ff•cts following oral exp~sure to chromiu~. 'lhus, no •••~~saenta,for carcinogenic risks from oral exp:>s.in t.o o;l\C',11iu111 have been conducted, Inhalation of chr0111iwa, however, is associated vi th an increased fr4,J•l'll'\<:)' of lung cancer in hwnans, ···

• EPA •s CAG ha& esti.111&ted the lifetillle cancer risk d11e to • co,iitant exposure to air contairung 1 ug/ml of ele~ental chrcniu.~ to be 1.2 x 10--2 (U.S. EPA, 1983).

'-,.

• Based on exposur~ to chr0111iwn via inhalation, lARC (1982) has claasifie~ chrOlll:iwn and certain chrOldWII compounds in Gro111> 1 (Chro.'liu11 vx>, sufficient evide~ce for eare.i~c.igenicity in hwaans and ani~~l••

• Applying the criteria described in l:PA's guidelines for asns!illll.,~ ~f carcinogenic risk (u.s. !:PA, \986), chromilU\ 111ay be classified in Group A: Human e~~r.i~o,-,n. This category is for agents for which

-,·l

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. i - : • ' • I I

·\

• I \

I l I

- •12- e there ls 1ufficient evidence to aupport the causal &saociaUo'\ h-tt.o1•u"I exp;>sure to the agents and c&ncer. Ho~ever, •• there &re inadequate data to conclude that chrClll\ium is carclnogenic via ingestion, chr0111iu~ is dealt with here•~ Gr~JP ~, Not classified. 'l'bis category is for agents with inadequate ani•&l evidence of carcinogenicity.

Ylo Q!'!_ER CRITERIA, GUIDANCE A?iD STANDAA.0S

Recanmended or established 1tandards for chrCllliUIII in the United States include:

• •

0

SO ug Cr VI per Ht':! .. r.-,r drinking water (u.s. J>HS, 1962) •

so ug total chromiwn per llt~r for drihkin9 water (NAS, 19741 U.s, EPA, 1916).

1 ug/ml for carcinogenic fornis of Cr V1 in workplace air (NIOSH, 1915}.

25 :Jg/113 Nil or ~O ug/1113 ceiling for non-carcinogenic forms of Cr VI it1 .,,:,r\place air (NIOSH, 197~).

• 1"he re:.>111-;ie•, l"c· ! ,111bient i.ratel" quality criterion for Cr VI is so ug/L (U,S, EPA, 1980).

0 A.•1 .;istipiate1 adequate an:! safe intake ro,. c~rc:r.iu .. of SO to 200 ug/day f~r adults has bee, e~t-1blished (NAS, 1980a,bJ~ 'Ibis range is based on the ab$en:~ o! si~,s of chromiUJn deficiency in the major portion of the u.s. population which consu11u -.1·> -t,·~r-1;<1? of 60 ug or chromiur.i per da:,:.

• l'he OStt,; 8-hour timeMJe;.ghtej average exposure 1i111i t for ci11· >11i,n, solu~le chr01111c, and chroaous salts as _chrcni~~ is o.s ag/ml (OSP.;, 198~).

vn. A~A!.YrlC~L METHODS ---• Deter:aination of chroniwn ii by atomic &ba;,,r,,t:.t,,1 (AA) using tit.her

direct aspiration into a flne (U.S. tJ>A, 19'9•) or• furnace technique tu.s. EPA, 19?9bl.

• Tne direct aapiration AA procedur• ia I physical 111ethod baaed on the absorption of radiation at 3S"l.9 rva by chrwWII. 'l'l• -s-t~l\e is aspirated into an air•acetylene flue and ltaDized. ~ lt9~~ ~it• is d1r•cte3 through the flame into a aonochromator, and cnto a detector that measures the Mount of light ab1orbe~. M>sorbctnce is proportio~a! to the concentration of chrolll,1,, in the sample. The detectioll li111it ia 50 us/L using t.his procedure.

• 'Jbe furna:~ ~; ,,.. 1,-:P.tl•1re i& sin1ilar to direct aspiration AA except Utat a furnace, rather than• flue, is used to &tOC'll~Ze t~~ ~4•ple. The detection liMit is 1 ug/L u~in9 this procedure.

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i I

l I

I I i i I i i

-VJ J J • TIU:AT~N't TtCHN':>LOGitS

• 'tile tre1t111ent technolo9ie1 that •re available to r•ovt chrcaiu~ fr011 vat.er i~clud• coagulation/filtration, lime t6ftaninc,, ion exchanca• an:S reverse 011101h. However, the type of treatMnt. that MY be applied b dependent on th• 1pecie1 of chrcaJwa trtHAt.

I •. Laboratory and pilot plant studies indicated thlt usihg ferric sulfate,

Cr Ill removals were near 100 percent in the range of pH 6.5 to 9,$. Alum was less effective between pH ?,Sand a.i, vith re111oval1 around 90 percent or better. Above and below thia pH tange, removal• were slightly lower, 80 to 90 percent. In r .. oVift9 Cr VI, laboratory and p1lot-plant. tests confil"llled that of the t.hret coagulant• used, only ferrous sulfate w~s effective. With 1lwn and ferric sultate, Cr Vl r•ovals did not exceed 30 percent. &y c0111pari1on, ferrous aulfate coagulation achieved 90 percent removal or better cu.s. EPA, 1977).

• Re.sill ts of jar and pilot•phnt tests indicate ~at. Cr lll removal efficiencies with lime softening were approxiMttly 72 percent at pH 6.S to 9.S and greater than 99 percent at pH 11 to t1.s. kesults with Cr VJ in the sa~e tests in all cases were less than 10 percent (U.S. tPA, 19771 Sorg, 1979).

• Since CP llI occurs in cationic species &nd Cr V1 in anionic species, a cation exchanger in series with an anion exchanger may be required for their removal. ~emoval of C~ Vl frCIII sewage CSor9, 1979), in~ostrial wastewater, rinse waters from chromiu~ plating operations {Miller an4 ~un~ler, 1978), cooling tower blowdown (kicnardson et al., 19681 Miller and ~~ndler, 1978), and •etal recovery (Sussman et al., 1945) has been demonstrated, Laboratory test& on a siliulated Aritona well wa~er (TDS 174 mg/L, pH 7,8S) having o.019 mg/Lo! Cr VI showed a breakthrough of er VI at roughly 12,000 bed volunies (U,s. EPA, 1982), ~eport, concerning industrial wastewater tte&~T.ent indicate that ion exehange can auccessfully remove Cr Ill to belov o.os ag/L (tatterson, 191~). Stron; acid cationic resins have been used for removing Cr lII u a contaminant fror:i 111etal plating rinse v&ttr., and from chrOlll&te traate~ cooling waters. Vendor information il'dicates that operating pH levels of between 6 and 8 are adequate for c: Ill reaoval with pH above 7 being slightly better than pH below ? Oohll and Haas Co., 1980). Ion exchange softening using 1taftdard strong acid 1ynthetic resins opetatJ.nq in the sodi\1111 cycle 1hould effectively remove er tII with 90 percent or greater efficiency (bore, 1971). In tests of ho1ne 1ofteners Vi.th tap vat.er apiked 11it.h 1 ag/1, of c:hrcniwr. nitrate, the chrcmium content continued to be r~uced to 0.020 ttg/~ after 192 cycles, at Which point the test vaa d11continued.

• Revers• 01•osl1 (RO) meabranea c&n efficiently re11ove frcm 82 to 99 perce)it of the chromiwo in a feed water source (l'ox, no d.tte, Mixon, 19,3, Johnston et al,, 1918). J>ilot plant tests using bot.h cellulose acetate and hollow fiber (polyamide) •••branes dtaon1trate~ their effectiveness in reMoving both er JU and er VI. Cr JU re111oval ranged from 90 to 98 percent and er VI re•ova1 r•nged from 82 to 9' percent. Slightly better z-emoval was achieved vith the hollow fiber than with the cellulose acetate membranes (Fox, ftO date),

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This Document Has Missing Pages

Bates 003320.001 - 003320.003

(Original Pages 14, 15 &16)

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: " ~ ... ' • • • ~ ' ~ I t ~ ,

I

lchroecler, N,A,, _,,,a.lnH &nd V,H, Y1nMtn, Ir. tA., ~r•a.u, edaitaa 1.IMI lud ln U\ts £Uaeu °" Uh lptDt Ll&aon ud Un111 hvtlt• 11 INU, 861 •'•H,

•chroeder, 1>.c,, a.n4 o.r. a..,. u11. ,.,.,.u,1 uuderaauena .r chr•i• In natural wat.1r1. Wat.er Mr loll Jtollu\, 41111•J65,

layt.h, M,r,, C,P, Carp.n\tr, c.1. Vail, u.c. tN~anl, ~.A, lt.rlet•l arMI ~.s. Nyc\111, 1969, 1'an91 filUSln9 t.oxlclty da\lt L11t viz. AA, Ind, ky9. Aa1oc, Journal, 30,,,0.

i

Sor9, T,J. 1979. Tr111ia,nt ttchnol09y to ht\ Ill• 1n,1r&.a prlaarr drlMint water r19ul1tion1 for lnor91nic11 f&rl 4, JAWA. 71(1)14l4•66,

lu11•1n, s., r,c, Nachocl t\ al. 1941, H1t.11 recovery ~Y anion 1xch1nt•• lnd~1trlal and En9in11rln9 O\aaJ.atry, 37(7)1611•22,

u.s. EP~ •• ,,,. U,S, Dlvironaental Protection A91ncy, National lnt.tri• priaary dr1nlt1ni vater r19ul1tion1, EPA $7O/9•7&-00J, W11bintton, DC:1 pp. 63-64,

u,s. EPA, 1977. u.s. EnviroMtnLal Protection A91ncy. Manu1l of tre11A1nt tec~nique1 f~r •••ting the interi• prtaary drinkin9 water r19ul1tion1, revisej. tPA•6O0/8-77-OO~.

u.s. EPA, 1979a, u.s. tnvironr.iental Protection A9ency. Met.hod a,,.,. Atooic Absorpti~n, dire:t as9ir1tion. ln, Mlt.hoda tor Oaeaical Analy•l• o( ~ater an! ~11tt1, EPA•6O~/4•79•O2O, March, 1979.

c.s. t~A. 1979:. u.s • .Environaental Protect.ion A9ency. Kfthod 211.2. Ato-uc Al;i•~rption, furnace technique. Ins Hetho4s for Chesical An1ly1l1 of ~Ater an! ~,stes. tPA-6~0/4•79-020, March, 1919,

u,s. EPA, 1960, u.s. Environmenul Protection A~ency, Allbient water quality criteria for chrca;iua, £PA 440/5•80•035, Washington, D.C.

u,s, EPA, 1982, u.s. tnvironm,~tal Protection A91ncy, Peraonal coa~unicat.io~. ~Jnici~al Enviro11r.1ent•l Research Laboratory,

u.s. EPA. 1983. u.s. tnviroNDental Protection Atency. Health ••••••••nt docu1111nt for chrcrdus, Review Draft, EPA 600/8•62.014A, V.uh1ntton, D,C.

u.s, tPA, 1985, u.s. Environ11ental Protection A9ency, Health lffecu Criteria Docuaent for c· rotaiua. criteria and St1ftdard1 Divi1ion. Office of Drinking Water. W11hih9ton, DC,

u.s, EPA. 1986, u.s. F.nvironiaent&l Protection A9ency. GUidtllne1 for carcinogen risk assessment. Ftd•ral Re9l1ter. S1(1a,1133992•3•OOJ. Se ptem:>er 24.

u.s. EPA, 1987, u.s. Envi.·oMent.al Protection A9ency. tst.i•attd nat.iond occurrence and exposure to chromiWII 1n public drinking water 1uprlie1. cso. Office of Drin>db; Water.

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003321

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WunA. ,., P, .. bulU, I>, ltltlHft., J, ltMtU, •••• M>Nt. &nd ...... ,. • 1u1, lhlUt1n111.t.y et a urlH •t hlu,..r.Uuu -.,._.,. (UU coa• ,._,., .,.,, ..... to,,,,.,,.. ~-, .. ,,·,,; "i·.•.'oi. ~i·' '.ll.''·l': ,;

v,an, a.e,, u. ""· lllftd)NMI). •• Otwnry ,,,. fllratea. Had Id, ~ mu, Cltvlla.nd, OH IP• 1-H, ••U•••, l•I U, t•U1,

lflM-.1&, ••, ••• u,,. lht 111111k ?Mu• An ... ,110,..u et 1h1a1Hh a.a, ... ,, tu. •• llilbwar, I-la tltrtk 1116 C.,, 1ft1, If• Hl•21t,