FINAL REMEDIAL INVESTIGATION REPORT VOLUME III OF III ...

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R-33-2-9-27

FINALREMEDIAL INVESTIGATION

REPORT

VOLUME III OF III: APPENDICES

C&R BATTERY SITECHESTERFIELD COUNTY, VIRGINIA

EPA WORK ASSIGNMENT NUMBER 37-01-3LP4CONTRACT NUMBER 68-W8-0037

NUS PROJECT NUMBER 9851

JANUARY 1990

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APPENDIX F

LABORATORY ANALYTICAL RESULTS

TABLE OF CONTENTS

TABLES

NUMBER ... .., , —

F-1 Debris Pile Samples - TAL ResultsF-2 Debris Pile Samples-EPToxicityF-3 Soil Samples-TAL ResultsF-4 Soil Samples^EPToxicityF-5 Monitoring WeTTs - TAL Total Metals ResultsF-6 Monitoring Wells - TAL Dissolved Metals ResultsF-7 Domestic Wells-TAL Total MetalsF-8 Surface Water Samples - TAL Total Metals ResultsF-9 Surface Water Samples - TAL Dissolved Metals ResultsF-10 Sediment Samples - TAL ResultsF-11 Sediment Samples - EP ToxicityF-12 Blank SamplesF-13 Summary of XRF and CLP Lead Results for Soi I SamplesF-14 Summary of XRF Lead Results (March 1989}

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DEBRIS PILE SAMPLES - TAL RESULTS

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TABLE F-4

SOIL SAMPLES - EP TOXICITY

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TABLE F-5

MONITORING WELLS - TAL TOTAL METALS RESULTS

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TABLE F-6

MONITORING WELLS - TAL DISSOLVED METALS RESULTS

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TABLE F-7

DOMESTIC WELLS - TAL TOTAL METALS

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TABLE F-8

SURFACE WATER SAMPLES - TAL TOTAL METALS RESULTS

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TABLE F-9

SURFACE WATER SAMPLES - TAL DISSOLVED METALS RESULTS

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TABLE F-10

SEDIMENT SAMPLES - TAL RESULTS

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TABLE F-11

SEDIMENT SAMPLES • EP TOXICITY

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TABLE F-12

BLANK SAMPLES

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TABLE M 3

SUMMARY OF XRF AND CLP LEAD RESULTS FOR SOIL SAMPLESC & R BATTERY SITE

CHESTERFIELD COUNTY. VIRGINIA

BoringNo.

SO-01SO-02SO-03SO-04SO-05SO-06SO-07SO-08SO-09SO- 10SO-11SO- 12SO- 13SO- 14SO- 15SO- 16SO-17SO- 18SO- 19SO-20SO-21SO-22SO-23SO-24SO-25SO-26SO-2750-28SO-29SO-30

Sample Depth (feet)

2,30010,290650NDNO

5,11021,98076,4102,29020,89092,2607,280127,100134,50022,520120,4004,86014,86014,260870350

21,010NDND3,880NDNA

1,750NDND

1,67013,5008221683202,78019,00043,0003,38023,80036,8004,51050,200122,00029,40075,10017,40023,2008,9408252949383716

2,620101NA

2,0907554

6,670290NDND8,460630680"NDND

17,53020,67065020,36017,2001,58023,600ND640ND

NDND7,050NDND

3,180NDNA880NANA

2,80044742NA7,2003698414240

13,90019,4001,27016,40014,50092010,40043

23,6008356681

3,700108NA4,220NANA

41,400NANA

ND1,240NDND350ND5101,780ND3,87015,5206501,3609706,83013,680ND560ND80NDNDNDNDNDNDNANDNANA

39180NANA38317799

1,480NA

1,8407,7205545,4206547,51079,400NA

1,130NA

212NA26NANA91NANA28NANA

ND90NDNDNDND90590ND830NO150ND910ND470NDNDND60NDNDNDNDNDNANANDNANA

88NANA23NA141737NA94414877

312137622NA42NA

112NANANANANANANANANANA

NDNDNDND70NDND110ND

ND910NDNDNDNDNDNDNDNDNDNDNDNDNANDNANA

NA129NA

NANANA341247NA2783423NA

1,110NA1815NA

270NANANANANANANANANA

flR30!98U

TABLE F-13SUMMARY OF XRF AND CLP LEAD RESULTS FOR SOIL SAMPLESC & R BATTERY SITECHESTERFIELD COUNTY, VIRGINIAPAGE TWO

BoringNo.

SO-01SO-02SO-03SO-04SO-05SO-06SO-07SO-08SO-09SO- 10SO-11SO- 12SO-13SO- 14SO- 15SO- 16SO-17SO-18SO-19SO-20SO-21SO-22SO-23SO-24SO-25SO-26SO-27SO-28SO-29SO-30

Sample Depth (feet)

NANANANANDNANA

NANANANANDNA

NANANDNANA

NANANDNANA300NDNANDNA

NANANANANANANANANANANANANANANANA

NANANANANANA70NANANANANA

NANANANA

90NANANANANANANANDNANANA80NANANANANDNANAND170NA80NANA

NANANANA

67NANANANANANANA56NANANA

157NANANANANANANANANA3988NANA

NANANANANDNANA

NANDNANANANDNANANANANDNANA330NDNANDNANA

NANANANA19NANANA

NANANANANANANANA23NANANANANDNANA263NA41NANANA

NANANANA

NDNANA

NANANANANDNANANANDNANANANANDNANAND130NANDNANA

NANANANA20NANANANANANANA,NANANANA96NANANANA

NANANDNANA

NANANA

NDNANANANDNANANANANDNANANDNDNANDNANA

NANANANANANA

NANANA

NANANANANANANANANANANANANANANA

B301985'

TABLE F-13SUMMARY OF XRF AND CLP LEAD RESULTS FOR SOIL SAMPLESC&R BATTERY SITECHESTERFIELD COUNTY, VIRGINIAPAGE THREE ^ ,- _ - .___ —

Notes:

XRF X-ray fluorescence analytical result (detection limifapprbximately 120 mg/kg)CLP Contract Laboratory Program analytical resultND Not DetectedNA Not Analyzed , - - - - -

ti—-

TABLE F-14

SUMMARY OF XRF LEAD RESULTS (MARCH 1989)

HR30S987

TABLE F-14

SUMMARY OF XRF LEAD RESULTS (MARCH 1989)C&R BATTERY SITE

CHESTERFIELD COUNTY. VIRGINIA

BoringNo.

SO-14A

Sample Depth (feet)

27,200[7,680]

20,100[24,600]

200(368]

120[43.6]

ND[156]

ND[33.8]

30-32-

Samples analyzed by the EPA Region III Central Regional Laboratory (CRL).All results reported in mg/kg.ND - Not detected. Detection limit =100 mg/kg.NA - Notanafyzed, ....._ ... ... ...[7,680] - CLP lead value for same sampling interval.

TABLE F-8

SURFACE WATER SAMPLES - TAL TOTAL METALS RESULTS

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TABLE F-9

SURFACE WATER SAMPLES - TAL DISSOLVED METALS RESULTS

ftR30!992

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TABLE F-10

SEDIMENT SAMPLES • TAL RESULTS

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TABLE F-11

SEDIMENT SAMPLES - EP TOXICITY

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TABLE F-12

BLANK SAMPLES

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TABLE F-13

SUMMARY OF XRF AND CLP LEAD RESULTS FOR SOIL SAMPLES

flR302029

TABLE F-13

SUMMARY OF XRF AND CLP LEAD RESULTS FOR SOIL SAMPLESC & R BATTERY SITE

CHESTERFIELD COUNTY, VIRGINIA

BoringNo.

SO-01SO-02SO-03SO-04SO-05SO-06SO-07SO-08SO-09SO-10SO- 11SO- 12SO- 13SO- 14SO- 15SO- 16SO-17SO-18SO-19SO-20SO-21SO-22SO-23SO-24SO-2550-2650-27SO-28SO-29SO-30

Sample Depth (feet)

2,30010,290650NDND

5,11021,98076,4102,29020,89092,2607,280127,100134,50022,520120,4004,86014,86014,260870350

21,010NDND3.880NDNA

1,750NDND

1,67013,5008221683202,78019,00043,0003,38023,80036,8004,51050,200122,00029,40075,10017,40023,2008,9408252949383716

2,620101NA2,0907554

6,670290NDND8,460630680NDND

17,53020,67065020,36017,2001,58023,600ND640NDNDND7,050NDND

3,180NDNA880NANA

2,80044742NA7,2003698414240

13,90019,4001,27016,40014,50092010,40043

23,60083566813,700108NA

4,220NANA

41,400NANA

ND1,240NDND350ND510

1,780ND3,87015,5206501,3609706,83013,680ND560ND80NDNDNDNDNDNDNANDNANA

39180NA

NA38317799

1,480NA

1,8407,7205545,420654

7,51079,400NA

1,130NA212NA26NANA91NANA28NANA

NDNDNDND90590ND830ND150ND910ND470NDNDND60NDNDNDNDNDNANANDNANA

88NANA

23NA141737NA9441487777312137622NA42NA112NANANANANANANANANANA

NDND70NDND110NDND910NDNDNDNDNDNDNDNDNDNDNDNDNANDNANA

NANANANA

NA2783423NA

1,110NA1815NA

NA270NANANANANANANANA

ftR302030

TABLE F-13SUMMARY OF XRF AND CLP LEAD RESULTS FOR SOIL SAMPLESC & R BATTERY SITECHESTERFIELD COUNTY, VIRGINIAPAGE TWO

BoringNo.

SO-01SO-0250-03SO-04SO-05SO-06SO-07SO-08SO-0950-10SO-11SO- 12SO- 13SO- 14SO- 15SO-16SO-17SO-18SO-19SO-20SO-21SO-22SO-23SO-24SO-25SO-2650-27SO-28SO-29SO-30

Sam pie Depth (feet)

NANANANANDNANANA

NANANANANDNA

NDNANA

NANANDNANA300NDNANDNANA

NANANANANANANANANANANANANANANANA

NANANANANANANANA70NANANANANA

NANANANA90NANANANANANANANDNANANA

80NANA

NANANDNANAND170NA80NANA

NANANANA67NANANANANANANA56NANANA157NANANANANANANANANA3988NANA

NANANANAND

NANANANANDNANANANONANA

NANANDNANA330NDNANDNANA

NANA19NANANA

NANANANANANANA23NANANANANDNANA263NA41NANANA

NANANANANDNANANANANANANANDNANANANDNANA

NANANDNANAND130NANDNANA

NANANDNANANA

NANANANA20NANANANANANANANANA

NANA96NANANANANA

NANANANANDNANANANANAhJA

NANDNANANANDNANANANANDNANANDNDNANDNANA

NANANANANANANANANANANANANANANANANANANANANANANANANANANANA

TABLE F-13SUMMARY OF XRF AND CLP LEAD RESULTS FOR SOIL SAMPLESC&RBATTERYSITECHESTERFIELD COUNTY, VIRGINIAPAGE THREE

Notes: ,

XRF X-ray fluorescence analytical result (detection limit approximately 120 mg/kg)CLP Contract Laboratory Program analytical resultND Not DetectedNA Not Analyzed

R3Q2032

TABLE F-14

SUMMARY OF XRF LEAD RESULTS (MARCH 1989)

fiR302033

TABLE F-14

SUMMARY OF XRF LEAD RESULTS (MARCH 1989)C&R BATTERY SITE

SoringNo.

SO-14A

Sample Depth (feet)

27,200[7,6803

20,100[24,600]

200[368]

120[43.6]

ND[156]

ND[33.8]

Samples analyzed by the EPA Region III Central Regional Laboratory (CRL).All results reported in mg/kg.ND - Not detected. Detection limit = 100 mg/kg.NA - Not analyzed.[7,680] - CLP lead value for same sampling interval.

flR3G203!*

APPENDIX G

TOXICOLOGICAL PROFILES

flR302035

SECTION

TABLE OF CONTENTS

TABLES

ANTIMONY ...............................

A DC CMI r

CADMIUM ................................

LEAD ........................ .... ,.,,.-,....

NICKEL ...................................

SILVER ....................................

ZINC .....,..........,,..,.,,.,......,,.. ,,

................................. G-1

,,...,.,,....,,,....,..........,. G-2

................................. G-3

................................. G-5

................................. G-6

,,,,..,.....,,.,.,..,,,,.,..,.,.. G-8

0332927 -- —-———- -- ,...-.H---- —-HR302036

G.1 ANTIMONY (Clement Associates, Inc., 1985)

G.1.1 Health Effects ... .... . _ _ _ _ _ _

Antimony production has been associated with an increase in lung cancer among exposed workers,and one inhalation study in rats also indicated that antimony trioxide might produce lung and livertumors. Several studies in bacterial test systems report that various antimony compounds, includingantimony trioxide, antimony trichloride, and antimony pentachloride, may be mutagenic. Reports ofeffects oh reproduction are limited. Among the effects on reproduction reported for humans areimpairments tcTthe female reproductive system. Female workers exposed to metallic antimony dust,antimony trioxide, and antimony pentoxide had an increased incidence of gynecological disordersand late spontaneous abortions. Antimony was found in the breast milk, placental tissue, amnioticfluid, and blood of the umbilical cord in exposed workers. Decreased weight gain was observed inchildren born of workers exposed to antimony. The same paper reports a study in whichintraperitoneal administration of antimony produced changes in rats that support the findings ofhuman reproductive effects.

Cardiovascular changes associated with exposure to antimony represent a serious health effect.Exposure to either trivalent or pentavalent antimonial compounds can produce electrocardiogram(ECG) changes in humans. Histopathological evidence of cardiac edema, myocardial fibrosis, andother signs of myocardial structural damage indicates that antimony may produce even more severe,possibly permanent myocardTai damage in humans. Parallel findings of functional changes in ECGpatterns and of histopathological evidence of myocardial structural damage have also been obtainedin animal toxicity studies. Pneumoconiosis in response tb Inhalation exposure and dermatitis inresponse to skin exposure have also been observed among individuals exposed to antimony or itscompounds. . ......... ... ....

G.1.2 Toxicity to Wildlife and Domestic Animals

Tests with antimony potassium tartrate and antimony trichloride in Daohnia magna reveal nodifference in the toxicity of these two compounds. The LCso and ECgo values for Daphnia maqna andthe fathead minnow, both freshwater species, range from 9,000 to 21,900 ug/'iter. Chronic values forthe fathead minnow and Daphnia maqna are 1,600 and 5,400 ug/liter, respectively. Acute-chronicratios'for the fathead minnow and Daphnia maqna are 14 and 3.5, respectively. The freshwater algaSelenastrum capricornutum is more, sensitive than the_an_imarspecies tested, with a 96-hour ECso of610 jig/liter for inhibition of the synthesis of chlorophyll a. No detectable bioconcentration of

R332927 flR302037

antimony by the bluegill was observed. No definitive data concerning the toxicity of antimony tosaltwater species or to other wildlife or domestic animals are available.

G.2 ARSENIC (Clement Associates, I nc.r 1985)

G.2.1 Health Effects .. ___....._-

Arsenic has been implicated in the production of skin cancer in humans. There is also extensiveevidence that inhalation of arsenic compounds causes lung cancer in workers. Arsenic compoundscause chromosome damage in animals, and humans exposed to arsenic compounds have beenreported to have an elevated incidence of chromosome aberrations. Arsenic compounds have beenreported to be teratogenic, fetotoxic, and embryotoxic in several animal species, and an increasedincidence of multiple malformations among children born to women occupationaily exposed toarsenic has been reported. Arsenic compounds also cause noncancerous, possibly precancerous, skinchanges in exposed individuals. Several cases of progressive polyneuropathy involving motor andsensory nerves and particularly affecting the extremities arid myelinated long-axon neurons havebeen reported in individuals occupationaily exposed to inorganic arsenic. Polyneuropathies have alsobeen reported after the ingestion of arsenic-contaminated foods.

G.2.2 Toxicitv to Wildlife and Domestic Animals

Various inorganic forms of arsenic appear to have similar levels of toxicity; they all seem to be muchmore toxic than organic forms. Acute toxicity to adult freshwater animals occurs at levels of arsenictrioxide as low as 812yg/liter and at levels as low as 40 ug/liter in early life stages of aquaticorganisms. Acute "toxicity" to saltwater fish occurs, at levels around 15mg/!iter, while someinvertebrates are affected at much lower levels (508yg/liter). Arsenic toxicity does not appear toincrease greatly with chronic exposure, and it does not seem that arsenic is bioconcentrated to a greatdegree. - - ...,..._ .... ........... ^___;._ _ =.._.. ,.. . _ , _ _ = , . : _ - - . . -

Arsenic poisbn'ihg is a ranFbut not uncommon toxic syndrome among domestic animals. Arseniccauses pyperemia and edema of the gastrointestinal tract, hemorrhage of the cardiac aerosal surfacesand peritoneum, and pulmonary congestion and edema; and it may cause liver necrosis, informationon arsenic toxTcttyTciTerTeitria! wildlife was not reported in the literature reviewed.

R332927 - __ - .:::. " : _ ._ . G-2 SR3020

G.3 CADMIUM (Clement Associates, Inc., 1985)

G-3-1 Health Effects ..._._..,_ ,_ ... ____^___

There is suggestive evidence linking cadmium with cancer of the prostate in humans. In animalstudies, inhalation exposure to cadmium caused lung tumors in rats, and exposure by injectionproduced injection-site sarcomas and/or Leydig-cell tumors. An increased incidence of tumors has notbeen seen in animals exposed to cadmium orally, but four of the five available studies wereinadequate by current standards.

The evidence from a large number of studies on the_mutagenicity of cadmium is equivocal, and it hasbeen hypothesized that cadmium is not directly mutagenicbutjmpedes repair. Cadmium is a knownanimal teratogen and reproductive toxin. It has been shown to cause renal dysfunction in bothhumans and animals. Other toxic effects attributed to cadmium include immunosuppression (inanimals), anemia (in humans), pulmonary disease (in humans), possible effects on the endocrine

system, defects in sensory function, and bone damage. The oral LD5o in the rat was 225 mg/kg.

Laboratory experiments suggest that cadmium may have adverse effects on reproduction in fish atlevels present in lightly to moderately polluted waters.

The acute LCso for freshwater fish and invertebrates, generally.. ranged from 100 to 1,000 ug/Hter;saimonids are much more sensitive than other organisms. Saltwater species were in general 10-timesmore tolerant to the acute effects of cadmium. Chronic tests have been performed and show thatcadmium has cumulative toxicity and acute-chronic ratios that range from 66 to 431.BioconcentratiorTfactors were generally less than 1,000 but were as high as 10,000 for somefreshwater fish species. - - - . .... —

No adverse effects on domestic or wild animals were reported. - ...— -

G.4 LEAD(Ciement Associates, Inc., 1985)

G.4.1 Health Effects

There is evidence that several lead salts are carcinogenic in mice or rats, causing tumors of the kidneysafter either oral or parenteral administration. EPA has classified lead as a probable human

ftR302039R332927 . . - .._„_..... -- G_3

carcinogen via the inhalation route of exposure. There is equivocal evidence that exposure to leadcauses genotoxicTty in humans and animals. The available evidence indicates that lead presents ahazard to reproduction and exerts a toxic effect on conception, pregnancy, and the fetus in humans

and experimental animals.

Many lead compounds are sufficiently soluble in body fluids to be toxic. Exposure of humans orexperimental animals to lead can result in toxic effects in the brain and central nervous system, theperipheral nervous system, the kidneys, and the hematopoietk system. Chronic exposure to inorganiclead by ingestion or inhalation can. cause lead encephalopathy, and severe cases can result inpermanent brain damage. Lead poisoning may cause peripheral neuropathy in adults and children,and permanent learning disabilities that are clinically undetectable in children may be caused byexposure to relatively low levels. Short-term exposure to lead can cause reversible kidney damage,but prolonged exposure at high concentrations may result in progressive kidney damage and possiblykidney failure..Anemia, due to inhibition of hemoglobin synthesis and a reduction in the life span ofcirculating red blood cells, is an early manifestation of lead poisoning. Several studies withexperimental animals suggest that lead may interfere with various aspects of the immune response..

Freshwater vertebrates and invertebrates are more sensitive to lead in soft water than in hard water.At a hardness of about 50 mg/liter CaCOs, the median effect concentrations for nine families rangefrom 140g/liter to 236,600 ug/liter. Chronic values for Daohnia maqna and the rainbow trout are12.26and 83.08 yg/liter, respectively, at a hardness of about 50 mg/liter. Acute-chronic ratioscalculated for three freshwater species ranged from 18 to 62. Bioconcentration factors, ranging from42 for young brook trout to 1,700 for a snail, were reported. Freshwater algae show an inhibition ofgrowth at concentrations above 500 ug/liter.

Acute values for twelve saltwater species range from 476 ug/liter for the common mussel to27,000 ug/titer for the soft-shell clam. Chronic exposure to lead causes adverse effects in mysidshrimp at 37 ug/liter, but not at 17yg/llter. The acute-chronic ratio for this species is 118. Reportedbioconcentration factors range from 17,5 for the Quahog clam to 2,570 for the blue mussel.Saltwater algae are adversely affected at approximate lead concentrations as low as 15.8 ug/liter.

Although lead is known to occur in the tissue of many free-living wild animals, including birds,mammals, fishes, and invertebrates, reports of poisoning usually involve waterfowl There is evidencethat lead, at concentrations occasionally found near roadsides and smelters, can eliminate or reduce

R332927 - - - - - _-- . _ . ._ . _ G-4

populations of bacteria and fungi on leaf surfaces and in soil. Many of these microorganisms play keyroles in the decomposer food chain.

Cases of lead poisoning have been reported for a variety of domestic animals, including cattle, horses,dogs, and cats. Several types of anthropogenic sources are cited as the source of lead in these reports.Because of their curiosity and their indiscriminate eating habits, cattle experience the greatestincidence of lead toxicity among domestic animals.

G.5 NICKEL (Clement Associates, Inc., 1985)

G.5;1 Health Effects

There is extensTve~epiderniological evidence indicating excess cancer of the lung and nasal cavity forworkers at nickel refineries arid smelters, and weaker evidence for excess risk in workers at nickelelectroplating and polishing operations. Nickel is a Class A carcinogen. Respiratory tract cancers haveoccurred in excess at industrial facilities that are metallurgical ly diverse in their operations. The nickelcompounds that have been implicated as having carcinogenic potential are insoluble dusts of nickelsubsulfide and nickel oxides, the vapor of nickel carbonyl, and soluble aerosols of nickel sulfate,nitrate, or chloride. Inhalation studies with experimental animals suggest that nickel subsulfide andnickel carbonyl are carcinogenic in rats. Evidence for the carcinpgenicity of nickel metal and othercompounds is relatively weak or inconclusive. Studies with" experimental animals indicate that nickelcompounds can also produce various types of malignant tumors in experimental animals afteradministration by other routes, including subcutaneous, intramuscular, implantation, intravenous,intrarenal, and intrapieural. Carcinogenic potential is not strongly dependent on route or site ofadministration, but appears to be inversely related to the solubility of the compounds in aqueousmedia. Insoluble compounds, such as nickel dust, nickel suifide. nickel carbonate, nickel oxide, nickelcarbonyl, and nickelocene are carcinogenic, whereas soluble nickel salts such as nickel chloride, nickelsulfate, and nickel ammonium sulfate, are not. . ._

Mammalian cell transformation data indicate that several nickel compounds are mutagenic and cancause chromosomal alterations. The available information is inadequate for assessing teratogenicand reproductive effects of nickel in humans and experimental animals.

Dermatitis and other dermatological effects are the most frequent effects of exposure to nickel andnickel-containing compounds. The dermatitis is'a sensitizatiori reaction. Most information regardingacute toxicity of nickel involves inhalation exposure to nickel carbonyl. Clinical manifestations ofacute poisoning include both immediate and delayed symptoms. Acute chemical pneumonitis is

R332927 ——— G-5 flR3020UI

produced, and death may occur at exposures of 107mg/m3 for 30 minutes. Rhinitis, nasal sinusitis,and nasal mucosal injury are among the effects reported among workers chronically exposed tovarious nickel compounds. Studies with experimental animals suggest that nickel and nickel

compounds have relatively low acute and chronic oral toxicity.

G.5,2 Toxicity to Wildlife and Domestic Animals

in freshwater, toxicity depends on hardness; nickel tends to be more toxic in softer water. Acutevalues for exposure to a variety of nickel salts, expressed as nickel, range from 510 ug/liter forDaphnia maqna to 46,200 ug/liter for banded killifish at comparable hardness levels. Chronic valuesrange from 14.8 ug/liter for Daphnia maqna in soft water to 530 ug/liter for the fathead minnow inhard water. Acute-chronic ratios for Daphnia maqna range from 14 in hard water to 83 in soft water,and are approximately 50 in both hard and soft water for the fathead minnow. Residue data for thefathead minnow indicate a bioconcentration factor of 61. Freshwater algae experience reducedgrowth at nickel concentrations as low as 10_0 ug/liter.

Acute values for saltwater species range from 152 ug/liter for mysid shrimp to 350,000 ug/liter for themummichog. A chronic value of 92,7 ug/liter is reported for the mysid shrimp, which gives an acute-chronic ratio of 5.5 for the species. Reduced growth is seen in saltwater algae at concentrations aslow as 1,000 ug/liter. Bioconcentration factors ranging from 299 to 416 have been reported for theoyster and mussel. _ .

G.6 SILVER (Clement Associates, Inc., 1985)

Only equivocal evidence exists to suggest that silver has carcinogenic activity in experimental animals.Silver implants and injected colloidal suspensions are reported to produce tumors or hyperplasis atthe site of application in several studies. However, it is suggested that the effects are due to thephysical form of the metal or to its action as an exogenous irritant. There are no studies to sugge_stthat silver is carcinogenic in humans. Silver does not appear to have significant mutagenic orteratogenic activity in humans or experimental animals.

Silver can be absorbed in humans by inhalation or ingestion. The most common and most noticeableeffects of excessive absorption are a local or generalized impregnation of the tissues referred to asargyria. In case_s of argyria, accumulation of silver can result in a blue-gray pigmentation of the skin,hair, internal "organs, and" conjunctiva of the eye. Large oral does of silver compounds may produce

R332927 _ .:. ..._ __ - .. G-6 &R302QI42

serious effects in humans. For example, silver nitrate can cause violent abdominal pain, vomiting, andconvulsions, and ingestion of 10 grams is reported to usually be fatal. Lesions of the liver, kidney,bone marrow, and lungs have also been attributed to industrial or medicinal exposure.

Intravenous administration of silver nitrateTs reported to produce pulmonary edema and congestionin experimental "animals. Liver and kidney damage, central nervous system effects, and death havealso been reported in experimental animals exposed to various silver compounds. The intraperitonealLD5o (30 days) for silver as the nitrate in male Swiss albino mice ts _1_3.9.mg/kg. Rats exposed to silver intheir drinking water for 11 months showed no. toxic effects at .concentrations less than 0.4 mg/liter.Hemorrhaging occurred in the kidneys at 0.4 mg/liter. Conditioned reflex activity and immunologicalresistance were lowered, and brain nucleic acid content was increased at 0.5 mg/liter. Numerousphysiological changes, including growth depression, and pathomorphologica! changes in the liver,kidney, stomach, and small intestine were evicleriTin rats exposed to 20 mg/liter for 5 months.

Acute toxicity values for freshwater invertebrates range from 0.25 ug/liter for Daphnia maqna to4,500 ug/liter for the scud Gammarus pseudolimnaeus. Acute values for fish range from 3.9 ug/literfor the fathead minnow in soft water to 280 ug/liter for rainbow trout in hard water. In fresh water,the acute toxicity of silver appears to decrease as hardness increases. Soluble compounds, such assilver nitrate, are generally much more toxic than insoluble compounds. Chronic values ranging from2.6 to 29 ug/Mter are reported for Daphnia maqna. Two early life stage studies with rainbow troutreport chronic values of 0.12 ug/liter. Acute-chronic ratios for Daphnia maqna and rainbow trout are2.0 and 54, respectively. Fresh water aquatic plaints appear to be more resistant to silver than themore sensitive animals.

Acute values for saltwater organisms range from 4.7 ug/liter for the summer flounder to 1,400 ug/literfor the sheepshead minnow. A chronic value of 18 ug/liter, and an acute-chronic ratio of 14 isreported for the mysid shrimp.

Reduced cell numbers are observed in the saltwater alga Skeletonema costatum after exposure to130 ug/liter of silver.

Excess silver can induce selenium, vitamin E, and copper deficiency symptoms in animals fed adequatediets, and can aggravate deficiency symptoms in animals whose diets lack one or more of thesenutrients. These effects are reported in dogs, sheep, pigs, chicks, turkey poults, and ducklings.

"32927 - G-7 flR3020H3

G.7 ZINC (Clement Associates, Inc., 1985)

Testicular tumors have been produced in rats and chickens when zinc salts are injectedintratesticularly, but not when other routes of administration are used. Zinc may be indirectlyimportant with regard to cancer since its presence seems to be necessary for the growth of tumors.Laboratory studies suggest that although zinc-deficient animals may be more susceptible to chemicalinduction of cancer/tumor growth is slower in these animals. There is no evidence that zincdeficiency has any etiological role in human, cancer There are no data available to suggest that zinc ismutagenicorteratogeriicihanimalsorhurnans. ..__ . ... .T : .t ...

Zinc is an essential trace eferhent that is involved fn enzyme functions, protein synthesis, andcarbohydrate metabolism. Ingestion of excessive amounts of zinc may cause fever, vomiting, stomachcramps, and diarrhea. Fumes of freshly formed zinc oxide can penetrate deep into the alveoli andcause metal fume fever. Zinc oxide dust does not produce this disorder. Contact with zinc chloridecan cause skin and eye irritation. Inhalation of mists or fumes may irritate the respiratory andgastrointestinal tracts. Zinc in excess of 0.25 percent in the diet of rats causes growth retardation,hypochromic anemia, arid defective mineralization of bone. No zinc toxicity is observed at dietarylevels below 0.25 percent.

Studies with animals and humans indicate that metabolic changes may occur due to the interaction ofzinc and other metals in the diet. Exposure to cadmium can cause changes in the distribution of zinc,with increases in the liver and kidneys, organs where cadmium also accumulates. Excessive intake ofzinc rfiay cause copper deficiencies and result in anemia. Interaction of zinc with iron or lead may alsolead to changes that are not produced when the metals are ingested individually.

Zinc produces acute toxicity in freshwater organisms over a range of concentrations from 90 to58,100 ug/liter and appears to be less toxic in harder water. Acute toxicity is similar for freshwaterfish and invertebrates. Chronic toxicity values range from 47 to 852 ug/liter and appear to berelatively unaffected by hardness. A final acute-chronic ratio for freshwater species of 3.0 has beenreported. Although most freshwater plants appear to be insensitive to zinc, one species, the algaSeienastrum capricornutum. exhibited toxic effects at concentrations from 30to 700 ug/liter.Reported acute toxicity values range from 2,730 to 83,000 ug/liter for saltwater fish and from 166 to55,000 ug/liter for invertebrate saltwater species. Zinc produces chronic toxicity in the mysid shrimp

R332927 ' ~ G-8 R302QH

at 166 ug/liter. The final acute-chronic ratio for saltwater species is 3.0, Toxic effects are observed insaltwater plant species at zinc concentrations of 50 to 25,000 ug/liter Bioconcentration factors ofedible portions of aquatic organisms"range from 43 for the soft-shell clam to 16,700 for the oyster.

Zinc poisoning has occurred in catt|e_,Mn_ one outbreak, poisoning was caused by food accidentallycontaminated with zinc at a concentration of 20 g/kg. An estimated intake of 140 g of zinc per cowper day for about 2 days was reported. The exposed cows exhibited severe enteritis, and some died orhad to be slaughtered. Postmortem findings showed severe pulmonary emphysema with changes inthe myocardium, kidneys^and liver. Zinc concentrations in the liver were extremely high. Based onrelatively limited data, some researchers have speculated that exposure to excessive amounts of zincmay constitute a hazard to horses. Laboratory studies and findings in foals living near lead-zincsmelters suggest that excessive exposure to zinc may produce bone changes, joint afflictions, andlameness. In pigs given dietary zinc at concentrations greater than 1,000 mg/kg, decreased foodintake and weight gain were observed. At dietary levels greater than 2,000 mg/kg, deaths occurredas soon as 2 weeks after exposure. Severe gastrointestinal changes and brain damage, both of whichwere accompanied by hemorrhages, were observed, as well as changes in the joints. Highconcentrations of zinc were found in the liver.

R332927

APPENDIX H

RISK ASSESSMENT CALCULATIONS

TABLE OF CONTENTS

SECTION __.__. _

H.1 RISKS FROM EXPOSURE TO FUGITIVE DUST

H.2 RISK FROM INGESTION OF SOIL

H.3 RISKS FROM GROUNDWATER USE

O332927

RR3020U7

APPENDIX H.1

RISK FROM EXPOSURE TO FUGITIVE DUST

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RISK FROM INGEST1ON OF SOIL

RR302051

APPENDIX H.2.1

INGEST.ON OF SOIL- SURFACE SOILS

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APPENDIX H.3

RISK FROM GROUNDWATER USE

TABLE OF CONTENTS

SECTION _. ... . ............... ._.__. . , __..._—...

H.3.1 CONTAMINANT CONCENTRATIONS AT DOWNGRADIENT RECEPTOR • RELEVANTEQUATIONS

H.3.2 GROUNDWATER EXPOSURE - ONSITE SOILS

H.3.3 GROUNDWATER EXPOSURE - DEBRIS PILES

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APPENDIX H.3.1

CONTAMINANT CONCENTRATIONS AT DOWNGRADIENTRECEPTOR - RELEVANT EQUATIONS

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APPENDIX I

C&R BATTERY AIR QUALITYMODELING ANALYSIS FORFUGITIVE DUST EMISSIONS

1.1 INTRODUCTION

This section presents a description of the air quality modeling study conducted to estimate ambientlead and arsenic concentrations at exposure points located beyond the C&R Battery propertyboundary. Ambient concentrations were estimated using a predictive air quality model approved bythe U.S. Environmental Protection Agency (ERA). The environmental exposure pathway addressed inthis study pertains to the erosion of contaminated surface soil by wind to offsite locations.

I.2 MODELING PROTOCOL

1,2.1 Model Selection . . . . . . . . ._

The C&R Battery Site is located on essentially flat terrain in Chesterfiefd County, Virginia,approximately 6 miles southeast of Richmond, as shown in Figure 1-1. The site is located on a 4.5-acretract of land, approximately 1,260 feet in the north-south direction, and between 100 and 190 feetwide. Figure 1-2 depicts the general site layout.

The purpose of this Study is to address site soil emissions that will result from wind erosion. Emissionsof this nature are commonly referred to as fugitive dust. Fugitive dust usually refers to the dust putinto the atmosphere by the wind blowing over areas with little or no vegetation. Fugitive emissionsinclude emissions resulting from a site, such as the C&R Battery Site. Where such fugitive emissionscan be properly specified, the Industrial Source Complex (ISC) model is recommended (ERA, 1986,1987).

The fSC dispersion model combines various algorithms that can be used to assess the air quality impactof emissions from a wide variety of sources associated with an industrial complex. The ISC model canbe used to estimate ambient particulate concentrations and dry deposition. The model can be used ineither the short-term or the long-term modes. For the purpose of this study, the ISC long-term (ISCLT)mode has been selected because it can calculate concentration values relative to long-term (annual)National Ambient Exposure and Applicable Air Quality Standards (NAAQS). At the present time, leadis regulated on a calendar quarter basis. Quarterly ambient concentrations of iead cannot exceed1.5 yg/m3. Mo NAAQS currently exists for arsenic.

The ISCLT is a sector-averaged model that uses statistical wind summaries to calculate seasonal(quarterly) and/or annual concentration or deposition values. The model will accept the followingsource types: stack, area, and volume.

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The ISCLT model contains a number of options that are designed to consider complicated sourceconfigurations and special atmospheric effects. In this study, the regulatory default option wasselected. This option automatically selects stack tip downwash, final-plume rise, buoyancy-induceddispersion, the default vertical potential temperature gradient and appropriate wind profileexponents. . ..- ....,=.-..= --.-.—^—--—-- — ----- -,,== ---

The ISCLT model can be used in either the rural or urban mode. Each option assigns rural or urbandispersion coefficients. Two procedures, based on land use or population density, are used todetermine the application of urban or rural dispersion coefficients (EPA, 1986).

Land use characteristics within a one(1) kilometer (km) square area of the C&R Battery Site werereviewed in accordance with procedures specified by EPA using the Auer Method (EPA, 1986). Areview of the area using the Drewrys Bluff, Virginia, 7.5 minute series topographic map indicate thatless than 25 percent of the total area within one (1) square km can be classified as urban. Therefore,the rural option was used to model fugitive emissions from the site.

1.2.3 Source Emissions . _ _

As discussed previously, the source of emissions examined in this study pertains to wind erosion oflead and arsenic from contaminated surface soil. Results of onsite and laboratory analysis of surfacesoil lead and arsenic concentrations were used to estimate emissions from various locations within thesite area. Because of the large spatial variation of surface soil lead concentrations, it was decided todivide the entire site into fifty-four 100-square-foot areas and assign individual emission rates(g/sec/m ) to each area source. An illustration of the 54 area sources overlying the site is shown inFigure!-3. : -- —-————--•--- -:. _^=-—-. - - - - -

Lead concentrations are shown in Figure !-4 and ranged from 120 mg/kg to 122,000 mg/kg. Arsenicconcentrations ranged from 2.9 mg/kg to 68 mg/kg and are depicted in Figure 1-5. Furtherinformation regarding the surface soil analyses are contained in Sections 4.1 and 4.2 of this report.

Individual emission rates for each area source were developed in a stepwise manner. Methods(EPA, 1985) are available for estimating the total suspended particuiate (TSP) emissions that resultduring disturbances by strong winds over open ground areas. For emissions from wind erosion, thefollowing TSP emission factor equation is recommended:

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where . E = TSP emission factor (Ib/day/acre)s = silt content of soil (%) = 75%p = number of days with 0.25mm (0.01 inch)of precipitation = 114daysf =. percentage of time that the unobstructed wind speed exceeds 5.4m/sec (12mph)

= 12.4%

The coefficient in the above equation is based on sampling of emissions from a sand and gravel area.Silt content was obtained from surface soil samples using the ASTM-C-136 method and was assumedto be uniform over the site area. The number of days with precipitation 0.01 in was obtained fromclimatological data compiled for Richmond, Virginia (Ruffner and Bair, 1977). The frequency of windspeed exceeding 12 mph was obtained from a 10-year (1964-1973) statistical summary compiled forRichmond, Virginia. Substitution of these values into the above equation resulted in an emissionfactor of 75.05 pound/day/acre (0.39 g/sec/acre). This TSP emission factor converts to 9.8 E-05 g/sec-m2for each 100-square-foot area.

Estimates of lead and arsenic emissions for each area source were made by multiplying the TSPemission factor by the mean percent lead and arsenic content estimated for each area source. Meanpercent content was determined by averaging the actual soil analysis concentrations reported withineach individual area source. When soil analysis points did not fall within the 100-square-foot area,lead content was estimated from isoconcentrations drawn within the area source. A listing of themean percent lead and arsenic for each area source is given in Tables 1-1 and 1-2, respectively. Therespective emission rate for lead and arsenic input into the ISCLT model for each of the 54areasources is presented in Tables 1-3 and 1-4.

1.2.4 Meteorological Data

The ISCLT mode! can use seasonal or annual "STAR" summaries to satisfy meteorological inputrequirements. STAR summaries are statistical tabulations of the joint frequency of occurrence ofwind speed and wind direction categories, classified according to Pasquill stability categories.

The closest available source of meteorological data to the C&R Battery Site is Byrd Field Airport inRichmond. The airport is approximately 20 miles northeast of the C&R Battery Site. A 10-yearseasonal STAR summary for the period 1964-1973 was obtained from the National Climatic Data

0332927 " - - |_g flR302

TABLE 1-1

MEAN PERCENT LEAD CONTENTFOR INDIVIDUAL C&R BATTERY AREA SOURCES

Area Source

A3A9A10A11A12B182B3B4B5B6B7B389810811B12

CIC2C3C4C5C6C7

Mean PercentLead

0.102.700.100.100.100.020.100.080.070.12

0.020.090.570.570.24

0.690.540.27

0.100.140.060.090.040.031.122.380.45

Area Source

C10C11C12D1020304D50607

0809010011D12ElE2E3E4E5E6E7

E10£11E12

Mean PercentLead

8.617.511.740.131.850.810.420.02

1.232.35

0.234.053.601.021.340.01

0.010.01

0.190.040.260.080.900.010.17

1.651.74

D332927 1-9 SR3Q2HG

TABLE 1-2

MEAN PERCENT ARSENIC CONTENTFOR INDIVIDUAL C&R BATTERY AREA SOURCES

Area Source

A9A10A11A12

8182838485

868788

89810811

812 'C1C2

C5C6C7

Mean PercentLead

0.00080,00110.00110.00100.00150.001 10.00030.00030.00030.00050.00080.00080.00350.00160.00130.00190.0022

0.00050.00030.00030.00050.00080.00120.00150.00160.00120.0010

Area Source

C10C11C12010203D4OS060708

09010D11012E1E2E3E4

E5E6E7

E8E9E10E11E12

Mean PercentLead

0.00260.00580.00330.00100.00110.00040.00070.00060.00060.00100.00200.00350.0019

0.00310.00230.00030.00030.00030.00030.00030.00030.00030.00030.0008

0.00100.00100.0008

D332927 1-10 flR302! i i

TABLE 1-3

C&R BATTERY AREA SOURCELEAD EMISSION RATES INPUT INTO THE ISCLT MODEL

{g/sec-m2}C&R BATTERY SITE

Area Source

A8A9A10A11A12818283848586878889810811B12C1C2C3C4CSC6C7

EmissionRate

9.8E-082.7E-069.8E-089.8E-089.8E-08

1.6E-089.6E-087.4E-086.8E-081. IE-07

1.8E-088.7E-085.6E-075.5E-072.3E-076.8E-075.3E-Q72.6E-079.8E-081.3E-07

5.7E-089.2E-083.9E-082.7E-081. IE-062.3E-064.4E-07

Area Source

C10C11C1201D20304

050607

010011012E1E2

E3E4E5

E6E7E8E9E10E11

EmissionRate

8.4E-06

7.4E-061.7E-061 .2E-061 .8E-068.0E-074. IE-072.8E-08

1.2E-062.3E-062.3E-074.0E-063.5E-061.0E-061.3E-061.2E-081.2E-081 .2E-081.9E-074.0E-082.SE-07

7.6E-088.8E-071.2E-081.7E-071.6E-061.7E-06

D332927 " ' 1-11 flR302l

TABLE 1-4

C&R BATTERY AREA SOURCEARSENIC EMISSION RATES INPUT INTO THE ISCLT MODEL

(g/sec-m2)C&R BATTERY SITE

Area Source

A9A10A11A1281828384

8586B7

B889810811

812C1aC3C4

C5C6C7

EmissionRate

7.84E-101 .07E-09

1.07E-099.80E-101.47E-091.07E-092.94E-102.94E-102.94E-104.90E-107.84E-107.84E-103.43E-10

1.57E-091.25E-09

1.86E-092.16E-094.90E-102.94E-102.94E-104.90E-107.84E-101.18E-091.47E-091.57E-091.18E-099.8E-10

Area Source

C10C11

020304OS06D7

0809010011

012E1E2E3E4E5E6E7E8

E9E10E11

EmissionRate

2.55E-095.68E-09

3.23E-099.80E-101.08E-093.92E-106.86E-105.88E-105.88E-109.80E-10

1.96E-093.43E-091.86E-093.04E-092.25E-09

2.94E-102.94E-10

2.94E-102.94E-102.94E-102.94E-102.94E-102.94E-107.84E-109.80E-109.80E-107.84E-10

D332927 " " j-12RR302M3

Center for use with the ISCLT model. The summary contained joint frequencies for six (6) stabilitycategories (A-F) and six wind speed groups over 16 radial sectors.

Additional meteorological data was obtained for input into the ISCLT model pertaining to meanseasonal ambient air temperatures and seasonal mixing heights from pertinent ciimatologicalreferences (Ruffner and Bair, 1977; EPA, 1972).

I.2.5 Receptor Network _

Ambient concentrations of les-i and arsenic were calculated at 97 receptors within a 1-km square areasurrounding the C&R Battery site. The receptor network was based on a Cartesian coordinate systemextending outward from the center of the site at increment of 100 meters. Ambient concentrationswere reported only for receptors that were located outside of the source area shown in Figure 1-4.Because the maximum ambient impact from ground-level fugitive dust sources is usually within a fewhundred meters of the sources, it was decided that a 1 km square receptor grid was adequate todefine the maximum ambient impact.

In addition to the receptor points described above, one (1) discrete receptor point was also included.The Drewrys Bluff topographic map was reviewed to locate the nearest public school building. Theclosest public school to the C&R Battery Site was found in Chimney Corner, approximately 2.3 kmsouthwest of the site. Ambient concentrations at all receptors were reported in micrograms per cubicmeter. . . . . _ _ .

1.3 MODELING RESULTS

The ISCLT model was run using the C&R Battery Site lead and arsenic inventories given in Tables 1-3and 1-4 and the 10-year meteorological STAR summary for Richmond, Virginia. Ambient leadconcentrations were calculated on a seasonal (quarterly) and annual basis, whereas ambient arsenicconcentrations were calculated onfy for the annual period.

The maximum ambient ground-level lead and arsenic concentrations calculated within the1-km-square receptor grid and the Chimney Corner Public School are reported in Tables t-5 and i-6.Results in Table 1-5 indicate that the maximum ground-level lead concentration was found to occurnortheast (NE) of the site at coordinate point 100,100 for both the seasonal and annual averagingperiods. The maximum annual lead concentration for the 1-km receptor grid was 0.0026 yg/m3. Themaximum annual lead concentration at the Chimney Corner Public School was 0.00024 vg/m3. The

W32927 1-13 AR3Q21 1

TABLE 1-5

RESULTS OF ISCLT MODEL FOR MAXIMUM SEASONAL ANDANNUAL LEAD CONCENTRATIONS

Receptor x,y (meters)

NE(100,100)

Chimney Corner School

Maximum Concentration (ug/m3)

Seasonal

0.0029

0.00028

Annual

0.0026

0.00024

0332927 1-14 a R 3 0 2 ! ! 5

TABLE 1-6

RESULTS OF ISCLT MODEL FOR MAXIMUM ANNUAL ANDAMBIENT ARSENIC CONCENTRATIONS

Receptor x,y (meters)

South (0,-200)

Chimney Corner School

Maximum Concentration(ug/m3)

0.00820

0.0000249

D332927 1-15

* maximum seasonal concentrations of 0.0029 yg/m3 at receptor point 100,100 and 0.00028 yg/m3 atChimney Corner Public School occurred during the July, August, September seasonal quarter.

Table I-6 indicates that the maximum arsenic ground- level concentration was found to occur south ofthe site at coordinate 0,-200 for the annual period. The maximum annual lead concentration forarsenic was 0.0082 yg/m3. The maximum annual arsenic concentration at the Chimney Corner Schoolwas 0.000025 yg/m3.

03329.7 ,.16 BR3Q2! 17

APPENDIX I

REFERENCES

EPA (U.S. Environmental Protection Agency), 1987. Industrial Source Complex (ISO Dispersion ModelUsers Guide - Volume I & II - Section Edition (Revised). EPA-450/4-88-0022, Research Triangle Park,North Carolina. --- - - ...__._ -_ ..._._-

EPA (U.S. Environmental Protection Agency), 1986. Guideline on Air Quality Models (Revised) andSupplement A (1987). EPA-450/2-78-027R, Research Triangle Park, North Carolina.

EPA (U.S. Environmental Protection Agency), 1985. Compilation of Air Pollutant Emission Factors.Volume 1: Stationary Poinl.and Area Sources. AP-42, Office of Air Quality Planning and Standards,Research Triangle Park, North Carolina.

EPA (U.S. Environmental Protection Agency), 1972. Mixing Heights, Wind Speeds, and Potential forUrban Air Pollution Throughout the Contiguous United States. Research Triangle Park,North Carolina. _ . ... ^

Ruffner, James A., and Frank E. Bair, 1977. The Weather Almanac. Gale Research Company, BookTower, Detroit, Michigan.

0332927 -- -M7- SR302! 18

APPENDIX J

DEBRIS PILE AND TANK FARM DIKE VOLUME CALCULATIONS

NUS CORPORA T/ON AND SUBSIDIARIES STANDARD CALCULAT/OMonce /

CUENT:

SUBJECT:C <* R

FILE NO.:

' : ' " •" ~~" '

RTH/SIC*CHECKED BY:. - 1 _

PAGE OF

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L Pfl " -SUBJECT:

C + R. ' '

FILE NO.:

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CHECKED BY: , .,__/Xt

PAGE^OF

DATE:3-3/-V

NUS 156A REVISCO 0385 flR302i2

NUS CORPORA TION AND SUBSIDIARIES -_ STANDARD CALCULATIONorTCC /

CLIENT:£"PA

SUBJECT:«-A £ G£ Oefi

FILE NO.:<n^/^ i s p/t e

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FINAL REMEDIAL INVESTIGATION REPORT VOLUME III OF III ...

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