nus · table of contents volume ii - appendices section a industrial lane database a.i area a data...

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FINAL

FOCUSED FEASIBILITY STUDY(GROUNDWATER)

IIIIII

_ INDUSTRIAL LANE SITE| | NORTHHAMPTON COUNTY, PENNSYLVANIA

• • EPA WORK ASSIGNMENT NUMBER 37-24-3L99• • CONTRACT NUMBER 68-W8-0037

I • NUS PROJECT NUMBER 2771

| MARCH 1991I

NUSS~n • ___ CORPORATION

1 B• ^JA Halliburton Company1 * flR30i979

TABLE OF CONTENTS

VOLUME II - APPENDICES

SECTION

A INDUSTRIAL LANE DATABASE

A.I AREA A DATA

A.2 AREA B DATA

A.3 AREA C DATA

A.4 AREA D DATA

A.5 AREA E DATA

B TOXICOLOGICAL PROFILES

C RISK ASSESSMENT CALCULATIONS

C.I REPRESENTATIVE CONTAMINANT CONCENTRATIONS

C.2 RISK ANALYSIS RESULTS

C.3 CLEANUP LEVEL CALCULATIONS

D ALTERNATIVE CALCULATIONS

D.I GENERAL CALCULATIONS

D.2 AIR STRIPPER MODEL OUTPUT FILES

E REMEDIAL ALTERNATIVE COSTS

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APPENDIX A

INDUSTRIAL LANE DATABASE

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APPENDIX A.I

AREA A DATA

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The following footnotes apply to the analytical results presentedin this database:

•J1 - Estimated value.

'B1 - Concentration is within 5-10 times theconcentration reported for qualityassurance samples.

'D'1 - Value presented is 1/2 the methoddetection limit.

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APPENDIX B

TOXZOOLOGICAL PROFILES

TABLE OF CONTENTS

SECTION PAGE

B.1.0 BENZENE (Clement Associates/ Inc.) B-l

B.I.I HEALTH EFFECTS. B-l

B.I. 2 TOXICITY TO WILDLIFE AND DOMESTIC ANIMALS B-l

B.2.0 CHLOROBENZENE (Clement Associates, Inc.) B-2

B.2.1 HEALTH EFFECTS B-2

B.2.2 TOXICITY OF WILDLIFE AND DOMESTIC ANIMALS B-2

B.3.0 CHLOROFORM (Clement Associates, Inc.) B-2


B.3.2 TOXICITY TO WILDLIFE AND DOMESTIC ANIMALS B-3

B.4.0 1,1-DICHLOROETHANE (Clement Associates, Inc.) B-3


B.4.2 .TOXICITY TO WILDLIFE AND DOMESTIC ANIMALS B-3

B.5.0 1,2-DICHLOROETHANE (Clement Associates, Inc.) B-4


B.5.2 TOXICITY TO WILDLIFE AND DOMESTIC ANIjMALS B-4

B.6.0 1,2-DICHLOROPROPANE (Clement Associates, Inc.) B-4



B.7.0 TETRACHLOROETHENE (PCE) (Clement Associates, Inc.) B-5


B.7.2- TOXICITY TO WILDLIFE AND DOMESTIC ANIMALS B-5

B.8.0 1,1,1-TRICHLOROETHANE (1,1,1-TCA) B-6(Clement Associates, Inc.)



D334906 fiR3Q2IQ2

TABLE OF CONTENTS (Continued)

SECTION PAGE

B.9.0 TRICHLOROETHENE (TCE) (Clement Associates, Inc.) B-7

B.9.1 HEALTH EFFECTS . B-7


B.10.0 VINYL CHLORIDE (Clement Associates, Inc.) B-7


B.10.2 TOXICITY TO WILDLIFE AND DOMESTIC ANIMALS- 'B-8

B.11.0 BIS(2-ETHYLHEXYL)PHTHALATE (BEHP) B-8(Clement Associates, Inc.)

B.ll.l HEALTH EFFECTS B-8


B.12.0 DICHLOROBENZENE (Clement Associates, Inc.) B-9



B.13.0 ISOPHORONE (ACGIH, 1980) " B-10

B. 13.1 HEALTH EFFECTS • B-10


B.14.0 METHYLENE CHLORIDE (Clement Associates, Inc.) B-10

. B. 1.4.1 HEALTH EFFECTS B-10

B.14.2 TOXICITY TO WILDLIFE AND DOMESTIC ANIMALS 'B-ll

B.15.0 1,1-DICHLOROETHYLENE (Clement Associates, Inc.) B-ll

B.I5.1 HEALTH EFFECTS B-ll

B."l5.2 TOXICITY TO WILDLIFE AND DOMESTIC ANIMALS B-l2

B.16.0 1,2-DICHLOROETHENE (Clement Associates, Inc.) B-12

B.I6.1 HEALTH EFFECTS B-12


0334906 iiiAR302I03

TABLE OF CONTENTS (Continued)

SECTION PAGE

B.17.0 CARBON TETRACHLORIDE (Clement Associates, Inc.) B-13



B.18.0 CHROMIUM (Clement Associates, Inc.) B-13



B.19.0 LEAD (Clement Associates, Inc.) B-14



B.20.0 MERCURY (Clement Associates, Inc.) B-15

B.20.1 HEALTH EFFECTS B-l6


B.21.0 MANGANESE (Clement Associates, Inc.) B-17



0334906 AR302I01*

APPENDIX B

TOXICOLOGICAL PROFILES

B.1.0 BENZENE (Clement Associates, Inc.)

B.I.I HEALTH EFFECTS

Benzene is a recognized human carcinogen (Class A). Severalepidemiological studies provide sufficient evidence of a causalrelationship between benzene exposure and leukemia in humans.Benzene is a known inducer of aplastic anemia in humans, with alatent period of up to 10 years. It produces leukopenia andthrombocytopenia, which may progress to pancytopenia. Similaradverse effects on the blood-cell-producing system occur inanimals exposed to benzene. In both humans and animals, benzeneexposure is associated with chromosomal damage, although it isnot mutagenic in microorganisms. Benzene was fetotoxic andcaused embryo lethality in experimental animals.

Exposure to very high concentrations of benzene (66,000 ing/m-*)I can be fatal within minutes. The prominent, signs are central•s nervous system depression and convulsions, with death usuallyI following as a consequence of cardiovascular collapse. Milderf ^.4 exposures can produce vertigo, drowsiness, headache, nausea, and

eventually unconsciousness if exposure continues. Deaths fromcardiac sensitization and cardiac arrhythmias have also beenreported after exposure to unknown concentrations. Althoughmost benzene hazards are associated with inhalation exposure,dermal absorption of liquid benzene may occur, and prolonged orrepeated skin contact may produce blistering, erythema, and adry, scaly dermatitis.

B.I. 2 TOXICITY TO WILDLIFE'AND D-X-IESTIC ANIMALS

The ECso values for benzene in a variety of invertebrate andvertebrate freshwater aquatic species range from 5,300 ug/L to386,000 ug/L. However, only values for the rainbow trout(5,300 ug/L) were obtained from a flow-through test and werebased on measured concentrations. Results based on unmeasuredconcentrations in static tests are likely to underestimatetoxicity for relatively volatile compounds like benzene. Achronic test with Daphnia maqna was incomplete,' with no adverseeffects observed at test concentrations as high as 98,000

For saltwater species, acute values for one fish and fiveinvertebrate species range from 10,900 ug/L to 924,000 ug/L.Freshwater and saltwater plant species that have been studiedexhibit toxic effects at benzene concentrations ranging from20,000 ug/L to 525,000 ug/L.

0334906 B-l

B.2.0 CHLOROBENZENE (Clement Associates, Inc.)

B.2.1 HEALTH EFFECTS

A carcinogenicity study showed that chlorobenzene causedneoplastic nodules in the liver of male rats but was notcarcinogenic in female rats or in mice. Occupational studiessuggest that chronic exposure to monochlorobenzene vapor maycause blood dyscrasia, hyperlipidemia, and cardiac dysfunction'in humans. Like many organic solvents, monochlorobenzene is acentral nervous system depressant in overexposed humans, but nochronic neurotoxic effects have been reported. Animals exposedto chlorobenzene have exhibited liver and kidney damage andatrophy of the seminiferous tubules in the testes. The oral LDgovalue for rats was 2,910 mg/kg

B.2.2 TOXICITY OF WILDLIFE AND DOMESTIC ANIMALS

Chlorobenzene was acutely toxic to fish at levels greater than25 mg/L and to aquatic invertebrates at levels greater than10 mg/L. No chronic studies on the toxicity of chlorobenzene toaquatic life were found in the literature reviewed.Monochlorobenzene was shown to have a bioaccumulation factor ofabout 1,000 in freshwater species. No studies on terrestrialwildlife or domestic animals were reported'.

B.3.0 CHLOROFORM (Clement Associates, Inc.)


Chronic administration of chloroform by gavage is reported toproduce a dose-related increase in the incidence of kidneyepithelial tumors in rats and a dose-related increase in theincidence of hepatpcellular carcinomas in mice. It is a Class Bcarcinogen. Epidemiological studies suggest that higherconcentrations of chloroform and other trihalomethanes in watersupplies may be associated with an increased frequency ofbladder cancer in humans. However, these results are notsufficient to establish causality. An increased incidence, offetal abnormalities was reported in offspring of pregnant ratsexposed to chloroform by inhalation. Oral doses' of chloroformthat caused, maternal toxicity produced relatively mild fetaltoxicity in the form of reduced birth weights. There arelimited data suggesting that chloroform has mutagenic activityin some test systems. However, negative results have beenreported for bacterial mutagenesis assays.

Humans may be exposed to chloroform by inhalation, ingestion, orskin contact. Toxic effects include local irritation of theskin or eyes, central nervous system depression,gastrointestinal irritation, liver and kidney damage, cardiacarrhythmia, ventricular tachycardia, and brachycardia. Deathfrom chloroform overdosing can occur and is attributed toventricular fibrillation. Chloroform anesthesia can producedelayed death as a result of liver necrosis.

D334906 B-2 m AR302I06

*

Exposure to chloroform by inhalation, intragastricadministration, or intraperitoneal injection produces liver andkidney damage in laboratory animals. The oral LDso andinhalation LCt,o values for the rat are 908 mg/kg and 39,000 mg/m3per 4 hours, respectively.

B.3.2 TOXICITY TO WILDLIFE AND DOMESTIC ANIMALS

Limited information is available concerning the toxicity ofchloroform to organisms exposed at known concentrations. Medianeffect concentrations for two freshwater and one invertebratespecies range from 28,900 to 115,000 ug/L. Twenty-seven day LCsovalues of 2,030 and 1,240 ug/L were reported for embryo-larvaltests with rainbow trout in water at two levels of hardness.The only reliable result concerning the toxicity of chloroformto saltwater aquatic life is a 96-hour LCso value of 81,500 ug/Lfor pink shrimp.

An equilibrium bioconcentration factor of six with a tissuehalf-life of less than 1 day was determined for the bluegill.Although chloroform is not strongly bioaccumulated, it isthought to be widely distributed in the environment and can bedetected in fish, water birds, marine mammals, and variouscrops.

B.4.0 1,1-DICHLOROETHANE (Clement Associates, Inc. )

B.-4.1 HEALTH EFFECTS

Limited toxicological testing of 1,1-dichloroethane has beenconducted, although the literature indicates that1,1-dichloroethane is one of the least toxic of the chlorinatedethanes. An NCI bioassay on 1,1-dichloroethane was limited bypoor survival of test animals, but some marginal tumorigeniceffects were seen. Inhalation exposure to high doses of1,1-dichloroethane (over 16,000 '.ag/m3) caused retarded fetaldevelopment in rats. 1,1-Dichloroethane was not found to bemutagenic, using the Ames assay. '1,1-Dichloroethane causescentral nervous system depression when inhaled at highconcentrations, and evidence suggests that the compound ishepatotoxic in humans. Kidney and liver damage was. seen inanimals exposed to high levels of 1,1-dichloroethane. The oral

value in the rat is 725 mg/kg.


No information on the toxicity of 1,1-dichloroethane to aquaticspecies was reported in the literature reviewed. However, theavailable information on the chloroethanes indicates thattoxicity declines with decreases in chlorination, and that the1,1,1-isomer is less active than the 1,1,2-isomer. Therefore,1,1-dichloroethane is probably no more toxic than1,2-dichloroethane, - which is acutely toxic at levels of

0334906 B-3

100-500 mg/L and has a chronic toxicity beginning at about20 mg/L.No information on the toxicity of 1,1-dichloroethane toterrestrial wildlife or domestic animals was found in thesources reviewed.

B.5.0 1,2-DICHLOROETH4ANE (Clement Associates, Inc.)


1,2-Dichloroethane is carcinogenic in rats and mice, producing avariety of tumors. When administered by gavage, it producedcarcinomas of the forestomach and hemangiosarcomas of thecirculatory system in male rats; adenocarcinomas of the mammarygland in female rats; lung adenomas in male mice; and lungadenomas, •mammary adenocarcinomas, and endometrial tumors infemale mice. It is mutagenic when tested using bacterial testsystems. Human exposure by inhalation to 1,2-dichloroethane hasbeen shown to cause headache, dizziness, nausea, vomiting,abdominal pain, irritation of the mucous membranes, and liverand kidney dysfunction. Dermatitis may be produced by skincontact. In severe cases, leukocyte-sis (an excess of whiteblood cells) may be diagnosed; and internal hemorrhaging andpulmonary edema leading to death may occur. Similar effects -areproduced in experimental animals.


1,2-Dichloroethane is one of the chlorinated ethanes least toxicto aquatic life. For both fresh- and saltwater species, it isacutely toxic at concentrations greater than 118 mg/L, whilechronic toxicity has been observed at 20 mg/L.1,2-Dichloroethane is not likely to bioconcentrate, as, itssteady state bioconcentration factor was 2 and its eliminationhalf-life was less than 2 days ir bluegill.

No information on the toxicity of 1,2-dichloroethane to domesticanimals or terrestrial wildlife was 'available in the literaturereviewed.

B.6.0 1,2-DICHLOROPROPANE (Clement Associates, Inc.)


1,2-Dichloropropane caused an increased incidence of combinedadenomas and carcinomas of the liver in male and female mice andcaused a slight increase in mammary adenocarcinomas in femalerats. In an earlier study, 80 C3H mice were exposed to1,850 mg/m3 of 1,2-dichloropropane for 4 to 7 hours per day37 times and were then observed for the next 7 months; only3 mice survived, but all of these developed multiple hepatomas.1,2-Dichloropropane was found to be mutagenic using the Amesassay both with and without metabolic activation. It alsoincreased the frequency of 8 azaguanine-resistant mutants in the

0334906 B-4

flR3Q2i08

Asperqillus nidulans spot test. No information was available onthe reproductive or teratogenic effects of this compound.

High concentrations of 1,2-dichlbropropane cause central nervoussystem depression and narcosis in humans. Other human symptomsinclude headache, vertigo, lacrimation, and irritation of themucous membranes. Studies indicate that exposure to highconcentrations may affect the rate of growth in rats and guineapigs, and cause fatty degeneration and multilobular orcentrilobular necrosis of the liver. Histopathological changeswere also observed in the kidneys, adrenals, and heart.1,2-Dichloropropane is a mild skin irritant. It is moderatelyirritating to the eye but does not cause permanent injury.

The oral LDso for rats is 1,900 mg/kg; the oral LDso for mice is860 mg/kg. The dermal LDso f°r rabbits is 8,750 mg/kg.


Only limited data are available on the effects of1,2-dichloropropane on wildlife and domestic animals. The48-hour ECso is 52 mg/L in Daphnia maqna. The 96-hour ECso forthe bluegill is 300 mg/L; for the fathead minnow, it is139.3 .mg/L; and for the tidewater sliverside-, it is 240 mg/L.In an embryo-larval test, using the fathead minnow, chroniceffects developed at 8,100 ug/L.

B.7.0 TETRACHLOROETHENE (PCE) (Clement Associates, Inc.)


PCE was found to produce liver cancer in male and female micewhen administered orally by gavage. It is a Class B2carcinogen. Unpublished gavage studies in rats and miceperformed by the National Toxicology Program (NTP) showedhepatocellular carcinomas in mice and a slight, statisticallyinsignificant increase in a rare type of kidney tumor. Elevatedmutagenic activity was found in Salmonella strains treated withPCE* Delayed ossification of skull bones and sternebrae werereported in offspring of pregnant mice exposed to 2,000 mg/m3 ofPCE for 7 hours/day on days 6-15 of gestation. Increased fetal'resorptions were observed after exposure of pregnant rats totetrachloroethene. Renal toxicity and hepatotoxicity have beennoted following chronic inhalation exposure of rats to PCElevels of 1,356 mg/m3. During the first 2 weeks of a subchronicinhalatioa study, exposure to concentrations of 10,867 mg/m3 ofPCE .produced signs of central nervous system depression, andcholinerg.ic stimulation was observed among rabbits, monkeys,rats and guinea pigs.


PCE is the most toxic of the chloroethenes to aquatic organismsbut is only moderately toxic relative to other types ofcompounds. The limited acute toxicity data indicate that the

flR302!09

LCgo value for saltwater and freshwater species are similar,around 10,000 ug/L; the trout was the most sensitive(LCso = 4,800 ug/L). Chronic values were 840 and 450 ug/L forfreshwater and saltwater species, respectively, and an acute-chronic ratio of 19 was calculated. No information on thetoxicity of PCE to terrestrial wildlife or domestic animals wasavailable.

B.8.0 1,1,1-TRICHLOROETHANE ( 1,1,1-TCA)(Clement Associates, Inc.)


1,1,1-TCA was re-tested for carcinogenicity because earlylethality in a previous study precluded an assessment ofcarcinogenicity. Preliminary results indicate that 1,1,1-TCAincreased the incidence of combined hepatocellular carcinomasand adenomas in female mice when administered by gavage. Thereis evidence that 1,1,1-TCA is mutagenic in Salmonellatyphimurium and causes transformation in cultured rat embryocells. These data suggest that the chemical may becarcinogenic.

Other.toxic effects of 1,1,1-TCA are seen only at concentrationswell above those likely in an open environment. The mostnotable toxic . effects of 1,1,1-TCA in humans and animals arecentral nervous system depression, including anesthesia, at veryhigh concentrations and impairment of coordination, equilibrium,and judgment at lower concentrations (350 ppm and above);cardiovascular effects, including premature ventricularcontractions, decreased blood pressure, and sensitization toepinephrine-induced arrhythmia; and adverse effects on thelungs, liver, and kidneys. Irritation of the skin and mucousmembranes resulting from exposure to 1,1,1-TCA has also beenreported. The oral LDso value of 1,1,1-TCA in rats is about11,000 mg/kg.


The acute toxicity of 1,1,1-TCA to aquatic species is ratherlow, with_the LCso concentration for the most sensitive speciestested being 52.8 mg/L. No chronic toxicity studies have beendone on 1,1,1-TCA, but acute-chronic ratios for the otherchlorinated ethanes ranged from 2.8 to 8.7. 1,1,1-TCA was onlyslightly bioaccumulated with a steady-state 'bioconcentrationfactor of 9 and an elimination half-life of 2 days.

No information on the toxicity of 1,1,1-TCA to terrestrialwildlife or domestic animals was available in the literaturereviewed.

flR302MO

B.9.0 TRICHLOROETHENE (TCE) (Clement Associates, Inc.)


TCE is carcinogenic (Class B2) to mice after oraladministration, producing hepatocellular carcinomas. It wasfound to be mutagenic using several microbial assay systems.TCE does not appear to cause reproductive toxicity orteratogenicity. TCE has been shown to cause renal toxicity,hepatotoxicity, neurotoxicity, and dermatological reactions inanimals following chronic exposure to levels greater than2,000 mg/m3 for 6 months. TCE has low acute toxicity; the acuteoral LDso value in several species ranged from 6,000 to7,000 mg/kg.

B.9.2 TOXICITY TO WILDLIFE AND. DOMESTIC ANIMALS

There was only limited data on the toxicity of' TCE to aquaticorganisms. The acute toxicity to freshwater species was similarin the three species tested, with LCso values of about 50 mg/L.No LCso values were available for saltwater species. However, adose of 2 mg/L caused erratic swimming and loss of equilibriumin the grass shrimp. No chronic toxicity tests were reported.No information on the toxicity of TCE to domestic animals orterrestrial wildlife was available.

B.10.0. VINYL CHLORIDE '(Clement Associates, Inc.)


Vinyl chloride is considered to be a Class A human carcinogen,causing angiosarcomas of the liver and tumors of the brain,lung, and nemolymphopoietic system in humans. Vinyl chloride iscarcinogenic, in mice, rats, and hamsters; it produces tumors atseveral sites, including angiosarcomas of the liver, after oralor inhalation exposure. Vinyl chloride, both as a vapor and insolution, is mutagenic in several biological assay systems. Inaddition, chromosome aberrations including fragments, dicenticsand rings, breaks, and gaps have been found in workersoccupationally exposed to vinyl chloride. The evidence on itsteratogenic and reproductive effects is equivocal. Minorskeletal abnormalities and increased fetal death rates have beenobserved in the offspring of experimental animals exposed byinhalation to vinyl chloride. In humans, a significant increasein fetal deaths was seen in women whose husbands were exposed tovinyl chloride. Also, an excess number of central nervoussystem disorders and deformities of the upper alimentary tract,genital organs, and feet were observed in stillborn and livechildren born in cities with vinyl chloride facilities.However, further research is necessary before the link betweenvinyl chloride and these observed effects can be positivelyestablished. .

Acute occupational exposure to high concentrations of vinylchloride can produce symptoms of narcosis in humans.

0334906 B-7

AR302IM

Respiratory tract irritation, bronchitis, headache,irritability, memory disturbances, and tingling sensations mayalso occur. Chronic exposure to vinyl chloride is associatedwith multiple systemic disorders, including a scleroticsyndrome, acro-osteolysis, thrombocytopenia, and liver damageconsisting of damage to parenchymal cells, fibrosis of the livercapsule, periportal fibrosis associated with hepatomegaly, andsplenomegaly. Concentrations encountered by workers inindustries using or producing vinyl chloride are reportedlyquite variable and may range from less ' than the limit ofdetection to several grams per cubic meter.

Acute inhalation exposure of experimental animals to highconcentrations of vinyl chloride can result in narcosis anddeath. The 2-hour LCso value for rats is 390 g/m3. Chronicexposure of experimental animals can result in growthdisturbances and histopathological and histochemical lesions inthe liver, kidneys, spleen, and lungs.


No information is available concerning the toxicity of vinylchloride to domestic animals or wildlife.

B.11.0 BIS(2-ETHYLHEXYL)PHTHALATE (BEHP) .(Clement Associates, Inc.)

B.I1.1 HEALTH EFFECTS

BEHP is reported to be carcinogenic in rats and mice, causingincreased incidences of hepatocellular carcinomas or neoplasticnodules after oral administration. • • Its status as a humancarcinogen (Class B2) is considered indeterminate by theInternational Agency for Research on Cancer (IARC). The resultsof dominant lethal experiments with mice suggest that BEHP ismutagenic when injected intraperitoneally. However, mostexperiments conducted with microorganisms and mammalian cellshave failed to demonstrate genotoxic activity. Teratogenic andfetotoxic effects have been observed in experimental animalsafter oral. and intraperitoneal administration. Otherreproductive effects, including testicular changes in rats andmice, have also been reported. .

BEHP appears to have a relatively low toxicity in experimentalanimals. The oral, intraperitoneal, and intravenous LDso valuesreported for BEHP in rats are 31 g/kg, 30.7 g/kg, and 0.25 g/kg,respectively. BEHP is poorly absorbed through the skin, and noirritant 'response or sensitizing potential from dermalapplication has been noted in experimental animals or humans.

Chronic exposure to relatively high concentrations of BEHP inthe diet has caused' retardation of growth and increased liverand kidney weights in experimental animals.

0334906 B-8flR302M2


Acute median effect values ranged from 1,000 to 11,100 ug/L BEHPfor the freshwater cladoceran Daphnia maqna. The LCso values forthe midge, scud, and bluegill all exceeded the highestconcentrations tested, which were 18,000, 32,000, and770,000 ug/Lr respectively. As these values are greater thanthe water solubility of the chemical, it is unlikely that BEHPwill be acutely toxic to organisms in natural waters. In achronic toxicity test with Daphnia maqna, significantreproductive impairment was found at the lowest concentrationtested, 3 ug/L. A chronic toxicity value of 8.4 ug/L wasreported for the rainbow trout. No acute or chronic values werereported for saltwater invertebrates or vertebrates. Reportedbioconcentration factors for BEHP in fish and invertebratesrange from 14 to 2,680.

Although insufficient data were presented to calculate theacute-chronic ratio for BEHP, it is apparently on the order of100 to 1,000. Therefore, acute exposure to the chemical isunlikely to affect aquatic organisms adversely, but chronicexposure may have detrimental effects on the environment.

B.12.0 DICHLOROBENZENE (Clement Associates, Inc.)


It is generally thought that the available data are inadequatefor assessing the carcinogenic potential of DCB in animals andhumans. One case study suggests an association between exposureto dichlorobenzene and several cases of leukemia. DCB isreported to be nonmutagenic in Salmonella typhimurium testerstrains. Mutagenic and clastogenic activity reportedly occursin some plant test systems. No data are available forevaluating the teratogenic or reproductive effects in animals orhumans.

Symptoms of acute inhalation intoxication in humans includeheadache, nausea, and throat irritation. DCB is also a skin andeye irritant.

A variety of :other symptoms, including weakness, fatigue, andanemia, have been observed after chronic dermal and inhalationexposure to dichlorobenzene.

Inhalation of DCB causes eye and upper respiratory tractirritation, central nervous system depression, and liver andkidney damage in experimental animals. An LC20 of approximately4,900 mg/m3/7 hours is reported :for the rat. No toxic effectswere observed after daily 7-hour inhalation exposures of up to560 mg/m3 for as much as 7 months in several species ofexperimental animals. Hepatic porphyria is reported to occur inrats after daily tracheal intubation of 455 mg/m3 for up to15 days. Oral exposure results in stimulation of livermicrosomal enzyme systems and cumulative toxicity. The oral

0334906 3-9 '•

&R302M3

for the rat is 500 mg/kg. Chronic oral exposure to188 mg/kg/day causes liver and kidney damage in rats. Exposureto 0.01-0.1 mg/kg/day produces changes in the hematopoieticsystem, increased prothrombin time, and altered conditionedreflexes and enzyme activities in chronically exposed rats. Ingeneral, toxicity increases in the order 1,4-DCB, 1,3-DCB,1,2-DCB.


The 48-hour and 96-hour LCso values for daphnia and bluegills,respectively, tested under static conditions, we're 2,440 and5,590 ug/L (1,2-DCB); 28,100 and 5,020 ug/L (1,3-DCB); and11,000 and 4,280 ug/L (1,4-DCB). Two flow-through 96-hour LCsotests using fathead minnows and rainbow trout gave values ofabout 3,000 ug/L. A freshwater chronic value of 2,000 ug/L isreported for the fathead minnow. Acute values for threesaltwater species ranged from 1,970'ug/L for the mysid shrimp to9,660 ug/L for the sheepshead minnow. No saltwater chronicvalues are available. A whole body bioconcentration factor ofabout 8 is reported for the bluegill.

The 96-hour median effect levels for chlorophyll A and the cellnumber are 179,000 and 149,000 ug/L, respectively, in thefreshwater alga Selenastrum capricornutum. In the saltwateralga Skeletonema costatum the corresponding values are 44,200and 44,100 ]iq/L, respectively.

B.13.0 ISOPHORONE (ACGIH, 1980)


Exposure in the workplace to isophorone at concentrations of40 to 400 ppm resulted in eye, nose, and throat irritation,nausea, headache, dizziness, faintness, and inebriation. Atime-weighted average threshold limit value of 5 ppm (25 mg/m3)was recommended to. prevent fatigue and malaise. Nocarcinogenic, mutagenic, or teratogenic effects are reported forhumans.


No studies on the toxicity of isophorone to domestic animals orwildlife were found in the literature reviewed.

B.14.0 METHYLENE CHLORIDE (Clement Associates, Inc.)

B.I4.1 HEALTH- EFFECTS

Methylene chloride is currently under review by the NationalToxicology Program (NTP 1984, USEPA 1985). Preliminary resultsindicate that it produced an increased incidence of lung andliver tumors in mice and mammary tumors in female and male rats.In a chronic inhalation study, male rats exhibited an increasedincidence of sarcomas in the ventral neck region (Burek,

AR302II1,

et al.r 1984). However, the authors suggested that therelevance and toxicological significance of this finding wereuncertain in light of available toxicity data. Methylenechloride is reported to be mutagenic in bacterial test systems.It also has produced positive results in the Fischer rat embryocell transformation test. However, it has been suggested thatthe observed cell-transforming capability may have been due toimpurities in the test material. There is no conclusiveevidence that methylene chloride can produce teratogeniceffects.In humans, direct contact with methylene chloride produces eye,respiratory passage, and skin irritation (USEPA 1985). Mildpoisonings due to inhalation exposure produce somnolence,lassitude, numbness and tingling of the limbs, anorexia, andlightheadedness, followed by rapid and complete recovery. Moresevere poisonings generally involve correspondingly greaterdisturbances of the central and peripheral nervous systems.Methylene chloride also has acute toxic effects on the heart,including the induction of arrhythmia. Fatalities reportedlydue to methylene chloride exposure have been attributed tocardiac injury and heart failure. Methylene chloride ismetabolized _to carbon monoxide in vivo, and levels ofcarboxyhemoglobin in the blood are elevated after acuteexposures. In experimental animals, methylene chloride isreported to cause kidney and liver damage, convulsions, anddistal paresis. An oral LDso value of 2,136 mg/kg, and aninhalation LCso value of 88,000 mg/m3/30 min are reported for therat.

B.I 4. 2 TOXICITY TO WILDLIFE AND DOMESTIC ANIMALS

Very little information concerning the toxicity 'of methylenechloride to domestic animals and wildlife exists (USEPA 1980).Acute values for the freshwater species Daphnia maqna, thefathead minnow, and the blueg-11 are 224,000, 193,000, and224,000 ug/L, respectively. Acute values for the saltwaterspecies, mysid shrimp and sheepshead minnow, are 256,000 and331,000 ug/L,- respectively. No data concerning chronic toxicityare available. The 96-hour ECso values for both freshwater andsaltwater algae are greater than the highest test concentration,662,000

B.15.0 1 , 1-DICHLOROETHYLENE (Clements Associates, Inc.)

B.I 5.1 HEALTH EFFECTS

1,1-Dichloroethylene caused kidney tumors in males and leukemiain males and females in one study of mice exposed by inhalation,gave equivocal results in other inhalation studies, and gavenegative results in rats and mice following oral exposure and inhamsters following inhalation exposure. VDC was mutagenic inseveral bacterial assays. 1,1-Dichloroethylene did not appearto be teratogenic but did cause embryotoxicity and fetotoxicitywhen administered to rats and rabbits by inhalation. Chronic

D334906 . B-ll flR3Q2l15

exposure to oral doses of VDC as low as 5 mg/kg/day caused liverchanges in rats. Acute exposure to high doses causes centralnervous system depression, but neurotoxicity has not beenassociated with low-level chronic exposure. The oral LDso valuefor the rat is 1,500 mg/kg, and for the mouse it is 200 mg/kg.


1,1-Dichloroethylene is not very toxic to freshwater orsaltwater species, with acute LCso values generally ranging from80 to 200 mg/liter. A chronic study in which no adverse effectswere observed indicated that the acute-chronic ratio was lessthan 40; a 13-day study that produced an LCso of 29 mg/literindicated that the acute-chronic ratio is greater than 4.

No reports of the toxicity of 1,1-dichloroethylene toterrestrial wildlife or domestic animals were found in theliterature reviewed.

B.16.0 1,2-DICHLOROETHENE (Clements Associates, Inc.)


Very little information concerning exposure - only to 1,2-trans-DCE is available. There are no reports of carcinogenic orteratogenic activity by 1,2-trans-DCE in animals or humans. Itis reportedly nonmutagenic in a variety of test systems. Likeother members of the chlorinated ethylene series, 1,2-trans-DCEhas anesthetic properties. Exposure to high vaporconcentrations has been found to cause nausea, vomiting,weakness, tremor, and cramps in humans. Repeated exposure viainhalation of 800 mg/m3 (8 hours/day, 5 days/week, for 16 weeks)was reported to produce fatty degeneration of the'liver in rats.The intraperitoneal injection LD50 value for the rat is7,536 mg/kg.

Although nephrotoxic and cardiac sensitizing effects areassociated with exposure to 1,1-dichloroethylene, the 1,2-DCEisoraers have not been investigated with respect to this type ofeffects. 1,2-trans-Dichloroethylene can inhibit aminopyrinedemethylation in rat liver microsomes in vitro, and it may thusinteract with the hepatic drug-metabolizing monooxygenasesystem.


Practically no information concerning the toxicity of 1,2-trans-DCE to wildlife' and domestic animals exists. The reported96-hour LCSO value under static conditions is 135,000 ug/literfor the bluegill. Under the same test conditions, the LC5<> valuefor ' 1,1-dichloroethylene is 73,900 ug/liter. Recommendedcriteria for protection of aquatic life are based primarily ondata concerning 1,1-dichloroethylene.

0334906 B-12 AR302M6

B.17.0 CARBON TETRACHLORIDE (Clement Associates. Inc.)


Carbon Tetrachloride was carcinogenic in mice, rats, andhamsters; in all cases liver tumors were induced (IARC 1979,USEPA 1980). In addition, mice also displayed a high incidenceof tumors of the adrenal gland (Weisburger 1977). Studiesdiscussed by EPA (1980) on the mutagenic and teratogenic effectsof carbon tetrachloride and its impact on reproduction areinconclusive. Carbon tetrachloride also causes both liver andkidney damage in animals and humans. One study in which guineapigs were repeatedly exposed to carbon tetrachloride vapor forseveral months provided evidence of damage to the optic nerveand degeneration of the myelin sheath of the sciatic nerve(Smyth et al,, 1936).


Carbon tetrachloride has been shown to be acutely toxic toaquatic species at concentrations as low as 35 mg/liter. Nodata on chronic toxicity to aquatic life were reported in theliterature reviewed. Fish bioconcentrate carbon tetrachlorideby a factor of less than 50. No studies on the toxicity ofcarbon tetrachloride to domestic animals or terrestrial wildlifewere found in the literature reviewed.

B.18.0 CHROMIUM (Clement Associates, Inc.)


The hexavalent form of chromium is of major toxicologicalimportance in higher organisms. A variety of chromate (Cr VI)salts are carcinogenic in rats and an excess of lung cancer hasbeen observed among workers in the chromate-producing industry.Cr VI compounds can cause DNA ar.-i chromosome damage in animalsand humans, and Cr (VI) trioxide is teratogenic in the hamster.Inhalation of hexavalent chromium salts causes irritation andinflammation of the nasal mucosa, and. ulceration and perforationof the nasal septum. Cr VI also produces kidney damage inanimals and humans. The liver, is also sensitive to the toxiceffects of hexavalent Cr, but apparently less so than thekidneys or respiratory system. Cr III is less toxic than Cr VI;its main effect in humans is a form of contact dermatitis insensitive individuals.


Chromium is an essential nutrient and is accumulated in. avariety of aquatic and marine biota, • especially benthicorganisms, to levels much higher than in ambient water. Levelsin biota, however, usually are lower than levels in thesediments. Passage_of chromium through the food chain can bedemonstrated. The food chain appears to be a more efficientpathway for chromium uptake than direct uptake from seawater.

0334906 . B-13

Water hardness, temperature, dissolved oxygen, species, and ageof the test organism all modify the toxic effects of chromium onaquatic life. Cr III appears to be more acutely toxic to fishthan Cr VI; the reverse is true in long term chronic exposurestudies.None of the plants normally used as food or animal feed arechromium accumulators. Chromium absorbed by plants tends toremain primarily in the roots and is poorly translocated to theleaves. There is little tendency for chromium to accumulatealong food chains in the trivalent inorganic form. Organicchromium compounds, about which little is known, can havesignificantly different bioaccumulation tendencies. Littleinformation concerning the toxic effects of chromium onmammalian wildlife and domestic animal species is available.

B.19.0 LEAD (Clement Associates, Inc.)


There is evidence that several lead salts are carcinogenic inmice or rats, causing tumors of the kidneys after either oral orparenteral administration. Data concerning the carcinogenicityof lead in humans are inconclusive. The available data are notsufficient to evaluate the carcinogenicity of organic leadcompounds or metallic lead. There is equivocal evidence thatexposure to lead causes genotoxicity in humans and animals. Theavailable evidence indicates that lead presents a hazard toreproduction 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 tobe toxic. Exposure of humans or experimental animals to .leadcan result in toxic effects in. the brain and central nervoussystem, the peripheral nervous . system, the kidneys, and thehematopoietic system. Chronic exposure to inorganic lead byingestion or inhalation can cause lead encephalopathy, andsevere cases can result in permanent brain damage. Leadpoisoning may cause peripheral neuropathy in adults andchildren, and permanent learning .disabilities that- areclinically undetectable in children may be caused by exposure' torelatively low levels. Short-term exposure to lead can causereversible kidney damage, but prolonged exposure at highconcentrations may result in progressive kidney damage andpossibly kidney failure. Anemia, due to inhibition ofhemoglobin- synthesis and a reduction in the life span ofcirculating red blood cells, is an early manifestation of leadpoisoning. Several studies with experimental animals suggestthat lead may interfere with various aspects of the immuneresponse.

1R302II8


Freshwater vertebrates and invertebrates are more sensitive tolead in soft water than in hard -water. At a hardness of about50 mg/L CaCOs, the median effect concentrations for ninefamilies range from 140 ug/L to 236,600 ug/L. Chronic valuesfor Daphnia maqna and the rainbow trout are 12.26 and83.08 ug/L, respectively, at a hardness of about 50 mg/L.Acute-chronic ratios calculated for three freshwater speciesranged 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 of growth at concentrationsabove 500 ug/L.

Acute values for ' twelve saltwater species range from 476 ug/Lfor the common mussel to 27,000 ug/L for the soft-shell clam.Chronic exposure to lead causes adverse effects in mysid shrimpat 37 ug/L, but not at 17 ug/L. The acute-chronic ratio forthis species is 118. Reported bioconcentration factors rangefrom 17.5 for the Quahog clam to 2,570 for the blue mussel.Saltwater algae are adversely affected at approximate leadconcentrations as low as 15.8 ug/L.Although lead is known to occur in the tissue of many free-living wild animals, including birds, mammals, fishes, andinvertebrates, reports of poisoning usually involve waterfowl.There is evidence that lead, at concentrations occasionallyfound near roadsides and smelters, can eliminate or reducepopulations of bacteria and fungi on leaf surfaces and in soil.Many of these microorganisms play key roles in the decomposerfood chain.

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

B.20.0 MERCURY (Clement Associates, Inc.)


When administered by intraperitoneal injection, metallic mercuryproduces implantation site sarcomas in rats. No other studieswere found- connecting mercury exposure with carcinogenic effectsin animals or humans.- Several mercury compounds exhibit avariety of genotoxic effects in eukaryotes. In general, organicmercury compounds are more toxic than inorganic compounds.Although brain damage due to prenatal exposure to methylmercuryhas occurred in human populations, no conclusive evidence isavailable to suggest that mercury causes anatomical defects inhumans. Embryotoxicity and teratogenicity of methylmercury hasbeen reported for a variety of experimental animals. Mercuricchloride is reported .to be teratogenic in experimental animals.

0334906 B-15

AR3Q2I IS

No conclusive results concerning the teratogenic effects ofmercury vapor are available.

In humans, alkyl mercury compounds pass through the blood brainbarrier and the placenta very rapidly, in contrast to inorganicmercury compounds. Major target organs are the central andperipheral nervous systems, and the kidney. Methylmercury isparticularly hazardous because of the difficulty of eliminatingit from the body. In experimental animals, organic mercurycompounds can produce toxic effects in the gastrointestinaltract, pancreas, liver, heart, and gonads, with involvement ofthe endocrine, immunocompetent, and central nervous-systems.

Elemental mercury is not highly toxic as an acute poison.However, inhalation of high concentrations of mercury vapor cancause pneumonitis, bronchitis, .chest pains, dyspnea, coughing,stomatitis, gingivitis, salivation, and diarrhea. Solublemercuric salts are highly poisonous on ingestion, with oral LDsovalues of 20 to 60 mg/kg reported. Mercurous compounds are lesstoxic when administered orally. Acute exposure to. mercurycompounds at high . concentrations causes a variety ofgastrointestinal symptoms and severe anuria with uremia. Signsand symptoms associated with chronic exposure involve thecentral nervous system and include behavioral and neurologicaldisturbances.


The toxicity of mercury compounds has been tested in a , widevariety of aquatic organisms. Although methylmercury appears tobe more toxic than inorganic mercuric salts, few acute orchronic toxicity tests have been conducted with it. Amongfreshwater species, the 96-hour LCso values for inorganicmercuric salts range from 0.02 ug/L for crayfish to 2,000 ug/Lfor caddisfly larvae. Acute values for methylmercurie compoundsand other mercury compounds are -nly available for fishes. Inrainbow trout, methylmercuric chloride is about ten times moretoxic to rainbow trout than mercuric chloride, which is acutelytoxic at about 300 ug/L at 10°C. Methylmercury is the mostchronically toxic of the tested compounds, with chronic valuesfor Daphnia maqna and brook trout of 1.00 and 0.52 ug/L,respectively. The .acute-chronic ratio for Daphnia maqna is 3.2.

Mean acute values for saltwater species range from 3.5 to1,680 ug/L. In general, molluscs and crustaceans are moresensitive than fish to the acute toxic effects of mercury. Alife-cycle - experiment with the mysid shrimp showed thatinorganic mercury at a concentration of 1.6 ug/L significantlyinfluences time of appearance of first brook, time of first-spawn, and productivity. The acute-chronic ratio for the mysidshrimp is 2.9.

0334906 B-16AR302120

B.21.0 MANGANESE (Clement Associates, Inc.)

B.21.1 HEALTH EFFECTS .-

There are no epidemiological studies suggesting that manganeseor its compounds are carcinogenic or have teratogenic orreproductive effects in humans. Exposure to manganese chlorideby intraperitoneal or subcutaneous routes was reported to causelymphomas in mice. Manganese sulfate wasfound to producetumors after intraperitoneal administration in mice. No otherreports of unequivocal carcinogenic activity are available forcommon manganese compounds. Some manganese compounds, notablymanganese chloride, have exhibited mutagenic activity in avariety of test .systems. Manganese compounds do not appear tobe teratogenic, however.

In humans, manganese dusts and compounds have relatively loworal and dermal toxicity, but they can cause a variety of toxiceffects after inhalation exposure. Acute exposure to very highconcentrations can cause manganese pneumonitis, increasedsusceptibility to respiratory disease, and pathway changesincluding epithelial necrosis. Chronic manganese poisoning ismore common, but generally occurs only among personsoccupationally exposed to manganese compounds. Degenerativechanges in the central nervous system are the major toxiceffects. Early symptoms include emotional changes, followed bya masklike face, retropulsion or propulsion and a Parkinson'slike syndrome. Liver changes are also frequently seen.Individuals with an iron deficiency may be more susceptible tochronic poisoning.

•Duplication of human exposure symptoms' in experimental animalshas only been partially successful. In rabbits exposure byinhalation to manganese dust, manganese pneumonitis did notdevelop, but fibrotic changes in the lungs were observed.Central nervous system effects characteristic of chronicexposure in humans have only been reproduced in monkeys.


Adequate data for characterization of the toxicity of manganeseto wildlife or domestic animals are not available.

A 48-hour LCso value of 16 mg/liter of manganese is reported forembryos of the oyster Crassostrea virqinica. For the softshellclam Mva --arenaria a 168-hour CC50 value of 300 mg/liter isreported. • .

0334906 B-17 AR302I2I

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APPENDIX C

RISK ASSESSMENT CALCULATIONS

D33490&

APPENDIX C.I

REPRESENTATIVE CONTAMINANT CONCENTRATIONS

30

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The W test developed by Shapiro and WHk (1965) is an effective method fortesting whether a data set hasbeen drawn from an underlying normal distribution.Furthermore, by conducting the test on the logarithms of the data, it is anequally effective way of evaluating the hypothesis of a lotmormai distribution.

We suppose that n £ 50 data. *•, *-,. . . . , jc_. have been drawn at randomfrom some population." The null hypothesis to be tested is

H0: The population has a normal distribution

versus

HA: The population does not have a normal distribution

If H0 is rejected, then HA is accepted. If H0 is not rejected, the data set isconsistent with the HO distribution, although a retest using additional data couldresult in rejecting HO-

The W test of this Hp is conducted as follows:

1. Compute the denominator d of the W test statistic, using the n data.

d - i: & - j):»i: *? - - f i *\ • 12.3i.i 1-1 n V• - /

2. Order the n data from smallest to largest to obtain the sample order statistics*•„ * xm * • • • * .r,.,.

3. Compute k. where, n ., .k ** - if n is even

_ iif n is odd

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4. Turn to Table A6 and for the observed n find the .coefficients a,. a:.. . . . at-

5. Then computei r * fW~-\ Z a-U,..-.-- -*,,,) 12.4a U - ' J

6. Reject H0 at the a significance level if W is less than the quantile given inTable A7.

To test the null hypothesisH0: The population has a lognormal distribution

versusHA: The population does not have a lognormal distribution

the preceding procedure is used on the logarithms of the data. That is. wecompute d (Eq. 12.3), using y,, -y,, . . . , y_. where y- « In x,, and we usethe sample order statistics of the logarithms >-()- £ y-2- s. • • • z >-,„, in placeof the *•-, in Eq. 12.4.

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