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PETITIONED PUBLIC HEALTH ASSESSMENT

SOUTHERN MARYLAND WOOD TREATING
NATIONAL PRIORITIES LIST (NPL) SITE
HOLLYWOOD, ST. MARY'S COUNTY, MARYLAND


APPENDIX 1 - FIGURES


Figure 1. USGS Map - Site Location


Figure 2. Site-Related Surface Waters


Figure 3. Tanks and Buildings Map


Figure 4. Groundwater Flow Direction Shallow Aquifer


Figure 5. Groundwater Flow Direction Upper Chesapeake Aquifer


Figure 6. Wind Rose


Figure 7. Monitoring Wells and Soil Sampling Locations


Figure 8. Soils to Be Remediated


Figure 9. Stream Sampling Locations


Figure 10. EPA Residential Well Sampling Locations



APPENDIX 2 - TABLES

TABLE 1. CONTAMINANTS IN ON-SITE SOILS & SEDIMENTS AT SMWT1

Table 1.

Human Health Effects at Various Hydrogen Sulfide Concentrations in Air
CONTAMINANT MAXIMUM CONCENTRATION (ppm)2COMPARISON VALUE
SOILSSTREAM
SEDIMENT
CONCENTRATION
(ppm)
REFERENCES2,3
SURFACESUBSURFACE
BenzeneNDNDNDNANA
2,4-DimethylphenolND0.92ND1,000RfD Child
Ethylbenzene12.*NDND5,000RfD Child
2-MethylphenolND0.97ND2,500RfD Child
4-Methylphenol100.J*4.9ND2,500RfD Child
Pentachlorophenol13090.J795.8CREG
Styrene8.8*NDND10,000RfD Child
Toluene 8.3*NDND10,000RfD Child
Total Xylenes42.*NDND100,000RfD Child
Carcinogenic PAHs1,2373,33424.6 J0.29EPA4
Noncarcinogenic PAHs3,01925,34061.1200RfD Child5
2,3,7,8-TCDD62.8 x 10-5*NDND5 x 10-5EMEG Child
2,3,7,8-TCDD Toxic
Equivalent 3
3.5 x 10-5*ND0.9 x 10-55 x 10-5EMEG Child
METALS
Chromium, Total21.*18.215.2250RfD Child
Lead13411.8167500ATSDR-19911
Mercury, Total0.15*0.530.1115RfD
1 References used: 1, 10, 19, 21, 22, 23, 26
2 See Appendix 3 for definitions.
3 See Appendix 3A for comparison value calculations.
4 Used benzo(a)pyrene comparison value for the group (interim cancer slope factor).
5 Used naphthalene comparison value for the group.
6 2,3,7,8-Tetrachloro-di-benzo-p-dioxin
NA = none available     ND = none detected     J = Analyte present but reported value is estimated     * Composite boring samples.


TABLE 2.

CONTAMINANTS IN ON-SITE WATER AT SMWT1
CONTAMINANT MAXIMUM CONCENTRATION (ppb)2 COMPARISON VALUE
AQUIFERS POND CONCENTRATION
(ppb)
REFERENCES2,3
SHALLOW UPPER CHESAPEAKE
Benzene 1,400 ND 10 1.2 CREG
2,4-Dimethylphenol 12,000 ND 40 200 RfD Child
Ethylbenzene 220 ND 5 1,000 RfD Child
2-Methylphenol 28,900 ND 60.J 500 RfD Child
4-Methylphenol 89,100 ND 31 500 RfD Child
Pentachlorophenol 5,000 ND 120 0.3 CREG
Styrene 240 ND ND 1.17 CREG
Toluene 900 ND 13 2,000 RfD Child
Total Xylenes 480 ND 10.J 2,000 RfD Child
Carcinogenic PAHs 11,800 ND 41 0.2 MCL4
Noncarcinogenic PAHs 79,200 ND 187 100 DWEL5
2,3,7,8-TCDD6 39.5 x 10-5 NA

ND

1 x 10-5 EMEG Child
2,3,7,8-TCDD Toxic
Equivalent 3
54.6 x 10-5 NA

ND

1 x 10-5 EMEG Child
METALS (filtered samples)
Chromium, Total 156 75 ND 50 EMEG Child
Lead 52 ND ND 50 MCL
Mercury, Total 2.3 0.9 ND 2 MCLG
1 References used: 1, 10, 19, 21, 22, 23, 26
2 See Appendix 3 for definitions.
3 See Appendix 3A for comparison value calculations.
4 Used benzo(a)pyrene comparison value for the group.
5 Used naphthalene comparison value for the group.
6 2,3,7,8-Tetrachloro-di-benzo-p-dioxin
NA = none available     ND = none detected     J = Analyte present but reported value is estimated.


TABLE 3.

CONTAMINANTS IN WASTES AT SMWT1
CONTAMINANT MAXIMUM CONCENTRATION
TANK LIQUIDS
(ppb)2,3
TANK SOLIDS
(ppm)2,4
Benzene 11,000 ND
2,4-Dimethylphenol 560 ND
Ethylbenzene 75,000 3.3
2-Methylphenol 3,310 ND
4-Methylphenol 385,000 ND
Pentachlorophenol 4,200,000 21,000
Styrene 26,000 3.6
Toluene 39,000 ND
Total Xylenes 73,000 12
Carcinogenic PAHs 20,000,000 21,800
Noncarcinogenic PAHs 34,910,000 43,500
2,3,7,8-TCDD5 ND ND
2,3,7,8-TCDD Toxic Equivalent 3 58 0.087 x 10-5
METALS
Chromium, Total 100,000 23.3
Lead 732,000 186.
Mercury, Total 40,000 9.6
1 References used: 1, 10, 19, 21, 22, 23, 26
2 See Appendix 3 for definitions.
ND = none detected
3 Use comparison values in Table 2.
4 Use comparison values in Table 1.
5 2,3,7,8-Tetrachloro-di-benzo-p-dioxin



TABLE 4. CONTAMINANTS IN OFF-SITE SOILS & SEDIMENTS AT SMWT1

Table 1.

Human Health Effects at Various Hydrogen Sulfide Concentrations in Air
CONTAMINANT MAXIMUM CONCENTRATION (ppm)2 COMPARISON VALUE
SOILS STREAM SEDIMENTS CONCENTRATION
(ppm)
REFERENCES2,3
SURFACE SUBSURFACE
Benzene

ND

ND ND NA NA
2,4-Dimethylphenol

ND

ND ND 1,000 RfD Child
Ethylbenzene

ND

ND ND 5,000 RfD Child
2-Methylphenol

ND

ND ND 2,500 RfD Child
4-Methylphenol

ND

ND ND 2,500 RfD Child
Pentachlorophenol

ND

ND 240 5.8 CREG
Styrene

ND

ND ND 10,000 RfD Child
Toluene

ND

ND ND 10,000 RfD Child
Total Xylenes

ND

ND 15.J 100,000 RfD Child
Carcinogenic PAHs 25.2 0.68 7.78 0.29 EPA4
Noncarcinogenic PAHs 4.88 0.09 15.08 200 RfD Child5
2,3,7,8-TCDD6

NA

NA ND 5 x 10-5 EMEG Child
2,3,7,8-TCDD Toxic
Equivalent 3

NA

NA 1 x 10-5 5 x 10-5 EMEG Child
METALS
Chromium, Total 15 8.9* 28 250 RfD Child
Lead 13 7.7* 167 500 ATSDR-1991
Mercury, Total 0.88 0.53 J* 0.2 15 RfD
1 References used: 1, 10, 19, 21, 22, 23, 26
2 See Appendix 3 for definitions.
3 See Appendix 3A for comparison value calculations
4 Used benzo(a)pyrene comparison value for the group (interim cancer slope factor).
5 Used naphthalene comparison value for the group.
6 2,3,7,8-Tetrachloro-di-benzo-p-dioxin value.
NA = none available     ND = none detected     J = Analyte present but reported value is estimated.     * Composite sample from Monitoring Well 07.


Table 5.

CONTAMINANTS IN OFF-SITE WATER AT SMWT1
CONTAMINANT MAXIMUM CONCENTRATION (ppb)2 COMPARISON VALUE
AQUIFERS STREAMS CONCENTRATION
(ppb)
REFERENCES2,3
SHALLOW UPPER CHESAPEAKE
Benzene

ND

ND

ND

1.2 CREG
2,4-Dimethylphenol

ND

ND

47 200 RfD Child
Ethylbenzene

ND

ND

ND

1,000 RfD Child
2-Methylphenol

ND

ND

ND

500 RfD Child
4-Methylphenol

ND

ND

ND

500 RfD Child
Pentachlorophenol

ND

ND

82 0.3 CREG
Styrene

ND

ND

ND

1.17 CREG
Toluene

ND

ND

ND

2,000 RfD Child
Total Xylenes

ND

ND

ND

2,000 RfD Child
Carcinogenic PAHs 5 J

ND

ND

0.2 MCL4
Noncarcinogenic PAHs 16 J

ND

44 100 DWEL5
2,3,7,8-TCDD6

NA

NA

ND

1 x 10-5 EMEG Child
2,3,7,8-TCDD Toxic
Equivalent 3

NA

NA

ND

1 x 10-5 EMEG Child
METALS (filtered samples)
Chromium, Total 290

ND

ND

50 EMEG-Child
Lead 110

ND

12* 50 MCL
Mercury, Total 2.9

NA

0.3 J 2 MCLG
1 References used: 1, 10, 19, 21, 22, 23, 26
2 See Appendix 3 for definitions.
3 See Appendix 3A for comparison value calculations.
4 Used benzo(a)pyrene comparison value for the group.
5 Used naphthalene comparison value for the group.
6 2,3,7,8-Tetrachloro-di-benzo-p-dioxin
NA = none available     ND = none detected     J = Analyte present but reported value is estimated.
* Only lead detected in stream sample was at T24 (inlet to pond at Morgan Road).


Table 6.

EXPOSURE PATHWAYS AT SMWT
Pathway Name Exposure Pathway ElementsTime
Source COCs1MediaPoint of ExposureRoute of
Exposure
Exposed Population
Completed Exposure Pathways
On-site workersWood-treating chemicals-unknown concentrationsAir - direct contact withchemicalsPlant operationsDermalInhalationIngestionSMWT plant employees - unknown numberPast
Off-site airEmissions from SMWT plantoperationsAirResidue on houses
Air emissions
Dermal
Inhalation
Nearby residents - unknown numberPast
Potential Exposure Pathways
On-site mediaPhenolic compounds
PAHs2, VOCs3, metals
Soil, air, surface water,sediments Direct contact withcontaminated mediaDermalInhalationIngestionTrespassers - unknown number and unknown activities.Past
Off-site sedimentsPCP4, cPAHs2Stream sedimentsOld Tom's Run (see Fig. 6)DermalIngestionChildren playing in stream - unknown number, unknownfrequency and duration of exposure.Past,present,future
Off-site groundwaterVOCs3, phenolic compounds,PAHs2, PCDD5, metalsGroundwater - presently,shallow aquifer affectedResidential wells downgradientof SMWT siteDermalInhalation IngestionResidents using private wells downgradient of the siteshould deeper aquifers become contaminated.Future
Eliminated Exposure Pathways
Remedial workersVOCs3, phenolic compounds,PAHs2, PCDD5, metalsSoil, air, surface water,sediments, groundwaterSampling of all media and otherremedial activitiesDermalInhalationIngestionRemedial workers - unlikely because appropriate safetyprocedures and PPE6 are required for on-site activities.Past,present,future
On-site buildingsPAHs2, PCP4Building surfacesDirect contact with buildingsDermalInhalationNone - Building samples were collected from treatedtimbers which do not pose a health concern.Past
Off-site soilsPAHs2Surface soilsDirect contactDermalIngestionChildren playing in the area with contaminated surface soil.Exposure is unlikely as the area is covered with grass,briars, and thorny locust saplings.Past,present,future
Food chainPAHs2, PCP4, mercuryFishOld Tom's RunIngestionNone - no edible fish populations exist.Past,present,future
1. COCs = contaminants of concern   2. PAHs = polynuclear aromatic hydrocarbons   3. VOCs = volatile organic compounds   4. PCP = pentachlorophenol   5. PCDD = polychlorinated-di-benzo-p-dioxin 6. PPE = personal protective equipment.


APPENDIX 3 - COMPARISON VALUES

Comparison values for ATSDR public health assessments arecontaminant concentrations in specific media (soil, air, andwater) that are used to select contaminants for furtherevaluation. The values provide guidelines for estimating dosesat which adverse health effects might occur. Comparison valuesand the units used to quantitate contaminant concentrations thatappear in the Environmental Contamination and Other Hazards andthe Public Health Implications sections of this public healthassessment are listed and described below.

Comparison Values
* CREG= Cancer Risk Evaluation Guides
* DWEL= Drinking Water Equivalent Level (µg/L)
* EMEG= Environmental Media Evaluation Guides
* MCL= Maximum Contaminant Level (µg/L)
* MCLG= Maximum Contaminant Level Goal (µg/L)
* MRL= Minimal Risk Level (mg/kg/day)
* PEL= Permissible Exposure Limit (mg/m3)
* RfD= Reference Dose (mg/kg/day)


Units
* ppm= milligrams per liter (mg/L water)
    milligrams per kilogram (mg/kg soil)
* ppb= micrograms per liter (µg/L water)
    micrograms per kilogram (µg/kg soil)
* kg= kilogram
* mg= milligram
* µg= microgram
* pg= picogram
* L= liter
* m3= meters cubed

Cancer Risk Evaluation Guides (CREGs) are estimated contaminantconcentrations that are expected to cause no more than one excesscancer in a million (10E-6) persons exposed over a lifetime (70years). CREGs are calculated from EPA's cancer slope factors.

EPA has not established a final cancer slope factor forbenzo(a)pyrene. Therefore, the comparison value used forcarcinogenic PAHs is based on an interim cancer slope factor.

The drinking water equivalent level (DWEL) is a lifetime exposurelevel specific for drinking water (assuming that all exposure isfrom that medium) at which adverse, noncarcinogenic healtheffects are not expected to occur.

Environmental Media Evaluation Guides (EMEGs) are based on ATSDRminimal risk levels (MRLs) and factor in body weight andingestion rates.

Maximum Contaminant Levels (MCLs) represent chemicalconcentrations that EPA deems protective of public health(considering the availability and economics of water treatmenttechnology) over a lifetime (70 years) at an exposure rate of 2liters of water per day (for an adult).

Maximum Contaminant Level Goals (MCLGs) are drinking water healthgoals set at levels at which no known or anticipated adverseeffects on the health of persons occurs and which allows anadequate margin of safety. Such levels consider the possibleimpact of synergistic effects, long-term and multi-stageexposures, and the existence of more susceptible groups in thepopulation. When there is no safe threshold for a contaminant,the MCLG should be set at zero.

A Minimal Risk Level (MRL) is an estimate of daily human exposureto a chemical (in mg/kg/day) that is not likely to cause anappreciable risk of deleterious effects (noncarcinogenic) over aspecified duration of exposure. MRLs are based on human andanimal studies and are reported for acute (< 14 days),intermediate (15-364 days), and chronic (> 365 days) exposures. MRLs are published in ATSDR Toxicological Profiles for specificchemicals.

The Occupational Safety and Health Administration's PermissibleExposure Limit (PEL) in air is an 8-hour, time-weighted averagedeveloped for the workplace. The level may be exceeded, but thesum of the exposure levels averaged over 8 hours must not exceedthe limit.

EPA's Reference Dose (RfD) is an estimate of the daily exposureto a contaminant that is unlikely to cause adverse healtheffects. However, RfDs do not consider carcinogenic effects.

APPENDIX 3A. Comparison Value Calculations

The following formula was used to calculate soil comparisonvalues from RfDs for volatile and semivolatile organic compoundsand metals; and MRLs for PAHS and 2,3,7,8-TCDD and congeners. Soil ingestion of 0.0002 kg/day for a reference child weighing 10kg was assumed.

Cs (mg/kg)   =10(kg) x RfD or MRL (mg/kg/day)
0.0002 (kg/day)
(1)

2,3,7,8-TCDD Toxic Equivalent

The 2,3,7,8-TCDD toxic equivalent is a weighted concentration oftotal polychlorinated dibenzo-p-dioxins (PCDDs)in a mixture thatcompensates for the differences in toxicity among the 2,3,7,8-TCDD analogs. The relative weight of 2,3,7,8-TCDD (tetra) is 1;2,3,7,8-PeCDD (penta) is 0.5; 2,3,7,8-HxCDD (hexa) is 0.1;2,3,7,8-HpCDD (hepta) is 0.001; and other PCDDs are 0. Usingthat convention, the concentration of each isomer in a mixture ismultiplied by the appropriate factor (listed above) and the sumof all the weighted PCDDs in the mixture is represented by the2,3,7,8-TCDD Toxic Equivalent (2).


COMPARISON VALUE REFERENCES

  1. Agency for Toxic Substances and Disease Registry. Health Assessment Guidance Manual. Atlanta: ATSDR, March 1992.
  2. Final Remedial Investigation/Feasibility Study Report forthe Southern Maryland Wood Treating Site, Hollywood,Maryland, Volume I, CDM Federal Programs Corporation, May1988.

APPENDIX 4 - TOXICOLOGICAL PROFILE SUMMARIES

TOXICOLOGICAL PROFILE SUMMARIES

NOTE OF EXPLANATION:

Brief discussions of the toxicology of existing contaminants atthe SMWT site are included in this appendix. Under presentconditions, the contaminants associated with the SMWT site arenot expected to cause illness or disease either in the localpopulations or in properly protected remedial workers. Thehealth effects described in this appendix result from higherdoses than those associated with possible exposure at the SMWTsite. Because access to the site is restricted, even exposure atlower doses is unlikely.

BENZENE

Benzene is released into the atmosphere from both natural andartificial processes. The most significant source appears to befrom the burning of gasoline. Levels of benzene measured in theatmosphere range from 1.3 ppb (parts per billion) in rural areasto 64.619 ppb in urban areas.

Benzene is one of the few compounds for which sufficient evidence exists of its ability to cause cancer in humans. Benzene has been associated with increases in leukemia, and itcauses a deficiency in all cells in the blood and anemia (failureof the bone marrow to make blood cells). Those effects are seenat levels of 20 ppm (parts per million - 1 ppm equals 1000 ppb).Benzene is also known to cause menstrual disturbances in women atdoses of 31 ppm. In animals, it interferes with fertility.

Benzene is considered sufficiently toxic that its use has beencurtailed. Previously one of the most common industrialsolvents, it is now rarely used. The main reason for thereduction in use has been concern about its ability to causeleukemia after long-term, low-level exposures. Benzene affectsthe blood, the central nervous system, the skin, the bonemarrow's ability to generate new white blood cells, the eyes, andthe respiratory system. Acute benzene exposure can causeirritation of the upper respiratory tract, dermatitis, and localirritation. Chronic exposure can result in anemia (leading toleukemia) and immunodepression. Benzene also causes increasedmammary tumors and chromosomal damage in bone marrow cells. Benzene is toxic to the fetus and embryo.

CREOSOTE

The toxicology of creosote is difficult to assess because it isactually a complex mixture of substances. Creosote is known tocontain polynuclear aromatic hydrocarbons (PAHs). Some of thesubstances in it are known to be carcinogens. However, thecancer-causing potential of the complex mixture referred to ascreosote is not known.

Dermal contact accounts for the majority of exposures tocreosote. Creosote can cause conjunctivitis and dermatitis(which is mild in 70% of reported cases). It is phototoxic,causing sunburn at low levels of sun exposure. It is uncertainwhether chronic occupational exposure causes skin cancers. Thereare very few data on cresote's toxicity to humans or animalsfollowing ingestion or inhalation.

PENTACHLOROPHENOL

Data on the toxicity of pentachlorophenol (PCP) are limited. Most exposure to PCP is by skin contact. It is known to causedermatitis and ulcers of the cornea, and it is reported to beassociated with the skin condition pemphigus vulgaris. Aplasticanemia (failure of the bone marrow to make all types of bloodcells), elevated body temperature, abdominal pain, and swellingand congestion of the lungs are effects that have been seen atvery high, but not fully characterized, levels of exposure.

Data on PCP's toxicity following inhalation or ingestion arelimited. Levels of 0.09 ppm are associated with eye irritation,and the Occupational Safety and Health Administration (OSHA) hasset a standard of 0.05 ppm as the threshold limit value (TLV) forexposure of workers during an eight-hour shift.

Based on animal hematologic (blood) effects, a minimal risk level(MRL) has been established at 0.05 mg/kg/day orally for acuteingestion and 0.002 mg/kg/day orally for intermediate ingestionexposures. The MRL is the level at which there is expected to beno toxicity for noncancer outcomes. PCP can be detected by smellat levels of 1.6 ppm in water.

Some animal tests suggest that PCP may cause cancer followingdermal exposure. The data in humans or animals are insufficient,however, to determine its carcinogenic potential.

CHROMIUM

Chromium is used in plating and making special steels, andchromium salts are used as dye mordants, tanning agents,pigments, wood preservatives, anticorrosives, and cleaningagents. Industrial usage and combustion of fossil fuels (autoand power plant emissions) are the major sources of chromiumrelease into the environment. Various ionic states occur insalts between +2 and +6, but only +3 and +6 are biologicallyactive. Trivalent (+3) chromium ions are virtually non-toxic,while hexavalent (+6) forms are irritants, corrosive, andcarcinogenic. Trivalent salts are poorly absorbed into the body;hexavalent salts are very well absorbed. Hexavalent forms areconverted to the trivalent state in cells after crossing the cellmembrane, and may bind cellular components during thisconversion. However, trivalent ions are not converted tohexavalent forms. Chromium is an essential element inmaintaining the integrity of blood vessels, RNA, insulin action,and carbohydrate metabolism. Chromium deficiency can causeincreased levels of serum cholesterol. Chromium and many of itssalts cause severe contact dermatitis. Dermatitis can resultfrom a single high dose or repeated low doses over years ofexposure. Chromium also sensitizes the skin to contactdermatitis; thus, a second dose can cause much greater damage. In addition, chromium can cause stomach and lung irritation. Nasal irritation, bronchitis, asthma, and cancer of the nasaltract can result from high or repeated doses. Liver and kidneytoxicity (necrosis of proximal tubule; sensitization to furtherdamage) may occur. Chromium causes both immunodepression andimmunosensitization. Some persons have allergic responses tochromium. Hexavalent chromium is highly water soluble and canleach into groundwater.

LEAD

Lead accumulates in body reservoirs from which it is releasedslowly over time in small amounts, or, under stress, more rapidlyin larger amounts. Lead primarily affects the peripheral andcentral nervous systems, blood cells, and vitamin D and calciummetabolism. Severe lead intoxication can cause death. Effects oflead on the nervous system include decreased nerve conductionspeeds, lowered IQ, damage to nerve cells, lowered coordinationand motor skills, and seizures. Kidney damage also occurs, withproximal tubular impairment leading to a gout-like condition. Lead affects reproduction by reducing sperm counts and motility. Lead crosses the placenta, increases the number of miscarriagesand stillbirths, and affects the viability and development of thefetus. Lead affects the blood, producing anemia, hypertension,and reduced hemoglobin synthesis. It also affects vitamin Dhormonal activities regulating calcium storage and mobilization. Lead may be a renal carcinogen. The development of lead toxicityand its effects depend upon the dose received, the duration ofexposure, and individual variation. However, lead effects areoften independent of the route of exposure. Lead is particularlytoxic to children, because it affects physiologic systemsimportant to their development and maturation.

MERCURY

Mercury exists in two forms with different biologic effects. Inorganic, metallic mercury (often absorbed as a vapor) is themore acute threat because it can cross the tissue barrier betweenthe blood and the brain, causing central nervous system effects. Organic mercury is in a different ionic state and cannot crossthe blood-brain barrier. In soil, the two forms interconvert. Low doses of inorganic mercury are generally not damaging to thecentral nervous system because the inorganic mercury can bemetabolized to the organic form, and is then unable to cross theblood-brain barrier. However, larger doses of inorganic mercurycan saturate the metabolic system and not be converted to organicmercury, thus allowing inorganic mercury to enter the brain. Solubility, biotransformation, and tissue distribution depend onvalence (salt form); the mechanism of toxicity depends on thecationic mercury itself, regardless of valence. Organicmercurials are generally more toxic in parts of the body otherthan the brain.

Mercury bioaccumulates and bioconcentrates in the food chain. Natural sources of mercury release much greater amounts thanindustrial sources. Mercury is used as an industrial catalyst insmelting and paper pulping. Burning of coal and petroleum mayrelease large amounts of mercury. Mercury is fetotoxic,neurotoxic (both peripheral and central), and affects thekidneys. It is not, however, considered carcinogenic. Toxicityvaries with dose, route, duration of exposure, and individualsusceptibilities.

High-dose exposure to inorganic, metallic mercury can result indeath due to respiratory edema, shock, acute renal failure, andcardiovascular collapse. Severe gastrointestinal damage maycontribute to death. Damage to the lungs and degeneration andnecrosis of heart muscle may occur; damage to blood cells isinfrequent. Inorganic mercury poisoning can cause anorexia,abdominal cramps, nausea, gingivitis, damage to the mucosa of thestomach, and liver necrosis. The kidney concentrates mercury,resulting in reduced kidney function, degeneration of convolutedtubules, reduced filtration, and edema. Kidney damage appears tobe the result of an immune response. Mercury can also have toxiceffects in the skin and eye. Neurologic signs may beirreversible, and may include tremors, insomnia, shyness,emotional instability, decreased motor function, decreasedmuscular reflexes, headaches, irregular brain wave patterns,lowering of peripheral nerve conduction velocities, and loss ofshort-term memory. Central nervous system effects are very dose-specific because metabolism tends to lower the ability ofinorganic mercury to enter the brain. Inorganic mercury also hasreproductive effects.

Exposure to large amounts of organic mercury has resulted indeath, but the cause is uncertain. The major toxicity of organicmercury exposure is degeneration of nerve cells in the brain.That nerve damage can be observed as tingling of extremities,tunnel and impaired vision, altered senses of taste, hearing, andsmell, slurred speech, unsteadiness of gait, muscle weakness andincoordination, irritability, memory loss, and depression. Kidney damage may include tubular necrosis, fibrosis, andinflammation. Changes in blood pressure occur, along withdecreased thymus and spleen weights, and immunodepression. Organic mercury can be fetotoxic, causing derangement of basiccentral nervous system development, and a reduction in fetalsurvival rates. Neonatal death can occur, as can alterations andderangements in postnatal development of the eye, behavioralmaturation, and learning ability.

POLYNUCLEAR AROMATIC HYDROCARBONS
(PNAs, PAHs, or Polycyclic Aromatic Hydrocarbons)

In general, PAHs are formed as products of ordinary combustionand thus are ubiquitous. They are found in smoke, tobacco smoke,soot, and coal. They are generally natural products, have noknown use, and are slowly biodegraded. Carcinogenic PAHs tend tobe metabolized into more reactive forms. Little is known aboutnoncancer toxicity, although some PAHs are fetotoxic, andreproductive toxicity may occur at high doses. Some carcinogenicforms are immunosuppressive and/or genotoxic in in vitro tests. PAHs generally have low water solubility and strong absorption tosoil, and thus do not migrate in the environment. PAHsbioaccumulate and bioconcentrate in the food chain, but arefairly rapidly excreted. They may interact with each other,enhancing or reducing carcinogenic potential (reduction is themore common experimental result), but those interactions are ill-defined for most PAHs.

NONCARCINOGENIC PAHs

Certain PAHs are not known to cause cancer. They includeacenaphthene, acenaphthylene, anthracene, fluoranthene, fluorene,methylated naphthalenes, naphthalene, phenanthrene, and pyrene.

ACENAPHTHENE

Acenaphthene affects skin, liver, kidneys, and lungs, resultingin weight loss, vomiting, changes in peripheral blood, andincreased serum aminotransferase. Morphologic changes occur inliver and kidneys. Bronchitis and inflammation of peribronchialtissue, lung hyperplasia, and metaplasia of bronchial epitheliummay be long-term consequences of acenaphthene exposure.

ACENAPHTHYLENE

Acenaphthylene affects the liver, kidneys, and lungs, resultingin weight loss, changes in peripheral blood, increased serumaminotransferase, a non-specific pneumonia, and changes in kidneyfunction.

ANTHRACENE

Anthracene affects skin, blood, and the eyes. This PAH interactswith light, causing phototoxicity and photoallergenic responses. On skin, anthracene may cause dermatitis, burning, itching, andedema. In the eyes, it may cause tearing, increased sensitivityto light, and swelling of the eye lids. It has low gastrictoxicity. Anthracene can increase skin pigmentation andhardening. Other known effects include headache, nausea, andloss of appetite.

FLORANTHENE

Floranthene can cause skin irritation and photosensitization, eyeirritation, and liver enzyme induction.

FLUORENE

Fluorene has been little studied, and its effects are largelyundetermined. It is considered noncarcinogenic, but is a liverenzyme inducer.

NAPHTHALENE

Naphthalene affects the eyes, skin, liver, kidney, and centralnervous system. It can cause jaundice, fever, oliguria, liverand kidney damage (renal tubule blockage), malaise, nausea,abdominal pains, and bladder irritation. Nervous system effectsinclude convulsions, headache, and confusion. Toxicity in theeyes results in lens opacity and cataracts. Blood effectsinclude red cell fragmentation, decreased hemoglobin, and reducedred blood cell count and hematocrit. Skin effects includerepeated reddening and dermatitis. Fetuses can be damaged aswell. No birth defects are known to occur.

PHENANTHRENE

Phenanthrene primarily causes skin damage, such as irritation,photosensitization, and allergic responses. Phenanthrene is onlyslightly toxic orally. It causes no known terata (birthdefects), fetotoxicity, or reproductive toxicity.

PYRENE

There are limited data on the toxicity of pyrene. Pyrene is askin irritant and it may cause liver damage. It is considerednon-carcinogenic.

CARCINOGENIC PAHs

Sufficient evidence exists to accept that the following PAHs arecarcinogenic: benz(a)anthracene, benzo(a)pyrene, anddibenzo(a,h)anthracene by the oral route; benz(a)anthracene,benzo(a)pyrene, benzo(b)fluoranthene, benzo(k)fluoranthene,chrysene, dibenzo(a,h)anthracene, and indeno(1,2,3-cd)pyrene bydermal contact.

Benz(a)anthracene is a common combustion residue found in tobaccosmoke. Skin cancer develops following intermediate dermalexposure. Cancer by other routes of exposure has not beenstudied. Its metabolites bind DNA. Toxicity other thancarcinogenesis is largely unstudied. It is genotoxic whenmetabolically activated in approximately half the trialsundertaken. Benz(a)anthracene is strongly sorbed onto soilparticles and has low water solubility.

Benzo(a)pyrene is a common combustion residue, found in tobaccosmoke. It is carcinogenic when applied to the skin, and, it cancause upper gastrointestinal tumors, stomach tumors, lungadenomas, leukemia following bone marrow suppression, nasaltumors, and respiratory tract neoplasms in the larynx, trachea,and pharynx. It affects skin and the reproductive system. Benzo(a)pyrene causes developmental toxicity, decreased fertilityindex, sterility in progeny, increased incidence of stillbirths,and increased terata. It is genotoxic in in vitro assays. Itcan be metabolized to more reactive forms. Benzo(a)pyrene haslow water solubility and strong sorption to soil particles, andthus limited leaching potential.

Dibenzo(a,h)anthracene is a combustion product, found in smokeand soot, and in tobacco smoke. It is also found in creosoteused to preserve wood. Dibenzo(a,h)anthracene is a carcinogenwhen applied to the skin, and a probable carcinogen when inhaled,taken orally, or placed under the skin. Like many carcinogenicPAHs, dibenzo(a,h)anthracene is metabolized to more reactiveforms. It is immunosuppressive. There are limited data on toxiceffects, although some fetal toxicity has been suggested. Dibenzo(a,h)anthracene is genotoxic in most in vitro assays,except human cell lines. The compound has low water solubilityand strong sorption to soils.

Chrysene is considered carcinogenic following long-term dermalexposure. It is metabolized to reactive forms that bind DNA, andis a weak mutagen in in vitro tests with activation. It causesincreased skin and liver tumors, but not much acute lethality.Little other toxicity is known. Chrysene is a combustionproduct, found in tobacco smoke, and in creosote used inpreserving wood. It has low water solubility and strong soilsorption characteristics.

Benzo(b)fluoranthene, benzo(k)fluoranthene, and indeno(1,2,3-cd)pyrene are considered carcinogenic, but there islittle other information about its toxicity.

DIOXINS AND FURANS

Dioxins and furans are related classes of compounds formed in manufacturing various chlorinated products, including herbicidessuch as 2,4,5-T (a component of Agent Orange) and otherchlorinated cyclic hydrocarbons, and in paper bleaching. Theycan also be formed by combustion (of various chemicals andindustrial and municipal wastes). They are formed naturally inmost combustion processes, and forest fires have generated a lowbackground level throughout the world. Dioxins and furans includecompounds with various levels of chlorination from 0 to 8,referred to as isomers. The arrangement of the chlorines on thebasic molecule determines the specific congener. Isomers withfour chlorine molecules are the most toxic forms, and congenerswith chlorines in the 2,3,7 and 8 positions are the most toxicforms within each isomer group. The most toxic form is 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD); the related furan isonly slightly less toxic. Other dioxins and furans can rangefrom slightly less toxic to 1,000 times less toxic. For dealingwith mixtures of dioxins and furans, a system has been developedthat weighs concentrations of congeners and isomers by factorsthat relate their toxicity to that of 2,3,7,8-TCDD, generating"TCDD equivalency factors." Those factors are then used toassess the health risks of a dioxin/furan mixture.

2,3,7,8-TCDD is considered one of the most potent man-madetoxicants known. It is 1,000 times as potent a toxicant as arePCBs, but considerably less toxic than some of the microbialtoxins, such as botulinum toxin. The most sensitive species(guinea pig) has an LD50 (the dose of a chemical that has beencalculated to cause death in 50% of a defined experimental animalpopulation) of approximately 0.6 µg/kg, but there are alsospecies, such as the hamster, that are highly resistant to TCDD(LD50 > 5,000 µg/kg). The sensitivity of humans to TCDD-inducedlethality is uncertain. TCDD is also a potent teratogen, atdoses 400 times lower than the LD50. In addition to lethality,TCDD causes reproductive failure, teratogenicity (cleft palate,hydronephrosis), immunosuppression, thymic atrophy, liver damageand enzyme induction, "wasting" (severe loss of weight and bodyfat over several weeks), changes in iron in the blood,hyperkeratinization of the skin (a rapid response), and hormonalchanges. The actual cause of death is, as yet, unknown, but mayinvolve alterations in the hormonal systems. Development ofintoxication signs may be delayed, and death may not occur forseveral weeks. While many of the effects are seen in animals,there are wide species differences in effect and levels needed tocause particular effects (e.g., the resistant hamster developsmany of the same signs of intoxication as the sensitive guineapig, but does not die from the effects of TCDD intoxication). Further, undefined factors cause many individual differences insusceptibility. In humans, few of the effects described arecertified; the only proven effect of TCDD in humans isdevelopment of a severe skin condition known as chloracne.

Other isomers and congeners can cause many of the same symptoms,but usually at much higher doses. The furans are roughly thesame as the related dioxin. Brominated forms of dioxins are alsonearly identical to the related chlorinated forms. For example,octa-chlorinated dioxin can cause most of the effects of 2,3,7,8-TCDD, but only at a much higher dose. Teratogenic effectsassociated with octa-chlorinated dioxin, however, appear toresult at lower doses.

TOXICOLOGICAL PROFILE REFERENCES

Agency for Toxic Substances and Disease Registry. ToxicologicalProfile for Benz(a)anthrene. Atlanta: ATSDR, March 1990.

Agency for Toxic Substances and Disease Registry. ToxicologicalProfile for Benzo(a)pyrene. Atlanta: ATSDR, May 1990.

Agency for Toxic Substances and Disease Registry. ToxicologicalProfile for Chrysene. Atlanta: ATSDR, March 1990.

Agency for Toxic Substances and Disease Registry. ToxicologicalProfile for Lead. Atlanta: ATSDR, June 1990.

Agency for Toxic Substances and Disease Registry. ToxicologicalProfile for Mercury. Atlanta: ATSDR, December 1989.

Agency for Toxic Substances and Disease Registry. DraftToxicological Profile for Polycyclic Aromatic Hydrocarbons. Atlanta: ATSDR, February 1990.

Agency for Toxic Substances and Disease Registry. ToxicologicalProfile for Creosote. Atlanta: ATSDR, February 1990.

Agency for Toxic Substances and Disease Registry. ToxicologicalProfile for Pentachlorophenol. Atlanta: ATSDR, December 1989.

Agency for Toxic Substances and Disease Registry. ToxicologicalProfile for Benzene. Atlanta: ATSDR, May 1989.

Agency for Toxic Substances and Disease Registry. ToxicologicalProfile for 2,3,7,8-Tetrachlorodibenzo-p-dioxin. Atlanta: ATSDR, June 1989.

Agency for Toxic Substances and Disease Registry. ToxicologicalProfile for Chromium. Atlanta: ATSDR, July 1989.

Klaassen, C.D., M.O. Amdur, J. Doull. 1986. Casarett and Doull'sToxicology: The Basic Science of Poisons. 3rd edition. Macmillan Publishing Company, NY.


APPENDIX 5 - APRIL 1989 HEALTH ASSESSMENT

The following appendix was not available in electronic format for conversion to HTML at the time of preparation of this document. To obtain a hard copy of the document, please contact:

Agency for Toxic Substances and Disease Registry
Division of Health Assessment and Consultation
Attn: Chief, Program Evaluation, Records, and Information Services
Branch, E-56
1600 Clifton Road NE, Atlanta, Georgia 30333



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