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1. ATSDR > Public Health Assessments & Consultations

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 2. CONTAMINANTS IN ON-SITE WATER AT SMWT¹

TABLE 3. CONTAMINANTS IN WASTES AT SMWT¹

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

TABLE 5. CONTAMINANTS IN OFF-SITE WATER AT SMWT¹

TABLE 6. EXPOSURE PATHWAYS AT SMWT

Pathway Name	Exposure Pathway Elements					Time
	Source COCs1	Media	Point of Exposure	Route of Exposure	Exposed Population
Completed Exposure Pathways
On-site workers	Wood-treating chemicals-unknown concentrations	Air - direct contact with chemicals	Plant operations	Dermal Inhalation Ingestion	SMWT plant employees - unknown number	Past
Off-site air	Emissions from SMWT plant operations	Air	Residue on houses Air emissions	Dermal Inhalation	Nearby residents - unknown number	Past
Potential Exposure Pathways
On-site media	Phenolic compounds PAHs2, VOCs3, metals	Soil, air, surface water, sediments	Direct contact with contaminated media	Dermal Inhalation Ingestion	Trespassers - unknown number and unknown activities.	Past
Off-site sediments	PCP4, cPAHs2	Stream sediments	Old Tom's Run (see Fig. 6)	Dermal Ingestion	Children playing in stream - unknown number, unknown frequency and duration of exposure.	Past, present, future
Off-site groundwater	VOCs3, phenolic compounds, PAHs2, PCDD5, metals	Groundwater - presently, shallow aquifer affected	Residential wells downgradient of SMWT site	Dermal Inhalation Ingestion	Residents using private wells downgradient of the site should deeper aquifers become contaminated.	Future
Eliminated Exposure Pathways
Remedial workers	VOCs3, phenolic compounds, PAHs2, PCDD5, metals	Soil, air, surface water, sediments, groundwater	Sampling of all media and other remedial activities	Dermal Inhalation Ingestion	Remedial workers - unlikely because appropriate safety procedures and PPE6 are required for on-site activities.	Past, present, future
On-site buildings	PAHs2, PCP4	Building surfaces	Direct contact with buildings	Dermal Inhalation	None - Building samples were collected from treated timbers which do not pose a health concern.	Past
Off-site soils	PAHs2	Surface soils	Direct contact	Dermal Ingestion	Children 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 chain	PAHs2, PCP4, mercury	Fish	Old Tom's Run	Ingestion	None - 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 are contaminant concentrations in specific media (soil, air, and water) that are used to select contaminants for further evaluation. The values provide guidelines for estimating doses at which adverse health effects might occur. Comparison values and the units used to quantitate contaminant concentrations that appear in the Environmental Contamination and Other Hazards and the Public Health Implications sections of this public health assessment 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 contaminant concentrations that are expected to cause no more than one excess cancer in a million (10E-6) persons exposed over a lifetime (70 years). CREGs are calculated from EPA's cancer slope factors.

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

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

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

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

Maximum Contaminant Level Goals (MCLGs) are drinking water health goals set at levels at which no known or anticipated adverse effects on the health of persons occurs and which allows an adequate margin of safety. Such levels consider the possible impact of synergistic effects, long-term and multi-stage exposures, and the existence of more susceptible groups in the population. 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 exposure to a chemical (in mg/kg/day) that is not likely to cause an appreciable risk of deleterious effects (noncarcinogenic) over a specified duration of exposure. MRLs are based on human and animal 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 specific chemicals.

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

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

APPENDIX 3A. Comparison Value Calculations

The following formula was used to calculate soil comparison values from RfDs for volatile and semivolatile organic compounds and 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 10 kg 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 of total polychlorinated dibenzo-p-dioxins (PCDDs)in a mixture that compensates 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. Using that convention, the concentration of each isomer in a mixture is multiplied by the appropriate factor (listed above) and the sum of all the weighted PCDDs in the mixture is represented by the 2,3,7,8-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 for the Southern Maryland Wood Treating Site, Hollywood, Maryland, Volume I, CDM Federal Programs Corporation, May 1988.

APPENDIX 4 - TOXICOLOGICAL PROFILE SUMMARIES

TOXICOLOGICAL PROFILE SUMMARIES

NOTE OF EXPLANATION:

Brief discussions of the toxicology of existing contaminants at the SMWT site are included in this appendix. Under present conditions, the contaminants associated with the SMWT site are not expected to cause illness or disease either in the local populations or in properly protected remedial workers. The health effects described in this appendix result from higher doses than those associated with possible exposure at the SMWT site. Because access to the site is restricted, even exposure at lower doses is unlikely.

BENZENE

Benzene is released into the atmosphere from both natural and artificial processes. The most significant source appears to be from the burning of gasoline. Levels of benzene measured in the atmosphere range from 1.3 ppb (parts per billion) in rural areas to 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 it causes a deficiency in all cells in the blood and anemia (failure of the bone marrow to make blood cells). Those effects are seen at levels of 20 ppm (parts per million - 1 ppm equals 1000 ppb). Benzene is also known to cause menstrual disturbances in women at doses of 31 ppm. In animals, it interferes with fertility.

Benzene is considered sufficiently toxic that its use has been curtailed. Previously one of the most common industrial solvents, it is now rarely used. The main reason for the reduction in use has been concern about its ability to cause leukemia after long-term, low-level exposures. Benzene affects the blood, the central nervous system, the skin, the bone marrow's ability to generate new white blood cells, the eyes, and the respiratory system. Acute benzene exposure can cause irritation of the upper respiratory tract, dermatitis, and local irritation. Chronic exposure can result in anemia (leading to leukemia) and immunodepression. Benzene also causes increased mammary 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 is actually a complex mixture of substances. Creosote is known to contain polynuclear aromatic hydrocarbons (PAHs). Some of the substances in it are known to be carcinogens. However, the cancer-causing potential of the complex mixture referred to as creosote is not known.

Dermal contact accounts for the majority of exposures to creosote. 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 uncertain whether chronic occupational exposure causes skin cancers. There are very few data on cresote's toxicity to humans or animals following 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 cause dermatitis and ulcers of the cornea, and it is reported to be associated with the skin condition pemphigus vulgaris. Aplastic anemia (failure of the bone marrow to make all types of blood cells), elevated body temperature, abdominal pain, and swelling and congestion of the lungs are effects that have been seen at very high, but not fully characterized, levels of exposure.

Data on PCP's toxicity following inhalation or ingestion are limited. Levels of 0.09 ppm are associated with eye irritation, and the Occupational Safety and Health Administration (OSHA) has set a standard of 0.05 ppm as the threshold limit value (TLV) for exposure 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 acute ingestion and 0.002 mg/kg/day orally for intermediate ingestion exposures. The MRL is the level at which there is expected to be no toxicity for noncancer outcomes. PCP can be detected by smell at levels of 1.6 ppm in water.

Some animal tests suggest that PCP may cause cancer following dermal 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, and chromium salts are used as dye mordants, tanning agents, pigments, wood preservatives, anticorrosives, and cleaning agents. Industrial usage and combustion of fossil fuels (auto and power plant emissions) are the major sources of chromium release into the environment. Various ionic states occur in salts between +2 and +6, but only +3 and +6 are biologically active. Trivalent (+3) chromium ions are virtually non-toxic, while hexavalent (+6) forms are irritants, corrosive, and carcinogenic. Trivalent salts are poorly absorbed into the body; hexavalent salts are very well absorbed. Hexavalent forms are converted to the trivalent state in cells after crossing the cell membrane, and may bind cellular components during this conversion. However, trivalent ions are not converted to hexavalent forms. Chromium is an essential element in maintaining the integrity of blood vessels, RNA, insulin action, and carbohydrate metabolism. Chromium deficiency can cause increased levels of serum cholesterol. Chromium and many of its salts cause severe contact dermatitis. Dermatitis can result from a single high dose or repeated low doses over years of exposure. Chromium also sensitizes the skin to contact dermatitis; 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 nasal tract can result from high or repeated doses. Liver and kidney toxicity (necrosis of proximal tubule; sensitization to further damage) may occur. Chromium causes both immunodepression and immunosensitization. Some persons have allergic responses to chromium. Hexavalent chromium is highly water soluble and can leach into groundwater.

LEAD

Lead accumulates in body reservoirs from which it is released slowly over time in small amounts, or, under stress, more rapidly in larger amounts. Lead primarily affects the peripheral and central nervous systems, blood cells, and vitamin D and calcium metabolism. Severe lead intoxication can cause death. Effects of lead on the nervous system include decreased nerve conduction speeds, lowered IQ, damage to nerve cells, lowered coordination and motor skills, and seizures. Kidney damage also occurs, with proximal 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 miscarriages and stillbirths, and affects the viability and development of the fetus. Lead affects the blood, producing anemia, hypertension, and reduced hemoglobin synthesis. It also affects vitamin D hormonal activities regulating calcium storage and mobilization. Lead may be a renal carcinogen. The development of lead toxicity and its effects depend upon the dose received, the duration of exposure, and individual variation. However, lead effects are often independent of the route of exposure. Lead is particularly toxic to children, because it affects physiologic systems important to their development and maturation.

MERCURY

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

Mercury bioaccumulates and bioconcentrates in the food chain. Natural sources of mercury release much greater amounts than industrial sources. Mercury is used as an industrial catalyst in smelting and paper pulping. Burning of coal and petroleum may release large amounts of mercury. Mercury is fetotoxic, neurotoxic (both peripheral and central), and affects the kidneys. It is not, however, considered carcinogenic. Toxicity varies with dose, route, duration of exposure, and individual susceptibilities.

High-dose exposure to inorganic, metallic mercury can result in death due to respiratory edema, shock, acute renal failure, and cardiovascular collapse. Severe gastrointestinal damage may contribute to death. Damage to the lungs and degeneration and necrosis of heart muscle may occur; damage to blood cells is infrequent. Inorganic mercury poisoning can cause anorexia, abdominal cramps, nausea, gingivitis, damage to the mucosa of the stomach, and liver necrosis. The kidney concentrates mercury, resulting in reduced kidney function, degeneration of convoluted tubules, reduced filtration, and edema. Kidney damage appears to be the result of an immune response. Mercury can also have toxic effects in the skin and eye. Neurologic signs may be irreversible, and may include tremors, insomnia, shyness, emotional instability, decreased motor function, decreased muscular reflexes, headaches, irregular brain wave patterns, lowering of peripheral nerve conduction velocities, and loss of short-term memory. Central nervous system effects are very dose-specific because metabolism tends to lower the ability of inorganic mercury to enter the brain. Inorganic mercury also has reproductive effects.

Exposure to large amounts of organic mercury has resulted in death, but the cause is uncertain. The major toxicity of organic mercury 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, and smell, slurred speech, unsteadiness of gait, muscle weakness and incoordination, irritability, memory loss, and depression. Kidney damage may include tubular necrosis, fibrosis, and inflammation. Changes in blood pressure occur, along with decreased thymus and spleen weights, and immunodepression. Organic mercury can be fetotoxic, causing derangement of basic central nervous system development, and a reduction in fetal survival rates. Neonatal death can occur, as can alterations and derangements in postnatal development of the eye, behavioral maturation, and learning ability.

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

In general, PAHs are formed as products of ordinary combustion and thus are ubiquitous. They are found in smoke, tobacco smoke, soot, and coal. They are generally natural products, have no known use, and are slowly biodegraded. Carcinogenic PAHs tend to be metabolized into more reactive forms. Little is known about noncancer toxicity, although some PAHs are fetotoxic, and reproductive toxicity may occur at high doses. Some carcinogenic forms are immunosuppressive and/or genotoxic in in vitro tests. PAHs generally have low water solubility and strong absorption to soil, and thus do not migrate in the environment. PAHs bioaccumulate and bioconcentrate in the food chain, but are fairly rapidly excreted. They may interact with each other, enhancing or reducing carcinogenic potential (reduction is the more common experimental result), but those interactions are ill-defined for most PAHs.

NONCARCINOGENIC PAHs

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

ACENAPHTHENE

Acenaphthene affects skin, liver, kidneys, and lungs, resulting in weight loss, vomiting, changes in peripheral blood, and increased serum aminotransferase. Morphologic changes occur in liver and kidneys. Bronchitis and inflammation of peribronchial tissue, lung hyperplasia, and metaplasia of bronchial epithelium may be long-term consequences of acenaphthene exposure.

ACENAPHTHYLENE

Acenaphthylene affects the liver, kidneys, and lungs, resulting in weight loss, changes in peripheral blood, increased serum aminotransferase, a non-specific pneumonia, and changes in kidney function.

ANTHRACENE

Anthracene affects skin, blood, and the eyes. This PAH interacts with light, causing phototoxicity and photoallergenic responses. On skin, anthracene may cause dermatitis, burning, itching, and edema. In the eyes, it may cause tearing, increased sensitivity to light, and swelling of the eye lids. It has low gastric toxicity. Anthracene can increase skin pigmentation and hardening. Other known effects include headache, nausea, and loss of appetite.

FLORANTHENE

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

FLUORENE

Fluorene has been little studied, and its effects are largely undetermined. It is considered noncarcinogenic, but is a liver enzyme inducer.

NAPHTHALENE

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

PHENANTHRENE

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

PYRENE

There are limited data on the toxicity of pyrene. Pyrene is a skin irritant and it may cause liver damage. It is considered non-carcinogenic.

CARCINOGENIC PAHs

Sufficient evidence exists to accept that the following PAHs are carcinogenic: benz(a)anthracene, benzo(a)pyrene, and dibenzo(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 by dermal contact.

Benz(a)anthracene is a common combustion residue found in tobacco smoke. Skin cancer develops following intermediate dermal exposure. Cancer by other routes of exposure has not been studied. Its metabolites bind DNA. Toxicity other than carcinogenesis is largely unstudied. It is genotoxic when metabolically activated in approximately half the trials undertaken. Benz(a)anthracene is strongly sorbed onto soil particles and has low water solubility.

Benzo(a)pyrene is a common combustion residue, found in tobacco smoke. It is carcinogenic when applied to the skin, and, it can cause upper gastrointestinal tumors, stomach tumors, lung adenomas, leukemia following bone marrow suppression, nasal tumors, and respiratory tract neoplasms in the larynx, trachea, and pharynx. It affects skin and the reproductive system. Benzo(a)pyrene causes developmental toxicity, decreased fertility index, sterility in progeny, increased incidence of stillbirths, and increased terata. It is genotoxic in in vitro assays. It can be metabolized to more reactive forms. Benzo(a)pyrene has low water solubility and strong sorption to soil particles, and thus limited leaching potential.

Dibenzo(a,h)anthracene is a combustion product, found in smoke and soot, and in tobacco smoke. It is also found in creosote used to preserve wood. Dibenzo(a,h)anthracene is a carcinogen when applied to the skin, and a probable carcinogen when inhaled, taken orally, or placed under the skin. Like many carcinogenic PAHs, dibenzo(a,h)anthracene is metabolized to more reactive forms. It is immunosuppressive. There are limited data on toxic effects, 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 solubility and strong sorption to soils.

Chrysene is considered carcinogenic following long-term dermal exposure. It is metabolized to reactive forms that bind DNA, and is a weak mutagen in in vitro tests with activation. It causes increased skin and liver tumors, but not much acute lethality. Little other toxicity is known. Chrysene is a combustion product, found in tobacco smoke, and in creosote used in preserving wood. It has low water solubility and strong soil sorption characteristics.

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

DIOXINS AND FURANS

Dioxins and furans are related classes of compounds formed in manufacturing various chlorinated products, including herbicides such as 2,4,5-T (a component of Agent Orange) and other chlorinated cyclic hydrocarbons, and in paper bleaching. They can also be formed by combustion (of various chemicals and industrial and municipal wastes). They are formed naturally in most combustion processes, and forest fires have generated a low background level throughout the world. Dioxins and furans include compounds with various levels of chlorination from 0 to 8, referred to as isomers. The arrangement of the chlorines on the basic molecule determines the specific congener. Isomers with four chlorine molecules are the most toxic forms, and congeners with chlorines in the 2,3,7 and 8 positions are the most toxic forms within each isomer group. The most toxic form is 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD); the related furan is only slightly less toxic. Other dioxins and furans can range from slightly less toxic to 1,000 times less toxic. For dealing with mixtures of dioxins and furans, a system has been developed that weighs concentrations of congeners and isomers by factors that relate their toxicity to that of 2,3,7,8-TCDD, generating "TCDD equivalency factors." Those factors are then used to assess the health risks of a dioxin/furan mixture.

2,3,7,8-TCDD is considered one of the most potent man-made toxicants known. It is 1,000 times as potent a toxicant as are PCBs, but considerably less toxic than some of the microbial toxins, such as botulinum toxin. The most sensitive species (guinea pig) has an LD50 (the dose of a chemical that has been calculated to cause death in 50% of a defined experimental animal population) of approximately 0.6 µg/kg, but there are also species, such as the hamster, that are highly resistant to TCDD (LD50 > 5,000 µg/kg). The sensitivity of humans to TCDD-induced lethality is uncertain. TCDD is also a potent teratogen, at doses 400 times lower than the LD50. In addition to lethality, TCDD causes reproductive failure, teratogenicity (cleft palate, hydronephrosis), immunosuppression, thymic atrophy, liver damage and enzyme induction, "wasting" (severe loss of weight and body fat over several weeks), changes in iron in the blood, hyperkeratinization of the skin (a rapid response), and hormonal changes. The actual cause of death is, as yet, unknown, but may involve alterations in the hormonal systems. Development of intoxication signs may be delayed, and death may not occur for several weeks. While many of the effects are seen in animals, there are wide species differences in effect and levels needed to cause particular effects (e.g., the resistant hamster develops many of the same signs of intoxication as the sensitive guinea pig, but does not die from the effects of TCDD intoxication). Further, undefined factors cause many individual differences in susceptibility. In humans, few of the effects described are certified; the only proven effect of TCDD in humans is development 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 the same as the related dioxin. Brominated forms of dioxins are also nearly 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 effects associated with octa-chlorinated dioxin, however, appear to result at lower doses.

TOXICOLOGICAL PROFILE REFERENCES

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

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

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

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

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

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

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

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

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

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

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

Klaassen, C.D., M.O. Amdur, J. Doull. 1986. Casarett and Doull's Toxicology: 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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Agency for Toxic Substances and Disease Registry, 1825 Century Blvd, Atlanta, GA 30345
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