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PUBLIC HEALTH ASSESSMENT

HIPPS ROAD LANDFILL
JACKSONVILLE, DUVAL COUNTY, FLORIDA


PUBLIC HEALTH IMPLICATIONS

In this section, we discuss the risk of illness and possible health effects for persons exposed to specific contaminants, evaluate state and local health databases, and address specific community health concerns.

Risk of Illness

In this health assessment, the risk of illness is the chance that exposure to a hazardous contaminant is associated with a harmful health effect or illness. The risk of illness is not a measure of cause and effect; only an in-depth health study may identify a cause and effect relationship. Instead, we use the risk of illness to indicate whether or not a follow-up health study is needed, and to provide possible associations to be addressed in a follow-up health study if the study is needed.

In general, the greater the exposure to a hazardous contaminant, the greater the risk of illness. However, the risk of illness is also determined by the amount of a substance that is required to harm a person's health. In theory, everyone who is exposed to a hazardous contaminant above a minimum level has an increased risk of illness, but only in unusual circumstances do many people actually become ill. Individual risks of illness usually are measured and reported as an expression of chance. Consequently, scientists discuss the likelihood of becoming ill, and may express the chance of becoming ill as a fraction. For example, in the 1930's and 1940's, some workers exposed to very high levels of asbestos in asbestos factories had an estimated cancer risk of one chance in one hundred (1/100). However, the estimated cancer risk from exposure to the lower levels of asbestos in air outside of these plants was one chance in ten thousand (1 in 10,000). Sometimes, scientists compare the severity of different risks by looking at the expected occurrences of an illness for the total exposed population. For example, in 100,000 workers exposed to high levels of asbestos in the 1930's and 1940's, scientists would expect to see 1,000 (= 100,000 x 1/100) extra cancer cases. If 100,000 people were exposed only to the low levels of asbestos, scientists would expect to see 10 (= 100,000 x 1/10,000) extra cases of cancer (EPA 1990b).

Information from human studies provides the strongest evidence that exposure to a hazardous contaminant is related to a particular illness. Some of this evidence comes from doctors reporting unusual incidences of a specific illness in exposed individuals. More formal studies compare illnesses in people with different levels of exposure. However, human information is very limited for most hazardous contaminants, and scientists frequently must depend upon data from animal studies. Animal studies are used to estimate risk of illness in humans because hazardous contaminants that are associated with harmful health effects in humans often also are associated with harmful health effects in other animal species. There are limits to relying only on animal studies, however. For example, scientists have found some hazardous contaminants are associated with cancer in mammals, but lack evidence of a similar association in humans. In addition, human and animals have differing abilities to protect themselves against low levels of contaminants. Furthermore, most animal studies test the possible health effects of high exposure levels only. Consequently, the possible effects of a hazardous contaminant on humans is uncertain when there is information only from animal experiments (EPA 1990b).

Dose-Response and Threshold Concepts

The focus of toxicological studies in humans or animals is identification of the relationship between exposure to different doses of a specific contaminant and the chance of having a health effect from each exposure level. This dose-response relationship provides a mathematical formula or graph that is used to estimate a person's risk of illness. The actual shape of the dose-response curve requires scientific knowledge of how a hazardous substance affects different cells in the human body. There is one important difference between the dose-response curves used to estimate the risk of noncancer illnesses and those used to estimate the risk of cancer: the existence of a threshold dose. The threshold dose is the highest exposure dose at which there is no risk of illness. The dose-response curves for noncancer illnesses include a threshold dose that is greater than zero. Scientists include a threshold dose in these models because of the observation that the human body is capable of adjusting to varying amounts of other types of cell damage without showing signs of illness. The threshold dose differs for different contaminants and different exposure routes, and is estimated from information gathered in human and animal studies. In contrast, the dose-response curves used to estimate the risk of cancer assume there is no threshold dose (or, the cancer threshold dose is zero). This assumes a single cancer cell may be sufficient to cause a clinical case of cancer (EPA 1990b). This assumption is very conservative, and many scientists believe a threshold dose greater than zero also exists for the development of cancer.

Uncertainty in Health Assessments

All health assessments require the use of assumptions, judgements, and incomplete data to varying degrees. These contribute to the uncertainty of the final risk estimates. Some of the more important sources of uncertainty in this public health assessment include environmental sampling and analysis, exposure parameter estimation, use of modeled data, and present toxicological knowledge. These uncertainties may cause risk to be overestimated or underestimated to different extents (EPA 1993a). As a result of the uncertainties described below, this public health assessment should not be construed as representing an absolute estimate of risk to persons potentially exposed to chemicals at or near the Hipps Road Landfill Site.

Environmental chemistry analysis errors can arise from random errors in the sampling and analytical processes, resulting in either an over- or under-estimation of risk. These errors can be controlled to some extent by increasing the number of samples collected and analyses performed, and by sampling the same locations over several different time periods. These actions tend to make uncertainty contributed from random sampling errors small (EPA 1993a). However, only a small number of samples were collected for some contaminants, and many sample locations were not sampled more than once. The limited data from these areas may not be representative of the presence or concentrations of contaminants across the entire area. Consequently, the risk of illness for these contaminants may be over- or under-estimated.

There are two areas of uncertainty related to exposure parameter estimation. The first is related to exposure point concentration estimation. The second is related to the parameter values used to estimate chemical exposures (EPA 1993a). In this assessment we used maximum detected concentrations as the exposure point concentration. We believe using the maximum measured value to be appropriate because we cannot be certain what the peak contaminant concentrations are, and we cannot statistically predict peak values because the sample numbers and distribution are unsuitable for this type of analysis. Nevertheless, this assumption introduces uncertainty into the health assessment that may over- or under-estimate the actual risk of illness. When selecting parameter values to estimate exposure dose, we used default assumptions and values within the ranges recommended by ATSDR or EPA. These default assumptions and values are designed to be conservative and may contribute to the over-estimation of risk of illness. Similarly, we assumed exposures took place from the time the landfill opened and that exposure occurred on a regular basis for each selected pathway. Both of these assumptions are likely to contribute to the over-estimation of risk of illness

For some of the identified data gaps we used modeled data to obtain exposure dose estimates. In particular, we used modeled data to estimate past contaminant concentrations in air and in some foods. ATSDR does not support using modeled data for evaluating possible health effects; rather, they recommend these data be used only to support a need for more sampling. Nevertheless, we believe we are justified in using modeled data in this public health assessment for two reasons. First, the maximum groundwater concentrations in the past generally are much higher than those in the present, and no amount of present-day sampling will yield past concentration data (unless other models are used). Second, nearby residents are greatly concerned their exposure from solvent volatilization will be ignored; they have specifically asked us to address this concern in the public health assessment to account for their total probable exposure to these contaminants. Still, using modeled data introduces uncertainties into the exposure dose estimates that may over- or under-estimate the actual risk of illness.

There are also data gaps and uncertainties in the design, extrapolation, and interpretation of toxicological experimental studies (EPA 1993a). Data gaps contribute uncertainty because information is either not available or must be addressed qualitatively. For example, possible health effects related to skin absorption represents a data gap for most contaminants in this public health assessment. Moreover, the available information on the interaction among chemicals found at the site, when present, is qualitative (that is, a description instead of a number) and cannot be applied mathematically to the dose estimates. These kinds of data gaps may tend to underestimate the actual risk of illness. In addition, there are great uncertainties in extrapolating from high to low doses, and from animal to human populations. Extrapolating from animals to humans is uncertain because of the differences in the uptake, metabolism, distribution, and body organ susceptibility between different species. Human populations are also variable because of differences in genetic constitution, diet, home and occupational environment, activity patterns, and other factors. These uncertainties can result in an over- or under-estimation of risk of illness. Finally, there are great uncertainties in extrapolating from high to low doses, and controversy in interpreting these results. Because the models used to estimate dose-response relationships in experimental studies are conservative, the risk estimates resulting from these models tend to be over-estimated. Currently, there is much debate in the scientific community as to how much the actual risks are over-estimated and what the risk estimates really mean.

A. Toxicological Evaluation

Introduction

In this subsection, we discuss exposure levels and possible health effects that might occur in people exposed to the 35 contaminants of concern at the site. To evaluate exposure, we estimated the daily dose of each contaminant of concern found at the site. Kamrin (1988) explains a dose in this manner:

    "...all chemicals, no matter what their characteristics, are toxic in large enough quantities. Thus the amount of a chemical a person is exposed to is crucial in determining the extent of toxicity that will occur. In attempting to place an exact number on the amount of a particular compound that is harmful, scientists recognize that the size of an organism has to be taken into account. It is unlikely, for example, that the same amount of a particular chemical that will cause toxic effects in a 1-pound rat will also cause toxicity in a 1-ton elephant.

    Thus instead of using the amount that is administered or to which an organism is exposed, it is more realistic to use the amount per weight of organism. Thus it could be said that an amount of 1 ounce administered to a 1-pound rat is equivalent to 2000 ounces to a 2000-pound (1-ton) elephant. In each case, the amount per weight is the same: 1 ounce for each pound of animal.

    This amount per weight is known as the dose. It is used to determine the amount of drug to prescribe to patients of differing weights and is used in toxicology to compare the toxicity of different chemicals in different animals."

In expressing the daily dose, we used the units of milligrams of contaminant per kilogram of body weight per day (mg/kg/day).

To calculate the daily dose of each contaminant, we used standard assumptions about body weight, ingestion and inhalation rates, exposure time length, and other factors needed for dose calculation (Tables 16-19, Appendix B). The standard values and dose-related equations we used originated from ATSDR and EPA guidance manuals (ATSDR 1992a, 1993a; EPA 1990a). In calculating the dose, we assumed residents were exposed to the maximum concentration measured for each contaminant in each medium (Tables 4-13, Appendix B). To calculate daily doses, we used the computer software, Risk*Assistant (1993). Using this software enabled us to estimate doses from skin contact, and gave us modeled dose estimates for other potential routes of exposure we would not have been able to evaluate otherwise including inhalation of shower vapors and ambient air, ingestion of fish, and ingestion of homegrown vegetables. Still, we did not have models available to evaluate potential inhalation of vapors from the fill material; skin absorption from contact with organic materials in soil, especially contact with the fill material at the site; or skin absorption of contaminants from household uses of water, other than showering.

Because some body functions work differently in adults and children, we estimated contaminant doses for three hypothetical individuals: a young child, an average child, and an adult. We defined a young child as a child from 0-6 years of age who exhibited pica behavior, the abnormal ingestion of large amounts of non-food substances including soil. Although all children inadvertently ingest soil as a part of normal mouthing behavior, this activity usually stops around 18 months of age. Pica behavior is rare. However, when it occurs, pica behavior is usually established by 18 months of age and may persist until a child is six years old (EPA 1990a). In terms of exposure, pica children are likely to ingest abnormally large amounts of soil, making their daily dose of a soil-borne contaminant much higher than that of other children or adults. We defined an average child by using mid-range values for all parameters for children between 0-18 years of age. We assumed average children did not exhibit pica behavior. To estimate contaminant exposure during swimming, we assumed swimming in area ponds and creeks began at 6 years of age, and average children had more opportunities to swim than adults. For adults, we assumed exposure to contaminants took place from 1967-1993, unless we knew a specific exposure pathway (such as swimming in on-site ponds) ceased to exist beforehand. For all individuals, we assumed exposure to air-stripper contaminants will last for ten years, twice the proposed length of operation, in case operation of this device continues longer than expected.

For each of the three hypothetical individuals, we estimated human exposure from incidental ingestion of contaminated soil and sediment, incidental ingestion of contaminated surface water during swimming, ingestion of contaminated groundwater used for domestic purposes, skin absorption of contaminants while swimming or showering, and inhalation of contaminants from the air stripper. Because there are no existing data on contaminant exposure from eating locally harvested food, inhaling vapors while showering, or breathing air inside and outside the home, we used Risk*Assistant's model data to evaluate the residents' exposure from these pathways.

In some cases, contaminants were found in monitor wells but not private wells. When this occurred, we considered the exposure pathway likely to be complete for three reasons. First, there were not enough samples to adequately characterize shallow groundwater in on-site private wells; consequently, we could not eliminate the possibility that a substance found in a bore hole or on-site monitor well might also be in an on-site private well. Second, off-site private well water quality was largely unknown prior to 1990, and we could not identify all contaminants nearby residents were exposed to during the time when few samples were taken. Third, both on- and off-site monitor wells and private wells drew water from the same aquifer, and in some cases the monitor wells are in residential yards. Therefore, it seemed likely that a substance detected in a monitor well but not in a private well was a sampling artifact. As a result, we used the highest contaminant concentration found in either monitoring or private wells to predict possible health effects from groundwater exposure.

To evaluate possible noncancerous health effects at these doses, we compared the calculated dose to contaminant-specific MRLs or RfDs, when they existed, for each type of exposure route (inhalation, ingestion, and skin contact) and length of exposure (chronic - greater than 364 days of exposure, intermediate - 15 to 364 days of exposure, and acute - less than 15 days of exposure). An MRL is an estimate of the daily dose of a contaminant below which non-cancer illnesses are unlikely to occur. ATSDR develops MRLs from scientific studies found in the toxicological literature, and publishes them in a series of chemical-specific documents called toxicological profiles. These documents contain not only MRLs, but also information on possible health effects, environmental transport, human exposure, and regulatory status of contaminants. EPA publishes similar minimal risk doses, called RfDs, below which non-cancer illnesses are unlikely to occur. In evaluating the dose data for contaminants at this site, we used the MRL for comparison when both an MRL and a RfD were available. In some cases, there are no MRLs or RFDs for comparison. In these cases, we compared the estimated doses we calculated to doses in published human or animal studies in order to estimate possible health effects. Our conclusions from these comparisons are judgements based on: what we know about the quality of the study, natural disease rates in the test organisms, and how close our estimated doses are to published experimental doses. These judgements always contain some uncertainty because of natural variation within human and animal populations, and because of species differences among humans and animals. Humans and animal differences are particularly important because a given test animal species may be either more or less sensitive to a particular contaminant than humans, and often the direction of this sensitivity difference is unknown.

To evaluate possible cancerous health effects, we used standard equations to calculate an individual's additional risk of developing cancer over a lifetime after exposure to a potentially cancer-causing contaminant. This calculated probability is known as the cancer risk, the number of excess cancer cases that could develop per unit of population if the exposure assumptions are met for a specific contaminant. Usually, an excess cancer risk of 1 in 10,000 to 1 in 1,000,000 is considered a negligible increase in cancer risk. There are three things to consider when evaluating cancer risk. First, when examining the numeric cancer risk value, it is important to recognize there is a background cancer rate of around 25% in the United States (ATSDR 1993b). This means that in a group of a million people, 250,000 people can be expected to develop cancer in their lifetime without exposure to contaminants at a particular site. Within the negligible cancer risk range of 1 in 1,000,000 to 1 in 10,000 excess cancer cases for a specific contaminant, 250,001 - 250,100 people in this same group might develop cancer in their lifetime if they are exposed to that contaminant at the specified dose and exposure period. Because these cancer risk calculations are made for a lifetime, and because some cancers don't develop until many years after exposure, we do not calculate a separate cancer risk for children. Second, when interpreting the associated cancer information, it is important to note whether or not the associated cancers have been looked for and found to occur in humans. This is because a given test animal species can be more or less likely to develop cancer than humans. When only animal studies of cancer are available, we present the suggestive evidence from the animal studies, but cannot necessarily conclude human exposure will be linked to cancer. Third, there is much scientific controversy about the validity of adding cancer risks from different exposure routes together. Some scientists believe exposure to a cancer-causing chemical via multiple pathways seems likely to increase the overall cancer risk. Other scientists believe cancer risks can be added only if the cancer-causing agent affects the same cell type within the same organ, and works through the same cellular mechanism within the common cell type. In this document, we support the principle that a common mechanism is required. Often, cellular mechanisms of action are not known; in these cases, the suitability of adding estimated cancer risks together cannot be determined. In this subsection, we present the estimated cancer risks from different exposure pathways separately. In the Community Health Concerns Evaluation subsection, we discuss additive cancer risks, when appropriate.

After examining the dose-related calculations for the 35 contaminants of concern and making the appropriate comparisons, we divided the contaminants among two categories: a minimal risk category and a possible risk category.

The minimal risk category identifies those contaminants whose dose-related value is very close to or below the applicable MRL, RfD, or within the negligible cancer risk range for a medium (soil, water, or air); or significantly below exposure levels associated with noncancer illnesses in a medium; or both. In defining "close to" values, we included contaminant doses that slightly exceeded a health value in this group for three reasons. First, the estimated dose values are not known with great precision due to the uncertainty inherent in exposure parameter estimation. Second, the conservative assumptions behind our calculations are likely to cause us to overestimate contaminant doses, and consequently to overestimate the public health risk. Third, our evaluation of the toxicological literature used to estimate the RfDs or MRLs for these specific contaminants supports this categorization. Therefore, we consider the actual risk of becoming ill from exposure to these contaminants to be minimal. The 15 minimal risk contaminants are:

Minimal Risk Contaminants

Beryllium
Chlorobenzene
Chlorodibromomethane
Chloroform
Cobalt
Cyanide
DDT
1,4-Dichlorobenzene
1,2-Dichloropropane
1,2-Diphenylhydrazine
Mercury
Naphthalene
Nickel
Selenium
Tin

The possible risk category includes those contaminants whose dose-related value is significantly greater than either the MRL or RfD, or is greater than the negligible cancer risk range in at least one medium, or has too few studies for evaluation. The 20 possible risk contaminants are:

Possible Risk Contaminants

Arsenic
Barium
Benzene
Bromodichloromethane
Cadmium
Chromium(VI)
Cresol
1,1-Dichloroethane
1,2-Dichloroethane
Di(2-ethylhexyl)phthalate
Hexachloroethane
Lead
Manganese
Methylene Chloride
n-Nitrosodiphenylamine
PCBs (total)
1,1,2,2-Tetrachloroethane
Tetrachloroethene
Trichloroethene
Vinyl Chloride

It is important to understand that contaminants in the possible risk category are not necessarily threats to public health; they are simply selected for further evaluation. For some contaminants in this category, there simply isn't enough reliable toxicological data to fully evaluate the potential health effects from exposure.

In addition to evaluating contaminants in the latter two categories, we also examined data for contaminants we had earlier classified as contaminants with drinking water standards. The chemicals in this category include pH and inorganic chemicals with established drinking water standards but without other comparison values. In our evaluation, we compared the maximum groundwater measurements for these substances with Florida's primary and secondary drinking water MCL values. Dose calculations were not necessary. The substances and measurements in this category are:

Contaminants with Drinking Water Standards

Aluminum
Copper
Fluoride
Iron
Nitrate
Nitrite
pH
Sodium
Sulfate

Below, we discuss the concentration or estimated doses of contaminants in each category, the known interactive effects, and the possible health effects from exposure. When we have enough information, we evaluate past, present, and future exposures individually. In our evaluation, past exposure includes data collected before May 1993, present exposure includes data collected from May-October 1993, and future exposure includes the time period after October 1993.

When providing information on how close our estimated doses were to experimental doses reported in toxicological studies, we used several different terms to indicate the degree of closeness (smaller or larger) to an observed experimental dose. "Similar to" means an estimated dose value is very close to the lower values in a range of comparison doses, usually within a fraction less than one (for example, 3.4 compared to 4.0). "Slightly" means an estimated dose value is a little farther away than a fraction from the lower values of the comparison doses, such as by a factor of two or three (for example, two or three times smaller than the comparison doses). "Somewhat" means an estimated dose value is still farther away from the lower values of the comparison doses, usually by a factor close to ten (for example, nine or ten times smaller than the comparison doses). "Much" means an estimated dose value is greater than a factor of ten from the lower values of the comparison doses (for example 30 or 100 times smaller than the comparison doses). As a dose value becomes much smaller than the lower values of the comparison doses, the uncertainty of an association between the estimated dose and possible health effects increases.

Contaminants with Drinking Water Standards

Some inorganic contaminants that do not have toxicological comparison values but do have primary drinking water standards (including sodium, fluoride, sulfate, nitrate, and nitrite) were found in the shallow groundwater surrounding the site. None of these contaminants were found in concentrations exceeding their respective maximum contaminant levels. Therefore, we do not expect illnesses to result from ingestion of these substances.

The shallow groundwater concentrations of aluminum, copper, and iron, as well as the lower range for pH violate Florida's secondary drinking water standards (Table 20, Appendix B). A comparison of the range of values between the on-site boreholes and monitoring wells and the off-site private wells suggests the landfill is a possible source of these contaminants. Secondary drinking water standards are established to provide consumers with water that is aesthetically pleasing in taste, smell, and appearance. The contaminants violating secondary drinking water standards in the Hipps Road area will not cause illnesses; however, these contaminants are found in concentrations which can contribute to the taste and odor problems reported by residents.

Minimal Risk Contaminants

Based on our comparison of the doses of these contaminants to studies in the toxicological literature, we do not believe exposure to any contaminant in this category is likely to be associated with illnesses. Nevertheless, it is important to consider the interactive effects these contaminants might have with each other, with other contaminants found at the site, and with chemicals from other common sources such as cigarette smoking, alcohol consumption, or food nutrients when this information is known. Frequently, interactive effects are grouped into one of four categories: additive effects, synergistic effects, potentiation, and antagonistic effects. Additive effects occur when the combined effects of two contaminants equals the sum of their individual effects; thus neither contaminant enhances or diminishes the effect the other (for example, 2 + 3 = 5). Additive effects are the most common interactive effects. Synergistic effects occur when the combined effects of two contaminants are much greater than the sum of their individual effects; thus each contaminant amplifies the effects of other (for example, 2 + 2 = 20). Potentiation occurs when one contaminant does not have a toxic effect on a certain body organ or system; however, when combined with another contaminant, it makes the latter much more toxic (for example, 0 + 2 = 10). Antagonistic effects occur when the combined effects of two contaminants are less than the sum of their individual effects; the effects are reduced by one contaminant interfering with the other, or both contaminants interfering with each other (for example, 4 + 6 = 8; 4 + (-4) = 0; 4 + 0 = 1) (Amdur et al. 1991).

ATSDR or EPA has published information on all 15 of the minimal risk contaminants found at the Hipps Road Landfill site:

  1. Beryllium - Beryllium is a hard, grayish element that occurs as a chemical component of certain rocks, coal and oil, soil, and volcanic dust. Beryllium is used to make making electrical and electronic parts, machinery, molds for plastics, nuclear weapons and reactors, aircraft, space vehicles, x-ray machines, and mirrors. Ingesting beryllium usually does not harm health because very little enters the body from the digestive system. Most of the small amount of beryllium that does enter the bloodstream is carried to the kidneys where it leaves the body within a few days through urination. Animal studies suggest beryllium exposure is not likely to affect reproduction. It is not known if beryllium ingestion affects the development of unborn babies. The potential interactive effects between beryllium and other substances found at the site are unknown. Beryllium ingestion is not known to be associated with cancer in humans or animals (ATSDR 1993f).

    In the past, nearby residents were exposed to beryllium through ingestion of groundwater. Present-day analyses indicate beryllium may no longer be present in well water. The past beryllium ingestion doses we estimated for all age groups are slightly smaller than EPA's RfD (IRIS 1994), indicating noncancer illnesses are unlikely to be associated with this exposure.

  2. Chlorobenzene - Chlorobenzene is a colorless liquid with an almond-like odor. It is manufactured as a solvent and is used in the production of other chemicals. Chlorobenzene can enter the body through ingestion, inhalation, and skin absorption. Once in the body, most chlorobenzene is expelled by exhaling and urinating. Harm to human health from ingesting chlorobenzene has not been established. In animals, exposure to high levels of chlorobenzene is associated with adverse effects on the brain, liver, and kidneys. Other animal studies suggest chlorobenzene exposure does not adversely affect reproduction or the development of unborn babies. The potential interactive effects between chlorobenzene and other substances found at the site are not known (ATSDR 1990b). Chlorobenzene is not classified as a potential cancer-causing agent (ATSDR 1993a).

    In the past, nearby residents were exposed to chlorobenzene through incidental ingestion of on-site subsurface soils and ingestion of groundwater. Present-day analyses indicate chlorobenzene may no longer be present in well water. The past chlorobenzene ingestion doses we estimated for all age groups are similar to or somewhat smaller than EPA's RfD (IRIS 1994), and the modeled chlorobenzene inhalation doses we estimated for all age groups are much smaller than the doses associated with noncancer illnesses in the animal studies we reviewed (ATSDR 1990b). These results indicate noncancer illnesses are unlikely to be associated with ingestion or inhalation exposure. There are no human or animal studies of the potential health effects from skin absorption of chlorobenzene (ATSDR 1990b); therefore, we cannot evaluate any potential association between this exposure route and noncancer illnesses.

  3. Chlorodibromomethane - Chlorodibromomethane is a colorless liquid with a sweetish odor. In the past, chlorodibromomethane was used to make other chemicals such as fire extinguisher fluids, spray can propellants, refrigerator fluid, and pesticides. Today, it is produced only in small quantities for use in laboratories. Chlorodibromomethane is also formed as an unwanted byproduct of chlorinating drinking water. Once chlorodibromomethane enters the body, it is quickly removed by exhalation. Human and animal studies indicate ingestion of large amounts of chlorodibromomethane can affect the brain, liver, and kidneys. Exposure to low levels of this compound does not seem to be associated with serious effects on these organs. Animal studies suggest chlorodibromomethane is not likely to adversely affect reproduction or the development of unborn babies at typical human exposure levels. Studies of chlorodibromomethane's interactive effects show acetone, and possibly other ketones, potentiate the toxic effects chlorodibromomethane has on the liver. Animal studies indicate long-term intake may be associated with cancer (ATSDR 1990a).

    In the past and present, nearby residents were and are exposed to chlorodibromomethane through use of their well water. In addition, nearby residents may have been coexposed to acetone and chlorodibromomethane in their drinking water in the past, and may be exposed to acetone in the air and chlorodibromomethane in their drinking water in the future. Still, the past chlorodibromomethane ingestion doses we estimated for all age groups are much smaller than EPA's RfD (IRIS 1994), and the modeled chlorodibromomethane inhalation doses we estimated for all age groups are much smaller than ATSDR's chronic MRL (ATSDR 1990a). These results indicate noncancer illnesses are unlikely to be associated with ingestion or inhalation exposure, even if interactions with acetone occur. There are no human or animal studies of the potential health effects from skin absorption of chlorodibromomethane (ATSDR 1990a); therefore, we cannot evaluate any potential association between this exposure route and noncancer illnesses. We estimated the increased cancer risk from chlorodibromomethane exposure to be negligible.

  4. Chloroform - Chloroform is a colorless liquid with a pleasant odor and a slightly sweet taste. In the past, hospitals used chloroform as an anesthetic. Today, it is used to make other chemicals and is an unwanted byproduct of chlorinating drinking water. Chloroform is found in air from all areas of the United States, and in nearly all drinking water supplies. Once inside the body, travels to body organs and can collect in body fat. Some of the chloroform in the body is exhaled, and the rest is broken down into other chemicals. Some of these breakdown products are excreted, and others can attach to chemicals inside cells where they may cause harmful effects to the liver and kidneys. In humans, ingestion or inhalation of high doses of chloroform can have adverse effects on the brain, liver, and kidneys. Ingestion or inhalation of small doses of chloroform can be associated with harm to the liver and kidneys. Animal studies indicate inhaling moderate amounts of chloroform may adversely affect reproduction and may be associated with birth defects in rats and mice. Similar reproductive and developmental effects have not been associated with chloroform ingestion in animals (ATSDR 1993h). Several animal studies indicate chloroform may interact with other chemicals inside the body. In rats, exposure to ketones and ethanol (drinking alcohol) can increase chloroform's toxic effects on the liver and kidneys. Similarly, experiments with rat liver cells suggest cadmium and chloroform may potentiated the toxic effects of each other on these cells (ATSDR 1989b, 1993h). Human studies indicate ingesting chlorinated drinking water, which contains chloroform and other chlorination by-products, may be linked with colon and urinary bladder cancer. Animal studies indicate ingestion of small amounts of chloroform for long time periods is associated with liver and kidney cancer, but it is not known if chloroform exposure is associated with these same cancers in humans (ATSDR 1993h).

    In the past, nearby residents were exposed to chloroform through household uses of well water. Present-day analyses indicate chloroform may no longer be present in well water, and chloroform was not detected in the air stripper's influent or effluent (Golder Associates 1993a). The past chloroform ingestion doses we estimated for all age groups are much smaller than EPA's RfD for this contaminant (IRIS 1994), and the modeled past chloroform inhalation doses we estimated for all age groups are much smaller than the doses associated with noncancer illnesses in the human and animal studies we reviewed (ATSDR 1993h). These results indicate noncancer illnesses are unlikely to be associated with ingestion or inhalation exposure even if coexposure with ethanol, ketones, or cadmium occurred. There are no human or animal studies of the potential internal health effects from skin absorption of low doses of chloroform (ATSDR 1993h); therefore, we cannot evaluate any potential association between this exposure route and noncancer illnesses. We estimated the increased cancer risk from chloroform exposure to be negligible.

  5. Cobalt - Cobalt is an element that naturally occurs in rocks, soil, surface water, groundwater, plants, and animals. It is used to make alloys and colored pigments, and as a drier for paint and porcelain enameling. Ingestion is the most likely route for cobalt exposure. Small amounts of cobalt are found in tea, coffee, many fruits and vegetables, and some fish. Some of the cobalt entering the body quickly leaves in the feces; the rest is absorbed into the blood where it travels throughout the body, particularly to the liver, kidneys, and bones. This cobalt leaves the body slowly, mainly through urination. Cobalt has both beneficial and harmful effects on human health. Vitamin B12 is a cobalt-containing compound essential for good health. Cobalt is also used as a treatment of anemia (a decrease in the number of red blood cells) because it causes red blood cells to be produced. However, too much cobalt may have harmful health effects. In some people, treatment with cobalt has been associated with adverse effects on the thyroid gland. In addition, some people can develop dermatitis after skin exposure to cobalt-containing compounds. It is not known if cobalt ingestion adversely affects human reproduction. Animal studies suggest high levels of cobalt may be associated with health effects in unborn babies; however, birth defects have not been seen in human babies whose mothers took cobalt for anemia during pregnancy. In other animal studies, cobalt ingestion is associated with adverse effects on the blood, liver, kidneys, and heart. When cobalt is administered in conjunction with the anti-tumor antibiotic bleomycin, these compounds interact to amplify each other's anti-tumor effects. In addition, there is some evidence that people with nickel sensitization may develop an allergy to cobalt under some circumstances. Cobalt ingestion is not known to be associated with cancer in humans or animals (ATSDR 1992c).

    In the past, nearby residents were exposed to cobalt through incidental ingestion of on-site sediment and off-site surface water, through ingestion of groundwater. There are no present-day analyses of cobalt, and it is not known if exposure to this substance is continuing. The cobalt ingestion doses we estimated for all age groups are much smaller than the levels associated with noncancer illnesses in the human and animal studies we reviewed (ATSDR 1992c).

  6. Cyanide - Cyanides are a group of compounds naturally produced by certain bacteria, fungi, and algae; they are naturally found in a number of foods (for example, cassava roots, lima beans, and almonds). Most cyanides in the soil and water, however, come from industrial sources. Cyanides are also found in vehicle exhaust. Once in the body, cyanide can quickly enter the bloodstream. The health effects of cyanide depend on the chemical form it is in. Inhaling or ingesting large amounts of cyanide harms the brain, heart, and lungs, and can result in coma or death. Nevertheless, small amounts of some cyanide compounds are always present in the body. Animal studies suggest cyanide ingestion does not adversely affect reproduction, but may affect the development of unborn babies. In the body, some of the cyanide is changed to a harmless chemical that is excreted in the urine, some interacts with a different body chemical to form vitamin B12, and some is converted to carbon dioxide and exhaled. Most of the ingested cyanide will leave the body within 24 hours after exposure. One study found synergism between potassium cyanide and vitamin C in guinea pigs, resulting in increased tremors, muscle incoordination, and muscle twitches in these animals. Antagonists stabilizing cyanide into nonharmful compounds include sodium nitrite, amyl nitrite, hydroxylamine, and cobalt containing compounds (ATSDR 1993c). Cyanide is not classified as a potential cancer-causing agent (ATSDR 1993a).

    In the past, nearby residents were exposed to cyanide through incidental ingestion of on-site subsurface soils, on-site sediments, and ingestion of groundwater. In addition, nearby residents may have been coexposed to cyanide and dietary vitamin C, and to cyanide and nitrates and cobalt in their drinking water in the past. There are no present-day analyses of cyanide, and it is not known if exposure to this substance is continuing. The degree of interaction of ingested vitamin C with ingested cyanide is unknown, but such interactions might occur in humans. Ingestion of nitrates and cobalt with cyanide could somewhat lessen the health effects from cyanide exposure. The past cyanide ingestion doses we estimated for all age groups are similar to or somewhat smaller than EPA's RfD (IRIS 1994), indicating noncancer illnesses are unlikely to be associated with this exposure.

  7. DDT - DDT, a widely used pesticide in the past, is sometimes found in food. It is also found at many waste sites, and releases from these sites can be additional sources of human exposure. DDT does not enter the body through the skin easily. Once in the body, DDT can be broken down and excreted in the urine. Nevertheless, DDT is readily stored in body fat, where levels may increase if exposure continues, or decrease slowly over time if exposure decreases. Short-term exposure to high DDT doses is associated primarily with effects on the nervous system. Long-term exposure to low doses is associated with temporary changes in liver enzyme levels. Although there is no indication DDT adversely affects human reproduction, animal studies suggest DDT ingestion may affect the development of unborn babies. DDT seems to have broad interactive effects by changing the effects of other chemicals. DDT reportedly promotes the tumor-forming effects of some cancer-causing agents, but inhibits the tumor-forming effects of other cancer-causing agents. Similarly, some pharmaceutical drugs prevent DDT's toxic effects on the nervous system, while other drugs enhance DDT's toxicity to the nervous system. The potential interactive effects between DDT and other substances found at the site are unknown. In some animal studies, DDT ingestion has been associated with liver cancer. It is not known if DDT ingestion is associated with cancer in humans (ATSDR 1992e).

    In the past, nearby residents were exposed to DDT through incidental ingestion while swimming in on-site ponds. Because these ponds no longer exist, exposure via this route has stopped. The past DDT ingestion doses we estimated for all age groups are much smaller than EPA's RfD (IRIS 1994), indicating noncancer illnesses are unlikely to be associated with this exposure. We estimated the increased cancer risk from DDT ingestion to be negligible.

  8. 1,4-Dichlorobenzene - At room temperature, 1,4-dichlorobenzene is a white solid with the strong odor of mothballs. 1,4-Dichlorobenzene is produced by chemical industries to make mothballs, deodorant blocks, and resins. Most people are exposed to 1,4-dichlorobenzene from breathing household products containing this compound such as mothballs and toilet deodorizer blocks. Because 1,4-dichlorobenzene is sometimes used to control odor in animal stalls, it can be found pork, chicken, and eggs. It may also be found in fish and human breast milk. After exposure, most 1,4-dichlorobenzene enters the bloodstream. Almost all 1,4-dichlorobenzene entering the body is broken down into the chemical 2,5-dichlorophenol. It is not known if this breakdown product is more or less harmful than 1,4-dichlorobenzene itself. Almost all of 1,4-dichlorobenzene leaves the body within a week through urination. Tiny amounts remain in body fat, and may stay there for a long time (ATSDR 1993j). There is no evidence moderate use of household products containing 1,4-dichlorobenzene is associated with illnesses. There are cases of people eating sweet-tasting 1,4-dichlorobenzene products and subsequently experiencing skin blotches and blood illnesses, such as anemia. In animal studies, breathing or eating 1,4-dichlorobenzene can be associated with illnesses of the liver, kidneys, and blood. Concentrations of 1,4-dichlorobenzene typically found around hazardous waste sites are not likely to adversely affect human reproduction or the development of unborn babies. The potential interactive effects between 1,4-dichlorobenzene and other substances found at the site are unknown. Studies of rats and mice suggest life-long ingestion of 1,4-dichlorobenzene may be associated with in higher incidences of cancer, but these studies are not conclusive (ATSDR 1993j).

    In the past, nearby residents were exposed to 1,4-dichlorobenzene through incidental ingestion of on-site subsurface soils and household uses of groundwater. The limited number of present-day samples indicate 1,4-dichlorobenzene is no longer found in the groundwater. The 1,4-dichlorobenzene ingestion and modeled inhalation doses we estimated for all age groups are, respectively, much smaller than and similar to their corresponding intermediate MRLs, and much smaller than the levels associated with noncancer illnesses in the acute and chronic human and animal studies we reviewed. There were no skin absorption studies available for evaluation (ATSDR 1993j). There is no apparent increased risk of cancer from 1,4-dichlorobenzene ingestion. It is not known if 1,4-dichlorobenzene inhalation or skin absorption is associated with cancer in humans or animals (ATSDR 1993j).

  9. 1,2-Dichloropropane - 1,2- Dichloropropane is a colorless liquid that evaporates easily at room temperature. It is now used only in research and industry. Before 1980, it was used as a soil fumigant for farming and was a component of some paint strippers, varnishes, and furniture finish removers. 1,2-Dichloropropane released into the environment usually ends up in the groundwater or air where it breaks down slowly. Once in the body, 1,2-dichloropropane quickly leaves the body through urination, defecation, and exhalation. Drinking or breathing very high levels of 1,2-dichloropropane is associated with poisoning in humans, but there are no reports of any human health effects associated with short or long term exposure to low-levels of this chemical. However, in animal studies, low-level exposure for short or long time periods is associated with liver, kidney, and respiratory damage. One animal study suggests ingestion of high amounts of 1,2-dichloropropane may be associated with harmful effects on sperm formation. Skin contact with 1,2-dichloropropane is associated with skin irritation in both humans and animals. 1,2-Dichloropropane is not associated with birth defects in humans or animals, but studies of rats indicate delayed bone growth in unborn babies may be associated with maternal exposure to 1,2-dichloropropane during pregnancy. Animals studies indicate inhalation of 1,2-dichloropropane with tetrachloroethene can have additive effects on the liver, lung, and nervous system. Human studies of short-term ingestion or inhalation of 1,2-dichloropropane have not found an association with cancer. However, in animals, long-term ingestion of 1,2-dichloropropane may be associated with liver cancer in mice and breast cancer in female rats. The significance of the animal cancer findings to humans is not well understood (ATSDR 1989c).

    In the past, nearby residents were exposed to 1,2-dichloropropane through household uses of well water. Present-day analyses indicate exposure is continuing for residents still using private well water from areas next to the groundwater contaminant plume. In addition, the air stripper's trial run demonstrated this device will successfully remove 1,2-dichloropropane from groundwater and expel it into the air. Furthermore, nearby residents may have been coexposed to tetrachloroethene and 1,2-dichloropropane in their drinking water and air in the past, and may be exposed to tetrachloroethene and 1,2-dichloroethane in the drinking water and air in the present and future. Still, the past and present 1,2-dichloropropane ingestion doses we estimated for all age groups are much smaller than ATSDR's intermediate MRL for this contaminant. Chronic ingestion studies were not available for review. The modeled past and present 1,2-dichloropropane inhalation doses we estimated for all age groups are much smaller than the doses associated with noncancer illnesses in the animal studies we reviewed (ATSDR 1989c). These results indicate noncancer illnesses are unlikely to be associated with ingestion or inhalation exposure even if coexposure with tetrachloroethene occurred or occurs. Nevertheless, several case studies indicate some people are allergic to 1,2-dichloropropane-containing products and may develop contact dermatitis upon skin contact with these products in sensitized individuals. It is not known at what exposure level the allergic response develops. There are no human studies of the potential internal effects from skin absorption of 1,2-dichloropropane, but the two available animal studies did not find an association between skin exposure to 1,2-dichloropropane and internal noncancer illnesses (ATSDR 1989c). We estimated the increased cancer risk from 1,2-dichloropropane ingestion to be negligible. It is not clear if 1,2-dichloropropane inhalation is associated with cancer in animals. There are no human or animal studies of the potential association between skin absorption of 1,2-dichloropropane and cancer (ATSDR 1989c).

  10. 1,2-Diphenylhydrazine - 1,2-Diphenylhydrazine is a white solid that tends to stick to soil. 1,2-Diphenylhydrazine is used to make fabric dyes and to make certain medicines. Most people are exposed to 1,2-diphenylhydrazine by incidentally ingesting dirt or breathing in dust in areas where 1,2-diphenylhydrazine has been recently spilled or uncovered. Not much is known about how 1,2-diphenylhydrazine enters the body or how the body breaks down 1,2-diphenylhydrazine. Still, two of the known breakdown products, aniline and benzidine, may contribute to 1,2-diphenylhydrazine's toxicity. Animal studies indicate at least some 1,2-diphenylhydrazine leaves the body through urination. The health effects of 1,2-diphenylhydrazine have not been studied in humans. Animals studies indicate chronic oral exposure to low doses of 1,2-diphenylhydrazine may be associated with liver damage. It is not known if exposure to 1,2-diphenylhydrazine has adverse effects on reproduction or the development of unborn babies. The potential interactive effects between 1,2-diphenylhydrazine and other substances found at the site are unknown. In addition, it is not known if 1,2-diphenylhydrazine is associated with cancer in humans. However, in rats and mice, chronic oral exposure to 1,2-diphenylhydrazine is associated with liver and breast cancer (ATSDR 1990d).

    In the past, nearby residents were exposed to 1,2-diphenylhydrazine through incidental ingestion of on-site subsurface soils and sediments. There are no present-day analyses of 1,2-diphenylhydrazine, and it is not known if exposure to this substance is continuing. The 1,2-diphenylhydrazine ingestion doses we estimated for all age groups are much smaller than the levels associated with noncancer illnesses in the animal studies we reviewed (ATSDR 1990d). There is no apparent increased risk of cancer from past 1,2-diphenylhydrazine ingestion.

  11. Mercury - Mercury is a naturally occurring metal found throughout the environment as a result of normal breakdown of the earth's crust by wind and water. Mercury can occur in metallic, organic and inorganic forms. All forms of mercury are considered poisonous. Mercury has many different uses. Metallic mercury is used in thermometers, barometers, batteries, and tooth fillings. Inorganic mercury is used in electrical equipment, skin care and medicinal products, and some fungicides. Organic mercury can be found in some paints and fungicides. A natural form of organic mercury is sometimes found in fish. Mercury found in air, water, and soil is thought to be mostly in the inorganic form. Inorganic mercury can enter the body through the digestive system and subsequently reach many tissues. It can stay in the kidneys for a relatively long time. Inorganic mercury leaves the body through urination or defecation after several weeks or months. The kidneys seem to be the most sensitive target of low-level exposure to inorganic mercury. Long-term exposure to higher than normal levels of inorganic mercury may be associated with kidney and brain damage in some people. In animals, short- and long-term exposure to low inorganic mercury levels is associated with adverse kidney and brain effects, and may be associated with adverse effects on unborn babies. It is not known if ingestion of inorganic mercury adversely affects reproduction. Vitamin D, vitamin E, selenium, and copper are antagonistic to the toxic effects of mercury. In rats, pretreatment with zinc seems to be protective against inorganic mercury's effects on the kidneys. In contrast, ethanol (drinking alcohol) consumption appears to increase the toxicity of mercury. Mercury ingestion is not known to be associated with cancer in humans or animals (ATSDR 1992i).

    Based on information we have about the site and the chemical analyses run, we presume the mercury detected around the site to be in the inorganic form. In the past, nearby residents were exposed to inorganic mercury through incidental ingestion of on-site subsurface soils and sediments, incidental ingestion of on-site surface water, and ingestion of groundwater. Present-day analyses indicate inorganic mercury may no longer be present in well water. The inorganic mercury ingestion doses we estimated for all age groups are somewhat smaller than and similar to ATSDR's acute and intermediate MRL's, respectively, and much smaller than the levels associated with noncancer illnesses in the chronic animal studies we reviewed. Nevertheless, several case studies indicate some people are allergic to mercury-containing products and may develop contact dermatitis, rashes or blisters upon skin contact with these products in sensitized individuals. It is not known at what exposure level the allergic response develops (ATSDR 1992i).

  12. Naphthalene - Naphthalene is a white solid with a strong odor that evaporates easily. It is used to make moth repellents, deodorizing blocks, dyes, resins, leather tanning agents, and insecticides. Naphthalene enters the body by breathing air, smoking, drinking water, or touching products containing this chemical. These exposure routes include breathing in vapors or wearing clothes stored in naphthalene-containing mothballs. Once in the blood, naphthalene travels to the liver and other organs where it is changed into other chemicals, some of which can be harmful to health. Naphthalene is able to cross a pregnant woman's placenta and get into a baby's blood. Most breakdown products of naphthalene are excreted in the urine. Smaller amounts are excreted in feces, and some can be excreted in mother's milk. It may take several weeks for all traces of naphthalene to leave the body. In humans, exposure to a high amount of naphthalene can cause hemolytic anemia, a condition in which unusual numbers of red blood cells are damaged or destroyed as they move through the circulatory system, as well as nausea, vomiting, diarrhea, blood in the urine, and yellow-colored skin. Pregnant women who develop naphthalene-induced anemia can have anemic children. Animal studies suggest inhaling naphthalene vapors can be associated with nose and lung inflammation, and ingesting naphthalene can be associated with weight reduction in the thymus and spleen or with cataract (cloudiness) development in the eyes. Some animal studies also suggest naphthalene ingestion may adversely affect reproduction. The potential interactive effects between naphthalene and other substances found at the site are unknown (ATSDR 1993n). Naphthalene is not classified as a cancer-causing agent (ATSDR 1993a).

    In the past, nearby residents were exposed to naphthalene through incidental ingestion of on-site subsurface soil and ingestion of groundwater. A limited number of present-day samples indicate naphthalene is no longer found in the groundwater. The past ingestion, inhalation, and skin absorption doses we estimated for all age groups are much smaller than the doses associated with noncancer illnesses in the animal studies we reviewed (ATSDR 1993n). These results indicate noncancer illnesses are unlikely to be associated with naphthalene exposure.

  13. Nickel - Nickel is a hard, silvery white metal that naturally occurs in the earth's crust. Nickel is commonly mixed with other metals to make metal coins, jewelry, stainless steel, industrial valves, and heat exchangers. Nickel compounds are used in hairdressing, nickel plating, coloring ceramics, making batteries, and forming enzymes used in chemical reactions. Nickel that enters the bloodstream leaves the body in the urine. In one study, some workers who drank high amounts of nickel from a water fountain developed stomach aches, increased numbers of red blood cells, and protein in the urine. In humans, skin exposure to nickel can cause an allergic reaction characterized by skin rashes and asthma. Eating nickel can cause this skin rash to return in sensitive people. In animals, ingesting large amounts of nickel has been associated with lung disease in dogs and rats, and with adverse effects on the stomach, liver, blood, kidneys, and immune system in rats and mice. Animal data suggest nickel ingestion may have adverse effects on reproduction and the development of unborn babies. Manganese appears to interact and reduce nickel's deposition in the liver, kidney, and lung while increasing its elimination through the urine. Pretreatment with cadmium, on the other hand, appears to enhance nickel's toxic effects on the kidney and liver. In iron deficient rats, nickel enhanced the absorption of one form of iron (ferric sulfate), but not others. Nickel ingestion is not known to be associated with cancer in humans or animals (ATSDR 1993o).

    In the past, nearby residents were exposed to nickel through incidental ingestion of on-site subsurface soil and ingestion of groundwater. Present-day analyses indicate nickel may no longer be present in groundwater. The past nickel ingestion doses we estimated for all age groups are similar to EPA's RfD (IRIS 1994), indicating noncancer illnesses are unlikely to be associated with this exposure. Nevertheless, several case studies indicate some people are allergic to nickel-containing products and may develop contact dermatitis upon skin contact with these products in sensitized individuals. It is not known at what exposure level the allergic response develops.

  14. Selenium - Selenium is an essential nutrient found in grains, cereals, and meat. It is commonly found in drinking water and sometimes found at hazardous waste sites. Selenium can be harmful in daily levels only somewhat larger than needed for good nutrition. Selenium exposure can lead to brittle hair, deformed nails, and in extreme cases, loss of feeling and control in arms and legs. Some animal studies suggest selenium ingestion may adversely affect female fertility. Animal data associating selenium ingestion with birth defects are inconclusive. Once ingested, selenium leaves the body mostly through urination. Interactions between selenium and other metals, vitamins, and nutrients usually lead to a reduced toxicity of selenium and/or the interacting substance. Selenium reduces the toxicity of many metals including cadmium, lead, mercury, silver, and to some extent copper. Arsenic decreases the toxicity of selenium in most cases (ATSDR 1989d). Selenium is not classified as a cancer-causing agent (ATSDR 1993a).

    In the past, nearby residents were exposed to selenium through ingestion of groundwater. Present-day analyses indicate selenium may no longer be present in groundwater. The past selenium ingestion doses we estimated for all age groups are similar to or much smaller than EPA's RfD (IRIS 1994), indicating noncancer illnesses are unlikely to be associated with this exposure.

  15. Tin - Tin is a soft, white metal found in small amounts in the earth's crust. It is also found in food containers, plastics, and a wide variety of industrial and household products. Because tin is naturally found in soil and water, it is normally present in plants and animals. Tin is sometimes found in elevated concentrations around hazardous waste sites, and people living near these sites may be exposed to higher-than-normal levels of this metal. Most ingested tin leaves the body in the feces, and some leaves the body in the urine. Very little tin can enter the body through unbroken skin. Although inorganic tin compounds tend to leave the body quickly, very small amounts stay in some body tissues, such as the bones, for longer periods of time. Exposure to large amounts of inorganic tin compounds is associated with stomach aches, anemia (a decrease in the number of red blood cells), liver and kidney problems, and skin and eye irritation. Inorganic tin compounds are not associated with adverse reproductive effects, birth defects, or cancer. Tin can interact with other essential metals needed in the diet. In rats, iron and copper lessen tin's effects on blood hemoglobin (proteins that carry oxygen in the blood). In humans, zinc uptake seems to decrease when administered with equal amounts of tin and iron (ATSDR 1992g). Tin is not classified as a cancer-causing agent (ATSDR 1993a).

    In the past, nearby residents were exposed to tin through incidental ingestion of on-site subsurface soils, incidental ingestion of surface water while swimming in on-site ponds, and ingestion of well water. There are no present-day analyses of tin, and it is not known if exposure is continuing. The past tin ingestion doses we estimated for all age groups are much smaller than EPA's RfD (IRIS 1994), indicating noncancer illnesses are unlikely to be associated with this exposure.

Possible Risk Contaminants

Contaminants included in this category have estimated doses above the MRL, RfD, or negligible cancer risk range; have estimated doses relatively close to doses associated with health effects in humans or animals; or do not have enough information for evaluation. Being above a health value does not necessarily mean exposure to a contaminant will cause illnesses; it simply means the contaminant needs further evaluation. We perform this evaluation by comparing the doses we estimated for different age groups of residents with doses found in human or animal studies published in the toxicological literature. In examining this literature, we relied heavily on the study summaries presented in the ATSDR toxicological profiles and in EPA's IRIS (Integrated Risk Information System) database. IRIS contains toxicological information for many contaminants commonly found at hazardous waste sites.

Likely health effects are influenced not only by exposure dose (how much), but also by exposure duration (how long), and exposure route (breathing, eating and drinking, or skin contact). Once exposure occurs, a person's individual characteristics such as age, sex, diet, general health, lifestyle, chemical exposure history, and genetics also influence how the body absorbs, distributes, metabolizes, and excretes a chemical. Together these factors determine health effects exposed people might have.

Overall, the doses we estimate for some contaminants may be associated with illness, while the estimated doses for other contaminants are unlikely to be associated with illness. For many contaminants, we do not have sufficient information to fully estimate the potential health effects a particular contaminant might have.

For each of the 20 contaminants below, we present a summary of our findings, followed by more detailed information about the contaminant. This more detailed information includes a summary of the contaminant's use and likely route(s) of exposure, as well as general information on known health effects. In many cases, health effects for a specific contaminant are only associated with high exposure doses, and it can be inappropriate to assume these effects will also associated with the low exposure doses estimated for the residents. Nevertheless, we intentionally present high exposure dose information in this assessment so that the description of a contaminant's interactive effects can be better understood. Because the interactive effects information is not quantitative, we can only address these effects qualitatively in our discussion. Under site-specific health effects, we discuss the human or animal illnesses associated with exposure doses close to the doses estimated for the residents. We discuss noncancer and cancer illnesses separately. At the end of each discussion, we present information known about groups of people likely to be unusually sensitive to the contaminant.

  1. Arsenic

    Summary - In human studies, arsenic ingestion doses similar to past doses we estimated for young children have been associated with symptoms of digestive system irritation, mild symptoms of nerve dysfunction, various skin changes, liver enlargement, or a thickening of blood vessel walls that eventually may lead to vessel damage. The past arsenic ingestion doses we estimated for average children and adults are much smaller than the doses associated with noncancer illnesses in the human studies we reviewed. We estimate the increased cancer risk from past arsenic ingestion to be moderate.

    Use and Human Exposure - Because arsenic is a natural element, low levels of this metal are commonly present in water, soil, food, and air. Commercially, arsenic is used as a wood preservative and is found component in some insecticides and weed killers. Most arsenic compounds can dissolve in water. Although arsenic is not broken down or destroyed in the environment, it can change from one form to another through chemical reactions with natural substances, including bacteria. Some fish build up arsenic in their tissues, but most of it is in a form that is not toxic. Arsenic does not pass through the skin easily, and exposure to this element usually occurs through ingestion. Once in the body, the liver changes some of the arsenic to a less harmful form. Most of the arsenic that enters body leaves through urination within several days. However, some remains in the body for several months or longer (ATSDR 1993d).

    General Health Effects - Arsenic has been known to be a human poison since ancient times. In very high doses, it can cause death. At lower doses, it can irritate the stomach, impair blood formation, cause skin changes, and affect the functioning of the heart, blood vessels, and nerves. It is not known if arsenic adversely affects reproduction or the development of unborn children. Arsenic exposure has been linked with skin cancer, and may also increase the risk of cancer in the liver, bladder, lung, and kidney. Arsenic is classified as a known cancer-causing agent in humans via ingestion (ATSDR 1993a, 1993d).

    Interactions with Other Chemicals - Arsenic compounds tend to decrease the toxic effects of selenium. The interaction between arsenic and smoking has not been extensively investigated, although there seems to be a positive interaction (either additive or synergistic) between the two in increasing lung cancer risk. Similarly, experiments with hamsters suggest a positive interaction between arsenic and benzo(a)pyrene in increasing lung cancer risk (ATSDR 1993d).

    Site-specific Noncancer Health Effects - In the past, nearby residents were exposed to arsenic through incidental ingestion of on-site subsurface soils and sediment, and ingestion of groundwater. Present-day analyses indicate arsenic may no longer be present in well water, but we do have enough groundwater, surface soil, or sediment samples to confirm exposure has stopped. In human studies, arsenic ingestion doses similar to past doses we estimated for young children have been associated with symptoms of digestive system irritation including nausea, vomiting, diarrhea, and abdominal pain; mild symptoms of nerve dysfunction, initially appearing as numbness in the hands and feet which may later develop into a painful "pins and needles" sensation; a thickening of the skin, as well as wart or corn formation on the palms or soles; skin pigmentation changes on the face, neck, and back; tenderness or enlargement of the liver; or a thickening of blood vessel walls that can lead to vessel damage. The past arsenic ingestion doses we estimated for average children and adults are much smaller than the doses associated with noncancer illnesses in the human studies we reviewed (ATSDR 1993d).

    Site-specific Cancer Risk - There is convincing evidence that arsenic ingestion can increase the risk of developing skin cancer. The most common lesions appear to develop from some of the warts and corns described above, although other sources of arsenic-induced skin cancer occur. In addition to the risk of skin cancer, there is mounting evidence that arsenic ingestion may increase the risks of several internal cancers, including bladder, kidney, liver, and lung cancer (ATSDR 1993d). Consequently, EPA, the U.S. Department of Health and Human Services' National Toxicology Program (NTP), and the International Agency for Research on Cancer (IARC) each have classified arsenic as a known human cancer-causing agent via ingestion of drinking water; EPA and NTP each have classified arsenic as a known human cancer-causing agent via ingestion of soil (ATSDR 1993a). Based on the exposure and dose information we have, we estimate the increased cancer risk from past arsenic ingestion to be moderate at 4 in 1,000. This means the risk of developing cancer, above the background rate, could rise from 250 cases per 1,000 people to 254 cases in a 70-year lifetime.

    Sensitive Populations - ATSDR's toxicological profile for arsenic did not cite any studies concerning groups of people that were unusually sensitive to arsenic. However, because methylation of arsenic in the liver is a detoxification mechanism, it seems likely that some members of the population who have a lower than normal methylating capacity may be especially susceptible to the toxic effects of arsenic (ATSDR 1993d).

  2. Barium

    Summary - The past barium ingestion doses we estimated for all age groups are much smaller than the doses associated with noncancer illnesses in nearly all studies we reviewed. It is not clear if the barium ingestion doses we estimated for all age groups might be associated with increased blood pressure. Barium's potential to cause cancer via any exposure route is unknown.

    Use and Human Exposure - Barium is a silvery-white metal that occurs in nature in many different forms or compounds. Barium and its compounds are used to make drilling muds, paints, bricks, tiles, glass, rubber, insect and rat poisons, and fuel additives. Doctors sometimes use barium compounds to perform medical tests and take x-ray photographs of the stomach and small intestine. Background levels of barium in the environment tend to be very low. Industrial operations can release barium into the air, soil, and water where they may be inhaled or ingested by people. Some foods such as Brazil nuts, seaweed, fish, and certain plants may contain high amounts of barium. Only a small amount of barium can enter the body through skin contact with barium compounds. Most of the barium that enters the body leaves within a few days in the feces and urine. The small amount of barium that stays in the body mostly goes into bones and teeth (ATSDR 1992b).

    General Health Effects - The potential health effects of different barium compounds depends on how well they dissolve in water. Water-insoluble barium compounds have few health effects, but water-soluble barium compounds can cause illnesses. Most of what is known about water-soluble barium's effects in people come from studies of short-term exposure at fairly large doses. Eating or drinking very high doses of barium compounds can cause paralysis or death. At somewhat lower doses, barium ingestion is associated with breathing difficulties, increased blood pressure, changes in heart rhythm, stomach irritation, minor changes in the blood, muscle weakness, changes in nerve reflexes, swelling of the brain, and damage to the liver, kidney, heart, and spleen. The long-term effects of barium that stays in the body are unknown. Similarly, barium's effects on reproduction or the development of unborn children are unknown, as is its potential to cause cancer (ATSDR 1992b).

    Interactions with Other Chemicals - Barium may interact with potassium, magnesium, and calcium normally present in the body. In animals, potassium is a powerful antagonist of paralysis and heart effects caused by barium. In other experiments, magnesium and calcium suppress the uptake of barium in pancreas cells grown in an artificial environment. In addition, barium interacts with components found in several prescription drugs. In rats, barium increases the depressive effects drugs containing sodium pentobarbital and phenobarbital have on the heart. In mice, atropine and naloxone inhibit the lethal toxicity of barium. In rabbits, verapamil and doxepin seem to offer some protection against barium-induced heart rhythm abnormalities. The interactive effects between barium and other substances found at the site are unknown (ATSDR 1992b).

    Site-specific Noncancer Health Effects - Nearby residents were exposed to barium through incidental ingestion of off-site sediments and ingestion of groundwater. Present-day analyses indicate barium may no longer be present in well water, but we do not have enough groundwater, surface soil, or sediment samples to confirm exposure has stopped. The past barium ingestion doses we estimated for all age groups are much smaller than the doses associated with noncancer illnesses in nearly all studies we reviewed. In the one human study available, the barium ingestion doses we estimated for all ages were close to the "no observed adverse effects level" (NOAEL) for circulatory system effects presented in the study. However, this study is limited by a small sample size and some flaws in its methodology. There are no other human studies available for review or confirmation of the NOAEL value. Similarly, the barium ingestion doses we estimated for all age groups were much smaller than the levels associated with circulatory system effects in most animal studies we reviewed. In one chronic ingestion study of rats, however, barium doses slightly larger than the past doses we estimated for all age groups have been associated with increased blood pressure (ATSDR 1992b). It is not clear what either of these studies means for humans ingesting very low doses of barium. More studies examining the potential association between low-dose barium ingestion and circulatory system effects are needed before we can make reliable comparisons with our estimated doses.

    Site-specific Cancer Risk - There are no studies of barium's likelihood to cause cancer in humans. In two animal studies, rats and mice exposed to barium in drinking water for a lifetime did not show an increased incidence of tumors. However, these studies had design and methodology errors making them inadequate for determining if an association exists between barium ingestion and cancer (ATSDR 1992b).

    Sensitive Populations - Because barium seems to be related to increased blood pressure, residents with hypertension or other heart problems could be at increased risk of becoming ill from exposure to barium. Similarly, since barium appears to interact with sodium pentobarbital and phenobarbital by enhancing these drugs' depressive effect on the heart, individuals on this medication may experience an increased risk of heart problems if exposed to barium. In addition, children may be at increased risk after exposure to barium since animal studies have shown a higher barium absorption rate in young animals than in older animals. One study indicated people who drink large quantities of milk, including children and pregnant women, may also have an increased barium absorption. Finally, people who smoke, have a history of lung disease, or take diuretics may be more susceptible to barium toxicity (ATSDR 1992b).

  3. Benzene  

    Summary - The past and present benzene ingestion and modeled inhalation doses we estimated for all age groups are much smaller than the doses associated with noncancer illnesses in the human and animal studies we reviewed. It is not known if skin absorption of benzene is associated with internal health effects. We estimate the increased risk of digestive system cancer from past benzene ingestion to be low. Using modeled inhalation data, we estimate the increased risk of developing leukemia (blood cancer) from past benzene inhalation to be moderate if actual exposure conditions are close to the estimated conditions used in the model. We estimate the increased cancer risk from present-day benzene ingestion and inhalation to be negligible. There is not have enough information to estimate the increased cancer risk from past or present skin exposure to benzene.

    Use and Human Exposure - Benzene is a colorless, flammable liquid with a sweet odor. Most benzene is made from petroleum sources, although small amounts occur naturally. Benzene is used to make other chemicals, rubber, lubricants, dyes, glues, paints, furniture wax, detergents, drugs, and pesticides. Most people are exposed to a small amount of benzene daily, mainly through breathing in tobacco smoke, gas station vapors, motor vehicle exhaust, industrial emissions, and household vapors from benzene-containing products. Benzene dissolves easily in water and leakage from gas stations, landfills, or hazardous waste sites containing benzene can contaminate well water. People using benzene-contaminated tap water can be exposed to benzene through drinking the water, eating foods prepared with the water, or breathing in benzene while bathing or cooking. A small amount of benzene can enter the body through skin contact with benzene-containing compounds. At high levels of air-borne benzene, about half of the inhaled benzene is subsequently exhaled, and the rest goes into the bloodstream. Ingested benzene also goes into the bloodstream. Once in the bloodstream, benzene travels throughout the body and can be temporarily stored in bone marrow and fat. The bone marrow and liver change benzene into breakdown products. Most benzene breakdown products leave the body within two days, but some remain in the body longer. Several of benzene's harmful effects are believed to be caused by these breakdown products in the body (ATSDR 1993e).

    General Health Effects - The potential health effects of benzene depend upon the exposure amount and length. Most information on the health effects of long-term benzene exposure are from studies of industrial workers exposed to very high levels in air. Exposure to high benzene levels in air can cause drowsiness, dizziness, rapid heart rate, headaches, tremors, confusion, and unconsciousness. In most cases, these symptoms stop once exposure ends and the individual breathes fresh air. However, people who breathe benzene for a long period of time may experience harmful effects in the tissues that form blood cells. These effects can disrupt normal blood production and cause a decrease in important blood components. Eventually, this disruption may lead to anemia (a decrease in the number of red blood cells) or excessive bleeding (caused by a decrease in the number of clotting components in blood). Exposure to benzene in air can also harm the immune system and has been linked with damage to chromosomes, the parts of cells responsible for hereditary characteristics. Exposure to air-borne benzene may also harm the reproductive organs and, in animals, has been associated with adverse effects on unborn babies. Long-term exposure to relatively high benzene in the air levels has been linked to leukemia (blood cancer). Eating or drinking high amounts of benzene can cause vomiting, stomach irritation, dizziness, sleepiness, convulsions, rapid heart rate, coma, and death. The health effects of ingesting lower levels of benzene are unknown. Benzene irritates the skin and can cause redness and sores. Benzene is classified as a known cancer-causing agent in humans via ingestion and inhalation (ATSDR 1993a, 1993e).

    Interactions with Other Chemicals - Benzene metabolism is complex, and agents that alter benzene metabolism may also alter benzene toxicity. In animals, ethanol (drinking alcohol) enhances both the metabolism and toxicity of benzene, particularly the toxic effects on blood. Likewise, benzene can interfere with ethanol metabolism, thereby increasing ethanol-induced effects on the brain. In rats and mice, treatment with the prescription drugs containing phenobarbital before exposure to very high levels of benzene in air increases their benzene metabolism. In contrast, experiments with rat cells grown in an artificial environment and pretreated with phenobarbital show no metabolic effects at lower benzene levels. Coadministration of toluene with benzene inhibits the metabolism of benzene in rats, but pretreatment with phenobarbital alleviates toluene's suppressive effect on benzene (ATSDR 1993e).

    Site-specific Noncancer Health Effects - In the past, nearby residents were exposed to benzene through incidental ingestion of on-site subsurface soils and household uses of well water. Present-day groundwater analyses indicate exposure is continuing for residents still using private well water. In addition, the air stripper's trial run demonstrated this device will successfully remove benzene from groundwater and expel it into the air. We used modeled data to estimate past inhalation exposure to benzene volatilized in the shower and present in ambient air. The past and present benzene ingestion and modeled inhalation doses we estimated for all age groups are much smaller than the levels associated with noncancer illness in the human and animal studies we reviewed. Benzene is a known skin irritant, but there are no studies of benzene's effects on internal body systems resulting from skin absorption (ATSDR 1993e).

    Site-specific Cancer Risk - There are no human studies examining benzene's cancer-causing potential from chronic oral exposure. However, animal studies indicate chronic oral exposure at high doses can cause cancer in various parts of the digestive system, particularly the mouth (ATSDR 1993e). EPA, NTP, and IARC each have classified benzene as a known human cancer-causing agent via ingestion (ATSDR 1993a). Based on the exposure and dose estimates we have, we estimate the increased cancer risk from past benzene ingestion to be low at 1 in 10,000. This means the risk of developing cancer, above the background rate, could rise from 2,500 cases per 10,000 people to 2,501 cases in a 70-year lifetime. We estimate the present-day increased cancer risk from oral exposure to be negligible.

    In addition, EPA, NTP, and IARC each have classified benzene as a known cancer-causing agent via inhalation (ATSDR 1993a). Chronic inhalation of benzene can cause leukemia in humans (ATSDR 1993e). Since we did not have actual measurements of past benzene concentrations in air, we used known groundwater concentrations to estimate the cancer risk from inhaling benzene vapors in the shower and in the ambient air inside and outside the home. Based on the modeled exposure and dose information we have, we estimate the increased cancer risk from past benzene inhalation to be moderate at 12 in 10,000. This means the risk of developing cancer, above the background rate, could rise from 2,500 cases per 10,000 people to 2,512 cases in a 70-year lifetime if the actual inhalation exposure conditions were similar to that predicted by the model. We estimate the present-day increased cancer risk from benzene inhalation to be negligible.

    There are no human studies of benzene's cancer-causing potential from skin exposure. One animal study found benzene did not induce skin tumors in mice after intermediate or chronic exposure lengths, but the study's authors concluded mouse skin may not be the best study system for this experiment. Therefore, it is not known if skin exposure to benzene is associated with cancer (ATSDR 1993e).

    Sensitive Populations - People who drink alcohol and are exposed to benzene may be more susceptible to the benzene's toxic effects on blood. In addition, individuals with viral hepatitis may have accelerated occurrences of aplastic anemia (low red blood cell count). Similarly, individuals with thalassemia (abnormal blood hemoglobin) may experience an increase in the harmful effects of benzene on the blood. Finally, children and unborn babies may also be more susceptible to benzene's harmful effects because their blood cell populations are growing, and rapidly dividing cells are at greater risk than slowly dividing cells (ATSDR 1993e).

  4. Bromodichloromethane

    Summary - Past and present bromodichloromethane ingestion is unlikely to be associated with noncancer illnesses. There is not enough toxicological information to determine if noncancer illnesses have been associated with bromodichloromethane inhalation or skin absorption doses similar to those we estimated for all age groups. We estimate the increased cancer risk from past or present bromodichloromethane ingestion to be negligible. There is not enough toxicological information to determine if past or present inhalation or skin absorption could be associated with cancer.

    Use and Human Exposure - Bromodichloromethane is a colorless liquid produced for laboratory use and chemical manufacturing. Most bromodichloromethane found in the environment is formed as an unwanted byproduct of chlorinating drinking water. Bromodichloromethane in water or air slowly breaks down into other substances. Most people are exposed to bromodichloromethane through drinking chlorinated water or swimming in chlorinated swimming pools. Small amounts can occur in foods made with chlorinated water such as ice cream and soft drinks. Almost all ingested bromodichloromethane moves from the digestive system into the blood. Because bromodichloromethane evaporates easily, people can inhale its vapors from household water, swimming pools, and hazardous waste sites. In addition, bromodichloromethane can cross the skin and people may be exposed while showering, swimming, or touching soil containing this compound. Once in the body, most bromodichloromethane rapidly leaves the body through exhalation, but small amounts are excreted in urine and feces. Little builds up in the body (ATSDR 1989a).

    General Health Effects - In animal studies, eating or drinking large amounts of this compound is associated with injury to the liver and kidneys, and with adverse affects on the brain leading to incoordination and sleepiness. In addition, there is some animal evidence high doses of bromodichloromethane may adversely affect unborn babies (ATSDR 1989a). Bromodichloromethane is classified as a suspected cancer-causing agent in humans via ingestion and inhalation (ATSDR 1993a).

    Interactions with Other Chemicals - In rats, pretreatment with oral doses of acetone dramatically increases ingested bromodichloromethane's toxic effects on the liver and kidneys (ATSDR 1989a).

    Site-specific Noncancer Health Effects - In the past, nearby residents were exposed to bromodichloromethane through household uses of well water. Present-day groundwater analyses indicate exposure is continuing for residents still using private well water. In addition, nearby residents may have been coexposed to acetone and bromodichloromethane in their drinking water in the past, and may be exposed to acetone in the air and bromodichloromethane in the drinking water in the present and future. Still, the past and present bromodichloromethane ingestion doses we estimated for all age groups are much smaller than EPA's RfD (IRIS 1994), indicating noncancer illnesses are unlikely to be associated with this exposure, even if interactions with acetone occur. There are no human or animal studies of the health effects from bromodichloromethane inhalation or skin absorption (ATSDR 1989a).

    Site-specific Cancer Risk - There are no human studies specifically examining bromodichloromethane's cancer-causing potential from chronic exposure. However, animal studies indicate chronic oral exposure to high doses of bromodichloromethane is associated with increased incidences of liver and kidney tumors (ATSDR 1989a). EPA and NTP each classified bromodichloromethane as a suspected cancer-causing agent in humans via ingestion (ATSDR 1993a). Based on the exposure and dose information we have, we estimate the increased cancer risk from past or present bromodichloromethane ingestion to be negligible. NTP has also classified bromodichloromethane as a suspected cancer-causing agent via inhalation. However, there are no studies examining the potential association between bromodichloromethane inhalation or skin absorption and cancer (ATSDR 1989a).

    Sensitive Populations - ATSDR's toxicological profile for bromodichloromethane did not cite any studies concerning groups of people that were unusually sensitive to this compound. However, because bromodichloromethane exposure is associated with adverse effects on the kidneys and liver, people with pre-existing kidney or liver disease may be unusually sensitive to this compound (ATSDR 1989a).

  5. Cadmium

    Summary - Cadmium ingestion doses much smaller than the past doses we estimated for all age groups have been associated with excreting abnormal amounts of protein in the urine, a symptom suggestive of mild kidney tubule dysfunction, in the human studies we reviewed. Kidney tubule dysfunction can result in a secondary loss of calcium which, in turn, may be associated with a variety of bone disorders. In a few animal studies, cadmium ingestion doses similar to past doses we estimated for all age groups have been associated with high blood pressure, but is not clear if cadmium exposure affects human blood pressure. In one animal study, a cadmium ingestion dose similar to the past dose we estimated for adults has been associated with effects on the nervous system of unborn baby rats. However, it is uncertain if maternal cadmium exposure has effects on unborn human babies. It is not known if oral exposure to cadmium causes cancer.

    Use and Human Exposure - Cadmium is a soft, silvery white metal that occurs naturally in the earth's crust. It is found in all soils and rocks, including coal and mineral fertilizers, and is commonly present as small particles in air. Cadmium is found in many industrial and consumer product uses, including batteries, pigments, metal coatings, and plastics. People can breathe in air-borne cadmium from industrial sources, the burning of coal or household wastes, and smoking tobacco. Workers who solder or weld metal may also be exposed to air-borne cadmium. People may also be exposed to cadmium through ingestion. Cadmium can enter drinking water supplies from disposal of household or industrial wastewater, use of fertilizers, or leaks from hazardous waste sites containing cadmium. Cadmium is commonly found in food, and most people ingest small amounts of cadmium daily from the things they eat. Very little cadmium enters the body through the skin. The body quickly absorbs about 25% of inhaled cadmium and 5% of ingested cadmium. Once in the body, cadmium stays in the liver and kidneys. Most of this cadmium is in a form that is not harmful, but too much cadmium can overload the kidneys' storage system and harm human health. Cadmium slowly leaves the body through urine and feces (ATSDR 1993g).

    General Health Effects - Cadmium is not known to have any beneficial health effects. Breathing very high levels of cadmium can cause severe lung damage and death. Breathing lower levels of cadmium for years can cause kidney disease, lung damage, and fragile bones. Workers who inhale cadmium over a long period of time have an increased risk of getting lung cancer. Eating very high cadmium levels severely irritates the stomach. Eating lower levels for a long time period is associated with kidney damage and fragile bones. It is not known if breathing or eating cadmium adversely affects reproduction or the development of unborn children; however, cadmium exposure is associated with these effects in laboratory rats. Similarly, it is not known if eating or breathing cadmium harms the liver, heart, nervous system, or immune system of humans. Cadmium is classified as a suspected cancer-causing agent in humans via inhalation. (ATSDR 1993a, 1993g).

    Interactions with Other Chemicals - Oral cadmium toxicity can be influenced by a wide variety of substances. In humans, dietary deficiencies of calcium, protein, and vitamin D likely account for cadmium's effects on bone. Similarly, iron deficiency increases cadmium's absorption from the digestive system. In quail, cadmium toxicity is intensified by zinc, copper, iron, calcium, and protein deficiencies. In other animal experiments, dietary calcium deficiencies aggravate cadmium's toxic effects on the immune system and on fetuses. In rats, coexposure of cadmium and ethanol (drinking alcohol) in a liquid diet produces liver damage at doses that are not toxic by themselves. Simultaneous administration of garlic decreases cadmium's toxic effects on rat kidneys, but pretreatment with drugs containing acetaminophen increases rat sensitivities to these effects. Coadministration of cadmium and lead in rat diets has an additive effect on reducing body weight, but an antagonistic effect on nervous system toxicity. Coexposure with selenium reduced cadmium's effects on mouse bone marrow (ATSDR 1993g).

    Site-specific Noncancer Health Effects - In the past, nearby residents were exposed to cadmium through incidental ingestion of on-site subsurface soils and ingestion of groundwater. The limited number of present-day samples indicate cadmium is no longer found in the groundwater, but we do not have enough groundwater, surface soil, or sediment samples to confirm exposure has stopped. In one human study, cadmium ingestion doses much smaller than the past doses we estimated for all age groups have been associated with excess protein in the urine, a symptom suggestive of mild kidney tubule dysfunction. Findings in animal studies support the probable existence of an association between cadmium exposure and the functioning of the kidney tubules. In addition, human and animal data indicate excess protein in the urine can develop only after a specific threshold of cadmium in the kidney is exceeded. Because small amounts of cadmium are normally present in the American diet and in tobacco smoke, people may not have a large margin of safety with respect to cadmium intake from other sources. Two studies indicate having excess protein in the urine may not decrease when cadmium exposure stops; rather, kidney tubule dysfunction and decreased filtration may continue to increase in severity. Moreover, there is some evidence cadmium exposure may affect kidney vitamin D metabolism with subsequent disturbances in calcium balance and bone density. Increased calcium excretion may increase the risk of osteoporosis, particularly in post-menopausal women. In addition, bone disorders such as osteomalacia (softening of the bones) and spontaneous bone fracture have been observed in some humans chronically exposed to unspecified amounts of cadmium in their diets (ATSDR 1993g).

    In a few animal studies, cadmium ingestion doses similar to past doses we estimated for all age groups have been associated with high blood pressure. However, cadmium's potential toxic effects on the human circulatory system are not clear, and, after several human studies, it is still unknown if cadmium exposure adversely affects human blood pressure. In addition, there is evidence cadmium exposure can affect the development of unborn babies of animals. In one animal study, a cadmium ingestion dose similar to the past dose we estimated for adults has been associated with pregnant rats having babies with reduced body movement ability and impaired balance. Cadmium's potential effects on the development of human babies is uncertain (ATSDR 1993g).

    Site-specific Cancer Risk - Although there is strong evidence that breathing cadmium dust for prolonged time periods can cause lung cancer in rats, the human evidence of cadmium's cancer-causing potential from ingestion is more limited. Neither human nor animal data provide sufficient evidence to determine if cadmium ingestion is associated with cancer (ATSDR 1993g).

    Sensitive Populations - ATSDR's toxicological profile for cadmium did not cite any studies concerning groups of people that were unusually sensitive to this element. Still, based on what is known about cadmium toxicity, people with depleted stores of calcium, iron, or other dietary components are likely to have an increased cadmium absorption from the digestive system. Likewise, people with kidney damage are likely to experience toxic effects on the kidneys at lower exposures than the general population (ATSDR 1993g).

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