Skip directly to search Skip directly to A to Z list Skip directly to site content

PUBLIC HEALTH ASSESSMENT

HIPPS ROAD LANDFILL
JACKSONVILLE, DUVAL COUNTY, FLORIDA


  1. Chromium(VI)

    Summary - Direct skin contact with chromium containing compounds can elicit an allergic response in humans, characterized by eczema and dermatitis. Chromium ingestion doses similar to past doses we estimated for all age groups have been associated with a worsening of chromium-induced dermatitis in sensitized individuals in a couple of the human studies we reviewed. There is not enough information to estimate an increased cancer risk from chromium ingestion.

    Use and Human Exposure - Chromium is a naturally occurring element found in rocks, soil, plants, and animals. It is present in the environment in several different forms. Chromium(III) occurs naturally in many fresh vegetables, fruits, meat, yeast, and grain. It is an essential nutrient required by the body for the metabolism of sugars, fats, and proteins. Chromium (III) is also used as brick lining for high temperature industrial furnaces. Chromium(0) and chromium(VI) are usually produced by industrial processes. Chromium(0) is used for making steel and other alloys. Both chromium(III) and chromium(VI) are used for plating, manufacturing dyes and pigments, tanning leather, and preserving wood. Smaller amounts are found in drilling muds, rust and corrosion inhibitors, textiles, and copy machine toner. People can breathe in air-borne chromium from industrial sources and tobacco. However, most people are exposed to chromium in their diets. Chromium is not only found in many fresh foods, but is also present in steel and can leach out of stainless steel cans containing acidic foods. Chromium can enter drinking water supplies from hazardous waste sites containing chromium. Very little chromium enters the body through the skin. Inhaled chromium particles are either coughed up and swallowed or slowly absorbed from the lungs into the bloodstream. Only a small amount of ingested chromium is absorbed from the intestines into the bloodstream; most leaves the body through the feces. The small amount of chromium that does enter the bloodstream is distributed throughout the body where it is used to carry out essential functions. Chromium then passes through the kidneys and is eliminated in the urine within a few days (ATSDR 1993i).

    General Health Effects - Breathing in large amounts of chromium can irritate the nose, and chronic exposure to very high amounts of chromium has been associated with lung cancer. Breathing in small amounts of chromium(VI) for short or long time periods does not seem to be associated with harmful effects. Ingesting small amounts of chromium(III) is essential for good nutrition, and ingesting small amounts of chromium(VI) does not seem to be harmful; however, ingesting large amount of either chromium(III) or chromium(VI) may cause health problems. Swallowing large amounts of chromium(VI) may cause upset stomachs and ulcers, convulsions, and kidney or liver damage. Some people are very sensitive to chromium(III) or chromium(VI), and may develop an allergic reaction characterized by redness and swelling of the skin. Not much is known about the health effects of chromium(0). There is no reliable information about chromium's effects on reproduction or unborn babies. Chromium is classified as a known cancer-causing agent in humans via ingestion and inhalation. (ATSDR 1993a, 1993i).

    Interactions with Other Chemicals - There are a few animal studies of chromium's interaction with other chemicals in rats. One study indicates chromium potentiates mercury's toxic effects on the kidneys. Another study suggests oral ingestion of both selenium and chromium has serious adverse effects on the liver, but these effects could be due solely to chromium, a possibility the study did not investigate. Vitamin C seems to have a protective effect against skin ulcerations produced from skin exposure to a chromium-containing compound, and against toxic kidney effects produced by ingesting this same compound. Vitamin E protected against, while vitamin B2 enhanced, chromium's toxicity to hamster cells grown in an artificial environment (ATSDR 1993i).

    Site-specific Noncancer Health Effects - In the past, nearby residents were exposed to chromium through incidental ingestion of on-site subsurface soils, on- and off-site sediments, off-site surface water, and ingestion of groundwater. The limited number of present-day samples indicate chromium is no longer found in the groundwater, but we do not have enough groundwater, surface soil, or sediment samples to confirm exposure has stopped. Direct skin contact with chromium-containing compounds can elicit an allergic response in humans, characterized by eczema and dermatitis in sensitized individuals. In a couple of human studies, chromium ingestion doses similar to past doses we estimated for all age groups have been associated with a worsening of chromium-induced dermatitis in sensitized individuals. The study of the interaction between chromium and selenium is inconclusive (ATSDR 1993i); therefore, we cannot evaluate selenium's potential effect on oral exposure to chromium.

    Site-specific Cancer Risk - Although there is sufficient human epidemiological and animal evidence that inhalation of chromium(VI) compounds can cause lung and nasal cancer, human evidence of chromium's cancer-causing potential from ingestion is more limited. A retrospective mortality study in China indicated increased incidences of stomach and lung cancer in people living near a chromium smelting plant, but the residents were likely exposed through air, drinking water, food and soil. Therefore, it is not known if these effects could be caused by chromium(VI) ingestion alone. There is no evidence of chromium(VI) causing cancer in mice chronically exposed to chromium in drinking water or in rats chronically exposed to chromium in their food (ATSDR 1993i). Nevertheless, NTP has classified chromium(VI) as a known human cancer-causing agent via ingestion (ATSDR 1993a). However, EPA has not classified chromium(VI) as a cancer-causing agent; consequently, the agency has not derived the toxicity values needed to estimate an increased cancer risk from chromium(VI) ingestion (ATSDR 1993a; IRIS 1994).

    Sensitive Populations - Acute inhalation studies and some oral and skin absorption studies suggest female animals are more sensitive than males to the lethal effects of chromium(VI) compounds. However, it is not known if human females are more sensitive than males to chromium's toxic effects. Some individuals have less ability than others to reduce chromium(VI) to chromium(III) in their bloodstream and are more likely to become ill from chromium exposure. This ability to reduce chromium(VI) in the bloodstream may be related to vitamin C levels in plasma. Limited findings in human and animal studies suggest youths may be more susceptible to chromium's toxic effects than adults (ATSDR 1993i).

  2. Cresol

    Summary - The past cresol ingestion doses we estimated for all age groups are much smaller than the doses associated with noncancer illnesses in the animal studies we reviewed. There is not enough toxicological information to determine if noncancer illnesses have been associated with cresol inhalation or skin absorption doses similar to those we estimated for all age groups. Cresols are suspected cancer tumor promoters, but there is not enough toxicological information to determine an increased cancer risk from exposure to these compounds.

    Use and Human Exposure - Pure cresols are colorless chemicals that occur in three different forms: o-cresol, m-cresol, and p-cresol. Cresols have a medicinal smell and can give water a medicinal smell and taste. Cresols are naturally present in many foods, and are also found in human and animal urine, wood and tobacco smoke, crude oil, and coal tar. In addition, cresols are used in human-made products such as wood preservatives (such as creosote and cresylic acid), disinfectants, and deodorants. Cresols do not evaporate quickly from surface waters, but can be quickly removed from rivers and lakes by bacteria. However, cresols dissolved in groundwater can persist for months without changing. People can be exposed to cresols by breathing air, drinking water and eating foods containing these compounds. The main sources of cresol in air are emissions from motor vehicles, in homes heated with coal or wood, from factories burning trash or garbage, and from industrial smokestacks. Cresols in the air quickly break down into smaller chemicals, some of which irritate the eyes. People can ingest cresols found in foods such as tomatoes, ketchup, asparagus, cheeses, butter, bacon, smoked foods, coffee, black tea, wine, whiskey, brandy, and rum. People who live near garbage dumps or hazardous waste sites may have large amounts of cresols in their water. Cresols can also be formed in the body from other compounds such as toluene and the amino acid tyrosine, a component of most proteins. Most of the cresols that enter the body are quickly changed to other substances and leave the body through urination within a day (ATSDR 1992d).

    General Health Effects - Ingestion of high levels of cresol can cause a burning feeling in the throat or mouth as well as stomach pains. Skin contact with high concentrations of cresol may result in a rash, severe skin irritation, or a chemical burn. Ingestion of or skin contact with high cresol levels can result in anemia, kidney problems, unconsciousness, or even death. Long-term exposure to low doses in humans may be associated with anemia and kidney problems. In animals, low levels of cresol have been associated with loss of coordination and muscle twitching; it is not known if these effects occur in humans. Animal studies suggest cresols probably are not associated with reproductive problems or birth defects in humans. There is animal evidence that cresols may enhance the cancer-causing ability of other chemicals to produce tumors in animals, but cresols themselves have not been found to cause cancer in humans or animals. Still, cresols are classified as suspected cancer-causing agents in humans (ATSDR 1992d).

    Interactions with Other Chemicals - Cresols may promote tumor development after tumor initiation by other chemicals. Although no evidence is available, it seems likely cresols could interact with phenols to affect the central nervous system, and on red blood cells to produce methemoglobinemia (the presence of an altered form of hemoglobin in the blood that cannot deliver oxygen to body tissues) (ATSDR 1992d).

    Site-specific Noncancer Health Effects - In the past, nearby residents were exposed to cresols through incidental ingestion of on- and off-site sediments and ingestion of groundwater. There are no present-day analyses of cresols; therefore, we do not know if exposure has stopped because we do not have groundwater, surface soil, sediment, or air samples to evaluate. The past cresol ingestion doses we estimated for all age groups are much smaller than the levels associated with noncancer illnesses in the animal studies we reviewed. Human ingestion studies were not available (ATSDR 1992d). We used modeled data to estimate past inhalation exposure to cresols volatilized in the shower and present in ambient air. However, studies of cresols' toxicity via inhalation were not sufficiently detailed to make reliable comparisons with our inhalation dose estimates. Finally, the past doses we estimated for cresol skin absorption while showering are much smaller than the doses associated with noncancer illnesses in the human and animal studies we reviewed. However, all of these studies used high cresol doses; the potential human health effects associated with chronic, low-dose skin exposure to cresol are not known (ATSDR 1992d). More studies examining the potential health effects of low-dose skin exposure to cresol are needed before we can make reliable comparisons with our estimated doses.

    Site-specific Cancer Risk - There have been no human studies of cresols' ability to cause cancer in humans. In one animal study, hamsters exposed to p-cresol in their feed had an increased incidence of nontumor stomach cells, suggesting p-cresol may act as a promoter of stomach tumors in hamsters. A similar study on rats had negative results, but rats may be less sensitive to stomach tumor initiators than other animals. Cresols' tumor promotion potential has also been studied in mice. In one study, mice were first given one skin application of a known tumor initiator, followed by application of all three forms of cresol. This resulted in increased numbers of skin growths that had the potential to develop into cancer. Still, researchers did not observe cancers developing from these growths. Based on this latter study, EPA has classified all three forms of cresol as possible human cancer-causing agents (ATSDR 1993f). However, EPA has not derived the toxicity values needed to estimate an increased cancer risk from cresol exposure (ATSDR 1993a; IRIS 1994).

    Sensitive Populations - There is some evidence individuals with glucose-6-phosphate dehydrogenase deficiency may have increased susceptibility to cresols' effects on the blood. Infants may also be unusually susceptible to the effects of cresols. Furthermore, people with immune deficiencies might be unusually susceptible to the apparent cancer promotional effects of cresols. In addition, individuals with seizure disorders might be more vulnerable to cresols' effects on the central nervous system, such as convulsions and coma, than other people.

  3. 1,1-Dichloroethane

    Summary - The past and present 1,1-dichloroethane ingestion doses we estimated for all age groups are much smaller than the EPA's 1989 RfD. The modeled past and present 1,1-dichloroethane 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. There is not enough toxicological information to determine if noncancer illnesses have been associated with 1,1-dichloroethane skin absorption doses similar to those we estimated for all age groups. Studies pertaining to 1,1-dichloroethane's cancer-causing potential from ingestion are inconclusive. There is not enough toxicological information to determine if 1,1-dichloroethane inhalation or skin absorption could be associated with cancer.

    Use and Human Exposure - 1,1-Dichloroethane is a colorless, oily liquid having an ether-like odor. It is used to make other chemicals and to dissolve other substances such as paint and varnish, and to remove grease. In the past, this chemical was used as a surgical anesthetic, but it is no longer used for this purpose. Because 1,1-dichloroethane evaporates easily into air, it is usually present in the environment as a vapor rather than a liquid. These vapors can be broken down by sunlight. Although 1,1-dichloroethane does not easily dissolve easily in water, small amounts of this compound may be found in water. In soil, 1,1-dichloroethane tends to either evaporate into the air or move into the groundwater. Most people are exposed to 1,1-dichloroethane by breathing air containing its vapors or drinking water contaminated with this compound. Inhaled or ingested 1,1-dichloroethane is believed to enter the body rapidly. Animal studies indicate 1,1-dichloroethane can also enter the body through the skin. Once in the body, 1,1-dichloroethane may go to many organs. Animal experiments indicate most 1,1-dichloroethane entering the body is removed unchanged within a couple of days by exhaling. The small portion remaining in the body is broken down, and the breakdown products quickly leave the body through exhalation and urination (ATSDR 1990c).

    General Health Effects - There is no reliable information on how 1,1-dichloroethane affects human health. One study of cats found 1,1-dichloroethane is associated with kidney disease after long-term, high-dose exposure in air. Comparable effects have not been found in other animals tested, suggesting cats may be uniquely sensitive to this compound. Similarly, delayed growth in offspring of mother rats inhaling high concentrations of 1,1-dichloroethane during pregnancy; still, the study indicates humans are unlikely to experience adverse developmental effects after low-level exposure to this compound. The evidence pertaining to 1,1-dichloroethane's cancer-causing potential is inconclusive (ATSDR 1990c).

    Interactions with Other Chemicals - Some evidence exists suggesting that 1,1-dichloroethane be enhanced by chlorinated hydrocarbons and acetaminophen. In addition, ethanol (drinking alcohol) increases the breakdown of 1,1-dichloroethane in the body and might affect its toxicity (ATSDR 1990c).

    Site-specific Noncancer Health Effects - Nearby residents were exposed to 1,1-dichloroethane through 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 1,1-dichloroethane from groundwater and expel it into the air. The past and present 1,1-dichloroethane ingestion doses we estimated for all age groups are much smaller than the EPA's 1989 RfD, currently under review (IRIS 1994; Risk*Assistant 1993). The modeled past and present 1,1-dichloroethane 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 1990c). 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 1,1-dichloroethane (ATSDR 1990c); consequently, we cannot evaluate any potential association between this exposure route and noncancer illnesses.

    Site-specific Cancer Risk - There are no human studies examining 1,1-dichloroethane's cancer-causing potential in humans. However, one animal study with rats suggests ingestion of very high doses of 1,1-dichloroethane may be associated with cancer, but this study had several flaws making the results questionable. Another study with mice and a different study with rat liver cells indicate 1,1-dichloroethane is not carcinogenic, but neither of these studies is conclusive. This limited evidence neither confirms nor dispels the cancer-causing potential of 1,1-dichloroethane. There are no studies examining the potential association between 1,1-dichloroethane inhalation or skin absorption and cancer (ATSDR 1990c).

    Sensitive Populations - ATSDR's toxicological profile for 1,1-dichloroethane did not cite any studies concerning groups of people that were unusually sensitive to this compound (ATSDR 1990c).

  4. 1,2-Dichloroethane

    Summary - The past and present 1,2-dichloroethane ingestion doses we estimated for all age groups are much smaller than the levels associated with noncancer illnesses in the animal studies we reviewed. 1,2-Dichloroethane inhalation doses similar to modeled doses we estimated for all ages have been associated with suppressed immune response in one animal study, but similar associations have not been found in other animal species. It is not known if 1,2-dichloroethane inhalation is associated with adverse effects on the human immune system. It is not known if skin contact with 1,2-dichloroethane is associated with changes in the skin or with noncancer illnesses in humans. There is no apparent increased risk of cancer from past 1,2-dichloroethane ingestion. Using modeled inhalation data, we estimate the increased risk of developing cancer from 1,2 -dichloroethane inhalation to be low if actual exposure conditions are close to the estimated conditions used in the model. We estimate the increased cancer risk from present-day 1,2-dichloroethane ingestion and inhalation to be negligible. We did not have enough information to estimate an increased cancer risk from past or present skin exposure to 1,2-dichloroethane.

    Use and Human Exposure - 1,2-Dichloroethane is a clear liquid with a sweet smell and taste that evaporates at room temperature. 1,2-Dichloroethane is used to make vinyl chloride and chemicals that dissolve grease, glue, and dirt. It is also added to gasoline to remove lead. In the past, 1,2-dichloroethane was a component of some cleaning solutions, pesticides, adhesives, paint, varnish, and finish removers. Because 1,2-dichloroethane evaporates easily into air, it is usually present in the environment as a vapor rather than a liquid. 1,2-Dichloroethane does not remain in the air for long because sunlight breaks it down. Small amounts of 1,2-dichloroethane can be found in water. In soil, 1,2-dichloroethane usually evaporates or travels downwards and enters groundwater. Small organisms in the soil and groundwater break down 1,2-dichloroethane very slowly. Most people are exposed to 1,2-dichloroethane by breathing air containing its vapors, drinking water contaminated with this compound, using old household products made with 1,2-dichloroethane, or coming in contact with gasoline or gasoline vapors. Animal studies show 1,2-dichloroethane may also enter the body through the skin. Animal experiments show 1,2-dichloroethane may go to many body organs after ingestion or inhalation. However, most 1,2-dichloroethane entering the body is removed by exhalation within two days. A small portion is broken down, and the breakdown products quickly leave the body through exhalation and urination (ATSDR 1992h).

    General Health Effects - People who accidentally inhale or ingest large amounts of 1,2-dichloroethane can develop nervous system disorders and liver and kidney disease. At very high levels, they can die of heart failure. The 1,2-dichloroethane levels causing these effects are unknown. In animals, inhalation or ingestion of large amounts of 1,2-dichloroethane is associated with nervous system disorders, kidney disease. Longer-term exposure to lower doses also is associated with kidney disease in animals. Furthermore, animal studies indicate exposure to high levels of 1,2-dichloroethane may reduce infection-fighting ability; however, there is no evidence 1,2-dichloroethane causes a similar immune reduction in humans. Animal studies indicate 1,2-dichloroethane does not affect reproduction or cause birth defects. So far, 1,2-dichloroethane has not been associated with cancer in humans. However, eating large doses of this chemical or having it applied to the skin has been linked with cancer in animals. Breathing 1,2-dichloroethane may also be linked with cancer in animals. Based on animal studies, 1,2-dichloroethane is classified as a suspected cancer-causing agent in humans via ingestion and inhalation (ATSDR 1992h, 1993a).

    Interactions with Other Chemicals - There are several studies of 1,2-dichloroethane's interaction with other chemicals in animals. Prescription drugs containing phenobarbital increase the breakdown of 1,2-dichloroethane and may increase its toxicity. One study shows ethanol's (drinking alcohol) effects on metabolism depend on existing tissue concentration of ethanol at the time of 1,2-dichloroethane exposure. If tissue ethanol concentration is low, 1,2-dichloroethane break down increases; if tissue ethanol concentration is high, 1,2-dichloroethane break down decreases. These findings are important because changes in 1,2-dichloroethane breakdown rate can have broad effects on 1,2-dichloroethane toxicity. Another study showed chronic coexposure to ethanol in rats had no effect on 1,2-dichloroethane's breakdown or toxicity. Coadministration of disulfiram, a component of prescription drugs that treat alcoholism, in diet and 1,2-dichloroethane in air greatly increased 1,2-dichloroethane's liver toxicity, and increased the tissue growths in the liver, the testes, mammary glands, and skin that have the potential to cause cancer. Cotreatment with 1,2-dichloroethene had slightly greater than additive effects on the liver (ATSDR 1992h, 1993a).

    Site-specific Noncancer Health Effects - Nearby residents were exposed to 1,2-dichloroethane through household uses of well water. Present-day groundwater 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-dichloroethane from groundwater and expel it into the air. For our health effects evaluation, we had only animal studies to review. The past and present 1,2-dichloroethane ingestion doses we estimated for all age groups are much smaller than the doses associated with noncancer illnesses in the animal studies we reviewed (ATSDR 1992h).

    We used modeled data to estimate past inhalation exposure to 1,2-dichloroethane volatilized in the shower and present in ambient air. In one study of mice, 1,2-dichloroethane inhalation doses similar to the past doses we estimated for all age groups have been associated with a decreased ability to fight infections after inhaling disease-causing microorganisms. This association has not been found in any of the inhalation studies with rats we examined. Human studies were not available for review (ATSDR 1992h), and it is not known if 1,2-dichloroethane is associated with adverse effects on the human immune system.

    Eye contact with concentrated 1,2-dichloroethane vapors has been associated with eye irritation and clouding of the cornea in humans and animals. Similarly, direct skin contact with concentrated solutions of 1,2-dichloroethane has been associated with cellular changes in the skin of guinea pigs. Nevertheless, the potential human health effects associated with chronic, low-dose skin exposure to 1,2-dichloroethane are not known (ATSDR 1992h).

    Site-specific Cancer Risk - There are no reliable human studies examining 1,2-dichloroethane's cancer-causing potential after chronic oral exposure. However, one animal study indicates chronic oral exposure at high doses may be associated with cancer in various parts of the body including the spleen, liver, pancreas, adrenal gland, stomach, breast, and lung (ATSDR 1992h). EPA, NTP, and IARC each have classified 1,2-dichloroethane as a probable human cancer-causing agent via ingestion of drinking water or soil (ATSDR 1993a). Based on the exposure and dose information we have, there is no apparent increased cancer risk from past 1,2-dichloroethane ingestion. We estimate the present-day increased cancer risk from 1,2-dichloroethane ingestion to be negligible.

    Similarly, there is little evidence associating chronic inhalation of 1,2-dichloroethane with cancer in humans (ATSDR 1992h). Nevertheless, EPA, NTP, and IARC each have classified 1,2-dichloroethane as a probable human cancer-causing agent via inhalation (ATSDR 1993a) from the ingestion data (IRIS 1994). In two animal studies, chronic inhalation exposure in rats did not show cancer, but design errors in and limitations of these studies make the results indeterminate. Because we did not have actual measurements of past 1,2-dichloroethane concentrations in air, we used known groundwater concentrations to estimate the cancer risk from inhaling 1,2-dichloroethane vapors in the shower and in ambient air inside and outside the home. Based on the exposure and dose information we have from the model, we estimate the increased cancer risk from past 1,2-dichloroethane inhalation to be low at 24 in 100,000. This means the risk of developing cancer, above the background rate, could rise from 25,000 cases per 100,000 people to 25,024 cases in a 70-year lifetime if the actual inhalation exposure was similar to that predicted by the model. We estimate the present-day increased cancer risk from 1,2-dichloroethane inhalation to be negligible.

    There are no human studies examining 1,2-dichloroethane's cancer-causing potential from skin exposure. One animal study found chronic skin exposure to 1,2-dichloroethane significantly increased the incidence of benign lung tumors in mice. This study provides supportive evidence that 1,2-dichloroethane causes cancer and can penetrate through the skin and move into the circulatory system (ATSDR 1992h). Nevertheless, it is not known if skin absorption of 1,2-dichloroethane is associated with an increased lung cancer risk in humans, and we did not have adequate information to estimate an increased cancer risk from skin exposure.

    Sensitive Populations - People who drink alcohol or take prescription drugs containing phenobarbital or disulfiram may be unusually sensitive to the toxic effects of 1,2-dichloroethane. People who smoke or passively breathe cigarette smoke may be more susceptible to lung emphysema after repeated exposure to 1,2-dichloroethane than nonsmokers. In addition, people with impaired liver or immune function, or alcoholics may be unusually susceptible to the effects of 1,2-dichloroethane (ATSDR 1992h).

  5. Di(2-ethylhexyl)phthalate

    Summary - Past di(2-ethylhexyl)phthalate ingestion is unlikely to be associated with noncancer illnesses. There is not enough toxicological information to determine if noncancer illnesses have been associated with di(2-ethylhexyl)phthalate inhalation or skin absorption doses similar to those we estimated for all age groups. We estimate the increased cancer risk from past di(2-ethylhexyl)phthalate ingestion to be low. It is not known if di(2-ethylhexyl)phthalate inhalation or skin absorption is associated with cancer.

    Use and Human Exposure - Di(2-ethylhexyl)phthalate is a colorless, odorless liquid added to many plastics to make them flexible. It is present in plastic products such as rainwear, footwear, upholstery materials, tablecloths, shower curtains, food packaging, floor tiles, toys, paints, flexible tubing, plastic bags, pesticides, and cosmetics. Di(2-ethylhexyl)phthalate is commonly present throughout the environment. It enters the environment from industrial releases and the burning of plastics. Over a long period of time, di(2-ethylhexyl)phthalate can also leach out of plastic products buried in the ground. Once in the environment, di(2-ethylhexyl)phthalate attaches strongly to soils and does not move far away from its release site. It does not break down very easily in deep soils or sediments. Small amounts of di(2-ethylhexyl)phthalate have been found in fish and other animals, and may be found in some plants. Most people are exposed to small amounts of di(2-ethylhexyl)phthalate daily in their food and drinking water. People can be exposed to elevated levels of di(2-ethylhexyl)phthalate in drinking water near landfills containing buried plastics, or in air from cities or industrial areas. People may also be exposed to this compound through medical procedures using plastic products. It is not known if di(2-ethylhexyl)phthalate can cross the skin; however, if transfer occurs, it is probably low. Once in the body, most di(2-ethylhexyl)phthalate is quickly broken down into products having toxicities similar to di(2-ethylhexyl)phthalate. These compounds travel through the blood to the liver, kidneys, and testes. Small amounts are stored in fat or secreted in breast milk. Most of the di(2-ethylhexyl)phthalate and its breakdown products leave the body in the urine and feces within 24 hours (ATSDR 1993k).

    General Health Effects - Most of what is known about di(2-ethylhexyl)phthalate comes from studies of rats and mice fed high doses of this compound. Because both rats and mice seem to be more sensitive than humans to the effects of di(2-ethylhexyl)phthalate exposure, it is difficult to predict human health effects from the animal study information. In rats and mice, short-term exposure to high levels of di(2-ethylhexyl)phthalate have been associated with problems in sperm formation. Exposure before puberty is associated with delayed sexual maturation and reversible changes in testicular structure in male rats. Nevertheless, long-term exposure to high di(2-ethylhexyl)phthalate doses is associated with decreased fertility of both male and female rats. However, these associations are not seen in nonrodent species, including monkeys and rabbits. In pregnant rats and mice, exposure to high levels of di(2-ethylhexyl)phthalate has been associated with offspring having low birth weight and survivorship, as well as malformations in the skeleton, heart, kidneys, brain, and blood vessels. It is not known if di(2-ethylhexyl)phthalate exposure is associated with similar effects in humans. In addition, long-term exposure of rats to di(2-ethylhexyl)phthalate is associated with structural and functional changes in the kidney. Such kidney changes are of special concern to humans because kidney dialysis procedures use flexible tubing containing di(2-ethylhexyl)phthalate. It is not known if di(2-ethylhexyl)phthalate causes cancer in humans; however, long-term exposure to high doses of this substance has been linked with liver cancer in rats and mice. Based on animal studies, di(2-ethylhexyl)phthalate is classified as a suspected cancer-causing agent in humans via ingestion (ATSDR 1993a, 1993k).

    Interactions with Other Chemicals - There are limited data concerning di(2-ethylhexyl)phthalate's interaction with other chemicals in humans. One study suggests di(2-ethylhexyl)phthalate may interact with the -adrenergic class of pharmaceutical drugs, although the nature of this interaction is not clear.

    There are several studies of di(2-ethylhexyl)phthalate's interactive effects with other chemical compounds in rats. Di(2-ethylhexyl)phthalate seems to affect the rat liver's metabolism of ethanol (drinking alcohol), depending on the frequency of di(2-ethylhexyl)phthalate administration. A single dose of di(2-ethylhexyl)phthalate given to rats 18 hours prior to ethanol exposure seems to decrease ethanol metabolism, making ethanol's effects last longer. In contrast, when the same dose of di(2-ethylhexyl)phthalate is given to rats for seven days prior to ethanol exposure, ethanol metabolism rates increased. These differences may be related to the liver's compensation for certain di(2-ethylhexyl)phthalate breakdown products. In addition, high doses of di(2-ethylhexyl)phthalate appear to affect rat thyroid cell structure and decrease the circulating amounts of the thyroid hormone T4. When large doses of di(2-ethylhexyl)phthalate are combined with dietary exposure to Aroclor-1254 (one of the PCBs known to have similar effects on the thyroid), there is an apparent additive effect on the thyroid in changing the cell structure and in decreasing the circulating levels of thyroid hormones T3 and T4. However, at low di(2-ethylhexyl)phthalate doses combined with Aroclor-1254, these apparent additive effects are not seen. Finally, di(2-ethylhexyl)phthalate may interact with caffeine to adversely affect pregnancy and the development of unborn babies in rats. One study indicates a high dose of caffeine injected into pregnant rats with a very high dose of di(2-ethylhexyl)phthalate during the critical period of baby organ development can increase the numbers of dead or malformed offspring. All of these interactive studies with rats must be interpreted with great caution because rats are much more sensitive to the health effects of di(2-ethylhexyl)phthalate than humans. Although these studies suggest similar di(2-ethylhexyl)phthalate interactions are possible in humans, they do not indicate the likelihood of these interactions (ATSDR 1993k).

    Site-specific Noncancer Health Effects - In the past, nearby residents were exposed to di(2-ethylhexyl)phthalate through incidental ingestion of on-site subsurface soils and ingestion of groundwater. The limited number of present-day samples indicate di(2-ethylhexyl)phthalate is no longer found in the groundwater, but we do not have enough groundwater, surface soil, or sediment samples to confirm exposure has stopped. The past di(2-ethylhexyl)phthalate ingestion doses we estimated for all age groups are much smaller than ATSDR's acute MRL, somewhat smaller than ATSDR's intermediate MRL, and somewhat smaller than the doses associated with noncancer illnesses in the chronic animal studies we reviewed. This finding suggests noncancer illnesses are unlikely to be associated with ingestion of this contaminant. Similarly, the modeled past di(2-ethylhexyl)phthalate inhalation doses we estimated for all age groups are much smaller than the doses associated with noncancer illnesses in the few animal studies we reviewed. There were no human inhalation studies available for review (ATSDR 1993k), and more studies examining potential health effects from low-dose di(2-ethylhexyl)phthalate inhalation are needed before we can make reliable comparisons with our estimated doses. Similarly, there was only one skin absorption study available to review. The study results suggested di(2-ethylhexyl)phthalate may not be a skin irritant at very high doses. There were no studies of the potential internal effects from di(2-ethylhexyl)phthalate skin absorption (ATSDR 1993k). More studies examining the potential health effects of low-dose skin absorption are needed before we can make reliable comparisons with our estimated doses.

    Site-specific Cancer Risk - There are no human studies concerning di(2-ethylhexyl)phthalate's ability to cause cancer. However, several chronic oral exposure studies in rats and mice indicate there may be a link between di(2-ethylhexyl)phthalate and liver cancer (ATSDR 1993k). After reviewing these studies, EPA and NTP each classified di(2-ethylhexyl)phthalate as a suspected cancer-causing agent in humans via ingestion of drinking water or soil (ATSDR 1993a). Based on the exposure and dose information we have, we estimate the increased cancer risk from past di(2-ethylhexyl)phthalate ingestion to be low at 11 in 100,000. This means the risk of getting cancer, above the background rate, could rise from 25,000 cases per 100,000 people to 25,011 cases in a 70-year lifetime. There are no reliable studies associating di(2-ethylhexyl)phthalate inhalation or skin absorption with cancer.

    Sensitive Populations - The very young and the elderly may have an increased susceptibility to the metabolic, reproductive, and nervous effects of di(2-ethylhexyl)phthalate if human response is similar to that in rats and mice. In addition, individuals with impaired liver function may be more sensitive to the effects of di(2-ethylhexyl)phthalate.

  6. Hexachloroethane

    Summary - Past hexachloroethane ingestion is unlikely to be associated with noncancer illnesses. There is not enough toxicological information to determine if noncancer illnesses may be associated with inhalation or skin absorption of this compound. We estimate the increased cancer risk from past hexachloroethane ingestion to be negligible. There is not enough toxicological information to determine if past hexachloroethane inhalation or skin absorption could be associated with cancer.

    Use and Human Exposure - Hexachloroethane is a colorless crystal with a camphor-like odor. It is used as a solvent, as a retarding agent in fermentation, and in the synthesis of other chemicals. It is also found in pyrotechnics and smoke devices, and in explosives. People can be exposed to hexachloroethane through ingestion, inhalation, and skin absorption (Lewis 1993). It is not known how hexachloroethane is absorbed, broken down, or eliminated by the body.

    General Health Effects - There are no studies of hexachloroethane's potential effects in humans. In animal studies, ingesting very high doses of this compound is associated with kidney damage, decreased litter size, and behavioral changes. In other animal studies, inhaling very large quantities of hexachloroethane is associated with behavioral changes in dogs and rats, and liver enlargement in the guinea pigs. Lower doses have not been associated with similar effects (IRIS 1994). Hexachloroethane's potential health effects via skin absorption are not known. Animal studies indicate inhalation of small amounts of hexachloroethane for long time periods is associated with liver and kidney cancer, but it is not known if hexachloroethane exposure is associated with these same cancers in humans (IRIS 1994).

    Interactions with Other Chemicals - The potential interactive effects between hexachloroethane and other substances found at the site are unknown.

    Site-specific Noncancer Health Effects - In the past, nearby residents were exposed to hexachloroethane through household uses of well water. There are no present-day analyses of hexachloroethane; therefore, we do not know if exposure has stopped because we do not have groundwater, surface soil, sediment, or air samples to evaluate. The past hexachloroethane ingestion doses we estimated for all age groups are somewhat smaller than EPA's RfD indicating noncancer illnesses are unlikely to be associated with this exposure. In addition, the modeled hexachloroethane inhalation doses we estimated for all age groups are much smaller than the levels associated with noncancer illnesses in rats, dogs, or guinea pigs in the one animal study available (IRIS 1994). However, more studies examining potential health effects from low-dose hexachloroethane inhalation are needed before we can make reliable comparisons with our estimated doses. There are no available human or animal studies examining the potential health effects from skin absorption of hexachloroethane (IRIS 1994).

    Site-specific Cancer Risk - There are no human studies concerning hexachloroethane's ability to cause cancer. However, one study of rats and mice indicates there may be a link between chronic ingestion of hexachloroethane and liver cancer in mice (IRIS 1994). EPA has classified hexachloroethane 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 hexachloroethane ingestion to be negligible. In addition, EPA has also classified hexachloroethane as a suspected cancer-causing agent via inhalation, based upon the ingestion data. However, there are no human or animal studies examining the potential association between hexachloroethane inhalation or skin absorption and cancer (IRIS 1994).

    Sensitive Populations - We did not find any studies or other documents identifying populations unusually sensitive to hexachloroethane.

  7. Lead

    Summary - Lead ingestion doses similar to past doses we estimated for all age groups have been associated with blood formation and blood pressure problems in the human and animal studies we reviewed. Young children appear to be more sensitive than adults to lead exposure. The present-day lead ingestion doses we estimated for young children are somewhat smaller than the doses associated with the blood problems in these studies. In animal studies, lead ingestion doses similar to past doses we estimated for all age groups have been associated with changes in the eye structures important in night vision, for young children have been associated with learning problems in young animals, and for adults have been associated with adverse effects on unborn baby animals and reproductive problems in adult animals. There is not enough information to estimate an increased cancer risk from lead ingestion.

    Use and Human Exposure - Lead is a naturally occurring bluish-gray metal found in small quantities in the earth's crust. Most lead used by industry comes from mined ores or from recycled scrap metal. Lead is used to produce some types of batteries, ammunition, and electronic devices. It is used as radiation shields (from x-rays, for example), and is found in sheet lead, solder, pipes, caulking, paints, ceramic glazes, and gasoline. In recent years, the amount of lead added to solder, paints, ceramic products, caulking, and gasoline has been reduced because of its harmful health effects; however, its use in ammunition and roofing has increased. Human activities, particularly the use of leaded gasoline, have spread lead to all parts of the environment (ATSDR 1993l).

    People can be exposed to lead by breathing air, drinking water, eating foods, or ingesting dirt or dust containing lead. Foods such as fruits, vegetables, meats, grains, seafood, soft drinks, and wine may have lead in them. This lead can come from deposition of lead-containing dust on crops or during food processing, plant uptake of lead from soil, use of improperly glazed ceramics or leaded-crystal glassware, lead-soldered cans containing acidic foods, or lead-soldered kettles used to boil water. Communities with acidic water may have increased lead levels in water as the metal leaches out of lead pipes, lead-based solder, and brass faucets. Children can ingest lead-based paint chips. Lead enters the air from industrial releases, the weathering or burning of lead-based paints, or the burning of leaded gasoline, solid wastes, or tobacco. Consequently, tobacco smokers can be exposed to more lead than nonsmokers. Although skin contact with lead-containing dust and dirt occurs every day, not much lead passes through intact skin (ATSDR 1993l).

    Most lead enters the body through ingestion. The amount of lead entering the body after ingestion depends upon when the last meal was eaten, as well as the person's age and how well the lead particles are dissolved in the stomach juices. Children tend to absorb more lead than adults, and more is absorbed from an empty stomach than from a full stomach. Frequent skin contact with lead in soil and dust can result in young children's swallowing high lead through hand-to-mouth behavior. In adults, only a small amount of lead can enter the body through intact skin if it is not washed off after skin contact. Lead can also enter the body through breathing in dust or chemicals containing lead, or through smoking tobacco products. Once in the body, lead first travels to body organs such as the liver, kidneys, lungs, brain, spleen, muscles, and heart. In adults, almost all of the lead entering the body leaves within a couple of weeks through urination or defecation. However, in children, only about a third of ingested lead leaves the body in waste. Lead that does not leave the body will, after several weeks, move to the bones and teeth where it can stay for decades. Some of the lead stored in bones and teeth may leave these tissues and reenter the blood and body organs at a later date. In adults, 94% of the total body lead is stored in bones and teeth. In children, only 73% is stored in bones and teeth; the rest is in body organs and blood.

    General Health Effects - At high levels of exposure, lead can damage the brain or kidneys of adults or children. Unborn children are particularly sensitive to lead exposure during development. Exposure during pregnancy can lead to premature birth, smaller babies, and decreased mental abilities in the infant. Young children are also more sensitive to lead exposure than are adults. Lead exposure can decrease IQ scores and reduce the growth of young children. These effects are more often seen after exposure to high lead levels rather than low lead levels. In adults, high levels of lead exposure may decrease reaction time; affect the memory; cause weakness in the fingers, wrists, or ankles; increase blood pressure in men; cause anemia; cause miscarriages; or damage the male reproductive system. It is not known if lead exposure causes cancer in humans. Some studies show rats and mice given very large doses of lead develop kidney tumors. However, the results of these animal studies are questionable because of the study methods used. Still, lead is classified as a suspected cancer-causing agent via ingestion (ATSDR 1993l).

    Interactions with Other Chemicals - A number of studies of humans have found undernourished individuals are more susceptible to the effects of lead exposure because deficiencies in calcium, phosphorus, copper, iron, and zinc can increase lead absorption. Several animal studies have supported these findings by showing that sufficient dietary intake of calcium, magnesium, phosphorus, copper, iron, and zinc protects against the harmful effects of various lead compounds. A few animal studies show cadmium increases lead's toxic effects on mortality, behavior, and the male reproductive system. In addition, lead may worsen mercury's effects on the kidneys and liver. Another animal study indicates lead blocks intestinal responses to vitamin D and its by-products. In a different study, coexposure of lead and ethanol (drinking alcohol) in rats increased the rat's susceptibility to lead's toxic effects on the liver, brain, and nervous system. However, another study investigating the interactive effects of lead and ethanol during pregnancy found no interaction between these substances on reproduction or learning in rats (ATSDR 1993l).

    Site-specific Noncancer Health Effects - In the past, nearby residents were exposed to lead through incidental ingestion of on-site subsurface soils, incidental ingestion of on- and off-site sediments, incidental ingestion of off-site surface water, and ingestion of groundwater. Present-day groundwater analyses indicate exposure may be continuing for some residents still using private well water. In the human and animal studies we reviewed, lead ingestion doses similar to past doses we estimated for all age groups have been associated with increased blood pressure and adverse effects on blood formation that may lead to anemia and decreased blood hemoglobin formation (ATSDR 1993l). Some human evidence suggests males may be more likely to experience lead-induced blood pressure increases than females (Amdur et al. 1991; ATSDR 1993l). Lead ingestion doses somewhat larger than the present-day doses we estimated for young children have been associated with effects on blood formation and blood pressure in these studies (ATSDR 1993l).

    In the animal studies we reviewed, lead ingestion doses slightly larger than the past doses we estimated for all age groups have been associated with changes in the rods of the eye (structures involved with night vision). Presumably, these changes could lead to a decreased ability to see well at night. Visual effects associated with lead exposure have been noted in humans, but are not well documented. In addition, lead ingestion doses similar to past doses we estimated for young children have been associated with learning problems in animals. In some studies, low level lead exposure before or shortly after birth has been associated with learning impairments in young monkeys. Other studies indicated these learning problems may continue for months or years after exposure has stopped. Studies of rats also have found associations between low level lead exposure and learning impairment. In contrast, human studies of children exposed to low lead levels have mixed results. Some studies indicate low-level lead exposure may be associated with 4-5 point decreases in IQ scores, but a couple of studies show no association between learning and low-level lead exposure. Still, overall, the data suggest children are more sensitive than adults to low-level lead exposure, and animals are affected at roughly the same blood levels as humans (ATSDR 1993l).

    Finally, lead ingestion doses similar to past doses we estimated for adults have been associated with adverse effects on reproduction and unborn babies in the animal studies we reviewed. In one study of female monkeys, chronic lead ingestion doses slightly larger than those estimated for adults have been associated with menstrual cycle irregularities and ovarian cyst development. Other studies of rats indicated an association between low level lead exposure before or shortly after birth and delayed sexual maturation in female offspring. In some male rats, exposure to low lead levels has been associated with decreased sperm counts, low sperm movement, increased prostate gland weight, and impotence. In humans, there are qualitative data indicating exposure to high lead levels adversely affects reproduction, but there are no data concerning the effects of low lead doses. Besides affecting reproduction, animal studies suggest low level lead exposure may be associated with blood formation problems in unborn babies, as well as the already mentioned learning behavior and sexual maturation problems after birth. There is no evidence low-level lead exposure is associated with body malformations (ATSDR 1993l).

    The potential health effects of lead for adults need to be interpreted with caution. In estimating our doses, we used the maximum groundwater concentration which was found in an on-site borehole. The maximum concentrations found in on-site private wells was 10 times smaller and in off-site wells was 20 times smaller than the maximum borehole value. At either of these drinking water well concentrations, our projected blood lead concentrations for adults are below the blood lead levels associated with health effects in adults.

    Site-specific Cancer Risk - There are no reliable studies available to evaluate lead's cancer-causing potential in humans. However, animal studies indicate very high doses of lead may be associated with kidney cancer (ATSDR 1993l). Based on the animal data, EPA, IARC, and NTP each have classified lead as a possible human cancer-causing agent via ingestion (ATSDR 1993a, 1993l). Nevertheless, limitations in the animal studies do not permit derivation of the toxicity values needed to estimate an increased cancer risk due to lead ingestion (ATSDR 1993l).

    Sensitive Populations - Preschool age children (under six years old), pregnant women, the elderly, smokers, alcoholics, and people with diseases affecting blood formation, nutrient uptake, and nerve or kidney function may be more susceptible to the toxic effects of lead exposure. Children are at the greatest risk for experiencing the toxic effects of lead exposure. Recent data suggest pregnant women, nursing mothers, and individuals with osteoporosis may have increased bone mobilization, resulting in increased levels of lead throughout the body. In addition, people with genetic diseases affecting the blood (such a thalassemia or sickle cell anemia), certain body enzymes, metabolic disorders (such as porphyria) may also be unusually sensitive to lead exposure.

  8. Manganese

    Summary - The manganese ingestion doses we estimated for adults and average children are much smaller than the doses associated with noncancer illnesses in the animal studies we reviewed. Young children may be more sensitive than adults to the effects of manganese exposure on the nervous system. Still, it is not clear if manganese ingestion doses similar to those we estimated for young children have been associated with biochemical changes in the nervous system. It is not known if manganese ingestion is associated with cancer.

    Use and Human Exposure - Manganese is a naturally occurring metal found in rock and fossil fuels. Manganese compounds can exist in air as dust particles. Some manganese compounds can dissolve in water, and low levels of these compounds are normally present in lakes, streams, and the ocean. Manganese is also normally present in plants and animals. Manganese metal, once purified from mined rocks, is used to make various kinds of steel and some types of batteries. Manganese is also an ingredient in some ceramics, pesticides, fertilizers, and dietary supplements. Because manganese is commonly present in the environment, most people are exposed to small amounts of it daily in air, water, soil, and food. Food is the largest manganese source for most people. However, people living near coal- or oil-burning factories, or close to a major highway may breathe in higher than normal amounts of manganese. In addition, people living next to waste sites releasing manganese may also be exposed to unusually high amounts of this element in water or soil. Little manganese enters the body through intact skin. Inhaled manganese particles are coughed up and swallowed or slowly absorbed from the lungs into the bloodstream. Only a small amount of ingested manganese is absorbed from the intestines into the bloodstream; most leaves the body through the feces. Because manganese is a normal part of the body, the body ordinarily controls the amount of manganese that is absorbed and retained. Therefore, the total amount of manganese in the body tends to remain relatively constant, even if exposure rates are higher or lower than usual. However, if too much manganese is taken in, the body may not be able to adjust for the added amount (ATSDR 1992f).

    General Health Effects - Eating a normal diet seems to provide the required daily amount of manganese needed for good health, and there are no reported cases in humans of illnesses from eating too little manganese. However, eating too much manganese can cause serious illness. Miners and steel workers inhaling very high amounts of manganese dust for many months or years sometimes develop a disease called manganism. This disease is characterized by mental and emotional disturbances, and slow and clumsy body movements resulting from injury to the part of the brain that helps control body movements. It is not certain if eating or drinking too much manganese is associated with manganism. Impotence is also a common effect in men who breathe in very high amounts of manganese dust. Animal studies indicate too much manganese may be associated with harm to the testes. Not much is known about the effects of too much manganese in women. Animal studies suggest females may be less sensitive than males to the effects of manganese; however, this is not certain for humans. It is not known if too much manganese is associated with birth defects or cancer (ATSDR 1992f).

    Interactions with Other Chemicals - Animal studies clearly show that intestinal absorption of manganese is inversely related to dietary iron intake. That is, high iron intake leads to decreased manganese absorption and toxicity, and low iron intake leads to increased manganese absorption and toxicity. Conversely, high dietary manganese leads to low iron absorption. Cadmium seems to have a similar inhibitory effect on the uptake of manganese. In addition, manganese appears to decrease cadmium's toxicity. There is limited animal evidence that ethanol (drinking alcohol) may increase human susceptibility to cadmium toxicity. There is also some animal evidence that chronic administration of prescription drugs containing chlorpromazine may increase manganese levels in the brain (ATSDR 1992f).

    Site-specific Noncancer Health Effects - In the past, nearby residents were exposed to manganese through incidental ingestion of on-site subsurface soils and sediments, incidental ingestion of on- and off-site surface water, and ingestion of groundwater. Low concentrations of manganese appear to be naturally present in the local groundwater, and present-day groundwater analyses indicate exposure is continuing for residents still using private well water. The past manganese ingestion doses we estimated for adults and average children are much smaller than the doses associated with noncancer illnesses in the animal studies we reviewed. However, in one study of newborn rats, manganese ingestion doses somewhat larger than the dose estimated for young children have been associated with biochemical changes in the nervous system. This study suggests young animals may be more susceptible than adults to manganese's toxic effects on the nervous system. In contrast, another study of rats did not find any association between such low doses of manganese and nervous system changes. Moreover, there is evidence rats may respond differently from humans to manganese exposure, making the interpretation of the health effects in the former study uncertain. Present-day ingestion dose estimates are below levels of concern and are not likely to contribute significantly to past exposures. There are no reliable human studies available for comparison (ATSDR 1992f).

    Site-specific Cancer Risk - Information on the cancer-causing potential of manganese is limited and difficult to interpret with certainty. Animal studies suggest the potential association between manganese and cancer in humans is probably small (ATSDR 1992f).

    Sensitive Populations - There seems to be a wide range in individual susceptibility to nervous system effects from inhaling manganese dust. Newborn babies seem to retain a higher percentage of ingested manganese than adults, resulting in higher tissue levels of manganese, particularly in the brain. Still, it is not clear if this results in increased susceptibility to manganese-induced toxicity in infants. Elderly people may be somewhat more susceptible to manganese's toxic effects on the nervous system than the general population, perhaps because of loss of nerve cells due to aging or to accumulated damage from other environmental toxins acting on the nervous system. Because manganese is excreted through the liver, people with liver disease may have a decreased ability to handle excess manganese (ATSDR 1992f).

  9. Methylene Chloride

    Summary - There is not enough toxicological information to determine if noncancer illnesses may be associated with methylene chloride ingestion. The modeled past and present methylene chloride 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. Skin contact with liquid methylene chloride can cause chemical burns, but it is not known if skin absorption of methylene chloride is associated with internal health effects. We estimate the increased risk of liver cancer from past methylene chloride ingestion to be low. Using modeled inhalation data, we estimate the increased risk of developing lung or liver cancer from past methylene chloride 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 methylene chloride ingestion and inhalation to be negligible. We did not have enough information to estimate an increased cancer risk from past or present skin exposure to methylene chloride.

    Use and Human Exposure - Methylene chloride is a human-made, colorless liquid with a sweetish odor. It is widely used as an industrial solvent and as a paint stripper. Methylene chloride is also used to manufacture photographic film, and can be found in some aerosols, pesticides, spray paints, automotive cleaners, and other household products. Because it evaporates easily, most methylene chloride enters the environment in air where it is subsequently broken down by sunlight and other air-borne chemicals into carbon dioxide. Sometimes small amounts are found in drinking water where it is broken down by bacteria and water-borne chemicals. Because methylene chloride is so widely used, most people are exposed to this compound daily in air, water, food, or consumer products. Near hazardous waste sites, the most likely exposure route is by breathing in contaminated air. A majority of the methylene chloride that is inhaled enters the bloodstream and is quickly carried throughout the body. The methylene chloride uptake rate from the digestive system into the bloodstream is unknown, but is likely to be fast. Skin absorption is usually small. Once in the bloodstream, most of the methylene chloride goes to the liver, kidney, brain, lungs, and fatty tissue. Increased physical activity or increased body fat tends to increase the amount of methylene chloride that remains in the body. Within 40 minutes, about half of the methylene chloride leaves the blood as it is broken down into other chemicals, including carbon monoxide, a compound normally present in the body in small amounts from the periodic breakdown of blood hemoglobin. Most unchanged methylene chloride and its breakdown products leave the body by exhalation within 48 hours. Small amounts leave in the urine (ATSDR 1993m).

    General Health Effects - Breathing in moderate amounts of methylene chloride for a few hours may temporarily impair hearing and vision. Inhaling larger amounts may temporarily impair reaction time, balance, and coordination. Breathing in methylene chloride for longer time periods may cause nausea, dizziness, drunkenness, and tingling or numbness in the fingers and toes. Animal studies suggest inhaling moderate amounts of methylene chloride is associated with changes in the liver and kidney. A limited number of studies have not found similar associations in humans. Animal studies also indicate exposure to high concentrations of methylene chloride vapors is associated with eye irritation and corneal changes; these effects appear to be reversible. In contrast, animal studies have not found an association between inhaling high concentrations of methylene chloride vapors and reproductive problems or birth defects. In humans, skin contact with liquid methylene chloride can cause chemical burn. Inhaling high methylene chloride concentrations has not been associated with cancer in humans; however, chronic inhalation of high methylene chloride concentrations has been associated with an increased occurrence of cancer in mice. Based on animal studies, methylene chloride is classified as a suspected cancer-causing agent in humans via ingestion and inhalation (ATSDR 1993m).

    Interactions with Other Chemicals - In rats, methylene chloride can interact with carbon monoxide to produce additive increases in carboxyhemoglobin (carbon monoxide bound to blood hemoglobin) formation (ATSDR 1993m). This can decrease the blood's ability to carry oxygen and deliver oxygen to body tissues (Wilson et al. 1991). In animals, methylene chloride can interact with ethanol (drinking alcohol) to produce an additive decrease in the conduction of nerve impulses (ATSDR 1993m).

    Site-specific Noncancer Health Effects - In the past, nearby residents were exposed to methylene chloride through incidental ingestion of on-site subsurface soil and household uses of groundwater. 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 methylene chloride from groundwater and expel it into the air. The past and present methylene chloride ingestion doses we estimated for all age groups are much smaller than the doses associated with noncancer illnesses in the few animal studies we reviewed (ATSDR 1993m). More studies examining potential health effects from low-dose methylene chloride ingestion are needed before we can make reliable comparisons with our estimated doses.

    We used modeled data to estimate past inhalation exposure to methylene chloride volatilized in the shower and present in ambient air. The past and present methylene chloride inhalation doses we estimated for all age groups are much smaller than the doses associated with noncancer illness in the few human studies we reviewed. However, methylene chloride inhalation doses smaller than past doses we estimated for all age groups have been associated with a reversible increase in liver fat content in studies of rats and mice. Although human study suggests the liver may not be a major target organ for methylene chloride in humans, little is known about methylene chloride's effects on the human liver or the significance of these findings. Present-day exposure doses from both the air stripper and from breathing methylene chloride vapors during household water use are below levels of concern (ATSDR 1993m).

    Finally, liquid methylene chloride is a known skin irritant, and can cause chemical burns at unknown doses. There are no human or animal studies examining methylene chloride's potential effects on internal body systems from skin absorption (ATSDR 1993m).

    Site-specific Cancer Risk - There are no human studies examining methylene chloride's cancer-causing potential after chronic oral exposure. However, animal studies indicate chronic oral exposure to high doses of methylene chloride is associated with liver cancer (ATSDR 1993m). EPA, NTP, and IARC each have classified methylene chloride as a suspected human cancer-causing agent via ingestion (ATSDR 1993a). Based on the exposure and dose estimates we have, we estimate adult residents' increased risk of cancer from past methylene chloride ingestion to be low at 52 in 100,000. This means the risk of getting cancer, above the background rate, could rise from 25,000 cases per 100,000 people to 250,052 cases in a 70-year lifetime. We estimate the present-day increased cancer risk from methylene chloride ingestion to be negligible.

    Epidemiological studies have not identified a causal relationship between occupational exposure to airborne methylene chloride and cancer in humans. However, these studies are limited in their ability to detect small increases in cancer. Animal studies suggest inhalation of high doses of methylene chloride is associated with lung and liver cancer in rats and mice, and is associated with an increased number of noncancerous breast tumors (in female mice and both sexes of rats) (ATSDR 1993m). EPA, NTP, and IARC each have classified methylene chloride as a suspected cancer-causing agent via inhalation (ATSDR 1993a). Since we did not have actual measurements of past methylene chloride concentrations in air, we used known groundwater concentrations to estimate the cancer risk from inhaling methylene chloride vapors in the shower and in ambient air inside and outside the home. Based on the modeled exposure and dose information we have, we estimate adult residents' increased risk of cancer from past methylene chloride inhalation to be moderate at 9 in 1,000. This means the risk of getting cancer, above the background rate, could rise from 250 cases per 1,000 people to 259 cases in a 70-year lifetime. We estimate the present-day increased cancer risk from methylene chloride inhalation to be negligible.

    Finally, there are no human or animal studies of the potential association between methylene chloride skin absorption and cancer (ATSDR 1993m).

    Sensitive Populations - People likely to be unusually sensitive to the effects of methylene chloride are those with pre-existing increased amounts of carboxyhemoglobin in their blood. This group includes smokers (who constantly maintain higher levels of carboxyhemoglobin in their blood) and people with cardiovascular disease (ATSDR 1993m).

  10. n-Nitrosodiphenylamine

    Summary - The past n-nitrosodiphenylamine ingestion doses we estimated for all age groups are much smaller than the doses associated with noncancer illnesses in the animal studies we reviewed. It is not known if inhalation or skin absorption of n-nitrosodiphenylamine is associated with noncancer illnesses. We estimate the increased cancer risk from past n-nitrosodiphenylamine ingestion to be negligible. There is not enough toxicological information to determine if past n-nitrosodiphenylamine inhalation or skin absorption could be associated with cancer.

    Use and Human Exposure - n-Nitrosodiphenylamine is a orange-brown or yellow solid that evaporates slowly into the air, dissolves in water, and attaches to soil. There is evidence that some microorganisms may make small amounts of this compound in nature. Human-made n-nitrosodiphenylamine is used to produce rubber products and other chemicals. It enters the environment from industrial discharges or from hazardous waste site releases into air, water, or soil. Once in the environment, n-nitrosodiphenylamine breaks down into other substances. It is not known if any of these breakdown products are harmful. Most n-nitrosodiphenylamine disappears from water or soil within several weeks. Because n-nitrosodiphenylamine is not normally found in the environment, people are usually exposed to this chemical only at work or at hazardous waste sites. Animal studies indicate n-nitrosodiphenylamine can enter the body through ingestion or skin contact. It is not known if n-nitrosodiphenylamine can enter the body through the lungs. Once in the body, animals break this chemical down into other chemicals that can harm their health. One animal study shows that n-nitrosodiphenylamine rapidly leaves the body in the urine. Some is probably excreted in the feces as well. Based on the animal data, it is likely humans have similar intake, breakdown, and elimination mechanisms (ATSDR 1993p).

    General Health Effects - Very little is known about the possible health effects of n-nitrosodiphenylamine. In animals, ingesting very large amounts of this compound can cause death. In other studies, animals eating moderate to high doses of n-nitrosodiphenylamine for a long time developed swelling, changes in body weight, and bladder cancer. It is not known if this chemical has comparable effects in humans. Similarly, it is not known if n-nitrosodiphenylamine affects reproduction or causes birth defects. Based on the animal studies, n-nitrosodiphenylamine is classified as a suspected cancer-causing agent in humans via ingestion (ATSDR 1993a; IRIS 1994).

    Interactions with Other Chemicals - In mice, n-nitrosodiphenylamine can interact with pentobarbital, a component of some prescription drugs, to decrease the drug's sedative effects (that is, sleeping time) (ATSDR 1993p).

    Site-specific Noncancer Health Effects - In the past, nearby residents were exposed to n-nitrosodiphenylamine through ingestion of groundwater. The limited number of present-day samples indicate n-nitrosodiphenylamine is no longer found in the groundwater, but we do not have enough groundwater, surface soil, or sediment samples to confirm exposure has stopped. The past n-nitrosodiphenylamine ingestion doses we estimated for all age groups are much smaller than the doses associated with noncancer illnesses in the animal studies we reviewed. There are no human or reliable animal studies examining the health effects associated with n-nitrosodiphenylamine inhalation or skin absorption (ATSDR 1993p). More studies examining the potential health effects from these exposure routes are needed before we can make reliable comparisons with our estimated doses.

    Site-specific Cancer Risk - There are no human studies examining n-nitrosodiphenylamine's cancer-causing potential after oral exposure. However, there is a weak association between high-dose n-nitrosodiphenylamine ingestion and an increased frequency in bladder cancer in rats (ATSDR 1993p). EPA has classified n- nitrosodiphenylamine as a suspected human cancer-causing agent via ingestion (ATSDR 1993a). Based on the exposure and dose information we have, we estimate adult residents' increased risk of cancer from past exposure to n-nitrosodiphenylamine to be negligible. There are no human or reliable animal studies examining the potential association between n-nitrosodiphenylamine inhalation or skin absorption and cancer (ATSDR 1993p).

    Sensitive Populations - Because of the limited toxicity data for n-nitrosodiphenylamine, it is difficult to identify persons likely to be unusually sensitive to this compound. It is possible people with bladder dysfunction or disease will be unusually sensitive to n-nitrosodiphenylamine exposure. It also seems likely n-nitrosodiphenylamine may affect the body's breakdown of some prescription drugs and ethanol (drinking alcohol) in unspecified ways (ATSDR 1993p).

  11. PCBs  

    Summary - There is not enough toxicological information to determine if noncancer illnesses may be associated with PCB ingestion, inhalation, or skin absorption doses similar to the past doses we estimated for all age groups. We estimate the increased liver cancer risk from past PCB ingestion to be moderate. There is not enough toxicological information to determine if past PCB inhalation or skin absorption could be associated with cancer.

    Use and Human Exposure - PCBs (polychlorinated biphenyls) are a group of human-made organic chemicals, consisting of over 200 individual compounds. PCBs are either oily liquids or solids that range in color from clear to light yellow. They have no smell or taste. Some PCB mixtures are called by their commercial name, Aroclor. Because they are a good insulating material and don't burn easily, PCBs were widely used as coolants and lubricants in transformers, capacitors, and other electrical equipment. In the United States, the manufacture of PCBs stopped in 1977 because of evidence that they built up in the environment and caused harmful effects. Still, consumer products made prior to October 1977, such as fluorescent lighting fixtures, electrical devices or appliances, microscope oil, and hydraulic fluids may contain PCBs. In the past, PCBs entered the air, water, and soil during their manufacture, use, and disposal. Today, PCBs enter the environment from poorly maintained hazardous waste sites containing PCBs, improper dumping of PCB wastes, leaks from electrical transformers containing PCBs, and disposal of PCB-containing consumer products into municipal landfills. In the air, PCBs can be present as solid or liquid aerosols, or as vapors. PCBs in the air can travel long distances away from their source, but eventually settle on the land or water. Only small amounts of PCBs remain dissolved in water, and most stick strongly to soils or sediments. In soils, PCBs usually don't travel downwards very deeply with rainwater. In sediments, fish may ingest PCBs, and these compounds can build up in their bodies until the PCB concentration is thousands of times larger than the concentration found in the water. The breakdown of PCBs in water and soil takes several years. In the sediments of permanent lakes and rivers, PCBs usually don't break down; instead, they are released back into the water in small amounts over time (ATSDR 1993q).

    Because PCBs remain in the environment for a long time and because many pieces of electrical equipment containing PCBs are still in use, it is still possible to be exposed to these compounds. Small amounts of PCBs can be found in almost all outdoor air, indoor air, soil surfaces, and surface waters. PCBs may also be found in fish. The concentration of PCBs in air, water soil and food have generally decreased since production stopped in 1977. Eating fish and breathing air in buildings using PCB-containing electrical equipment are the most likely sources of PCB exposure for most people. People living around hazardous waste sites containing PCBs are usually exposed by breathing air containing PCBs. Children playing at or near these sites may also be exposed by touching and eating soils containing PCBs. Infants are most likely exposed through breast milk containing PCBs (ATSDR 1993q).

    Nearly all of the ingested PCBs are likely to be absorbed quickly into the bloodstream. It is not known how much or how quickly PCBs are absorbed into the body through inhalation or skin absorption. Once in the body, some PCBs are broken down into other chemicals that are eliminated in the feces within a few days. However, some PCBs and their breakdown products remain stored in body fat for months and perhaps years. Some of the stored PCBs build up in breast milk and can be passed to infants through breast-feeding. It is not known if any of the PCB breakdown products are harmful to human health (ATSDR 1993q).

    General Health Effects - Human studies have shown workers exposed to relatively high concentrations of PCB vapors can develop skin irritations, such as rashes and acne, as well as nose, lung, and eye irritation. There are no studies of PCB ingestion in humans. In animal studies, ingestion of large amounts of PCBs for a short time period has been associated with mild liver damage and death in rats. In other animal experiments, ingestion of smaller amounts of PCBs over several weeks or months has been associated with many serious health effects including: liver, stomach, and thyroid gland injuries; anemia; acne; and damaged reproduction. These effects were seen in many different kinds of animals and in their offspring. PCB ingestion has not been associated with birth defects. There is limited information on health effects from skin or inhalation exposure to PCBs. In one experiment, skin exposure to moderate amounts of PCBs has been associated with liver, kidney, and skin damage in rabbits. In different experiments, breathing in large amounts of PCBs over several months has been associated with liver and kidney damage in rats and other animals. It is not known if PCBs cause cancer in humans. Experiments in rats indicate PCB exposure may be associated with liver cancer in these animals. Based on the animal data, PCBs are classified as a suspected human carcinogen (ATSDR 1993a, 1993q).

    Interactions with Other Chemicals - Studies indicate PCBs can interact with pentobarbital, a component of some prescription drugs, to decrease the drug's sedative effects (that is, sleeping time). In animals, pretreatment with PCB mixtures can increase the toxic effects trichloroethene and tetrachloroethene have on the liver. In rats, pretreatment with Aroclor-1254 protected against the toxic effects on the liver due to 1,1-dichloroethene inhalation. Increased dietary vitamin C intake may have similar protective effects. In rats, coadministration of cadmium and Aroclor-1248 have additive effects on growth retardation and blood cholesterol. PCBs can interact with cancer-causing agents in various ways, depending on the interacting chemical used. In animals, several oral exposure studies indicate PCBs may work as cancer cell promoters, and one skin absorption study suggests PCBs may have weak cancer cell initiation abilities. Other studies suggest PCBs may act as cancer inhibitors (ATSDR 1993q).

    Site-specific Noncancer Health Effects - In the past, nearby residents were exposed to PCBs through incidental ingestion of on- and off-site sediments, incidental ingestion of off-site surface waters, and ingestion of groundwater. The limited number of present-day samples indicate PCBs 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 two studies of monkeys, chronic PCB ingestion doses similar to those we estimated for all age groups have been associated with a decrease in the numbers of two kinds of antibodies. However, other immune system parameters measured in these studies were not affected, and there was no change in overall immune response (ATSDR 1993q). Nevertheless, animal studies also indicate PCB exposure at higher doses is associated with suppression of the immune system (Amdur et al. 1991; ATSDR 1993q). More studies examining potential immune system effects from low-dose PCB ingestion are needed before we can make reliable comparisons with our estimated doses.

    We used modeled data to estimate past inhalation exposure to PCBs volatilized in the shower and present in ambient air. PCB inhalation doses similar to the past inhalation doses we estimated for all age groups have been associated with effects on the liver and kidney in the one animal study available. In this study, the severity of the liver effects ranged from increased numbers of storage compartments inside liver cells to fatty changes and other degenerative lesions, depending on the species of animal tested. Although epidemiologic studies of Aroclor-exposed workers indicate an association may exist between PCB exposure and increased activity of some liver enzymes, there is no conclusive evidence that PCBs are toxic to the human liver. The available study also reported an association between low-dose PCB inhalation and slight degeneration of the kidney tubules in rats, but an invalid analytical method made the PCB concentrations uncertain (ATSDR 1993q). More studies examining potential health effects from low-dose PCB inhalation are needed before we can make reliable comparisons with our estimated doses.

    Finally, the doses we estimated for PCB skin absorption while showering or swimming were much smaller than the doses associated with noncancer illnesses in the few animal studies we reviewed. However, these studies did not investigate the potential health effects associated with chronic, low-dose skin exposure to PCBs. More studies are needed before we can make reliable comparisons with our estimated skin absorption doses (ATSDR 1993q).

    Site-specific Cancer Risk - Studies of PCB-exposed workers provide inconclusive evidence that PCB exposure is associated with cancer in humans. However, animal studies indicate the cancer-causing potential of PCB mixtures depends on the degree of chlorination, and ingestion of PCBs that are at least 60% chlorine by weight is associated with liver cancer in rats. In addition, studies with rats and mice indicate that PCBs with lower chlorine content can act as tumor promoters once these cells have been treated with chemicals acting as tumor initiators (ATSDR 1993q). Based on the animal evidence, EPA, NTP, and IARC each have classified PCBs 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 PCB ingestion to be moderate at 6 in 1,000. This means the risk of developing cancer, above the background rate, could rise from 250 cases per 1,000 people to 256 cases in a 70-year lifetime. There are no reliable studies examining the potential association between PCB inhalation or skin absorption and cancer (ATSDR 1993q).

    Sensitive Populations - Unborn and newborn children are potentially susceptible to the health effects of PCBs because their underdeveloped enzyme systems do not eliminate chemicals from the body as easily as in adults. In addition, breast-fed infants may have additional risk because of a steroid excreted in human milk that can inhibit PCB elimination from the body. Children exposed to the antibiotic novobiocin may also be more susceptible to the health effects of PCBs because the drug may interact with the mechanism responsible for eliminating PCBs from the body. People with liver infection, dysfunction, or disease may also be more susceptible to PCB toxicity (ATSDR 1993q).

  12. 1,1,2,2-Tetrachloroethane

    Summary - There is not enough toxicological information to determine if noncancer illnesses may be associated with 1,1,2,2-tetrachloroethane ingestion or skin absorption doses similar to the past doses we estimated for all age groups. The past 1,1,2,2-tetrachloroethane 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. There is no apparent increased cancer risk from past 1,1,2,2-tetrachloroethane ingestion. There is not enough toxicological information to determine if past 1,1,2,2-tetrachloroethane inhalation or skin absorption could be associated with cancer.

    Use and Human Exposure - 1,1,2,2-Tetrachloroethane is a human-made, colorless liquid with a sweet, chloroform-like odor. In the past, 1,1,2,2-tetrachloroethane was used in large quantities to produce other chemicals and as an industrial solvent. It was also used to separate other substances, to clean and degrease metals, and to manufacture paints and pesticides. In the present, 1,1,2,2-tetrachloroethane's use appears to be limited, but information about its use is not available. Most 1,1,2,2-tetrachloroethane released into the environment moves into air or groundwater where breakdown is slow. Low levels of 1,1,2,2-tetrachloroethane can be present in both indoor and outdoor air, and higher concentrations may be present in workplaces where this substance is used. Studies show 1,1,2,2-tetrachloroethane in groundwater or landfills slowly changes to other chemicals, including vinyl chloride. Exposure to 1,1,2,2-tetrachloroethane most commonly occurs through inhalation of or skin contact with 1,1,2,2-tetrachloroethane vapors. It is rare for individuals to be exposed to 1,1,2,2-tetrachloroethane in drinking water, and this substance is not normally found in soil or food. The body seems to absorb 1,1,2,2-tetrachloroethane easily through inhalation, ingestion, or skin absorption. Animal studies indicate 1,1,2,2-tetrachloroethane, once in the body, can be broken down into other substances that may be toxic, such as vinyl chloride. 1,1,2,2-Tetrachloroethane leaves the body within a few days through exhalation and urination (ATSDR 1989e).

    General Health Effects - Exposure to 1,1,2,2-tetrachloroethane can be life threatening if a person is exposed to very large amounts of this chemical. Breathing in 1,1,2,2-tetrachloroethane fumes at concentrations high enough to notice its sickeningly sweet smell can cause fatigue, vomiting, dizziness, and possibly unconsciousness. Most people will recover once they are in fresh air. Breathing or drinking smaller amounts (but still enough to have an odor) has been associated with dizziness, stomach aches, and liver damage. The human health effects of chronic exposure to very small doses are not known. Similarly, there is not enough information to determine if exposure to 1,1,2,2-tetrachloroethane is associated with reproductive effects or birth defects (ATSDR 1989e). 1,1,2,2-Tetrachloroethane is a suspected cancer-causing agent via ingestion (ATSDR 1993a).

    Interactions with Other Chemicals - In animals, survival times are increased if 1,1,2,2-tetrachloroethane is administered with carbon or castor oil, but are decreased when administered with milk, mineral oil, or paraffin. It is not known if similar interactive effects occur in humans. Ethanol (drinking alcohol) increases the breakdown of 1,1,2,2-tetrachloroethane, and may intensify its toxic effects (ATSDR 1989e).

    Site-specific Noncancer Health Effects - In the past, nearby residents were exposed to 1,1,2,2-tetrachloroethane through ingestion of groundwater. The limited number of present-day samples indicate 1,1,2,2-tetrachloroethane is no longer found in the groundwater, but we do not have enough groundwater, surface soil, or sediment samples to confirm exposure has stopped. The past 1,1,2,2-tetrachloroethane ingestion doses we estimated for all age groups are much smaller than the doses associated with noncancer illnesses in the few animal studies we reviewed (ATSDR 1989e). More studies examining potential health effects from low-dose 1,1,2,2-tetrachloroethane ingestion are needed before we can make reliable comparisons with our estimated doses.

    We used modeled data to estimate past inhalation exposure to 1,1,2,2-tetrachloroethane volatilized in the shower and present in ambient air. The past 1,1,2,2-tetrachloroethane inhalation doses we estimated for all age groups are much smaller than the doses associated with noncancer illness in the human and animal studies we reviewed (ATSDR 1989e).

    There are very few quantitative studies of 1,1,2,2-tetrachloroethane's health effects from skin absorption. The two human studies we reviewed are confounded by multiple exposure routes. The one quantitative animal study cited found skin damage in guinea pigs after exposure to very high doses. There were no studies concerning health effects from low-dose skin exposure to 1,1,2,2-tetrachloroethane (ATSDR 1989e). More studies examining potential health effects from low-dose 1,1,2,2-tetrachloroethane skin absorption are needed before we can make reliable comparisons with our estimated doses.

    Site-specific Cancer Risk - Epidemiologic evidence associating 1,1,2,2-tetrachloroethane ingestion with cancer in humans is inconclusive. In one animal study, one strain of mice chronically ingesting high levels of 1,1,2,2-tetrachloroethane had a significant increase in the incidence of liver cancer. There is some evidence that liver cancers are not unusual in this strain of mice, making interpretation of these data uncertain. Nevertheless, EPA has classified 1,1,2,2-tetrachloroethane as a suspected human cancer-causing agent via ingestion (ATSDR 1989e, 1993a). Based on the exposure and dose estimates we have, there is no apparent increased risk of developing cancer from past 1,1,2,2-tetrachloroethane exposure. There are no reliable human or animal studies examining the potential association between 1,1,2,2-tetrachloroethane inhalation or skin absorption and cancer (ATSDR 1989e).

    Sensitive Populations - People who consume ethanol may be at increased risk of the toxic effects of 1,1,2,2-tetrachloroethane (ATSDR 1989e).

  13. Tetrachloroethene

    Summary - The past and present tetrachloroethene ingestion doses we estimated for all age groups are much smaller than EPA's RfD, indicating noncancer illnesses are unlikely to be associated with oral exposure to this contaminant. In a few human studies, tetrachloroethene inhalation doses similar to past doses we estimated for all age groups have been associated with nervous system/behavioral changes and excretion of excess protein in the urine, a symptom of mild kidney tubule dysfunction. In addition, our estimated past inhalation doses are similar to doses associated with liver enlargement in one study of mice. Present-day exposure doses from both the air stripper and from breathing tetrachloroethene vapors during household water use are much smaller than the doses associated with noncancer illnesses in these human and animal studies. Although tetrachloroethene is a skin irritant, there is not enough toxicological information to determine if noncancer illnesses may be associated with skin absorption of this compound. There is not enough toxicological information to determine if past or present tetrachloroethene ingestion, inhalation, or skin absorption could be associated with cancer.

    Use and Human Exposure - Tetrachloroethene is a human-made chemical with a sharp, sweet odor that evaporates easily. It is widely used for dry cleaning fabrics and metal degreasing operations. Tetrachloroethene is also used to make other chemicals and is found in consumer products such as auto brake quieters and cleaners, water repellents, silicone lubricants, some aerosol cleaners, fabric finishers, spot removers, adhesives, and wood cleaners. In addition, at one time, tetrachloroethene was used as a general anesthetic agent. Other common names for tetrachloroethene are tetrachloroethylene, perchloroethylene, PCE, perclene, and perchlor. Tetrachloroethene enters the air through evaporation during use, evaporation from water or soil, and evaporation or leakage from storage or waste sites containing this compound. It can stay in the air for several months before it is broken down into other chemicals, some of which may be harmful, or it settles in soil or water. Tetrachloroethene entering water supplies can stay there for many months before being broken down. Under the right conditions, bacteria will break tetrachloroethene down into other chemicals, some of which may also be harmful. Tetrachloroethene does not seem to build up in fish (ATSDR 1993r).

    People can be exposed to tetrachloroethene from environmental and occupational sources and from consumer product use. Because it is used so widely, tetrachloroethene is often present in ambient air in very low concentrations. In general, it is present in higher concentrations in urban or industrial areas than in rural or remote areas. When tetrachloroethene is found in water, its concentrations are usually small, although they tend to be higher around waste sites. Although uncommon, small amounts of tetrachloroethene may be found in food. Tetrachloroethene may also be found in breast milk of mothers who have been exposed to this chemical (ATSDR 1993r).

    Tetrachloroethene can enter the body through breathing in air, drinking water, or eating food containing this chemical. The amount entering the body depends upon breathing rate, and food and water intake rate. Tetrachloroethene does not cross the skin easily. Once in the body, most tetrachloroethene is removed by exhaling. Some is changed into other chemicals and are removed in urine within a few days. One of these chemicals, trichloroacetic acid, may be harmful. A small amount of the tetrachloroethene taken in remains in body tissues. Some of this amount is stored in body fat where it can remain for several days or months (ATSDR 1993r).

    General Health Effects - Exposure to high tetrachloroethene concentrations, especially in poorly ventilated areas, can cause dizziness, headache, sleepiness, confusion, nausea, difficulty in speaking and walking, and possibly unconsciousness and death. Exposure to lower airborne concentrations can also result in dizziness, sleepiness, and other nervous system effects. The human health effects of breathing in or drinking low levels of tetrachloroethene are unknown. Similarly, the effects of exposing babies to tetrachloroethene in their mothers' milk are also unknown. This chemical does not seem to be associated with birth defects in humans. Repeated or prolonged skin contact with tetrachloroethene can irritate the skin. In animals, ingesting high doses of tetrachloroethene has been associated with liver or kidney damage, as well as liver and kidney cancers. Tetrachloroethene has not been associated with cancer in humans. Still, based on the animal data, tetrachloroethene is classified as a suspected human carcinogen (ATSDR 1993r).

    Interactions with Other Chemicals - In humans, tetrachloroethene does not seem to interact with ethanol (drinking alcohol) or prescription drugs containing diazepam. In a study of Chinese dry cleaning workers, coexposure to mixtures of tetrachloroethene and trichloroethene resulted in a decreased number of tetrachloroethene breakdown products in the urine. In mice, coexposure to tetrachloroethene and trichloroethene did not have any additive or synergistic effects on the liver. In rats, pretreatment with PCBs increased the break down of tetrachloroethene, and enhanced its toxicity to the liver. There is some evidence tetrachloroethene may make heart muscle more sensitive to the effects of other chemicals, such as epinephrine that is introduced into the body along with injected tetrachloroethene. Tetrachloroethene may also have a direct effect on the heart. In rats, there is evidence tetrachloroethene has a synergistic effect with ethanol and too little oxygen in the blood on heart rate (ATSDR 1993r).

    Site-specific Noncancer Health Effects - In the past, nearby residents were exposed to tetrachloroethene through household uses of groundwater. Present-day groundwater analyses have not detected this compound; however, the air stripper's trial run demonstrated this device will successfully remove tetrachloroethene from groundwater and expel it into the air. The past tetrachloroethene 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. Because present-day tetrachloroethene groundwater concentrations are below the detection limit, they are below levels of concern for oral exposure.

    We used modeled data to estimate past inhalation exposure to past tetrachloroethene volatilized in the shower and present in ambient air. In a couple of human studies, tetrachloroethene inhalation doses similar to those we estimated for all age groups have been associated with nervous system/behavioral changes such as impaired perception, attention, and intellectual function; and excretion of excess protein in the urine, a symptom suggestive of mild damage to kidney tubules. In one animal study, tetrachloroethene inhalation doses similar to past doses we estimated for all age groups have been associated with liver enlargement in mice. The liver is a target organ for tetrachloroethene toxicity in humans, possibly at higher levels than indicated in the mice study. Present-day exposure doses from both the air stripper and from breathing tetrachloroethene vapors during household water use are much smaller than the doses associated with noncancer illnesses in these human and animal studies (ATSDR 1993r).

    Tetrachloroethene can be a skin and eye irritant, and can cause chemical burns at very high concentrations. However, there are no studies of tetrachloroethene's effects on internal body systems resulting from skin absorption (ATSDR 1993r).

    Site-specific Cancer Risk - There are no reliable human studies associating tetrachloroethene ingestion or inhalation with cancer. Available studies of residential exposure to solvent mixtures in drinking water wells are confounded by the presence of other potential cancer-causing agents in the drinking water. Epidemiological studies of dry cleaning workers inhaling tetrachloroethene in solvent mixtures have similar confounding factors, preventing the identification of any potential cancer risk from tetrachloroethene. However, animal studies suggest tetrachloroethene inhalation and ingestion may be associated with liver cancer in mice. In addition, studies of rats suggest tetrachloroethene inhalation may be associated with leukemia in both sexes and kidney cancer in males. It is not known if tetrachloroethene ingestion is associated with these cancers in humans (ATSDR 1993r). Still, based on the animal data, EPA, NTP, and IARC each have classified tetrachloroethene as a suspected human cancer-causing agent via ingestion and inhalation (ATSDR 1993a, 1993r). However, EPA has not derived the toxicity values needed to estimate an increased cancer risk from past or present tetrachloroethane ingestion or inhalation (IRIS 1994).

    There are no human studies examining tetrachloroethene's cancer causing potential from skin absorption. In one study, skin application of tetrachloroethene did not produce tumors in mice (ATSDR 1993r). More studies examining the potential association between tetrachloroethene skin absorption and cancer are needed before we can make reliable comparisons with our estimated doses.

    Sensitive Populations - People with prior exposure to tetrachloroethene or having detectable blood levels of different solvents may be especially sensitive to exposure to tetrachloroethene. Some adults appear to have increased heart sensitivity to tetrachloroethene. Children and unborn babies may also be unusually sensitive to tetrachloroethene exposure, especially to possible effects on the blood and immune system (ATSDR 1993r).

  14. Trichloroethene

    Summary - Past and present trichloroethene ingestion and inhalation are unlikely to be associated with noncancer illnesses. Although trichloroethene is a skin irritant, there is not enough toxicological information to determine if noncancer illnesses may be associated with skin absorption of this compound. There is not enough toxicological information to determine if past or present trichloroethene ingestion, inhalation, or skin absorption is associated with an increased cancer risk.

    Use and Human Exposure - Trichloroethene is a colorless, human-made chemical with a sweet chloroform-like odor that evaporates easily. It is widely used to remove grease from metal parts and in other solvent operations. Trichloroethene is also used to make other chemicals and is found in consumer products such as typewriter correction fluid, paint removers, adhesives, and spot removers. In addition, at one time, trichloroethene was used as a general anesthetic agent. Other common names for trichloroethene are trichloroethylene, Triclene, Vitran, and other industrial trade names. The largest source of trichloroethene in the environment is evaporation from factories using it as a degreaser. It can also enter the air and water from disposal at chemical waste sites. Once in the air, about half of the trichloroethene breaks down within a week. The breakdown products in air can include phosgene, a lung irritant, as well as other chemicals that may be harmful. In surface waters, trichloroethene tends to evaporate into the air; it can take days or weeks to break down in the surface water body. Trichloroethene can also be found in groundwater or soil where breakdown is much slower. Trichloroethene is sometimes found in food using contaminated water sources during processing. Trichloroethene can also be found in fish tissue, but does not seem to build up to large quantities (ATSDR 1993s).

    People can be exposed to trichloroethene from environmental and occupational sources and from consumer product use. Because it is used so widely, trichloroethene is often present in ambient air in very low concentrations. It is sometimes found in water supplies. Trichloroethene easily enters the body through ingestion and inhalation. About half of the inhaled and most of the ingested trichloroethene enters the bloodstream where it travels to other body organs. Trichloroethene enters the body less easily through skin absorption. Once in the bloodstream, the liver changes most of the trichloroethene into breakdown products that leave the body through urination within a day. Some of these breakdown products may be harmful. Trichloroethene also leaves the body by exhaling. Some trichloroethene is stored in body fat for a brief time, but it is not likely to build up in the body (ATSDR 1993s).

    General Health Effects - Humans have reported health effects after trichloroethene exposure to levels at which its odor is noticeable or at higher levels. Exposure to high trichloroethene concentrations in air can cause dizziness, sleepiness, and unconsciousness or death. Inhaling high levels of trichloroethene has been associated with damage to facial nerves in some people. Inhaling moderate airborne concentrations of trichloroethene can also result in dizziness or sleepiness. Some people who get concentrated trichloroethene on their skin develop skin rashes. It is not known if trichloroethene is associated with reproductive problems or birth defects in humans. In animals, ingestion or inhalation of moderate doses of trichloroethene has been associated with liver enlargement, and high doses have been associated with liver or kidney damage. In some animal studies, trichloroethene has been associated with heart abnormalities in unborn babies. It is uncertain if trichloroethene is associated with cancer in humans. In rats and mice, high dose ingestion of trichloroethene has been associated with liver and kidney tumors, and high dose inhalation has been associated with lung, liver, and testicular tumors. Based on the animal data, trichloroethene is classified as a suspected human carcinogen (ATSDR 1993s).

    Interactions with Other Chemicals - Ethanol (drinking alcohol) can affect the body's breakdown of trichloroethene, depending on the time interval between ethanol and trichloroethene administration, and the doses administered. In human volunteers, simultaneous exposure to trichloroethene and ethanol increased the trichloroethene concentration in the blood. This finding has also been seen in rabbits. Alternatively, if trichloroethene is administered a long time after ethanol exposure, the trichloroethene breakdown rate is expected to increase. Furthermore, high ethanol concentrations may decrease the breakdown of trichloroethene, whereas low ethanol concentrations may enhance its breakdown. Other types of alcohols or compounds that inhibit the ethanol breakdown system in the liver may also influence the blood levels of trichloroethene. Pretreatment with prescription drugs containing phenobarbital may increase the extent of liver injury following trichloroethene exposure. Animal studies indicate trichloroethene can sensitize the heart to rhythm disruptions caused by epinephrine. In rabbits, phenobarbital administration decreased these trichloroethene-epinephrine-caused disruptions. In contrast, caffeine increased the incidence of epinephrine-induced heart rhythm disruptions in rabbits exposed to trichloroethene. In mice, coexposure to trichloroethene and tetrachloroethene did not result in additive or synergistic effects on the liver. Finally, coexposure to carbon monoxide, common in some degreasing operations, may worsen the symptoms of headache, nausea, dizziness, and chest pain reported by workers (ATSDR 1993s).

    Site-specific Noncancer Health Effects - In the past, nearby residents were exposed to trichloroethene through household uses of groundwater. Present-day groundwater analyses have not detected this compound; however, the air stripper's trial run demonstrated this device will successfully remove trichloroethene from groundwater and expel it into the air. The past tetrachloroethene ingestion doses we estimated for all age groups are much smaller than ATSDR's intermediate MRL and much smaller than the acute and chronic doses associated with noncancer illnesses in animals, suggesting illnesses are unlikely to be associated with this exposure. Because present-day trichloroethene groundwater concentrations are below the detection limit, they are below levels of concern for ingestion. To evaluate inhalation exposure, we used modeled data to estimate past inhalation doses from trichloroethene volatilized in the shower and present in ambient air. The past and present modeled tetrachloroethene inhalation doses we estimated for all age groups are much smaller than ATSDR's intermediate MRL and much smaller than the acute doses associated with noncancer illnesses in animals, suggesting illnesses are unlikely to be associated with this exposure. Chronic inhalation data are not available for review. Finally, trichloroethene can be a skin and eye irritant, and can cause chemical burns at very high concentrations. However, there are no studies of trichloroethene's effects on internal body systems resulting from skin absorption (ATSDR 1993s).

    Site-specific Cancer Risk - There are no reliable human studies associating trichloroethene ingestion or inhalation with cancer. Although several epidemiological studies have examined the potential association between trichloroethene and cancer, these studies are limited by their methodology and the presence of confounding factors, such as exposure to several potential cancer-causing agents in the solvent mixtures containing trichloroethene. However, trichloroethene ingestion and inhalation have been associated with liver, lung, and stomach cancer in mice, and with kidney and testicular cancer in rats (ATSDR 1993s). It is not known if trichloroethene is associated with these cancers in humans. Still, based on the animal data, EPA has classified trichloroethene as a suspected human cancer-causing agent via ingestion and inhalation (ATSDR 1993a, 1993s). Nevertheless, EPA has not derived the toxicity values needed to estimate an increased cancer risk from past or present trichloroethene ingestion or inhalation (IRIS 1994).

    There are no human studies examining trichloroethene's cancer causing potential from skin absorption. In one study, skin application of trichloroethene did not produce tumors in mice (ATSDR 1993s). More studies examining the potential association between trichloroethene skin absorption and cancer are needed before we can make reliable comparisons with our estimated doses.

    Sensitive Populations - Some people who have worked with trichloroethene for long periods of time may develop an allergy to it or become especially sensitive to its effects on the skin. People who drink ethanol or take drugs containing disulfiram may be at increased risk of trichloroethene poisoning because both of these drugs can decrease the breakdown of trichloroethene and cause it to accumulate in the blood. Accumulation in the blood may potentiate trichloroethene's effects on the nervous system. In addition, people with compromised liver or kidney function, or those with a history of heart rhythm disturbances, may be unusually sensitive to trichloroethene exposure (ATSDR 1993s).

  15. Vinyl Chloride

    Summary - In one study of rats, vinyl chloride ingestion doses somewhat larger than the past doses we estimated for all age groups has been associated with mild changes in liver cells. The physiological significance of these changes was not reported. The present-day vinyl chloride ingestion doses we estimated for all age groups is similar to ATSDR's chronic MRL, indicating illnesses are unlikely to be associated with this exposure. The past and present modeled vinyl chloride 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. Although vinyl chloride can be a skin irritant and can cause skin changes or chemical burns at very high concentrations, it is not believed to enter the body through the skin. We estimate the increased risk of liver cancer from past vinyl chloride ingestion to be moderate. Using modeled inhalation data, we estimate the increased risk of developing liver or other cancers from past vinyl chloride inhalation to be moderate if actual exposure conditions are close to the estimated conditions used in the model. There is no apparent increased cancer risk from present-day ingestion or inhalation of vinyl chloride.

    Use and Human Exposure - Vinyl chloride is a colorless vapor at room temperature with a mild, sweet odor. Almost all vinyl chloride is human-made. In the United States, most vinyl chloride is used to produce PVC (polyvinyl chloride). PVC is used to make a variety of plastic products including pipes, wire and cable coatings, and packaging materials. It is also used in furniture and automobile upholstery, wall coverings, housewares, and automotive parts. In the past, vinyl chloride was used as a coolant, a propellant in spray cans, and in some cosmetics. Other common names for vinyl chloride are chloroethene, chloroethylene, monochloroethylene, or ethylene monochloride. Most of the vinyl chloride in the environment comes from plastics industries that release this chemical into air or wastewater. Vinyl chloride also can enter the environment as a breakdown product of other human-made chemicals already in the environment, from improper disposal at waste sites, or from spills or leaking containers. Vinyl chloride evaporates easily from the surface of water or soil. Once in the air, vinyl chloride breaks down within a few days. A limited amount of vinyl chloride can dissolve in water. If this chemical enters the groundwater, it can persist for years. Vinyl chloride is unlikely to build up in the plants or animals people eat (ATSDR 1993t).

    People are usually exposed to vinyl chloride in the air. Vinyl chloride is not normally found in the environment, but people who live near plastics industries, hazardous waste sites, or landfills containing this material may be exposed to it. Vinyl chloride is found in tobacco, and smokers are also likely to be exposed to this chemical. Vinyl chloride is sometimes found in water supplies. Some PVC pipes may release small quantities of vinyl chloride into the water inside. In the past, some food packages were made of PVC, and vinyl chloride may have entered the enclosed food from this packaging material. People who work in industries using vinyl chloride or PVC products are also exposed to this compound (ATSDR 1993t).

    Vinyl chloride easily enters the body through ingestion and inhalation. Most of the inhaled or ingested vinyl chloride enters the bloodstream where it travels to body organs. Vinyl chloride is not believed to enter the body through the skin. Once in the bloodstream, the liver changes most of the vinyl chloride into breakdown products that leave the body through urination within a day. However, some of the breakdown products stay in the body and may be more harmful than the vinyl chloride. Eventually, these remaining products also leave the body. Vinyl chloride can also leave the body through exhalation (ATSDR 1993t).

    General Health Effects - In humans, exposure to high vinyl chloride concentrations in air can cause dizziness or sleepiness. Exposure to very high concentrations in air can cause unconsciousness. Most people recover from these effects once they breathe fresh air, although some develop a headache immediately upon breathing fresh air. Some people exposed to high vinyl chloride concentrations have had changes in their liver structure, nerve damage, and immune reactions. Others have reported problems with blood flow and unusual cold sensitivity in their hands. In some of these people, skin changes have appeared on their hands and forearms, and the bone tips at the end of their fingers have broken down. Some men exposed to high vinyl chloride concentrations in air have complained of a lack of sex drive. Some women exposed to high concentrations of vinyl chloride in air have had irregular menstrual cycles, and have developed high blood pressure during pregnancy. The lowest levels at which these effects occur is not known, and some people appear to be more sensitive than others to vinyl chloride exposure. The human health effects from ingesting high concentrations of vinyl chloride are unknown. People having skin contact with liquid vinyl chloride have reported numbness, redness, and blisters (ATSDR 1993t).

    In animals, breathing in extremely high doses of vinyl chloride is associated with kidney, liver, lung, and heart damage, as well as a prevention of blood clotting. At more moderate airborne levels, vinyl chloride exposure in animals is associated with testicle damage and decreased sperm production; increased numbers of miscarriages; harmful effects on unborn babies; and decreased weight and delayed skeletal development in babies (ATSDR 1993t).

    Studies of workers exposed to vinyl chloride for many years show it can cause liver cancer. In addition, vinyl chloride exposure may be associated with brain lung, and some blood cancers. Animal studies indicate long term exposure to very low vinyl chloride levels in air or drinking water is associated with cancer. Based on the existing data, vinyl chloride is classified as a known cancer-causing agent in humans (ATSDR 1993t).

    Interactions with Other Chemicals - Studies of rats indicate pretreatment with phenobarbital or Aroclor-1254 (a type of PCB) can enhance vinyl chloride's liver toxicity. However, treatment with the amino acid cysteine may provide partial protection against the toxic effects produced by Aroclor-1254 and vinyl chloride. Other experiments indicate ethanol (drinking alcohol) may enhance the incidence of liver tumors in rats (ATSDR 1993t).

    Site-specific Noncancer Health Effects - In the past, nearby residents were exposed to vinyl chloride through ingestion of groundwater. 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 vinyl chloride from groundwater and expel it into the air. In one study of rats, vinyl chloride ingestion doses somewhat larger than the past doses we estimated for all age groups has been associated with mild changes in liver cells. The physiological significance of these changes was not reported (ATSDR 1993t). The present-day vinyl chloride ingestion doses we estimated for all age groups is similar to ATSDR's chronic MRL, indicating illnesses are unlikely to be associated with this exposure. To evaluate inhalation exposure, we used modeled data to estimate past inhalation doses from vinyl chloride volatilized in the shower and present in ambient air. The past and present modeled vinyl chloride 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. Finally, vinyl chloride can be a skin irritant and can cause skin changes or chemical burns at very high concentrations. However, this chemical is not believed to enter the body through the skin (ATSDR 1993t).

    Site-specific Cancer Risk - There are no human studies examining vinyl chloride's cancer-causing potential from ingestion. However, animal studies indicate chronic vinyl chloride ingestion is associated with liver cancer, including angiosarcoma of the liver (ATSDR 1993t). EPA, NTP, and IARC each have classified vinyl chloride as a known human cancer-causing agent via ingestion (ATSDR 1993a, 1993t). Based on the exposure and dose estimates we have, we estimate adult residents' increased risk of cancer from past vinyl chloride ingestion to be moderate at 21 in 10,000. This means the risk of getting cancer, above the background rate, could rise from 2,500 cases per 10,000 people to 2,521 cases in a 70-year lifetime. There is no apparent increased cancer risk from present-day ingestion of vinyl chloride.

    Vinyl chloride is also classified as a known cancer-causing agent via inhalation. Epidemiological studies of workers exposed to vinyl chloride vapors indicate this chemical can cause angiosarcoma of the liver, a rare type of liver cancer. In addition, exposure may be associated with cancers of the brain and central nervous system, lung and respiratory tract, and lymphatic/blood forming system. Most of these studies were in male workers, and little is known about vinyl chloride's cancer-causing potential in females. However, one study suggests female workers may have higher incidences of stomach and lung cancers, leukemia (blood cancer), and lymphomas than male workers. Animal data support the conclusion that vinyl chloride can cause cancer (ATSDR 1993t). EPA, NTP, and IARC each have classified vinyl chloride as a known human cancer-causing agent via inhalation (ATSDR 1993a, 1993t). Since we did not have actual measurements of past vinyl chloride concentrations in air, we used known groundwater concentrations to estimate the cancer risk from inhaling vinyl chloride vapors in the shower and in ambient air inside and outside the home. Based on modeled exposure information, we estimate adult residents' increased risk of cancer from past vinyl chloride inhalation to be moderate at 24 in 10,000. This means the risk of getting cancer, above the background rate, could rise from 2,500 cases per 10,000 people to 2,524 cases in a 70-year lifetime if the actual inhalation exposure was similar to that predicted by the model. There is no apparent increased cancer risk from present-day inhalation of vinyl chloride.

    Sensitive Populations - Several subpopulations may be unusually sensitive to the effects of vinyl chloride, including: unborn children, infants, and young children; people with liver disease, irregular heart rhythms, impaired circulation in the limbs, or systemic sclerosis; people exposed to organic pesticides containing chlorine; and people who ingest ethanol, barbiturates, or taking prescription drugs containing disulfiram (ATSDR 1993t).

Next Section    Table of Contents

 
 
USA.gov: The U.S. Government's Official Web PortalDepartment of Health and Human Services
Agency for Toxic Substances and Disease Registry, 4770 Buford Hwy NE, Atlanta, GA 30341
Contact CDC: 800-232-4636 / TTY: 888-232-6348

A-Z Index

  1. A
  2. B
  3. C
  4. D
  5. E
  6. F
  7. G
  8. H
  9. I
  10. J
  11. K
  12. L
  13. M
  14. N
  15. O
  16. P
  17. Q
  18. R
  19. S
  20. T
  21. U
  22. V
  23. W
  24. X
  25. Y
  26. Z
  27. #