Risk Analysis, Vol. 10, No. 4, 1990
Editorial
Background Exposure to Chemicals: What Is the Risk?' Curtis C. Travis2 and Sheri T. HesterZ 1. INTRODUCTION
2.2. Trichloroethylene
This issue of Risk Analysis contains two articles that maintain that the background cancer risk from chloroform in drinking and shower water is high. We expand upon this idea by discussing human exposure to other commonplace carcinogenic chemicals. We do not claim to have done a comprehensive survey, but rather to have chosen examples where data are readily at hand. Our hypothesis is that the cancer risk from background exposure to organic chemicals, as computed by EPA (Environmental Protection Agency) methodologies, is higher than the generally accepted target range of 10-7-10-4 lifetime cancer risk.
Trichloroethylene is widely used as an industrial solvent, particularly in metal degreasing. Other applications include dry-cleaning, fumigating, use as a lowtemperature heat exchange fluid, and use as a diluent in paints and adhesives. Assuming a mean concentration in personal air of 1.9 kg/m3,(') an adult inhalation rate of 20 m3/day, and a cancer potency estimate of 1.3 x lo-? (mg/kg/day)- ', the corresponding lifetime cancer risk from background exposure to trichloroethylene is 0.26 x 10-4.
2.3. Tetrachloroethylene 2. INDOOR AIR EXPOSURE
Tetrachloroethylene (perchloroethylene, PCE) is a nonflammable, colorless liquid, with a chloroform-like odor. PCE is extensively used in the textile industry as a dry-cleaning aid, constituting more than 65% of the total dry-cleaning solvent usage in the United States. Assuming a mean concentration of tetrachloroethylene in personal air of 24 pg/m3,(') an adult inhalation rate of 20 m3/day, and a cancer potency estimate of 1.7 x (mg/kg/day)-', the corresponding lifetime cancer risk from background exposure to tetrachloroethylene is 0.12 x 10-4.
Humans are constantly exposed to trace levels of indoor air pollutants for which personal air concentrations (the air that humans breathe) are several times higher than outdoor concentrations. The EPA has surveyed these exposures,(') and we have computed risk estimates for those that are carcinogenic. 2.1. Benzene
Benzene is used in the synthesis of other organic compounds. It is a widely occurring environmental pollutant which is known to cause leukemia in humans. Assuming a mean concentration of benzene in personal air of 13.7 pg/m3,(') and adult inhalation rate of 20 m3/ day, and a cancer potency estimate for benzene of 2.6 x lo-* (mg/kg/day)- the corresponding lifetime cancer risk from background exposure to benzene is 1 x
2.4. Carbon Tetrachloride
Carbon tetrachloride is used primarily in the production of fluorocarbons. Assuming a mean concentration in personal air of 3.1 kg/m3,(') an adult inhalation rate of 20 m3/day, and a cancer potency estimate of 1.3 x lo-' (mg/kg/day)-', the corresponding lifetime cancer risk from background exposure to carbon tetrachloride is 1.2 x
10-4.
' Received August 8, 1990. Office of Risk Analysis, Oak Ridge National Laboratory, Health and Safety Research Division, Oak Ridge, Tennesscc 37831-6109.
463
0272-4332/90/1200-0463$06.00/1 Q 1990 Society for Risk Analysis
Travis and Hester
464 2.5. Formaldehyde
The major sources of background indoor formaldehyde are resins found in structural materials, insulation, and furnishing. Assuming a mean indoor formaldehyde concentration of 74.5 ppb,m and using the formaldehyde potency data published by U S . EPA,(3) the lifetime cancer risk from background exposure to formaldehyde is 0.65 x lod4. 2.6. Xylenes
Commercial xylene is a mixture of the ortho-, rneta-, and para-isomers. The xylenes are widely used as fuel components, intermediates in the chemical industry, and solvents. Using a cancer potency estimate of 9.9 x 10-4,(4)for each of these isomers, a mean concentration in personal air of 10.1 @m3 for orthoxylene and 28.3 @m3 for meta- and paraxylene combined,“) the corresponding lifetime cancer risk from background exposure to xylenes is 0.37 x lod4.
3. WATER EXPOSURE
Most organics that humans are exposed to are either very volatile or very lipophilic with the result that background concentrations of organics in drinking water are low. Chloroform is the pollutant in water with the highest risk. The articles by Jo er al. in this issue of Risk Analysis examine the ingestion, inhalation, and dermal exposure risks to chloroform in ordinary tap water. 3.1. Chloroform
Most chloroform in tap water results from the water chlorination process, although concentrations have been measured in raw water used for drinking water. The dose of chloroform from a single, 10-min shower is 0.46 kg/ kg/day, which includes 0.24 p,gikg/day for inhalation exposure and 0.22 p,g/kg/day for dermal exposure. The resulting risk estimate is 1.22 x The chloroform dose from daily tap-water ingestion is 0.7 p,,g/kg/day for a daily 2 L water ingestion, with a risk of 1.8 x
4. FOOD-CHAIN EXPOSURE
The food chain is the primary pathway for human exposure to many pollutants. The following risk esti-
mates are based on direct measurement of dietary intake, except in the one case noted. 4.1. Dioxins and Furans
2,3,7,8-Tetrachlorodibenzo-p-dioxin(TCDD, commonly referred to as “dioxin”) is the most potent chernical carcinogen ever evaluated by EPA. Polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzo-furans (PCDFs), which are isomers of dioxin, have been found in virtually all media, including air, soil, meat, milk, fish, vegetation, fruits, and human biological samples. The primary path of human exposure is through the food chain. The toxicity of different PCDD and PCDF isomers is typically expressed in terms of toxic equivalent factors (TEFs), which relate the toxicity of all PCDDPCDF compounds to the known toxicity of TCDD using one of several weighing schemes. Market basket studies in Germany, Japan, and Canada estimate the mean background dietary intake (with meat and dairy products accounting for the majority of dietary intake) of PCDDs and PCDFs (expressed in TEFs) as 1.3 pg/ k g / d a ~ . ( ~Using ) a cancer potency estimate of 1.56 x (mg/kg/day)-’, the lifetime cancer risk from ingestion of food items contaminated with background levels of dioxin and furans is 2.1 x 4.2. Dieldrin
Dieldrin is a highly persistent, synthetic compound with a higher acute toxicity than DDT. It was used as a pesticide until its manufacture was banned in the United States in 1974; however, human exposure through the food chain continues. Market basket studies show a background daily intake of 0.0049 kg/kg/day.@) Using a cancer potency estimate of 1.6 x l O - l , the lifetime cancer risk from background intake of dieldrin is 0.78 x 10-4. 4.3. Ethylenebisdithiocarbamates (EBDCs)
EBDCs are a versatile group of chemicals widely used to control fungal diseases on fruits, vegetables, field crops, and seeds. Approximately one third of all fruits and vegetables in the United States are treated with EBDCs. The National Academy of Sciences,(’) using estimated exposures rather than measured residue data, from estimated a lifetime cancer risk of 3.4 x background ingestion of EBDCs.
Background Exposure to Chemicals 4.4. Polychlorinated Biphenyls (PCBs)
PCBs are synthetic chlorinated compounds with a wide number of industrial applications. Commercial production of PCBs was banned in 1977 following highly publicized incidents of environmental contamination. However, PCBs are extremely stable in the environment and human exposure continues. Market basket studies mg/kg/ show a background daily intake of 1.4 x day.(*) Using a cancer potency estimate of 7.7 (mg/kg/ day)-’, the lifetime cancer risk of background PCB intake is 1.1 x 5. CONCLUSION
The above calculations, all but one of which are based on measured exposures, indicate a total background cancer risk from the pollutants considered of 1.4 x This is an underestimate of the total background cancer risk because a comprehensive survey of food-chain exposures was not performed. However, it is doubtful that the total background cancer risk from enunless vironmental chemicals exceeds 2 or 5 x there is an extremely toxic environmental pollutant that has thus far escaped detection. Thus, background cancer risk based on measured exposures can account for 1-2% of actual annual cancer deaths, a number consistent with other estimates of the contribution of chemical pollution to background cancer rates. It is interesting to note that these estimates provide indirect evidence that EPA cancer potency estimates are not overly conservative, as is often maintained. If cancer potency estimates, which are based primarily on animal data, vastly overestimate human risk, one would expect the background cancer risk estimates produced above to overpredict the contribution of chemical pollution to background cancer rates. However, the estimates are consistent with human data, providing further confirmation of the Allen et u L . ( ~ ) observation that human risk estimates derived from animal data are consistent with epidemiological data and the Zapponi(lo) analysis that animal and human data for seven known human carcinogens fall within a factor of three of each other. The high background cancer risk estimated in this paper raises the question of how effective EPA can be in reducing the overall cancer risk from environmental chemicals. EPA’s regulatory focus is on controlling local exposure to large point sources of pollutants. These sources typically have maximum individual risks in the to range, but because risk drops off rapidly with distance from the source, risk to the average individual is
465
typically in the to lo-’ range. Thus, the majority of EPA regulations, while protective of the maximum exposed individual, do little to reduce the overall cancer rate in the U.S. population resulting from background exposure to chemical pollutants. The difficulty with regulating background cancer risk is that it results from widespread global pollution from a multitude of widely dispersed sources. This pollution cannot be reduced significantly by controlling emissions associated with production and use. When these chemicals are produced and not destroyed naturally or by man, they will eventually reach the environment. Once they reach the environment, even relatively nonvolatile compounds like PCB and dioxin are atmospherically transported on a global scale, resulting in global chemical pollution. If we do not want to change our style of living, the only way to reduce global chemical pollution is to make production and consumption processes more efficient, thereby lowering the necessary levels of production of these toxic chemicals. Thus, the only reasonable solution to global pollution is not increased environmental regulation of emissions, but rather decreased production, achieved through improved process design, waste reduction, and material recycling. Until we focus on these issues, we will continue to experience background chemical risk in the range.
ACKNOWLEDGMENTS
Oak Ridge National Laboratory is operated by Martin Marietta Energy Systems, Inc., Contract No. DEAC05-840R21400 with the U.S. Department of Energy.
REFERENCES 1. L. Wallace, “Personal Exposures, Indoor and Outdoor Air Con-
2.
3. 4. 5.
centrations, and Exhaled Breath Concentrations of Selectcd Volatile Organic Compounds Measured for 600 Residents of New Jersey, North Dakota, North Carolina, and California,” Toxicol. Environ. Chem. 12, 215-236 (1986). A. R. Hawthorn, R. B. Gammage, C. S. Dudney, B. E. Hingcrty, D. D. Schuresko, D. C. Parzyck, D. R. Womack, S. A. Morris, R. R. Westley, D. A. White, and J. M. Schrimsher, An IndooiAir Qualiw Study of Fory East Tennessee Homes (Oak Ridge National Laboratory, Oak Ridge, Tennessec, ORNL-5965, 1984). U.S. EPA (United States Environniental Protection Agency), “Formaldehyde Determination of Significant Risk,” Federal Register 49, 21870 (1984). M. Tancrede, R. Wilson, L. Zeise, E. A. C. Crouch, “The Carcinogenic Risk of Some Organic Vapors Indoors: A Theorctical Survey,” Atmospheric Environment 21( lo), 2187-2205 (1987). C. C. Travis and H. A. Hattemer-Frey, “Human Exposure to Dioxin,” Science of the Total Environnienf (in press).
466 6. U.S. FDA (United States Food and Drug Administration), “Food and Drug Administration Pesticidc Program: Residucs in Foods1988,” J. Assoc. 08 Anal. Chem. 72(5), 133A-152A (1989). 7. NAS (National Academy of Sciences), ReguZafing Pesticides in Food: The Deluney Paradox (National Academy Press, Washington, D. C., 1987). 8. M. J. Gartrell, J. C. Craun, D. S. Podrebarac, and E. L. Gunderson, “Pesticides, Selected Elements, and Other Chemicals in
Travis and Hester Adult Total Diet Samples, October 1980-March 1982,”J. Assoc. Ofl Anal. Chem. 69(1), 146-159 (1986). 9. B. C. Allen, K. S. Crump, and A. M. Shipp, “Corrclation Between Carcinogenic Potency of Chemicals in Animals and Humans,” Risk Analysis 8(6), 531-544 (1988). 10. G. A. Zapponi, A. Loizzo, and P. Valente, “Carcinogenic Risk Assessment: Some Comparisons Bctween Risk Estirnatcs Derived from Human and Animal Data,” Exp. Parhol. 37, 1-4 (1989).
Editorial
Background Exposure to Chemicals: What Is the Risk?' Curtis C. Travis2 and Sheri T. HesterZ 1. INTRODUCTION
2.2. Trichloroethylene
This issue of Risk Analysis contains two articles that maintain that the background cancer risk from chloroform in drinking and shower water is high. We expand upon this idea by discussing human exposure to other commonplace carcinogenic chemicals. We do not claim to have done a comprehensive survey, but rather to have chosen examples where data are readily at hand. Our hypothesis is that the cancer risk from background exposure to organic chemicals, as computed by EPA (Environmental Protection Agency) methodologies, is higher than the generally accepted target range of 10-7-10-4 lifetime cancer risk.
Trichloroethylene is widely used as an industrial solvent, particularly in metal degreasing. Other applications include dry-cleaning, fumigating, use as a lowtemperature heat exchange fluid, and use as a diluent in paints and adhesives. Assuming a mean concentration in personal air of 1.9 kg/m3,(') an adult inhalation rate of 20 m3/day, and a cancer potency estimate of 1.3 x lo-? (mg/kg/day)- ', the corresponding lifetime cancer risk from background exposure to trichloroethylene is 0.26 x 10-4.
2.3. Tetrachloroethylene 2. INDOOR AIR EXPOSURE
Tetrachloroethylene (perchloroethylene, PCE) is a nonflammable, colorless liquid, with a chloroform-like odor. PCE is extensively used in the textile industry as a dry-cleaning aid, constituting more than 65% of the total dry-cleaning solvent usage in the United States. Assuming a mean concentration of tetrachloroethylene in personal air of 24 pg/m3,(') an adult inhalation rate of 20 m3/day, and a cancer potency estimate of 1.7 x (mg/kg/day)-', the corresponding lifetime cancer risk from background exposure to tetrachloroethylene is 0.12 x 10-4.
Humans are constantly exposed to trace levels of indoor air pollutants for which personal air concentrations (the air that humans breathe) are several times higher than outdoor concentrations. The EPA has surveyed these exposures,(') and we have computed risk estimates for those that are carcinogenic. 2.1. Benzene
Benzene is used in the synthesis of other organic compounds. It is a widely occurring environmental pollutant which is known to cause leukemia in humans. Assuming a mean concentration of benzene in personal air of 13.7 pg/m3,(') and adult inhalation rate of 20 m3/ day, and a cancer potency estimate for benzene of 2.6 x lo-* (mg/kg/day)- the corresponding lifetime cancer risk from background exposure to benzene is 1 x
2.4. Carbon Tetrachloride
Carbon tetrachloride is used primarily in the production of fluorocarbons. Assuming a mean concentration in personal air of 3.1 kg/m3,(') an adult inhalation rate of 20 m3/day, and a cancer potency estimate of 1.3 x lo-' (mg/kg/day)-', the corresponding lifetime cancer risk from background exposure to carbon tetrachloride is 1.2 x
10-4.
' Received August 8, 1990. Office of Risk Analysis, Oak Ridge National Laboratory, Health and Safety Research Division, Oak Ridge, Tennesscc 37831-6109.
463
0272-4332/90/1200-0463$06.00/1 Q 1990 Society for Risk Analysis
Travis and Hester
464 2.5. Formaldehyde
The major sources of background indoor formaldehyde are resins found in structural materials, insulation, and furnishing. Assuming a mean indoor formaldehyde concentration of 74.5 ppb,m and using the formaldehyde potency data published by U S . EPA,(3) the lifetime cancer risk from background exposure to formaldehyde is 0.65 x lod4. 2.6. Xylenes
Commercial xylene is a mixture of the ortho-, rneta-, and para-isomers. The xylenes are widely used as fuel components, intermediates in the chemical industry, and solvents. Using a cancer potency estimate of 9.9 x 10-4,(4)for each of these isomers, a mean concentration in personal air of 10.1 @m3 for orthoxylene and 28.3 @m3 for meta- and paraxylene combined,“) the corresponding lifetime cancer risk from background exposure to xylenes is 0.37 x lod4.
3. WATER EXPOSURE
Most organics that humans are exposed to are either very volatile or very lipophilic with the result that background concentrations of organics in drinking water are low. Chloroform is the pollutant in water with the highest risk. The articles by Jo er al. in this issue of Risk Analysis examine the ingestion, inhalation, and dermal exposure risks to chloroform in ordinary tap water. 3.1. Chloroform
Most chloroform in tap water results from the water chlorination process, although concentrations have been measured in raw water used for drinking water. The dose of chloroform from a single, 10-min shower is 0.46 kg/ kg/day, which includes 0.24 p,gikg/day for inhalation exposure and 0.22 p,g/kg/day for dermal exposure. The resulting risk estimate is 1.22 x The chloroform dose from daily tap-water ingestion is 0.7 p,,g/kg/day for a daily 2 L water ingestion, with a risk of 1.8 x
4. FOOD-CHAIN EXPOSURE
The food chain is the primary pathway for human exposure to many pollutants. The following risk esti-
mates are based on direct measurement of dietary intake, except in the one case noted. 4.1. Dioxins and Furans
2,3,7,8-Tetrachlorodibenzo-p-dioxin(TCDD, commonly referred to as “dioxin”) is the most potent chernical carcinogen ever evaluated by EPA. Polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzo-furans (PCDFs), which are isomers of dioxin, have been found in virtually all media, including air, soil, meat, milk, fish, vegetation, fruits, and human biological samples. The primary path of human exposure is through the food chain. The toxicity of different PCDD and PCDF isomers is typically expressed in terms of toxic equivalent factors (TEFs), which relate the toxicity of all PCDDPCDF compounds to the known toxicity of TCDD using one of several weighing schemes. Market basket studies in Germany, Japan, and Canada estimate the mean background dietary intake (with meat and dairy products accounting for the majority of dietary intake) of PCDDs and PCDFs (expressed in TEFs) as 1.3 pg/ k g / d a ~ . ( ~Using ) a cancer potency estimate of 1.56 x (mg/kg/day)-’, the lifetime cancer risk from ingestion of food items contaminated with background levels of dioxin and furans is 2.1 x 4.2. Dieldrin
Dieldrin is a highly persistent, synthetic compound with a higher acute toxicity than DDT. It was used as a pesticide until its manufacture was banned in the United States in 1974; however, human exposure through the food chain continues. Market basket studies show a background daily intake of 0.0049 kg/kg/day.@) Using a cancer potency estimate of 1.6 x l O - l , the lifetime cancer risk from background intake of dieldrin is 0.78 x 10-4. 4.3. Ethylenebisdithiocarbamates (EBDCs)
EBDCs are a versatile group of chemicals widely used to control fungal diseases on fruits, vegetables, field crops, and seeds. Approximately one third of all fruits and vegetables in the United States are treated with EBDCs. The National Academy of Sciences,(’) using estimated exposures rather than measured residue data, from estimated a lifetime cancer risk of 3.4 x background ingestion of EBDCs.
Background Exposure to Chemicals 4.4. Polychlorinated Biphenyls (PCBs)
PCBs are synthetic chlorinated compounds with a wide number of industrial applications. Commercial production of PCBs was banned in 1977 following highly publicized incidents of environmental contamination. However, PCBs are extremely stable in the environment and human exposure continues. Market basket studies mg/kg/ show a background daily intake of 1.4 x day.(*) Using a cancer potency estimate of 7.7 (mg/kg/ day)-’, the lifetime cancer risk of background PCB intake is 1.1 x 5. CONCLUSION
The above calculations, all but one of which are based on measured exposures, indicate a total background cancer risk from the pollutants considered of 1.4 x This is an underestimate of the total background cancer risk because a comprehensive survey of food-chain exposures was not performed. However, it is doubtful that the total background cancer risk from enunless vironmental chemicals exceeds 2 or 5 x there is an extremely toxic environmental pollutant that has thus far escaped detection. Thus, background cancer risk based on measured exposures can account for 1-2% of actual annual cancer deaths, a number consistent with other estimates of the contribution of chemical pollution to background cancer rates. It is interesting to note that these estimates provide indirect evidence that EPA cancer potency estimates are not overly conservative, as is often maintained. If cancer potency estimates, which are based primarily on animal data, vastly overestimate human risk, one would expect the background cancer risk estimates produced above to overpredict the contribution of chemical pollution to background cancer rates. However, the estimates are consistent with human data, providing further confirmation of the Allen et u L . ( ~ ) observation that human risk estimates derived from animal data are consistent with epidemiological data and the Zapponi(lo) analysis that animal and human data for seven known human carcinogens fall within a factor of three of each other. The high background cancer risk estimated in this paper raises the question of how effective EPA can be in reducing the overall cancer risk from environmental chemicals. EPA’s regulatory focus is on controlling local exposure to large point sources of pollutants. These sources typically have maximum individual risks in the to range, but because risk drops off rapidly with distance from the source, risk to the average individual is
465
typically in the to lo-’ range. Thus, the majority of EPA regulations, while protective of the maximum exposed individual, do little to reduce the overall cancer rate in the U.S. population resulting from background exposure to chemical pollutants. The difficulty with regulating background cancer risk is that it results from widespread global pollution from a multitude of widely dispersed sources. This pollution cannot be reduced significantly by controlling emissions associated with production and use. When these chemicals are produced and not destroyed naturally or by man, they will eventually reach the environment. Once they reach the environment, even relatively nonvolatile compounds like PCB and dioxin are atmospherically transported on a global scale, resulting in global chemical pollution. If we do not want to change our style of living, the only way to reduce global chemical pollution is to make production and consumption processes more efficient, thereby lowering the necessary levels of production of these toxic chemicals. Thus, the only reasonable solution to global pollution is not increased environmental regulation of emissions, but rather decreased production, achieved through improved process design, waste reduction, and material recycling. Until we focus on these issues, we will continue to experience background chemical risk in the range.
ACKNOWLEDGMENTS
Oak Ridge National Laboratory is operated by Martin Marietta Energy Systems, Inc., Contract No. DEAC05-840R21400 with the U.S. Department of Energy.
REFERENCES 1. L. Wallace, “Personal Exposures, Indoor and Outdoor Air Con-
2.
3. 4. 5.
centrations, and Exhaled Breath Concentrations of Selectcd Volatile Organic Compounds Measured for 600 Residents of New Jersey, North Dakota, North Carolina, and California,” Toxicol. Environ. Chem. 12, 215-236 (1986). A. R. Hawthorn, R. B. Gammage, C. S. Dudney, B. E. Hingcrty, D. D. Schuresko, D. C. Parzyck, D. R. Womack, S. A. Morris, R. R. Westley, D. A. White, and J. M. Schrimsher, An IndooiAir Qualiw Study of Fory East Tennessee Homes (Oak Ridge National Laboratory, Oak Ridge, Tennessec, ORNL-5965, 1984). U.S. EPA (United States Environniental Protection Agency), “Formaldehyde Determination of Significant Risk,” Federal Register 49, 21870 (1984). M. Tancrede, R. Wilson, L. Zeise, E. A. C. Crouch, “The Carcinogenic Risk of Some Organic Vapors Indoors: A Theorctical Survey,” Atmospheric Environment 21( lo), 2187-2205 (1987). C. C. Travis and H. A. Hattemer-Frey, “Human Exposure to Dioxin,” Science of the Total Environnienf (in press).
466 6. U.S. FDA (United States Food and Drug Administration), “Food and Drug Administration Pesticidc Program: Residucs in Foods1988,” J. Assoc. 08 Anal. Chem. 72(5), 133A-152A (1989). 7. NAS (National Academy of Sciences), ReguZafing Pesticides in Food: The Deluney Paradox (National Academy Press, Washington, D. C., 1987). 8. M. J. Gartrell, J. C. Craun, D. S. Podrebarac, and E. L. Gunderson, “Pesticides, Selected Elements, and Other Chemicals in
Travis and Hester Adult Total Diet Samples, October 1980-March 1982,”J. Assoc. Ofl Anal. Chem. 69(1), 146-159 (1986). 9. B. C. Allen, K. S. Crump, and A. M. Shipp, “Corrclation Between Carcinogenic Potency of Chemicals in Animals and Humans,” Risk Analysis 8(6), 531-544 (1988). 10. G. A. Zapponi, A. Loizzo, and P. Valente, “Carcinogenic Risk Assessment: Some Comparisons Bctween Risk Estirnatcs Derived from Human and Animal Data,” Exp. Parhol. 37, 1-4 (1989).
