Abstract
This paper describes risk assessment methods for two chronic exposure pathways involving arsenic contaminated soil, namely inhalation of fugitive dust emissions over a lifetime, and inadvertent soil/house dust ingestion. The endpoint in the first case is assumed to be lung cancer and in the second case skin cancer. In order to estimate exposures, inhalation rates and soil/dust ingestion rates are estimated for different age groups; indoor/outdoor time budgets for different age groups are developed; and indoor surface dust and air arsenic concentrations are estimated based on outdoor concentration measurements. Differences observed in indoor/outdoor ratios and arsenic containing dust particle size among different types of communities are noted, as well as possible relationship of particle size to bioavailability. Calculations of risk are presented using cancer potency factors developed by the U.S. Environmental Protection Agency, and uncertainties in these toxicity estimates are described based on: (1) evidence that arsenic may be neither a cancer initiator nor promotor, but may act instead as a late stage carcinogen and (2) evidence that the arsenic dose-response relationship for ingestion may be nonlinear at low doses due to increasing methylation of inorganic arsenic. The first of these considerations influences the relative importance ascribed to arsenic doses in different age groups. The latter consideration indicates that the risk estimates described here are probably very conservative.
Similar content being viewed by others
References
Alzona, J., Cohen, B.L., Rudolph, H., Jow, H.N. and Frohlinger, J.O. 1979. Indoor-outdoor relationships for paniculate matter of outdoor origin.Atmospheric Environment,13, 55–60.
Anderson E., Browne, N., Duletsky, S.,et al. 1985Development of Statistical Distributions or Ranges of Standard Factors Used in Exposure Assessments. EPA-600/8-85/010. Report to U.S. EPA Office of Health and Environmental Assessment. Washington, D.C.
Barltrop, D. 1966. The prevalence of pica.American Journal of Disease in Children,112, 116–123.
Barltrop, D., Thorton, I., Strehlow, C.D., and Webb, J.S. 1975. Absorption of lead from dust and soil.Postgraduate Medical Journal,5, 801–804.
Barltrop, D. and Strehlow, C.D. 1988. The contribution from soil and house dust lead to lead burden in childhood. Presented at Conference on Lead in Soil: Issues and Guidelines, March 7–9, at Chapel Hill, N.C.
Binder, S., Sokal, D., and Maughan, D. 1986. Estimating soil ingestion: the use of tracer elements in estimating the amount of soil ingested by young children.Archives of Environmental Health,41, 341–345.
Binder, S. (U.S. Department of Health and Human Services) March 3, 1987. Memo regarding Mill Creek pre- and post-move urinary arsenic levels.
Brown, C.C. and Chu, K.C. 1983. A new method for the analysis of cohort studies: implications of the multistage theory of carcinogenesis applied to occupational arsenic exposure.Environmental Health Perspectives,50, 293–308.
Calabrese, E.J., Pastides, H., Barnes, R. et al. 1988.How Much Soil Do Young Children Ingest: an Epidemiologic study. Draft Report to Syntex Corp. Amherst: University of Massachusetts.
Clausing P., Brunekreff, B. and van Wijnen, J.H. 1987. A method for estimating soil ingestion by children.Interational Archives for Occupational and Environmental Health,59, 73–82.
Cohen, A.F. and Cohen, B.L. 1980. Protection from being indoors against inhalation of suspended paniculate matter of outdoor origin.Atmospheric Environment,14, 183–184.
Diemel, J.A.L., Brunekreef, B., Boley, J.S.M., Biersteker, K. and Veenstra, S.J. 1981. The Amhem lead study, II: indoor pollution and indoor/outdoor relationship.Environmental Research,25, 449.
Doull, J., Klaasen, C.D. and Amdur, M.O. 1980.Casarett and Doull's Toxicology. The Basic Science of Poisons. Macmillan Publishing Co., Inc., New York.
Freed, J.R., Chambers, T., Christie, W.N. and Carpenter, C.E. 1983.Method for assessing exposure to chemical substance. U.S. EPA Office of Toxic Substances, EPA 560/5-83-015.
Franzen,D., Sackman, A., Oale, R. and Chapin, M. 1988.Analytical Results Report for Ambient Air and Residental Characterisation at Prospect Square, Park City, Utah. Report Prepared for EPA Hazardous Site Evaluation Division.
Hawley, J.K. 1985. “Assessment of Health Risk from Exposure to Contaminated Soil.”Risk Analysis,5(4), 289.
International Commission on Radiological Protection. 1984.Report of the Task Group on Reference Man. Oxford: Pergamon Press.
Lee, T.C., Tanaka, N., Lamb, P.W., Gilmer, T.M. and Barrett, J.C. 1988. Induction of gene amplification by arsenic.Science,241, 79.
Lefcoe, N.M. and Inculet, I.I. 1975. Particulates in domestic premises.Archives of Environmental Health,30, 565.
Mahaffey, K.R. 1977. Quantities of lead producing health effects in humans: sources and bioavailability.Environmental Health Perspectives,19, 285–295.
Marafante, E. and Vahter, M. 1984. The effect of methyltransferase inhibition on the metabolism of [74As] arsenite in mice and rabbits.Chemical and Biological Interactions,50, 49–57.
Moschandreas, D.J., J.W. Winchester, J.W. Nelson and R.M. Burton. 1979. Fine particle residential indoor air pollution.Atmospheric Environment,13, 1413.
Roberts, T.M. 1974. Lead contamination around secondary smelters: estimation of dispersal and accumulation.Science,186, 1120.
Schilling R., Rass, D., Sokal, D., Inez R., Brokopp, C. and Maughan, A.D. 1984. Children's exposure to smelter-associated lead, Montana and Idaho. Proceedings of the 5th National Conference on Management of Uncontrolled Hazardous Waste Sites, November 7–9, Washington, D.C. p. 239.
Steele, M.J., Beck, B.D., Murphy, B.L. and Strauss, H.S. 1989. Assessing the contribution from lead in mining wastes to blood lead. Submitted toRegulatory Toxicology and Pharmacology.
Tetra Tech. 1987. Unpublished data.
U.S. Department of Health and Human Services (Agency of Toxic Substances and Disease Registry). 1988.The Nature and Extent of Lead Poisoning in Children in the United States: A Report to Congress.
U.S. Environmental Protection Agency (Office of Health and Environmental Assessment). 1984.Health Assessment Document for Arsenic. EPA-600/8-83-021F.
U.S. Environmental Protection Agency (Region VIII). 1986a.Endangerment Assessment: Mill Creek/Montana Smelter Site. Revised Final Report.
U.S. Environmental Protection Agency (Office of Air Quality Planning and Standards). 1986b.Review of National Ambient Air Quality Standards for Lead: Assessment of Scientific and Technical Information. Draft Report.
U.S. Environmental Protection Agency (Office of Remedial Response). 1988a.Superfund Exposure Assessment Manual. EPA 540/1-88/001.
U.S. Environmental Protection Agency. 1988b.Special report on ingested inorganic arsenic: Skin cancer Nutritional Essentiality. EPA-625/3-87/013P.
U.S. Environmental Protection Agency. 1989a.Integrated Risk Information System (IRIS) (U.S. EPA Online Chemical Potency Information).
U.S. Environmental Protection Agency 1989b.Exposure Factors Handbook. EPA-600/8-89/043.
Vahter, M. 1983. Metabolism of arsenic. In: Fowler, B.A. (ed.),Biological and Environmental Effects of Arsenic. Elsevier Science Publishers, B.V.
Yankel, A.J., Von Lindem, I.H. and Walter, S.D. 1977. The Silver Valley lead study: the relationship between childhood blood levels and environmental exposure.Journal of the Air Pollution Control Association,27, 766.
Yocom, J.E., W.A Cote, and F.B. Benson. 1977. As cited in: Walden R.A. and Schett P.A., (eds.):Indoor Air Pollution. John Wiley & Sons, New York. 1983.
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Murphy, B.L., Toole, A.P. & Bergstrom, P.D. Health risk assessment for arsenic contaminated soil. Environ Geochem Health 11, 163–169 (1989). https://doi.org/10.1007/BF01758667
Received:
Accepted:
Issue Date:
DOI: https://doi.org/10.1007/BF01758667