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BIOGRAPHY FOR BARBARA D. BECK
Dr. Beck is an expert in toxicology and in health risk assessment for environmental chemicals, especially metals and air pollutants, and the author of over 30 book chapters and journal articles on these topics. Dr. Beck directs Gradient's toxicology and risk assessment practice. She has performed more than 100 site-specific risk assessments, developed risk assessment methodologies, e.g., for cumulative risk assessment, and presented the results to different audiences including regulatory agencies, the U.S. Congress and the public. Before joining Gradient, she was Chief of Air Toxics Staff in Region I EPA. Prior to that she was a Fellow in the Interdisciplinary Programs in Health at the Harvard School of Public Health. She is at present a Lecturer in Toxicology at Harvard. Dr. Beck has a Ph.D. in Molecular Biology from Tufts University and an A.B. in Biology from Bryn Mawr College, and is a diplomate of the American Board of Toxicology.
PUBLICATIONS
Topic: Arsenic
Articles
Abernathy, C.O., Y.-P. Liu, D. Longfellow, H.V. Aposhian, B. Beck, B. Fowler, R. Goyer, R. Menzer, T. Rossman, C. Thompson, and M. Waalkes. 1999. Arsenic: health effects, mechanisms of actions, and research issues. Environmental Health Perspectives 107(7):593–597.
Goering, P.L., H.V. Aposhian, M.J. Mass, M. Cebrian, B.D. Beck, and M. Waalkes. 1999. The enigma of arsenic carcinogenesis: role of metabolism. Toxicological Sciences 49:5–14.
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Cohen, J.T., B.D. Beck, T.S. Bowers, R.L. Bornschein, and E.J. Calabrese. 1998. An arsenic exposure model: probabilistic validation using empirical data. Human and Ecological Risk Assessment 4(2):341–377.
Valberg, P.A., B.D. Beck, P.D. Boardman, and J.T. Cohen. 1998. Likelihood ratio analysis of skin cancer prevalence t t associated with arsenic in drinking water in the USA. Env. Geochemistry and Health 20(2):61–66.
Valberg, P.A., B.D. Beck, T.S. Bowers, J.L. Keating, P.D. Bergstrom, and P.D. Boardman. 1997. Issues in setting health-based cleanup levels for arsenic in soil. Reg. Toxicol. and Pharm. 26:219–229.
Chappell, W.R., B.D. Beck, K.G. Brown, R. Chaney, C.R. Cothern, K.J. North, I. Thornton, and T.A. Tsongas. 1997. Inorganic arsenic: a need and an opportunity to improve risk assessment. Env. Health Perspect. 105(10):1060–1067. October.
Brown, K.G. and B.D. Beck. 1996. Arsenic and bladder cancer mortality. Epidemiol. 7:557–558.
Slayton, T.M., B.D. Beck, K.A. Reynolds, S.D. Chapnick, P.A. Valberg, L.J. Yost, R.A. Schoof, T.D. Gauthier, and L. Jones. 1996. Issues in arsenic cancer risk assessment. Env. Health Perspect. 1104:2–4.
Rudel, R., T.M. Slayton, and B.D. Beck. 1996. Implications of arsenic genotoxicity for dose-response of carcinogenic effects. Regul. Toxicol. Pharmacol. 23:87–105.
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Carlson-Lynch, H., B.D. Beck, and P.D. Boardman. 1994. Arsenic risk assessment. Env. Health Pers. 102(4):354–356.
Petito, C.T. and B.D. Beck. 1991. Evaluation of evidence of non-linearities in the dose-response curve for arsenic carcinogenesis. Proceedings of the 24th Annual Conference on Trace Substances in Environmental Health and Annual Meeting of the Society for Environmental Geochemistry and Health, July 9–12, pp. 143–176.
Abstracts
Slayton, T.M. and B.D. Beck. 2001. Mechanistic differences between low dose and high dose effects of arsenic. The Toxicologist 60(1):76.
Slayton, T.M., B.D. Beck and J.W. Yager. 2000. EPRI-sponsored arsenic research program—application to arsenic cancer risk assessment. SEGH Fourth International Conference on Arsenic Exposure and Health Effects, Book of Abstracts, San Diego, CA, June 18–22, 2000, p. 171.
Kitchin, K.T. and B.D. Beck. 2000. Arsenic: carcinogenic mechanisms, risk assessment and the maximum contaminant level (MCL). The Toxicologist 54(1):356.
Beck, B.D. and T.M. Slayton. 1998. Impact of arsenic (Asi) metabolism on human populations: dose-response relationships in arsenic-induced cancers. The Toxicologist 42(1–S):354.
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Beck, B.D., L.A. Beyer, C. Price, J. Robertson, and D. Hiller. 1998. An exposure assessment for inorganic arsenic in vegetables using site-specific data from a tailings site in Ontario. Presented at the Third International Conference on Arsenic Exposure and Health Effect, San Diego, CA.
Cohen, J.T., B.D. Beck, and T.S. Bowers. 1996. Validation of an arsenic model through urine and fecal measurements. The Toxicologist 30:49.
Cohen, J.T., B.D. Beck, P.D. Boardman, L.A. Beyer, and D. Hiller. 1995. Use of an arsenic exposure model at a gold mining and milling site. Presented at 1995 International Conference on Arsenic, San Diego, CA.
Beck, B.D., P.D. Boardman, L.A. Beyer, J.T. Cohen, and D. Hiller. 1995. Validation of an arsenic exposure model at a mining and milling site through urinalysis. Presented at 1995 International Conference on Arsenic, San Diego, CA.
Beck, B.D., P.D. Boardman, and A. Watson. 1995. Urinalysis study for evaluating arsenic exposure in a population residing on mill tailings. The Toxicologist 15:87.
Schoof, R.A., L.J. Yost, P.A. Valberg, and B.D. Beck. 1994. Recalculation of the oral arsenic reference dose and cancer slope factor using revised assumptions in inorganic arsenic intake from food. The Toxicologist 14:37.
Petito, C.T. and B.D. Beck. 1990. Evaluation of non-linearities in the dose response curve for arsenic carcinogenesis. Proceedings of the 24th Annual Conference on Trace Substances in Environmental Health.
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Other Publications/Reports
Valberg, P.A., B.D. Beck. 1993. ''Recalculation of the Arsenic Cancer Slope Factor.'' Submitted to IRIS Information Submission Desk (U.S. EPA) on August 9, 1993.
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BIOGRAPHY FOR SCOTT J. RUBIN
Scott Rubin is an independent attorney and consultant, working exclusively on issues affecting the public utility industry. From 1983 until January 1994, he was an attorney and policy expert with the Pennsylvania Office of Consumer Advocate. From 1990 until he left the OCA, Mr. Rubin chaired the Water Committee of the National Association of State Utility Consumer Advocates. In that capacity, he served on EPA's Federal Advisory Committee to negotiate new regulations for disinfectants and disinfection by-products in drinking water.
i Since establishing his own practice in 1994, Mr. Rubin has testified as an expert witness before public utility commissions and legislative committees in more than a dozen states in matters involving the regulation of electric, gas, water, and telecommunications utilities. Mr. Rubin has given speeches throughout the country, published technical papers, and contributed to books on issues affecting the utility industry. His clients include consumer advocates, attorneys general, labor unions, state and local governments, consumer groups, and several private businesses and research foundations. Since 2000, he has served on the faculty of the Annual Regulatory Studies Program at the Institute for Public Utilities at Michigan State University. Mr. Rubin received his Bachelor's degree with distinction from Pennsylvania State University and his law degree with honors from George Washington University. He lives and works in Selinsgrove, Pennsylvania.
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Selected Publications
''Are Water Rates Becoming Unaffordable?,'' Journal American Water Works Association, Vol. 86, No. 2 (February 1994), pages 79–86.
''How much should we spend to save a life?,'' Seattle Journal of Commerce, August 18, 1994 (Protecting the Environment Supplement), pages B–4 to B–5.
''Water Rates: An Affordable Housing Issue?,'' Home Energy, Vol. 12 No. 4 (July/August 1995), page 37.
''A Nationwide Look at the Affordability of Water Service,'' Proceedings of the 1998 Annual Conference of the American Water Works Association, Water Research, Vol. C, No. 3, pages 113–129 (American Water Works Association, 1998).
''Assessing the Effect of the Proposed Radon Rule on the Affordability of Water Service,'' prepared for the American Water Works Association. 1999.
''Estimating the Effect of Different Arsenic Maximum Contaminant Levels on the Affordability of Water Service,'' prepared for the American Water Works Association. 2000.
''Viewpoint: Change Sickening Attitudes,'' Engineering News-Record, Dec. 18, 2000.
White Paper for National Rural Water Association: Affordability of Water Service. 2001.
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BIOGRAPHY FOR ERIK D. OLSON
Erik D. Olson joined the Natural Resources Defense Council (NRDC) in 1991 as a Senior Attorney, specializing in public health issues including drinking water, pesticides, toxics, and food safety. Mr. Olson is the national Coordinator of the Campaign for Safe and Affordable Drinking Water, a coalition of over 300 public health, environmental, consumer, and other groups dedicated to improved drinking water protection. Mr. Olson also sits on the EPA-American Water Works Association Research Foundation Microbial and Disinfection By-Products Research Committee. Until 1997, he served as the national environmental group representative on the Congressionally-chartered National Drinking Water Advisory Council.
From 1986–1991, he was counsel for the Environmental Quality division at the National Wildlife Federation (NWT), the largest environmental group in the country, where he worked on pollution issues. He teaches an environmental law seminar at the University of Virginia School of Law, and has taught courses in environmental law at the University of Maryland.
Previously (from 1984–1986), he was an attorney at the Office of General Counsel, of the U.S. Environmental Protection Agency, where he litigated environmental cases in numerous courts. At EPA's General Counsel's office, he worked on the Safe Drinking Water Act, hazardous waste, and the Clean Water Act.
Mr. Olson received his J.D. from the University of Virginia; he was inducted into the Order of The Coif legal honor society, was on the editorial board for the VIRGINIA JOURNAL OF NATURAL RESOURCES LAW (since renamed the VIRGINIA ENVIRONMENTAL LAW JOURNAL) and was a National Conservation Fellow. He received his B.A. in an independently-created major, Environmental Biology and Management, from Columbia University in New York City.
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Appendix 2:
Additional Material for the Record
SUBMITTED TESTIMONY OF GEORGE E. PARRIS
Arsenic in Drinking Water
George E. Parris, Ph.D., Director of Environmental and Regulatory Affairs, American Wood Preservers Institute
Introduction
Thank you for this opportunity to address the House Science Committee's Subcommittee on Environment, Technology and Standards. I represent the American wood preservers Institute, which is one of the organizations that has challenged the arsenic MCL set by the U.S. EPA on January 22, 2001. Most of our members are small and middle-size businesses that have been instrumental in the economic growth of this country by making railroads, marine shipping, rural electric utilities, telecommunications and house construction reliable and economically feasible while conserving our forest resources.
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I should explain that the wood preserving, mining and other industries may be more severely impacted by the U.S. EPA's ongoing setting of water standards for arsenic than are water utilities. Obviously, the U.S. EPA will use the dose-response curve developed in setting the drinking water standards in its risk assessment activities across many other programs. We make a product known as chromated copper arsenate- (CCA-) preserved wood that has been safely used for decades to make utility poles, pilings, timbers and lumber. CCA-preserved lumber is used in construction of houses, decks, fences, walkways and other outdoor applications where decay or insect attack is relevant to the economy, durability and structural integrity (safety) of the product.
The Economic Impact on Industries Other Than Water Utilities
Unlike the water utilities, any increase in cost of manufacture of preserved wood cannot automatically be passed along to the consumers because of aggressive competition from non-wood materials. Moreover, private water utilities may receive government grants to facilitate upgrade of their water systems to meet new standards. That is not likely to happen for wood preservers. You are probably not cognizant of the economic impact on our industry or industries in similar situations because the U.S. EPA has not analyzed those impacts. The AWN has argued that the U.S. EPA should have conducted a broad Regulatory Impact Analysis (RIA) in their promulgation of new MCL standards to show how wood preserving, mining and other industries will be impacted. Executive Order 12866 requiring regulatory impact analyses is independent of the narrow statutory basis for setting the MCLs under the Safe Drinking Water Act (SDWA section 1412(b) ). The U.S. EPA has chosen to limit their regulatory impact analysis to water utilities, i.e., the entities considered in the narrow statutory language. If the U.S. EPA fully disclosed the impacts of their new arsenic MCL on all industries and even private citizens who will have their real estate stigmatized (devalued) by the current regulatory agenda(see footnote 23), I believe that the Congress would be more circumspect about allowing the U.S. EPA to use their arbitrary default policies in risk projection.
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Arsenic is a Threshold Carcinogen
This brings me to the heart of my testimony. Contrary to the inflammatory public rhetoric concerning arsenic-related risks, the U.S. EPA's panel on arsenic (1997), the original NRC subcommittee (1999) and the recent NRC subcommittee (2001) have all found that there is no evidence that arsenic is a direct acting carcinogen. Thus, they have concluded that arsenic must follow a non-linear (S-shaped) dose-response curve, which (at some point) will have a threshold. However, the policy position taken by the original NRC subcommittee (1999, p. 206) was that because a specific mode of action was not identified, they would assume that the dose-response curve was linear with no-threshold. This approach meant that the much-publicized (inflammatory) calculations in the 1999 NRC report were little more than a ''what-if'' exercise. That is, ''what would the risk of low-dose exposure to arsenic be, if the dose-response curve were linear with no threshold?''
The linear no-threshold (LNT) model for extrapolating risk has been the policy of the U.S. EPA for several decades. We do not agree that the policy position taken by the NRC and the U.S. EPA meets the criteria of best peer-reviewed science required under the SDWA. This policy has its roots in the so-called ''target theory of cancer causation,'' which was proposed in the 1930s and was still plausible in 1970, but which has now clearly outlived its usefulness.(see footnote 24) The general application of the ''target theory'' to predict cancer rates from chemical exposure is theoretically implausible based on what we have learned about cells over the last 30 years. Moreover, in the specific case of arsenic, there are substantial data that would allow one to affirmatively reject application of the ''target theory.''(see footnote 25) For example, (i) the target theory requires direct damage to DNA, which has been shown (to a scientific certainty) not to happen with any relevant arsenic species at physiologically assessable concentrations (See for example, Ng et al., 2000; Mass et al., 2001); and (ii) the target theory requires a linear relationship between total/cumulative-dose and effects, which was not observed in controlled studies in Taiwan (Chiou et al., 2001)(see footnote 26) or in Utah by the U.S. EPA (Lewis et al., 1999).(see footnote 27)
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If you take away the historical bias for the linear no-threshold (LNT) model of extrapolation, there is no scientific reason not to believe that cancer incidence follows a typical S-shaped dose-response like other toxicological and pharmacological effects. Indeed, the recent NRC subcommittee report (2001, pp. 94–97) seems to acknowledge that fact; but at the same time, they conjurer up reasons why they could not or should not find a threshold that would have regulatory significance. For example, they claim that they do not know where they are on the S-shaped curve. However, it is clear that the epidemiological data used by the NRC and U.S. EPA to project risk must be on the ''upper plateau'' of the S-shaped curve on theoretical grounds (i.e., Michaelis-Menten kinetics) and the observation that cancer rates do not rapidly accelerate at higher doses. Indeed, most epidemiologists have seen fit to simply pool all the drinking water data above 100 ppb (Chiou et al., 2001) or 600 ppb (Tseng, 1977).(see footnote 28) Also, do not forget the very high doses used in various animal studies, which have generally failed to show any excess incidence of cancer at all much less an acceleration at high doses.(see footnote 29) The NRC's own analysis of the biologically relevant concentrations of arsenic suggests that 1 mM (e.g., 75 ppb) arsenic in tissue should fully a activate the relevant mechanisms of action (leading to non-linear/threshold dose-response curves).
Another approached used by the NRC subcommittee (2001) to avoid accepting a relevant threshold (i.e., one above the proposed regulatory level) is to argue that even if there is a biochemical threshold, at background dose rates, we are already above the threshold; and, thus, the dose-response should be linear at higher doses. In other words, they postulate that the threshold is very near ''zero'' dose, so that a linear extrapolation to that threshold is essentially identical to a linear extrapolation from observed data to ''zero.'' The argument(see footnote 30) that appears on page 6 of the Executive Summary and in the section entitled ''Implications of the Mode-of-Action of Arsenic in Drinking Water to Human Carcinogenesis'' (pages 94–97) in the ''2001 Update'' compares the concentration of arsenic in urine to the levels of arsenic in vitro that cause cellular effects:
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''(Page 6) Furthermore, in laboratory studies, cellular effects of arsenic occur at concentrations below those found in the urine of people who had ingested drinking water with arsenic at concentrations as low as 10 mg/L. Therefore, even if the curve is sublinear at some point (e.g., if a threshold exists), the available data showing cellular effects at arsenic concentrations in the range of those measured in U.S. populations suggest that any hypothetical threshold would likely occur below concentrations that are relevant to U.S. populations.''(see footnote 31)
In this case, note these points:
For starters, the particular ''cellular effects'' at low doses alluded to in the NRC report are not likely to lead to cancer.(see footnote 32) But fundamentally, the fact that the lining of the bladder is exposed to some level of arsenic-containing liquid is irrelevant. The blood must control the biochemistry in VIABLE cells in vivo. Only viable cells can produce clones of cancerous cells in vivo. Oxygen and nutrients that are essential to the growth of normal tissue (and even more critical to rapidly growing cancer clones) come from the blood, not from the urine. If a cell is detached from the lining of the bladder to the extent that it is significantly affected by the content of the urine, it is by definition being shed and excreted and cannot found a clone that will invade the bladder as a cancer. Comparing the concentration of arsenic in urine to the concentrations that cause effects in vivo or in vitro is a fundamental error. Obviously, how would it explain lung or skin cancers? These tissues are not bathed in urine. Why is drinking water-related cancer reported in the skin and not in the G.I. tract?(see footnote 33)
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Cohen (June 2000. The carcinogenicity of dimethylarsenic acid (DMA) in rats, SEGH Fourth International Conference on Arsenic Exposure and Health Effects, p. 38) and Arnold et al. (June 2000. Early effects of dietary treatment with dimethylarsenic acid on the bladder epithelium of female F344 rats, SEGH Fourth International Conference on Arsenic Exposure and Health Effects, p. 177) have demonstrated that proliferation of bladder epithelial tissues associated with DMA exposure is the result of cytotoxicity and subsequent regenerative hyperplasia.
Proliferation of cells (hyperplasia) is often associated with expression of a biomarker protein AP–1. By monitoring AP–1 expression, a dose-response curve for arsenic hyperplasia can be developed. In preliminary studies, Simeonova et al. (2001. Quantitative relationship between arsenic exposure and AP–1 Activity in mouse urinary bladder epithelium. Toxicological Sciences 60, 279–284) found that
''While AP–1 is a functionally pleomorphic transcription factor regulating diverse gene activities, numerous studies have indicated that activation of the MAP kinase pathway and subsequently increased AP–1 binding activities, is a precursor for arsenic-induced cancers of internal organs as well as the skin. We observed previously that within 8 weeks of exposure AP–1 activation occurs in urinary bladder tissue of mice exposed to arsenic in the drinking water.''
Simeonova et al. (2001) observed a non-linear dose-response relationship between As(III) concentration in drinking water and AP–1 DNA-binding activity in the bladder tissues of mice (C57BL/6):
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''In the present studies, C57BL/6 mice were exposed to sodium arsenite at various concentrations in the drinking water for 8 consecutive weeks. Minimal but observable AP–1 activity occurred in bladder tissue at exposure levels below which histopathological changes or arsenic tissue accumulation was detected. Marked AP–1 DNA-binding activity only occurred at exposure levels of sodium arsenite above 20 mg/ml, where histopathological changes and accumulation of arsenic in the urinary bladder epithelium occurred. Although the experimental design did not allow statistical modeling of the entire dose-response curve, the general shape of the dose-response curve is not inconsistent with the previously proposed hypothesis that arsenic-induced cancer follows a non-linear dose-response model.''
Please note that the minimum concentration in drinking water where (i) substantial increase in the AP–1 activity occurred, (ii) increase in arsenic accumulation in tissue occurred and (iii) histopathological evidence of tissue changes occurred was 20 mg/ml in drinking water, which is 20,000 mg/L or 20,000 ppb.
What is the Threshold?
There are actually three independent lines of argument that lead to a threshold for ''arsenic'' in drinking water above 100 ppb (e.g., 3mg/kg/day).
(1) In trial calculations, I have combined the ideas that you cannot have cancer without genoticicity and rudimentary pharmocodynamics to derive a numerical minimum (not most likely) threshold in drinking water of about 19 mg/L, and a likely threshold over 300 mg/L.
(2) Some epidemiologists who accept that there is a threshold, and thus, have tried to identify it statistically have analyzed the epidemiological data and find evidence for a threshold (in normal populations) over 100 mg/L.(see footnote 34)
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(3) Histologists (Cohen et al., 2000) have looks that the phenomena of cytotoxicity and regeneration of tissue and are led to conclude that concentrations that cause bladder epithelial tissues to die (over 100 mg/L in drinking water) would be required to initiate the chain of events leading to cancer.
I will also add that some scientists at the U.S. EPA (Kitchen et al., 1999) have examined induction of the HO–1 gene (a marker for arsenic toxicity) and found that it has a threshold (above 100 mg/L) and non-linear dose-response curve for biological effects in rats.(see footnote 35)
A Word About Epidemiology
Remember that the only evidence that ''arsenic'' is a carcinogen is based on epidemiology. Why have the epidemiologists and risk analysts focused on ''arsenic'' when we know that there are many different arsenic species (iAs(III), iAs(V), etc.). Perhaps this statement in the NRC report (2001) holds the answer:
''(p. 125) Because the most appropriate dose metric for arsenic-induced cancer is still not known, the choice of metric adds uncertainty to arsenic risk assessments.''
Contrary to this statement, it is the theory of cancer causation that determines the appropriate dose metric to consider not whether the chemical of concern is ''arsenic,'' iAs(Ia), iAs(V), tannins, etc. If epidemiologists are allowed to manipulate the measure of exposure (i.e., dose metric) until they get a positive dose-response correlation, then there is no science in the processes.(see footnote 36) Exactly how does the NRC subcommittee know a priori that arsenic or any chemical is a carcinogen? Does the NRC panel believe that all chemicals are carcinogens and that the job of epidemiologists is to find the correct dose metric to achieve a positive correlation? The fact is that the database that represents the doses in all the Southwestern Taiwan studies (see NRC 1999, pp. Table A10–1) consist of only about 150 individual measurements of dubious quality(see footnote 37) and relevance. The statistical power of the analysis can be no greater than the statistical power of the dose metric. While epidemiologists have been focusing on the 40,000+ participants (i.e., responses) in this study, they really should be focusing on the fact that we have no idea what they were exposed to and statistics do not help when you only have 150 measurements.
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Developing an MCL for a Threshold Carcinogen
If the U.S. EPA were to accept that there is a threshold for arsenite (iAs(III) ) at 100 ppb in drinking water (e.g., 3 mg/kg/day), I envision cost-effective regulation being implemented as follows: First, the MCL would, of course, not be set at the threshold but rather a ''safety factor'' would be applied to ensure that regulated water utilities stayed safely below the threshold considering variability in source concentrations and background (dietary uptake). For example, with a threshold of 100 ppb for arsenite, I would expect the MCL for arsenite to be around 10 ppb. If it were economically feasible for a water utility to meet this standard, they could accept the 10-ppb iAs(III) standard as a ''total-arsenic'' standard and conduct their monitoring for total arsenic (as currently done). However, if total-arsenic concentrations exceeded the arsenite MCL and proved to be an economic burden, the utility would have the option of determining and monitoring for arsenite (iAs(III) ) and arsenate (iAs(V) ) and use the less restrictive threshold(see footnote 38) and corresponding MCL for iAs(V). If the combined concentration of iAs(III/V) in the water was still above one of the respective thresholds, they could consider oxidizing iAs(III) to iAs(V) without precipitation with flocculating agent as an economical treatment alternative.
It particularly troubles me that the money that would be spent under the regulatory scheme proposed by the U.S. EPA does nothing to reduce exposure to people with private wells who are likely the individuals facing the highest daily doses in the country. Some of these people even display hyperkeratosis and are undoubtedly above the thresholds for cancer and non-cancer diseases described by the NRC (1999, 2001), whereas I am not aware of any water system subject to the MCL that is currently clearly above the thresholds for non-cancer effects. Money that the Congress might appropriate for compliance assistance to water utilities under the U.S. EPA's current regulatory concept would be more appropriately targeted to getting private homeowners below the non-cancer and cancer thresholds.
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BIOGRAPHY FOR GEORGE E. PARRIS
Dr. George E. Parris began working with arsenic as an undergraduate in 1966 and published several papers on arsenic chemistry from his undergraduate work at North Carolina State University (B.S. 1969).
He received his Ph.D. in organic chemistry in 1974 from the Georgia Institute of Technology as a Fannie and John Hertz Fellow. He then received a National Research Council Post-doctoral fellowship to pursue research in the environmental and analytical chemistry of arsenic, antimony and other metals at the National Bureau of Standards (now NIST). This work resulted in additional publications on the environmental chemistry of arsenic and antimony.
Upon completion of his post-doc, he moved to the U.S. Environmental Protection Agency where he managed several projects to monitor environmental contaminants during initial implementation of the Toxic Substances Control Act. He then moved to the Food and Drug Administration (Bureau of Foods) where he was a technical expert for environmental contamination of the food chain.
Upon leaving government service, he joined a consulting firm (1980–1988) and supported the U.S. EPA in a number of programs including identifying chemicals that warrant further testing (bioassays) under TSCA and identifying hazardous waste under the Resources Conservation and Recovery Act (RCRA). His expertise included exposure assessments and metabolism of xenobiotic chemicals. He also published several papers on risk assessment. From there, he spent two years (1989–1991) with an engineering firm discovering and cleaning up hazardous waste sites. He then accepted a job as a program manager for an international A&E firm (1991–1996) where he coordinated the analysis of various installation restoration alternatives for the Programmatic Environmental Impact Statement by the U.S. Department of Energy for its nuclear sites. Concurrently, he was the project manager for the Installation Wide Site Assessment for Fort Riley, Kansas for the Corps of Engineers. In both of these roles he was involved in risk and cost analyses and environmental monitoring.
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In 1996 he joined the American Wood Preservers Institute as their Director of Environmental and Regulatory Affairs. In this role he has conducted a thorough review of the recent studies of arsenic biochemistry and toxicology.
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Next Hearing Segment(6)
(Footnote 23 return)
Homes that depend upon private wells with arsenic concentrations below the old standard (50 ppb) but above the new standard (e.g., 10 ppb) will potentially lose market value equal to the cost of bring the water to the perceived (official) ''safe'' level. The U.S. EPA (June 22, 2000) has estimated that the cost to treat water for an individual house to exceed $360/year or $30/month. If this is subtracted from a typical affordable mortgage payment of e.g., $1000, the affordable mortgage decreases by about 3% implying a decrease is the properly value of about 3% of a property valued at about $150,000 or $4,500/household lost property value. Even in states like Florida where natural arsenic levels in groundwater are considered to be low, the USGS has found many counties where a significant fraction of the wells exceed 10 ppb.
(Footnote 24 return)
See Appendix I of the accompanying report, Arsenic: Dose-response of a Threshold Carcinogen.
(Footnote 25 return)
While most critics of the NRC/U.S. EPA positions have limited themselves to arguing that the S-shaped dose-response curve is equally valid as the linear, no-threshold model, it should be pointed out that general application of the linear no-threshold model can be affirmatively rejected on theoretical grounds and specifically rejected in the case of arsenic because of arsenic-specific observations. Thus, the focus must shift from arguing about the shape of the curve to determining the quantitative threshold.
(Footnote 26 return)
In this study where concentration and duration of exposure could actually be measured for individuals, it was found that there was a correlation between current exposure level and cancer incidence (as one would expect for a normal S-shaped dose response curve), but there was no correlation with duration of exposure (and hence total/cumulative-dose).
(Footnote 27 return)
The U.S. EPA likes to discredit this study on the basis of inadequate statistical power to be relevant for decision-making at low doses. However, they do not mention that there were effects seen at low total-doses that were not statistically significant at high total-doses.
(Footnote 28 return)
One of my objections to these studies is that data that are classified as ''>100 ppb'' may actually average much higher (e.g., 424 ppb in Chiou, 2001).
(Footnote 29 return)
Of course, the epidemiological analyses of Dr. Byrd (September 20, 2000) and Dr. Lamm submitted as various comments (see Section 7.3.1 of the attached report) show that the observed data are best interpreted with a threshold at 100 mg/L arsenic in drinking water or higher (i.e., the steep part of the curve is found above 100 ppb).
(Footnote 30 return)
This argument is constructed upon a fallacious concept introduced in the March 1999 report (Chapter 11 and the Executive Summary).
(Footnote 31 return)
This same strategy/argument has been used to justify the continued use of the linear no-threshold model for risk projection of ''dioxin'' in the face of a widely-accepted mode of action that clear requires a threshold.
(Footnote 32 return)
See Chapter 7 of the attached report for a summary of in vitro thresholds.
(Footnote 33 return)
For more details, I call your attention to Section 7.2.1 of my report. The following discussion can be found there:
(Footnote 34 return)
Chiou et al. (2001) using a population in which all the members were over 40 years old with poor nutrition, and extensive tobacco and alcohol exposure found a statistically significant increases in cancer above 100 ppb.
(Footnote 35 return)
I would like to mention, by the way, that I have critically reviewed a number of papers from U.S. EPA scientists and I have found the experimental technique and observations to be among the best published in the literature. However, sometimes the interpretations seem to have been written to pass a censor.
(Footnote 36 return)
A purely empirical mathematical correlation based on an arbitrary dose metric might have practical use at predicting risk within the range of experimental observation, but it does not confirm any particular model that would allow extrapolation outside the range of experimental data.
(Footnote 37 return)
No quality control or indications of precision and accuracy.
(Footnote 38 return)
In Appendix II of the attached report. I estimate the threshold for iAs(V) to be about 7 times higher than the threshold for iAs(III).