Environmental Protection Agency Science Advisory Research Articles

Climate change doubters are finalists for Environmental Protection Agency Science Advisory Board

Climate change doubters are finalists for Environmental Protection Agency Science Advisory Board

Estimating sediment and nutrient delivery ratios in the Big Sunflower Watershed using a multiple linear regression model

This study is part of an effort to analyze the nutrient load reductions obtained from current and future best management practices implementations in the Big Sunflower Watershed to meet the 45% nutrient reduction goal set for the watershed based on the US Environmental Protection Agency Science Advisory Board9s (USEPA 2007) Gulf of Mexico hypoxia report. This paper describes the identification of dominant pollutant delivery mechanisms in the watershed, estimation of instream pollutant delivery ratios (DR) from subbasins to watershed outlet, and development of a tool to estimate changes in instream pollutant DR for what-if scenarios. The Big Sunflower Watershed is a 7,800 km² intensively cultivated agricultural watershed in the State of Mississippi. The Comprehensive Environmental and Economic Optimization Tool (CEEOT) modeling system, consisting of the Soil and Water Assessment Tool (SWAT) and Agricultural Policy and Environmental Extender (APEX) models, was used to develop a multiple regression equation to estimate the sediment and nutrient DRs for this watershed. The models used 32 years of weather data from 1981 to 2012. The explanatory variables considered for the DR are distance to watershed outlet, flow, and pollutant loads leaving subbasins. They were chosen based on their strength of correlations and type of relationship with DR. Our results indicate that flow from each subbasin is the dominant factor affecting DR for this watershed. Together, the explanatory variables considered under the multiple linear regression framework were able to estimate sediment and nutrient DRs with satisfactory regression parameters. The <i>R</i>² values for the regression relationship between the pollutant DRs and their counterparts estimated with multiple linear regression method were 0.8 for sediment, 0.96 for total nitrogen (N), and 0.9 for total phosphorus (P). The corresponding standard errors were 0.01 for sediment, 0.03 for total N, and 0.07 for total P. The explanatory variables were more strongly correlated to sediment DR than to nutrient DR. The tool developed to analyze changes in DRs for alternative scenarios appears to be useful for watershed managers.

Tiered on-the-ground implementation projects for Gulf of Mexico water quality improvements

B oth the Gulf Hypoxia Action Plan for Reducing, Mitigating, and Controlling Hypoxia in the Northern Gulf of Mexico and Improving Water Quality in the Mississippi River Basin (USEPA 2008) and the GOMA Governors' Action Plan II for Healthy and Resilient Coasts (GOMA 2009) call for the development and implementation of nutrient reduction strategies to reduce excess nutrient loads to the Gulf of Mexico. However, it is not just the Gulf of Mexico waters that are impacted by excess nutrients. The US Environmental Protection Agency Wadeable Streams Assessment (USEPA 2006) and the National Lakes Assessment (USEPA 2010) indicated almost one-third of the nation's stream miles and 20% of the lakes contain high total phosphorus (P) and total nitrogen (N) concentrations. Over 6,000 waterbodies in the United States are impaired by nutrients (USEPA 2011). The US Environmental Protection Agency Science Advisory Board has called for a 45% reduction of both N and P loads from the Mississippi River Basin to achieve the goal of a 5,000 km2 (1,930 mi2) hypoxic zone in the Gulf of Mexico (USEPA 2007). The approach taken by several states, including Mississippi, involves reduction of excess nutrients to attain the designated uses of state waterbodies for cumulative benefits…

Enhancing the ecological risk assessment process

The Ecological Processes and Effects Committee of the US Environmental Protection Agency Science Advisory Board conducted a self-initiated study and convened a public workshop to characterize the state of the ecological risk assessment (ERA), with a view toward advancing the science and application of the process. That survey and analysis of ERA in decision making shows that such assessments have been most effective when clear management goals were included in the problem formulation; translated into information needs; and developed in collaboration with decision makers, assessors, scientists, and stakeholders. This process is best facilitated when risk managers, risk assessors, and stakeholders are engaged in an ongoing dialogue about problem formulation. Identification and acknowledgment of uncertainties that have the potential to profoundly affect the results and outcome of risk assessments also improves assessment effectiveness. Thus we suggest 1) through peer review of ERAs be conducted at the problem formulation stage and 2) the predictive power of risk-based decision making be expanded to reduce uncertainties through analytical and methodological approaches like life cycle analysis. Risk assessment and monitoring programs need better integration to reduce uncertainty and to evaluate risk management decision outcomes. Postdecision audit programs should be initiated to evaluate the environmental outcomes of risk-based decisions. In addition, a process should be developed to demonstrate how monitoring data can be used to reduce uncertainties. Ecological risk assessments should include the effects of chemical and nonchemical stressors at multiple levels of biological organization and spatial scale, and the extent and resolution of the pertinent scales and levels of organization should be explicitly considered during problem formulation. An approach to interpreting lines of evidence and weight of evidence is critically needed for complex assessments, and it would be useful to develop case studies and/or standards of practice for interpreting lines of evidence. In addition, tools for cumulative risk assessment should be developed because contaminants are often released into stressed environments.

A Conflict-of-Interest Policy for Epidemiology

W /hen I arrived at the Environmental Protection Agency (EPA) as the Assistant Administrator for Research and Development, I was faced with a report from the General Accounting Office titled Science Advisory Board Panels: Improved Policies and Procedures Needed to Ensure Independence and Balance. The EPA's Science Advisory Board was in the midst of revising a form from the Office of Government Ethics for federal employees to determine whether their activities constituted a conflict of interest. The Science Advisory Board had used that same form and now it was apparent that something more detailed was necessary. The evaluation of conflict of interest was not new to me. As a nominee going through Senate confirmation, I had filled out forms for the White House, the Senate, and the EPA. I had also overseen these evaluations as a staff person for the National Research Council (NRC) where all participants in NRC activities have these evaluations. new form was eventually developed and extended throughout the various advisory boards of the EPA. It was then incorporated into the peer review activities for all major science activities at the EPA. These peer reviews, done through independent contractors along with the work of the formal advisory boards, results in over 600 reviews in any given year. Thus, reporting and evaluations related to conflict of interest are now done not just for federal employees engaged in the conduct and use of science in federal agencies, but for peer reviewers of that science as well. How does any of this relate to whether EPIDEMIOLOGY should have a conflict-of interest policy for its authors? Ralph Waldo Emerson should have included policymakers when he said A foolish consistency is the hobgoblin of little minds, adored by little statesmen and philosophers and divines. So we will abandon a justification based on consistency. How about going back to the basics? The EPA and other regulatory agencies are constantly urged to use the best available science in formulating environmental and human health regulations. Most of that science is not generated internally. Most of it comes from research conducted outside federal agencies. During my time inside the EPA, a new set of guidelines was developed for determining what information is used in the formulation of regulations (the Guidelines for Ensuring and Maximizing the Quality, Objectivity, Utility, and Integrity of Informa tion Disseminated by Federal Agencies). These guidelines place a premium on the use of peer-reviewed literature as a mechanism for quality assurance. Organizations who view themselves as watchdogs of the regulatory process have for some time opposed the use of science funded by entities that are the object of regulation. This applies to science performed by a corporate scientist or even an academic who has been funded by a corporate entity. In their view, this research is tainted even if it appears in a peer-reviewed journal. There is also a growing movement among these watchdog groups to restrict the participation of scientists and engineers as reviewers of regulation related science if they have been funded by entities that are the object of the regulation. Is all this concern misplaced? Perhaps it is, and, then again, perhaps it is not. Take the example of a recently published epidemiologic study of a compound that has been the subject of intense regulatory interest. Should the journal publishing the paper have refused to review it

Dose–response implications of the University of Alabama study of lymphohematopoietic cancer among workers exposed to 1,3-butadiene and styrene in the synthetic rubber industry

New quantitative cancer risk estimates for exposure to 1,3-butadiene are presented. These estimates are based on the most recent human epidemiologic data developed by Drs Delzell and Macaluso and their colleagues at the University of Alabama at Birmingham. The implications of Poisson regression analyses of the relative rate for leukemia are explored using their updated dose estimates and lymphohematopoietic cancer data. The Poisson regression model in these analyses has the same form as in the U.S. Environmental Protection Agency (EPA)'s draft risk assessment of 1,3-butadiene [U.S. Environmental Protection Agency, Health Risk Assessment of 1,3-Butadiene — External Review Draft, National Center for Environmental Assessment, Office of Research and Development, 63 Fed. Reg. 7167 (February 12, 1998) Publication NCEA-W-0267, Washington, 1998]. Consistent with the proposed cancer risk assessment guidelines of the EPA and the EPA's draft risk assessment, the exploration includes the maximum likelihood estimate of the ‘effective concentration’ (EC 01) corresponding to an extra risk of leukemia of 0.01 (1%) from a lifetime continuous exposure to 1,3-butadiene based on a linear dose–response model and the cumulative 1,3-butadiene dose metric (ppm-years). The incorporation of the most recent exposure estimates results in a 2.5-fold decrease in the estimates of leukemia risks computed by EPA. In addition, three changes proposed by the American Chemistry Council (formerly the Chemical Manufacturers Association) to the EPA's Science Advisory Board (SAB) for EPA's draft risk assessment of 1,3-butadiene are incorporated into the calculation. This results in approximately an additional fivefold decrease in the risk estimates of leukemia. The leukemia cancer risk estimates in the EPA's draft risk assessment of 1,3-butadiene decrease by approximately a factor of 13-fold when the updated epidemiologic data and the alternative numbers proposed by industry to the SAB are both incorporated. Specifically, the maximum likelihood estimate of the EC 01 increases from EPA's 1.2 ppm to 2.8 ppm on the basis of the updated epidemiologic data and increases further to 15.1 ppm when the CMA's proposed changes are also incorporated.

Ecosystem Management of South Florida

and Atmospheric Science, University of Miami, 4600 Rickenbacker Causeway, Miami, FL 33149. He is an ecosystems ecologist specializing in methods for ecological risk assessment and ecosystem management. He is also chair of the US Environmental Protection Agency Science Advisory Board (SAB) Ecological Processes and Effects Committee and chair of the US Man and the Biosphere Program (US MAB) Human-Dominated Systems Directorate. The time has come to

Exposure to Methylene Chloride

James Huff, John Bucher, and J. Carl Barrett state in their letter of 24 May (p. [p. 1083][1]) that new, possibly exculpating, evidence (Meeting Briefs, [12 Apr., p. 200][2]) should not be taken into account in reassessing the potential cancer risk posed by methylene chloride. This research was thought sufficiently important that the Occupational Safety and Health Administration reopened the record in its methylene chloride rulemaking ([1][3]), and the Environmental Protection Agency (EPA) is considering a reassessment of methylene chloride under its revised guidelines for carcinogen risk assessment. This is significant because EPA's Science Advisory Board and other reviewers have considered the rat results discussed by Huff et al . to be largely irrelevant to assessing methylene chloride's potential risk to humans ([2][4]). As for the criticisms of research showing that mice are unusually susceptible to this chemical, the results of experiments cited by Huff et al . do not show that the increase in lung tumors observed in the mice occurred by a mechanism that would also be operating in humans, as one of the authors (R. R. Maronpot) of a paper by F. W. Kari et al . ([3][5]) acknowledged at the summer 1993 Toxicology Forum ([4][6]). Huff et al . [paraphrasing the results of Kari et al . ([3][5])] state that “mice exposed to only 2000 parts per million of methylene chloride … showed eventual lung and liver cancers …,” implying that this is a low exposure. In fact, 2000 parts per million is a very high exposure that far exceeds the saturation limits of the P450 pathway. 1. 1.[↵][7] Fed. Regist. 60, 54462 (1995). [OpenUrl][8] 2. 2.[↵][9] For example, letter from EPA's Science Advisory Board and report to William D. Ruckelshaus, EPA Administrator (18 July 1984). 3. 3.[↵][10] 1. F. W. Kari, 2. F. J. Foley, 3. S. K. Seilkop, 4. R. R. Maronpot, 5. M. W. Anderson , Carcinogenesis 14, 819 (1993). [OpenUrl][11][Abstract/FREE Full Text][12] 4. 4.[↵][13] “Methylene chloride mechanistic and bioassay studies,” Toxicology Forum, National Institute of Environmental Health Sciences, Aspen, CO, summer 1993, transcript, p. 350. [1]: /lookup/doi/10.1126/science.272.5265.1083b [2]: /lookup/doi/10.1126/science.272.5259.200 [3]: #ref-1 [4]: #ref-2 [5]: #ref-3 [6]: #ref-4 [7]: #xref-ref-1-1 View reference 1. in text [8]: {openurl}?query=rft.jtitle%253DFed.%2BRegist.%26rft.volume%253D60%26rft.spage%253D54462%26rft.atitle%253DFED%2BREGIST%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx [9]: #xref-ref-2-1 View reference 2. in text [10]: #xref-ref-3-1 View reference 3. in text [11]: {openurl}?query=rft.jtitle%253DCarcinogenesis%26rft.stitle%253DCarcinogenesis%26rft.issn%253D0143-3334%26rft.aulast%253DKari%26rft.auinit1%253DF.W.%26rft.volume%253D14%26rft.issue%253D5%26rft.spage%253D819%26rft.epage%253D826%26rft.atitle%253DEffect%2Bof%2Bvarying%2Bexposure%2Bregimens%2Bon%2Bmethylene%2Bchloride-induced%2Blung%2Band%2Bliver%2Btumors%2Bin%2Bfemale%2BB6C3F1%2Bmice%26rft_id%253Dinfo%253Adoi%252F10.1093%252Fcarcin%252F14.5.819%26rft_id%253Dinfo%253Apmid%252F8504473%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx [12]: /lookup/ijlink/YTozOntzOjQ6InBhdGgiO3M6MTQ6Ii9sb29rdXAvaWpsaW5rIjtzOjU6InF1ZXJ5IjthOjQ6e3M6ODoibGlua1R5cGUiO3M6NDoiQUJTVCI7czoxMToiam91cm5hbENvZGUiO3M6NjoiY2FyY2luIjtzOjU6InJlc2lkIjtzOjg6IjE0LzUvODE5IjtzOjQ6ImF0b20iO3M6MjQ6Ii9zY2kvMjc0LzUyODYvMzI0LjUuYXRvbSI7fXM6ODoiZnJhZ21lbnQiO3M6MDoiIjt9 [13]: #xref-ref-4-1 View reference 4. in text

Tobacco industry response to a risk assessment of environmental tobacco smoke

Tobacco industry response to a risk assessment of environmental tobacco smoke

Regulatory Focus: Improving health-related risk assessments

The Office of Research and Development (ORD) at the Environmental Protection Agency (EPA) has prepared a plan for a comprehensive and broad research program to improve health risk assessments. ORD presented its plan to the executive committee of EPA's Science Advisory Board in April. This plan was developed in response to congressional direction to begin such an integrated and systematic program in 1988. The proposed budget is $3 million in fiscal year 1988 and $7 million in fiscal year 1989, and EPA plans to spend $7 million a year for at least five years.

Role of Science Advisory Groups in Eastablishing Standards for Ambient Air Pollutants

The scientific data bases on the sources, transport, transformations, sampling and analytical technology, exposures and effects of ubiquitous air pollutants have been essential resources in the development of the National Ambient Air Quality Standards (NAAQSs), and the Clean Air Scientific Advisory Committee (CASAC) has provided critical review and oversight of the Environmental Protection Agency (EPA) staffs use of the data in developing proposed standards for the Administrator. It has also provided guidance to EPA in planning research needed to address critical knowledge gaps. This paper provides a review of the development of the current process used in developing ambient air standards, a chronology of some landmark events, a critique of the current process, and a summary of CASAC's recent recommendations for improving the process. Standards for point source pollutants are developed by a process that differs in many respects from those used for the more ubiquitous “criteria” pollutants. The health assessment documents for the “hazardous” pollutants from point sources receive critical review from the Environmental Health Committee of the EPA's Science Advisory Board (SAB). They contain quantitative probability estimates of cancer risk based on animal toxicology and human epidemiology studies. While exposure assessments developed for NAAQSs are subject to CASAC review, those for hazardous air pollutants have not been subjected to SAB review. The National Emissions Standards For Hazardous Air Pollutants (NESHAPs) are based primarily on the application of specific source control technologies. There is currently no established procedure for SAB review of the scientific basis for EPA's proposals for NESHAPs. A chronology of some landmark events in the development of regulatory controls for point source pollutants is presented and discussed.

Advisory Committees in OSHA and EPA: Their Use in Regulatory Decisionmaking

Federal agencies regulating the production and use of toxic substances increasingly have utilized citizen advisory committees to help shape the form of that regulation. Both the U.S. Occupational Safety and Health Administration (OSHA) and the U.S. Environmental Protection Agency (EPA) turn to such committees for recommendations on a variety of subjects, and the advisory committee has become an especially important source of federal policy on toxic substances. Recently, the discovery of a Reagan administration hit list naming many members of EPA's Science Advisory Board (SAB) whose views were no longer acceptable raised concern about questionable political manipulation of government advisory committees in general.' This article examines the creation and use of advisory committees in the regulation of toxic substances in manufacturing, and suggests mechanisms to insure and improve the effectiveness and public service functions of of these and similar committees.