| Literature DB >> 20920952 |
Maureen R Gwinn1, Jeneva Craig, Daniel A Axelrad, Rich Cook, Chris Dockins, Neal Fann, Robert Fegley, David E Guinnup, Gloria Helfand, Bryan Hubbell, Sarah L Mazur, Ted Palma, Roy L Smith, John Vandenberg, Babasaheb Sonawane.
Abstract
BACKGROUND: Quantifying the benefits of reducing hazardous air pollutants (HAPs, or air toxics) has been limited by gaps in toxicological data, uncertainties in extrapolating results from high-dose animal experiments to estimate human effects at lower doses, limited ambient and personal exposure monitoring data, and insufficient economic research to support valuation of the health impacts often associated with exposure to individual air toxics.Entities:
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Year: 2010 PMID: 20920952 PMCID: PMC3018491 DOI: 10.1289/ehp.1002468
Source DB: PubMed Journal: Environ Health Perspect ISSN: 0091-6765 Impact factor: 9.031
Overview of case studies that explored various methodologies for benefits analysis of regulating air toxics.
| Chemical name | Dose–response data | Health end point(s) analyzed | Methods for risk evaluation | Methods for valuation | Size of benefit/potential utility | Uncertainties | Reference |
|---|---|---|---|---|---|---|---|
| Benzene | Human epidemiological studies (occupational cohort) | Leukemias (fatal and nonfatal) | Life table approach | VSL for fatal leukemias; approximation of willingness to pay for nonfatal leukemias | Model demonstrated percent reduction in risk by 2020 from 72 to 98% depending on county | Model sensitive to inputs; only quantified leukemias and not other health effects; low-dose extrapolation issues | |
| Acrolein | Analysis of existing animal studies with dose conversion to human equivalents | Respiratory effects (noncancer) | Dose–response functions combined with modeled ambient acrolein concentrations to estimate risks of adverse effects | Not carried out in this study; further analysis needed to relate respiratory outcomes observed in animals to likely human effects | Method used animal data to inform benefits of reduction in exposure in human populations | Assumptions based on low-dose extrapolation and human interpretation of end point (adverse effects as general indicators of potential human lung function changes) | |
| Toluene | Meta-analysis of human epidemiology studies on toluene and ethanol effects | Neurobehavioral effects | Dose-scaling comparison for acute effects of toluene exposure with those of ethanol intake | Effect of toluene scaled to that of ethanol; used costs of ethanol intoxication (e.g., automobile crashes) | Comparison with another toxicant with the same mechanism of action that has been monetized can yield a quantitative benefits estimate | Assumptions needed for mechanisms of both toxicants and dose–response comparisons | |
| Lead | Human epidemiology studies | IQ | Model changes in lead air quality for the exposed population and translated these into changes in blood lead | Present value of lifetime loss in earnings per IQ point lost | Provide a credible estimate of the human health benefits of attaining alternate lead NAAQS | Uncertainties in air-lead to blood-lead relationship; valuation method had substantial limitations |
Abbreviations: IQ, intelligence quotient; NAAQS, National Ambient Air Quality Standards.