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Air Toxics Exposure: Relevance to Risk Assessment

Air Toxics Exposure: Relevance to Risk Assessment. TCEQ/NUATRC Air Toxics Workshop October 17, 2005 Tina Bahadori, D. Sc. Long-Range Research Initiative American Chemistry Council. GPRA Goals (source: EPA Air Toxics Research Strategy draft 2002).

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Air Toxics Exposure: Relevance to Risk Assessment

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  1. Air Toxics Exposure:Relevance to Risk Assessment TCEQ/NUATRC Air Toxics Workshop October 17, 2005 Tina Bahadori, D. Sc. Long-Range Research Initiative American Chemistry Council

  2. GPRA Goals (source: EPA Air Toxics Research Strategy draft 2002) • “By 2010, reduce air toxics emissions by 75% from 1993 levels.” • “By 2020, eliminate unacceptable risks of cancer and other significant health problems from air toxics emissions for at least 95% of the population, with particular attention to children and other sensitive subpopulations…”

  3. Risk Assessment/Risk Management Framework

  4. Foundation for Decision-Making MACT Std’s Residual Risk Std’s Urban Area Source Std’s Community Initiatives Utility Determination & Actions Mobile Source Std’s Combustion Std’s NATA HEALTH RISK INFORMATION Is it sufficient?

  5. “Individual” Air Toxics 188 CAA 34 NATA 21 Mobile Source 18 Indoor Air The Conundrum Facility SOURCE 1 SOURCE 2 SOURCE 3 8-9 Yr after MACT: Residual Risk? Ample margin of safety test.

  6. Sources of Air Toxics

  7. RfC Lifetime continuous exposure Adverse effects unlikely in sensitive groups NOAEL/BMD (human adj)/UF’s: NOAEL, interspecies, intraspecies, chronic, database Linear Multi-Stage Model Lifetime continuous exposure Upper bound excess lifetime cancer risk Risk unlikely to exceed upper bound Risk likely to be somewhere between 0 and upper bound

  8. Current and Future Needs • Improve risk assessment methodologies • consideration of real-world exposures (e.g., dose-rate, intermittent) • reduced reliance on generic defaults, • harmonization of cancer and noncancer methods • Expand research on complex mixtures of air toxics • Use available health information in state-of-the-science assessments, in time for regulatory use • Prioritize and fill chemical-specific health data gaps in context of the risk “wheel”

  9. The ACC’s Long-Range Research Initiative (LRI) • Goal: Provide fundamental research essential to improving chemical testing and risk assessment practices and policies • Research independence • PIs select chemicals • PIs “own” data and publish in peer-reviewed literature without ACC approval • Research conducted according to • MOU with CIIT Centers for Health Research • Competitive RfP program, often with other federal agencies

  10. LRI Air Toxics Program • Human Exposure Studies • Atmospheric formation of air toxics mixtures, with identification of toxic components (UNC) • Measurement of indoor, outdoor, and personal exposures to VOCs in several areas of Boston and Detroit (Harvard,U.MI) • Improve air toxics exposure models (EOHSI with EPA/NERL & OAQPS)

  11. LRI Air Toxics Program • Dose Studies • Respiratory tract dosimetry modeling, reactive gases and particles (CIIT) • Animal-to-human extrapolation • Human age models • Age-dependent pharmacokinetic modeling for systemically acting chemicals (CIIT, ENVIRON) • Chlorine dosimetry (CIIT)

  12. LRI Air Toxics Program • Health Effects and Assessment Studies • Chlorine dose-response modeling (CIIT) • Mechanisms of acute lung injury (CIIT) • Lung biomarkers (CIIT) • Methods for developmental effects (EPA, Cornell, TNO, CIIT) • Chloroform computational modeling (CIIT) • Functional genomics (CIIT) • BB-DR modeling (CIIT, Colorado State, Gradient)

  13. For more information on LRI www.uslri.org Tina_Bahadori@americanchemistry.com

  14. Far More Advanced Assessment Methods Available, if Database Rich • Noncancer • Expert judgment (e.g., EPA ozone) • Advanced BMD and Bayesian analyses (e.g., EPA Mn) • Probabilistic UF’s (e.g., pubs, mostly for RfD’s) • 1999/2003 EPA’s Draft Revised Cancer Guidelines • Mode of action • Biologically-based dose-response modeling • Margin of exposure • 2003 supplement for early-life exposure

  15. Research Causes Evolution of Formaldehyde Cancer Assessment • Early 80’s, nasal cancers in rodents, >6ppm • Later • rat-human nasal dose models • mode of action (DPX & CRCP) • 2-stage clonal growth model link of DPX & CRCP with tumors

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