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Bioavailability of Contaminants in Soil: Considerations for Human Health Risk Assessment

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1 Introduction
1 Introduction Overview
1.1 Using Bioavailability Information
1.2 Background
1.3 Definition of Terms
2 Regulatory Background
2 Regulatory Background Overview
2.1 Current Practices: Survey of State Regulators
3 Technical Background
3 Technical Background Overview
3.1 Soil Mineral Phases
3.2 Soil pH, Organic Matter, and Reactive Clay Minerals
3.3 Soil Particle Size
4 Decision Process
4 Decision Process Overview
4.1 Decision Process Flowchart
4.2 Is there a Method Available?
4.3 Could Bioavailability Assessment Affect the Remedial Decisions?
4.4 Do the Benefits of Bioavailability Assessment Justify the Costs?
4.5 Further Considerations
5 Methodology
5 Methodology for Evaluating Contaminant Oral Bioavailability Overview
5.1 In Vivo Approach
5.2 In Vitro Approach
6 Lead
6 Lead Overview
6.1 Fate and Transport
6.2 Toxicology and Exposure
6.3 Methodology for Quantifying RBA of Lead in Soil
6.4 When Does a Bioavailability Study Make Sense?
6.5 Case Studies
6.6 Using Bioavailability Methods to Evaluate Remedies (Bioavailability-Based Remediation)
7 Arsenic
7 Arsenic Overview
7.1 Fate and Transport
7.2 Toxicology and Exposure
7.3 Methodology for Evaluating Arsenic Bioavailability
7.4 When Does It Make Sense to Use Bioavailability?
7.5 Case Studies
7.6 Using Bioavailability Methods to Evaluate Remedies (Bioavailability Based Remediation)
8 PAHs
8 Polycyclic Aromatic Hydrocarbons (PAHs) Overview
8.1 PAH Sources and Exposure
8.2 General Toxicity of PAHs
8.3 Influences of Soil on Bioavailability of PAH
8.4 Methodology for Evaluating PAH Bioavailability
8.5 Dermal Absorption
8.6 Amendment Strategies and Permanence of Bioavailability
8.7 Case Study
9 Risk Assessment
9 Using Bioavailability Information in Risk Assessment Overview
9.1 Risk Calculations
9.2 Other Considerations and Limitations
10 Stakeholder Perspectives
10 Stakeholder Perspectives Overview
10.1 Stakeholder Concerns
10.2 Specific Tribal Stakeholder Concerns
10.3 Stakeholder Engagement
11 Case Studies
11 Case Studies Overview
11.1 Arsenic, Mining, CA
11.2 Arsenic, Pesticide, AR
11.3 Arsenic, Naturally occurring, UT
11.4 Arsenic, Smelter, AZ
11.5 Arsenic-contaminated tailings, OR
11.6 Lead, Industrial, Midwest US
11.7 PAH, Skeet targets, TX
11.8 Arsenic, Copper precipitation, UT
11.9 Arsenic, CCA wood preservative, CA
11.10 Arsenic, MGP coal ash, MI
11.11 Lead, Mining MT
11.12 Lead, Mining, MT
11.13 Lead, Smelter, UT
Additional Information
Review Checklist
Appendix A: Detailed Survey Responses
Appendix B: Chemical Reactions of Metals
Acronyms
Glossary
Acknowledgments
Team Contacts
Document Feedback

 

Bioavailability of Contaminants in Soil
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8.1 PAH Sources and Exposure

PAHs are ubiquitous environmental contaminants, originating from both natural and anthropogenic sources.  Anthropogenic sources dominate, and include incomplete combustion of organic materials, notably carbon fuels such as coal or petroleum.  Natural sources include volcanic eruptions and forest fires. PAHs are distributed widely in the environment, generally as complex mixtures, and concentrations are often elevated in urban soils due to the presence of such mixtures. Exposures to these mixtures can occur through inhalation, ingestion, and dermal contact.

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Motor vehicle exhaust, industrial emissions and smoke from burning wood, charcoal, and tobacco all contain high levels of PAHs. PAH formation from combustion depends in part on combustion temperature. In general, more PAHs form when organic materials burn at low temperatures, such as in wood fires or cigarettes. High-temperature furnaces produce fewer PAHs. PAHs formed from combustion can bind to particulates in smoke or exhaust, and dispersion of suspended particulates in air can move PAHs over long distances. PAHs are also found in a wide range of products, including coal tar, crude oil, creosote, roofing tar, and mothballs, medicines, dyes, plastics, and pesticides, which can be additional sources of PAHs in the environment.

PAHs are relatively insoluble in water and are mostly associated with particulate matter, either in air as mentioned above, or in soils and sediments in the environment. Inhalation exposure to PAHs occurs from breathing polluted air, wood smoke, vehicle exhaust, or cigarette smoke. Ingestion of PAHs can occur from food sources, contaminated drinking water, and from incidental ingestion of soil near areas where coal, wood, gasoline, or other products have been burned. Incidental ingestion can also result from the soil at hazardous waste sites, former manufactured gas plant sites, and wood-preserving facilities. Dermal exposure can occur from contact with PAH-contaminated soil or commercial products containing PAHs, such as coal tar shampoos.

Although this guidance focuses on oral bioavailability, dermal absorption of PAHs has carcinogenic effects, both systemically and at the site of contact on the skin. Using standard USEPA default exposure values and the current oral cancer slope factor for the index PAH, benzo(a)pyrene (BaP), the ingestion route of exposure accounts for 72% and dermal route of exposure accounts for 28% of the potential cancer risk from direct contact with soil PAH.

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