Naturally Occurring Asbestos (NOA) General Overview

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1 Naturally Occurring Asbestos (NOA) General Overview Lee R. Shull PhD Health, Ecology and Risk Practice MWH Global Sacramento, CA CASH NOA Workshop January 24, 2006 Presentation Outline Brief background Current status - main issues & questions Exposure Health effects State of the science Assessing risk Managing NOA

2 Asbestos What is it? Types: Serpentine - chrysotile Amphibole - tremolite, actinolite, crocidolite, amosite, anthophylite Physical Properties: Fibrous silicate minerals µm in size Not visible (naked eye) Strong, indestructible Resistant to chemicals Chrysotile -- more flexible, jagged, curly Amphibole -- more brittle, smooth NOA Evolution of the issue in California Early 1900s Processed asbestos introduced into commerce (Ex. buildings, products, ships) 1930s Asbestos related illnesses identified (asbestosis, mesothelioma, lung cancer) 1960s Libby, MT vermiculite mine (NOA) 1980s Fairfax County, VA tremolite in soil 1990s CA foothill Counties (El Dorado, etc) tremolite in serpentine rocks, homeowners issue 2000s California Schools (Oak Ridge HS, El Dorado Hills) NOA found in road-cuts near school soccer field

3 NOA Many issues, concerns, & questions Science How serious of a public health threat is it? How accurately can we quantify exposure? What s the dose-response relationship? How does NOA do what it does in the body? How accurately can we assess health risks? Who are the most sensitive in the population? Regulatory/policy What should comprise an optimized NOA risk management program? What role can/should government agencies play in NOA risk management? What laws and regulations are needed to optimize risk management? What risk management measures should be recommended and/or required to manage risk? NOA Many issues, concerns, & questions Regulated entities Employer s responsibility to workers (educating, informing, protecting)? Liability (e.g., homebuilders, school districts)? Managing risk? Sociologic Deciding whether or not to live in an NOA area? What life-style factors affect NOA exposure potential? Understanding the real deal on NOA -- what information sources to believe?

4 NOA in California Current status of the issue Knowledge of NOA occurrence in CA improving Quantifying NOA exposure a major challenge -- soil to air relationship Sampling and laboratory methods slowly improving; NOA vs cleavage fragments not yet resolved No confirmed deaths from NOA in CA; indications? Good epidemiological data are lacking; except for mesotheolioma, asbestos mortality difficult to track Regulatory programs emerging (e.g., Cal/EPA schools) Risk assessment methods still too crude, unsubstantiated, thus precautionary principle applied General public confused and concerned about exposure, potential health impacts, how/whether to self-protect Everyone wonders -- are the $$$ spent to mitigate theoretical, unconfirmed health risks justified? From Rocks and Soil to Air Exposure prerequisite Natural Rock weathering Wind erosion Anthropogenic Construction activities Vehicular traffic Land clearing Logging Farming Recreational activities Gardening activities

5 Asbestos in Air Typical reported levels Typical environmental levels in the US: Rural air ~ f/ml or ~10 f/m 3 Urban air ~100 f/m 3 Indoor air ~100 f/m 3 Bldgs with asbestos ,000 f/m 3 Air near asbestos mine or factory: up to 10,000 f/m 3 USEPA 2005 study in El Dorado Hills: Background in air (PCME): f/m 3 Sport activities, air: ,600 f/m 3 Managing Exposure Regulations and standards National air stds: ACGIH TLV-TWA: 100,000 f/m 3, ave. inhalation rate ~1 m 3 /hr NIOSH (>5 µm): 100,000 f/m 3 OSHA: PEL (8-hr TWA) ,000 f/m 3 PEL (30-min excursion TWA) -- 1,000,000 f/m 3 EAWG World Trade Center monitoring levels: Reoccupation level: 10,000 f/m 3 Long-term monitoring = 900 f/m 3 (10-4 risk) California regulations and stds: Toxic air contaminant (TAC) Prop 65 listed substance Listed hazardous substance Hazardous waste -- TTLC (wet-wt) = 1.0%

6 Measuring Exposure Medical/analytical methods Best: Lung tissue biopsy: detection of fibers, very invasive Lung lavage: detection of fibers, discomfort Others: Fiber analysis in other biological fluids: saliva, mucus, urine; not much value Chest X-ray: detects tissue changes, only good for high/known asbestos exposure Gallium 67 lung scanning and high-resolution computed tomography: detects non-specific tissue changes Overview of Health Effects The human lung

7 Overview of Health Effects Pulmonary region of the human lung Overview of Health Effects Fate of NOA in the lungs Upper respiratory: mostly removed -- mucociliary transport Pulmonary region: engulfed by macrophages and removed engulfed by macrophages and not removed penetrates into lymph system and transported to pleura and peritoneum not removed -- accumulates Factors determining fate: fibers thickness (>2 µm) fiber length (5-10 µm most problematic)

8 Overview of Health Effects Those incredible macrophages Overview of Health Effects Confirmed effects Malignant mesothelioma Pleura Peritoneum Lung cancer (bronchogenic carcinoma) Noncancer effects: Asbestosis -- scarring Pleural plaques -- localized pleura thickening Diffuse pleura thickening -- widespread Pleura calcification -- calcium deposition Pleura effusions -- fluid buildup

9 Overview of Health Effects Scientific consensus Exposure-effects well established in humans: Exposure to any asbestos type can increase likelihood of lung cancer, mesothelioma, and nonmalignant lung and pleural disorders Determinants of toxicity: Exposure concentration (EC), exposure duration (ED), exposure frequency (EF), and fiber dimension are main determinants Fiber potency differs: Amphibole fibers (e.g., tremolite) are retained longer in the lower respiratory tract than chrysotile fibers of similar dimension -- likely accounts for their greater potency Overview of Health Effects Scientific consensus Pulmonary interstitial fibrosis: Confirmed -- collagen deposition, progressive lung stiffening and impaired gas exchange, disability, possibly death Long time between exposure and effects (latency period): Asbestosis: 15 or more years Mesothelioma: 30 or more years Additive risk: Asbestos-exposed tobacco smokers are at greater than additive lung cancer risk

10 Overview of Health Effects Fibers can lodge in lung tissue Overview of Health Effects Lung tissue with asbestosis

11 Overview of Health Effects How does it do what it does? Not yet completely known Why its important to figure it out Scientific consensus: Multiple cellular and molecular responses No single mechanism explains all asbestos-related diseases Steps leading to disease not fully established Fiber structural and chemical properties are important factors Overview of Health Effects How does it do what it does? Two working hypotheses: Older: Fibers activate alveolar macrophages and other cells to produce reactive oxygen species that cause cellular damage, which leads to cellular changes, ending in injury (non-cancer, cancer). More Recent: Fibers activate certain genes in certain cell types causing these cells to produce specific chemical factors that control cell growth, resulting in harmful cellular changes.

12 Assessing Health Risk Dose-Response Relationship R e s p o n s e Observable Range Range of Inference 0 Dose Assessing Health Risk Cancer and non-cancer risk Measured: Incidence of asbestos-related lung disease (cancer, non-cancer): f-yr/ml = f/ml for 40 years = 125,000-30,000,000 f/m 3 Compare: OSHA 8-hr TWA std = 100,000 f/m 3 Estimated: USEPA estimate of cancer risk associated with lifetime exposure to 100 fibers (>5 µm)/m 3 of air: 2-4 excess cases/100,000 exposed people

13 Assessing Health Risk No completely adequate method USEPA unit risk factor (IRIS, 2005; 1993 last revised): Combines lung cancer and mesothelioma URF = 0.23 (f/ml) f/ml (400 f/m 3 ) = 1/10,000 risk f/ml (40 f/m 3 ) = 100,000 risk f/ml (4 f/m 3 ) = 1/1,000,000 risk Berman and Crump (2001) Modified Elutriator Method Separate unit risk factors for chrysotile and amphibole Methods currently under review by USEPA State of the Science Seeking answers to key questions Main question: What is the extent of NOAinduced disease caused by different fiber types and sizes? Are amphibole fiber types more potent than chrysotile in inducing asbestosis and lung cancer? What is the best regulatory definition of an asbestos fiber (length, width) for purposes of quantifying exposure levels and risk? What is the mechanism of action involved in asbestos-induced respiratory and pleural effects, and how are they influenced by fiber dimensions and mineral type?

14 State of the Science Seeking answers to key questions Other important questions: How much more sensitive are children to asbestos-induced respiratory effects than adults? What are the actual risks for respiratory diseases at low exposure levels (< fibers/m 3 )? Can NOA fibers induce lung cancer without first inducing pulmonary fibrosis, regardless of fiber type? Does exposure to asbestos increase the risk of gastrointestinal cancer? Managing NOA It IS manageable Understand NOA: Research Knowledge Utilize resources: Local air district State agencies Federal agencies Understand your NOA issue: Sampling, analysis, monitoring, record keeping Responsibilities, requirements, liabilities Develop and implement a management plan: Identify, implement practical mitigation measures Minimize exposure to the degree practicable

15 Thank You! Lee R. Shull (916)

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