BISC 312 ASBESTOS What is asbestos a group

BISC 312 ASBESTOS

What is asbestos? § a group of fibrous, naturally occurring silicate minerals that generally exist in nature as metamorphic or igneous rocks § classified into 2 groups according to their physical characteristics 1) Serpentine asbestos - develops in a layered or tiered form 2) Amphibole asbestos - has chain like structures § the three common types of asbestos fibres are: Chrysotile, Amosite and Crocidolite

Asbestos Types Name Shape/ Colour Compsition Group Crysotile* Curly/ White Magnesium silicate Serpentine Amosite Straight/ Grey Iron and Magnesium Amphibole Crocidolite Straight/ Blue sodium, iron, magnesium silicate Amphibole Picture * Crysotile is the most used form toxicity ranking: chrysotile < crocidolite < amosite

History § the word asbestos is derived from the Greek word “αμίαντος” meaning inextinguishable or indestructive § first used in 4000 BC by the Romans in cremation, cloths and lamp wicks § commercially mined in 1800's § found in rock formations in USA, Canada, South Africa, and the former Soviet Union

Uses § heavily used due to its high tensile strength, thermal stability/resistance, and electrical resistance § fibers can be spun into material that is flame retardant and chemically inert § Examples: § § § household appliances handheld hair dryers insulation (in walls and piping) Uses of Asbestos in 1999

Airborne (friable) asbestos § only dangerous if in this form § form of asbestos released from the manufacturing process § exposure/dose = risk of disease § risks associated with low-level non-occupational exposure are not well established § biggest concern: diameter < 3 µm

Uptake of Asbestos Respiratory: § friable asbestos can be deposited in both the upper and lower respiratory tracts § smaller fibres have greater probability of deposition in lower respiratory tract § fibre geometry and anatomy of the animal affect successful entrance into the body § fibres deposited in lungs may penetrate respiratory membrane and be transported to other sites of body via circulatory and lymphatic systems

Uptake of Asbestos Gastro-Intestinal: § Ingestion § human water supply can be contaminated due to mine runoff into lakes and streams § airborne asbestos may settle on crops and be ingested § then crosses the GI mucosa and can be transported to other sites in body

Fibre persistence the retention of fibres in the lung over time § depends on the relative insolubility of fibres § long fibres generally have more biological activity greater pathogenicity § most carcinogenic fibres for the mesothelium have fibre lengths > 8 µm and diameters < 0. 25 µm. § fibres that split longitudinally produce thinner and longer respirable fibres that are more pathogenic § non-biodegradable by aquatic organisms

Clearance of asbestos § clearance of inhaled asbestos occurs via the sputum (mucociliary transport) § ingested asbestos cleared from the body via feces no evidence for 100% clearance

Asbestos Effects on other Organisms Bacteria § addition of asbestos dust to soil reduced the total population of soil microflora Plants § dumping of asbestos-bearing wastes onto soil results in areas devoid of vegetation

Asbestos Effects on Humans § biochemical alterations § genetic impairment § changes in the immune response and kidney damage § pulmonary functions are adversely affected § impairment of gas exchange, vital capacity and ventilation capacity changes § asbestos can contain the carcinogen, Benzopyrene found to facilitate the transfer of Benzo(a)pyrene to phospholipid vesicles

Diseases Associated with Asbestos § latency period between date of first exposure and the time when the disorder becomes clinically apparent. § lung disease from asbestos can be divided into three main types: 1) 2) 3) asbestosis mesothelioma lung cancer

Asbestosis § § Disease of the lung lining causes inflammation, tissue damage, and scarring around the asbestos fibers scarring can continue to grow and form plaques at the surface of the lungs and in the tissue lining latency period of 15 -30 years often lethal symptoms include: - dyspnea - basilar interstitial opacities - inspiratory crackles - difficulty breathing - enlarged heart - dry cough - decreased blood flow to lungs

Mesothelioma § § Cancer of the pleural lining a rare cancer exclusively related to asbestos exposure affects thin membranes, surrounding lungs & other internal organs latency period: 30 -40 years by time it is diagnosed, almost always fatal (no treatment) symptoms include: - dyspnea - lasting cough - pleuritic pain - fatigue - weight loss - chest pain - opacification Dose (mg/rat) 0. 5 1 2 4 8 # of Rats 12 11 12 12 12 # with mesothe lioma 1 3 5 4 8 Mean survival (days) 784 729 664 762 692 Lung with Mesothelioma Healthy Lung

Lung Cancer § persistence of asbestos fibers in the lung tissue and the resulting inflammation seem to initiate the process of cancer formation. § starts in the lining of the bronchi, bronchioles, trachea, or alveoli § forms malignant tumor and can spread to other parts of the body smoking increases the risk of lung cancer (synergistic effect with asbestos) § due to the weakening of the mucocilliary defence mechanism of the lungs caused by smoking

Other Effects Immune system § Impaired cell-mediated immune response noted in asbestosis and mesothelioma patients Chromosome abnormalities eg) Chinese hamster cells exposed in vitro to 0. 01 mg/ml chrysotile, crocidolite, amosite or anthophyllite

Who is at Risk? Industries commonly associated with asbestos exposure § § § § mining and milling manufacturing construction industry ship building industry insulation workers brake repair and maintenance building demolition workers asbestos abatement workers

Factors in determining risk of asbestos exposure: § fibre characteristics (type, physical properties, length to width ratio) § § dose and duration of exposure confounding variable (i. e. smoking) biopersistence of the fibre surface reactivity of the material (wet, dry, in concrete, in insulation, etc. )

Two hypotheses of asbestos exposure 1) The “One Hit” hypothesis: § assumes cancer is an expression of a permanent replicable change in cellular genetics resulting from the interaction of one molecule of carcinogen with a critical receptor in one cell. § thus the curve passes through zero and any dose above zero will exert an effect 2) The “Threshold” hypothesis: § assumes a no effect dose of carcinogen below which cancer cannot occur (occurs with near zero probability). § an exposure to small amounts is considered hazard-free

Exposure Dose What is a safe amount of asbestos? § experimenters expose animals to high doses and extrapolate data to humans who typically receive low doses Exposure risk is difficult to quantify: § humans are exposed repeatedly and to varying mixtures of fibres § the mortality and disease presently being studied is the result of exposure 20 to 50 years ago when fibre levels were unregulated and exposure levels were much higher § individuals respond differently to a given dose

Protection § Two main ways: 1) respiratory masks § § half-face mask full-face mask helmet hooded respirator Levels of protection: half mask < full mask < helmets < hooded respirators 2) protective clothing § § disposable coveralls hard hats safety shoes/boots eye protection

Regulations § Environmental Protection Agency (EPA) require that all asbestos be thoroughly wet with a water and surfactant mixture (low pressure water stream spraying) prior to removal § 1970’s: began regulation of asbestos use § Occupational Safety and Health Administration (OSHA) has set Permissible Exposure Limit (PEL) at 0. 1 fibers per cubic centimeter (f/cc) for an 8 hour time weighted average

Regulations § Under EPA and OSHA, asbestos containing waste must be properly containerized with warning labels

SUMMARY 1. 2. 3. 4. 5. asbestos is extremely persistent problems mostly in humans hard to study because its effects can take decades to show can be effectively protected against with the right equipment and handling still being used today in a more controlled manner

References: § Associate Committee on Scientific Criteria for Environmental Quality, Effects of Asbestos in The Canadian Environment, NRCC NO. 16452 13, (19, 106)1979 § Kamp DW, Weitzman SA. Asbestosis: clinical spectrums and pathogenic mechanisms. Proc Soc Exp Biol Med 214: 12 -26 (1997) § Jaurand M. Mechanisms of fiber-induced genotoxicity. Environ Health Perspect 105(suppl 5): 1073 -1084 (1997) § Vu VT, Lai DY. Approaches to characterizing human health risks of exposure to fibers. Environ Health Perspect 105(suppl 5): 1329 -1336 (1997) § http: //www. bigclassaction. com/asbestos/descriptive. html § http: //www. findarticles. com/p/articles/mi_m 0984/is_2_124/ai_107395165 § http: //www. asbestosnetwork. com/asbestos/de_history_usage. htm § http: //www. asbestosnetwork. com/asbestos/de_type. htm § http: //www. co. fairfax. va. us/service/hd/atphotos. htm http: //www. active§ asbestos. co. uk/frame_centre_about_history. html § http: //www. asbestosresource. com/asbestos/ § http: //www. nsc. org/library/chemical/asbestos. htm § http: //www. dnr. state. wi. us/org/aw/air/reg/asbestos/asbes 3. htm

THANK YOU GROUP #9 § § § Douglas Campbell Wesley Chan Rebecca Eastman Ann Ho Beth O’Donoghue Linda Tang § § § Andy Chan Don Dang Nassim Ghani Mirian Lee Devika Sharma