physical hazard ii suspended particles n.
Download
Skip this Video
Loading SlideShow in 5 Seconds..
Physical hazard II: Suspended particles PowerPoint Presentation
Download Presentation
Physical hazard II: Suspended particles

Loading in 2 Seconds...

play fullscreen
1 / 45
julio

Physical hazard II: Suspended particles - PowerPoint PPT Presentation

193 Views
Download Presentation
Physical hazard II: Suspended particles
An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.

- - - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript

  1. Physical hazard II: Suspended particles Occupational Health EOH3202 Environmental & Occupational Health Faculty of Medicine and Health Sciences University Putra of Malaysia

  2. Learning goals • Able to identify work tasks associated with high exposures to suspended particles • Able to characterise the physical and chemical properties of suspended particulates • Able to understand particle size distribution and its relationship with site deposition and mechanisms of particle deposition in the lung • Able to identify health outcomes related to exposure of particulates

  3. Classification of hazards: Recap • Physical - noise, heat, vibration, ionizing radiation, pressure, poor lighting, electricity, mechanical injury, particulate emissions • Chemical • - solid, liquid, semisolid, gas • - heavy metal, solvents, etc. • Biological – Bacteria, virus, parasite • Psychosocial – stress, violence • Ergonomic problem – lifting heavy objects, repetitive movements, poor posture

  4. Examples of tasks at risk for high exposures to suspended particulates • Sandblasting work • http://www.youtube.com/watch?v=-TjqtXB8BtY&feature=related • http://www.youtube.com/user/allweldsandblasting?v=g-726Qa7Pco&feature=pyv&ad=6850597350&kw=industrial%20sandblasting • Quarry operation • http://www.youtube.com/watch?v=vAW_Vvu2nYI • Asbestos-related work • http://www.youtube.com/watch?v=RZm7u6z6tLI • Cotton processing workers • Laboratory workers – animal handlers • Welding work

  5. Cotton processing workers Typical setting of grinding the pieces of cotton and mixed garments in the recycling industry in Nepal A duvet maker beating the recycled cotton to make mattress in Nepal

  6. Physical hazard: suspended particles • Aerosol is the dispersion of solid or liquid in the gasesousmedium • –Cigarette smoke • –Welding fume • –Sea mist • DUST • Solid aerosols generated by the handling, grinding, abrasion, or cutting of a bulk material, with individual particle diameter being 0.1 µm or above • Dust particle size is related to the amount of energy involved in creation; the higher the energy—the smaller the particle created; the lower the energy—the larger the particle created • Examples: Saw dust, coal dust • FUMES • Solid aerosols generated by the condensation of vapors or gases from combustion or other high temperature processes • Usually very small and spherical • Sources: Welding, foundry and smelting operations, hot cutting or burning operations

  7. Aerosol cont. • MISTS • Liquid aerosols generated by condensation from a gaseous state or by the breaking up of a bulk liquid into a dispersed state • Droplet size related to energy input as in dusts and fibers • Examples: Metal working fluid from lathe, paint spray, liquid mixing operations • SMOKE • Solid aerosols resulting from the incomplete combustion of carbonaceous materials • Wide range of particle sizes • Size related to combustion efficiency • High efficiency = smaller particles, Low efficiency = larger particles • Examples: Wood smoke, diesel exhaust

  8. Aerosol cont. • FIBERS • A special (based on toxicological properties) kind of dust that is fibrous in nature (i.e., longer than it is wide) • Aspect ratio (L:W) defined as 3:1 or 5:1 • Toxicity a function of composition, size, and number of fibers • Examples: Asbestos, fiberglass, refractory ceramic fibers • BIOAEROSOLS • Solid or liquid aerosols from biological sources • May be infectious, allergenic, and/or irritating • Wide range of particle sizes • –Virus (0.002–0.03 um) • –Tree pollen (10–100um) • Examples: Mold spores, animal allergens, anthrax

  9. Physical and chemical properties of suspended particulates • 6 properties: • Particles size • Shape and aspect ratio • Surface area and volume • Solubility • Composition • Reactivity • These properties also determine its toxicity

  10. Particle size: Aerodynamic Equivalent Diameter • The Aerodynamic Equivalent Diameter (AED) of a particle is the diameter of a unit density sphere that would have the identical settling velocity as the particle • Measure of behavior of particle in air • Function of particle diameter, density, shape, and surface characteristics • Determines site of deposition in lung • Effects air sampling characteristics • Referenced to spherical drop of water with identical settling velocity

  11. Physical and chemical properties cont. • Shape and aspect ratio • important when dealing with fiber: egasbestos • Respirabilityfunction: depend on diameter and not the length • Surface area and volume • reactivity increase when size reduce because the relative surface area rapidly increase • Solubility • This influence the rate of absorption in the body • Water or liquid soluble: the effect is generally systemically – ammonia (very soluble) • While the insoluble the effect is at the point of contact or deposited – eg deposited at nasopharynx can cause nasopharyngeal cancer

  12. Physical and chemical properties cont. • Composition • Chemical composition has direct bearing on resulting health effect due to differing properties or chemical interaction • Ega particulate with 10 % of silica bears less health effect compared to a particulate with 90% silica • Reactivity • Under certain conditions, chemical in particulates could give rise to dangerous reaction or decomposition • Release of toxic, flammable or combustible gases with release of heat

  13. Cumulative log-normal size distribution of particles

  14. Particle size distribution • Inhalable fraction (<100 μmAED) • Fraction of dust which can be breathed into nose or mouth • Thoracic fraction (<25 μmAED) • Fraction of dust which can penetrate head airways and enter lung airways • Respirable fraction (<10 μmAED) • Fraction of dust which can penetrate beyond terminal bronchioles to gas exchange region • Fine fraction (<2.5 μmAED) • Fraction of dust which can penetrate the alveoli or cross membranes to enter the bloodstream • Ultrafine fraction (<0.1 μm AED) • Fraction of dust which are smaller than 0.1 µm

  15. Regional Particle Deposition

  16. Routes of entry • Inhalation: very significant route • 50 µm AED will be filtered at the nose • 7 – 20 µmAED: deposited at the nasopharynx • 5 – 7 µmAED: deposited at tracheo-bronchial air ways • 0.5 – 5 µmAED: alveolar region

  17. Pulmonary alveoli

  18. Site of Particle Deposition

  19. Mechanisms of Particle Deposition in the Lung • Inertial impactions • Function of particle velocity and mass, deposition by impaction is greatest in the bronchial region • Interception • Function of particle diameter and is most significant for fibers, which easily contact airway surfaces do to their length. Fibershave small aerodynamic diameters relative to their size, so they can often reach the smallest airways • Sedimentation (gravitational settling) • Function of particle velocity (residence time) and mass, sedimentation plays a greater role in the deposition of particles with larger aerodynamic diameters • Diffusion • Function of particle diameter, concentration, velocity (time), and distance. Diffusional deposition occurs mostly when the particles have just entered the nasopharynx, and is also most likely to occur in the smaller airways of the pulmonary(alveolar) region, where air flow is low

  20. Mechanism of particle deposition in lung cont. http://www.mfg.mtu.edu/cyberman/environment/air/depos.html

  21. Particle deposition in lung

  22. Pneumoconiosis • Pneumoconiosis causes inflammation of the lungs • silicosis, asbestosis and coal worker's pneumoconiosis • The lung tissue in normal people is very elastic • This allows it to expand and contract while breathing • In the common types of pneumoconiosis, fibrous tissue gets deposited in the lungs, the condition being called fibrosis • Fibrosis tends to stiffen the lung tissue and restrict its expansion

  23. Suspended particles: Asbestos • Asbestos – mineral fiber - used for 2500 years and have been commercially used since mid-1850’s • Among of it uses – boilers, steam pipe, insulation for locomotive and ships, fire blankets and fabrics, brake pads, roof top, special purpose clothing etc. Asbestos insulated ship being dismantled Asbestos Mills 1900′s Asbestos Insulated Locomotive

  24. Asbestos • Exists in two groups: • Serpentine group: chrysotile – white asbestos – thin, long and snake-like • Amphibole group: crocodolite, amosite, actinolie, remolite and anthopylite – a.k.a. blue asbestos – thin, long and needle shape Left: chrysotile Right: Crocidolite

  25. Asbestos cont. • Historically, name was derived from Greek word – asbestos, meaning ‘inextinguishable’ • Asbestos had low thermal conductivity or resistant to fire, acids and is pliable • Early 1920’s, large number of deaths were observed in mining towns • Asbestos miners were observed to die unnaturally young – one woman, worked with asbestos since 13 yrs old, died at 33 in 1924 - first asbestosis case • Asbestos, Canada where chrysotile is mined - particularly Quebec, show that individuals who live in the mine areas have a greater incidence of developing an asbestos-related disease • Banned in EU, US and other western countries except Canada

  26. National Asbestos Bans Latest update: Malaysia’s ban expected by 2015 through a voluntary phase-out plan developed in 2009

  27. Asbestos related lung disease: Asbestosis • Types of disease • Specific – example such as asbestosis, mesothelioma, pleural plaques • Non-specific – example such as lung cancer, diffuse pleural thickening, pleural effusion, rounded atelectasis • Asbestosis – fibrotic - non-malignant lung disease – development depends on amount and duration of exposure • Symptoms – cough and shortness of breath on exertion • Treatment does not reverseprogression of disease • Occurrence of asbestosis is Dose-dependent

  28. Asbestos related lung disease: Lung cancer and mesothelioma • Increased risk of lung cancer in asbestos exposed workers – up to 5x • Direct and linear relationship between RR of lung cancer and cumulative exposure to chrysotile and amphiboles – no safe dose • Lung cancer attributable to asbestos is under recognised • Mesothelioma – cancer of pleural and peritoneal – tissues that lines lungs, stomach • Exposure for 15-50 years • No threshold dose for the occurrence • Symptoms – persistent coughing, fatigue, sob etc

  29. Factories and Machineries (Asbestos Process) Regulations, 1986 • Establishes a PEL of 1 fiber/ml of air over 8 hour period • Requires exhaust equipment (Local Exhaust Ventilation) to be provided in order to keep exposures below PEL • Requires equipment to be examined and tested at specified intervals by a competent person • Provide PPE in the prescribed area or where concentrations exceed PEL • Obligation on employees to use PPE • Cleaning and housekeeping • Personal monitoring at least at 3 monthly intervals to comply with regulations • Medical examination of employees at least every 2 years (lung function test) - Specify details of the test

  30. Factories and Machineries (Asbestos Process) Regulations, 1986 • Provide employees with training on the process, controls, PPE and medical surveillance • Medical records kept for 20 years • Remove employees from work area if there is indications of asbestos related diseases • Example of asbestos removal task http://www.youtube.com/watch?v=5f7medwuIMA&feature=related

  31. Silicosis • When small silica dust particles inhaled • Embed deeply into alveolus and ducts in the lungs - lungs cannot clear out the dust by mucous or coughing • Bilateral pulmonary fibrosis caused by • inhalation and deposition of dust containing silicon dioxide (SiO2) in crystalline form – either quartz, cristobalite and tridymite • Sources of exposure: • quarries, foundries (mold made from sand), porcelain factories, cement factories, glass making, sandblasting

  32. Silicosis cont. • Simple, chronic, complicated silicosis • Signs: obstructive lung disease or fibrosis in advanced stage of disease • Symptoms few or none – dry cough, sputum production, symptoms of pulmonary insufficiency with advancing disease • Exposure between 20-30 years • Accelerated silicosis • Simple nodular silicosis rapidly develops into massive fibrosis • Developed between 5-10 years of exposure • Acute silicosis • Rapidly developing breathlessness, coughing, asthenia, weight loss, progressive respiratory insufficiency • Developed between 1-3 years of exposure

  33. FMA 1967 (Mineral Dust Regulations) • PEL of 0.1 mg/m3 quartz and 0.5 mg/m3TWA forcristobalite and trydimite • Employers provide and employees required to use protective clothing, respiratory equipment and PPE • Report any defects in the equipment • Sand blasting is prohibited unless written approval from DOSH is obtained

  34. Occupational asthma • Variable airflow limitation and airway hyper responsiveness • due to causes and conditions attributable to a particular occupational environment • not to a stimuli encountered outside the workplace • Present in 2 types • OA that begins after preceding asymptomatic period of work exposure (latency period) to causative agent (allergic sensitisation) • Irritant-induced asthma or RADS or Reactive Airways Dysfunction Syndrome (no latency)

  35. Occupational Asthma • Risk factor for IgE mediated OA caused by High Molecular Weight agents – natural/plant sources and LMW chemicals • Prevalence of OA is higher in atopics – • Microbial enzymes - Protein allergens in rubber latex gloves, detergent workers • Epidermal/urinary proteins – animal handlers • Atopy? – hyper reactive – propensity to produce specific IgE to environmental allergens • 30% of population is atopic • Prevalence : 2-5% of all occupational cases • Bakers – 7-9% - alpha amylase • Lab workers – 8-12% • Manufacturing workers – diisocyanates 1 to 10%

  36. Mechanism of OA • Exposure • IgE mediated sensitisation in skin and airway mucosa – antigens processing by dendritic cells and B cells present antigens to TH cells • Activated t cells produce cytokines and stimulate B cells to produce IgE antibodies • Following sensitisation, clinical manifestation occur on re-exposure • Mast cells release histamine an other mediators – early allergic response • Secreted cytokines stimulate influx of inflammatory cells in late phase response

  37. Allergic asthma and irritant-induced asthma • Airway inflammation: infiltration of bronchiol mucosa with activated lymphocytes, neutrophils and mast cells • Irritant effects: airway injury by exposure to high levels of irritants • Disrupt intercellular tight junctions between bronchoepitheliel cells • Disruption of epithelial barrier • Penetration of chemical antigens into Submucosa where IgE produced

  38. Byssinosis • Acute or chronic lung disease characterised by chest tightness and breathlessness caused by exposure to cotton, flax, hemp, jute and sisal • Decline in FEV1 within few hours exposureto cotton dust after 48 hours separation from cotton dust • How to measure? • 6 hour or work shift decrease FEV1 is the objective measure of response to cotton dust

  39. Prevention and control • Screening to eliminate highly susceptible potential workers from exposure • Workers informed of additive effects of cigarette smoking • Relocate workers who develop hyperreactivity of hypersusceptibility • Fair and adequate compensation for those with byssinosis related pulmonary impairment

  40. Hyper sensitivity pneumonitis/ extrinsic allergic alveolitis • Allergic lung disease due to sensitisation and recurrent exposure to allergens usually in agriculture settings • Acute form presents as recurrent influenza like illness and chronic form as insidious exertionaldyspnea

  41. Agents causing hypersensitivity pneumonitis • Thermophyllicactinomycetes • Micropolysporafaeni – farmers lung from moldy compost • Thermoactinomucesvulgars – mushroom workers lung • Thermoactniomycessacharii – bagassosis – sugar cane • Fungi • Aspergillusclavatus – malt worker lung – moldy lung • Penicillumcasee – cheese worker lung – cheese mold • Hair dust – furriers lung from animal proteins • Altered humidified water – humidifier lung

  42. Hypersensitivity pneumonitis cont. • Bacterial, fungi and serum protein antigens causing HP have small AED <5micron presenting as aeroallergens in lung • Reach terminal bronchioles and alveoli • Clinical response depends on particle size, antigen load and concentration of aerosol • Symptoms – fever, cough, dyspnea, malaise • Management – avoidance of contaminated areas

  43. Thank You