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

Physical hazard II: Suspended particles

Occupational Health EOH3202

Environmental & Occupational HealthFaculty of Medicine and Health SciencesUniversity Putra of Malaysia

Learning goals1. Able to identify work tasks associated with

high exposures to suspended particles2. Able to characterise the physical and chemical

properties of suspended particulates3. Able to understand particle size distribution

and its relationship with site deposition and mechanisms of particle deposition in the lung

4. Able to identify health outcomes related to exposure of particulates

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

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

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

Physical hazard: suspended particles Aerosol is the dispersion of solid or liquid in the gasesous medium• –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

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

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

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

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

Physical and chemical properties cont. Shape and aspect ratio

important when dealing with fiber: eg asbestos Respirability function: 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

Physical and chemical properties cont. Composition

Chemical composition has direct bearing on resulting health effect due to differing properties or chemical interaction

Eg a 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

Cumulative log-normal size distribution of particles

Particle size distribution Inhalable fraction (<100 μm AED)

Fraction of dust which can be breathed into nose or mouth

Thoracic fraction (<25 μm AED) Fraction of dust which can penetrate head airways

and enter lung airways Respirable fraction (<10 μm AED)

Fraction of dust which can penetrate beyond terminal bronchioles to gas exchange region

Fine fraction (<2.5 μm AED) 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

Regional Particle Deposition

Routes of entry

Inhalation: very significant route 50 µm AED will be filtered at the nose 7 – 20 µm AED: deposited at the

nasopharynx 5 – 7 µm AED: deposited at tracheo-

bronchial air ways 0.5 – 5 µm AED: alveolar region

Pulmonary alveoli

Site of Particle Deposition

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. Fibers have 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

Mechanism of particle deposition in lung cont.

http://www.mfg.mtu.edu/cyberman/environment/air/depos.html

Particle deposition in lung

Particle size Example Site of injury

>10 micron Dust from earth crust Upper airways

2.5 – 6 micron Fire smoke particles Lower airways

< 2.5 micron Metal fumes, asbestos powder

Lung parenchyma

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

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 Locomotive

Asbestos insulated ship being dismantled

Asbestos Mills 1900′s

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

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

National Asbestos Bans

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

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 reverse progression of disease▫ Occurrence of asbestosis is Dose-dependent

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

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

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

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

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

FMA 1967 (Mineral Dust Regulations)

•PEL of 0.1 mg/m3 quartz and 0.5 mg/m3 TWA for cristobalite 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

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)

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%

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

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

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 exposure to 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

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

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 exertional dyspnea

Agents causing hypersensitivity pneumonitis• Thermophyllic actinomycetes

▫ Micropolyspora faeni – farmers lung from moldy compost

▫ Thermoactinomuces vulgars – mushroom workers lung▫ Thermoactniomyces sacharii – bagassosis – sugar cane

• Fungi▫ Aspergillus clavatus – malt worker lung – moldy lung▫ Penicillum casee – cheese worker lung – cheese mold

• Hair dust – furriers lung from animal proteins▫ Altered humidified water – humidifier lung

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

Thank You