Occupational Diseases in Quarries and Mines in Ireland

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Presentation transcript:

Occupational Diseases in Quarries and Mines in Ireland Dr Tom Donnelly

Learning objectives Historical Occupational Disease from Quarrying and Mines Understand How Lungs Work. What is crystalline Silica and its adverse effects Control Measures Other Issues in Quarries related to the lungs.

Historical Cases Withdrawal off Nitrates and Angina: Wet dynamite (TNT) in contact with skin, angina when on holidays Crow (Tapping) Bar Blasted out of Dynamite hole with resultant head injury and change of character (Frontal Lobe), Phineas Gage 25 yrs old in 1848, railway construction worker with resultant change of character, he eventually died from epilepsy

Anatomy of the Lungs Medulla controls diaphragm- CO2 drive Pharynx is common junction (Aspiration) Tongue attached to Jaw Bone Surface Area 120M2 (Tennis Court) C02 out, O2 in Site of disease Route of entry 5 Lobes(3R,2L) 5 lobes air enter mouth nostils warmed and cleared large particle dust large surface area very suceptable to damage Fibre size crutial respirable Or if gaseous can reach gas exchange alveoli

Natural Protection Hairs, turbinates Humidication & filtration, Smell Narrow nostrils, large nasal cavity 90 degree bend of nasopharynx Wet mucous & tonsils Reflexes – cough,sneeze,gag, swallow Macrophages – White Blood cells and find an eat bacteria Cilary hairs down to bronchioles(escalator)

Definition and types of dust Dusts are solid particles, ranging in size from below 1 µm up to at least 100 µm, which may be or become airborne, depending on their origin, physical characteristics and ambient conditions (WHO definition), Industrial dusts have different biological effect depending on their physico-chemical characteristics, size of particles and conditions of exposure, Absorption and deposition of dust in the human dirways depend on the diameter of the particle, level of fragmentation of particles and minute ventilation, According to biological effect dusts are divided into irritant, allergic, carcinogenic and fibrous.

Types of pneumoconioses according to pathological changes in the lungs Collagen pneumoconioses may be caused by an exposure to fibrinogenic dusts or by an altered tissue response to a non fibrogenic dust (sillicosis, asbestosis):: permanent alteration or destruction of alveolar architecture, collagenous stromal reaction of moderate to maximal degree, permanent scarring of lung. Non-collagen pneumoconioses may be caused by an exposure to non-fibrogenic dusts (stannosis): the alveolar architecture remains intact, the stromal reaction is minimal and consists mainly of reticulin fibres, the dust reaction is potentially reversible. Pneumoconioses caused by an exposure to mixed dust – coal worker’s pneumoconiosis (CWP) =anthracosis.

Occupational Lung Diseases In Ireland (ROI) Occupational physicians’ reports (SWORD, 2007-2012) N = 45

Site and Diseases Airways – asthma and bronchitis Lung substance (Parenchyma) – farmers lung, silicosis, asbestosis Lining of Lung – mesothelioma (cancer) Toxic inhalations – chlorine, carbon monoxide, hydrogen sulphide Infections – TB, pneumonia

Lung Reaction Highly water soluble substances affect upper airways Inflammatory response eg bronchitis Allergic – asthma and rhinitis Fibrotic – scarring, silica or spores Neoplastic – cancer of nasal cavity,pleura Wilfred Owen (Dulce et Decorum est) – Chlorine attack 1917

Medical Classification Obstructive disorders – Partial blockage of the air passages Restrictive disorders – change the nature of the lung substance (fibrosis) or chest wall (pleura) Lung function testing by measuring amount of air/given time helps differentiate the two types

Types of Occupational Lung Fibrosis Sillicosis Coal-worker pneumoconiosis (CWP) Pneumoconiosis - tuberculosis Welders’ pneumoconiosis Asbestosis Talcosis Graphitosis Pneumoconioses caused by a metal dusts

Silicosis Silica 2nd most common element in Earths Crust (after oxygen) If < 10 um (microns) in diameter it will reach Alveoli of lungs It inactivates Macrophages which are lungs last line of defense Exposure to Silica and development of Silicosis is associated with high levels of TB Granite, Sandstone and Slate and Sand (not black lough Neagh sand) – main component of Flint and Glass Crystalline (deadly) and Amorphous (benign) Quartz is 2nd commonest mineral in world (1st=Feldspar)

Silica Asbestos is made from silica It is a poor conductor of electricity but when Boron and other compounds added it is used in Computer Chips Spines of nettles are made of silica Macrophages try to ingest it

Silicosis OELV for respirable crystalline silica is 0.1mg/m3 Chronic Silicosis > 10 yrs exposure to low levels of silica Accelerated Silicosis – 5-10 years exposure to high levels Acute Silicosis - Few weeks up to 5 yrs to develop FFP3 particulate filter mask Substituting Crystalline Silica with alternative Dust suppression by damping Dust extraction

Symptoms & Signs Symptoms = Complaints Signs=physical findings Cough Shortness of Breath Wheeze Chest Pain Weight Loss Fatique Blood in Spit Signs=physical findings Wheeze Rapid Breathing Cyanosis (Blue) Finger Clubbing Accessory muscles

Asthma Reversible Airways Obstruction PyeRadius 2 1cm2 4cm2 Reversible Airways Obstruction Workplace Sensitiser < 10um diameter Chemicals labelled R42 Biological origin (foreign proteins and enzymes) Prevent exposure (2ary antiinflmmatory , broncho dilators)

Symptoms of exposure to respiratory sensitisers Asthma Coughing wheezing chest tightness Rhinitis conjunctivitis Immediate or late symptoms Continued exposure once sentised permenant lung damage substitution……..Control Risk assessment Health surveillance

Occupational Asthma Isocyanates Floor/grain Solder flux – pine rosin Resins Lab animals Wood dust Plants Welding fumes Glutaraldehyde Fish Protein Car painter Bakers Electronics Boat manufacture Research students Joiners Florists Welders Nurses Prawns

Occupational Asthma Recurrent Wheeze Cough – esp night time Shortness of breath Chest tightness Test – pulmonary function measures rate of flow (indirect measure of diameter)

Occupational asthma Onset after starting job Improvement at weekends/holidays Exacerbations with heavy exposure Presence of recognized asthma inducer in the workplace Suspision that undue number of other workers affected