مرکز تخصصی پایش طب کار البرز http://www.payeshteb.ir مرکز تخصصی پایش طب کار البرز http://www.payeshteb.ir

Occupational lung diseases Ali naserbakht , MD مرکز تخصصی پایش طب کار البرز www.payeshteb.ir

INHALATION EXPOSURE Airways Bronchioles Alveoli Interstitium Blood Systemic effects paraquat

Site & intensity of the injury Physico-chemical properties Particle size…<5u go deeper Concentration… Solubility Density… lighter (as) go deeper Reactivity… higher (NH4) more damage Duration of exposure Rate / depth of breathing Host response variability / susceptibility Host defense mechanisms

Site of respiratory tract deposition Water solubility examples Site of injury High Moderate low Ammonia Chlorine Nitrogen dioxide Upper airway Lower airway Lung paranchyma Particle size >10µm 2. 5-6µm <2.5µm Dust from earth crust Some fire smoke particles Metal fume, asbestos fiber

Mechanisms Irritant : chemicals Allergic : flour (bakers) fibrogenic : silicosis Carcinogenic uranium,asbestosis

local systemic BRONCHITIS ASTHMA PULM EDEMA PNEUMONITIS FIBROSIS AIRWAYS BRONCHITIS ASTHMA local PULM EDEMA PNEUMONITIS FIBROSIS EXPOSURE ALVEOLI SYSTEMIC systemic NEUROTOXINS FEVERS

Evaluation of patient History Physical exam Imaging studies Pulmonary function testing

Symptoms Cough Hemoptysis Dyspnea at rest and/or on exertion Wheezing Chest tightness / pain Upper airways symptoms Fever, chills

Pulmonary function test Spirometry values: FVC(FEV6): forced vital capacity - total amount air exhaled FEV1: amount of air exhaled during the first second of forced expiration FEV1/FVC% :The ratio of FEV1 to FVC, expressed as a percentage

Interpretation Normal: both the FVC and the FEV1/VC ratio are normal.FEV1& FVC≥ 80 FEV1/VC ≥ 70 Obstructive: FEV1/FVC ratio is below the normal range. Restrictive: reduction in the FVC without reduction of the FEV1/FVC ratio. This is most reliably interpreted on the basis of TLC.

Toxic inhalation injury Irritation Inflammetion Decreased mucociliary clearance Edema Asphyxiation

Simple Carbomonoxide-fires Methane, CO2-manure pits Chemical H cyanide-burning plastics H sulfide-manure pits

Occupational diseases Asthma Bronchitis Silicosis HP,MMF Acute Chronic Progressive Regressive Intermitent Reversible Irreversible

Occupational Asthma Types of Work-Related Asthma : Work-aggravated asthma Reactive airway dysfunction syndrome (RADS) Allergic occupational asthma

Definition Occupational asthma Diagnosed Asthma Onset after entering workplace C. Association of symptoms to workplace D1. Agent known to cause OA or D2. Work-related changes in lung function

Agents of Reactive Airway Dysfunction Syndrome Hydrochloric acid Hydrogen sulfide Locomotive/diesel exhaust Phosgene Phosphoric acid Sodium hydroxide Sulfuric acid Tear gas Toluene diisocyanate Welding fumes Zinc chloride

Agents of Allergic Occupational Asthma High-molecular-weight substances Animal & and plant proteines Latex Grain dusts low-molecular-weight substances Diisocyanates Colophony Western red cedar Metals (chromium, platinum, nickel) Glutaraldehyde, formaldehyde

Hypersensitivity pneumonitis Lung disease resulting from sensitization and recurrent exposures to organic dusts Symptoms: HP presents acutely, as flu-like illness with cough; subacutely, as recurrent "pneumonia"; and chronically, as exertional dyspnea, productive cough and weight loss. Latency: few weeks to years; Onset of symptoms after acute exposure: 4 to 12 hours Repeated exposure to: 1) bioaerosols of microbial or animal antigens; or 2) a few reactive chemicals

Hypersensitivity Pneumonitis Microbial Bacteria Thermophiles NonThermophiles P. fluorescens B. cereus, B subtilis Fungi : Aspergillus sp,Penicillium, Amebae Mycobacteria avium Animal Birds, rats dander,feathers, droppings, urine Insects:weevil Chemicals Metal fluid Diisocyanates Pyrethrum

PROGNOSIS- OUTCOME Treatment Resolve Recurrent disease= outcome determinant Fibrosis / COPD Fatal,progressive Treatment Avoidance of exposure Corticosteroids

Inhalation fever Metal fumes, polymer fumes Contaminated water sources Contaminated agricultural dusts

pneumoconiosis A type of O-ILDs. Due to inhalation and deposition of mineral dust within lung parenchyma. Induce tissue reaction May cause disruption of alveolar architecture or collagen fibrosis.

Common features of all pneumoconiosis Deposition of mineral dusts in lung tissue. Presence of parenchymaL tissue reaction Positive chest x-ray findings

Silicosis A collagenous pneumoconiosis caused by inhalation of respirable (0.2 – 10 µm ) free crystalline silicon dioxide ( SiO2 ). Chronic diffuse interstitial fibro nodular lung disease. High-dose and long-time inhalation is required.

Silica exposure Minning Foundry work Sand blasting Ceramics HOST

Silicosis Calcified lymph nodes Upper lobe nodules

Silicosis

Asbestosis

Products that can contain asbestos Pipe covering Asbestos cloth Cements Roofing materials

Asbestos related lung disease Clinical presentation: exertional dyspnea,, cough, chest pain, clubbing • X Ray: reticular veiling lower lobes, ground glass pleural changes, PMF in mixed exposure, • Lung fx: restrictive, diffusion↓, art hypoxemia,

Coal worker pneumoconiosis Coal worker's pneumoconiosis (CWP) can be defined as the accumulation of coal dust in the lungs and the tissue's reaction to its presence: simple CWP (SCWP) pulmonary massive fibrosis (PMF)

Coal workers pneumoconiosis Radiology: nodular veiling upper lung zones, nodules > 1 cm indicative of PMF • Lungfx: normal – simple type restrictive – complicated type • Prognosis: simple type – good complicated type – cardio-respiratory failure

Coal worker pneumoconiosis

OCCUPATIONAL LUNG DISEASES ARE PREVENTABLE

مرکز تخصصی پایش طب کار البرز http://www.payeshteb.ir مرکز تخصصی پایش طب کار البرز http://www.payeshteb.ir

مرکز تخصصی پایش طب کار البرز http://www.payeshteb.ir مرکز تخصصی پایش طب کار البرز http://www.payeshteb.ir

Complex exposures