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Occupational lung Diseases

Bahrami By : Dr.HamidOCUPATIONAL MEDICINE SPECIALIST

94ابان

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مایده 32سوره

 رامازینی سال دکتر آمد 1633در بدنیا ایتالیا در میالدی

بعنوان )) ای حرفه بهداشت در اش ارزنده خدمات بعلت پدر وکار .طب شد(( نامیده

که است فردی نخستین توصیه او پزشکان بهاز خود پرسشهای ضمن در کرد

، مورد شغلبیمار نیز را اومعتقد او زیرا ، دهند قرار پرسش

است که بود ارتباطی ممکنبیماری نزدیک و فرد شغل بین

باشد داشته وجود 4وی

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respiratory tract site of injury from occupational

exposures. widespread use of potentially toxic

materials in environment poses a major threat to both airways & lung parenchyma.

limited ways to respond to injury.

Introduction

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Introduction

OLD have three common characteristics:

(1) caused or aggravated by a workplace exposure,

(2) preventable, (3) potentially compensable.

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(l) detailed history, including occupational and environmental exposures,

(2) thorough physical examination, (3) appropriate imaging studies, (4) PFT_pulmonary function testing.

EVALUATION OF PATIENTS WITHOCCUPATIONAL LUNG DISEASE

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detailed history of both the patient's complaints & environmental/occupational exposures

types and durations of exposures, environmental controls , respiratory protective gear is used substance data sheets (SDSs) actual industrial hygiene data Condition of the patient's home, any

hobbies, and social habits

History

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OLD do not present with specific clinical findings.

It is difficult, for example, to distinguish asbestosis from IPF(idiopathic pulmonary fibrosis) or chronic beryllium disease from sarcoidosis.

Only in context of the exposure history will correct diagnosis be made.

Physical Examination

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Ph.Ex helpful if abnormal wheezing, rhonchi, or both airways

disease, Crackles presence of parenchymal disease.

Physical Examination

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CXR part of workup normal do not exclude significant damage to

lung. Immediately after toxic inhalational injury Dramatically abnormal in individuals without

significant lung injury who are exposed chronically to iron oxide or tin oxide

Imaging Studies

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Abnormalities do not correlate with degree of pulmonary impairment or disability.

These are better assessed by PFT and ABG dust-exposed, chest films interpreted

according to International Labor Organization (ILO)

classification for pneumoconiosis + routine interpretation

Provide a standardized, descriptive coding system for appearance and extent of radiographic change caused by pneumoconiosis.

Imaging Studies

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CT abnormalities of pleura & mediastinal because it is more sensitive to differences in density.

CTafter administration of intravenous contrast medium, choice for evaluation of pulmonary hila.

HRCT more sensitive for assessing the presence, character, and severity of diffuse lung processes such as emphysema & ILD.

Imaging Studies

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most valuable of all PFT are those obtained from spirometry FEV 1 , FVC, FEV1:FVC ratio.

best method of detecting presence and severity of airway obstruction

most reliable assessment of impairment.

Pulmonary Function Testing

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PEFR (peak expiratory flow rate) single-breath test reflects degree of airway obstruction

Serial peak-flow measurements are especially valuable in diagnosis of occupational asthma to document delayed responses after work shift is over.

Pulmonary Function Testing

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in diagnosis of occupational asthma. Pulmonary function responses to inhaled histamine and

methacholine are easy to measure and give an indication of presence and degree of nonspecific hyperresponsiveness of airways.

FEV1, obtained repeatedly after progressively increasing doses of histamine or methacholine to generate a dose-response curve.

test terminated after a 20% fall in FEV1• Patients with asthma typically respond with such a change in

lung function after a relatively low cumulative dose of methacholine.

Bronchoprovocation Tests

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TOXIC INHALATION-INJURY OCCUPATIONAL ASTHMA HYPERSENSITIVITY PNEUMONITIS INHALATION FEVERS METAL-INDUCED LUNG DISEASE PNEUMOCONIOSES CHRONIC OBSTRUCTIVE PULMONARY

DISEASE PLEURAL DIORDERS LUNG CANCER & MESOTHELIOMA

Occupational lung Diseases

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ESSENTIALS OF DIAGNOSIS lnhalational exposure to irritating agents

cause injury along respiratory tract. site of injury depends on physical & chemical

properties of inhaled agent( water solubility) severity of injury depends on the intensity &

duration of the exposure. (minute ventilation) Effects range from transient, mild irritation of

mucous membranes of upper airways to lifethreatening pulmonary edema.

TOXIC INHALATION-INJURY

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Short-term exposures to high concentrations of noxious gases, fumes, or mists generally are a result of industrial or transportation accidents or fires.

Inhalation injury from high-intensity exposures can result in severe respiratory impairment or death.

TOXIC INHALATION-INJURY

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concentration of an inhaled water-soluble gas such as ammonia is greatly reduced by time it reaches trachea because of efficient scrubbing mechanisms of moist surfaces of the nose and throat.

In contrast, a relatively water-insoluble gas, such as phosgene, is not well absorbed by upper airways and thus may penetrate to alveoli.

TOXIC INHALATION-INJURY

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Clinical Findings initial focus of Ph.ex on airway. If nose and throat are badly burned, or hoarseness or stridor,

chemical laryngitis. early wheezing suggests exposure heavy. Spirometry or peak-flow : airway obstruction relatively early. CXR usually normal. Chemical pneumonitis and pulmonary edema (ARDS) may develop within

4-8 hours of heavy exposure.

ABG hypoxemia prior to radiographic evidence of parenchymal injury.

Because of the relative lack of immediate signs and frequent delayed reactions to poorly water-soluble agents such as phosgene and oxides of nitrogen, patients exposed to significant concentrations of these agents observed for a minimum of 24 hours

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TOXIC INHALATION-INJURY

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Prognosis Controversy exists, potential for long term

pulmonary sequelae after toxic inhalation injury.

For example, there are well-documented reports of persisting airway obstruction, nonspecific airway hyperresponsiveness, and sequential reduction in residual volume following acute chlorine gas exposure.

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ESSENTIALS OF DIAGNOSIS complain of dyspnea, wheezing, and/or

cough that correlate with workplace exposures

report feeling better in evenings or during weekends and vacations.

Symptoms occur 4-8 hours after exposure or after patient left work or even at night. diagnosis confirmed with changes in lung

function (spirometry or peak flow).

OCCUPATIONAL ASTHMA

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Asthma is characterized by airway obstruction reversible(but not

completely), either spontaneously or with treatment,

airway inflammation, increased airway responsiveness to stimuli In occupational asthma, variable airway obstruction and/or airway

hyperresponsiveness as a consequence of workplace exposure(s).

More than 250 agents in the workplace cause asthma, and the list is

growing as new materials and processes are introduced.

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In US, asthma occurs in 5% of general population.

Work-related asthma (ie, both occupational asthma and work-aggravated asthma) estimated to be 15-20% of all adult asthma.

Work-aggravated asthma occurs when workplace exposures lead to exacerbations of preexisting non-occupational asthma.

OCCUPATIONAL ASTHMA

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Work-related asthma Work-aggravated asthma occupational asthma Irritant-induced asthma Sensitizer-induced asthma HMW-type I-IgE LMW

OCCUPATIONAL ASTHMA

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OCCUPATIONAL ASTHMA

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SIA is characterized by variable time during which sensitization to an agent

present in work site takes place.

IIA without a latent period after substantial exposure to an irritating dust, mist, vapor, or fume. Reactive airways dysfunction syndrome

RADS is a term used to describe irritant-induced asthma caused by a short-term, high-intensity exposure.

OCCUPATIONAL ASTHMA

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Pathogenesis Airway inflammation is now recognized as paramount

feature of asthma. Asthmatic airways are characterized by (1) infiltration with inflammatory cells, eosinophils, (2) edema, (3) loss of epithelial integrity.

OCCUPATIONAL ASTHMA

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SIA early response

trigger rapid-onset but self-limited bronchoconstriction

Mast-cell degranulation responsible for early response. late response 4-8 hours later,. dual response

OCCUPATIONAL ASTHMA

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OCCUPATIONAL ASTHMA

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diagnosis A) diagnosis of asthma and B) establishing a relationship between asthma and work

A)diagnosis of asthma made only when both intermittent respiratory symptoms and physiologic evidence of airways obstruction

OCCUPATIONAL ASTHMA

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B) relationship between asthma and workplace exposure fit any of following patterns:

(1) symptoms occur only at work (2) symptoms occur regularly after work shift (3) symptoms increase progressively over course of workweek, (4) symptoms improve on weekends or vacations (5) symptoms improve after a change in work environmet

OCCUPATIONAL ASTHMA

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At least one of symptoms : wheezing, shortness of breath, cough, & chest tightness while worker is at or within 4-8 hours of leaving workplace.

Often worker's symptoms improve during days off work or while away from the worker's usual job.

With persistent exposure, symptoms become chronic and lose an obvious relationship to workplace.

Concomitant eye and upper respiratory tract symptoms also noted.

A helpful clue to significant problem in a workplace is presence of coworkers with episodic respiratory symptoms.

OCCUPATIONAL ASTHMA

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Spirometry : FEV1 & FVC most reliable method for assessing airway obstruction.

reversible airway obstruction, normal lung function during intervals between acute attacks.

response to inhaled bronchodilator administration used as a measure of airway hyperresponsiveness.

12% improvementin FEV1 of at least 200 mL after inhaled bronchodilator is how ATS.

Across-work-shift spirometry, objective evidence of OA greater than I0% fall in FEV 1 across a work shift is

suggestive of an asthmatic response.

OCCUPATIONAL ASTHMA

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Serial recording of PEFR over a period of weeks to months is best way to document work-relatedness of asthma.

worker records his or her PEFR at least four times while awake & respiratory symptoms & medication .

When interpreting worker's log, attention given to any work-related pattern of change.

20% or greater diurnal variability in PEFR is considered evidence of an asthmatic response

OCCUPATIONAL ASTHMA

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OCCUPATIONAL ASTHMA

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MCT Methacholine or histamine challenge

nonspecific airway hyperresponsiveness suspected of OA has normal spirometry

OCCUPATIONAL ASTHMA

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Allergy skin tests with common aeroallergens used to establish whether or not worker is atopic.

Atopy is a risk factor for HMW sensitizer-induced asthma.

Extracts of materials such as flour, animal proteins, coffee give positive skin tests in specifically sensitized individuals.

OCCUPATIONAL ASTHMA

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Treatment Once diagnosis of OA is made,

primary intervention is reduce or eliminate worker's exposure through modifications in workplace

substitute offending agent with another safer one. Improved local exhaust ventilation and enclosure of specific

processes

IIA, use of personal protective equipment may lower exposures to levels that do not induce bronchospasm.

Workers who are allowed to continue in job regular follow-up visits, including monitoring of their lung function and nonspecific airway responsiveness.

SIA precluded from further exposure to sensitizing agent. necessary to completely remove worker from workplace because exposure to even minute quantities of offending agent may induce bronchospasm.

OCCUPATIONAL ASTHMA

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Prevention considered in all workplaces where cases are diagnosed.

environmental control of processes known to involve exposure to potential sensitizers and irritants.

Protection of workers substitution of other materials for asthma-inducing agents use of appropriate ventilation systems respiratory protective equipment worker education about appropriate procedures Avoidance of high-intensity exposures from leaks and spills

OCCUPATIONAL ASTHMA

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Medical surveillance for early detection contribute to reducing burden of impairment/disability

Factors that affect long-term prognosis

total duration of exposure, duration of exposure after onset of

symptoms, severity of asthma at time of diagnosis.

OCCUPATIONAL ASTHMA

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SPECIFIC AGENTS 1. Diisocyanatesused in manufacture of polyurethane

surface coatings, insulation materials, car upholstery, furniture.

most commonly used diisocyanate is toluene diisocyanate (TDI)

2. Vegetable Dusts, Cotton (Byssinosis),Flax, Hemp, & Jute Byssinosis in certain workers in cotton textile industry. chest

tightness ,cough , dyspnea l-2 hours after returns to work after several days off.

symptoms usually resolve overnight and on subsequent days become milder until by end of workweek worker may become asymptomatic

OCCUPATIONAL ASTHMA

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3. Metal Salts Complex salts of platinum used in electroplating,

platinum refinery operations, manufacture of fluorescent screens, jewelry

Specific IgE antibodies to platinum salts conjugated to human serum albumin found in sensitized workers by RAST.

Rhinitis and urticaria frequently accompany asthma, and this triad is sometimes called platinosis.

Nickel , vanadium, chromium, and cobalt

OCCUPATIONAL ASTHMA

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4. Acid Anhydrides Epoxy resins contain acid anhydrides as curing

or hardening Phthalic anhydride, trimellitic anhydride(TMA),

tetrachlorophthalic anhydride (TCP A) . OA occurs in a small percentage of exposed

workers serum of affected workers typically contains

specific IgE antibodies against acid anhydride-protein conjugates.

OCCUPATIONAL ASTHMA

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5. Wood Dusts A large number of wood dusts are known to

cause rhinitis and asthma. Western red cedar is best studied. This wood contains LMW compound plicatic

acid, which is believed to be responsible for causing asthma

OCCUPATIONAL ASTHMA

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ESSENTIALS OF DIAGNOSIS link between symptoms and antigen exposure obtained

from work or environmental history.

antigen : a microbial agent, animal protein, or chemical sensitizer.

clinical presentation : acute, subacute, chronic (insidious onset).

HYPERSENSITIVITY PNEUMONITIS

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OCCUPATIONAL ASTHMA

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an immunologically mediated inflammatory disease of lung parenchyma induced by inhalation of organic dusts that contain a variety of etiologic agents ( eg, bacteria, fungi, amebae, animal proteins, and several low-molecular-weight chemicals).

basic clinical and pathologic findings are similar regardless of nature of inhaled Continued antigen

exposure may lead to PIF

HYPERSENSITIVITY PNEUMONITIS

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acute more common form of HP occurs within 4-6 hours of an intense exposure.

Recurrent low-level exposure to an appropriate antigen result in insidious onset of chronic ILD with fibrosis.

Symptoms of chills, fever, malaise, myalgia, cough, headache, and dyspnea are noted commonly.

Ph.Ex : ill-appearing patient with bibasilar inspiratory crackles misdiagnosed acute viral syndrome or pneumonia Lab : leukocytosis with increased neutrophils and

lymphopenia ABG : hypoxemia

HYPERSENSITIVITY PNEUMONITIS

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CXR normal Reticulonodular pattern. Patchy densities are bilaterally distributed,

PFT decrease in FEV and FVC with an unchanged FEV1:FVC ratio consist tent with a restrictive impairment

acute decrease Dlco reflecting impaired gas exchange progresses for up to 18-24 hours and then begins to resolve.

Recurrence of the syndrome with reexposure to the antigen.

HYPERSENSITIVITY PNEUMONITIS

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Progressive respiratory impairment with symptoms of dyspnea, cough, excessive fatigue, and weight loss develop without acute episodes.

Ph.Ex reveal cyanosis, clubbing, and inspiratory crackles. CXR diffusely increased linear markings and reduced lung

size. HRCT PFT usually a restrictive impairment with a decrease DLco' some patients with a mixed or obstructive pattern.

HYPERSENSITIVITY PNEUMONITIS

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diagnosis with episodic respiratory symptoms and evidence of fleeting infiltrates on CXR or restrictive on PFT

temporal relationship of symptom development after exposure is crucial to diagnosis.

Additional supporting evidence remission of symptoms and signs after cessation of exposure and their reappearance on reexposure.

home environment can be a source of offending antigen. Workplace and home (eg, evidence of mold or water

damage). Serologic studies demonstrating specific IgG precipitating

antibodies by traditional double-immunodiffusion technique will be positive in most patients

HYPERSENSITIVITY PNEUMONITIS

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primary complication irreversible lung fibrosis key to successful treatment of is avoidance of antigen persistence of symptoms occurs despite engineering

control measures and respiratory protective equipment, complete removal of worker from exposure is necessary.

Prognosis frequent follow-up, If further exposure to agent is avoided, prognosis is good. Significant pulmonary morbidity occur if persistent

exposure is allowed.

HYPERSENSITIVITY PNEUMONITIS

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ESSENTIALS OF DIAGNOSIS lnhalational exposure to : organic dusts,

polymer fumes, and certain metals can cause a flu-like illness.

self-limited CXR Bilateral infiltrates In contrast to OA & HP, which require susceptibility

and/or sensitization, attack rate for inhalation fevers is high; that is, most people experience symptoms as a result of high level exposure

INHAlATION FEVERS

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Inhalation of certain freshly formed metal oxides can cause metal fume fever, an acute self-limiting flulike illness.

most common cause of this syndrome is inhalation of zinc oxide, which is generated from molten bronze or welding galvanized steel.

oxides of only two other metals, copper and magnesium, When zinc is heated to its melting point, zinc oxide fumes are

generated. clinical syndrome begins 3-10 hours after exposure to zinc

oxide. initial symptom a metallic taste associated with throat irritation and followed within several hours by the onset of fever, chills, myalgia, malaise, and a nonproductive cough.

MFF

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ESSENTIALS OF DIAGNOSIS lnhalational exposure to several

metals cause immune-mediated ILD clinical presentation is similar to other

types of ILD

METAL-INDUCED LUNG DISEASE

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1. Hard Metal alloy of tungsten carbide with cobalt other metals titanium, tantalum,chromium,

molybdenum, or nickel. use is in manufacture of cutting tools and drill-tip

surfaces. Workers exposed to hard metal are at risk for

developing ILD, so-called hard-metal disease, and OA. putative cause of both these disease processes is

cobalt.

METAL-INDUCED LUNG DISEASE

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in manufacture of alloy, grinders and sharpeners of hard metal tools, and diamond polishers and others who use disks containing cobalt and metal coaters who use powdered hard metal.

symptoms of dyspnea on exertion, cough, sputum production, chest tightness, and fatigue.

Ph.Ex crackles on chest auscultation, Reduced chest expansion, clubbing, and in advanced

cases, cyanosis. CXR : bilateral rounded and/or irregular opacities with no

pathognomonic features

METAL-INDUCED LUNG DISEASE

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PFT : restrictive & decreased DLco diagnosis basis of pathologic examination

of lung tissue. primary treatment is removal of affected

worker from further exposure.

METAL-INDUCED LUNG DISEASE

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2. Beryllium Used manufacture of fluorescent light tubes, ceramics,electronics,

aerospace, and nuclear weapons/power industries. Workers at risk : in processes that generate airborne beryllium,

including melting, casting, grinding, drilling, extracting, and smelting Acute beryllium-induced pneumonitis after high-intensity

exposure but has largely disappeared owing to improved workplace control of exposures.

Chronic beryllium disease, which involves sensitization to the metal through a cell-mediated (type IV) mechanism, still occurs after lower-level exposures in susceptible workers. is a granulomatous inflammatory disorder that is very similar to sarcoidosis.

METAL-INDUCED LUNG DISEASE

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Chronic beryllium disease affects only the lungs

present : with insidious onset of dyspnea on exertion, cough, and fatigue.

Anorexia, weight loss, fever, chest pain, and arthralgias also may occur.

Ph.Ex confined to lungs, with crackles being most common, but they may be absent with mild disease.

METAL-INDUCED LUNG DISEASE

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similarity between chronic beryllium disease and sarcoidosis , demonstration of beryllium sensitization is necessary

LPT specific blood lymphocyte proliferation test sensitivity of LPT for chronic beryllium

disease is greater than 90% when using peripheral blood lymphocytes and can be increased if lung lymphocytes obtained from BAL are used.

METAL-INDUCED LUNG DISEASE

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criteria for the diagnosis of chronic beryllium disease :

(1) a history of beryllium exposure, (2) a positive peripheral blood or BAL LPT, (3) presence of epithelioid granulomas and mononuclear

infiltrates, in absence of infection, in lung tissue This approach relies on LPT to confirm sensitization to

beryllium and transbronchial biopsy of lung tissue to confirm presence of disease.

worker with chronic beryllium disease should be completely removed

METAL-INDUCED LUNG DISEASE

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3. Other Metals Inhalation of relatively high concentrations of

cadmium, chromium, or nickel fumes or mercury vapor can cause toxic pneumonitis.

Occupational exposure to certain metals ( antimony, barium, iron, and tin) can lead to deposition of sufficient radiodense dust that chest radiographs demonstrate opacities in absence of lung parenchymal inflammation and fibrosis.

METAL-INDUCED LUNG DISEASE

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ESSENTIALS OF DIAGNOSIS Chronic exposure, years, to mineral dusts can cause

fibrotic ILD. Symptoms are typically progressive dyspnea and dry

cough. Diagnosis made on basis of radiographic

abnormalities, may proceed lung function impairment.

PNEUMOCONIOSES

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Diagnosis : based on chest imaging. Radiographically evident interstitial opacities may appear

before impairment of pulmonary function or symptoms. risk of disease associated with level of exposure. Chronic exposure (ie, years) is required for most types of

pneumoconiosis. long latent period >5 years between onset of exposure

and clinical manifestation of disease is also required

PNEUMOCONIOSES

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SPECIFIC PNEUMOCONIOSES 1. Silicosis 2. Asbestosis 3. Coal Workers' Pneumoconiosis 4. Other Pneumoconioses

PNEUMOCONIOSES

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1. Silicosis inhalation of silicon dioxide, or silica, in crystalline

form Silica is a major component of rock and sand. miners, sandblasters, foundry workers, tunnel drillers,

quarry workers, stone carvers, ceramic workers, and silica flour production workers.

Silicosis

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Silica

Refers to the chemical compound silicon dioxide Crystalline silica exists in

several forms Alpha quartz (often simply

referred to as quartz) Other forms (beta quartz,

keatite, coesite etc.) less common

Noncrystalline (amorphous)

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High Risk Occupations

MiningSandblasters, stone cutters, construction workers

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Classification

Chronic or Classic Silicosis Accelerated Silicosis Acute Silicosis(silicoproteinosis)

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Chronic Silicosis Most common form Exposure 20-40 yrs Hallmark of chronic

form is the silicotic nodule or islet

Silicotic islet develops in hilar lymph nodes & calcify

Disease progress to fibrosis of upper lobe

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three disease patterns: (1) chronic simple silicosis, follows more than 10

years of exposure to respirable dust with less than 30% quartz,

(2) subacute/accelerated silicosis, follows shorter, heavier exposures (ie, 2-5 years),

(3) acute silicosis, following intense exposure to fine dust of high silica content over a several month

Silicosis

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Chronic silicosis : silicotic nodules in pulmonary parenchyma and hilar lymph nodes

lesions in hilar lymph nodes may calcify in an "egg shell" pattern that, while only occurring in a small proportion of cases, is virtually pathognomonic for silicosis.

Lung parenchymal involvement upper lobes. coalescence of small silicotic nodules into larger fibrotic

masses, called progressive massive fibrosis (PMF), complicate a minority of cases.

PMF tends to occur in upper lung fields, may obliterate blood vessels and bronchioles, causes gross distortion of lung architecture, and leads to respiratory insufficiency.

Silicosis

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Accelerated silicosis is similar to chronic silicosis except that time span is shorter and complication of PMF more frequently.

Acute silicosis, rare , in exposed to very high concentrations of free silica dust with fine particle size. occur in absence of adequate respiratory protection.

characteristic findings differ from chronic silicosis consolidation without silicotic nodules, alveolar spaces are filled with fluid similar to that found in pulmonary alveolar proteinosis.

Acute silicosis leads to death in most cases.

Silicosis

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chronic simple silicosis : few symptoms and signs diagnosis chest radiographs,

small round opacities (<10 mm) in both lungs, upper lung zones.

PFT in simple silicosis is usually normal , occasionally mild restrictive and decreased lung compliance. mild obstructive

With complicated silicosis involving progressive fibrosis (nodules >10 mm), increasing dyspnea is noted, initially with exertion and then progressing to dyspnea at rest.

Complicated chronic silicosis is associated with greater reductions in lung volumes, decreased diffusing capacity, and hypoxemia with exercise.

PMF is end-stage of complicated chronic silicosis.

Silicosis

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Diagnosis of Silicosis

three key elements : A history of silica exposure sufficient

to cause degree of illness and appropriate latency from time of first exposure

CXR : opacities consistent with silicosis Absence of another diagnosis more

likely to be responsible for observed abnormalities

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Increased mycobacterial disease, both typical and atypical, in silicosis.

Fungal diseases (cryptococcosis, blastomycosis, and coccidioidomycosis).

No treatment, management : prevention of progression and development of

complications. Continued exposure avoided, and surveillance for tuberculosis. PPD positive persons with silicosis 30-fold greater risk for developing

TB and treated for latent tuberculosis. acute silicosis, therapeutic whole-lung lavage employed to physically

remove silica from alveoli. prognosis for chronic silicosis is good, especially if they are

removed from exposure. Mortality remains high, however, in those who develop PMF

Silicosis

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Simple silicosis

noal

chest

x-ray

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Accelerated Silicosis ( Progressive Massive Fibrosis)

normal chest x-ray PMF

Diagnosis of Silicosis: CXR

Coalescence of opacities

PMF

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Silicosis

Diagnosis of Silicosis: CXR

Egg shell appearance of

hilar lymph nodes

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ASBESTOSIS

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2. Asbestosis Asbestos is fibrous forms of a group of mineral silicates. types : chrysotile, amosite, crocidolite, anthophyllite,tremolite, and actinolite, chrysotile being the most commonly used. durability, heat resistance, and ability to be woven into textiles of asbestos Major occupational exposures

،ساختمان یا و ها کشتی برای عایق اندازی راه و نصب یا و تولید معدن، ،کالچ روکش و ترمز های لنت برای اصطکاکی مواد ساخت ،آزبست منسوجات تولید آزبست، سیمان تولید ، آزبست حاوی تزئینی برای اسپری محصوالت حریق ضد و ، بلندگو

Asbestosis

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Properties of Asbestos

Asbestos ore

Naturally occurring fibrous minerals

Good tensile strength

Flexible

Heat resistant

Electrical resistance

Good insulation

Chemical resistant

Asbestos fibers

Because of these unique properties, asbestos was used extensively in variety of

products.

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Populations At RiskPopulations At Risk

Past Exposures Current Exposures• Mechanics,

construction workers, shipyard workers, and military personnel

• Secondary exposure in the workplace

• Household contacts of workers

• Construction workers, mechanics (brake pads)

• People in homes with friable asbestos materials

• People in areas where asbestos-bearing rock is disturbed

.

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Asbestos: TypesAsbestos: Types

Serpentine(93% of commercial use)

Amphibole(7% of commercial use)

ChrysotileActinolite, Amosite,

Anthophyllite, Crocidolite, Richterite, Tremolite

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Types of Asbestos

- Chrysotile - “White asbestos”

- Amosite - “Brown asbestos”

- Crocidolite - “Blue asbestos”

Asbestos fibers, high

magnification

Most commonl

y used:

Others:

Tremolite (sometimes found in vermiculite)

Actinolite

Anthophyllite

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Crocidolite Asbestos

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Amosite & Chrysotile Asbestos

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Uses of Asbestos

Pipe insulation

Surfacing insulating materials

Reinforcement of materials

Fireproofing

Acoustic and decorative plaster

Textiles

Asbestos insulated pipe

Asbestos insulated boiler

Asbestos has been used for centuries, but greatly increased during and after World War II in ship insulation and the following:

Use has greatly declined since the late 1970’s

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Examples of Uses of Asbestos

Vinyl asbestos flooring

Sprayed-on fireproofing material

Sheet vinyl containing asbestos

These products may be found in homes and buildings constructed before 1981.

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Asbestos Mill Board

Asbestos millboard was used in the construction of walls and ceilings, especially around furnaces and wood-burning stoves, where insulation and fire protection was required. Most varieties of asbestos millboard typically contained between 80% and 85% asbestos.

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Asbestos shingles and siding

Found in older houses – not to be confused with newer asbestos-free cement siding.

There is little hazard unless disturbed. The top right hand picture shows a siding

replacement job with broken green asbestos shingles which would have released dust and fibers into the air if done incorrectly .

Removal done correctly

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Asbestos in joint compound and plaster

Some joint compound contained up to 5% asbestos

Joint compound

Plaster with asbestos

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Asbestos Exposure PathwaysAsbestos Exposure Pathways

Most common exposure pathway:

Inhalation of fibers

Minor pathways:

Ingestion

Dermal contact

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Asbestosis

Pulmonary fibrosis due to asbestos exposure Dose response and latency occur Increasingly a milder disease is being

recognised: probably due to better imaging and also a

trend to lower exposures in exposed populations that remain alive

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factors play a role in disease initiation and progression,

type and size of fiber intensity and duration of exposure history of cigarette smoking individual susceptibility

Asbestosis

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A dose-response relationship asbestosis is more common in a higher exposure level.

Once asbestosis begins, it may progress irrespective of removal from continued exposure.

latency period (usually at least 20 years) between onset of exposure and development of clinically apparent disease

Asbestosis

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diagnosis : thorough exposure history, clinical examination, appropriate imaging studies, and PFT.

symptoms indistinguishable from other gradually progressive interstitial pulmonary fibrosing disorder, with progressive dyspnea and nonproductive cough being most prominent.

Bibasilar crackles with a "Velcro" quality auscultated over posterolateral chest in middle to late phase of inspiration. crackles of asbestosis are unaffected by coughing.

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Imaging CXR and HRCT scan.

CXR characteristic small, irregular or linear opacities distributed throughout lung fields but more prominent in lower zones. loss of definition of heart border and hemidiaphragms.

most useful radiographic finding bilateral pleural thickening which does not occur commonly with other diseases-causing interstitial pulmonary fibroses

Diaphragmatic or pericardial calcification is almost a pathognomonic sign ILO classification system is often used in US to rate degree of profusion of

small, irregular opacities and of pleural thickening on chest radiograph. Conventional chest CT scanning is more sensitive than chest radiography

for detection of pleural disease but not for parenchymal disease. HRCT is most sensitive imaging method for detecting early asbestosis. PFT Depending on severity of disease, restrictive & decreased DLco

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As for silicosis, no treatment. Fortunately, only a minority of those exposed are likely to develop

radiographically evident disease, and among these, most do not develop significant respiratory impairment.

Workers with asbestosis should be removed from further asbestos exposure because risk that parenchymal scarring will progress appears to increase with cumulative asbestos exposure

other factors that contribute to respiratory disease be reduced or eliminated especially true of cigarette smoking because there is some evidence that contribute to initiation and progression of asbestosis.

substitution of other fibrous materials for asbestos and institution of strict environmental controls where it is still present have led to a dramatic reduction in occupational exposures to asbestos.

Asbestosis

124

3. Coal Workers' Pneumoconiosis by inhalation of coal dust. Miners in underground mining and drillers in surface mines are at

greatest risk heavy coal dust burden is required to induce coal workers' pneumoconiosis, and condition is seen rarely in those who have spent fewer than 20 years underground.

coal macule is primary lesion in coal workers‘ pneumoconiosis. predilection for the upper lung lobes simple (radiographic lesions <10 mm in diameter) or

complicated (lesions >10 mm in diameter). <5% develop complicated or progressive fibrotic disease. Progressive massive fibrosis, identical to that described earlier for silicosis,

may occur.

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symptoms of cough and sputum production are common among coal miners and often are result of chronic bronchitis from dust inhalation rather than coal workers' pneumoconiosis.

As with silicosis, simple coal workers' pneumoconiosis is often asymptomatic.

symptoms and signs of complicated disease are same as those described earlier for silicosis.

PMF almost invariably leads to respiratory insufficiency and death.

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Caplan syndrome occur in coal miners with RA and is characterized by appearance of rapidly evolving rounded densities on chest radiographs.

These have a propensity to cavitate and histologically are composed of layers of necrotic collagen and coal dust.

pulmonary manifestations of Caplan syndrome may precede or coincide with the onset of arthritis.

Simple coal workers' pneumoconiosis usually follows a benign course.

Unlike silicosis, no increase is seen in either pulmonary tuberculosis or fungal infections of the lung.

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4. Other Pneumoconioses graphite (disease similar to coal workers'

pneumoconiosis), kaolin and diatomaceous earth (silicosis-like

disease), talc and mica (features of both silicosis and

asbestosis). A metal dust that can cause pneumoconiosis is

aluminum oxide,

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4. Other Pneumoconioses A new cause of ILD reported involving a series of

cases of ILD from a single nylon flock manufacturing plant.

Finely cut nylon, called flock, is used to make fabric for upholstery, clothing, and automobiles.

Nylon flock fibers are 10-15 Jlm in diameter, but respirable-size particles are generated during cutting operations.

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COPD two main categories, chronic bronchitis and emphysema

although many patients with COPD have features of both. Work-related COPD is usually of chronic bronchitis although cadmium and coal dust have been associated with

emphysema.

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130

CHRONIC BRONCHITIS ESSENTIALS OF DIAGNOSIS History of chronic exposure to inhaled irritants at work is necessary for

diagnosis of occupational COPD. There may or may not be a history of coexistent cigarette smoking Chronic cough and sputum production are required for the diagnosis of

chronic bronchitis. Airflow limitation as evidenced by a decreased FEV1 :FVC ratio that

does not improve with inhaled bronchodilator is another essential feature of COPD

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

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·ESSENTIALS OF DIAGNOSIS History of exposure to known lung carcinogens, asbestos, radon,

chloromethyl ethers, polycyclic aromatic hydrocarbons, chromium, nickel, inorganic arsenic exposure.

Cigarette smoking or exposure to cigarette smoke. Cough, hemoptysis, dyspnea, weight loss. Mass lesion, pulmonary infiltrate, hilar or mediastinal

adenopathy on chest radiograph. Diagnosis with one or more of the follow-ing :

sputum cytology, bronchoscopy with brushings and biopsy, transthoracic needle biopsy; thoracotomy rarely required.

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Occupations at Risk • Asbestos-exposed workers, including miners, insulators, and

shipyard workers • Workers exposed to radon, for example, uranium miners • Chemical production workers exposed to chloromethyl ethers

- Workers exposed to diesel exhaust/diesel particulate matter • Workers exposed to polycyclic aromatic hydrocarbons, for

example, aluminum reduction workers, coke oven workers, roofers, and rubber production workers

• Workers exposed to hexavalent chromium compounds, for example, in chromate production

Lung cancer

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Lung Cancer & Asbestos

First recognized in 1930

Average latency period 20-30 yrs

Association of lung cancer with smokers & asbestos exposure is multiplicative

Adenocarcinoma & squamous cell carcinoma

Lung CancerLung cancer causes the largest number of deaths from asbestos

exposure. The risk greatly increases in workers who smoke.

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136

Asbestos and smoking – the multiplicative effect

20 pack years of smoking gives 10-fold increased risk of lung cancer over lifelong non-smoker

40 pack years gives 40-fold increased risk

Asbestos exposure increases these figures by 1.4 with light exposure (plaques only); and 8 times with heavy exposure (asbestosis)

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/ نادر تومورپلورالازبست% /80تا با درمواجهه/ خفیف مواجهه با/ نهفته 40-30دوره پتانسیل amosite, crocidoliteبیشترینNonpleuretic chest pain –dypnea اشتها ،کاهش ،خستگی

ووزنCXR کنترالترال شیفت بدون افیوژن پلورال

Mesothelioma

138

Mesothelioma

Arise in the pleura & peritoneum

80% occur in men exposed to asbestos in the workplace or living near the mines

Smoking does not enhance prevalence of disease

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Mesothelioma

Clinical Manifestation Mean age 60 yrs Most common symptom are chest pain & dyspnea Pleural thickening or interstitial fibrosis-20% of CXRs

Diagnosis-open lung biopsy Treatment

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