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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
106
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.
107
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
.
108
Asbestos: TypesAsbestos: Types
Serpentine(93% of commercial use)
Amphibole(7% of commercial use)
ChrysotileActinolite, Amosite,
Anthophyllite, Crocidolite, Richterite, Tremolite
109
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.
114
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
116
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
120
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.
Asbestosis
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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
Asbestosis
123
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.
Coal Workers' Pneumoconiosis
125
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.
Coal Workers' Pneumoconiosis
126
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.
Coal Workers' Pneumoconiosis
127
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,
Other Pneumoconiosess
128
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.
Other Pneumoconiosess
129
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.
CHRONIC OBSTRUCTIVE PULMONARY DISEASE
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
131
132
·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.
Lung cancer
133
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
134
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.
135
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)
137
/ 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
139
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
140
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