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Occupational lung Diseases

Occupational lung Diseases

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Occupational lung Diseases

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  1. Occupational lung Diseases BahramiBy : Dr.Hamid OCUPATIONAL MEDICINE SPECIALIST ابان 94

  2.  مَن قَتَلَ نَفْسًا بِغَيْرِ نَفْسٍ أَوْ فَسَادٍ فِي الْأَرْضِ فَكَأَنَّمَا قَتَلَ النَّاسَ جَمِيعًا وَمَنْ أَحْيَاهَا فَكَأَنَّمَا أَحْيَا النَّاسَ جَمِيعًا سوره مایده 32

  3. دکتر رامازینی در سال 1633 میلادی در ایتالیا بدنیا آمد و بعلت خدمات ارزنده اش در بهداشت حرفه ای بعنوان (( پدر طب کار)) نامیده شد.او نخستین فردی است که به پزشکان توصیه کرد در ضمن پرسشهای خود از بیمار ، شغل او را نیز مورد پرسش قرار دهند ، زیرا او معتقد بود که ممکن است ارتباطی نزدیک بین شغل فرد و بیماری وی وجود داشته باشد

  4. Introduction 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.

  5. Introduction • OLD have three common characteristics: • (1) caused or aggravated by a workplace exposure, • (2) preventable, • (3) potentially compensable.

  6. EVALUATION OF PATIENTS WITHOCCUPATIONAL LUNG DISEASE (l) detailed history, including occupational and environmental exposures, (2) thorough physical examination, (3) appropriate imaging studies, (4) PFT_pulmonaryfunction testing.

  7. History 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

  8. Physical Examination 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.

  9. Physical Examination Ph.Ex helpful if abnormal wheezing, rhonchi, or both airways disease, Cracklespresence of parenchymal disease.

  10. Imaging Studies CXRpart 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

  11. Imaging Studies Abnormalitiesdo 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.

  12. Imaging Studies CTabnormalities of pleura & mediastinalbecause it is more sensitive to differences in density. CTafteradministration of intravenous contrast medium, choicefor evaluation of pulmonary hila. HRCTmore sensitive for assessing the presence, character, and severity of diffuse lung processes such as emphysema & ILD.

  13. Pulmonary Function Testing 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.

  14. Pulmonary Function Testing 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.

  15. Bronchoprovocation Tests in diagnosis of occupational asthma. Pulmonary function responses to inhaled histamine and methacholineare easy to measure and give an indication of presence and degree of nonspecific hyperresponsivenessof 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.


  17. TOXIC INHALATION-INJURY ESSENTIALS OF DIAGNOSIS lnhalationalexposure to irritating agents cause injury along respiratory tract. site of injury depends on physical & chemical propertiesof inhaled agent( water solubility) severity of injury depends on the intensity & durationof the exposure. (minute ventilation) Effectsrange from transient, mild irritation of mucous membranes of upper airways to lifethreatening pulmonary edema.

  18. TOXIC INHALATION-INJURY 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.

  19. TOXIC INHALATION-INJURY 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.

  20. TOXIC INHALATION-INJURY Clinical Findings initial focus of Ph.exon airway. Ifnose and throat are badly burned, or hoarseness or stridor, chemical laryngitis. earlywheezing suggests exposure heavy. Spirometry or peak-flow : airway obstruction relatively early. CXRusually normal. Chemical pneumonitis and pulmonary edema (ARDS) may develop within 4-8 hours of heavy exposure. ABGhypoxemiaprior 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 phosgeneand oxides of nitrogen, patients exposed to significant concentrations of these agents observed for a minimum of 24 hours

  21. 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 chlorinegas exposure.

  22. OCCUPATIONAL ASTHMA ESSENTIALS OF DIAGNOSIS complainof dyspnea, wheezing, and/or cough that correlate with workplace exposures report feeling better in eveningsor during weekends and vacations. Symptomsoccur 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).

  23. 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 hyperresponsivenessas 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.

  24. OCCUPATIONAL ASTHMA 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.

  25. OCCUPATIONAL ASTHMA Work-related asthma Work-aggravated asthma occupational asthma Irritant-induced asthma Sensitizer-induced asthma HMW-type I-IgE LMW


  27. OCCUPATIONAL ASTHMA 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 RADSis a term used to describe irritant-induced asthma caused by a short-term, high-intensity exposure.

  28. OCCUPATIONAL ASTHMA 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.

  29. OCCUPATIONAL ASTHMA SIA early responsetrigger rapid-onset but self-limited bronchoconstriction Mast-cell degranulation responsible for early response. late response 4-8 hours later,. dual response


  31. OCCUPATIONAL ASTHMA diagnosis A) diagnosis of asthma and B) establishing a relationship between asthma and work A)diagnosis of asthma made only when both intermittent respiratory symptomsand physiologic evidence of airways obstruction

  32. OCCUPATIONAL ASTHMA B) relationshipbetween 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

  33. OCCUPATIONAL ASTHMA 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. Concomitanteye and upper respiratory tract symptoms also noted. A helpful clue to significant problem in a workplace is presence of coworkers with episodic respiratory symptoms.

  34. OCCUPATIONAL ASTHMA 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.

  35. OCCUPATIONAL ASTHMA 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


  37. OCCUPATIONAL ASTHMA MCT Methacholineor histamine challenge nonspecific airway hyperresponsiveness suspected of OA has normal spirometry

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

  39. OCCUPATIONAL ASTHMA 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.

  40. OCCUPATIONAL ASTHMA 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 substitutionof 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

  41. OCCUPATIONAL ASTHMA 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.