logging in or signing up Occupational Lung Diseases drriham Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: Embed: Flash iPad Dynamic Copy Does not support media & animations Automatically changes to Flash or non-Flash embed WordPress Embed Customize Embed URL: Copy Thumbnail: Copy The presentation is successfully added In Your Favorites. Views: 562 Category: Education License: All Rights Reserved Like it (0) Dislike it (0) Added: May 04, 2012 This Presentation is Public Favorites: 0 Presentation Description No description available. Comments Posting comment... Premium member Presentation Transcript Occupational and environmental lung diseases : Occupational and environmental lung diseases By Chest Department Ain Shams University Slide 2: What are occupational lung diseases? Repeated and long-term exposure to certain irritants on the job can lead to an array of lung diseases that may have lasting effects, even after exposure ceases. Certain occupations, because of the nature of their location, work, and environment, are more at risk for occupational lung diseases than others. Contrary to a popular misconception, coal miners are not the only ones at risk for occupational lung diseases. For instance, working in a car garage or textile factory can expose a person to hazardous chemicals, dusts, and fibers that may lead to a lifetime of lung problems if not properly diagnosed and treated. Slide 3: Consider these statistics from the American Lung Association: Occupational lung diseases are the number one cause of work-related illness. Most occupational lung diseases are caused by repeated, long-term exposure, but even a severe, single exposure to a hazardous agent can damage the lungs. Occupational lung diseases are preventable. Smoking can increase both the severity of an occupational lung disease and the risk of lung cancer. Slide 4: What are the symptoms of an occupational lung disease? The following are the most common symptoms of lung diseases, regardless of the cause. However, each individual may experience symptoms differently. Coughing shortness of breath chest pain chest tightness abnormal breathing pattern Slide 5: How are occupational lung diseases diagnosed? Occupational lung diseases, like other lung diseases, usually require an initial chest x-ray for preliminary diagnosis. In addition, various tests may be performed to determine the type and severity of the lung disease, including: pulmonary function tests - diagnostic tests that help to measure the lungs' ability to exchange oxygen and carbon dioxide appropriately. microscopic examination of tissue, cells, and fluids from the lungs biochemical and cellular studies of lung fluids measurement of respiratory or gas exchange functions examination of airway or bronchial activity Slide 6: What is the difference between inorganic and organic dust? Particles in the air may cause lung problems. Often called particulate matter (PM), particles can consist of a combination of dust, pollens, molds, dirt, soil, ashes, and soot. Particulate matter in the air comes from many sources, such as factories, smokestacks, exhaust, fires, mining, construction, and agriculture. The finer the particles are, the more damage they can do to the lungs, because they are easily inhaled deep into the lungs, where they are absorbed into the body. "Inorganic" refers to any substances that do not contain carbon , usually come from nonliving sources excluding certain simple carbon oxides, such as carbon monoxide and carbon dioxide. "Organic" refers that they are made of materials that contain carbon and are part of living organisms (such as grain dusts, cotton dust, or animal dander) excluding simple carbon oxides, sulfides, and metal carbonates Slide 7: Relevant Fundamentals of Lung Structure and Function The airways of the lung derive from the trachea downwards by progressive division into two (or more) branches. Those airways beyond the trachea that contain cartilage are called bronchi. The airways lacking in cartilage beyond the bronchi are the bronchioles. These lead into hollow spaces called alveoli which have a diameter of about 0.1 mm each. There are approximately 300 million alveoli and their total surface area is about 140 m2. The conducting airways are lined by cells with cilia. Interspersed between these cells are mucus secreting cells. Secreted mucus spreads over the cilia which direct it upwards to the larger airways by rhythmic undulating movements, thus helping to clear deposited dusts. Slide 8: The respiratory units, i.e. the alveoli and the smallest bronchioles called respiratory bronchioles are responsible for the exchange of gases. They are lined mainly by flat, extremely thin cells which permit easy diffusion of oxygen through them from the air in the alveolar spaces to the blood in the capillaries and easier diffusion of carbon dioxide in the opposite direction. Alveolar macrophages are very abundant, mobile and phagocytic cells mainly responsible amongst other functions for the ingestion of foreign matter. Slide 9: Deposition and host defense of inhaled dusts and mists Aerosol is an all-embracing term including all airborne particles small enough to float in the air. Dusts are solid particles dispersed in air. Mists are liquid droplets formed by the condensation of vapours, usually around appropriate nuclei or the 'atomisation' of liquids. The aerodynamic diameter of a particle is the diameter of a sphere of unit density that would settle at the same rate. When airborne particles come in contact with the wall of the conducting airway or a respiratory unit they do not become airborne again. This constitutes deposition and can be achieved in one of four ways: Slide 10: Sedimentation is settlement by gravity and tends to occur in larger airways. Inertial impaction occurs when an airstream changes direction especially in the nose but also in other large airways. Interception applies mainly to irregular particles such as asbestos or other fibrous dusts which by virtue of their shape can avoid sedimentation and inertial impaction. However they are intercepted by collision with walls of bronchioles especially at bifurcations or if the fibers are curved. Diffusion is the behavior of very small aerosol particles which are randomly bombarded by the molecules of air. It significantly influences deposition beyond the terminal bronchioles. Slide 11: Most compact particles larger than 20 microns aerodynamic diameter and about half of those of 5 micron aerodynamic diameter are filtered within the nose during breathing at rest. However there is a wide variation in the efficiency of this among apparently normal subjects. Moreover conditions which favor mouth breathing, (e.g. high ventilation rates and obstructive disease of the nasal airways) will cause large particles to bypass this filter. Alveolar deposition is appreciable at particle diameters of between 1 and 7 microns (respirable particles) and probably maximal at aerodynamic diameter of between 2 and 4 microns. During regular breathing at rest only about 10% of compact particles of 0.5 to 1 micron diameter are deposited in the lung (alveoli), the bulk being again exhaled. Slide 12: During exertion, increase in tidal volume and particularly in respiratory minute volume (i.e. the product of tidal volume and the respiratory rate) is the single most important determinant of the total load of particles in the alveoli and hence the total volume of particles deposited for a given aerosol. Several other factors may influence particle deposition. Insoluble particles deposited in the conducting airways are propelled towards the larger airways by the cilia and then rapidly coughed or swallowed. This may be delayed by factors such as tobacco smoking. In the respiratory units, ingestion by macrophages is necessary before the particles are carried to the larger airways. Particles may also penetrate the deeper lung tissue where they may stay for years or be transported by macrophages to the lymph nodes. Slide 13: Vapours and gases Vapours are substances in the gaseous phase at a temperature below their boiling point. Gases produce their harmful effects in the following ways (as described below): (1) They can cause asphyxiation (deprivation of oxygen to the tissues); (2) They can cause irritation of the airways and the lungs; (3) After entering the body through the lungs they can cause damage to other tissues of the body. Slide 14: Nano-particles: A New Cause of Environmental Lung Disease? Particles affect the lung differently depending on what substances they are made from. Particles of the same material also may have different effects depending on their size and shape. The nanotechnology industry creates extremely small particles of different substances, such as carbon, for various uses. These particles are called nano-particles when they are less than 100 nanometers in size. For comparison, a human hair is about 100,000 nanometers in diameter, so it would take 1000 nano-particles to equal the thickness of one hair. Animal and laboratory tests show that high concentrations of nano-particles can be dangerous. But doctors do not know for certain the effects of the amounts and types of nano-particles that workers in the nanotechnology industry are exposed to. Studies are being designed to evaluate the risks and to ensure that workers are protected. Slide 16: What is the difference between inorganic and organic dust? Particles in the air may cause lung problems. Often called particulate matter (PM), particles can consist of a combination of dust, pollens, molds, dirt, soil, ashes, and soot. Particulate matter in the air comes from many sources, such as factories, smokestacks, exhaust, fires, mining, construction, and agriculture. The finer the particles are, the more damage they can do to the lungs, because they are easily inhaled deep into the lungs, where they are absorbed into the body. "Inorganic" refers to any substance that do not contain carbon , usually come from nonliving sources excluding certain simple carbon oxides, such as carbon monoxide and carbon dioxide. "Organic" refers that they are made of materials that contain carbon and are part of living organisms (such as grain dusts, cotton dust, or animal dander) excluding simple carbon oxides, sulfides, and metal carbonates. Examples of inorganic dust diseases: : Examples of inorganic dust diseases: Asbestosis Asbestos is a mineral fiber that was added in the past to certain products for strengthening, heat insulation, and fire resistance. Most products today are not made with asbestos. Normally safe when combined with other materials, asbestos is hazardous to the lungs when the fibers become airborne (such as when a product deteriorates and crumbles). If the asbestos-containing materials are in good condition, they are generally safe if left alone. The risk of asbestos exposure is not just limited to the workplace. Since many homes were built with asbestos products. Asbestos fibers are naturally occurring long, thin fibers of silicon that come in 1 of 2 major varieties. The curved fibers are serpentine and the straight fibers are amphiboles (scanning electron micrograph shown). Due to their heat-resistant properties they were extensively used to insulate heating and cooling units in World War II ships and buildings. : Asbestos fibers are naturally occurring long, thin fibers of silicon that come in 1 of 2 major varieties. The curved fibers are serpentine and the straight fibers are amphiboles (scanning electron micrograph shown). Due to their heat-resistant properties they were extensively used to insulate heating and cooling units in World War II ships and buildings. The carcinogenicity and fibrinogenicity of asbestos fibers are related to the type of fiber, duration of exposure, and associated host risk factors. Although both types of asbestos fibers are fibrogenic, amphiboles are markedly more carcinogenic because their straight shape allows for better penetration of cell membranes. : The carcinogenicity and fibrinogenicity of asbestos fibers are related to the type of fiber, duration of exposure, and associated host risk factors. Although both types of asbestos fibers are fibrogenic, amphiboles are markedly more carcinogenic because their straight shape allows for better penetration of cell membranes. ● Smaller fibers penetrate cells inducing fibrosis, while long fibers are incompletely phagocytosed and stay in the lungs inducing cycles of inflammation and cytokine release. Damage to the lung parenchyma is the result of chronic, repetitive release of oxygen free radicals, plasminogen activators, and growth factors by the macrophages. ● Individuals who smoke have an increased risk for asbestosis progression because of their impaired muco-ciliary clearance mechanisms. The Prussian blue stained micrograph shows an asbestos body (arrow) within the lung parenchyma surrounded by macrophages; this is called a ferruginous body. : ● Smaller fibers penetrate cells inducing fibrosis, while long fibers are incompletely phagocytosed and stay in the lungs inducing cycles of inflammation and cytokine release. Damage to the lung parenchyma is the result of chronic, repetitive release of oxygen free radicals, plasminogen activators, and growth factors by the macrophages. ● Individuals who smoke have an increased risk for asbestosis progression because of their impaired muco-ciliary clearance mechanisms. The Prussian blue stained micrograph shows an asbestos body (arrow) within the lung parenchyma surrounded by macrophages; this is called a ferruginous body. Slide 21: Asbestos-related diseases may develop after a latency of up to 20 years. The most common presenting symptom is a dry nonproductive cough or nonspecific chest discomfort in advanced cases. On physical examination, persistent and dry inspiratory rales are the most important finding. Clubbing and reduced chest expansion may also be present. Formal diagnosis requires an exposure history, evidence of fibrosis on imaging, physical examination, and pulmonary function findings particularly low forced vital capacity and a low carbon monoxide diffusing capacity consistent with fibrosis, and the absence of another cause of interstitial fibrosis. Slide 22: Classic findings include reticulonodular infiltrates at the lung bases (shown), shaggy heart borders (shown), and calcified diaphragmatic pleural plaques that are commonly called "holly leaf." An abnormal chest x-ray shows extensive scarring of tissue in the lungs. This finding is typical of severe asbestosis Treatment focuses on removal of any ongoing asbestos exposure. Patients are advised to quit smoking. Prompt treatment of any subsequent respiratory infections and timely immunizations against influenza and pneumococcal pneumonia are warranted. Some patients may require supplemental home oxygen therapy. Corticosteroids and immunosuppressive drugs do not alter the course of the disease. : Treatment focuses on removal of any ongoing asbestos exposure. Patients are advised to quit smoking. Prompt treatment of any subsequent respiratory infections and timely immunizations against influenza and pneumococcal pneumonia are warranted. Some patients may require supplemental home oxygen therapy. Corticosteroids and immunosuppressive drugs do not alter the course of the disease. HRCTS may show intralobular opacities (black arrow), thickened septa (white arrows), subpleural curvilinear lines, parenchymal bands, peribronchial fibrosis, honeycombing, and calcified diaphragmatic pleural plaques (red arrow), depending on the extent of disease. The majority of mesothelioma cases are preceded by asbestos exposure, but the latency period may be up to 50 years. Tumor growth usually occurs along the lower part of the chest. The tumor often extends into the pulmonary parenchyma, brachial plexus, and superior vena cava. Treatment options have limited success and are based on the extent of disease progression. Combinations of chemotherapy, radiation therapy, and surgery are utilized. Median survival is only 11 months and the disease is almost always fatal. : The majority of mesothelioma cases are preceded by asbestos exposure, but the latency period may be up to 50 years. Tumor growth usually occurs along the lower part of the chest. The tumor often extends into the pulmonary parenchyma, brachial plexus, and superior vena cava. Treatment options have limited success and are based on the extent of disease progression. Combinations of chemotherapy, radiation therapy, and surgery are utilized. Median survival is only 11 months and the disease is almost always fatal. extensive pleural thickening, effusion, and lung volume reduction in the affected hemithorax. Slide 25: Coal workers' pneumoconiosis (black lung) is a lung disease caused by deposits of coal dust in the lungs. People generally have no symptoms, but people who have severe disease cough and become short of breath. Chest x-rays and computed tomography are used to make the diagnosis. Prevention by minimizing exposure is important. People may need to take drugs to keep the airways open and free of mucus. Slide 26: Coal workers' pneumoconiosis results from inhaling coal dust or graphite over a long time. Although coal dust is relatively inert and does not provoke much reaction, it spreads throughout the lungs and shows up as tiny spots on an x-ray. Coal dust may block the airways. In simple coal workers' pneumoconiosis, coal dust collects around bronchioles. Simple coal workers' pneumoconiosis may progress to a more serious form of the disease called progressive massive fibrosis, in which large scars (at least ½ inch in diameter) develop in the lungs as a reaction to the dust. PMF may worsen even after exposure to coal dust stops. Lung tissue and the blood vessels in the lungs can be destroyed by the scarring. Coal dust enters the alveoli and is ingested by macrophages which expel the particles through mucus or via the lymphatic system. When the system is overwhelmed, the accumulation of macrophages triggers an immune response leading to inflammation and fibrosis (shown). : Coal dust enters the alveoli and is ingested by macrophages which expel the particles through mucus or via the lymphatic system. When the system is overwhelmed, the accumulation of macrophages triggers an immune response leading to inflammation and fibrosis (shown). Slide 28: Coal worker's lung is a fibrotic pulmonary condition caused by the accumulation of coal dust in the lungs. Anthracosis in comparison is the asymptomatic accumulation of coal pigment without cellular reaction found in urban dwellers and tobacco smokers. Periarterial fibrosis can lead to strangulated vessels and ischemic necrosis. Focal areas of coal deposition produce coal macules, the hallmark or coal worker's pneumoconiosis, which can extend into one another leading to focal emphysematous changes. Slide 29: The degree of fibrosis is related to the duration of exposure, age at first exposure, and the quantity of inhaled silica within the coal dust. Patients with early disease are typically asymptomatic but may eventually report productive cough and dyspnea. Diagnosis is typically made based on history, physical examination findings, and evidence of fibrosis on radiographic imaging. Treatment is largely supportive and preventative. Mortality is related to the degree of fibrosis and oxygen requirement An abnormal chest x-ray shows severe scarring (arrows) in the lungs (L) caused by progressive massive fibrosis. This finding is seen in severe black lung disease caused by exposure to coal dust : An abnormal chest x-ray shows severe scarring (arrows) in the lungs (L) caused by progressive massive fibrosis. This finding is seen in severe black lung disease caused by exposure to coal dust Slide 31: Silicosis Silicosis is a lung fibronodular lung disease caused by inhalation of dust containing crystalline silica. The dust found in the air of mines, foundries, blasting operations, and stone, clay, and glass manufacturing facilities are at risk of developing disease without appropriate protection. Characterized by scarring of the lungs, silicosis itself can increase the risk for other lung diseases, including tuberculosis. Slide 32: Small silicon particles are inhaled into the distal alveoli where they generate silicon-based radicals that lead to the production of oxygen and hydrogen-based free radicals that damage cell membranes. Alveolar macrophages ingest the particles and release their own inflammatory mediators. The end result is inflammation that damages cells and the extracellular matrix leading to fibrosis. Silica particles outlive the alveolar macrophages, thus continuing the cycle of injury. The historical image from 1939 depicts workers shoveling finely ground quartz for the creation of clay without respiratory protection before the dangers of silicon inhalation were known. : The historical image from 1939 depicts workers shoveling finely ground quartz for the creation of clay without respiratory protection before the dangers of silicon inhalation were known. Slide 34: Acute silicosis Occurs following a brief massive exposure to silica while chronic silicosis develops after years of exposure. In both forms, physical examination findings are typically benign with respiratory difficulty and signs of hypoxemia only in severe cases. Diagnosis is based on a history of exposure, clinical symptoms, physical examination findings, and chest radiographic appearance. Chest radiographs are essential to the diagnosis of silicosis. Treatment focuses on exposure avoidance, smoking cessation, immunization, and prompt treatment of respiratory infections. Corticosteroids may benefit individuals with acute silicosis. Infection of cavities by fungal organisms is a potential complication. Overall mortality is quite low. Slide 35: Typical findings include bilateral alveolar filing, multiple diffuse small nodules predominately in the upper lung findings, calcification of hilar lymph nodes (red arrow), and rarely cavitation of coalescing nodules. Slide 36: Berillium: Inhalation of beryllium causes 2 distinct pulmonary syndromes: an acute chemical pneumonitis and a chronic granulomatous lung disease known as berylliosis. It is often confused with sarcoidosis as they have very similar chest radiographs. In acute beryllium disease, the metal acts as a direct chemical irritant causing an inflammatory reaction. Berylliosis occurs after exposure to beryllium dust or fumes, which can be found in numerous manufactured products: computer or automotive electronics, nuclear reactors, aircraft components, and nuclear reactors. The pathogenesis is a result of delayed-type hypersensitivity reaction stimulating proliferation of T cells leading to inflammatory, fibrosis, and granuloma formation. Patients may report cough, chest pain, arthralgias, fatigue, and weight loss. Other than inspiratory crackles, physical examination findings are uncommon. Treatment focuses on exposure avoidance and corticosteroid therapy for 4-6 weeks. Prognosis is highly variable and ranges from complete recovery to lung transplantation. Diagnosis is made by a beryllium lymphocyte proliferation test from blood or bronchoalveolar lavage and non-necrotizing granulomas on lung biopsy (black arrow on hematoxylin-and-eosin histopathology slide shown). : Diagnosis is made by a beryllium lymphocyte proliferation test from blood or bronchoalveolar lavage and non-necrotizing granulomas on lung biopsy (black arrow on hematoxylin-and-eosin histopathology slide shown). Examples of organic dust diseases: : Examples of organic dust diseases: Byssinosis Byssinosis is caused by dust from hemp, flax, and cotton processing. Also known as brown lung disease, the condition is chronic and characterized by chest tightness and shortness of breath. Byssinosis may cause wheezing and tightness in the chest, usually on the first day of work after a break. The diagnosis is made by detecting decrease lung capacity over the course of a workday. Exposure should be stopped, then wheezing and chest tightness can be treated with drugs used for asthma. Prolonged exposure to cotton dust increases the frequency of symptoms and leads to permanent lung disease, which can sometimes be disabling. Hypersensitivity pneumonitis : Hypersensitivity pneumonitis Slide 40: Building-related illnesses Are disorders that affect the lungs as well as other parts of the body and are caused by exposure to substances within modern airtight buildings. Are caused by exposure to substances within airtight buildings that have poor ventilation. Symptoms vary depending on the cause but may include fever, difficulty breathing, runny nose or congestion, headaches, skin problems, and difficulty concentrating. Diagnosis usually includes evaluating the air quality of the building and determining how many people experience building-related symptoms. Treatment is usually removal from the building or improving air quality within the building. Slide 41: Building-related illnesses can be specific or nonspecific. Specific Building-Related Illnesses Specific building-related illnesses are those illnesses for which a link between building-related exposure and illness is proved. Examples include Legionnaires' disease, occupational asthma, hypersensitivity, and inhalational fever. Slide 42: Nonspecific Building-Related Illnesses Nonspecific building-related illnesses are those for which a link between building-related exposure and illness is difficult to prove. The term sick building syndrome has been used to refer to illnesses that occur in clusters within a building. The symptoms are often very general and may include the following: Itchy, irritated, dry, or watery eyes Runny nose or nasal congestion Throat soreness or tightness Dry itchy skin or unexplained rashes Headache, lethargy, or difficulty concentrating Slide 43: Air Pollution–Related Illness The major components of air pollution in developed countries are nitrogen dioxide (from combustion of fossil fuels), ozone (from the effect of sunlight on nitrogen dioxide and hydrocarbons), and suspended solid or liquid particles. High levels of air pollution can trigger exacerbations in people with asthma or chronic obstructive pulmonary disease. People living in areas with high traffic are at particular risk. Most air pollutants cause airways to narrow (airway hyper-reactivity). Long-term exposure may increase respiratory infections and symptoms in the general population, especially children. Slide 44: Ozone, which is the major component of smog, is a strong lung irritant. Levels tend to be highest in the summer compared to other seasons and relatively higher in the late morning and early afternoon compared to other times of the day. Short-term exposures can cause breathing difficulties, chest pain, and airway hyper-reactivity. sulfur oxides, can cause the airways to become inflamed and constricted and increase the risk for chronic bronchitis. Particulate air pollution derived from fossil fuel combustion (especially diesel fuel) is a complex mixture. The particles can cause inflammation of the airways or can affect other parts of their body, such as the heart. Gas and Chemical Exposure : Gas and Chemical Exposure Symptoms depend on which gas or chemical is inhaled and how deeply and for how long it was inhaled. Symptoms may include irritation of the eyes or nose, cough, blood in the sputum, and shortness of breath. Chest x-rays, computed tomography, and breathing tests are used to determine how much lung damage has occurred. Oxygen and drugs to open the airways and decrease inflammation are given. Prevention is the main issue. Slide 46: Many types of gases—such as chlorine, phosgene, sulfur dioxide, hydrogen sulfide, nitrogen dioxide, and ammonia—may suddenly be released during industrial accidents and may severely irritate the lungs. Gases such as chlorine and ammonia easily dissolve and immediately irritate the mouth, nose, and throat. The more peripheral parts of the lungs are affected only when the gas is inhaled deeply. Radioactive gases, which may be released in a nuclear reactor accident, may cause lung and other cancers many years after the exposure. Slide 47: Silo filler's disease (which mostly affects farmers) results from inhaling fumes that contain nitrogen dioxide given off by moist silage. Fluid may develop in the lungs as late as 12 hours after exposure. The condition may temporarily improve and then recur 10 to 14 days later, even without further contact with the gas. A recurrence tends to affect the small airways (bronchioles). Occupational Asthma : Occupational Asthma OA is a reversible narrowing of the airways caused by inhaling work-related particles or vapors that act as irritants or cause an allergic reaction. Many substances in the workplace can cause narrowing of the airways, which makes breathing difficult. Some people are particularly sensitive to airborne allergens, some develop disease from very high exposures to airborne irritants even if they do not have an allergy, and some develop building-related illness. Examples of workers at risk for OA from exposure to allergens include animal handlers and bakers. Slide 49: Symptoms The same as asthma. Sometimes people show signs of allergy to dust at work, with symptoms of sneezing, runny nose, and watery eyes. For some people, wheezing at night is the only symptom. Symptoms may develop during work hours but often do not start until a few hours after work,; as much as 24 hours after exposure. Also, symptoms may come and go for a week or more after exposure. Commonly, people who have daytime exposures start having symptoms at nighttime. Thus, the link between the workplace and the symptoms is often obscured. Symptoms often become milder or disappear on weekends or over holidays. They worsen with repeated exposure. Slide 50: OA is different from occupationally aggravated asthma in which people who have a history of asthma have an increase in their symptoms while they are at work because they are exposed to a substance that triggers an asthma attack. Because the airways may begin to narrow before symptoms appear, a person with delayed symptoms may use a portable peak flow meter, that measures the speed at which a person can blow air out of the lungs. When the airways narrow, the rate slows significantly, suggesting occupational asthma. Reactive Airways Dysfunction Syndrome(RADS) : Reactive Airways Dysfunction Syndrome(RADS) What is RADS? Reactive Airways Dysfunction Syndrome, involves the development of asthma-like conditions from a single exposure to a respiratory irritant, such as a chemical, vapor, smoke, gas, or fume. RADS results in the development of persistent breathing problems in a previously healthy person within 24 hours of a single exposure to a respiratory irritant. The treatment of RADS is varied but many times involves steroids. Slide 52: The criteria for a diagnosis of RADS are: A documented absence of previous respiratory complaints. The onset of symptoms occurs after a single exposure. The exposure was to a gas, smoke, fume or vapor with irritant qualities that was present in high concentrations. The onset of symptoms occurs within 24 hours of exposure and persists for a minimum of 3 months. The symptoms simulate asthma with cough, wheezing and dyspnea. Methacholine challenge should be positive. Other types of pulmonary disease should be ruled out. Slide 53: Reactive Airways Dysfunction Syndrome (RADS) and Irritant Induced Asthma (IIA) are both forms of non-immunological asthma and both exhibit similar clinical pathological features caused by exposure to an irritating airborne agent and characterized by a negative history of asthma symptoms or treatment with asthma medications prior to exposure, persistence of asthma symptoms for at least three months, objective evidence of nonspecific bronchial hyper-responsiveness, and arguably, abnormal airway histopathology. Slide 54: A major difference between the clinical definition of RADS and IIA is that in the case of RADS, symptoms of asthma appear no later than 24 hours after initial (first) exposure to the causal irritating substance. However, in the case of IIA, symptoms (similar to those of RADS) do not appear within 24 hours of the initial exposure, but do appear after repeated, more-or-less tolerable exposures have continued for several days, weeks, or even months. Once symptoms do become clinically apparent, both RADS and IIA behave clinically like non-allergic asthma, which, of course is what they are. You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.